Nerve Surgery 9781588905130, 9781604062823, 2014014249

Table of contents :
Nerve Surgery
Media Center Information
Title Page
Copyright
Dedication
Contents
Menu of Accompanying Videos on Thieme's MediaCenter
Preface
Acknowledgments
List of Contributors
Chapter 1: Anatomy and Physiology for the Peripheral Nerve Surgeon
Chapter 2: Evaluation of the Patient with Nerve Injury or Nerve Compression
Chapter 3: The Electrodiagnostic Examination with Peripheral Nerve Injuries
Chapter 4: Nerve Repair and Grafting
Chapter 5: Nerve Transfer for the Forearm and Hand
Chapter 6: Nerve Transfer Procedures for Tetraplegia
Chapter 7: Nerve Autograft Substitutes: Conduits and Processed Allografts
Chapter 8: Peripheral Nerve Allotransplantation
Chapter 9: Median Nerve Entrapment and Injury
Chapter 10:Ulnar Nerve Entrapment and Injury
Chapter 11:Radial Nerve Entrapment and Injury
Chapter 12:Thoracic Outlet Syndrome
Chapter 13:Injury and Compression Neuropathy in the Lower Extremity
Chapter 14:Brachial Plexus Injuries
Chapter 15:Obstetrical Brachial Plexus Palsy
Chapter 16:Facial Nerve Injury
Chapter 17:Tendon Transfers for Functional Reconstruction
Chapter 18:Tumors of the Peripheral Nervous System
Chapter 19:Surgical Management of Chronic Headaches, Migraines, and Neuralgias
Chapter 20:Painful Sequelae of Peripheral Nerve Injuries
Index

Citation preview

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Nerve Surgery

Susan E. Mackinnon, MD, FACS, FRCS(C) Sydney M. Shoenberg Jr. and Robert H. Shoenberg Professor of Surgery Chief, Division of Plastic and Reconstructive Surgery Washington University School of Medicine St. Louis, Missouri

Contributing Editor Andrew Yee, BSc Senior Research Assistant Division of Plastic and Reconstructive Surgery Washington University School of Medicine St. Louis, Missouri

880 illustrations

Thieme New York • Stuttgart • Delhi • Rio de Janeiro

Executive Editor: Timothy Y. Hiscock Managing Editors: J. Owen Zurhellen IV and Judith Tomat Editorial Assistant: Kate Barron Production Editor: Mason Brown International Production Director: Andreas Schabert Senior Vice President, Editorial and E-Product Development: Vera Spillner International Marketing Director: Fiona Henderson Director of Sales, North America: Mike Roseman International Sales Director: Louisa Turrell Senior Vice President and Chief Operating Officer: Sarah Vanderbilt President: Brian D. Scanlan Printer: Replika Press Cover Illustration: Artist Terry Watkinson has illustrated the sensory/motor topography of the median nerve in the mid-arm. The understanding of fascicular specificity has propelled the success of modern nerve transfer surgery and a paradigm shift in the management of the nerve-injured patient. From 12 o'clock, clockwise the four groups are, pronator group, larger sensory, anterior interosseous, and flexor carpi radialis/flexor sublimis. Library of Congress Cataloging-in-Publication Data Nerve surgery / [edited by] Susan E. Mackinnon. p. ; cm. Includes bibliographical references. ISBN 978-1-58890-513-0 (hardback) – ISBN 978-1-60406-282-3 (ebook) I. Mackinnon, Susan E., 1950- editor. [DNLM: 1. Peripheral Nervous System Diseases–surgery. 2. Decompression, Surgical. 3. Nerve Transfer. 4. Peripheral Nerves–anatomy & histology. 5. Peripheral Nervous System–injuries. WL 520] RD595 617.4'83–dc23 2014014249

Important note: Medicine is an ever-changing science undergoing continual development. Research and clinical experience are continually expanding our knowledge, in particular our knowledge of proper treatment and drug therapy. Insofar as this book mentions any dosage or application, readers may rest assured that the authors, editors, and publishers have made every effort to ensure that such references are in accordance with the state of knowledge at the time of production of the book. Nevertheless, this does not involve, imply, or express any guarantee or responsibility on the part of the publishers in respect to any dosage instructions and forms of applications stated in the book. Every user is requested to examine carefully the manufacturers’ leaflets accompanying each drug and to check, if necessary in consultation with a physician or specialist, whether the dosage schedules mentioned therein or the contraindications stated by the manufacturers differ from the statements made in the present book. Such examination is particularly important with drugs that are either rarely used or have been newly released on the market. Every dosage schedule or every form of application used is entirely at the user’s own risk and responsibility. The authors and publishers request every user to report to the publishers any discrepancies or inaccuracies noticed. If errors in this work are found after publication, errata will be posted at www.thieme.com on the product description page. Some of the product names, patents, and registered designs referred to in this book are in fact registered trademarks or proprietary names even though specific reference to this fact is not always made in the text. Therefore, the appearance of a name without designation as proprietary is not to be construed as a representation by the publisher that it is in the public domain.

© 2015 Thieme Medical Publishers, Inc. Thieme Publishers New York 333 Seventh Avenue, New York, NY 10001 USA +1 800 782 3488, [email protected] Thieme Publishers Stuttgart Rüdigerstrasse 14, 70469 Stuttgart, Germany +49 [0]711 8931 421, [email protected] Thieme Publishers Delhi A-12, Second Floor, Sector-2, Noida-201301 Uttar Pradesh, India +91 120 45 566 00, [email protected] Thieme Publishers Rio, Thieme Publicações Ltda. Argentina Building 16th floor, Ala A, 228 Praia do Botafogo Rio de Janeiro 22250-040 Brazil +55 21 3736-3631 Printed in India ISBN 978-1-58890-513-0 Also available as an e-book: eISBN 978-1-60406-282-3

This book, including all parts thereof, is legally protected by copyright. Any use, exploitation, or commercialization outside the narrow limits set by copyright legislation without the publisher’s consent is illegal and liable to prosecution. This applies in particular to photostat reproduction, copying, mimeographing or duplication of any kind, translating, preparation of microfilms, and electronic data processing and storage.

My husband, Dr. Alec Patterson, Chief of Cardiothoracic Surgery at Washington University School of Medicine, has been my strongest advocate, mentor, and supporter and has allowed me to live nerve surgery 24/7 for over forty years. This book is dedicated to Alec, with love and gratitude.

Contents Menu of Accompanying Videos . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

ix

Preface . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

xi

Acknowledgments. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

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List of Contributors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

xiv

Chapter 1: Anatomy and Physiology for the Peripheral Nerve Surgeon . . . . . . . . . . . . . . . . . . .

1

Matthew D. Wood, Philip J. Johnson, and Terence M. Myckatyn

Chapter 2: Evaluation of the Patient with Nerve Injury or Nerve Compression . . . . . . . . . . . . .

41

Christine B. Novak

Chapter 3: The Electrodiagnostic Examination with Peripheral Nerve Injuries . . . . . . . . . . . . . .

59

Mark A. Ferrante and Asa J. Wilbourn

Chapter 4: Nerve Repair and Grafting . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

75

Kirsty U. Boyd and Ida K. Fox

Chapter 5: Nerve Transfer for the Forearm and Hand . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

101

Renata V. Weber and Kristen M. Davidge

Chapter 6: Nerve Transfer Procedures for Tetraplegia. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

157

Kristen M. Davidge and Ida K. Fox

Chapter 7: Nerve Autograft Substitutes: Conduits and Processed Allografts . . . . . . . . . . . . . .

169

Amy M. Moore, Wilson Z. Ray, Matthew D. Wood, and Philip J. Johnson

Chapter 8: Peripheral Nerve Allotransplantation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

193

Amy M. Moore, Wilson Z. Ray, and Philip J. Johnson

Chapter 9: Median Nerve Entrapment and Injury . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

207

Kristen M. Davidge and Douglas M. Sammer

Chapter 10: Ulnar Nerve Entrapment and Injury . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

251

Kristen M. Davidge and Kirsty U. Boyd

Chapter 11: Radial Nerve Entrapment and Injury . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

289

Kirsty U. Boyd, Linda T. Dvali, J. Megan Patterson, Brendan M. Patterson, and Kristen M. Davidge

Chapter 12: Thoracic Outlet Syndrome . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

311

Stephen H. Colbert

Chapter 13: Injury and Compression Neuropathy in the Lower Extremity . . . . . . . . . . . . . . . . .

338

Kirsty U. Boyd and Justin M. Brown

Chapter 14: Brachial Plexus Injuries. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Thomas H.H. Tung and Amy M. Moore

391

Contents

Chapter 15: Obstetrical Brachial Plexus Palsy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

468

Alison K. Snyder-Warwick and Gregory H. Borschel

Chapter 16: Facial Nerve Injury . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

481

Gregory H. Borschel, Tessa A. Hadlock, Christine B. Novak, and Alison K. Snyder-Warwick

Chapter 17: Tendon Transfers for Functional Reconstruction . . . . . . . . . . . . . . . . . . . . . . . . . . .

504

J. Megan Patterson, Martin I. Boyer, Charles A. Goldfarb, and Douglas M. Sammer

Chapter 18: Tumors of the Peripheral Nervous System . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

530

John R. Barbour and Kirsty U. Boyd

Chapter 19: Surgical Management of Chronic Headaches, Migraines, and Neuralgias . . . . . . . .

572

Ivica Ducic

Chapter 20: Painful Sequelae of Peripheral Nerve Injuries . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

591

Stephen H. Colbert

Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

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Menu of Accompanying Videos on Thieme’s MediaCenter The videos are organized by category and then by date created (most recent first). Note that most surgical tutorials include both a standard and an extended version.

Nerve Decompressions 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16.

Radial Nerve Release at the Spiral Groove Revision Carpal Tunnel Release in a Case of Persistent Symptoms and Incomplete Release Posterior Interosseous Nerve Release Carpal Tunnel Release Median Nerve Release in the Forearm Transmuscular Ulnar Nerve Transposition in a Case of Traumatic Medial Cord Injury Revision Carpal Tunnel Release in a Case of Proximal Median Nerve Hematoma Injury and Mild Compression Tarsal Tunnel Release Superficial Peroneal Nerve Release in the Lower Leg Common Peroneal Nerve Release at the Fibular Head Thoracic Outlet Decompression Tibial Nerve Decompression at the Soleus Median Nerve Forearm Decompression Carpal Tunnel Release Guyon’s Canal Release and Carpal Tunnel Release Submuscular Ulnar Nerve Transposition

[8:39] [16:11] [8:49] [16:31] [6:45] [15:56] [5:54] [9:17] [7:25] [17:07] [10:07] [24:17] [5:31] [12:58] [8:13] [17:32] [4:53] [10:17] [5:36] [11:09] [9:41] [23:34] [5:01] [8:29] [5:14] [9:37] [7:04] [5:20] [7:56] [5:50] [19:22]

Nerve Transfers 17. 18. 19. 20. 21. 22. 23. 24. 25. 26. 27. 28. 29.

Brachialis to Anterior Interosseous Nerve Transfer with Extended Forearm Incision Median {FCS/FDS) to Radial (PIN/ECRB) Nerve Transfers Posterior Approach – Spinal Accessory to Suprascapular Nerve Transfer Anterior Interosseous to Ulnar Motor Nerve Transfer Third Webspace to Sensory Component of Ulnar Nerve Transfer and PCM to DCU Nerve Transfer Anterior Interosseous to Ulnar Motor Supercharge Nerve Transfer Pectoral Fascicle of the Middle Trunk to Spinal Accessory Nerve Transfer Median (FCR/FDS) to Radial (PIN/ECRB) Nerve Transfer with Pronator Teres to ECRB Tendon Transfer Medial Triceps Branch to Axillary Nerve Transfer Flexor Digitorum Superficialis to Anterior Interosseous Nerve Transfer RETS AIN to Ulnar Motor Nerve Transfer Thoracodorsal to Long Thoracic Nerve Transfer Double Fascicular Nerve Transfer

[20:15] [47:35] [18:12] [39:34] [13:27] [27:00] [11:55] [29:28] [12:38] [36:51] [9:12] [22:29] [7:47] [16:16] [9:00] [10:21] [7:14] [17:03] [5:45] [14:18] [5:32] [18:49] [5:04] [10:16] [7:02] [21:29]

Tendon Transfers 30. 31.

Median to Radial Nerve Tendon Transfers: PT to ECRB, FCR to EDC, PL to EPL Flexor Digitorum Profundus Tenodesis (Median FDP to Ulnar FDP)

[12:37] [29:08] [4:05] [6:04]

Pain Management 32. 33.

Superficial Peroneal and Sural Neuroma Transposition Ulnar Index of Median to Medial Ring of Ulnar Sensory Nerve Transfer and Prevention of Proximal Neuroma

[18:26] [33:06] [10:22] [23:57]

ix

Menu of Accompanying Videos

Facial Reconstruction 34. 35.

Stage 1: Cross-Facial Nerve Grafting for Smile Segmental Gracilis Muscle Transfer for Smile in a Case of Mobius Syndrome

[10:07] [29:10] [26:31] [53:47]

Nerve Harvests 36.

Medial Antebrachial Cutaneous Nerve Graft Harvest

[5:27] [10:07]

Nerve Tumors 37.

Ganglion Cyst Removal in the Common Peroneal Nerve at the Fibular Head

[7:05] [16:43]

Microsurgical Techniques 38.

End-to-End Epineurial Nerve Repair in a Rat Model

[8:51]

Postoperative Management 39.

Robert Jones Dressing for the Lower Leg

[11:56]

Presentations 40. 41. 42. 43. 44. 45. 46. 47. 48. 49. 50. 51. 52.

2014 PRS: Supercharge Nerve Transfers 2014 ASSH: Median to Radial Nerve Transfers 2014 FRS: Jumping the Nerve Gap 2014 CRN: Nerve Transfers for the Hand 2014 CRN: Brachial Plexus Lesions 2014 CRN: Peripheral Nerve Surgery 2014 CRN: Nerve Transfers for the Shoulder and Elbow 2014 CRN: Compression Neuropathies 2013 PRS: Nerve Entrapment – CME Update 2012 CRN: Brachial Plexus Lesions – Presentation 2012 CRN: Supercharge Nerve Transfers and Nerve Transfers in the Hand 2012 CRN: Peripheral Nerve Surgery 2012 VuMedi: Transmuscular Ulnar Nerve Transposition

[26:31] [16:23] [19:44] [1:12:54] [41:38] [1:13:47] [52:04] [1:24:16] [22:11] [85:02] [56:30] [38:35] [10:11]

Clinical Examinations 53. 54. 55. 56.

Utility of Scratch Collapse Test in a Case of Failed Carpal Tunnel Release Hierarchical Scratch Collapse Test Localizing a Secondary Compression Point with the Hierarchical Scratch Collapse Test Examination Example of Non-Nerve Related Pain

[5:14] [5:15] [4:15] [4:56]

Physical Therapy 57. 58.

Motor Re-Education following Median to Radial Nerve Transfer Motor Re-Education following Reverse End-to-Side Anterior Interosseous Nerve Transfer

[17:57] [9:02]

Case Studies 59.

x

Long-Term (4 Years) Postoperative Outcome following Median to Radial Nerve Transfers

[3:21]

Preface In 1970, at Queens University in Kingston, Ontario, Canada, I fell in love with Alec Patterson and the peripheral nervous system. Four decades later, I am still passionately in love with both of them. In my surgical career, I have been fortunate to have seen two major paradigm shifts in nerve surgery: nerve repair to nerve graft and nerve graft to nerve transfer. These radical shifts in the management of nerve injuries illustrate Thomas Kuhn’s concept of scientific development as a succession of tradition bound periods that are punctuated by sudden breaks or paradigm shifts. He emphasized that for these shifts to occur, problems, cracks, and failures had to be identified in existing beliefs or procedures. Tracing these scientific paradigm shifts over time, he emphasizes that when they occur there is always controversy, debate, and heated discussion. I know that our first courses on nerve transfers were met with some degree of scepticism and Hanno Millesi, one of the earliest proponents of nerve grafting, recently shared his recollections of similar dissent with the shift from repair to grafting in the 1960s and 1970s. Sir Sydney Sunderland and Leonard Goldner were strong advocates for direct nerve repair, even with gaps up to 13 cm. Hanno Millesi and Algis Narakas popularized nerve grafting and the shift from nerve repair to nerve graft technique was met with serious debate. Hanno Millesi recalls: “In 1963, I was in the USA and met James Smith who had also started to perform nerve suture using a microscope. I returned to Vienna and started to do experiments with sutures using the microscope and it turned out that a good recovery occurred only if tension at the repair site was absolutely avoided. Only then the advantages of the optical magnification could be exploited. The only way to achieve this in a case of defect was to use a graft. I started to do clinical cases after having changed the technique and had surprisingly good results. The first presentations were received with hesitation and criticism. I had a discussion with Dr. Eric Moberg and after that he asked for a demonstration of the technique. He and Sir Donald Brooks came for a visit to Vienna. Sir Donald Brooks was a well known British surgeon who worked with Sir Herbert Seddon with cable grafts and knew about the poor results. Consequently he was especially critical. After that visit, Moberg and Brooks were convinced of the advantages of nerve grafts and started to support my work. In the US there was something like a bias against nerve grafting. Dr. Sterling Bunnell and Dr. Joseph Boyes had done some cases using cable grafts, apparently like Sir Seddon with poor results. Dr. Leonard Marmor, a surgeon from Los Angeles, was using irradiated nerve allografts. As far as I know, many of them had to be

excised and consequently the general reputation of nerve grafting was poor. A breakthrough was the 1978 symposium in Durham, North Carolina at a symposium organized by Dr. Leonard Goldner still emphasized a nerve repair even in cases of long defects. He presented a case of a boy having suffered a radial nerve defect of 10cm. He resected 10cm of the humeral shaft to be able to achieve a repair. At the same session, Dr. Raymond Curtis reported 25 cases of long defects of the radial nerve managed by grafts according to my technique with superior results.” The introduction of microsurgery and the popularization of nerve grafting techniques by the late 1970s and 1980s improved surgical results in patient outcome when a tension free direct repair was not possible. By the 1990s, synthetic conduits found a role in the management of short nerve gaps in small diameter sensory nerves and nerve allotransplantation had found a limited role for devastating, otherwise irreparable nerve injuries. However, for more than a decade innovation in peripheral nerve surgery was somewhat “stalled.” The next big shift to nerve transfer awaited a decade of basic research with incremental increase in our understanding of neuroregeneration and muscle reanimation. During April 1991, in my own surgical practice I expanded the use of nerve transfer for high ulnar nerve injuries and upper brachial plexus injuries with the anterior interosseous to deep ulnar and medial pectoral to musculocutaneous nerve transfers. Twenty years later, nerve transfers have become more sophisticated and elevated our expectations for functional recovery following major nerve injury. While new nerve transfers are described almost on a monthly basis, the concept of nerve transfer is now mainstream and considered a key component of modern nerve surgery. These procedures have changed the management of nerve injuries and the results can be truly spectacular. The impetus for Nerve Surgery is to prepare for a new era in the surgical management of nerve injuries. The University of Toronto and Washington University School of Medicine in St. Louis afforded me brilliant and talented colleagues to work with and a strong basic neuroscience research environment. Our research laboratory, funded initially by the Medical Research Council of Canada and now by the National Institutes of Health, allows us to ask and answer clinical questions and translate the results from the laboratory directly to clinical practice. Nerve transfers per say are not a new idea, but early nerve transfers did not successfully translate clinically because they were done without the “adjacent possibility” of microsurgery, internal neurolysis, and an understanding of the micro topography and internal anatomy of the peripheral nerve. For a decade

xi

Preface

and a half, my research focused on nerve allotransplantation and while it did not provide a “cure” for clinical nerve injury, it did provide the neurological platform for composite functional tissue transplantation and importantly, the laboratory techniques to investigate the types of nerve injury and reconstruction that essentially provided that “adjacent possibility” to investigate the nuances of nerve transfers. Importantly, the development of specific transgenic rats in our laboratory has allowed us to accurately visualize nerve transfer models in “real time.” This book has been written for all surgeons managing patients with nerve injury. Peripheral nerve surgery is somewhat of an “orphan” speciality being managed by plastic surgeons, orthopedic surgeons, hand surgeons, neuro surgeons, otolaryngologists, and general surgeons. Even the simple digital nerve injury repaired with tension can irreparably alter the patient’s life with painful sequelae. At the other extreme, the last decade of wars against terrorism have resulted in horrific extremity nerve injuries not previously seen. Yearly, over 360,000 nerve repairs are performed in the United States. It is estimated that 54% of all combat wounds are extremity wounds, with to date more than 52,000 direct combat wounds being reported due to ongoing American military operations. This text begins with a chapter on anatomy and physiology to emphasize the importance of laboratory work on advancing the clinical management of nerve injured patients. It then offers my “take” on the traditional concepts of evaluation of the nerve injured patient, nerve repairs, and issues specific to

xii

each major nerve. Most of our nerve transfers are detailed in this text. In May of 2010, we did the first nerve transfer for a C7 quadriplegic patient to restore some important hand function. Dr. Martin Robson brought his paralyzed lifelong friend since surgical internship to our clinic “for a nerve transfer procedure to give him some hand function.” A chapter on nerve transfers for patients with tetraplegia introduces an exciting new area for investigation and study. I have had a long-standing respect for painful sequelae associated with nerve injury and continue to be humbled by this life-altering problem; thus, a chapter is dedicated to this topic. In my bookcase is a copy of Hand Clinics on tendon transfers published in 1974 and I still refer to this frequently. Thus I have included a chapter on tendon transfers, which should always be considered, especially in late cases of nerve injury and are frequently useful as an adjunct to nerve reconstruction. There are specific chapters on facial reanimation, surgical management of headaches, peripheral nerve tumors, and of course our passion toward managing patients with brachial plexus injuries. Finally, my colleagues at Washington University School of Medicine in the Division of Plastic and Reconstruction Surgery, Dr. Ida Fox and Mr. Andrew Yee, have for many years worked to develop a website (nervesurgery.wustl.edu). On this website we continue to update surgical procedures and use this website as a forum for problematic clinical case presentations and the ongoing problems relating to this challenging clinical problem.

Acknowledgments The editorial team at Thieme Publishers has been the model of professionalism as they have waited with patience over the ten years it has taken to put the book manuscript together. J. Owen Zurhellen has brought precision and organization to shifting authors and chapters as the scope and the breadth of the text has matured over the years, and Executive Editor Kay Conerly and Managing Editor Judith Tomat were been essential and lenient as every chapter was updated in the last months before production. I am grateful to artist Terry Watkinson for his renderings in the initial stages of this text, especially the cover image of the intraneural topography of the median nerve. Thank you as well to Alexandra and David Baker, such talented medical artists, for the clarity and accuracy of their drawings, and especially to my Coeditor, Andrew Yee, for his talents with intraoperative illustrations, videos, figure layout and his deep passion for nerve surgery and surgical education. In the Peripheral Nerve Surgery laboratory, Senior Scientist, Dan Hunter, and all of the many researchers over three decades have asked and answered the important questions that have led to the many changes in the management of complex nerve injuries that are discussed in Nerve Surgery. James F. Murray and Alan R. Hudson trained me in hand surgery and nerve surgery so many years ago, their expertise in tendon transfers and brachial plexus nerve

grafting specifically sowed the seeds for the field of nerve transfers. My dear friend and colleague in physical therapy, Christine Novak, PT, PhD, has shared my passion for the nerve injured patient for three decades. I am grateful to my department Chairman, Timothy Eberlein, for his constant support of such an orphan area of surgery—nerve surgery— and to my colleagues, associates, and friends, in the Division of Plastic Surgery at Washington University School of Medicine, many of whom are authors in this textbook and share a passion toward the care of nerve injured patients. This text, for the most part, is authored by the talented surgeons, clinicians, and scientists who have initially trained with me and are now my peers with whom I still work very closely. I am so proud of their accomplishments and so appreciate their tolerance as this book was written, rewritten, edited, reedited, and rewritten again, to make it as good and as up to date as we possibly could. Finally, without the love, support, and happiness of my husband Alec and our children, Lachlan, Megan, Brendan, and Caitlan, and now their families, Cristin, Ganesh, Jenny, and Thomas, and their children, Lydia, Kiran, Noah, Emilia, Liliana, Rowan and Julian, it would have been impossible to complete Nerve Surgery with such great joy.

xiii

Contributors John R. Barbour, MD Assistant Professor of Plastic Surgery Department of Plastic Surgery Georgetown University School of Medicine Washington, DC Gregory H. Borschel, MD, FACS, FAAP Associate Professor Division of Plastic and Reconstructive Surgery University of Toronto and the Hospital for Sick Children Toronto, Ontario, Canada

Mark A. Ferrante, MD Professor of Neurology University of Tennessee Health Science Center Director, EMG Laboratory, VAMC Memphis, Tennessee

Kirsty U. Boyd, MD, FRCS(C) Assistant Professor, Division of Plastic Surgery Department of Surgery University of Ottawa The Ottawa Hospital - Civic Campus Ottawa, Ontario, Canada

Ida K. Fox, MD Assistant Professor of Plastic and Reconstructive Surgery Division of Plastic and Reconstructive Surgery Washington University School of Medicine St. Louis, Missouri

Martin I. Boyer, MD, MSc, FRCS(C) Carol B. and Jerome T. Loeb Professor of Orthopedic Surgery Department of Orthopedic Surgery Washington University School of Medicine Saint Louis, Missouri

Charles A. Goldfarb, MD Associate Professor of Orthopaedic Surgery Co-Chief, Hand Surgery Service Washington University School of Medicine St. Louis, MO

Justin M. Brown, MD Director, Neurosurgery Peripheral Nerve Program Associate Professor of Neurosurgery University of California, San Diego La Jolla, California

Tessa A. Hadlock, MD Associate Professor of Otology and Laryngology Harvard Medical School Director, Division of Facial Plastic and Reconstructive Surgery Massachusetts Eye and Ear Infirmary Boston, MA

Steven H. Colbert, MD Assistant Professor of Plastic Surgery Head, Hand and Microsurgery University of Missouri Columbia, Missouri Kristen M. Davidge, MD, FRCS(C) Fellow Division of Plastic and Reconstructive Surgery University of Toronto and the Hospital for Sick Children Toronto, Ontario, Canada Ivica Ducic, MD, PhD Professor of Plastic Surgery & Neurosurgery Director, Peripheral Nerve Surgery Institute Georgetown University Hospital Washington, DC

xiv

Linda Dvali, MD Assistant Professor Division of Plastic and Reconstructive Surgery Toronto Western Hospital University of Toronto Toronto, Ontario, Canada

Philip J. Johnson, PhD Division of Plastic and Reconstructive Surgery Washington University School of Medicine St. Louis, Missouri Susan E. Mackinnon, MD, FACS, FRCS(C) Sydney M. Shoenberg Jr. and Robert H. Shoenberg Professor of Surgery Chief, Division of Plastic and Reconstructive Surgery Washington University School of Medicine St. Louis, Missouri Amy M. Moore Assistant Professor of Plastic and Reconstructive Surgery Division of Plastic and Reconstructive Surgery Washington University School of Medicine St. Louis, Missouri

Contributors

Terence M. Myckatyn, MD Associate Professor of Plastic and Reconstructive Surgery Division of Plastic and Reconstructive Surgery Director, Cosmetic and Breast Plastic Surgery Washington University School of Medicine St. Louis, Missouri

Alison Snyder-Warwick, MD Assistant Professor of Plastic and Reconstructive Surgery Division of Plastic and Reconstructive Surgery Director, Facial Nerve Institute Washington University School of Medicine St. Louis, Missouri

Christine B. Novak, PT, PhD Associate Professor Division of Plastic and Reconstructive Surgery University of Toronto Toronto, Ontario, Canada

Thomas H.H. Tung, MD Associate Professor of Plastic and Reconstructive Surgery Division of Plastic and Reconstructive Surgery Washington University School of Medicine St. Louis, Missouri

J. Megan Patterson, MD Assistant Professor Department of Orthopaedics University of North Carolina Chapel Hill, North Carolina

Renata V. Weber, MD Department of Plastic Surgery Montefiore Medical Center Bronx, New York Asa J. Wilbourn, MD†

Brendan M. Patterson Resident, Department of Orthopaedics University of North Carolina Chapel Hill, North Carolina Wilson Z. Ray Assistant Professor Department of Neurological Surgery Washington University School of Medicine St. Louis, Missouri Douglas M. Sammer, MD Assistant Professor of Plastic Surgery University of Texas Southwestern Medical Center at Dallas Program Director Hand Surgery Fellowship Chief of Plastic Surgery, Parkland Hospital Dallas, Texas

Matthew D. Wood, PhD Assistant Professor Division of Plastic and Reconstructive Surgery Washington University School of Medicine St. Louis, Missouri Andrew Yee, BSc Senior Research Assistant Division of Plastic and Reconstructive Surgery Washington University School of Medicine St. Louis, Missouri

†

Deceased.

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Anatomy and Physiology for the Peripheral Nerve Surgeon

1 Anatomy and Physiology for the Peripheral Nerve Surgeon

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Matthew D. Wood, Philip J. Johnson, and Terence M. Myckatyn

1.1 Introduction At a macroscopic level, peripheral nerve anatomy has been extensively studied and documented, and our understanding of the fascicular arrangements of specific nerves has evolved with the development of nerve transfers. Our understanding of nerve anatomy and physiology at the subcellular level has grown at a remarkable rate and offers new insights into the mechanisms of neurodegeneration, regeneration, and novel therapeutic targets to manipulate.

1.2 Nerve Fiber Anatomy Uninjured peripheral nerves are composed of unmyelinated or myelinated mature axons (▶ Fig. 1.1) that are opposed by Schwann cells. Several unmyelinated axons are surrounded by one Schwann cell–derived double basement membrane, whereas myelinated axons are ensheathed by laminin-rich, multilaminated sheets of myelin (provided by a single Schwann cell). Individual axons

are immediately surrounded by thin collagen fibers forming an endoneurium and are further sorted into fascicles defined by a discrete connective tissue sheath known as the perineurium. Between these fascicles is the internal epineurium. A thicker, connective tissue sheath termed the external epineurium encompasses all the fascicles that group together to form a single nerve. Nerves accommodate shortening and lengthening during flexion and extension of an extremity by being bounded by the epineurium and delimited by areolar connective tissue, the mesoneurium, interspersed with a protective fatty tissue cocoon. When the full range of motion of an extremity is compromised, patients are more at risk for traction and compression neuropathies (▶ Fig. 1.2). This is becoming more common as our population becomes on average more obese, more deconditioned, and older.

1.2.1 Fascicular Anatomy Nerves in the proximal extremity are monofascicular, but even at this level, motor and sensory fibers are grouped together

Fig. 1.1 Peripheral nerve: morphology. (a) The normal peripheral nerve is composed of neural tissue and connective tissue components. The nerve fibers may be myelinated or unmyelinated. (b) A population of myelinated and unmyelinated nerve fibers are seen. The basement membrane of the Schwann cell is a double basement membrane (arrow) that can only be identified by electron microscopy. A, axon; C, endoneurial collagen; M, myelin; NR, node of Ranvier; SCN, Schwann cell nucleus; ua, unmyelinated axon (uranyl acetate, 4750x).

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Anatomy and Physiology for the Peripheral Nerve Surgeon

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Fig. 1.2 Peripheral nerve axon: anatomical organization. Axons are either myelinated or unmyelinated and are shown here as the small (yellow) fibers to the right. Myelinated axons are associated with a single Schwann cell, whereas unmyelinated axons are small, and multiple axons can be associated with one Schwann cell. Individual axons are immediately surrounded by thin collagen fibers forming an endoneurium and are further sorted into fascicles defined by a discrete connective tissue sheath known as the perineurium (green). Between these fascicles is the internal epineurium (dark yellow). A thicker connective tissue sheath, the external epineurium, encompasses all the fascicles that group together to form a single nerve. Nerves accommodate shortening and lengthening during flexion and extension of an extremity by being bounded by the epineurium and delimited by areolar connective tissue, the mesoneurium, interspersed with a protective fatty tissue cocoon. (Used with permission from Mackinnon SE, Dellon AL, eds. Surgery of the Peripheral Nerve. New York, NY: Thieme; 1988:21.)

topographically. There is considerable plexus formation between the fascicles in the proximal portion of the extremity that decreases in the distal extremity. As nerves progress distally, they become polyfascicular, but fascicles are differentiated into specific motor and sensory components even in proximal locations.1,2,3 In the proximal segment of the nerve, motor versus sensory fibers are distinguished by knowledge of the internal topography, which has come predominantly from intraoperative stimulation of normal nerves to identify motor and sensory topography.3,6 Using intraoperative stimulation techniques, we have seen a very specific motor response to stimulation of a single teased fasicle. Knowledge of the usual internal topography of the peripheral nerves can direct proper alignment of fascicles at the time of nerve repair to optimize the specificity of modality- and

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function-matched reinnervation. For example, the fascicles of the ulnar nerve in the mid- and distal forearm are divided into a dorsal sensory group, a volar sensory group, and a motor group (▶ Fig. 1.3). In the mid-forearm, the motor group is positioned between the ulnar dorsal sensory group and the radial volar sensory group. The dorsal sensory group separates from the main ulnar nerve ~ 8 cm proximal to the wrist. The motor group remains ulnar to the volar sensory group until reaching the Guyon canal, at which time it passes dorsal and radial to become the deep motor branch to the intrinsic muscles. The size match between the motor and sensory groups of the main ulnar nerve at this level is ~ 2:3. The median nerve topography is more complex because it contains more fascicles (▶ Fig. 1.4). In the forearm, the anterior interosseous nerve is situated in the radial or posterior aspect

Anatomy and Physiology for the Peripheral Nerve Surgeon

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Fig. 1.3 Internal topographical anatomy of the ulnar nerve. The ulnar nerve has a distinct fascicular pattern as it courses distally from the forearm into the hand. The motor component of the ulnar nerve is found between the sensory component and the dorsal cutaneous fascicles. Distal to the dorsal cutaneous nerve branch point, the motor component is identified on the medial aspect of the ulnar nerve. This motor component branches from the ulnar nerve on its medial/ulnar aspect to become the deep motor branch, then dives deep to the leading edge of the hypothenar muscles to course around the hook of the hamate and innervate the intrinsic muscles. The sensory component of the ulnar nerve is a larger fascicular group than the motor component and innervates the ulnar aspect of the ring finger, the small finger, and the fourth web space.

of the median nerve as a distinct group. The distal internal topography of the median nerve approximates the distal anatomy; the motor fascicles to the thenar muscles are on the radial side, and the sensory fibers to the third web space are on the ulnar side. In the leg, the motor fibers to the anterior tibialis are located medially within the peroneal nerve as it crosses the knee and turns abruptly around the head of the fibula. The motor component of the axillary nerve is located superiorly and the smaller sensory component inferiorly. Over the past 20 years, intraoperative direct stimulation of normal or recovering nerves has allowed us to define the discrete and consistent motor/sensory internal topography of the various nerves and is described in more detail throughout this text and in the accompanying videos. After the work of Sunderland,3,4,5 it was assumed that the motor and sensory fibers were diffusely scattered across the different fascicles and followed a tortuous course of plexus formation until they finally organized themselves into specific motor and sensory groups distally in the extremity. Recent work has contradicted this theory to show that fibers destined for a specific territory organize themselves into distinct groups even proximally within the nerve.1,7 Using retrograde labeling

techniques in a nonhuman primate model, Brushart studied median nerve topography at 1-cm cross sections from the radial digital nerves of the thumb, index, and long fingers all the way to the distal brachial plexus.8 Brushart found that digital nerve axons maintained discrete territories even in the upper arm, occupying one-third to one-sixth of the median nerve’s total diameter. Moreover, these territories were consistently maintained between left and right extremities, as well as between different animals. We have seen that a single fascicle in the axilla can be neurolysed to give a single specific movement in the hand. Although there is some territory separation at the proximal level, the internal topography is much more specific and constant than previously thought. This challenges the peripheral nerve surgeon to strive for an understanding of this anatomy for better functional recovery after neural repair.

1.3 The Basics of Nerve Injury Recovery following peripheral nerve trauma is influenced by the relative distance of the injury to the cell body, or soma, and characterized by specific changes both proximal and distal to the site of injury (▶ Fig. 1.5a).9 Proximally, axons retract a

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Anatomy and Physiology for the Peripheral Nerve Surgeon

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Fig. 1.4 Internal topographical anatomy of the median nerve. Proximal forearm: The median nerve is composed of several motor and sensory fascicles. In the proximal forearm, the pronator teres fascicle is on the most anterior aspect, followed medially by the flexor carpi radialis (FCR) and palmaris longus (PL) fascicles. Further medially, the flexor digitorum superficialis (FDS) fascicular group is identified. This fascicular group usually includes two fascicles that correspond to two branch points to the FDS. The anterior interosseous fascicle is on the posterior aspect of the ulnar nerve and continues distally to become lateral/radial before its branch point. This fascicle includes a small sensory articular component to the wrist joint. It is important to acknowledge a thenar motor component within the sensory component. Distal forearm: The anterior interosseous nerve includes three fascicles: flexor pollicis longus (FPL), flexor digitorum profundus (FDP), and pronator quadratus (PQ)/articular. The FPL and FDP fascicles are large compared to the PQ fascicle and have an anterior orientation. The median nerve includes a recurrent thenar fascicle that is found posterior and lateral. As the median nerve courses distally, the sensory fascicles are revealed to have three major groups: first web space and radial aspect of thumb, second web space, and third web space. These groups have a lateral, middle, and medial orientation, respectively. The palmar cutaneous nerve branches from the anterior and lateral aspect of the median nerve. Hand: The recurrent thenar nerve branches from the posterior and lateral aspect of the median nerve to innervate the thenar musculature. The three sensory fascicular groups branch from the median nerve to innervate their appropriate sensory territories. The lateral branch includes the first web space and radial aspect of the thumb fascicles before its respective branch point.

variable distance and undergo a brief dormant phase during which injury-induced molecular signaling cascades are initiated, and neurotrophic factors (NFs) are shuttled before formation of a regenerating unit (▶ Fig. 1.5b).10 The elongating regenerating unit has the appearance of a hydra, with an elongating single parent axon giving rise to multiple daughter axons (▶ Fig. 1.5c).11 In myelinated nerves, axons sprout through anatomical gaps in the myelin known as the nodes of Ranvier and progress to their sensory or motor targets (▶ Fig. 1.5d). Once a projection from a regenerating unit forms a functional synapse, the remaining daughter axons are “pruned back,” thus resulting in a one-to-one relationship between neuron and target end-organ. In the distal nerve segment, Schwann cells, fibroblasts, myocytes, and injured axons express a host of neurotrophic factors at discrete concentrations and time points as the degrading neural elements are phagocytosed in a process termed wallerian degeneration.12–18 Schwann cells assume a

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pro-regenerative phenotype instrumental in remyelinating and guiding regenerating axons to their appropriate targets along residual endoneurial tubes known as the band of Bungner.19–25 Neurotrophism, or nerve nourishment, refers to the ability of neurotrophins secreted in an autocrine or paracrine fashion to enhance the elongation and maturation of nerve fibers. Recovery, then, is dependent upon the number of motor fibers and sensory fibers that are properly matched with their respective motor end plates and sensory receptors. Regenerating nerve fibers also demonstrate neurotropism, or end-organ specificity, whereby nerve fibers grow toward an end-organ target and receive factors that prevent neuronal death.26,27 The importance of neurotropism in nerve regeneration has been demonstrated by the removal of end-organ contact following nerve injury and repair, resulting in significantly decreased axonal regeneration.28,29 The difference between neurotrophism and neurotropism is effectively demonstrated when cellular components

Anatomy and Physiology for the Peripheral Nerve Surgeon

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Fig. 1.5 Peripheral nerve regeneration. Unlike the central nervous system, peripheral nerves have the intrinsic ability to regenerate damaged axons. (a) Animation of an uninjured myelinated axon. (b) Following injury, axons retract to a node of Ranvier, and the neurons undergo a conformational change into a regenerative phenotype. Schwann cells in the distal stump dedifferentiate into a phagocytic pro-regenerative phenotype. These activated Schwann cells along with macrophages prepare the distal stump for regenerating axons from the proximal stump in a process called wallerian degeneration. (c) Regenerating axons then sprout from the node of Ranvier and resemble a hydra as they regenerate toward their end-organ target. (d) As axons regenerate further distally, Schwann cells began to myelinate the portions of the axons closer to the site of injury. (Used with permission from Mackinnon SE, Dellon AL, eds. Surgery of the Peripheral Nerve. New York, NY: Thieme; 1988:21-23.)

of the nerve are genetically modified to constitutively overexpress glial cell line–derived neurotrophic factor (GDNF), a factor normally expressed transiently in the injured distal stump and denervated muscle. The consistent overexpression of this growth factor in the nerve results in a strong neurotropic effect that traps axons and prevents end-organ reinnervation.30 When combined with an accurate history of the mechanism, location, and timing of peripheral nerve injury, a proper physical examination may determine the level and extent of peripheral nerve injury and susbsequent expectations for recovery and potential reconstruction. Evaluation for weakness, loss of function, and atrophy determines the extent of motor nerve injury. Moving and static two-point discrimination tests measure the innervation density and evaluate the number of fibers innervating sensory end-organs. Light moving touch, for example, evaluates the innervation of large Aβ fibers and fibers which

can be quickly screened with the valid and reliable Ten Test. 31 In this test, patients rank the quality of sensation in the affected digit with that in the normal contralateral digit using a scale from 0 to 10. Vibration instruments and Semmes-Weinstein monofilaments are also used as threshold tests to evaluate the performance level of nerve fibers and are useful when evaluating chronic compressive neuropathies. Testing should be performed after nerve repair to assess outcome and monitor recovery. These topics are covered in detail in Chapters 2 and 3.

1.3.1 Mechanisms of Nerve Injury Level of Injury The neuronal response to injury depends not only on the mechanism of injury, but whether it occurs in an adult, child, or

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Anatomy and Physiology for the Peripheral Nerve Surgeon neonate and the relative proximity of injury to the soma, or cell body. The more traumatic the injury, the greater the proximal and distal extent of the injury, and the closer to the cell body all increase the likelihood of soma death. Children but not adults or neonates have superlative functional recovery following nerve injury and repair. The mechanisms that regulate the response of the soma, lengthy axonal projection, and terminal arbors of a single neuron to injury are, at least in part, locally regulated. As such, compromise of a proximal nerve compartment component may not necessarily spell the demise of a more distal component. This so-called compartmental view of neurodegeneration, as termed by Gillingwater and Ribchester,32 is used to organize this summary of the multilevel response to a peripheral nerve injury. Injury to the motor neuron, either by avulsion, direct lesion, or a proximal axonal injury, represents the most devastating level of injury.33,34 This is particularly devastating in neonates, with the demise of 60 to 70% of involved motor neurons reported in murine models.35,36,38,39,40,41,42 Currently, distal nerve transfer reconstruction is favored in these proximal injuries with the potential demise of a functioning cell body, unavailable proximal stump for reconstruction, or the inability to reinnervate a distal target following a prolonged period of denervation.

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tmesis), he did describe axonotmesis as having complete (Sunderland II) or incomplete (Sunderland III) recovery. In addition, Seddon noted that a neurotmetic injury could be in-continuity (Sunderland IV) or a complete transection (Sunderland V) (▶ Fig. 1.6). Neurapraxia (first-degree) injury represents an ischemic injury that may have segmental demyelination but no interruption of axonal or connective tissue continuity. A localized conduction block is produced, but because the axons are not injured, regeneration is not required, and remyelination and evidence of recovery are anticipated in up to 12 weeks. Tourniquet palsies are typically acute conduction blocks and recover within 12 weeks. In chronic nerve compression or with radiation neuritis, a permanent conduction block may exist. Similarly, if an injury localizes to a known area of nerve compression, then a chronic conduction block can persist and be improved with surgical decompression at the site of superimposed nerve compression, for example, foot drop following traction, pressure during knee surgery, or prolonged bed rest. An axonotmetic (second-degree) injury is characterized by axonal disruption but intact connective tissue sheaths. The segment of axon distal to the injury undergoes wallerian degeneration, while proximally, nerve fibers regenerate at a rate of ~ 1 inch (2.5 cm) per month. By definition, the connective tissue layers are uninjured. Recovery will be complete as some uninjured axons are able to collaterally sprout at the distal motor end plates (motor unit potentials [MUPs] on elecromyogram [EMG]) to “babysit,” or protect, the muscle until the native, or parent, axons (nascent units on EMG) eventually reach their targets. The progress of regeneration can be followed by the advancing Tinel sign. First- and second-degree injuries are predominantly managed conservatively, based on highly convincing studies in animal models43 that are corroborated by a wealth of clinical experience.44 Still, promyelinating and neuroregenerative clinical therapies are on the horizon, and their use could be justified to treat an increasingly demanding patient population with proximal injuries that are known to have delayed, and in the case of third-degree injuries, poorer, results due to the time-dependent depletion of the available motor end plate pool. Third-degree injuries are uniquely characterized by fibrosis in the endoneurium that prevents the unencumbered regeneration of some injured axons. This leads to incomplete or mismatched end-organ innervation and can be helped with surgical decompression if the injury localizes to an area of entrapment. The recovery is uniformly better than that seen with a repair or graft unless it is associated with severe causalgia and, in these rare

1.3.2 Classifying Nerve Injury Seddon’s36,37 (▶ Table 1.1) and Sunderland’s3,4 (▶ Table 1.2) classification systems, proposed in 1947 and 1951, respectively, continue to guide the management of nerve-injured patients. These classifications guide expected time to recovery and reconstructive strategies and are organized below. Interestingly, in Seddon’s original classification (neurapraxia, axonotmesis, neuroTable 1.1 Classification of Nerve Injury Seddon

Sunderland (Degree)

favorable

recovery rate

Neurapraxia

I

+

quick

Axonotmesis

II

+

slow

III

+

partial slow

IV

-

-

V

-

-

VI (combination of any of Sunderland (I-V)

+/-

+/-

Neurotmesis

Table 1.2 Classification of Nerve Injury Histopathologic Changes

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Axon

Tinel Sign

Degree of Injury

Myelin

Endoneurium

Perineurium

I Neurapraxia

+ /-

II Axonotmesis

+

+

III

+

+

+

IV

+

+

+

+

V Neurotmesis

+

+

+

+

VI

Various fibers and fascicles demonstrate various pathologic changes

Epineurium

+

Present

Progresses Distally

-

-

+

+

+

+

+

-

+

-

+

+ /-

Anatomy and Physiology for the Peripheral Nerve Surgeon

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Fig. 1.6 Peripheral nerve organization and injury classification. (a) Schematic representation of the cross section of a normal peripheral nerve showing the connective tissue and nerve tissue components. (b) The cross section of the peripheral nerve demonstrates a mixed, or sixth-degree, injury pattern. The fascicle at the top left is normal. Moving in the counterclockwise direction, fascicle I is a first-degree injury (neurapraxia) with segmental demyelination. Fascicle II is a second-degree injury (axonotemesis). The second degree involves both the axon and the myelin. The endoneurial tissue is not damaged. Fascicle III demonstrate a third-degree injury, with injury to the axon, myelin, and endoneurium. The perineurium is intact and normal. Fascicle IV demonstrates a fourth-degree injury, with injury to the axon, myelin, endoneurium, and perineurium. The fascicle is marked by scarring across the nerve, with only the epineurium being intact. Fascicle V is a fifth-degree injury in which the nerve in not in continuity and is transected. The surgeon will separate the fourth- and fifth-degree injury patterns, which will require reconstruction from the normal fascicles and the fascicles demonstrating first-, second-, and third-degree injury patterns (such latter patterns of injury require, at most, neurolysis). (Modified with permission from Mackinnon SE, Dellon AL, eds. Surgery of the Peripheral Nerve. New York, NY: Thieme; 1988:36.)

situations, can be treated as a fourth-degree injury to control pain and causalgia. We have recently used a reverse (distal motor) end-to-side (RETS) nerve transfer in proximal second- or third-degree motor injuries to “babysit,” “supercharge,” or “protect” the distal muscle until the parent axons regenerate.45,46 We have also noted that as axons regenerate, they frequently “slow” at known areas of nerve entrapment. This can be determined with a scratch collapse test or a strong Tinel sign. In these cases, surgical decompression will enhance and/or speed up recovery of function. Fourth-degree injuries represent an in-continuity neuroma with no potential for spontaneous recovery, as the entire population of regenerating axons are blocked by scar. Neuroma excision with nerve graft repair is indicated. Neurotmetic (fifth-degree) injuries occur when the nerve fiber, and therefore both axons and all connective tissue elements, are divided. This mandates surgical repair. Mackinnon54 has popularized the term sixth-degree injury to describe nerve injuries demonstrating a mixed picture of

normal fascicles or two or more injury patterns at the same level of disruption. This sixth-degree injury was not well described until it had been shown that neurolysis was possible and safe, where the internal topography would permit the separation of major components into separate fascicles, a detailed clinical examination could parse out function in separate parts of a single nerve, and microinstruments and technique were perfected. This pattern is the most challenging because it requires differentially treating the various nerve fascicles based on their degree of injury. This complex reconstructive approach requires the highest level of judgment and technical skill so as to protect and not downgrade fascicles that are normal or have the potential to recover, yet excise and reconstruct the fourth- and fifthdegree component of the injury pattern.55

1.4 Injection Nerve Injury A special case of nerve injuries can be considered due to the insertion of a needle and chemicals intrafascicularly or

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Anatomy and Physiology for the Peripheral Nerve Surgeon

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Fig. 1.7 Injection injury to nerve. (a) Intrafascicular injection of local anesthetics can result in damage to nerve due to the physical disruption to axons caused by the needle and the application of toxic chemicals to the nerve. (b) Injection of a significant quantity of anesthetic agents to nerve results in a region of severe injury (denoted by black arrows) due to the toxic nature of the drugs. (Adapted with permission from Farber SF, Saheb-Al-Zamani M, et al. Peripheral nerve injury after local anesthetic injection. Anesth Analg 2013;117(3):731-739.)

extrafascicularly to nerve. Injection of local anesthetics is commonly used for the provision of analgesia in a wide variety of procedures and pain syndromes. The use of a needle causes traumatic injury to the nerve, but additionally a variety of drugs, including local anesthestics, have toxic and damaging effects to nerve due to activation of signaling cascades leading to cellular apoptosis and stress-induced damage of DNA. 47,48,49,50, 51 The incidence of peripheral nerve injury associated with local anesthetic agent injection based on retrospective studies is estimated at 1%,52 although a prospective study reports an incidence of approximately 10 to 15%.53 Farber et al re-evaluated the effect of currently utilized local anesthetic agents on the rat sciatic nerve, using histological assessment techniques (▶ Fig. 1.7a).54 Cross-sections of whole nerves injected with 8 µL of bupivacaine, lidocaine, ropivacaine, and saline (insufficient volume to cause extensive chemical toxicity) revealed that a comparable number of axons were affected as measured by mean total fiber count, fiber density, area of injury, and percent nerve (▶ Fig. 1.7b). However, administration of 50 µL of any local anesthetic agent resulted in areas of severe injury, defined by total loss of large myelinated fibers and extensive fibrosis. Regardless of the drug used, there was a significant decrease in number of fibers and percent nerve in severely-injured nerve zones as compared to non-injured zones and decrease in fiber area. No zone of severe injury was observed in salineinjected nerves. These results demonstrate that local anesthetic agents can cause fourth-degree injury, as perineurium was disrupted in the severe injury areas. Additionally, insertion of the needle alone can cause a small amount of fifth- or sixth-degree injuries.54

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1.5 Mechanisms of Neurodegeneration Axons, Schwann cells, macrophages, fibroblasts, and other cell types demonstrate significant changes in response to nerve injury. As noted above, the components of a single neuron differentially respond to nerve injury, suggesting a compartmentalized process.14,32 Avulsion and proximal axonal injuries lead to injury-induced cell death with loss of the soma and all of its projections. The soma is maintained following a more distal axonal injury with preservation of its regenerative potential. 56 Antegrade degeneration following axotomy, first described by Waller in 1850,57 is aptly named wallerian degeneration (▶ Fig. 1.8; ▶ Fig. 1.9).58 The loss of axonal continuity manifests as a loss of cellular integrity, trafficking of intracellular components, and impaired transmission of a depolarizing axon potential. The degeneration of neuromuscular synapses can precede wallerian degeneration by several hours59–63 and is now thought to be independent of wallerian degeneration, 32,64 thus lending further credence to the compartmentalized view of peripheral nerve injury. Intimately associated with neurons, Schwann cells remain intact but undergo phenotypic changes,22,23,25,65–68 whereas physiologic changes in endothelial permeability and the recruitment of macrophages enable the clearing of products of wallerian degeneration.69–72 Injury to the soma is the most proximal and severe form of nerve injury, with no potential for recovery and is most commonly seen clinically, and reproduced experimentally, with an avulsion injury. It may also be seen with direct mechanical or vascular insult to the soma or with particularly proximal peripheral nerve transection injuries.33,56

Anatomy and Physiology for the Peripheral Nerve Surgeon

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Fig. 1.8 Electron microscopy of transverse nerve sections. (a) A normal myelinated nerve fiber is noted (A, axon; M, myelin; SCN, Schwann cell) (uranyl acetate lead citrate, 13,000x). (b) Following nerve injury, wallerian degeneration occurs. The Schwann cells proliferate and become phagocytic. Myelin and axonal degeneration are noted, as well as frank areas of early myelin degeneration (M, early myelin degeneration; Y, endoneurium) (uranyl acetate lead citrate, 20,000x). (c) A classic regenerating unit containing myelinated and unmyelinated fibers surrounded by perineurium. (d) The process of regeneration and degeneration will occur simultaneously in the distal stump. A regenerating unit is noted on the left, and ongoing wallerian degeneration with myelin debris is noted on the right (M, degenerating myelin debris; R, regenerating unit). (Fig. 1.8c is used with permission from Mackinnon SE, Dellon AL, eds. Surgery of the Peripheral Nerve. New York, NY: Thieme; 1988:18.)

Significant insight into the mechanisms of wallerian degeneration has been gained by the serendipitous development and subsequent evaluation of the Wld(s) mouse.15,26 The outcome of a chance spontaneous mutation in a colony of commonly used C57Bl/6 mice at Oxford University,73–75 the Wld(s) strain manifests no outward phenotypic changes but demonstrates a 10fold delay in wallerian degeneration based on electrophysiologic and anatomical evaluation.14 To reveal the molecular mechanism of delayed nerve degeneration and identify therapeutic targets for subsequent antidegenerative therapies, the Wld(s) mutant has been thoroughly evaluated. It has been hypothesized that protein ubiquitination and deubiquitination regulate the rate of wallerian degeneration at a molecular level.1,2 Ubiquitin functions as a macromolecular tag that targets proteins for degradation by the 26S proteosome. The pattern and degree of protein ubiquitination regulate where, within a cell, a particular protein is proteolysed. If fewer than four ubiquitin subunits are associated with a particular protein, then it will typically facilitate posttranslational modification of another protein rather than being degraded by the 26S proteasome. As such, ubiquiti-

nation can facilitate the rapidity and location of proteasome degradation of specific intracellular proteins, whereas deubiquitination can affect gene transcription. The inhibition of ubiquitination has been associated with delayed wallerian degeneration. The Wld(s) gene is composed of fragments that include ubiquitination factor E4B (Ube4b) and nicotinamide mononucleotide adenylyltransferase-1 (Nmnat-1) (▶ Fig. 1.10a). It was initially felt that the Ube4b component conferred the neuroprotective phenotype in Wld(s) mutants.76 A series of elegant studies performed by Araki et al,12 however, show that Nmnat-1, an enzyme in the nicotinamide adenine dinucleotide (NAD) pathway that generates nuclear NAD, is responsible for axonal protection in Wld(s) mice (▶ Fig. 1.10b). Sertuin-1 (SIRT-1), a downstream effector of elevated nuclear NAD, functions as a deacetylase of histones and other proteins and is proposed to regulate a genetic program that protects injured axons (▶ Fig. 1.10c). Observations of wallerian degeneration have revealed that initial degradation of axonal components rapidly leads to recruitment and activation of nonneuronal cells that are crucial for regeneration. This process includes the dedifferentiation,

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Anatomy and Physiology for the Peripheral Nerve Surgeon

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Fig. 1.9 Wallerian degeneration observed with light microscopy. (a) A population of well-myelinated fibers is noted in the proximal normal nerve (toluidine blue, 400x). (b) After nerve transection, wallerian degeneration is noted in the distal nerve, with areas of myelin debris (arrows) noted within a population of cells, which are determined to be Schwann cells by electron microscopy (toluidine blue, 400x). (c) Each nerve fiber will sprout into a regenerating unit. A field of regenerating units is shown in this image. (d) Immediately distal to a nerve repair, a population of well-myelinated fibers is noted within the nerve (bottom left). In the extraepineurial space (top right), a population of regenerating units can be seen. These units represent both lost function and potential pain as a suture-line neuroma (toluidine blue, 400x).

proliferation, and migration of Schwann cells, along with the activation of macrophages within the endoneurium and the recruitment of complementary immune cells from the periphery.74,77–80 These cells prepare the distal nerve for regeneration by clearing myelin debris and other inhibitors to axonal regeneration during the neural wound-healing response.81–84 Recent studies suggest that activation of Schwann cells following injury is mediated in part through the involvement of the Toll-like receptor (TLR) family.85–87 TLRs are essential components of the innate immune response that bind specific peptide components conserved among microorganisms as well as endogenous ligands produced by necrotic cells, injured axons, and the extracellular matrix. Stimulation of Schwann cells in vitro by degenerated neural tissue stimulates the production of monocyte chemotactic protein-1 (MCP-1) partially through TLR2, -3,87 and -4.86 In vivo work demonstrated that the expression of interleukin-1β (IL-1β) is reduced in the distal segment of the injured sciatic nerve in mice lacking TLR2, -4, and the adapter protein myeloid differentiation primary response gene 88 (MyD88), and MCP-1 expression was reduced in mice lacking MyD88 after injury.85 These changes were accompanied by a decrease in macrophage recruitment and overall wallerian degeneration. However, the incomplete decreases in macrophage recruitment and wallerian degeneration suggest that the innate immune response only partially contributes to full recruitment of this healing response.

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The recruitment of Schwann cells and macrophages is also linked to the secretion of several other specific proinflammatory cytokines and chemokines.88–93 Tumor necrosis factor α (TNF-α) and IL-1α are also expressed by Schwann cells early after sciatic nerve injury, followed by IL-1β expression, suggesting that they all contribute to the early injury response.9,10,94,95,100 The secretion of these proinflammatory agents further stimulates the recruitment of macrophages and immune-competent cells from the periphery.90,92 Following recruitment and activation, macrophages likely perpetuate this activation through the expression of TNF-α, IL-1α, and IL-1β.94,95

1.6 Transcriptional Control of Nerve Regeneration The response to nerve injury is affected by processes both intrinsic and extrinsic to the neuron. A neuron senses axonal injury by unique and potentially cooperative molecular processes of which three types of signals have been identified.96,97 First, positive signals derived from retrograde transport of kinases, such as mitogen-activated protein kinases (MAPKs), are transported from the injury site to the cell body.96,98,99 These positive signals activate their associated MAPK transcription factors, leading to upregulation of regeneration-associated genes. Second, the injury to the axon leads to disruption of action poten-

Anatomy and Physiology for the Peripheral Nerve Surgeon

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Fig. 1.10 The components of the Wld(s) chimeric gene. (a) The Wld(s) gene contains a short fragment of the ubiquitin assembly protein Ube4b and the full-length nicotinamide adenine dinucleotide (NAD) synthetic enzyme nicotinamide mononucleotide adenylyltransferase-1 (Nmnat-1). (b) The mammalian NAD synthesis pathways. In mammalian cells, NAD could be synthesized from three different precursors, such as from tryptophan (the de novo synthesis), as well as from nicotinamide or nicotinic acid (the salvage synthesis). Nmnat-1 is an indispensable enzyme controlling the last step of both de novo and salvage NAD biosynthesis pathways. Nicotinamide represents the main source of NAD in most cells in mammals, including neurons, and it is also the product of NAD+ hydrolysis catalyzed by NAD+-consuming proteins. (c) The molecular pathway proposed to participate in axon degeneration of Wld(s) and normal mice.

tials, generating an large influx of calcium and a depolarizing wave.96,99 This influx of calcium leads to protein kinase C (PKC) activation within the cell body and the nuclear export of histone deacetylase 5 (HDAC5), a regeneration-associated gene repressor.99 Third, interruption of retrogradely transported trophic factors and negative regulators of axonal growth at the end-organ lead to the upregulation of regeneration-associated genes.96,97 This pathway has been described the least and the mechanisms of action involved in it are still being explored. Additionally, these peripheral-nerve-injury signals also result in elevated levels of cyclic adenosine monophosphate (cAMP) intrinsic to the injured neuron.101,102 Elevated cAMP activates protein kinase A (PKA) through a transcription-dependent process, which leads to axonal elongation by inactivating Rhoassociated kinases (▶ Fig. 1.11).103–106 Significant current research on the intrinisic capacity of neurons to regenerate focuses on the interplay between cytoskeletal assembly and blocking the inhibitory effects of myelin. Small guanine nucleotide guanosine triphosphate (GTP)ases of the Rho family control actin polymerization, cell growth and motility, cytokinesis, trafficking, and cytoskeletal architecture. Inhibition of the Rho-associated kinases (ROCKs) inhibits cytoskeletal assembly. This can be achieved by antagonizing signal-

ing mediators of myelin-associated inhibitory molecules. For example, binding of the neurite outgrowth inhibitor (Nogo) receptor by either myelin-associated glycoprotein (MAG) or myelin activates Rho and consequently ROCK, thus providing a molecular mechanism for the inhibitory influences of myelin on nerve regeneration.103 Elevated intracellular levels of cAMP not only antagonize Rho, but may also antagonize Rho activation by myelin-associated inhibitory molecules. A transcription factor strongly linked to the intrinsic capacity of neurons to regenerate is cAMP response element-binding protein (CREB). CREB can also stimulate a regenerating neuron to overcome the inhibitory influences of myelin.107 CREB phosphorylation may exert its regenerative effects by upregulating arginase-1-modulated polyamine synthesis.101,108 Polyamines can promote axonal elongation independently or by inducing the expression of other genes that promote cytoskeletal assembly, thus providing yet another mechanism for preventing cytoskeletal assembly inhibition by Rho (▶ Fig. 1.12).108 c-Jun, a component of the heterodimeric activator protein 1 (AP-1) transcription factor, is also significantly induced by nerve injury109 and may have a dual function in both cell death and regeneration of neurons.110 c-Jun activation is involved in growth factor–dependent apoptotic neuronal death, since

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Anatomy and Physiology for the Peripheral Nerve Surgeon

Fig. 1.11 Activation of intrinsic growth capacity by peripheral nerve injury. Peripheral nerve injury elevates intracellular cyclic adenosine monophosphate (cAMP) levels, which activates protein kinase A (PKA). PKA triggers gene expression through cAMP response element binding protein (CREB), resulting in transcriptional upregulation of regeneration-related genes such as arginase-1. Arginase-1 promotes the synthesis of polyamines, which may directly regulate cytoskeleton assembly or further induce gene expression necessary for regeneration. Activation of polyamines also inhibits Rhoantagonizing MAG or myelin-induced Rho inhibition of neurite growth. Peripheral injury additionally induces c-Jun transcription factor– dependent regeneration-related gene expression. Activation of the intrinsic growth capacity is regulated mainly at transcriptional level.

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Fig. 1.12 Schematic model showing the general configuration of laminin. The protein contains globular domains and a coiled-coil region in which laminin’s three chains are covalently linked by several disulfide bonds. Different sections of the globular region bind to cellsurface integrin and dystroglycan receptors to augment axonal growth.

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Anatomy and Physiology for the Peripheral Nerve Surgeon inhibition of c-Jun expression blocks cell death induced by deprivation of neurotrophic factors.111,112 On the other hand, some data suggest that activation of c-Jun is involved in neuroprotection and regeneration. Axotomized retinal ganglion cells regenerating through a peripheral nerve graft coexpress c-Jun and growth-associated protein 43 (GAP-43) for several weeks.113,114 More direct evidence of c-Jun involvement in nerve regeneration comes from analysis of injured motor neurons in conditional knock-out mice lacking c-Jun only in the central nervous system (CNS). Here, c-Jun signaling is required for efficient axonal regeneration.115 In addition, inhibition of c-Jun phosphorylation significantly reduces axonal outgrowth of adult sensory neurons.116 Nuclear translocation of c-Jun and subsequent gene transcription require the kinase activity of the cJun-N-terminalkinases (JNKs), which are also activated by axotomy concurrent with c-Jun.106 It has been suggested that JNKs participate in the initiation of the axonal response to nerve injury and can be transported on microtubules along axons via their association with motor proteins of the kinesin family.117,118 Therefore, the JNK/c-Jun pathway is a potential candidate for sensing and triggering the axonal response to injury.119 The fact that c-Jun induction mediates the divergent pathways of increasing the vulnerability of axotomized neurons to undergo apoptotic cell death, on the one hand, while promoting neuronal survival and regeneration, on the other, suggests that other signaling pathways must modulate its activities. Members of the activating transcription factor (ATF)/CREB family of transcription factors may key the selection of one c-Jun pathwaymediated pathway over another. Two members of this family, ATF2 and ATF3, can act as homodimers, but they can also form active heterodimers with c-Jun.110,120 Coordination of CREBand AP-1 transcription-factor-regulated gene expression may be required to control axonal regeneration. ATF2 and ATF3 respond differently to neuronal injury. ATF3 is not expressed in normal tissue, but instead is induced in a variety of stressed tissues and is dramatically upregulated in motor neurons and sensory neurons following axotomy.121,122 Overexpression of ATF3 inhibits JNK-induced death and induces neurite elongation in pheochromocytoma (PC) 12 cells and sympathetic cervical ganglion neurons.123,124 ATF2 is known to play a role in neuronal protection, but in contrast to ATF3, it is downregulated in injured adult neurons following axotomy. This suppression occurs in parallel with upregulation of c-Jun.110 Colocalization studies indicate that c-Jun, ATF3, and ATF2 are coexpressed at different periods postinjury, and for c-Jun, a switch in heterodimerizing partner (ATF3 vs ATF2) may occur.125,126 ATF3 homodimer functions as a transcriptional repressor for most target genes, such as gadd153/Chop10,127 whereas ATF3 heterodimer (with c-Jun, for instance) has been demonstrated to function as a transcriptional activator.120 But gadd153 in turn can bind ATF3 to form a nonfunctional heterodimer and negatively regulate ATF3 function (▶ Fig. 1.11).128

1.7 Schwann Cell-Based Signaling in Peripheral Nerve Injury Schwann cells are the primary extrinsic mediators of nerve regeneration in the peripheral nervous system. In contrast to the CNS, where glial cells lead to scarring and the persistence

of myelin-based inhibitory proteins, Schwann cells can phagocytose myelin debris and dedifferentiate into a migratory, proliferative, but nonmyelinating phenotype.129–131 Following nerve injury, and early in development, Schwann cells assume a dedifferentiated, proliferative phenotype characterized by markers such as p75 neurotrophin receptor (p75NTR),132 L1 cell adhesion molecule, and neural cell adhesion molecule (NCAM).133,134 At the subcellular level, selective activation of the extracellular signal-regulated kinase (Erk) pathways and specific activation of p38 mitogen-activated protein kinase (MAPK) prevents Schwann cell maturation and myelination.66–68,132,135 Upon maturation, Schwann cells can assume a nonmyelinating phenotype characterized by persistent L1, NCAM, and glial fibrillary-acidic protein (GFAP) expression or a myelinating phenotype characterized by 1:1 Schwann-cell-to-axonal relationships.136,137 Schwann-cell transformation from a nonmyelinating to myelinating phenotype may be reliant on a number of intracellular events. Selective phosphorylation of Akt 135 and activation of the cell cycle-regulator nuclear factor κβ (NF-κβ) both facilitate myelination,138 whereas selective inhibition of either process attenuates myelination. The axon-based signal neuregulin1, type III has also been shown to have a critical role in axonal ensheathment and myelination of postmigratory Schwann cells independent of axon caliber, and is associated with activation of phosphoinositide (PI) 3-kinase and the presence of suppressed cAMP-inducible POU (SCIP). 139 SCIP is a transcription factor that characterizes premyelinating Schwann cells and is influenced by upstream NF-κβ activity.138 Downstream from SCIP, the zinc-finger protein transcription factor Egr2 serves as a marker for myelinating Schwann cells 140,141 and is modulated by nerve-growth-factor inhibitory-A (NGFI-A)binding (Nab) proteins Nab1 and -2, which also play a significant role in Schwann cell maturation and the upregulation of myelinating genes.142 Mutations in Egr2 cause a number of myelinopathies, and interactions between Egr2 and the transcription factor Sox2 (SRY [sex determining region Y]–box 2) have a deleterious effect on myelination. 137 Schwann cell migration is most extensively studied in development, as Schwann cells do not need to migrate significant distances following nerve injury unless an allograft or conduit is used for reconstruction.80 Whether Schwann cells require dedifferentiation prior to migration also remains unclear. In vitro, activation of the neurotrophin-3 (NT-3) tyrosine kinase receptor (TrkC)—but not the ubiquitous neurotrophin receptor p75, which marks dedifferentiated Schwann cells—works through the guanine-nucleotide exchange factor (GEF) to activate the Rho GTPases Rac1 and Cdc42.143 In turn, these small GTPases activate the downstream JNK and regulate actin cytoskeleton formation, possibly to induce Schwann-cell motility.106,144 Strong evidence also suggests that Schwann-cell migration is influenced by interaction between neuregulins (Nrg) and their ErbB receptors on Schwann cells,104,119 and in the zebrafish model, nonproliferating Schwann cells can migrate.131 Further studies are forthcoming to evaluate whether ErbB–Nrg interaction confers the ability for Schwann cells to migrate or directly causes migration. Schwann-cell migration is also dependent on interactions between components of the extracellular matrix, including laminins, fibronectin, and tenascin, and a host of integrins, a group of heterodimeric molecules located on the

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Anatomy and Physiology for the Peripheral Nerve Surgeon Schwann cell that likely serve as receptors to modulate intracellular signaling programs.145–147 As Schwann cells proliferate and migrate in response to injury, they also come into direct contact with fibroblasts, which accumulate in the nerve injury site. Fibroblasts have been shown to actively organize Schwann-cell distribution to facilitate organized nerve regeneration. The process mediates the formation of multicellular cords of Schwann cells through the cell-surface interactions of ephrin-B and EphB with subsequent downstream activation of Sox2.148 The removal of this signaling process results in disorganized Schwann-cell migration and erratic axonal regeneration. To establish a uniform distribution of Schwann cells following proliferation and migration with appropriate myelinating and nonmyelinating Schwann-cell–axonal relationships, it is likely that redundant or misplaced Schwann cells will undergo apoptosis. Between birth and postnatal day 3, Schwann-cell proliferation is robust in postnatal rats and exceeds the number of available axons. Schwann cells devoid of axonal contact then undergo apoptosis,149 possibly modulated by selective inhibition of NF-κβ.150 The recent development of a transgenic mouse (S100-GFP) whose Schwann cells constitutively express green fluorescent protein (GFP), in combination with in vivo fluorescent imaging, provides a unique opportunity to study Schwann-cell migration into peripheral nerve allografts. 151 GFP-labeled Schwann cells from this homozygous host can be tracked into a nerve allograft devoid of fluorescence. Serial imaging of transgenic mice whose axons constitutively express chromophores provides a unique opportunity to study peripheral-nerve regeneration.25,65,152–154 Using such tools, it has been demonstrated that in an acellular nerve allograft or conduit, Schwann-cell migration precedes axonal sprouting, and that proliferation in the distal stump is more prolific. 155 Following peripheral-nerve injury and reconstruction, the prolonged time period required for the regenerating nerve to reach its target muscle is a major factor in predicting the likelihood of functional recovery. During this regenerative period, the denervated muscle begins to atrophy, resulting in profound, irreversible muscle damage and fibrosis manifested by poor functional recovery.89,156–160 Short-term denervated muscles recover well after reinnervation, but after longer periods of denervation (between 12 and 18 months in humans and 4 to 7 months in rats157,161), functional reinnervation is limited by the muscle. In addition to effects on the muscle, Schwann cells in the distal nerve stump become less supportive of regenerating axons.162,163 The Schwann cells of the distal stump progressively decrease in number when the regenerating axons fail to contact them in the distal nerve stumps.164 Furthermore, the Schwann cells that remain begin to downregulate the production of trophic factors that are essential to the support of regenerating axons.165 The combined effect of chronic denervation is fewer regenerating axons reaching degenerated muscle, resulting in poor functional recovery.

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1.8 Extracellular Matrix Molecules in Nerve Regeneration Components of the extracellular matrix, namely, laminins and their receptors—integrins and dystroglycans—also play a critical

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role in the extrinsic mediation of nerve regeneration (▶ Fig. 1.12). There are 15 described laminin isoforms, many of which are expressed in injured and uninjured nerves and are thought to promote nerve regeneration through the regulation of Schwann-cell phenotype, and by providing guidance cues and substrate for regenerating axons.166 The expression of laminins 2 (α2β1γ1) and 8 (α4β1γ1) is upregulated in the endoneurium following peripheralnerve injury.167,168 Successful impairment of axonal regeneration has been demonstrated in conditional gene knockout and antibody experiments where α2 or γ1 laminin chain expression was attenuated.169 Similar knockout experiments of endogenous integrin receptor expression also lead to reduced axonal regeneration that can be bolstered with exogenous induction of integrin receptor expression.170 The mechanisms by which laminins regulate axonal regeneration are not clearly elucidated but are likely to be mediated by integrins, and probably involve Akt phosphorylation.171 When regenerating axons and laminin are brought into close proximity, axonal PI-3 is activated and can phosphorylate Akt. Phospho-Akt is a known inhibitor of glycogen synthase kinase 3β (GSK-3β). Reduced GSK-3β activity results in the organization of cytoskeletal elongation, thus promoting axonal regeneration.172 Laminins and their receptors are also intimately involved with the regulation of Schwann–cell–axonal relationships. Laminins are integral components of a Schwann cell’s basal lamina and contribute to proper axonal ensheathment and myelination. When contact between Schwann cells and axons is lost during the period of wallerian degeneration, laminin expression is downregulated. Laminins are upregulated commensurate with maturation of Schwann cells to a differentiated, myelinating phenotype. The Schwann–cell–derived laminin receptors most likely to facilitate axonal sorting and orchestrate myelin folding are β1 integrin and dystroglycan. It is likely that β1 integrin expressed by promyelinating Schwann cells is the key player in axonal sorting, while dystroglycan173 subsequently regulates myelin folding and maintenance.174 In peripheral nerve surgery, fibrin glue has supplanted suture neurorrhaphy for some surgeons. However, fibrin is a known inhibitor of myelination, and a Schwann cell’s ability to lyse fibrin is an important step in the remyelination of regenerated axons.175 Fibrin maintains Schwann cells in a dedifferentiated state by inducing extracellular regulated kinase 1 and 2 activity, as well as p75 nerve-growth-factor (NGF) low-affinity receptor activity. 132 Following nerve injury, Schwann cells secrete increased levels of plasminogen activator, thereby facilitating the conversion of the plasminogen zymogen to plasmin. Plasminogen activator–mediated fibrinolysis enables Schwann-cell migration and remyelination by clearing fibrin that has infiltrated a peripheral nerve as part of the injury response. The above discussion of the importance of Schwann cells and extracellular matrix helps to put the relative merit of an autograft (Schwann cells and extracellular laminin matrix), acellular allograft (extracellular matrix alone), and empty conduit (no Schwann cells and no matrix) in context. Consistently, laboratory research has demonstrated that the differences between the three clinical treatments have a significant effect on nerve regeneration and functional outcome. 176, 177 Ignorance of these differences results in poor surgical outcomes.178

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Fig. 1.13 Growth factors that augment and mediate peripheral nerve regeneration. The neurotrophic factors NGF (nerve growth factor), NT4/5, BDNF (brain-derived neurotrophic factor), and NT3 all have affinities for the p75NTR coreceptor and differential affinities for the tyrosine kinase receptors (Trks). NGF selectively binds TrkA, NT4/5 and BDNF bind TrkB, and NT3 binds TrkC. Interaction with their specific Trk receptor and the ubiquitous p75 receptor stimulates downstream effectors that augments cell growth/regeneration (through the mitogen-activated protein kinase [MAPK] pathway) and cell survival (through the Akt pathway) and inhibits cell growth arrest (inhibition of Rho-associated kinase [ROCK]). The glial-derived neurotrophic factor (GDNF) family of growth factors have selective affinities for four GDNF-family receptor α (GFRα) receptors. Association of each GDNF family growth factor with its respective GFRα receptor and subsequent association with the Ret tyrosine kinase receptor can augment cytoskeleton organization (enigma), cell growth/regeneration (MAPK pathway), and cell survival (Akt pathway).

1.9 Neurotrophins and Neurotrophic Factors in Nerve Regeneration Neurotrophins and neurotrophic factors are distinct groups of molecules with specific receptor affinity and expression profiles involved in the regulation of axonal regeneration and Schwanncell behavior. Common to all four members of the neurotrophin family are their ubiquitous affinities for the p75NTR coreceptor and differential affinities for the Trk receptor tyrosine kinases. NGF selectively binds TrkA, brain-derived neurotrophic factor (BDNF) and NT4/5 (NT = neurotrophic factor) bind TrkB, and NT3 binds TrkC.179 Messenger RNA (mRNA) levels for the p75NTR receptor and BDNF are increased in distal stump Schwann cells following nerve injury, while NT-3 mRNA levels are decreased before normalizing 2 weeks later.79,180 In addition to regulating neuronal survival and differentiation, neurotrophins regulate myelination.181 Specifically, myelination is upregulated by BDNF

through its interactions with p75NTR but downregulated by NT3 via its interaction with TrkC (▶ Fig. 1.13). GDNF was first discovered as a potent survival factor for midbrain dopaminergic neurons182 and has subsequently been investigated as a treatment for neurodegenerative diseases.183,184 Three GDNF-related proteins were discovered, including neurturin (NRTN), a survival factor for sympathetic neurons, 185 followed by artemin (ARTN) and persephin (PSPN), which were identified on the basis of sequence homology.186,187 The receptor complex for GDNF family members is composed of a signaling component transmembrane Ret tyrosine kinase188–192 and one of four glycosylphosphatidylinositol (GPI)-linked high-affinity ligand-binding components designated as GFRα1–GFRα4. Each GDNF family member has a preferred binding receptor. GDNF primarily mediates its signals by binding Ret and GFRα1 receptor,193 NRTN by binding GFRα2,193–199 PSPN by binding GFRα4,200–205 and ARTN by binding GFRα3.206–208 Although each GDNF family member binds one preferred GFRα receptor in

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Anatomy and Physiology for the Peripheral Nerve Surgeon vitro, the coreceptors are less specific in their ligand-binding affinities and how they activate Ret (▶ Fig. 1.13).209,210 GDNF and other members of the GDNF family of ligands are important neurotrophic factors for the development, survival, and maintenance of distinct populations of central and peripheral neurons, including motoneurons.210 GDNF promotes embryonic motoneuron survival in vitro and in vivo211,212 and is 70-fold more potent in this model than BDNF, ciliary neurotrophic factor (CNTF), or insulin-like growth factor-2 (IGF-2).211 The local application of GDNF, NRTN, and PSPN to a transected nerve stump efficiently prevents axotomy-induced motoneuron death in neonatal rodents.187,212–214 All three factors are expressed in motoneuron target tissue (i.e., skeletal muscle) during development (▶ Fig. 1.13).215–218 Following neonatal and adult peripheral-nerve injury, expression of GDNF and its receptor complex is differentially regulated. Embryonic and adult motoneurons do not express GDNF,218–221 and following axotomy, the levels of GDNF in motoneurons is not upregulated.222 GDNF is expressed in peripheral nerves, and after nerve injury its expression is upregulated significantly in the distal stump of sciatic nerve223,224 and in muscle,223,224 but very little in the proximal nerve stump.222,225 Following axotomy in neonates, GFRα1 receptor expression is downregulated, while RET expression is slightly upregulated.226,227 By contrast, both GDNF receptors are substantially upregulated in injured adult motoneurons.216,222,223 GFRα1 mRNA is expressed in normal peripheral nerves, and its dramatic upregulation in the distal but not proximal stump of nerve is observed. Importantly, this increase is most pronounced in the more distal segments of the nerve, resulting in a distally increasing gradient of both GDNF and GFRα1 expression.223,224 Based on these findings, it is proposed that GFRα1 captures and presents soluble GDNF to function as a membrane-anchored trophic signal for RET-expressing regenerating motoneurons. Alternatively, it is proposed that soluble GFRα1 secreted by Schwann cells can bind GDNF and form a complex that can activate regenerating motor axons.223,224 Taken together, these results suggest that GDNF is important during axonal regeneration of motoneurons after nerve injury (▶ Fig. 1.13). The neuroregenerative effects of GDNF in vivo are strongly related to the location of its delivery. Following facial-nerve crush injury in a neonatal rat model, a neuroregenerative effect is detected when GDNF is incorporated into an adenovirus and injected into adjacent facial muscles but not when delivered into muscles of the lower extremity distant to the site of nerve injury.38 GDNF delivery into facial muscles is characterized by an increase in the number of surviving motoneurons within the facial nucleus after crush injury, more myelinated axons in the buccal branch of the facial nerve relative to contralateral controls, and a more rapid restoration of normal whisker movement compared to nerve-injured animals treated with placebo alone. In the adult mouse model, axotomy of nerves innervating muscle fibers singly transfected with GDNF leads to profuse axonal sprouting in the vicinity of the injury.224 This effect was not noted in intact adult nerves. Transected sciatic nerves repaired with neural conduits seeded with slow-release GDNF support significantly better axonal regeneration than untreated or NGF-treated conduits.228 Other investigators demonstrate that GDNF may accelerate sensory recovery229 and has a more significant neuroregenerative effect in chronic than acute

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peripheral nerve injury.165,230 This suggests that low levels of GDNF expression in chronic-nerve-injury models are responsible for the poorer results noted when peripheral-nerve injuries are reconstructed in a delayed rather than in an acute fashion.10,165,230

1.10 Preferential Motor Reinnervation When given equal access to motor and sensory pathways, the ability of regenerating motor axons to preferentially regenerate down a terminal motor pathway and reinnervate its muscle target is termed preferential motor reinnervation (PMR).231,232 and has been demonstrated in mice, rats, and primates.233–235 The femoral nerve is ideally suited for studying PMR, as proximally, its motor and sensory fibers are more heterogeneously distributed before assuming a more predictable topography distally that branches into the cutaneous saphenous nerve and the quadriceps motor branch.26,231,232,236–239 In a series of studies, Brushart, Madison, and colleagues demonstrated that regenerating motor axons,231,232,238 as well as afferents from the muscle spindle, preferentially regenerate down the quadriceps motor pathway even when deliberate attempts at mismatching sensory and motor paths are made.238 They postulated that trophic factors intrinsic to the motor and sensory pathways guide axons to their specific targets and demonstrated this further in mice whose dorsal-root ganglia were severed to enable assessment of motor axons exclusively.250 Unfortunately, deafferentation can affect motor-neuron function,251 and a lack of sensory fibers creates an artificial environment where motor axons no longer have to compete with sensory axons for the same endoneurial tubes. Although some investigators maintain that factors intrinsic to the pathway guide PMR,250 other work suggests that it is trophic support derived from contact with muscle (“targetderived”) that is most relevant. 29,252 Using the femoral-nerve model, contact between the quadriceps and its motor branch was severed. Under these conditions, motor axons preferentially occupied the cutaneous pathway, presumably because it was longer and had greater trophic support than its motor counterpart. Additionally, removal of the cellular component of the distal stump while maintaining end-organ contact did not affect PMR.29 These investigators conclude that the influence of target-derived trophic support on PMR was more powerful than that of “pathway-derived” trophic support. Mackinnon and coworkers conducted numerous laboratory studies evaluating pathway- versus target-derived mechanisms for PMR.253–257 In their initial studies, a rat tibial-nerve model found that motor-nerve grafts support significantly better nerve regeneration than sensory grafts alone.253,254 After the completion of these studies, others demonstrated that Schwann cells exhibit a motor and sensory phenotype that may contribute to PMR.24 In response, the Mackinnon group evaluated the contribution of cellular components of nerve grafts by isolating minced motor and sensory tissue in nerve conduits251 and by removing cellular components of motor and sensory nerves via decellularization processes.257 The pair of studies suggested that the cellular component of the grafts had no significant effect on nerve regeneration and that the differential size of the

Anatomy and Physiology for the Peripheral Nerve Surgeon

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Fig. 1.14 Differences in pure motor and sensory nerve architecture. Both images show laminin staining of harvested rodent nerve in red. (a) The endoneurial tubes shown in the cross section of the femoral motor branch are larger and more defined than (b) the tubes found in the femoral sensory branch. These images demonstrate the architectural difference between motor and sensory nerves which may contribute to differences in regeneration seen when used to reconstruct a mixed nerve.

extracellular matrix tubes of motor grafts enhanced nerve regeneration (▶ Fig. 1.14). A final study was conducted in the pure motor and sensory model of the femoral nerve. In this study, modality-matched and -mismatched grafts were evaluated (matched: femoral motor graft to femoral motor nerve; mismatched: femoral sensory graft to the femoral motor nerve). The researchers concluded that in a pure motor- or sensory-nerve modality, matching has no significant effect on nerve regeneration. 255 It was hypothesized that in a mixed nerve where end-organ signaling is mixed, the axons use the larger nerve architecture to enhance regeneration. In contrast, in a pure nerve, the singular end-organ signaling negates any architectural effects. Clinically, improved functional results have been noted when motor-nerve transfers are used instead of sensory grafts to reconstruct human motor-nerve injuries (▶ Fig. 1.15).258–262

1.11 Axonal Transport Transport of essential molecules such as neurotransmitters and organelles must take place within neurons, including the axons. Regardless of axons' length, axonal transport occurs to maintain normal cellular function and synaptic communication. Transport occurs bidirectionally along the axon: from soma to distal axon (anterograde), such as in the transport of neurotransmitters from the nucleus to the distal end of the axon, and from distal axon to soma (retrograde), such as with endocytosed growth factors produced in target tissue. Transport typically occurs at two different speeds in the axon: fast and slow. Additionally, the slow transport is separated further into two different speeds to be elucidated further in this section. Microtubules residing within the axons provide the infrastructure on which the transport can take place. Many different cellular components traverse these “axonal highways.” These structures include membrane proteins, organelles such as mitochondria and neurotransmitter-containing vesicles, and trophic

factors. Early studies by Dahlström et al with inhibitors of microtubule assembly demonstrated that it was in fact microtubules that contributed to axonal transport in the anterograde direction.263 Microtubules are oriented within the axon with positively charged (+) ends directed toward the distal endorgan. It was found that these microtubules could support transport in either direction, with the ATPase dynein providing the driving force in the retrograde direction and the ATPase kinesin providing the driving force in the anterograde direction (toward the (+) side).264 Kinesins, of which there are many types, contain two heavy chains and a variable number of light chains. The heavy chain provides the movement force, and the light chains function as attachments to the cargo. Through the conversion of adenosine triphosphate (ATP) to adenosine diphosphate (ADP), the kinesin, while attached to the cargo molecule, changes configuration, allowing it to progress down the microtubule.265 Ochs demonstrated fast axonal anterograde transport rates of about 400 mm/day using cat sciatic nerves.266 Dynein transport has been reported to move at rates around 100 mm/day.267 Items transported in the “fast” modality include mitochondria, neurotransmitter-containing vesicles, lysosomes, other organelles, membrane proteins, and trophic factors. Additional studies of axonal transport revealed that there were two “slow” speeds at which transport occurred.268 These two components of slowed transport were labeled A (SCa) and B (SCb). Group A contained neurofilament triplet proteins and tubulin. Group B was composed of mostly actin. The transport velocities for the two groups differed, with that of group A (SCa) being ~ 0.1 to 1.0 mm/d and that of group B (SCb) being ~ 5 to 10 mm/d. The SCa group used the microtubule/neurofilament network for transport, and the SCb group transported mostly peptides and soluble proteins using the microfilament network. The rates of both fast and slow axonal transport have been shown to decrease with age. Several studies using the peripheral nerves in rat models have been used to demonstrate this phenomenon. In one study, a reduction in speed of > 50% was

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Fig. 1.15 Preferential motor reinnervation. Following injury to a mixed motor and sensory nerve, regenerating axons will preferentially regenerate down a modality-matched terminal pathway. A small proportion of the regenerating axons will inappropriately innervate a mismatched sensory or muscle target. However, over time these inappropriate connections are pruned back, leaving only appropriate end-organ association. The mechanism underlying this specificity is mediated through “pathway,” “target,” or combined signals.

observed.269 It is known that fast axonal transport is an energydependent process. A possible explanation for decrease in transport speed is an age-related decrease in energy supply. Slow transport has been demonstrated to decrease in velocity as well. In one study using radiolabeled cytoskeletal proteins, both the rates of SCa and SCb were shown to decrease ~ 40% in aged rats.270 Another study demonstrated similar results, observing tubulin transport in rats.271 It is this change in axonal transport that may result in disorder of neuronal growth, innervation, and synaptic transmission with age.

1.12 Nerve Blood Supply Peripheral nerves receive their blood supply from major arteries branching into small vessels leading to the epineurium (extrinsic), perineurium, and endoneurium.240 The normal nerve is critically dependent upon the intrinsic blood supply and the perineurial and endoneurial vessels. This allows for the successful elevation of even large-diameter nerves over long distances, such as anterior transposition of the ulnar nerve in cubital-tunnel surgery. These intrinsic vessels are similar to

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other major vessels with the exception of having endothelial cells that contain tight junctions, no fenestration, and additional receptors to aid in diffusion and extrusion of compounds.240,241 This innermost layer of cells within the perineurium prevents the diffusion of large molecules and proteins to the endoneurium and has been termed the blood-nerve barrier or interface. 241,242,243 The endothelial cells lining this barrier act to maintain homeostasis through osmotic control, blockade of toxic metabolites, and incorporation of essential parenchymaassociated molecules using their specialized ultrastructure and receptors.241 This intrinisic blood supply is crucial during regeneration, as the blood–nerve barrier breaks down uniformly along the nerve within days of injury, allowing large molecules, such as growth factors and immune cells, to cross and enter the endoneurial space.244,245,246,247,248 Following regeneration, the blood–nerve barrier is gradually, but fully, restored, limiting the supply of proteins and foreign molecules to protect the nerve from potentially toxic substances and restore homeostasis.241,249 Evaluation of the intrinsic and extrinsic blood supplies of peripheral nerves has benefited from intravital light-microscopic techniques. Lundborg272 showed that a nerve supplied by only

Anatomy and Physiology for the Peripheral Nerve Surgeon one extrinsic blood vessel maintained normal intraneural microcirculation to a length:diameter ratio of 45:1. With the aid of radioactive microspheres, Maki et al273 built on Lundborg’s work in the rabbit sciatic nerve, demonstrating maximal length-to-diameter ratios of 63:1 with only the proximal intrinsic blood supply intact, and of 45:1 with a single extrinsic blood vessel intact. Moreover, incomplete revascularization of large-caliber but not small-caliber standard nerve grafts has been demonstrated using fluorescent vascular tracers and histomorphometric techniques in the ewe peroneal-nerve model.274 Clinically, Taylor and Ham reported the first vascularized nerve graft when they harvested the superficial branch of the radial nerve with a segment of microvascularly anastomosed radial artery to reconstruct a 22-cm median-nerve defect.275 Since that time, vascularized nerve grafts have been used to facilitate axonal regeneration through grafts traversing scarred wound beds, limiting central graft ischemia in larger diameter nerve trunks, and functioning as vascularized carriers for nonvascularized nerve grafts. The advantages of vascularized peripheral-nerve grafts have been identified in a number of animal studies. Vascularized nerve grafts decrease the concentrations of infiltrating fibroblasts and support increased myelination, nerve-fiber diameter, and functional recovery.276,277 Based on the theoretical advantages of vascularized nerve grafts and some favorable animal studies, patterns of blood supply to human peripheral nerves and candidate human vascularized peripheral-nerve grafts have been sought. Breidenbach and Terzis developed the first classification system, identifying three vascular patterns: no dominant pedicle, one dominant pedicle, and multiple dominant pedicles.278 More recently, el-Berrany and colleagues also classified arterial blood supply to the superficial branch of the radial nerve, ulnar nerve, sural nerve, saphenous nerve, and the deep and superficial peroneal nerves based on the presence or absence of dominant arterial pedicles.279 Defining usable vascularized nerve grafts in humans has enabled their successful clinical application in neural defects exceeding 20 cm in both the upper and lower extremity.280,281 Currently, vascularized nerve grafts are clinically indicated only when large-caliber nerve grafts, such as the ulnar nerve, are required,6 but are not needed if small-caliber grafts, such as the sural nerve, are used.

1.13 Accelerated Nerve Regeneration and FK-506 (Tacrolimus) Following peripheral-nerve injury and reconstruction, the time required for nerve regeneration is a major factor contributing to suboptimal return of motor function. During regeneration, the denervated muscle begins to atrophy, causing profound and irreversible muscle damage resulting in poor functional recovery.89,156–158 Thus, the ability to accelerate nerve regeneration increases the potential for positive functional outcomes following peripheral-nerve injury. Accordingly, identification and investigation of therapeutic strategies that accelerate nerve regeneration are essential to advancing the treatment of peripheral-nerve injury. One such strategy is use of the immunosuppressant drug FK-506 (tacrolimus) that, which was isolated in 1984 from a soil sample obtained in Tsukuba, Japan, containing the bacteria of the strain Streptomyces.282,283 It has been used primarily as an immuno-

suppressant in solid-organ transplant recipients. However, a fortuitous discovery revealed that FK-506 enhances nerve regeneration and functional recovery following nerve injury.284, 285 Subsequent investigation found that FK-506 demonstrates this effect in multiple types of peripheral-nerve injury (▶ Fig. 1.16).286–293 FK-506’s neuroenhancing effect is a dose-dependent response and significant even at subimmunosuppressive doses.291 It has been shown that the combination of therapeutic-dosed FK-506 with costimulatory blockade (CSB), another immunosuppressive regimen, abrogates the nerve-regenerationenhancing abilities of FK-506. In contrast, a subtherapeutic dose of FK-506, in combination with CSB, enhances nerve regeneration, demonstrating that combinations of immunomodulatory regimens affect nerve regeneration.292 The timing of FK-506 delivery affects its neuroenhancing activity. Delivery of FK-506 from 1 to 3 days before nerve injury enhances nerve regeneration as compared to administration at the time of nerve injury (▶ Fig. 1.17).286,289,293 Despite its positive neuroregenerative effects, the systemic immunosuppressive properties of FK-506 make it undesirable for long-term use in peripheral-nerve regeneration. As a result, the neuroenhancing properties of FK-506 can only be used in the treatment of patients with nerve allografts and limb-transplant procedures where the immunosuppressive effects are imperative to prevent rejections. Consequently, ongoing studies are directed toward separating the neuroenhancing properties of FK-506 from its immunosuppressive properties. FK-506 acts directly on neurons to enhance axonal regeneration through binding to heat shock protein 90 (Hsp-90) and disrupting the steroid-receptor complex.294 Disruption of the steroid-receptor complex leads to dissociation of p23, increased phosphorylation of extracellular signal-regulated kinase 1/2 (erk1/2),295 and ultimately accelerated growth of injured axons through expression of growth-associated protein 43 (GAP43) mRNA.296 In vitro studies of other nonimmunosuppressive agents that bind Hsp-90 have also shown enhanced neurite extension in neuronal cell cultures.297–299 These Hsp-90 binding agents have yet to be extensively evaluated for their ability to enhance peripheral nerve regeneration in vivo, although studies are ongoing. Other nonimmunosuppressant analogues of FK-506 that have shown promise in vitro have shown little ability to enhance nerve regeneration in vivo.297 Interestingly, increased levels of calcineurin (which FK-506 inhibits in vivo) reduce the activation of the innate immune response after peripheral-nerve injury.300 As was discussed in an earlier section devoted to the mechanisms of neurodegeneration, suppression of the innate immune response leads to decreased wallerian degeneration. Delays in wallerian degeneration in the distal nerve stump negatively affect nerve regeneration.77 This suggests that FK-506 may also stimulate nerve regeneration by enhancing the innate immune response’s role in wallerian degeneration through suppression of calcineurin.

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1.14 Electrical Stimulation and Nerve Regeneration The use of electrical stimulation has long been investigated as a potential means to accelerate or augment functional recovery

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Anatomy and Physiology for the Peripheral Nerve Surgeon

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Fig. 1.16 FK-506 accelerates nerve regeneration in all levels of nerve injury. (a) Walking track analysis and the measurement of print length factor (PLF) in rodents is an established method of evaluating functional recovery following nerve injury. PLF is inversely proportional to the return of function. FK-506 enhances functional recovery following (b) crush, (c) transection, and (d) nerve graft. (Fig. 1.16b is adapted with permission from Lee M, Doolabh VB, et al. FK506 promotes functional recovery in crushed rat sciatic nerve. Muscle Nerve 2000;23(4): 633−640. Fig. 1.16c is adapted with permission from Jost SC, et al. Acceleration of peripheral nerve regeneration following FK506 administration. Restor Neurol Neurosci 2000;17(1):39 −44. Fig. 1.16d is adapted with permission from Doolabh VB, et al. FK506 accelerates functional recovery following nerve grafting in a rat model. Plast Reconstr Surg 1999;103(7):1928−1936.)

following nerve injury. Its use as a therapeutic strategy evolved out of seminal studies by Hoffman, who demonstrated that ventral electrical stimulation of the lumbar spinal cord enhanced axonal sprouting from newly transected proximal sciatic nerve stumps.301 The effects demonstrated by Hoffman were presumably a result of activation of motoneurons that reside in the spinal cord. Subsequent studies built on these initial findings by investigating the effect of electrical stimulation administered directly to the injured nerve. Nix and Hopf stimulated the soleus nerve of a rabbit following a crush injury and were the first to report accelerated recovery of muscle function. 302 These early studies demonstrated that electric simulation has the potential to augment functional recovery and, because the depolarization of an axon initiates bidirectional action potentials, provided further evidence that its effect was mediated through electrical activation of motoneurons in the spinal cord. Unlike FK-506, electrical simulation has been shown to have only a temporary effect on regeneration. Gordon and colleagues demonstrated that electrical stimulation significantly increased the number of motoneurons after injury, but the acceleration

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was found to be due to enhanced axonal growth across the nerve-repair site and not due to an accelerated rate of axonal regeneration.303,304 Thus, electrical stimulation only elicits an effect early after nerve injury. These findings were later confirmed at the molecular level. Using qRT-PCR (quantitative reverse transcription polymerase chain reaction), electrical stimulation was shown to enhance expression of neural regenerative genes, such as GAP43, β-tubulin, and BDNF, in regenerating neurons temporarily for approximately 2 days postrepair.305,306 The 2-day time period is sufficient to enhance the ability of axons to traverse the injury site. For this reason, electrical stimulation’s ability to accelerate functional recovery is limited to decreasing the time axons require to cross the injury site. This time is minimal in crush injuries and can be up to 1 month in transection repairs. This limitation may explain why in a relatively short model of nerve regeneration, such as the rodent facial nerve, electrical stimulation has been shown to accelerate307 and have no beneficial effect309 on functional recovery. Therefore, electrical stimulation may provide the greatest benefits by enhancing axonal growth from neurons with limited

Anatomy and Physiology for the Peripheral Nerve Surgeon

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Fig. 1.17 Investigation of FK-506 has determined its neuroregenerative parameters. In this figure, experimental counts of the number of regenerative nerve fibers are compared under different parameters of FK-506 administration. (a) Administration of FK-506 3 days prior to nerve injury enhances nerve regeneration above that with FK-506 delivered immediately and that in controls receiving no FK-506. (b) Delaying the administration of FK-506 following nerve injury diminishes its neuroregenerative effect. (c) FK-506 administration is a dose-dependent effect and has been shown to enhance regeneration even at subimmunosuppressive levels. (Fig. 1.17a is adapted with permission from Snyder AK, et al. Neuroregenerative effects of preinjury FK-506 administration. Plast Reconstr Surg 2006;118(2):360−367. Fig. 1.17b is adapted with permission from Sobol JB, et al. Effects of delaying FK-506 administration on neuroregeneration in a rodent model. J Recon Micro 2003;19:113−118. Fig. 1.17c is adapted with permission from Yang RK, et al. Dose-dependent effects of FK-506 on neuroregeneration in a rat model. Plast Recon Surg 2003;112:1832−1840.)

ability to extend axons due to chronic axotomy and denervation308 or multiple suture sites in nerve grafting. When combined with other therapies, electrical stimulation provides an additive effect. Electrical stimulation in combination with exercise increases functional recovery following nerve injury above either treatment alone.310 The combination of gonadal steroids and electrical stimulation also demonstrates an additive effect on functional recovery that is above either treatment alone.311 Interestingly, either exercise or gonadal steroid treatment alone enhances functional recovery to a level similar to singular treatment with electrical stimulation. This suggests that in the clinic other routine, noninvasive treatments such as physical therapy may already provide the same functional benefit as invasive treatments with electrical stimulation. Furthermore, it may explain why clinical treatments using electrical stimulation have shown improvements in sensitive electrophysiological measure of functional recovery but no tangible increases in function for patients. 312 Electrical stimulation elicits its neuroenhancing effects by increasing the production of neurotrophic factors and tyrosine kinase (Trk) receptor expression in regenerating motoneurons early after injury.313 Using transgenic animals, investigators

demonstrated that neuroenhancement from electrical stimulation is dependent on the activation of TrkB on the surface of the neuron by its ligands (BDNF, NT-4, and NT-5) originating from motoneurons themselves.314 Thus, current data suggest that electrical simulation works in part through a motoneuronmediated, autocrine-like mechanism. In addition to the effects on motoneurons, electrical stimulation enhances the regenerative activity of Schwann cells following nerve injury. It potentiates myelin maturation after peripheral-nerve regeneration through enhanced BDNF signaling315 and causes a calciumdependent release of growth factors from Schwann cells. 316 Although less attention has been paid to the effect on Schwann cells, it is likely that they play a significant role on the neuroenhancing properties of electrical stimulation. As mentioned in the section on preferential motor reinnervation, the accurate reinnervation of the appropriate end-organ by regenerating axons is a significant impediment to functional recovery. Some investigators have suggested that electrical stimulation of the nerve following injury enhances preferential reinnervation of muscle by axons from motoneurons. Brushart and colleagues, using the femoral-nerve model of PMR, demonstrated that 1 hour of electrical stimulation was sufficient to

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Anatomy and Physiology for the Peripheral Nerve Surgeon enhance the normal reinnervation of muscle. The percentage of regenerating neurons that both originally served muscle and returned to muscle after nerve repair increased from 40% without simulation to 75% with stimulation.317 Although others using the same model have noted beneficial effects on functional recovery, they did not observe enhanced preferential reinnervation by motoneurons of muscle as opposed to skin.318 Hamilton et al observed that acute electrical stimulation promoted enhanced axon regeneration, but did so with decreased fidelity of muscle reinnervation and increased reinnervation of multiple muscle targets by the same motoneuron. They found that functional recovery was neither improved nor degraded, which suggests that compensatory changes in the inputs of the spinal circuits driving locomotion may mask the misdirection of regenerating axons in the periphery.319 The ability of electrical stimulation to preferentially guide axons to the appropriate end-organ has yet to be determined, and its potential to cause aberrant axonal sprouting and inappropriate reinnervation merits further exploration. Another application of electrical simulation following nerve injury that has been investigated is its administration to the denervated muscle. Some studies have shown that electrical stimulation of the muscle enhances functional recovery following peripheral nerve injury.320 Although others have demonstrated that stimulation of the muscle hinders functional recovery by reducing the number of innervated motor end plates, failing to reduce the proportion of polyinnervated motor end plates,321 decreasing muscle-fiber diameter, and increasing muscle atrophy.322 In conclusion, electrical stimulation has shown some promise as a potential therapeutic strategy to enhance function following nerve injury, but more extensive laboratory research is needed before it merits mass translation to the clinic.

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1.15 End-to-Side and Reverse Endto-Side Nerve Transfer End-to-side (ETS) nerve transfer, whereby the distal portion of a transected nerve is reinnervated by coapting it into the side of an intact donor nerve, represents a technique first described at the turn of the 19th century and subsequently reintroduced starting in the early 1990s.323 ETS transfer remains one of the more controversial areas within peripheral-nerve surgery, fueled by numerous contradictory studies. With this subject having been extensively investigated,324–328 some evidence suggests that ETS reconstruction will result in some sensory collateral sprouting. This phenomenon is seen daily in patients with sensory-nerve-graft donor sites recovering some sensation over time. By constrast, we have definitely shown that motor axons will sprout only if injured. Again, we see this clinically with the hypoglossal-facial nerve experience. The end-to-end repair gave “too much” power and was replaced with the ETS hypoglossal-to-facial nerve repair, but this reconstruction was underpowered. As a happy medium, a small neurectomy in the hypoglossal nerve diverts a sufficient number of axons to the distal facial nerve stump to provide sufficient but not excessive power to the facial mimetics. Studies regarding this technique include quantifying the number of axons recruited by ETS repair and the functional deficit inflicted upon the donor nerve.329 Some have suggested that collateral axonal sprouts

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repopulate the terminal limb without axotomy or functional consequence, attributing this spontaneous phenomenon to neurotrophic influences.330,331 Others suggest that an epineurotomy or perineurotomy, exposing but not injuring donor axons, facilitates spontaneous collateral sprouting.332 Other researchers have shown that regenerative sprouting induced by a deliberate axotomy is required to induce some terminal sprouts to regenerate down the recipient pathway rather than the original donor-nerve pathway.326 Interestingly, even if axotomy with donor-nerve injury is required, this may not significantly impact function, owing to the redundancy and plasticity of donor-nerve motor-end-plate innervation.328,333–338 We have taken advantage of transgenic mouse models coupled with high-resolution in vivo and confocal imaging to clearly determine if axotomy is a necessary component of effective ETS repair (▶ Fig. 1.18).328 The power of the fluorescent rodent model is clearly demonstrated in this study. In the conventional rodent model, the same investigator using the same repair techniques came to the conclusion that uninjured motor axons would spontaneously sprout without injury.339 The same investigator, using these techniques in the fluorescent protein-expressing mouse, was then able to unequivocally show that injury was a prerequisite for sprouting, corroborating this finding with real-time imaging, confocal microscopy, electron microscopy, transcutaneous imaging, Western blot analysis of myelin-based proteins, and staining for proregenerative transcription factors. Specifically, our data clearly show that to obtain significant morphologic evidence of nerve regeneration, motor-end-plate and cutaneous reinnervation, coupled with molecular markers of reinnervation, an injury is required. This is not surprising when the tenets of neuroscience are considered, in particular the fact that during development, a single neuron can initially extend numerous axonal projections that differentially respond to local guidance cues, but that one-to-one relationships between neurons and motor units are established after synapse elimination.340,341 Despite these findings, ETS nerve repair may still represent a viable reconstructive alternative in specific circumstances where other reconstructive options are unavailable, such as in the restoration of noncritical sensation in the hand. In these circumstances, the ETS repair is, in effect, a form of nerve transfer where axons are diverted through a modest neurectomy within a single fascicle of the donor nerve, rather than an entire fascicle. Donor morbidity is avoided by limiting the size of the neurectomy but must be tempered with producing a sufficiently large donor injury to stimulate sufficient sprouting. In this regard, ETS repair is simply a form of end-to-end repair that ultimately maintains one-to-one relationships between neurons and their targets. Another situation where ETS nerve repair is clinically indicated is in the context of harvesting a donor sensory nerve. We suggest that ETS suture of the distal stump of the divided donor sensory nerve to an adjacent uninjured sensory nerve will reinnervate the donor-site territory, thereby providing sensory recovery and reduced donor-site pain. 342 Unlike motor axons, which will only sprout with a transection (traumatic sprouting), sensory axons will spontaneously sprout without injury.328 In a RETS nerve transfer, an expendable donor nerve is transected distally, and the donor nerve is transferred to the side of

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Fig. 1.18 End-to-side (ETS) repair requires nerve injury to initiate graft innervation. In a study by Hayashi et al, the Mackinnon group investigated the parameters surrounding ETS nerve repair. (a,b,c) These images demonstrate the nerve-injury model in which the distal end of the peroneal nerve is sutured into the side of the tibial nerve in transgenic Thy-1 YFP mice whose axons express a fluorescent protein that allows the researchers to visually monitor axonal regeneration. (d) Depiction of the axons in an uninjured ETS repair failing to grow into the grafted peroneal nerve. (e,f) In contrast, a crush injury above the ETS graft site allows regenerating axons to grow into the grafter peroneal nerve. (Adapted with permission from Hayashi A, et al. Axotomy or compression is required for axonal sprouting following end-to-side neurorrhaphy. Exp Neurol 2008;211(2):539−550.)

the injured distal nerve, close to the target organ. This is distinguished from an ETS, where the distal end of an injured nerve is transferred to the side of an intact donor nerve. In theory, the RETS nerve transfer can provide additional motor

axons to “supercharge” the regenerating nerve, as well as provide earlier muscle reinnervation to “babysit” the target muscle until native axons from the muscle’s original motor nerve regenerate.

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Anatomy and Physiology for the Peripheral Nerve Surgeon Published data on RETS nerve transfer is relatively scarce. In 2005 Isaacs et al demonstrated that donor motor axons could grow through a RETS nerve transfer and successfully reinnervate target muscle, so long as the recipient nerve had been injured and the muscle had undergone denervation. 343 Fujiwara et al then performed a series of experiments attempting to “supercharge” a primary nerve repair with the addition of a RETS nerve transfer. In their model of a RETS transfer of the left sciatic nerve to the right sciatic nerve, they saw better sensory and motor functional recovery than with transection and repair of the right sciatic nerve without “supercharging.”344 Finally, Isaacs et al again published a study on RETS nerve repair comparing transection with primary repair to transection with primary repair plus RETS nerve transfer. By performing muscle force testing simultaneously with the transection of the tibial and peroneal nerves at various levels (thereby preferentially directing electrical stimulation), they determined that both tibial and peroneal axons had achieved significant reinnervation of the target muscle.345 Mackinnon and colleagues have developed a model of RETS that comprehensively evaluates the surgical technique in a rodent. The model uses the injured tibial nerve as the recipient and the transected peroneal nerve as the donor. It includes a true negative control consisting of a chronic denervation of the tibial nerve in which the proximal stump is doubly ligated and cauterized to prevent proximal contamination.346 With the inclusion of a true positive control consisting of an end-to-end (ETE) coaptation to evaluate maximum axonal input from the peroneal nerve, the model provides a comprehensive evaluation of the efficiency and success of RETS nerve transfers. Evaluation of this model demonstrated statistically similar numbers of regenerating nerve fibers in ETE and RETS animals with no regeneration in the chronically denervated negative controls.46 Muscle-mass preservation was similar in the ETE and RETS groups and significantly better than in negative controls. Additionally, a transgenic rat (Thy-1 GFP) whose axons express green fluorescent protein347 was used to visualize regenerating axons, and robust axonal regeneration across the RETS coaptation of Thy1-GFP rats was confirmed. To our knowledge, the study represents the first data to suggest that the RETS technique can result in an equivalent number of donated motor axons as a standard ETE transfer. If this should prove true in a clinical setting, RETS nerve transfer could replace ETE nerve transfer in cases where even the slightest chance of native axonal regeneration exists.45

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1.16 Neuromuscular Anatomy and Physiology Under normal, physiologic conditions, a small percentage of neuromuscular junctions are denervated due to synaptic instability or axonal dropout before becoming rapidly reinnervated.348 At baseline, adult acetylcholine receptors also demonstrate a surprising degree of dynamism. Having undergone a molecular and topologic switch from the γ-subunit-containing α2βδγ neonatal form to the homologous ε-subunit-containing α2βδε composition, adult acetylcholine receptors not only demonstrate altered Ca2+ permeability349–351 but are also more resistant to disassembly. Also, in adult mice, 9% of acetylcholine receptors are lost per day (or 0.4%/h) but are rapidly replaced, thus maintaining a net

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neutral number of receptors in active adult muscle.350 The activity of acetylcholine receptors is further supported by studies using fluorescent recovery after photobleaching studies showing that untethered acetylcholine receptors stay in the same place for as little as 8 hours, whereas clustered acetylcholine receptors are immobile and moored to the cystoskeleton so long as neuromuscular activity persists.350,351 This dynamic, background process is not considered pathologic, as there is a stable net number of innervated motor end plates and functional receptors. Following axotomy, or neuronal cell death, however, there is a dramatic increase in denervated motor end plates, leading to physiologic changes in muscle fibers occurring concurrent with nerve regeneration. Upon denervation, muscle fibers remain viable, but a series of proteasemediated processes regulated by the ubiquitin-proteosome pathway lead to the catabolization of myosin and actin filaments. Myofibrils are reabsorbed, resulting in myocyte atrophy, and the enlarging extracellular space fills with collagen. The persistent absence of myofibrils signals the demise of the myocyte, leading to a permanent deterioration in muscle function that cannot be salvaged with reinnervation alone.159 Denervation-induced differences are also observed at the receptor level. Denervated acetylcholine receptors recapitulate their development roots, reverting to the expression of the γinstead of ε-containing subunit. The persistence, distribution, and organization of acetylcholine receptors into clusters are also deleteriously affected by the loss of electrical activity that accompanies denervation. Whereas acetylcholine receptors are lost but rapidly replaced at 0.4% per hour with normal electrical activity, cessation of neurotransmission with pharmacologic blockade accelerates the loss of acetylcholine receptors to 4% per hour with no replacement at the crests of postsynaptic folds.350 Clusters of acetylcholine receptors located at the crests of postsynaptic folds migrate into perisynaptic regions, where they are subjected to the endocytotic machinery of the myocyte for recycling or degradation.352 Importantly, experimental evidence in mice suggests that the postsynaptic apparatus of adults is more stable than that found in neonates. Clusters of acetylcholine receptors that are quickly disassembled in neonates following denervation retain their organization for many weeks following denervation in adults in the face of ongoing myocyte atrophy.353,354 This difference is clearly unrelated to the composition of the acetylcholine receptor, which, as discussed above, reverts to its embryonic form during periods of denervation. Rather, differences in the adult versus neonatal basal lamina and cytoskeleton and their links to one another may be involved. The dystrophin-glycoprotein complex is a key candidate in this regard, given that mutations of laminin within the basal lamina, sarcoglycans in the membrane, and dystrophin in the cytoskeleton are implicated in the development of muscular dystrophy in humans and experimental animals.352,355 Denervation subjects myocytes not only to atrophy but also to a change in muscle-fiber composition. Normally, myocytes contain both type I (slow-twitch) and type II (fasttwitch) myosin heavy chains (MHCs). With 1 week of denervation, there is a significant shift toward type II MHCs that resemble type II fibers physiologically in terms of calcium regulation within the sarcoplasmic reticulum, contractility, and fatiguability.356 A specific complement of type II MHC

Anatomy and Physiology for the Peripheral Nerve Surgeon isoforms characteristic of denervation is also observed, suggesting that myocyte MHCs revert to a predetermined denervated phenotype that can be differentially regulated by motor-neuron reinnervation.357 Functional reinnervation depends on plasticity not only in the CNS, but also within muscle. A motor unit is defined as the neuromuscular territory innervated by a single motor neuron with a single neuron and axon with multiple terminal branches. Single motor units can enlarge up to about five times their original size, however, resulting in the ability to compensate for up to 80% (70–80% compensation) of motoneuron loss without a decrease in contractile muscle force.358 The myocyte end-organs of a single motor unit are spatially dispersed within a single muscle so that two myocytes belonging to a single motor unit are rarely in direct contact. Following a crush injury, the combination of intact endoneurial tubes and passive guidance cues facilitates motor-unit reinnervation that is ≥ 95% efficient.43 However, despite meticulous repair, transection injury leads to a disorganized pattern of reinnervation, whereby myocytes in close proximity to one another—rather than distant myocytes that were originally part of the motor unit—are reinnervated. Disparate myocytes are thus recruited and undergo an unintended shift in MHC isoform expression. Ultimately, groups of adjacent myocytes belonging to the same motor unit with similar MHC isoform expression (also known as fiber type grouping) replace the more heterogeneous normal anatomy. This change forces a latent period following reinnervation where muscle contractility is gradually re-established with restoration of muscle-fiber types capable of contracting appropriately.359 After prolonged periods of denervation, blood flow is reduced, as evidenced by an ~ 90% reduction in capillary density and a near-avascular state within 18 months of denervation.360,361 Regions of necrosis and areas of myofibrillar disorganization that are supplanted by collagen deposition lead to a reduction in the ability of muscle tissue to generate force per square area, resulting in a lower specific force capacity.362 The relatively poor functional recovery that accompanies prolonged periods of denervation may be due, in part, to a progressively waning affinity between regenerating axons and denervated myocytes. In the first 2 months after injury, denervated myocytes upregulate the expression of transcription factors, such as myogenin MRF4 (myogenenic factor 4), MyoD (myoblast determination protein), Myf-5 (myogenic factor 5), and ID-1 (DNA-binding protein inhibitor ID-1). 334, 363–366 In turn, these transcription factors orchestrate a phenotypic change in the pattern and distribution of surface molecules, such as neural cell adhesion molecules and acetylcholine receptors, to resemble the embryonic state. 366 However, if denervation persists beyond a 2-month “grace” period, the phenotypic profile of denervated muscle reverts to the adult state, and neuromuscular synapse formation can be impaired despite the presence of regenerated axons. When muscle contraction is not re-established in a timely manner, structural changes such as collagen deposition, fibrosis, and a hypovascular state progress so that impaired muscle function results from structural changes to the muscle itself, as well as its inadequate connection with the peripheral nervous system.

1.16.1 Pathophysiology of Compression Neuropathy

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Recent data at the cellular and subcellular levels support earlier experimental work that found that chronic nerve compression is a progressive problem beginning with blood–nerve barrier changes, followed by subperineurial edema and fibrosis, focal demylination localized to axons “seeing the greatest presence of ischemia,” and then progressing to diffuse demyelination and finally axonal degeneration.367–369 For example, chronic nerve compression does not result in wallerian degeneration, at least in the earlier phases; instead, it predominantly affects Schwann cells rather than axons.370 Clinically, compression neuropathy is more common in the setting of repeated episodes of compression that can lead to ischemia and edema formation in the subendoneurial space.371 Abnormally high fluid pressures surrounding the median nerve of patients diagnosed with carpal tunnel syndrome due to edema formation limit microvascular blood flow within the nerve, contributing to localized ischemia. The synovium, initially edematous, can become fibrotic, but there is little evidence of acute inflammation in biopsy specimens as compared to control specimens from healthy subjects.372,373 It is also likely that the affected nerve is tethered by scar tissue, which limits nerve gliding and contributes to ischemia by limiting the total number of nutrient blood vessels, by attenuating their diameter at rest, or, during movement, by causing kinking.374–376 Finally, localized mechanical pressures from structures such as the flexor retinaculum and the tendinous leading edge of muscles over nerves at joints may discretely cause localized areas of nerve compression (▶ Fig. 1.19).377 Increased tension on a nerve through positional or postural changes can significantly affect pressures around a nerve, leading to chronic nerve compression. In the carpal tunnel, for example, wrist extension increases carpal tunnel pressures to 40 mm Hg, and a finger pinch of 1.2 kg has the same effect. The mechanical effects of these postural changes have not been studied beyond 10 minutes, but during this limited time frame, no mechanism for alleviating these potentially damaging pressures has been identified.378–382 Even pressures as low as 20 mm Hg reduce venous outflow, and delayed nerve injury is observed when 30 mm Hg is applied to a rat sciatic nerve for 2 hours.383,384 Elbow flexion, knee extension, and ankle pronation increase tension in the ulnar, peroneal, and tibial nerves, respectively. The duration and intensity of nerve compression result in a spectrum of pathophysiologic processes ranging from an acute crush to chronic nerve compression (▶ Fig. 1.20). As such, findings from a report of the study of a more chronic nerve injury are unlikely to apply to an acute injury. Pressures of 20 to 30 mm Hg interfere with venous blood flow, whereas pressures of 35 to 50 mm Hg reduce capillary flow. If applied for 4 hours, pressures as low at 30 mm Hg increase endoneurial edema for at least 24 hours, as no lymphatic drainage mechanism functioning as a pressure release is available.385–387 Although this level of injury attenuates the microcirculation, a pressure of 70 mm Hg applied for 4 hours causes complete ischemia.388,389 When an inflatable cuff is used to apply 30 or 80 mm Hg of pressure to the rat sciatic nerve for 2 hours, detectable differences are also noted.383,384 Endoneurial edema, forming within 4 hours in the injured nerves, was found

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Anatomy and Physiology for the Peripheral Nerve Surgeon

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Fig. 1.19 Transverse section of a primate median nerve (toluidine blue). (a) Transverse section of a normal median nerve. The perineurium has a thin, healthy appearance (arrows) (100x). (b) At a higher magnification, a population of normal nerve fibers is seen (400x). (c) After 12 months of nerve compression, thickening of the internal epineurium and the perineurium is noted (100x). (d) At a higher magnification, nerve-fiber changes with thinning of the myelin are seen (400x).

to last for at least 28 days and was accompanied by early inflammation and fibrin deposition. This acute response was followed within days by the proliferation of endoneurial fibroblasts and capillary endothelium suggestive of angiogenesis.383,384 The development of animal models that more accurately simulate human nerve compression has significantly influenced our understanding of its pathophysiology. For example, some investigators have been critical of previous rodent models where a cuff was used because the degree of compressive pressure could not be controlled or easily quantified.390 To overcome this shortcoming, an externally adjustable small balloon catheter was implanted into the carpal tunnel of a rabbit model. Neuropathies resulting from applied pressures of 40 to 80 mm Hg were then evaluated.388,389 The rabbit model could also be used to study the effects of cumulative trauma by repeated loading. The rabbit carpal tunnel consists of the four flexor digitorum profundus tendons and the median nerve bounded by the flexor retinaculum. As such, the impact of precise stimulation of the rate and force of flexor digitorum profundus tendon contraction on the carpal tunnel could be controlled with a load cell. Not unexpectedly, 40 hours of loading to 15% of peak tetanic force at a 1-Hz repetition rate for 2 hours, 3

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days a week for 7 weeks, led to a significant increase in motor latency.391 The study of chronic nerve compression cannot rely solely on large-animal-model data, as the use of these animals for laboratory research is understandably limited by governing agencies. By extension, the majority of techniques and tools used to study molecular mechanisms have been optimized for the mouse or rat. The use of short silicone tubes secured loosely to the sciatic or sural nerves of the rat is probably the most common method in animal models of nerve compression.367,392 The key results from these studies were the development of pain and histologically demonstrable changes from 1 to 3 months following cuff application, with histopathologic changes that mimicked those seen in human compression-neuropathy specimens. In general, these studies showed the development of perineural edema and the breakdown of the blood–nerve barrier within days of injury, followed by the recruitment of macrophages, type I collagen deposition, and the development of subperineurial and then intrafascicular fibrosis. Localized demyelination followed by remyelination occurred within 14 to 28 days of injury. Nerve-fiber degeneration was considered a late outcome of chronic compressive neuropathy. This silicone-cuff model

Anatomy and Physiology for the Peripheral Nerve Surgeon

1

Fig. 1.20 Schematic diagram outlining the pathogenesis of chronic nerve compression. (a) The normal nerve is shown for comparison. (b) The changes with chronic nerve compression are noted. The initial changes involve changes in the blood–nerve barrier: endoneurial and subperineurial edema will be seen relating to increased endoneurial fluid pressure. The next histologic changes to occur are those involving the connective-tissue layers. Increased perineurial and epineurial thickening are noted. Localized nerve-fiber changes then occur. Some fascicles appear entirely normal; others demonstrate stressed segmental demyelination of the large fibers. The unmyelinated fibers show evidence of regeneration, with a new population of very small unmyelinated fibers noted. Central fascicles or the central fibers within a given fascicle are usually spared. With progression of either the degree of compression or the duration of the nerve compression, diffuse fiber changes are noted across all fascicles and degeneration is apparent in both the myelinated and the unmyelinated nerve fibers.

produced identical changes to those seen in human specimens of chronic nerve compression, which are rare. Important findings were the slow progression of pathologic findings from just blood–nerve barrier changes alone to localized demyelination, followed by diffuse degeneration and axonal injury. The localized nature of pathology, with some normal fascicles adjacent to others that showed pathology, explains the variability in patient presentation. For example, patients with carpal tunnel syndrome will eventually present with just long- and ringfinger numbness and later with index-finger and thumb complaints. Electron microscopy of the unmyelinated fibers in

patients with radial sensory-nerve compression showed that the unmyelinated fibers underwent changes before the myelinated fibers. Similarly, the pathologic changes occur before demyelination and axonal injury, in keeping with symptomatic patients with normal electrical studies. Using the silicone-cuff model, the merits of neurolysis were investigated. Although removal of the silicone tube reversed most histologic findings, internal neurolysis caused no damage but did not improve recovery over removal of the silicone cuff alone. A series of elegant studies by Gupta and colleagues has shed new light on the pathophysiology of chronic compressive

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Fig. 1.21 Transverse section of the sciatic nerve of a rat (toluidine blue). (a) After 2 months of compression with a 1.5-mm-internal-diameter silicone tube, the nerve looked essentially normal (400x). (b) After 2 months of compression with a 1.1-mm-internal-diameter tube, subperineurial edema is noted. A fallout in the large myelinated fiber group is noted at the periphery of the fascicle. EP, epineurium (400x).

neuropathy and has represented a paradigm shift from an axonal to Schwann cell–mediated disease process. To study this hypothesis, Gupta et al used a 1-cm-long compressive cuff with an internal diameter of 1.3 mm and an external diameter of 2.0 mm on the sciatic nerves of age- and size-matched adult SpragueDawley rats.369,393 This model was designed to simulate the forces of sheer stress, compression, and longitudinal stretch that play a role in chronic nerve compression (▶ Fig. 1.21). The chronicity of this injury model was confirmed by demonstrating significant reductions in nerve conduction velocity starting at 3 months that fell to 65% of those in uninjured controls by 6 months. Using this model of chronic nerve compression, Gupta et al refuted the long-held belief that wallerian degeneration occurs with chronic nerve compression. By 1 month, there was morphometric evidence for a significant reduction in myelin thickness along the peripheral diameter of a nerve’s cross section, and at 8 months, there was an overall 63% reduction in myelin thickness, which fit well with the electrophysiologic data. Even after recovery from compressive neuropathy, preinjury levels of myelin thickness and internodal distance were not restored, leading to delayed nerve conduction velocity. Internodal dis-

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tance measures the spacing between the nodes of Ranvier, or gaps in myelin where the axolemma is depolarized and saltatory conduction maintained. A reduction in internodal length increases the number of depolarizations that must occur along a particular axon to transmit a depolarizing action potential. This process would slow down nerve conduction velocity. 394 In fact, in periaxin knockout mice that are characterized by decreased internodal lengths but normal axonal diameters and myelin thickness, there is a 50% decrease in nerve conduction velocity.395 This suggests that the decrease in nerve conduction velocity associated with chronic nerve compression injury may be the result of a new population of phenotypically altered Schwann cells that produce myelin with decreased internodal lengths. In support of the notion that wallerian degeneration is not an outcome of chronic compressive neuropathy, no difference in the overall number of axons accompanied a reduction in myelin thickness. 395 Concurrent with a reduction in myelin thickness was inhibition of myelin-associated glycoprotein (MAG) expression and an increase in macrophage recruitment, Schwann-cell apoptosis, proliferation, and vascular endothelial growth factor (VEGF) expression.370,396–400

Anatomy and Physiology for the Peripheral Nerve Surgeon MAG expression, which reduces axonal sprouting by inhibiting CREB-mediated signaling,401,402 is downregulated by Schwann cells in response to sustained shear stress.400 This alteration in Schwann-cell phenotype occurs independent of neuronal signaling. The recruitment of macrophages occurs in a delayed fashion and may be triggered by VEGF signaling.399 Assays for inducible nitric oxide synthase (iNOS), a free-radical gas messenger common to many biologic systems and a product of macrophages, demonstrated its presence predominantly in the deeper perineurium of nerve cross sections. 403 The absence of iNOS in the periphery of nerve cross sections suggested that its induction was driven by ischemia, as its expression was initiated in the central watershed area of the nerve, where it would be most susceptible to reduced blood flow. Specific findings from this work suggested an increase in macrophages at 1 month after nerve compression that was localized to the peripheral one-third of the nerve before demonstrating a more homogeneous distribution in the ensuing months. Elevated levels of iNOS were noted in the perineurium of nerve cross sections proximal to the site of compression 3 months prior to injury, reached the site of compression at 5 months, and peaked at 9 months. By contrast, acute nerve injury resulting in wallerian degeneration is characterized by a rapid rise in macrophages that is significantly elevated within 24 to 96 hours and peaks at 14 days before declining at 21 days. Macrophage recruitment, as well as an increase in angiogenesis at the site of nerve compression injury, may be regulated by VEGF signaling.399 Schwann-cells are the primary source of VEGF in the peripheral nervous system, as VEGF mRNA transcripts colocalize to Schwann-cell nuclei during in situ hybridization when a VEGF riboprobe is used. Increased VEGF expression is noted to significantly rise 2 weeks following chronic nerve compression and peaks at 1 month, before demonstrating a drop-off at 2 months. Despite falling from peak values, VEGF is still elevated relative to baseline levels 6 months after injury. Although VEGF signaling probably contributes to angiogenesis in the vicinity of compressed nerve specimens 8 months after injury, it probably does not serve as the predominant Schwanncell mitogen. In fact, Gupta and Steward’s work has also demonstrated an intriguing interplay between Schwann-cell apoptosis and proliferation.393 A dramatic rise in Schwann-cell proliferation noted 1 month after chronic nerve compression occurs coincident with the elevation in VEGF levels, thus providing strong temporal evidence that VEGF is not a significant Schwann-cell mitogen. Rather than a molecular signal, then, Schwann-cell proliferation may be induced by low-level shear stress. The application of shear stress to cultured Schwann cells has a mitogenic effect and makes them more receptive to mechanical stimuli at various points during the cell cycle. Similarly, the persistence of intact axons and functional myelin also dissuades one from the previously held belief that wallerian degeneration was triggering this dramatic change in Schwann-cell turnover. By 8 months, Schwann-cell concentrations are still two- to three-fold higher than controls, but there is also a significant amount of apoptosis occurring at this point. Apoptosis, one of the most well-studied forms of programmed cell death, represents a series of molecular events that cause the cell to commit a systematic form of suicide that is triggered by a stimulus such as, in this case, chronic compression. Therefore,

the level of Schwann-cell proliferation is probably significantly higher than the two- to three-fold increase suggested by morphometric data when one considers that another population of Schwann cells is simultaneously dying. Still, even in the peripheral nervous system, this paradoxical increase in both cell proliferation and death is not unique and has been observed in both developmental models and models of wallerian degeneration.149,404

1

1.16.2 Transcutaneous Peripheral-Nerve Imaging Clinically, several diagnostic imaging modalities exist to visualize and evaluate peripheral-nerve injuries, including computed tomography,405,406 ultrasound,407–411 and magnetic resonance imaging.412–416 These modalities depend on changes to tissue morphology at an anatomical level and thus can be used to locate acute peripheral nerve injury. However, existing modalities are not capable of providing detailed information about the extent of injury, the state of chronic nerve injury, or the process of regeneration. Optical imaging modalities have the potential to overcome the shortcomings of existing noninvasive methods by imaging peripheral nerves at the molecular level to quantify the extent of peripheral-nerve injury and subsequent recovery. The potential was first demonstrated by Pan et al in 2003 through the use of Thy1-YFP (thymidylate synthase complementing protein 1– yellow fluorescent protein) transgenic mice in which axonal regeneration (and degeneration) could be visualized and quantified directly through the skin, sparing the need for surgical exposure and animal sacrifice: two factors that limit sampling frequency (▶ Fig. 1.22).153 Although these animals have provided contributions to the study and evaluation of therapeutic strategies for peripheral-nerve injury, their utility is limited.43, 153,155,328,339,347,417 These fluorescent proteins both absorb and emit light in the visible region of 400 to 700 nm, where biologic tissue naturally fluoresces (autofluorescence) 418–420 and scatters light, making transcutaneous imaging of nerves possible only in the small superficial nerves of the mouse. Thus, evaluation of nerve regeneration in large, more clinically relevant nerves through imaging of these proteins requires an invasive surgical procedure to expose the nerve. The need for nerve-specific fluorescent probes or contrast agents has been identified as an achievement that would be of immediate benefit to both patients and surgeons for nervesparing surgery.421 Initial efforts toward the design of both a myelin-specific contrast agent421 and a targeted optical probe422,423 have recently been published (▶ Fig. 1.23). Unfortunately, both the contrast agent and the probe emit light in the visible region, which is outside of the optical window preferred for optical-imaging applications, and they are incapable of providing information about the extent of axonal de- and regeneration, meaning they cannot be used to diagnose or evaluate peripheral-nerve injuries. To overcome the limitations imposed by fluorescent probes used by previous investigators,422–424 near-infrared (NIR) fluorescent optical probes that emit within the therapeutic window from 700 to 1,300 nm can be used. At these wavelengths, light has maximum depth penetration (up to a few centimeters, as compared to 2 mm or less for XFP [fluorescent protein] trans-

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Anatomy and Physiology for the Peripheral Nerve Surgeon

Fig. 1.22 In vivo images of the femoral nerve from Thy1-CFP mice. (a) Bright field image showing the two branches of the femoral nerve, with the motor branch on the bottom and the sensory branch on the top. In the bright field image, the distinct bands of Fontana are visible. (b) Under excitation with 488-nm light, the CFP expressed within the axons gives off light in the visual spectrum. The axons can be seen through the fascia of the nerve.

1

Fig. 1.23 In vivo fluorescent labeling of nerve for surgical reconstruction. (a) A bright field image of an exposed mouse sciatic nerve demonstrating the low visibility of nerve in situ. (b) Fluorescent image of the same sciatic nerve from a Thy1-YFP transgenic mouse whose axons express yellow fluorescent protein. When excited with a certain wavelength of light, YFP emits light in the visual spectrum, and the nerve glows “yellow.” (c) Demonstration of the myelin-specific probe developed by Whitney et al. The probe was injected intravenously into the bloodstream and selectively adheres to nerve tissue with reasonable specificity. (Adapted with permission from Whitney MA, et al. Fluorescent peptides highlight peripheral nerves during surgery in mice. Nat Biotechnol 2011;29:352−356.)

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Anatomy and Physiology for the Peripheral Nerve Surgeon

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Fig. 1.24 Near-infrared (NIR) fluorescent probes for transcutaneous imaging. (a) High-resolution imaging of NIR probes injected into the mouse bloodstream. The vasculature of the ear can be easily identified through the skin. The rate at which the fluorescent probe leaks out of the vasculature depends on the design of the NIR fluorescent cyanine probes. By changing the binding constant (BC) of each probe for bovine serum albumin (BSA, a carrier protein found in the blood), the rate of probe leakage can be controlled. The series of high-magnification images demonstrate this phenomena depicting dyes of decreased BSA binding strength moving from left to right. Decreased binding of BSA allows more of the probe to leak out into the tissue. (b) A similar dye injected into the paw of a rat subcutaneously migrates to the axillary lymph node (ALN) via the lymphatic vessels (LV). The migration of this probe demonstrates the clarity with which the probe can be imaged through the skin and the possible utility of the probe in imaging of nerve. (c) The same animal with the skin removed. (Adapted with permission from Berezin MY, et al. Rational approach to select small peptide molecular probes labeled with fluorescent cyanine dyes for in vivo optical imaging. Biochemistry 2011;50(13): 2691−2700.)

genic proteins) and light scattering by tissues and fluids is minimal, making NIR optical probes ideal for use in imaging applications in vivo (▶ Fig. 1.24).420,425–429 These probes generally consist of a targeting moiety—such as a peptide, protein, or antibody (which acts as a carrier)— coupled to a contrast agent (in this case, an NIR dye). The carrier must take advantage of the presence or upregulation of specific factors, such as cell-specific receptors, in tissues to deliver NIR dyes to a target of interest.420 Examples of this include the labeling of peptides420,425,428,429 or the use of antibodies,430,431 that target cell-surface receptors upregulated in cells, with NIR fluorescent dyes. These carriers bind to the targeted surface receptors, allowing identification of the tissue of interest through noninvasive imaging. An axon-targeted NIR optical probe may allow the evaluation of acute and chronic peripheral-nerve injuries by providing detailed information as to the location and

extent of injury, the state of nerve injury, and the process of axonal de- and regeneration during recovery. All of the aforementioned topics have significant relevance to the peripheral-nerve surgeon. There is no question that advances in basic neuroscience research will translate into more effective therapies for peripheral-nerve-injured patients.

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[398] Gupta R, Rummler LS, Palispis W, et al. Local down-regulation of myelin-associated glycoprotein permits axonal sprouting with chronic nerve compression injury. Exp Neurol 2006;200:418–429 [399] Gupta R, Gray M, Chao T, Bear D, Modafferi E, Mozaffar T. Schwann cells upregulate vascular endothelial growth factor secondary to chronic nerve compression injury. Muscle Nerve 2005;31:452–460 [400] Gupta R, Truong L, Bear D, Chafik D, Modafferi E, Hung CT. Shear stress alters the expression of myelin-associated glycoprotein (MAG) and myelin basic protein (MBP) in Schwann cells. J Orthop Res 2005;23:1232–1239 [401] Nave KA. Myelin-specific genes and their mutations in the mouse. In: Jessen KR, Richardson WD, eds. Glial Cell Development: Basic Principles and Clinical Relevance. New York: Oxford University Press; 2001 [402] McKerracher L, David S, Jackson DL, Kottis V, Dunn RJ, Braun PE. Identification of myelin-associated glycoprotein as a major myelin-derived inhibitor of neurite growth. Neuron 1994;13:805–811 [403] Gray M, Palispis W, Popovich PG, van Rooijen N, Gupta R. Macrophage depletion alters the blood-nerve barrier without affecting Schwann cell function after neural injury. J Neurosci Res 2007;85:766–777 [404] Trachtenberg JT, Thompson WJ. Schwann cell apoptosis at developing neuromuscular junctions is regulated by glial growth factor. Nature 1996;379:174– 177 [405] Baron B, Goldberg AL, Rothfus WE, Sherman RL. CT features of sarcoid infiltration of a lumbosacral nerve root. J Comput Assist Tomogr 1989;13:364– 365 [406] Yu YL, du Boulay GH, Stevens JM, Kendall BE. Computed tomography in cervical spondylotic myelopathy and radiculopathy: visualisation of structures, myelographic comparison, cord measurements and clinical utility. Neuroradiology 1986;28:221–236 [407] Ernberg LA, Adler RS, Lane J. Ultrasound in the detection and treatment of a painful stump neuroma. Skeletal Radiol 2003;32:306–309 [408] Gray AT, Collins AB, Schafhalter-Zoppoth I. Sciatic nerve block in a child: a sonographic approach. Anesth Analg 2003;97:1300–1302 [409] Gray AT, Schafhalter-Zoppoth I. Ultrasound guidance for ulnar nerve block in the forearm. Reg Anesth Pain Med 2003;28:335–339 [410] Sidhu MK, Perkins JA, Shaw DW, Bittles MA, Andrews RT. Ultrasound-guided endovenous diode laser in the treatment of congenital venous malformations: preliminary experience. J Vasc Interv Radiol 2005;16:879–884 [411] Spence BC, Sites BD, Beach ML. Ultrasound-guided musculocutaneous nerve block: a description of a novel technique. Reg Anesth Pain Med 2005;30:198– 201 [412] Howe FA, Filler AG, Bell BA, Griffiths JR. Magnetic resonance neurography. Magn Reson Med 1992;28:328–338 [413] Cudlip SA, Howe FA, Griffiths JR, Bell BA. Magnetic resonance neurography of peripheral nerve following experimental crush injury, and correlation with functional deficit. J Neurosurg 2002;96:755–759 [414] Gupta R, Villablanca PJ, Jones NF. Evaluation of an acute nerve compression injury with magnetic resonance neurography. J Hand Surg Am 2001;26:1093–1099 [415] Dailey AT, Tsuruda JS, Filler AG, Maravilla KR, Goodkin R, Kliot M. Magnetic resonance neurography of peripheral nerve degeneration and regeneration. Lancet 1997;350:1221–1222 [416] Maravilla KR, Bowen BC. Imaging of the peripheral nervous system: evaluation of peripheral neuropathy and plexopathy. AJNR Am J Neuroradiol 1998;19:1011–1023 [417] Magill CK, Tong A, Kawamura D, et al. Reinnervation of the tibialis anterior following sciatic nerve crush injury: a confocal microscopic study in transgenic mice. Exp Neurol 2007;207:64–74 [418] Frangioni JV. In vivo near-infrared fluorescence imaging. Curr Opin Chem Biol 2003;7:626–634 [419] Klohs J, Wunder A, Licha K. Near-infrared fluorescent probes for imaging vascular pathophysiology. Basic Res Cardiol 2008;103:144–151 [420] Achilefu S. Lighting up tumors with receptor-specific optical molecular probes. Technol Cancer Res Treat 2004;3:393–409 [421] Gibbs-Strauss SL, Nasr KA, Fish KM, et al. Nerve-highlighting fluorescent contrast agents for image-guided surgery. Mol Imaging 2011;10:91–101 [422] Whitney MA, Crisp JL, Nguyen LT, et al. Fluorescent peptides highlight peripheral nerves during surgery in mice. Nat Biotechnol 2011;29:352–356 [423] Wu AP, Whitney MA, Crisp JL, Friedman B, Tsien RY, Nguyen QT. Improved facial nerve identification with novel fluorescently labeled probe. Laryngoscope 2011;121:805–810 [424] Pan HC, Cheng FC, Chen CJ, et al. Post-injury regeneration in rat sciatic nerve facilitated by neurotrophic factors secreted by amniotic fluid mesenchymal stem cells. J Clin Neurosci 2007;14:1089–1098

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Evaluation of the Patient with Nerve Injury or Nerve Compression

2 Evaluation of the Patient with Nerve Injury or Nerve Compression Christine B. Novak

2.1 Introduction A thorough subjective and physical evaluation of the patient with nerve compression or following nerve injury will provide the information that is necessary to identify the level of the lesion (injury or compression), to document improvement or decline in motor and/or sensory function, and to determine treatment options. Numerous measures have been described in the assessment of patients with nerve injury/compression, and no one test has been universally accepted as the gold standard for assessment. The specific components of the comprehensive assessment for each patient should be determined by medical history, etiology, severity of nerve compression/nerve injury, and patient-specific factors.

2.2 Sensory and Motor Nerve Assessment 2.2.1 Sensory Evaluation Many instruments and measurement tools have been used for the evaluation of sensibility, but there has been little consensus on the gold standard for assessment.1–19 This in part relates to the fact that there are different stages of nerve compression and nerve injury and that no one measure may be optimal for the range of neural changes and patient symptoms. Because different sensory tests evaluate different parameters of neural function (▶ Fig. 2.1), some assessment tools will be more useful in the various stages of nerve compression than they will be for nerve injury and vice versa.

2 The sensory receptors in the glabrous skin of the hand have been classified by receptive-field and response qualities. The quickly and slowly adapting sensory receptors may be clinically evaluated with sensory testing. The slowly adapting receptors include the Merkel cell–neurite complex and Ruffini end-organ, which respond to static touch. The Merkel cell– neurite complexes are located within the basal layer of the epidermis, and the Ruffini end-organs have been recognized electrophysiologically but not histologically in the glabrous skin. The quickly adapting receptors include Meissner and Pacinian corpuscles, which respond to moving touch. The Pacinian corpuscles respond to the higher frequencies, and the Meissner corpuscles are most sensitive to frequencies up to 30 Hz. Clinical evaluation of the sensory receptors may include assessment of threshold (the minimum stimulus necessary to elicit a response) and innervation density (the number of innervated sensory receptors). The threshold of the quickly adapting receptors is assessed with vibration thresholds, and the slowly adapting receptors are evaluated with cutaneous pressure thresholds. Innervation density of the quickly and slowly adapting receptors may be assessed with moving and static two-point discrimination (2pd). The earliest changes that occur with chronic nerve compression may be detected with provocation testing, and all sensory testing may be normal. Abnormalities in the threshold testing of the sensory receptors will precede changes in innervation density.3,8,11,12,20–25 With more severe nerve compression, 2pd will become abnormal.24,26–28

Fig. 2.1 The spectrum of histopathologic changes that occur with chronic nerve compression will be reflected in patient symptoms and clinical testing. In the early stage of chronic nerve compression, intermittent sensory paresthesia or numbness may be the only symptom, and positional and pressure provocation maneuvers may be the only positive findings. With more severe chronic nerve compression and wallerian degeneration, patient complaints will include constant numbness and muscle atrophy. (Used with permission from Novak CB. Patient evaluation of nerve compression in the upper limb. In: Allieu Y, Mackinnon SE, eds. Nerve Compression Syndromes of the Upper Limb. London: Martin Dunitz; 2002.)

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Evaluation of the Patient with Nerve Injury or Nerve Compression

Light Moving Touch Light moving touch can provide a relatively simple assessment of the large Aβ fibers. As introduced by Strauch et al, the Ten Test is a method that allows the patient to subjectively compare the sensation between the affected neural distribution to a contralateral region of normal sensation.19 Strauch et al found sensory thresholds as measured by the Semmes-Weinstein monofilaments related well to the Ten Test, thus supporting the validity of this test.19 Patel and Bassini assessed the Weinstein Enhanced Sensory Test, 2pd, and the Ten Test in patients with carpal tunnel syndrome and found the Ten Test to be the most sensitive.29 To perform the Ten Test, the examiner applies a light moving touch stimulus to an area of normal sensation on the unaffected digit on the contralateral hand; this is classified as normal sensation, at 10/10 (▶ Fig. 2.2). A similar moving touch stimulus is applied simultaneously to the digit or sensory area to be tested, and the patient is asked to rank the sensation on a scale from 0 to 10 (0 being no sensation and 10 being perfect sensation). The value given by the patient is recorded as the moving touch sensory threshold. Additionally, when testing the hand there are certain territories exclusive to the median, the radial, and the ulnar nerve (▶ Fig. 2.3). This can help with the efficacy of the sensory testing.

2

Vibration Thresholds The threshold of the quickly adapting receptors may be assessed using vibration. This can be subjectively evaluated qualitatively or quantitatively. Qualitative assessment of vibratory sensation can be performed with a low- or high-frequency tuning fork, but limitations with this test have been described.3,30,31 For evaluation of sensory reinnervation following nerve injury, a low-frequency tuning fork (30 cps) may be used to indicate reinnervation of sensory receptors prior to the perception of light touch. The vibrating tuning fork is applied to the area to be assessed, and a positive response is indicated if the patient

senses the stimulus, thus indicating reinnervation of the lowfrequency quickly adapting receptors.3,4 With chronic nerve compression, the high-frequency quickly adapting receptors are first affected; therefore, evaluation with a low-frequency tuning fork will not be sensitive to the earliest changes.12 A high-frequency tuning fork (e.g., 256 cps) will be more useful to detect alterations in the early stages of nerve compression (▶ Fig. 2.4). The vibrating tuning fork is applied to the digit pulp and then applied to the contralateral area, and the patient reports if the stimulus feels the same, more intense, or less intense.3 Assessment with a tuning fork requires a comparison between the affected neural distribution and the contralateral region and thus is not useful in patients who present with bilateral upper or lower extremity nerve compression. There are several technical details that must be considered in the reliability of this test. The stimuli are not applied simultaneously, so the patient must recall the previously applied vibration for comparison, and the application of the tuning fork stimulus may vary with alteration of examiner technique. Reliable patient comparison requires that the examiner apply the same stimulus force each time; however, there have been published reports of variation in the application force.32 Therefore, this test for the documentation of chronic nerve compression has limited value. A number of vibrometers are available to quantitatively assess vibration thresholds. Each device requires the patient to detect the minimal vibratory stimulus.4,5,7,8,11,12,22 In general, the devices vary in the frequency of the vibrating stimulus. The Vibratron II (Physitemp Instruments Inc., Clifton, NJ) is a fixed frequency device (120 Hz) with two non-force-sensitive transducers.7,16 The digit to be assessed is placed lightly on one of the transducers, and the patient indicates when the vibration stimulus is perceived. Through a method of limits and force choice methodology, the vibration threshold is determined. 16 Although good reliability has been established for this device, the major limitation is that only a single frequency is available.16 In the early stages of chronic nerve compression, the

Fig. 2.2 To perform the Ten Test, the examiner applies a light moving touch stimulus to an area of normal sensation on the unaffected digit; this is classified as normal sensation, at 10/10. A similar moving touch stimulus is applied simultaneously to the digit to be tested, and the patient is asked to rank the sensation on a scale from 0 to 10 (0 being no sensation and 10 being perfect sensation).

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Evaluation of the Patient with Nerve Injury or Nerve Compression

2

Fig. 2.3 There are exclusive territories on the hand for sensory testing. The radial nerve can be tested using the dorsal radial aspect of the hand superficial to the thenar muscles. The ulnar nerve can be tested using the distal end of the little finger. The median nerve can be tested using the distal end of the index finger.

Fig. 2.4 A 256-cps tuning fork will be more useful than a low-frequency tuning fork to detect alterations in the early stages of nerve compression.

perception of higher vibration frequencies may become abnormal first and thus may not be detected at a single lower vibration frequency. However, when baseline measures are within normal limits, and only a single frequency vibrometer is available, provocation of symptoms preceding patient testing may be useful. We found that in patients with thoracic outlet syndrome (TOS), vibration thresholds in the small finger were significantly elevated following arms-elevated provocation. 24

However, as a single diagnostic criterion, baseline vibration thresholds were not significantly different in patients with TOS than in normal control subjects with no evidence of brachialplexus nerve compression.33 Vibration thresholds with multiple frequencies may be assessed with instruments such as the Bruel and Kjaer vibrometer (type 9627, Naerum, Denmark) which has a number of frequencies ranging from 8 to 500 Hz.11,12 The digit is lightly placed on

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Evaluation of the Patient with Nerve Injury or Nerve Compression

Two-Point Discrimination

2

Fig. 2.5 Semmes-Weinstein monofilaments are applied to the digit pulp in sequential order. The smallest filament that the patient can detect is the pressure threshold.

a 5-mm2 probe, and the intensity is increased and decreased by a control that the subject holds in the contralateral hand. Through a method of limits, the vibration threshold is calculated. Previous studies have demonstrated that the higher frequencies are affected in the earlier stages of chronic nerve compression and also with increasing age; thus, this evaluation may detect early alterations in neural function.12

Cutaneous Pressure Thresholds The threshold of the slowly adapting sensory receptors may be assessed using cutaneous pressure thresholds. Introduced by Von Frey, the original method used hair of varying diameters. Semmes-Weinstein monofilaments are now commonly used to evaluate cutaneous pressure thresholds.1,34 The nylon monofilaments are of various diameters, which produce different application forces (▶ Fig. 2.5). The force exerted by the set of 20 monofilaments incrementally increases on a logarithmic scale (log 10 force of 0.1 mg), and the smallest monofilament that is felt by the patient is recorded as the pressure threshold. Good reliability requires consistency in the testing protocol and in the monofilament dimensions and structure. Variability in either of these parameters will alter the application force and thus the pressure threshold.10,35 In a recent evaluation of normal subjects, agreement in repeated testing with Semmes-Weinstein monofilaments ranged from 27% (radial-nerve distribution) to 63% (median-nerve distribution), which emphasizes the need for consistent testing protocols.36 Others have questioned the use of a logarithmic scale between the monofilaments and the variability in the shape and size of the nylon filament, which may alter the force that is applied.10,37 The results of Semmes-Weinstein testing have been grouped and colored coded and may be illustrated on a body diagram. We have found that patients often appreciate the color-coded records as their sensation improves. To avoid the controversies associated with reporting and comparing pressure thresholds on a logarithmic scale, a computerized one-point discrimination system has been described for measurement of cutaneous pressure thresholds.38 We have not had personal experience with the use of this type of measurement system.

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Static and moving 2pd have been used to evaluate tactile discrimination; 2pd is hypothesized to indicate the quantity of innervated sensory receptors.4 As described by Moberg, static 2pd was initially measured using a paper clip.14,15,39 Although this measurement tool was very accessible, the variable blunt ends and potential inconsistency in the distance between the two points introduced an element of tester variability and made the paper clip less than ideal to evaluate 2pd. Other instruments, such as the Disk-Criminator (North Coast Medical Inc., Gilroy, CA) and the Two-Point Aesthesiometer, have provided tools with consistent distances between the probes and thus decreased the likelihood for testing variability in the distances between the two points. To ensure good reliability, consistency in the testing protocol is necessary and in those instruments that are not force-sensitive, it is necessary to apply only enough pressure to produce minimal skin deformation. 16 For the evaluation of static 2pd, one or two probes are placed on the digit pulp with minimal pressure, and the probes are held in one place for 5 seconds (▶ Fig. 2.6). The patient is asked to identify the number of probes that were applied, and the smallest gap at which the patient can correctly distinguish one from two probes is recorded in millimeters as the static 2pd. The test is begun by introducing the test by showing the patient the disk and narrow probes. With the stimulus applied, the patient is instructed to answer “one,” “two,” or “I don’t know”; this will minimize the risk of guessing as the 2pd is reached. Next, the test is performed on a digit with normal sensation to ensure that the patient understands the test. The 2pd is then assessed on the affected hand. Moving 2pd is evaluated by placing the probes on the distal digit pulp perpendicular to the long axis of the digit. The probes are moved slowly along the distal digit pulp from proximal to distal, and the patient is asked to identify if one or two probes were applied. With alternation between one stimulus and two stimuli, the smallest distance or gap between the two probes that the patient can correctly identify is recorded in millimeters as the moving 2pd. In patients with decreased sensibility, there is often a delayed response or the finger is moved toward the disk as the minimum 2pd is applied. Good intertester reliability has been shown using the Disk-Criminator, which permits 2pd measures of between 2 and 15 mm (▶ Fig. 2.6).16,40 In the original descriptions of static 2pd measurement, the direction of the placement of the probes was not specified, but from previous reports it is likely that the stimuli were applied parallel to the long axis of the digit.15,39,41,42 Onne42 reported the outcomes of patients following nerve injury as having large static 2pd values that could only have been attained by placing the probes parallel to the long axis of the digit. The original description of the measurement of moving 2pd specified that the probes be placed perpendicular to the digit pulp.2 In some patients with severe nerve compression or nerve injury, the diameter of the digit may be too small to permit sufficient distance between the two probes for the patient to correctly identify; therefore, the size of the digit pulp may limit the measurement of moving 2pd. However, in our experience, a 2pd that is greater than the digit pulp essentially represents nonfunctional tactile discrimination and may be classified as a lack of 2pd. We have therefore standardized our measurement of both static and moving 2pd to apply

Evaluation of the Patient with Nerve Injury or Nerve Compression

2

Fig. 2.6 Moving and static two-point discrimination (2pd) may be assessed using the Disk-Criminator (North Coast Medical Inc., Gilroy, CA). The probes are applied perpendicular to the long axis of the digit pulp. The smallest distance between the probes at which the patient can correctly discriminate two probes is recorded as the 2pd.

the probes perpendicular to the long axis of the digit pulp and to use two out of three trials for the correct response. In patients for whom the distance between the probes exceeds the size of the digit, this is recorded as the absence of 2pd. We use a disk that provides 2pd measurement at distances of up to 8 mm. When the patient cannot discriminate one from two points at 8 mm, we record this as > 8 mm and consider this as “no functional 2pd.” A criticism of the probe instrument is that there is variability in the application force because the instrument is not force sensitive.30,32 However, excellent intertester reliability has been shown with a consistent testing protocol.16,40 Therefore, we hypothesize that with tactile discrimination, there is a range of application force that may be applied and still achieve excellent reliability and consistency. We recommend applying just enough force to barely indent the skin. Patient fatigue may be an issue if the examination period is prolonged. Based on patient history and the results of the Ten Test, the measurement of 2pd can begin in the expected range and more quickly establish the limits of the patient’s 2pd. Using these clinical cues, the neurologic examination can be expedited and less burdensome to the patient.

Provocation Testing for Chronic Nerve Compression Compression of a sensory nerve will cause symptoms that range from occasional paresthesia to constant numbness. These

symptoms reflect the patient's histopathologic neural changes. In the early stages of nerve compression, provocation testing may be the only positive finding (▶ Fig. 2.1). The concept of increasing nerve tension and compression to evaluate chronic nerve compression has been established in the assessment of carpal tunnel syndrome and cubital tunnel syndrome and may be extrapolated to other sites of nerve compression.24,26,43–54 The double crush mechanism must be considered in the evaluation of patients with suspected nerve compression.55–59 Upton and McComas described the double crush mechanism and hypothesized that a proximal site of compression will cause the distal entrapment sites to be less tolerant to compression. 60 In their review, the authors presented a group of patients with a high prevalence of distal nerve compression and cervical-root lesions. They concluded that the summation of neural compression may alter axoplasmic flow, thus cumulatively resulting in patient symptoms. Evidence of the double crush and the effects of cumulative compressive forces along the nerve has been presented in a rodent chronic-nerve-compression model.61 Lundborg expanded this concept with the reverse double crush, where a distal nerve entrapment will alter neural transmission, thus affecting the more proximal entrapment sites.62 Because compression at the proximal sites may affect the more distal sites and vice versa, all entrapment sites in the upper extremity should be evaluated for nerve compression.60,63 Identification and treatment of all sites of nerve compression that are contri-

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Evaluation of the Patient with Nerve Injury or Nerve Compression

Fig. 2.7 Habitual postures and positions (wrist flexion/extension, elbow flexion, and arm elevation) may cause increased pressure on nerves, contributing to chronic nerve compression. These positions not only will affect nerves but will also place muscles in elongated or shortened positions. With prolonged positioning, weakness in some muscles will result in muscle imbalance, particularly in the cervicoscapular region. If a short, tight muscle crosses over a nerve, then increased compression may be placed on that nerve, such as occurs with the pronator teres muscle compressing the median nerve in the forearm or the pectoralis minor or scalene muscles compressing the brachial plexus. (Adapted from Mackinnon SE, Novak CB. Clinical commentary: pathogenesis of cumulative trauma disorder. Hand Surg Am 1994; 19: 873-883.)

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buting to patient symptoms will provide the best strategy for successful management. Certain postures and positions, such as wrist flexion and extension for carpal tunnel syndrome, elbow flexion for cubital tunnel syndrome, and arm elevation for brachial-plexus nerve compression, are believed to contribute to chronic nerve compression (▶ Fig. 2.7).55 The postures and positions that contribute to multiple sites of nerve compression may also place muscles in shortened positions and contribute to muscle tightness. These shortened muscles may then further compress nerves, such as the pronator teres compressing the median nerve in the forearm and the pectoralis minor and scalene muscles compressing the brachial plexus.55 Muscles that are placed in either shortened or lengthened positions will be weak. This weakness in some muscles will result in compensatory overuse of other muscles and muscle imbalance. This is most evident in the muscles in the cervicoscapular region and may contribute to complaints of diffuse discomfort in the upper back and suprascapular area (▶ Fig. 2.7). Tests of provocation may be used to identify the sites of nerve compression in the upper extremity. These tests include positional provocation, direct pressure, and the Tinel sign.24,48–50,54, 64–66 Because provocation of the more proximal entrapment sites may elicit patient discomfort, testing should begin at the more distal nerve entrapment sites and progress proximally. It is also necessary to ensure that only one entrapment site is provoked at one time to isolate the site that is producing symptoms. Therefore, each provocation test should be performed in isolation, and sufficient time should be allowed for the symptoms to subside prior to the next test. Patients should also clearly report the distribution of their symptoms to identify the specific source of symptoms. A Tinel sign is elicited by applying four to six digital taps at a specific entrapment site, and then repeating this at each site. This test is considered positive with elicitation of symptoms in the appropriate neural distribution. For carpal tunnel syndrome, the digital taps are applied on the median nerve just proximal to the carpal canal; for the median nerve in the forearm, the nerve is tapped in the region of the pronator teres. For the ulnar nerve at the cubital tunnel, digital taps are applied along the ulnar nerve beginning just proximal to the cubital tunnel

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and progressing distally through the cubital tunnel. For the brachial plexus, the digital taps are applied supraclavicularly between the scalene muscles. Many patients may have local tenderness in the region of the scalene muscles. This should be noted, but a positive Tinel sign is indicated with “electric shock”-type symptoms in the appropriate sensory distribution. Provocation tests that are elicited by position or pressure are held for a total of 1 minute and are positive with sensory complaints in the specific sensory distribution of that nerve. Positional maneuvers may be performed by increasing tension on the nerve (e.g., elbow flexion for the ulnar nerve) or increasing pressure around the nerve (e.g., wrist flexion for the median nerve). In the upper extremity, these tests should include the carpal tunnel (wrist flexion or extension), cubital tunnel (elbow flexion), and brachial plexus (arm elevation).24,48–50,54,64–66 There is increased tension of the pronator teres muscle with full forearm supination and elbow extension, thus placing pressure on the median nerve. Forearm pronation with wrist ulnar deviation increases tension on the radial sensory nerve between the extensor carpi radialis and the brachioradialis tendons in the forearm. Direct digital pressure on the nerve will also produce symptoms in a “compromised” nerve. Pressure provocation is performed by placing digital pressure at the specific entrapment site, including the carpal tunnel (median nerve proximal to the wrist crease), median nerve in the forearm (level of the pronator teres), cubital tunnel (ulnar nerve proximal to the cubital tunnel), and brachial plexus (supraclavicular between the scalene muscles).24,48–50,54,64,66 Provocation of the nerve can be increased by combining tension and digital pressure on the nerve (▶ Table 2.1). Symptoms arising from nerve compression of the cervical nerve root can be clinically evaluated using a Spurling test. 67 The patient’s head is placed in slight cervical extension and side flexion, and axial compression is applied to the patient’s head. A positive Spurling test is noted with a “spray” of symptoms into the arm. The test is then repeated with cervical side flexion to the contralateral side. Clinical provocative tests for the evaluation of patients with entrapment neuropathies are useful in confirming a diagnosis and also in establishing a treatment plan. A single nerve may be compressed at multiple levels in the same extremity,

Evaluation of the Patient with Nerve Injury or Nerve Compression Table 2.1 Provocative Tests for Nerve Compression in the Upper Extremity Nerve

Site of Entrapment

Provocative Test

Brachial plexus

Supra-/infraclavicular

Arm elevation Pressure on the brachial plexus between the scalene muscles

Radial nerve

Distal forearm

Forearm pronation with wrist ulnar deviation Pressure over the tendinous junction of the extensor carpi radialis and brachioradialis

Proximal forearm

Forearm pronation with pressure at the leading edge of the supinator muscle between the extensor carpi radialis and brachioradialis muscles

Cubital tunnel

Elbow flexion and pressure on the ulnar nerve at the cubital tunnel region

Guyon canal

Pressure at Guyon canal

Proximal forearm

Forearm supination with pressure in the region of the pronator teres

Carpal tunnel

Wrist flexion and/or extension with pressure proximal to the carpal tunnel

Ulnar nerve

Median nerve

and multiple nerves in an extremity can be affected by compression neuropathy. No single clinical test has 100% sensitivity, specificity, or predictive value even in patients with positive electrodiagnostic studies. Pressure or positional tests not only assist in the diagnosis of a compressed nerve but can also identify a specific anatomical location. To localize specific areas of nerve compression, it is important that only a single nervecompression point is provoked with any one test and that the patient specifically report paresthesia in the distribution of the nerve being tested. For example, if the elbow flexion test is used to evaluate cubital tunnel syndrome, then the wrist and forearm must be kept in neutral and the shoulder adducted to avoid increased tension on the ulnar nerve at the Guyon canal or the brachial plexus. When testing for carpal tunnel syndrome (with wrist flexion or extension), the forearm should be in neutral to avoid concomitant compression to the median nerve (at the level of the pronator teres) or to the radial sensory nerve. Because forearm pronation provokes the radial sensory nerve, and forearm supination compresses the median nerve, the forearm should be placed in neutral rotation. The addition of digital pressure on a nerve at the entrapment point with the positional provocative test will decrease the time of symptom onset. However, because symptoms come on very rapidly when digital pressure is added, the patient may not be able to differentiate the most provocative site. Thus, the establishment of the priority of compression problems is better achieved by the positional provocative test, without pressure, as this allows the patient to report which maneuvers elicit maximum symptoms. Differentiation between neural and nonneural symptoms is important, particularly in patients with brachial plexus nerve compression, which is frequently associated with muscular pain in the shoulder and cervicoscapular regions, as well as with paresthesia in the hand related to nerve compression.

Scratch Collapse Test The scratch collapse test (SCT) is another clinical test that may be used to identify sites of nerve compression. It has been shown to have good diagnostic parameters (positive and negative predictive values).68–70 This is a unique test that relies on a response independent of the compressed nerve, specifically the loss of shoulder external-rotation muscle strength, and may be used independently with each site of nerve compression. The

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SCT has been validated in patients with abnormal electrodiagnostic tests, but it is particularly helpful in identifying nerve compression when electrodiagnostic tests are normal and other provocative tests are negative. The SCT is also useful in patients with multiple levels of nerve compression and muscle imbalance, especially to prioritize multiple neuromuscular problems within the same extremity. The neurophysiologic basis for the test is not well defined and may be related to a response to the touch stimulus and increased substance P in an area of nerve irritation. To perform the SCT, the examiner should be positioned facing the patient (▶ Fig. 2.8). The patient’s arms are placed in neutral shoulder rotation, elbows flexed at 90 degrees, and wrist in neutral. The examiner applies a force to the dorsal aspect of the forearms, and the patient is asked to resist this force and maintain the arm in the same position. The isometric shoulder external rotation is assessed (▶ Fig. 2.8). The examiner then lightly scratches the patient’s skin over the site of nerve compression to be assessed; a similar force is again applied to the dorsal aspect of the forearm to resist isometric shoulder external rotation. A loss of shoulder externalrotation strength will result in “collapse” of the arm toward the abdomen. This is a positive response and indicative of nerve compression at the site of provocation. The SCT can be used to determine the most sensitive nerve compressive site. The loss of shoulder external-rotation strength will be most evident at the most irritable site, and patients will “collapse” more easily with less force applied by the examiner. For patients who have multiple sites of compression along the same nerve, as in cubital tunnel syndrome and TOS, the first provocative area can be cold sprayed with an agent such as ethyl chloride. This provocative site will temporarily disappear, allowing assessment of the next provocative site. This technique of cold spraying can also be used to determine the exact location of more or less compression over the ulnar nerve at the Guyon canal, at the thick fascial entrapment point just proximal to the wrist crease, or distally where the deep motor branch curves around the hook of the hamate under the tendinous leading edge of the short flexor muscle. This can be used to identify additional sites of compression prior to surgery. For example, the SCT may be used to identify patients with cubital tunnel syndrome who may benefit from a more complex surgical procedure rather than a simple decompression. In

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Evaluation of the Patient with Nerve Injury or Nerve Compression

Fig. 2.8 Directions for the scratch collapse test. (a) The patient’s arms are placed in neutral shoulder rotation and the elbows are flexed at 90 degrees. The examiner then applies resistance to produce an isometric contraction of shoulder external rotation. In this example, showing assessment for compression of the ulnar nerve at the cubital tunnel, (b) the examiner lightly scratches the patient’s skin over the region of the cubital tunnel, and (c) the isometric shoulder external-rotation muscle strength is then reexamined. A loss of shoulder external-rotation strength with “collapse” of the arm toward the abdomen is graded as a positive response. (Used with permission from Cheng CJ, MackinnonPatterson B, Beck JL, Mackinnon SE. Scratch Collapse Test for carpal and cubital tunnel syndrome. J Hand Surg Am 2008;33(9):15181524.)

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patients with cubital tunnel syndrome, the first scratch collapse point is usually at the tendinous edge of the flexor carpi ulnaris. If this single entrapment point is then cold sprayed with ethyl chloride, most patients will then collapse with a scratch directly behind the medial epicondyle, suggesting that while the decompression would relieve the distal entrapment by the tendinous portion of the flexor carpi ulnaris muscle, it would not address issues of neural tension on the ulnar nerve produced by elbow flexion. For surgeons who use a simple ulnar nerve decompression, the identification preoperatively of a second scratch collapse point on the ulnar nerve behind the medial epicondyle helps to identify which patients would benefit from a transposition procedure. A deeper pressure stimulus may be needed for nerve compression deep in the extremity, such as of the median nerve at the pronator arch or the posterior interosseous nerve at the arcade of Frohse. The SCT is useful in the evaluation of TOS to determine the relative contribution of brachial-plexus nerve compression between the scalene muscles and the common sites of nerve compression. In addition, the SCT may be used to evaluate the contributions of muscle imbalance associated with TOS by provocation along the medial border of the scapula. Patients who have muscle imbalance as well as direct nerve compression can be educated as to the importance of improved posture using the SCT and cold spray. With application of a cold spray to the brachial plexus between the scalene muscles, there is a collapse of the postural correction with stroking along the parascapular muscles. The patient is then asked to “correct” his or her posture in a more upright position. When the patient assumes a better posture, the positive SCT along the scapular muscles disappears. When the patient resumes a poor forward-flexed posture of the neck and shoulder, the SCT becomes positive again. This is a powerful demonstration for patients to experience and shows the importance of motor re-education, improved posture, and physical therapy that focuses on muscle balance. Patients who demonstrate improvement in postural correction may present with a negative SCT at the parascapular muscles but continuing brachial-plexus nerve compression at the scalene muscles. The use of a serial SCT with ethyl chloride spray provides a method of monitoring patient progress with complicated issues of muscle imbalance and multilevel areas of nerve

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compression, especially when TOS is a component of the clinical presentation. The SCT is also useful in the evaluation of lower extremity nerve compression. It is especially useful in patients with peroneal nerve compression to prioritize and differentiate multiple sites of compression (common peroneal nerve compression at the fibular head, superficial peroneal nerve compression at the leg, and compression of the deep peroneal nerve at the dorsum of the foot). It can also be used to prioritize tarsal tunnel compression at the lancinate ligament or more distally at the medial and lateral plantar tunnels. Deeper palpation as the stimulus to the SCT, rather than a superficial scratch, can help to distinguish tibial nerve compression at the soleus arch. Because the SCT is very sensitive to the entrapment point, the examiner must be extremely accurate in terms of the location at which the stimulus is applied to the nerve, or a false-negative scratch collapse for nerve compression may result. In the lower extremity, the peroneal nerve courses from behind the leg above the entrapment point, above the fibular head, and not distal to the fibular head. The examination is performed using a technique similar to that described for the upper extremity; resistance of shoulder external rotation with pressure on the forearms is used for this test of lower extremity nerve entrapment. The patient will typically collapse at the most irritable lower-extremity entrapment point. If a cold spray of ethyl chloride is applied to the previously tested entrapment point, the next site can be assessed. The entrapment point for superficial peroneal nerve compression is a long distance through the fascial tunnel, but typically the main scratch collapse point will be just as the peroneal nerve exits from this entrapment point in the distal leg at the level of the anterior crural intermuscular septum. As noted previously, when looking for entrapment of the tibial nerve at the soleus arch, deeper pressure needs to be used to elicit a response. The main entrapment point of the common peroneal nerve at the fibular head is the tendinous leading edge of the peroneus muscles or the posterior crural intermuscular ligament. There are, however, two other fascial septa between the anterior and lateral muscle compartments that can also compress the peroneal nerve. The lateral crural intermuscular ligament is between the peroneal muscles and the extensor hallucis longus

Evaluation of the Patient with Nerve Injury or Nerve Compression (EHL). A third septum can compress the nerve and is located between the EHL and the tibialis anterior muscle. By applying a cold spray of ethyl chloride specifically to that small area where the tendinous edge of the peroneus muscle is located, the location of the compression can be identified: entrapment at the septum between the peroneus and EHL and tibialis anterior muscles by the respective fibrous septa. There will be patients with painful shoulders or nerve injuries that involve the suprascapular nerve and preclude evaluation with resisted external rotation of the shoulder. For these patients, resistance to ankle eversion can be used as an alternative to shoulder external rotation. The patient dorsiflexes the ankles with the heels remaining on the ground and the toes off the ground, and the patient is then instructed to evert the ankles. The examiner then applies resistance against the lateral aspect of the patient's feet and asks the patient to resist as the examiner tries to invert the ankle. The examiner can then scratch the area of potential nerve compression, either on the upper or on the lower extremity. The patient’s ankle eversion will be weakened, and the ankle will collapse or give way. Although these provocation tests will assist in the identification of entrapment sites in the upper extremity that are compressing the nerve and contributing to patient symptoms, they do not provide quantification of the neural changes caused by the compression.

2.2.2 Motor Evaluation The status of muscle function can be assessed qualitatively or quantitatively. Visual assessment of muscle atrophy may be graded as mild, moderate, or severe. Decline in motor function occurs with severe nerve compression; therefore, many patients with mild nerve compression will have little evidence of muscle weakness or atrophy. Because patients often present in the early stages of nerve compression with complaints of paresthesia and/or numbness and no motor dysfunction, there may be no alteration in muscle performance detected. Following a traumatic nerve lesion, the patient may have abrupt loss of muscle function, but it may take several weeks for muscle atrophy to be visible. This delay in atrophy may complicate patient examination immediately after a nerve injury, particularly when more than one muscle provides a particular movement, and uninjured muscles may supply the muscle action for the denervated muscle (i.e., shoulder abduction and elbow flexion). Thus, individual muscle assessment is essential to determine the muscles that may be affected following injury.71,72 Musclegrading systems that are reviewed in this chapter may be useful to assess individual muscle strength. A number of hand dynamometers have been described for the assessment of muscle strength.73–78 Pinch and grip strength are commonly measured with closed hydraulic systems. The reliability of these instruments has been demonstrated by calculating the mean value of three trials using the same position. 76 Lateral key pinch is frequently used to evaluate the strength of the intrinsic muscles innervated by the ulnar nerve. Although this measure does isolate muscles innervated by the ulnar nerve, it provides only a general quantitative assessment of pinch strength. In patients with mild nerve compression, only sensory complaints may be present, and no muscle weakness may be detected. However, patients with weakness of the

muscles innvervated by the ulnar nerve may generate increased pinch strength with contraction of the flexor pollicis longus muscle, thus producing flexion of the interphalangeal (IP) joint of the thumb (the Froment sign). Simultaneous extension of the metacarpophalangeal joint may also be observed (the Jeanne sign). We describe a “pseudo” Froment sign where obvious IP joint flexion is not seen, but the positioning of the IP joint in the hand with weakness of muscle innervated by the ulnar nerve is not as extended as in the normal hand. With assessment of pinch strength, a note is made whether or not the patient exhibits a “Froment sign.“ Grip strength is commonly used to evaluate “hand function,” although it does provide a measure of general strength in the hand. Because many factors contribute to grip strength, it does not provide assessment of specific muscles or the structures that may be affected by compression (i.e., muscle, joint, tendon, bone, or nerve). Decreased grip strength will not be detected in the early stages of nerve compression. Because weakness and/or muscle atrophy may not be evident until the affected nerve has undergone considerable nerve degeneration, these assessments are of limited value in terms of grading nerve compression. Although many physical structures contribute to grip strength, patient effort and pain may influence maximal grip strength. The Rapid Exchange Grip (REG) was described as a method to detect submaximal effort with grip strength measurement.79 However, because of the variability in measurement of rapid alternating grip, some have reported that REG is not useful in detecting submaximal effort.80–83 The rapid simultaneous grip (RSG) test is similar in theory to the REG and has been shown to have good sensitivity and specificity.84 In the RSG, the patient holds one dynamometer in each hand and simultaneously maximally squeezes both dynamometers quickly and under the direction of the examiner for 10 to 15 repetitions. Comparisons are made to the maximum static grip strength measured in both hands. Submaximal effort may be detected with increased grip strength in the affected hand or decreased grip strength in the unaffected hand. When patients are asked to simultaneously grip both dynamometers quickly, it is difficult to produce a submaximal effort in one hand and full effort in the contralateral hand. The difference in maximal and submaximal grip strengths becomes evident. In the rare case of a true maligner, the patient will usually refuse to do the test. We have found measurement of simultaneous grip strength to be very useful in assessing maximal grip strength and degree of effort.

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2.2.3 Grading Systems The use of standardized grading systems provides the opportunity to classify muscle function in patients with nerve injury or compression. However, to ensure accurate comparisons between patients and outcomes, classification and grading systems depend on their consistent use with valid and reliable measures. Several grading classifications for the motor system have been based on the assessment of muscle strength. First published in 1943, the British Medical Research Council (MRC) grading system72 categorizes muscle strength on a scale of 0 to 5, with 0 = no muscle contraction, 1 = a flicker of contraction, 2 = movement with gravity eliminated, 3 = full range of motion against gravity, 4 = full range of motion with resistance, 5 = nor-

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Evaluation of the Patient with Nerve Injury or Nerve Compression mal muscle strength. Birch et al presented another MRC grading system derived from Highet that included categories from M0 to M5: M0 = no contraction, M1 = visible contraction in proximal muscles, M2 = visible contraction in proximal and distal muscles, M3 = all important muscles both proximally and distally contract against resistance, M4 = return of function such that all synergistic and independent movements are possible, M5 = complete recovery.85 Kline and Hudson titled this system Grading of the Entire Nerve and described another grading system of the entire nerve (American System) that included grades M0 to M6.86 Although reporting of outcome using a motorfunction grading system is helpful for patient comparison, standardized muscle-grading systems must be used to ensure consistency and accuracy.71,72 Numerous systems have been described to classify motor function. In contrast, classification of the sensory system is less defined. Highet’s scheme included classifications from S0 (no sensation) to S4 (complete recovery).85 As described by Dellon,37 this system was modified by Zachary and Holmes, and the classification was then adapted to include 2pd. 4 This sensory classification system includes the following: S0 = no sensation, S1 = recovery of deep pain sensibility, S1 + = recovery of superficial pain sensibility, S2 = recovery of pain and some touch sensibility, S2 + = recovery of pain and some touch sensibility with some overresponse, S3 = recovery of pain and some touch sensibility with no overresponse with 2pd > 15 mm, S3 + = sensory localization and 2pd recovery between 7 and 15 mm, S4 = complete recovery with 2pd between 2 and 6 mm.4

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2.3 Test Selection No one test has been universally accepted as the definitive measure for evaluation of sensibility in patients with nerve injury and nerve compression. Tests that possess the best parameters to detect nerve compression may not be the most useful to assess functional outcome following nerve injury. In the early stages of nerve compression when the neural changes are mild, threshold and tactile discrimination may be within normal limits, and provocation tests may be the only way to identify the site of compression (▶ Fig. 2.1). With more chronic nerve compression, vibration and pressure thresholds will become abnormal, and abnormalities in 2pd will then become evident. Because significant neural changes must be present for abnormal 2pd, this measure has very low sensitivity and positive predictive capacity in patients with mild or moderate chronic nerve compression.24,64 The progression of chronic nerve compression is related to longer duration of compression. Therefore, some compressive sites, such as the carpal tunnel and the cubital tunnel, which are relatively enclosed anatomical spaces, may have a greater tendency to cause compression that progresses to cause. Many patients with brachial-plexus nerve compression have concomitant pain with positions that compress the brachial plexus. To minimize the discomfort, these patients will decrease the duration of time spent in arm-elevated positions. In patients without anomalous bands compressing the brachial plexus, compression in this region does not commonly progress to the more severe stages of chronic nerve compression. Clinical testing will reflect these changes upon positive provocative maneuvers, perhaps with abnormal sensory thresholds, and normal 2pd.24,64

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In patients with nerve injury, 2pd may be a better indicator of functional recovery than threshold measures.16,87 Object identification is often used to evaluate functional outcome and patient recovery following median-, ulnar-, and radial-nerve reconstruction. A strong correlational relationship has been reported between object identification and 2pd in patients with median-nerve injuries.16,87,88 With respect to object identification, then, 2pd is a good predictor of function. A number of assessments that require combined motor and sensory function, such as the Moberg Pick-up, Valpar, Purdue Pegboard, Minnesota Rate of Manipulation, and Braille Pattern Identification tests, can provide information regarding functional outcome and dexterity.89–92 Some of these assessments have a greater emphasis on sensibility and others on motor function. The individual measures do not specifically indicate the origin of dysfunction but rather assessment of the sensorimotor function. To integrate all of the components, a composite-score assessment tool, which combines the sensory, motor, and pain domains, was introduced by Rosén and Lundborg.93 The selection of the most optimal test of sensibility should be based on the etiology and objective of the assessment. Tests of threshold and tactile discrimination are useful measures but provide different information in patients with nerve compression or nerve injury. Functional measures and patient-reported assessments will provide insight into the impact of a nerve injury on the patient’s life, disabilities, and health-related quality of life.

2.4 Evaluation of Muscle Imbalance and Neural Mobility Concomitant soft-tissue pathology, particularly in the cervicoscapular region, may be present following nerve injury or may be the result of postural abnormalities. This can contribute to pain and discomfort in the cervicoscapular region as a result of muscle imbalance. To identify movement abnormalities and muscle dysfunction, a comprehensive assessment of the cervical, scapular, and shoulder region should be included in patients who report symptoms arising from brachial-plexus nerve compression and in those with peripheral-nerve injuries following trauma. Posture should be evaluated in a standing and sitting position. A relaxed standing posture, when compared to the ideal posture,71 usually reveals a head-forward position with loss of cervical lordosis, increased thoracic flexion, scapulae abduction, and shoulder internal rotation. When these altered postures are maintained for prolonged periods of time, adaptation of the muscle length and compensatory muscle imbalance will result.94 Range of motion of the cervical spine and shoulder should be evaluated for the degrees of motion, in addition to associated pain and movement abnormalities. When assessing shoulder range of motion, scapular motion should also be assessed for abnormal movement patterns and winging. In cases of minimal weakness of the scapular muscles, full shoulder range of motion may be achieved, and it is with eccentric contraction of these scapular muscles that weakness will be apparent. Assessment of mild weakness of the serratus anterior muscle may be assessed with shoulder flexion and the

Evaluation of the Patient with Nerve Injury or Nerve Compression trapezius muscles with shoulder abduction. Scapular winging and/or abnormal motion will be noted with eccentric contraction as the arm is lowered against gravity. Individual muscles in the cervicoscapular region should also be assessed for weakness, tenderness and/or adaptive lengthening or shortening. In patients with upper extremity nerve compression, particularly in those with complaints of paresthesia and numbness, neural length and mobility should be assessed.95–97 Because the nerve is composed of neural and connective tissue, adaptive changes with prolonged positioning in either lengthened or shortened positions will result in relative adaptive length changes. Therefore, nerves placed in shortened positions for prolonged periods of time will undergo neural shortening. In patients with chronic nerve compression, increased fibrosis and adhesions at the entrapment sites may restrict mobility and tether the nerve at these sites. Increased patient symptoms may arise with relatively minor stretching of the nerve; thus excessive stretching will cause a significant increase of symptoms into the distal sensory distribution and/or proximally. The irritability of the patient’s condition will help to determine the time at which neural tension testing will provide the most useful information. The neural mobility tests for the upper quadrant proposed by Butler are important to identify decreased mobility of the neural tissues.96 However, if performed without knowledge of patient and tissue response, these tests can produce pain in “asymptomatic” individuals. Therefore, the examiner should become familiar with the various responses on asymptomatic individuals prior to testing patients with nerverelated symptoms. In our experience with patients who have multiple levels of nerve compression, these tests are best used once segmental mobility of the cervical spine, scapula, and shoulder has been achieved and the irritability of the condition has decreased.

2.5 Patient-Reported Assessment Measures of the physical impairments are more frequently used for assessment of motor and sensory dysfunction and treatment-related outcome. In the past, patient-reported outcomes were thought to be more subjective in nature and less often included in the comprehensive assessment either pre- or postoperatively. Because pain is a subjective experience, it has been universally assessed by self-report, and there are a number of unidimensional and multidimensional assessment tools to assess pain. More recently, patient-reported outcome measures and health-related quality of life have become important components of assessment to evaluate the impact of the pathology on the patient.

2.5.1 Pain Evaluation Pain following peripheral nerve injury or associated with nerve compression and/or muscle imbalance may be severe. A patient’s response to pain can significantly affect patient function and thus can directly influence outcome.98–100 Although recognition of severe neuropathic pain in patients with brachial plexus nerve injuries is documented, pain associated with multilevel nerve compression and cervicoscapular muscle imbalance is more controversial.55,56,101 In our survey of peripheral

nerve surgeons, 75% quantitatively assessed pain intensity (using verbal or numeric scales or the visual analogue scale [VAS]) in patients referred with pain, and assessment of pain decreased to 52% in patients referred with motor or sensory dysfunction.102 The use of multidimensional questionnaires was reported by very few surgeons. Because pain can negatively affect functional outcome and health-related quality of life, pain evaluation should be included in the comprehensive patient assessment.99 There are numerous methods described to assess pain intensity, including verbal scales, numeric scales, and the VAS. To evaluate pain qualities, multidimensional questionnaires have been used. The most widely cited multidimensional questionnaire is the McGill Pain Questionnaire (MPQ), which assesses pain intensity and pain qualities.103–105 The short-form MPQ consists of 15 adjectives (scored for the Pain Rating Index), a Present Pain Intensity score (ranked from 0 to 5), and pain intensity (measured from a 10-cm VAS). More recently, a modification of the short-form MPQ provides the opportunity to differentiate between neuropathic and nociceptive pain. Although the MPQ is an excellent measure of pain qualities, it does not indicate the impact of the pain on the patient’s life. We have developed a pain evaluation questionnaire (see Appendix of this chapter) that is composed of items from several other questionnaires.26,49,106–108 Our pain evaluation questionnaire consists of four parts, including questions (regarding work, home, medications, etc.), a body diagram, pain adjectives, and a 10-cm VAS (for pain intensity, stress, coping, anger, depression, and impact of injury on quality of life). Each part is scored separately and considered positive with a questionnaire score that is > 20, a body diagram that does not follow an anatomical pattern, and selection of more than three pain adjectives. When two or more of these parts are positive, the patient is referred for a more comprehensive psychological assessment. The first page, which consists of the body diagram, pain adjectives, and pain intensity (on a 10-cm VAS), can be quickly completed at each visit and may be used to monitor the patient’s progress (for surgeon and patient) at subsequent visits. The specific adjectives used (neurogenic vs. nonneurogenic) are also helpful in patient evaluation. For example, patients may choose “burning“ or “numbing“ but say that these are less important or frequent than “dull,“ “aching,“ and “throbbing.“ This would suggest that a nonneurologic source of pain is also important in their symptomatology. We have also added three VASs: depressive symptoms, anger, and the impact on overall quality of life. Optimal patient outcome can only be achieved if pain is successfully managed, and this must include the psychological component associated with this problem. Though outside the scope of practice of many surgeons and hand therapists, referral to the appropriate pain management center or psychologist/ psychiatrist can be extremely beneficial.

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2.5.2 Self-Report Questionnaires There are numerous self-report questionnaires that have been used for assessment of health status, health-related quality of life, and disability related specifically to upper extremity pathology. These questionnaires are useful to obtain patient-related outcomes and impact of the injury/pathology on the patient. No single questionnaire has been universally accepted, and the

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Evaluation of the Patient with Nerve Injury or Nerve Compression selection of the most appropriate questionnaire depends on the information or data required. Self-report questionnaires that are most commonly used in hand surgery are those that assess health status (SF-36) and general upper extremity disability, such as the Disabilities of the Arm, Shoulder, and Hand (DASH) and the Michigan Hand Outcomes Questionnaire (MHQ). There are also a number of disease-specific questionnaires, such as the Levine Carpal Tunnel Questionnaire, the Cold Intolerance Severity Scale, the Patient-Specific Functional Scale (PSFS), and other questionnaires specific to the shoulder and elbow regions. The DASH, a disease-specific self-report questionnaire to assess upper extremity disability, was developed as a joint effort of the American Academy of Orthopedic Surgeons, the Council of Musculoskeletal Specialty Societies, and the Institute of Work and Health.109 The DASH contains 30 items related to symptoms and physical function in addition to two subscales (work and recreation). Evidence regarding the validity, reliability, and responsiveness has been presented.110–118 DASH scores as an indicator of disability have been published in a variety of upper limb pathologies. In a large US population-based study, Hunsaker et al reported a mean DASH score of 10.10 ± 14.86 for the normative value.111 In our study of patients with upper extremity nerve injuries, the mean DASH score was 44 ± 22, with significantly higher scores in patients with brachial plexus injuries.100 Evaluation of the psychometric properties of the DASH has shown that this questionnaire has excellent validity, reliability, and responsiveness to measure disability in patients with upper extremity pathologies. The QuickDASH has 11 items and has been validated in a number of studies.119,120 The MHQ has the capacity to assess individual domains of hand function, activities, work, pain, appearance, and satisfaction and has shown evidence of good validity, reliability and responsiveness.121,122 The MHQ has 71 items, which may impose a burden on the patient and increased difficulty in completion and scoring. The brief MHQ has been developed with 12 items and showed good psychometric properties.123 The PSFS was developed to assess functional impairment specific to each patient.124,125 Validity and responsiveness to change have been shown in patients with back pain, neck pain, knee pain, and various hand pathologies.117,126–130 In our study of upper extremity nerve injury, we showed construct validity of the PSFS with moderate correlation with the DASH; also, the PSFS scores were significantly lower in patients with brachial plexus injuries compared to patients with distal nerve injuries.131 The PSFS was completed in a shorter time than the DASH and provides the opportunity to select items that are patient specific and thus more meaningful to the individual. Each patient identifies three items that he or she finds difficult or unable to perform, then indicates the level of difficulty on a 10-cm VAS. The PSFS may prove a more useful assessment tool for individual changes over time, but because patients choose their own items, it makes comparison between patients more difficult. Questionnaires such as the Levine Carpal Tunnel Questionnaire provide the opportunity for patients with a specific diagnosis of carpal tunnel syndrome to report both symptoms and function.132 There are a number of self-report questionnaires for specific diagnoses, but the usefulness of these questionnaires for clinical use may relate in part to the volume of patients seen in a surgical practice.

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2.6 Conclusion There is no single test or measure that will be adequate for comprehensive evaluation of all patients with nerve injury or nerve compression. The basis of the evaluation of patients with nerve compression and/or injury begins with an accurate history and patient subjective symptom description to determine the assessment tools that will be most informative. Motor and sensory evaluations are required in traumatic nerve injuries, but in patients with nerve compression, tests of provocation will provide the earliest signs of nerve compression and help in detecting the site of nerve entrapment. The use of a battery of available valid and reliable sensory and motor assessments in addition to patient self-report questionnaires will provide the most comprehensive information to formulate a treatment plan and more accurately reflect treatment-related outcomes.

2.7 References [1] Bell-Krotoski JA. Sensibility testing: current concepts. In: Hunter JM, Mackin EJ, Callahan AD, eds. Rehabilitation of the Hand: Surgery and Therapy. St. Louis, MO: CV Mosby; 1995:109–128 [2] Dellon AL. The moving two-point discrimination test: clinical evaluation of the quickly adapting fiber/receptor system. J Hand Surg Am 1978;3:474–481 [3] Dellon AL. Clinical use of vibratory stimuli to evaluate peripheral nerve injury and compression neuropathy. Plast Reconstr Surg 1980;65:466–476 [4] Dellon AL. Evaluation of Sensibility and Re-education of Sensation in the Hand. Baltimore, MD: Williams & Wilkins; 1981 [5] Dellon AL. The vibrometer. Plast Reconstr Surg 1983;71:427–431 [6] Dellon AL, Keller KM. Computer-assisted quantitative sensorimotor testing in patients with carpal and cubital tunnel syndromes. Ann Plast Surg 1997;38:493–502 [7] Gerr FE, Letz R. Reliability of a widely used test of peripheral cutaneous vibration sensitivity and a comparison of two testing protocols. Br J Ind Med 1988;45:635–639 [8] Grunert BK, Wertsch JJ, Matloub HS, McCallum-Burke S. Reliability of sensory threshold measurement using a digital vibrogram. J Occup Med 1990;32:100–102 [9] Hermann RP, Novak CB, Mackinnon SE. Establishing normal values of moving two-point discrimination in children and adolescents. Dev Med Child Neurol 1996;38:255–261 [10] Levin S, Pearsall G, Ruderman RJ. Von Frey’s methods of measuring pressure sensibility in the hand: an engineering analysis of the Weinstein-Semmes pressure aesthesiometer. J Hand Surg [Br] 1978;3:211–216 [11] Lundborg G, Lie-Stenström AK, Sollerman C, Strömberg T, Pyykkö I. Digital vibrogram: a new diagnostic tool for sensory testing in compression neuropathy. J Hand Surg Am 1986;11:693–699 [12] Lundborg G, Sollerman C, Strömberg T, Pyykkö I, Rosén B. A new principle for assessing vibrotactile sense in vibration-induced neuropathy. Scand J Work Environ Health 1987;13:375–379 [13] Mackinnon SE, Dellon AL. Two-point discrimination tester. J Hand Surg Am 1985;10:906–907 [14] Moberg E. Objective methods for determining the functional value of sensibility in the hand. J Bone Joint Surg Br 1958;40-B:454–476 [15] Moberg E. The unsolved problem: how to test the functional value of hand sensibility. J Hand Ther 1991;4:105–110 [16] Novak CB, Mackinnon SE, Williams JI, Kelly L. Establishment of reliability in the evaluation of hand sensibility. Plast Reconstr Surg 1993;92:311–322 [17] Rosén B, Lundborg G. A new tactile gnosis instrument in sensibility testing. J Hand Ther 1998;11:251–257 [18] Semmes J, Weinstein S, Ghent I, Teuber H. Somatosensory Changes after Penetrating Brain Wounds in Man. Cambridge, MA: Harvard University Press; 1960 [19] Strauch B, Lang A, Ferder M, Keyes-Ford M, Freeman K, Newstein D. The Ten Test. Plast Reconstr Surg 1997;99:1074–1078 [20] Doezie AM, Freehill AK, Novak CB, Dale AM, Mackinnon SE. Evaluation of cutaneous vibration thresholds in medical transcriptionists. J Hand Surg Am 1997;22:867–872

Evaluation of the Patient with Nerve Injury or Nerve Compression [21] Gelberman RH, Szabo RM, Williamson RV, Dimick MP. Sensibility testing in peripheral-nerve compression syndromes: an experimental study in humans. J Bone Joint Surg Am 1983;65:632–638 [22] Jetzer TC. Use of vibration testing in the early evaluation of workers with carpal tunnel syndrome. J Occup Med 1991;33:117–120 [23] Lundborg G, Dahlin LB, Lundström R, Necking LE, Strömberg T. Vibrotactile function of the hand in compression and vibration-induced neuropathy. Sensibility index—a new measure. Scand J Plast Reconstr Surg Hand Surg 1992;26:275–279 [24] Novak CB, Mackinnon SE, Patterson GA. Evaluation of patients with thoracic outlet syndrome. J Hand Surg Am 1993;18:292–299 [25] Werner RA, Franzblau A, Johnston E. Comparison of multiple frequency vibrometry testing and sensory nerve conduction measures in screening for carpal tunnel syndrome in an industrial setting. Am J Phys Med Rehabil 1995;74:101–106 [26] Mackinnon SE, Dellon AL. Surgery of the Peripheral Nerve. New York, NY: Thieme; 1988 [27] Szabo RM, Gelberman RH, Dimick MP. Sensibility testing in patients with carpal tunnel syndrome. J Bone Joint Surg Am 1984;66:60–64 [28] Szabo RM, Slater RR, Farver TB, Stanton DB, Sharman WK. The value of diagnostic testing in carpal tunnel syndrome. J Hand Surg Am 1999;24:704–714 [29] Patel MR, Bassini L. A comparison of five tests for determining hand sensibility. J Reconstr Microsurg 1999;15:523–526 [30] Bell-Krotoski JA, Weinstein S, Weinstein C. Testing sensibility, including touch-pressure, two-point discrimination, point localization, and vibration. J Hand Ther 1993;6:114–123 [31] Novak CB, Mackinnon SE. Evaluation of nerve injury and nerve compression in the upper quadrant. J Hand Ther 2005;18:230–240 [32] Bell-Krotoski JA, Buford WL. The force/time relationship of clinically used sensory testing instruments. J Hand Ther 1988;1:76–85 [33] Dale AM, Novak CB, Mackinnon SE. Utility of vibration thresholds in patients with brachial plexus nerve compression. Ann Plast Surg 1999;42:613–618 [34] Bell-Krotoski JA. Light touch-deep pressure testing using Semmes-Weinstein monofilaments. In: Hunter JM, Schneider LH, Mackin EJ, Callahan AD, eds. Rehabilitation of the Hand: Surgery and Therapy. St. Louis, MO: CV Mosby; 1990 [35] van Vliet D, Novak CB, Mackinnon SE. Duration of contact time alters cutaneous pressure threshold measurements. Ann Plast Surg 1993;31:335–339 [36] Massy-Westropp N. The effects of normal human variability and hand activity on sensory testing with the full Semmes-Weinstein monofilaments kit. J Hand Ther 2002;15:48–52 [37] Dellon AL. Somatosensory Testing and Rehabilitation. Bethesda, MD: American Occupational Therapy Association; 1999 [38] Dellon ES, Mourey R, Dellon AL. Human pressure perception values for constant and moving one- and two-point discrimination. Plast Reconstr Surg 1992;90:112–117 [39] Moberg E. Two-point discrimination test: a valuable part of hand surgical rehabilitation, e.g., in tetraplegia. Scand J Rehabil Med 1990;22:127–134 [40] Dellon AL, Mackinnon SE, Crosby PM. Reliability of two-point discrimination measurements. J Hand Surg Am 1987;12:693–696 [41] Aulicino PL. Clinical evaluation of the hand. In: Hunter JM, Mackin EJ, Callahan AD, eds. Rehabilitation of the Hand: Surgery and Therapy. St Louis, MO: Mosby; 1995:53–76 [42] Onne L. Recovery of sensibility and sudomotor activity in the hand after nerve suture. Acta Chir Scand Suppl 1962;300 Suppl 300:1–69 [43] de Krom MCTFM, Knipschild PG, Kester ADM, Spaans F. Efficacy of provocative tests for diagnosis of carpal tunnel syndrome. Lancet 1990;335:393–395 [44] Durkan JA. A new diagnostic test for carpal tunnel syndrome. J Bone Joint Surg Am 1991;73:535–538 [45] González del Pino J, Delgado-Martínez AD, González González I, Lovic A. Value of the carpal compression test in the diagnosis of carpal tunnel syndrome. J Hand Surg [Br] 1997;22:38–41 [46] Gunnarsson LG, Amilon A, Hellstrand P, Leissner P, Philipson L. The diagnosis of carpal tunnel syndrome: sensitivity and specificity of some clinical and electrophysiological tests. J Hand Surg [Br] 1997;22:34–37 [47] MacDermid JC. Accuracy of clinical tests used in the detection of carpal tunnel syndrome: a literature review. J Hand Ther 1991;4:169–176 [48] Novak CB, Lee GW, Mackinnon SE, Lay L. Provocative testing for cubital tunnel syndrome. J Hand Surg Am 1994;19:817–820 [49] Novak CB, Mackinnon SE. Evaluation of the patient with thoracic outlet syndrome. Chest Surg Clin N Am 1999;9:725–746

[50] Paley D, McMurtry RY. Median nerve compression test in carpal tunnel syndrome diagnosis. Reproduces signs and symptoms in affected wrist. Orthop Rev 1985;14:41–45 [51] Phalen GS. The carpal-tunnel syndrome: seventeen years’ experience in diagnosis and treatment of six hundred fifty-four hands. J Bone Joint Surg Am 1966;48:211–228 [52] Phalen GS. The carpal-tunnel syndrome: clinical evaluation of 598 hands. Clin Orthop Relat Res 1972;83:29–40 [53] Tetro AM, Evanoff BA, Hollstien SB, Gelberman RH. A new provocative test for carpal tunnel syndrome: assessment of wrist flexion and nerve compression. J Bone Joint Surg Br 1998;80:493–498 [54] Williams TM, Mackinnon SE, Novak CB, McCabe S, Kelly L. Verification of the pressure provocative test in carpal tunnel syndrome. Ann Plast Surg 1992;29:8–11 [55] Mackinnon SE, Novak CB. Clinical commentary: pathogenesis of cumulative trauma disorder. J Hand Surg Am 1994;19:873–883 [56] Mackinnon SE, Novak CB. Repetitive strain in the workplace. J Hand Surg Am 1997;22:2–18 [57] Novak CB, Mackinnon SE. Multilevel nerve compression and muscle imbalance in work-related neuromuscular disorders. Am J Ind Med 2002;41:343–352 [58] Omurtag M, Novak CB, Mackinnon SE. Multiple level nerve compression is frequently unrecognized. Can J Plast Surg 1996;4:165–167 [59] Vaught MS, Brismée J-M, Dedrick GS, Sizer PS, Sawyer SF. Association of disturbances in the thoracic outlet in subjects with carpal tunnel syndrome: a case-control study. J Hand Ther 2011;24:44–51, quiz 52 [60] Upton ARM, McComas AJ. The double crush in nerve entrapment syndromes. Lancet 1973;2:359–362 [61] Dellon AL, Mackinnon SE. Chronic nerve compression model for the double crush hypothesis. Ann Plast Surg 1991;26:259–264 [62] Lundborg G. Nerve Injury and Repair. New York, NY: Churchill Livingstone; 1988 [63] Lundborg G. Nerve Injury and Repair. 2nd ed. New York, NY: Churchill Livingstone; 2005 [64] Mackinnon SE. Double and multiple “crush” syndromes: double and multiple entrapment neuropathies. Hand Clin 1992;8:369–390 [65] Rayan GM, Jensen C, Duke J. Elbow flexion test in the normal population. J Hand Surg Am 1992;17:86–89 [66] Roos DB, Owens JC. Thoracic outlet syndrome. Arch Surg 1966;93:71–74 [67] Tong HC, Haig AJ, Yamakawa K. The Spurling test and cervical radiculopathy. Spine 2002;27:156–159 [68] Cheng CJ, Mackinnon-Patterson B, Beck JL, Mackinnon SE. Scratch collapse test for evaluation of carpal and cubital tunnel syndrome. J Hand Surg Am 2008;33:1518–1524 [69] Boyd K, Mackinnon SE. Scatch collapse test as an adjunct in the diagnosis of tarsal tunnel syndrome. Plast Reconstr Surg 2011;128:933–939 [70] Gillenwater J, Cheng J, Mackinnon SE. Evaluation of the scratch collapse test in peroneal nerve compression. Plast Reconstr Surg 2011;128:933–939 [71] Kendall FP, McCreary EK, Provance PG. Muscles: Testing and Function. Baltimor, MDe: Williams & Wilkins; 1993 [72] Medical Research Council of the U.K. Aids to the Examination of the Peripheral Nervous System. Palo Alto, CA: Pentagon House; 1976 [73] Schreuders TAR, Roebroeck ME, van der Kar TJ, Soeters JN, Hovius SE, Stam HJ. Strength of the intrinsic muscles of the hand measured with a hand-held dynamometer: reliability in patients with ulnar and median nerve paralysis. J Hand Surg [Br] 2000;25:560–565 [74] Mathiowetz V. Comparison of Rolyan and Jamar dynamometers for measuring grip strength. Occup Ther Int 2002;9:201–209 [75] Schreuders TAR, Roebroeck ME, Goumans J, van Nieuwenhuijzen JF, Stijnen TH, Stam HJ. Measurement error in grip and pinch force measurements in patients with hand injuries. Phys Ther 2003;83:806–815 [76] Mathiowetz V, Weber K, Volland G, Kashman N. Reliability and validity of grip and pinch strength evaluations. J Hand Surg Am 1984;9:222–226 [77] Schreuders TAR, Roebroeck ME, Jaquet J-B, Hovius SER, Stam HJ. Measuring the strength of the intrinsic muscles of the hand in patients with ulnar and median nerve injuries: reliability of the Rotterdam Intrinsic Hand Myometer (RIHM). J Hand Surg Am 2004;29:318–324 [78] Massy-Westropp N, Rankin W, Ahern M, Krishnan J, Hearn TC. Measuring grip strength in normal adults: reference ranges and a comparison of electronic and hydraulic instruments. J Hand Surg Am 2004;29:514–519 [79] Hildreth DH, Breidenbach WC, Lister GD, Hodges AD. Detection of submaximal effort by use of the rapid exchange grip. J Hand Surg Am 1989;14:742– 745

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Evaluation of the Patient with Nerve Injury or Nerve Compression [80] Shechtman O, Taylor C. The use of the rapid exchange grip test in detecting sincerity of effort: 2. Validity of the test. J Hand Ther 2000;13:203–210 [81] Tredgett MW, Davis TRC. Rapid repeat testing of grip strength for detection of faked hand weakness. J Hand Surg [Br] 2000;25:372–375 [82] Shechtman O, Taylor C. How do therapists administer the rapid exchange grip test? A survey. J Hand Ther 2002;15:53–61 [83] Shechtman O, Goodall SK. The administration and interpretation of the rapid exchange grip test: a national survey. J Hand Ther 2008;21:18–26, quiz 27 [84] Joughin K, Gulati P, Mackinnon SE, et al. An evaluation of rapid exchange and simultaneous grip tests. J Hand Surg Am 1993;18:245–252 [85] Birch R, Bonney G, Wynn Parry CB. Surgical Disorders of the Peripheral Nerves. London, England: Churchill Livingstone; 1998 [86] Kline DG, Hudson AR. Nerve Injuries: Operative Results for Major Nerve Injuries, Entrapment and Tumors. Philadelphia, PA: WB Saunders; 1995 [87] Novak CB, Mackinnon SE, Kelly L. Correlation of two-point discrimination and hand function following median nerve injury. Ann Plast Surg 1993;31:495–498 [88] Novak CB, Kelly L, Mackinnon SE. Sensory recovery after median nerve grafting. J Hand Surg Am 1992;17:59–68 [89] Amirjani N, Ashworth NL, Gordon T, Edwards DC, Chan KM. Normative values and the effects of age, gender, and handedness on the Moberg Pick-Up Test. Muscle Nerve 2007;35:788–792 [90] Jebsen RH, Taylor N, Trieschmann RB, Trotter MJ, Howard LA. An objective and standardized test of hand function. Arch Phys Med Rehabil 1969;50:311–319 [91] Novak CB, Mackinnon SE, Williams JI, Kelly L. Development of a new measure of fine sensory function. Plast Reconstr Surg 1993;92:301–310 [92] Tiffin J, Asher EJ. The Purdue pegboard: norms and studies of reliability and validity. J Appl Psychol 1948;32:234–247 [93] Rosén B, Lundborg G. A model instrument for the documentation of outcome after nerve repair. J Hand Surg Am 2000;25:535–543 [94] Sahrmann SA. Diagnosis and Treatment of Movement Impairment Syndromes. St. Louis, MO: Mosby; 2002 [95] Byl C, Puttlitz C, Byl N, Lotz J, Topp K. Strain in the median and ulnar nerves during upper-extremity positioning. J Hand Surg Am 2002;27:1032–1040 [96] Butler DS. Mobilisation of the Nervous System. Melbourne, Australia: Churchill Livingstone; 1991 [97] Totten PA, Hunter JM. Therapeutic techniques to enhance nerve gliding in thoracic outlet syndrome and carpal tunnel syndrome. Hand Clin 1991;7:505–520 [98] Jensen MP, Chodroff MJ, Dworkin RH. The impact of neuropathic pain on health-related quality of life: review and implications. Neurology 2007;68:1178–1182 [99] Novak CB, Katz J. Neuropathic pain in patients with upper-extremity nerve injury. Physiother Can 2010;62:190–201 [100] Novak CB, Anastakis DJ, Beaton DE, Mackinnon SE, Katz J. Biomedical and psychosocial factors associated with disability after peripheral nerve injury. J Bone Joint Surg Am 2011;93:929–936 [101] Hadler NM. Repetitive upper-extremity motions in the workplace are not hazardous. J Hand Surg Am 1997;22:19–29 [102] Novak CB, Anastakis DJ, Beaton DE, Katz J. Evaluation of pain measurement practices and opinions of peripheral nerve surgeons. Hand (NY) 2009;4:344– 349 [103] Melzack R. The McGill Pain Questionnaire: major properties and scoring methods. Pain 1975;1:277–299 [104] Melzack R. The short-form McGill Pain Questionnaire. Pain 1987;30:191–197 [105] Melzack R, Katz J. Assessment of pain in adult patients. In: McMahon SB, Koltzenburg M, eds. Wall & Melzack’s Textbook of Pain. New York, NY: ChurchillLivingstone; 2006:291–304 [106] Chen DL, Novak CB, Mackinnon SE, Weisenborn SA. Pain responses in patients with upper-extremity disorders. J Hand Surg Am 1998;23:70–75 [107] Melzack R. The McGill Pain Questionnaire: major properties and scoring methods. Pain 1975;1:277–299 [108] Hendler N, Viernstein M, Gucer P, Long D. A preoperative screening test for chronic back pain patients. Psychosomatics 1979;20:801–808 [109] Hudak PL, Amadio PC, Bombardier C, the Upper Extremity Collaborative Group (UECG). Development of an upper extremity outcome measure: the DASH (Disabilities of the Arm, Shoulder and Hand) [corrected]. Am J Ind Med 1996;29:602–608 [110] Beaton DE, Katz JN, Fossel AH, Wright JG, Tarasuk V, Bombardier C. Measuring the whole or the parts? Validity, reliability, and responsiveness of the Disabilities of the Arm, Shoulder and Hand outcome measure in different regions of the upper extremity. J Hand Ther 2001;14:128–146

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[111] Hunsaker FG, Cioffi DA, Amadio PC, Wright JG, Caughlin B. The American Academy of Orthopaedic Surgeons outcomes instruments: normative values from the general population. J Bone Joint Surg Am 2002;84-A:208–215 [112] Dias JJ, Bhowal B, Wildin CJ, Thompson JR. Assessing the outcome of disorders of the hand: is the patient evaluation measure reliable, valid, responsive and without bias? J Bone Joint Surg Br 2001;83:235–240 [113] Gay RE, Amadio PC, Johnson JC. Comparative responsiveness of the Disabilities of the Arm, Shoulder, and Hand, the cCarpal Tunnel Questionnaire, and the SF-36 to clinical change after carpal tunnel release. J Hand Surg Am 2003;28:250–254 [114] Horng Y-S, Lin M-C, Feng C-T, Huang C-H, Wu H-C, Wang J-D. Responsiveness of the Michigan Hand Outcomes Questionnaire and the Disabilities of the Arm, Shoulder, and Hand Questionnaire in patients with hand injury. J Hand Surg Am 2010;35:430–436 [115] MacDermid JC, Richards RS, Donner A, Bellamy N, Roth JH. Responsiveness of the short form-36, Disabilities of the Arm, Shoulder, and Hand Questionnaire, patient-rated wrist evaluation, and physical impairment measurements in evaluating recovery after a distal radius fracture. J Hand Surg Am 2000;25:330–340 [116] MacDermid JC, Tottenham V. Responsiveness of the Disabilities of the Arm, Shoulder, and Hand (DASH) and Patient-Rated Wrist/Hand Evaluation (PRWHE) in evaluating change after hand therapy. J Hand Ther 2004;17:18–23 [117] McMillan CR, Binhammer PA. Which outcome measure is the best? Evaluating responsiveness of the Disabilities of the Arm, Shoulder, and Hand Questionnaire, the Michigan Hand Questionnaire and the Patient-Specific Functional Scale following hand and wrist surgery. Hand (NY) 2009;4:311–318 [118] SooHoo NF, McDonald AP, Seiler JG, McGillivary GR. Evaluation of the construct validity of the DASH questionnaire by correlation to the SF-36. J Hand Surg Am 2002;27:537–541 [119] Beaton DE, Wright JG, Katz JN, Upper Extremity Collaborative Group. Development of the QuickDASH: comparison of three item-reduction approaches. J Bone Joint Surg Am 2005;87:1038–1046 [120] Gummesson C, Ward MM, Atroshi I. The shortened Disabilities of the Arm, Shoulder and Hand questionnaire (QuickDASH): Validity and reliability based on the responses within the full-length DASH. BMC Musculoskelet Disord 2006;7:44 [121] Chung KC, Kalliainen LK, Hayward RA. Type II (beta) errors in the hand literature: the importance of power. J Hand Surg Am 1998;23:20–25 [122] Chung KC, Pillsbury MS, Walters MR, Hayward RA. Reliability and validity testing of the Michigan Hand Outcomes Questionnaire. J Hand Surg Am 1998;23:575–587 [123] Waljee JF, Kim HM, Burns PB, Chung KC. Development of a brief, 12-item version of the Michigan Hand Questionnaire. Plast Reconstr Surg 2011;128:208– 220 [124] Stratford P, Gill C, Westaway M, Binkley J. Assessing disability and change on individual patients: a report of a patient-specific measure. Physiother Can 1995;47:258–262 [125] Stratford P, Spadoni G. Assessing improvement in patients who report small limitations in functional status on condition-specific measures. Physiother Can 2005;57:234–241 [126] Cleland JA, Fritz JM, Whitman JM, Palmer JA. The reliability and construct validity of the Neck Disability Index and Patient-Specific Functional Scale in patients with cervical radiculopathy. Spine 2006;31:598–602 [127] Pengel LHM, Refshauge KM, Maher CG. Responsiveness of pain, disability, and physical impairment outcomes in patients with low back pain. Spine 2004;29:879–883 [128] Westaway MD, Stratford PW, Binkley JM. The Patient-Specific Functional Scale: validation of its use in persons with neck dysfunction. J Orthop Sports Phys Ther 1998;27:331–338 [129] Gross DP, Battié MC, Asante AK. The Patient-Specific Functional Scale: validity in workers’ compensation claimants. Arch Phys Med Rehabil 2008;89:1294– 1299 [130] Rosengren J, Brodin N. Validity and reliability of the Swedish version of the Patient-Specific Functional Scale in patients treated surgically for carpometacarpal joint osteoarthritis. J Hand Ther 2013;26:53–60, quiz 61 [131] Novak CB, Anastakis DJ, Beaton DE, Mackinnon SE, Katz J. Validity of the Patient Specific Functional Scale in patients following upper extremity nerve injury. J Hand Surg [Br] 2012;37:45 [132] Levine DW, Simmons BP, Koris MJ, et al. A self-administered questionnaire for the assessment of severity of symptoms and functional status in carpal tunnel syndrome. J Bone Joint Surg Am 1993;75:1585–1592

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Evaluation of the Patient with Nerve Injury or Nerve Compression

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Evaluation of the Patient with Nerve Injury or Nerve Compression

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Evaluation of the Patient with Nerve Injury or Nerve Compression

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The Electrodiagnostic Examination with Peripheral Nerve Injuries

3 The Electrodiagnostic Examination with Peripheral Nerve Injuries Mark A. Ferrante and Asa J. Wilbourn

3.1 Introduction Peripheral nerve injuries generate substantial disability and, when improperly managed, impede functional recovery. The majority of these injuries follow trauma, the incidence of which exceeds that of both carpal tunnel syndrome (CTS) and diabetic polyneuropathy.1,2 These lesions may follow any force capable of disrupting the myelin coating or the axon of the nerve fiber, such as roadway accidents, falls, industrial injuries, lacerations, and (especially during wartime) penetrating damage from missiles and other objects.2,3 It is estimated that 54% of all combat wounds are extremity wounds, and to date more than 47,000 direct combat wounds have been reported due to ongoing US military operations.4,5 These extremity wounds have identified a new population of complex peripheral nerve injuries. During peacetime, most such lesions follow vehicular accidents. Over 360,000 nerve repairs are performed in the US each year.6 In a recent retrospective review, the mean patient age was 32.4 years, and the majority of nerve injuries occurred in men (74%), involved a single nerve (83%), and most commonly involved the upper extremity (73.5%).7 These findings are consistent with those of others.8 Most upper extremity nerve injuries involve the radial nerve, whereas the sciatic nerve is the more

commonly injured lower extremity nerve.2,8 Peripheral neuropathies may be divided into open (e.g., lacerations and gunshot wounds) and closed (e.g., traction) types, the exact ratio of which reflects the particular nerve involved. For example, with axillary neuropathies, closed traction injuries related to shoulder dislocations far outnumber direct injuries from other sources, such as gunshot wounds to the shoulder.9 Although nerve fiber injuries have a variety of origins, including mechanical (e.g., compression, traction, and laceration), entrapment, ischemic, thermal, chemical, and irradiation, their pathologic responses are limited to wallerian degeneration, termed axon loss, and demyelination. Both of these pathologies are associated with specific pathophysiologic responses. It is the latter that dictates the electrodiagnostic (EDX) and clinical manifestations observed (▶ Table 3.1). Before discussing these correlations, an understanding of pertinent anatomy, pathology, pathophysiology, EDX examination (and its limitations), and the sequence of events following nerve trauma is required. This permits a full appreciation of the EDX aspects of lesion localization, severity assessment, prognostication, and, perhaps most importantly, the optimal timing of EDX testing. Although this has been discussed in detail in Chapter 1, we will highlight the pertinent details as they affect the evaluation of EDX studies.

3

Table 3.1 Degree of Nerve Injury and Anticipated Recovery Chronic Nerve Injury

Acute Nerve Injury Degree of Nerve Injury

Spontaneous Recovery

Rate of Recovery

Surgery

Fibs

MUAPs

Fibs

MUAPs

I (neurapraxia)

Full

Occurs in days to 3 months following injury

None*

No

Yes (normal)

No

Yes (normal)

II (axonotmesis)

Full

Regenerates at the None* rate of 1 inch/month

Yes

Yes**

No

Yes (abnormal)

III

Partial

Regenerates at the None* rate of 1 inch/month

Yes

Yes**

No

Yes (abnormal)

IV

None

Following surgery at the rate of 1 inch/ month

Yes Nerve repair, graft or transfer (except for chronic injury)

No

No

No

V (neurotmesis)

None

Following surgery at the rate of 1 inch/ month

Yes Nerve repair, graft or transfer (except for chronic injury)

No

No

No

VI (mixed injury)

Recovery and type of surgery will depend on the injury and the combination of degrees of nerve injury

* Surgery to release or remove the pressure on the nerve, which has potential to speed up recovery or improve recovery in a third-degree injury. ** Early nerve regeneration = MUAPs secondary to collateral sprouting. Late nerve regeneration = nascent MUAPs secondary to axonal regeneration. Abbreviations: Fibs = fibrillation potentials; MUAPs = motor unit action potentials.

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The Electrodiagnostic Examination with Peripheral Nerve Injuries

3.2 Pertinent Anatomy The central nervous system (CNS) communicates with the fibers composing skeletal muscle and the various sensory receptors via the peripheral nervous system (PNS), thereby effecting movement and permitting sensation. The various neural elements of the PNS (i.e., the roots, plexuses, and nerve trunks) are formed by the intermingling and rearrangement of PNS nerve fibers as they proceed peripherally from the spinal cord. These nerve fibers are of two anatomical types, myelinated and unmyelinated, and are surrounded by endoneurial connective tissue, termed endoneurium. Individual nerve fibers are packaged into fascicles, which are surrounded by perineurial connective tissue, termed perineurium. The fascicles run individually or, more commonly, in groups within the internal epineurium. The external epineurial connective tissue is surrounded by loose connective tissue, which provides the nerve trunks with the mobility they require to traverse the various body joints. The smallest element of movement is the motor unit, which is defined as a single lower motor neuron (e.g., anterior horn cell) and all of the muscle fibers that it innervates.

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3.3 Pertinent Pathology and Pathophysiology As previously stated, the underlying pathology and pathophysiology of the peripheral nerve injury dictates its EDX and clinical manifestations. With intraneural microcirculation ischemia, such as when foot numbness follows peroneal nerve compression from leg crossing or hand numbness occurs at night during sleep, a metabolic conduction block occurs that is immediately reversible upon restoration of the circulation. In general, nerve fibers can tolerate up to 6 hours of ischemia before irreversible damage results.10–12 When forces produce focal myelin destruction, the term focal demyelination is applied. Because this type of pathology does not induce abnormalities distant to the lesion, it remains localized to the injury site (i.e., it is a focal pathologic insult).9,13,14 With forces large enough to disrupt the axon, however, the segment of nerve fiber distal to the disruption is detached from its cell body and thus undergoes degeneration in a series of steps termed wallerian degeneration.15,16 The latter process, which is referred to as axon loss, includes changes involving the distal nerve segment (e.g., intra-axonal fluid leakage, endoneurial edema, neurofibril loss, and fragmentation and digestion of the axon and myelin), the proximal nerve stump (e.g., variable degrees of retrograde degeneration), and the cell body (e.g., Nissl body breakdown and eccentric displacement of the nucleus and nucleolus).16 Because these changes involve the entire nerve fiber distal to the disruption, the EDX abnormalities associated with axon disruptions do not remain focal. In general, whenever focal injuries to large, heavily myelinated nerve fibers cause symptoms of greater than a few hours' duration, focal demyelination, axon loss, or some combination of the two is present. These two pathologic forms are associated with distinct pathophysiologies. Pathophysiologically, axon disruption is associated with conduction failure (related to wallerian degeneration), conduction block (prior to wallerian degeneration), and conduction slowing (following axon regeneration), whereas focal demyelination is associated

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with conduction block (when action potentials cannot traverse the lesion site) or conduction slowing (when action potentials traverse the lesion site at a slower rate). The EDX manifestations also reflect whether the lesion was abrupt or gradual in its onset.

3.4 The Electrodiagnostic Examination 3.4.1 Overview The EDX examination is an extension of the clinical neurologic examination and can be categorized as nerve conduction studies (NCSs), electromyography (EMG), and special studies. The motor NCSs and EMG assess the motor axons from their cell bodies of origin (i.e., lower motor neurons in the brainstem and spinal cord) to the muscle fibers that they innervate, whereas the sensory NCSs assess the sensory axons from their cell bodies of origin (i.e., dorsal root ganglia [DRG]) to the stimulating or recording site, whichever is more distal. Special studies, with the exception of the H-response (of value in the assessment of the S1-derived nerve fibers), are of limited value in the assessment of PNS injuries and will not be discussed. EDX studies yield information about the electrical status of assessable nerve and muscle fibers. When properly applied, EDX studies localize the lesion and determine the underlying pathophysiology and severity. This information, which often cannot be obtained in any other manner, has important diagnostic and prognostic implications of value in clinical management.

3.4.2 Nerve Conduction Studies There are three types of NCSs: sensory, motor, and mixed (▶ Fig. 3.1). With all three, bidirectionally propagating nerve fiber action potentials are generated by stimulus current applied percutaneously with the stimulating electrodes. With sensory and mixed NCSs, the recording electrodes are positioned over the nerve being studied, whereas with motor NCSs, they are placed over the motor point and tendon of one of the muscles innervated by the nerve being assessed. Like mixed responses, the sensory responses represent numerous nerve fiber action potentials traversing the larger diameter, more heavily myelinated nerve fibers; the action potentials generated along the smaller, lesser (or un-)myelinated nerve fibers do not contribute to these responses. Thus, the fibers that mediate pain are not measured with sensory NCSs. The recorded sensory responses are termed compound sensory nerve action potentials (SNAPs). Unlike sensory and mixed responses, recorded motor responses represent numerous muscle fiber action potentials. They are termed compound muscle fiber action potentials (CMAPs). These responses assess the larger, more heavily myelinated motor nerve fibers, the muscle fibers that they innervate, and their intervening neuromuscular junctions (NMJs). Each motor nerve fiber action potential generates multiple muscle fiber action potentials, the exact ratio of which is determined by the innervation ratio (the number of muscle fibers innervated per motor nerve fiber) of the muscle under study. For this reason, unlike sensory and mixed nerve responses, which are measured in microvolts, motor responses are measured in millivolts.

The Electrodiagnostic Examination with Peripheral Nerve Injuries positive phase to the peak of the subsequent negative phase when the response is triphasic. Biphasic SNAPs, like motor responses (CMAPs), are measured from the baseline to the initial negative peak (▶ Fig. 3.2). The amplitude is considered absolutely abnormal when it falls below the published or individual age-related laboratory control value for that response and relatively abnormal when it is less than half the value of the contralateral homologous response.9,17 Amplitudes reflect the number of functioning nerve fibers, the relative conduction rates of those fibers (i.e., their synchrony), and the distance between the stimulation and recording sites (longer distances produce temporal dispersion and lessen the amplitude). With PNS disorders, the amplitude value usually is the most informative response parameter measured because it reflects the number of functioning nerve fibers. Consequently, when surface recording electrodes are used (rather than needle electrodes), the CMAP amplitude provides a semiquantitative measure of the number of functioning nerve fibers. In addition, these values are directly related to negative clinical symptoms, such as muscle weakness and sensory loss. Despite their indispensability, amplitudes are the most neglected response parameter. Many clinicians ordering EDX examinations express little interest in them, and many electrodiagnosticians fail to record them.13,14,18

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3.4.5 Area

Fig. 3.1 The three types of nerve conduction studies (NCSs) performed in the electrodiagnostic laboratory: (a) motor, (b) sensory, and (c) mixed motor and sensory. With (a), the end point is a compound muscle action potential, whereas with (b) and (c), it is a nerve action potential, which is considerably smaller. (Used with permission from Isley MR, Kranss GL, Levin KH, Litt B, Shields RW, Wilbourn AJ. Electromyography/Electroencephalography. Redford, WA: SpaceLabs Medical; 1993.)

3.4.3 Evoked Response Parameters Whenever an NCS is performed, several attributes of the recorded response are analyzed, including the amplitude, area, latency, conduction velocity (CV), and duration. For each attribute, every EDX laboratory has its own set of normal values, which usually reflect patient age because they often vary considerably with age. In addition to these population-derived normal values, in the setting of a unilateral lesion, the best comparison for a given parameter is the value recorded when the same NCS is performed on the contralateral, asymptomatic side.

3.4.4 Amplitude This is the height of the evoked response. With sensory responses (SNAPs), it is measured from the trough of the initial

The area of the negative phase of the evoked response reflects its amplitude and duration and is expressed in millivolt-millisecond (CMAP) or microvolt-millisecond (SNAP) units (▶ Fig. 3.2). Most modern EMG machines calculate this value automatically. The area of the negative phase of the CMAP is a somewhat more accurate indicator than the amplitude for estimating the number of functioning motor nerve fibers in the studied nerve segment. It can be compromised by various factors, including axon loss, demyelinating conduction block, and temporal dispersion.

3.4.6 Latency Latency measurements reflect conduction velocities over fixed distances and are measured in milliseconds. With motor NCSs, the motor nerve fibers are stimulated at two sites along their course; thus two responses are generated. The response recorded with proximal stimulation is referred to as the proximal CMAP, whereas the one recorded with distal stimulation is the distal CMAP. With motor NCSs, the latency value of the distal CMAP (the time interval from the moment of nerve stimulation at the distal stimulation site to the onset of the distal CMAP) is reported as the distal latency. It indicates the CV along the fastest conducting motor nerve fibers and is reported (▶ Fig. 3.2). The onset latency of the proximal CMAP usually is not reported. Its value is used to calculate the CV along the fastest conducting motor nerve fibers. The distal motor latency also reflects the NMJ and muscle fiber action potential transmission times. With sensory NCSs, the sensory nerve fibers under study are stimulated at only one point, and the recorded latency value is reported as an onset or peak latency, depending on whether the time measurement is taken at the onset of the evoked response

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The Electrodiagnostic Examination with Peripheral Nerve Injuries

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Fig. 3.2 Compound muscle fiber action potential (CMAP) and sensory nerve action potential (SNAP) obtained by stimulating the median nerve at the wrist while recording, with surface electrodes, from the thenar eminence and the index finger. The amplitude, latency, and duration of each response are illustrated. (Used with permission from Isley MR, Kranss GL, Levin KH, Litt B, Shields RW, Wilbourn AJ. Electromyography/Electroencephalography. Redford, WA: SpaceLabs Medical; 1993.)

or at its first positive peak (▶ Fig. 3.2). Onset latencies reflect the fastest conducting fibers; peak latencies correspond to the average conduction rate of the fastest conducting fibers. These values do not provide accurate information about the number of functioning nerve fibers in the studied segment, and they underestimate the true conduction velocity.

3.4.7 Conduction Velocity Similar to latencies, conduction velocities reflect the speed of action potential propagation along the fastest conducting nerve fibers in the studied nerve segment. They are expressed in meters per second and are calculated by dividing the distance between the stimulating and recording electrodes (in millimeters) by the onset latency (in milliseconds). By expressing conduction rates in this manner, rather than as latencies, conduction velocities from different nerves within the same body segment (e.g., median and ulnar nerve forearm CVs) or from the same nerve in individuals with different body sizes (e.g., a child and a professional basketball player) can be compared regardless of the length of the nerve segment assessed. Like latency values, CV values reflect conduction rates and thus provide no information on the number of functioning nerve fibers in the studied segment. 13,14,18 Unfortunately, many physicians erroneously consider conduction velocity values to be the most informative response parameter, when in fact they are the least. With respect to peripheral nerve injuries, especially those of abrupt onset, CV values are insensitive.

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3.4.8 Duration The response duration is the time interval, in milliseconds, over which the negative phase occurs (see ▶ Fig. 3.2). It primarily reflects the uniformity of the conduction rates among the recorded action potentials.19 When the distance between the stimulating and recording electrodes is increased, phase cancellation due to physiologic dispersion results in response amplitude decrement. Because the duration of the negative phase of an individual muscle fiber action potential approaches that of the negative phase of the CMAP, and because the CVs of motor nerve fiber action potentials are more synchronous, physiologic dispersion is less of a problem with CMAPs than it is with SNAPs. Thus, longer segments of nerve can be evaluated with motor NCS techniques than with sensory ones. Whenever responses of low amplitude are recorded, it is important to assess their duration to determine whether the response is dispersed. Dispersion implies differential slowing and is a feature of demyelination.

3.4.9 Sensory Nerve Conduction Studies SNAPs are recorded proximal or distal to the stimulation site by using an orthodromic or antidromic technique, respectively. Of these, we prefer the antidromic technique because it yields higher SNAP amplitudes and is associated with less patient discomfort. Sensory NCSs are an indispensable part of the EDX assessment for several reasons. First, they are the only abnormal

The Electrodiagnostic Examination with Peripheral Nerve Injuries portion with disorders limited to sensory nerve fibers (e.g., sensory neuropathies) or neurons (e.g., paraneoplastic sensory neuropathy). Second, because only lesions at or distal to the DRG affect them, SNAP abnormalities have localizing value. They are observed with ganglionic and postganglionic lesions (plexopathies and neuropathies) but not with preganglionic ones (e.g., radiculopathies). Because the cell bodies of motor nerve fibers are located within the substance of the CNS, whenever normal SNAPs are associated with abnormal CMAPs from nerve fibers assessing the same portion of the PNS, a preganglionic (e.g., intraspinal canal or avulsion injury) axon loss lesion is implicated. (Although myopathies and NMJ disorders may demonstrate this same pattern of normal SNAPs and abnormal CMAPs, they usually are easily differentiated clinically.) Third, sensory NCSs are more sensitive than motor NCSs at identifying focal demyelination and axon loss lesions. With mild lesions, SNAP abnormalities may be the only NCS abnormality (i.e., the CMAPs are normal), whereas with more severe lesions, typically they are more pronounced than the CMAP abnormalities. For example, with early CTS, demyelinating conduction slowing is detectable along the sensory nerve fibers before the motor nerve fibers. With more severe disease, when axon loss is present, the SNAP amplitudes are either solely affected or more severely affected than the CMAP amplitudes. The major drawback of sensory NCS is the small size of the recorded responses, which renders them vulnerable to physiologic (e.g., age and dispersion), physical (e.g., temperature, obesity, and edema), and technical (e.g., electrode misplacement) factors, as well as to unrelated cutaneous neuropathies. In addition, individuals over the age of 60 years may have bilaterally absent lower extremity SNAPs. Moreover, because these studies do not assess the sensory receptors or the sensory nerve fiber segments distal to the surface electrodes, they do not identify disorders limited to these regions.13,20

3.4.10 Motor Nerve Conduction Studies Motor NCSs are orthodromic studies that differ considerably from sensory NCSs. Their distal latencies cannot be used to calculate the CV of the fastest conducting motor nerve fibers because these values reflect the motor nerve fiber, NMJ, and muscle fiber conduction times. For that reason, the motor nerve

fibers are stimulated at two points along their course, and two CMAPs are generated, a proximal CMAP and a distal CMAP (named for their relationship with the stimulation site, not the recording site). By measuring the distance and time differences between the two stimulation sites, the CV of the fastest conducting motor nerve fibers can be determined because the NMJ and muscle fiber conduction times are identical for the two responses and thus subtract out (▶ Fig. 3.3). Again, the major advantage of this technique is the magnification effect produced by the innervation ratio of the motor nerve fibers under study. This magnification reduces vulnerability to physiologic (e.g., temporal dispersion) and physical (e.g., obesity) factors and permits longer segments of nerve to be studied, thereby enhancing localization. Motor NCSs are also used to verify suspected malingering (or identify it when it is not suspected) because true weakness is associated with EDX abnormalities (on motor NCSs and EMG), whereas malingering is not. In addition, motor NCSs can be used to separate pure motor disorders (e.g., motor neuron disease, NMJ disorders, and myopathies) from sensorimotor ones (e.g., plexopathies and polyneuropathies), to identify peripheral nerve anomalies (e.g., Martin-Gruber anastomosis), and to differentiate acquired from hereditary demyelination. 14,21

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3.4.11 Mixed Nerve Conduction Studies With mixed NCSs, motor and sensory nerve fibers are stimulated simultaneously, and the mixed nerve action potential generated is recorded proximally (e.g., palmar studies for CTS). In general, with the exception of focal trauma to the palmar or plantar nerves, mixed NCSs have little to offer when assessing PNS injuries.9,14,18

3.4.12 Electromyography (Needle Electrode Examination) The standard EMG samples distal, middle, and proximal limb muscles, including paraspinal muscles, that are innervated by motor nerve fibers traversing different roots, plexus elements, and nerve trunks. The electrical activity from each of the studied muscles is recorded during one of three phases: insertion, rest, and activation.

Fig. 3.3 The procedure for determining a motor conduction velocity (in this instance, the median motor forearm conduction velocity, recording thenar eminence). (Used with permission from Isley MR, Kranss GL, Levin KH, Litt B, Shields RW, Wilbourn AJ. Electromyography/Electroencephalography. Redford, WA: SpaceLabs Medical; 1993.)

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The Electrodiagnostic Examination with Peripheral Nerve Injuries

3.4.13 Insertion Phase After penetrating the skin, the needle electrode lies in the substance of the muscle under study. At this point, it is advanced in small increments in multiple directions. Typically, each advancement is associated with a brief (less than one-third of a second) burst of electrical activity, termed insertional activity, which is related to electrode-induced mechanical excitation of the encountered muscle fibers. The amount of insertional activity recorded may be quantitatively abnormal. When fat or connective tissue replaces muscle fibers, the amount of insertional activity is pathologically decreased. Increased insertional activity may be normal (e.g., snap-crackle-pop potentials) or abnormal (e.g., brief trains of insertional positive waves that precede fibrillation potentials by ~ 1 week).22

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3.4.14 Rest Phase During the rest phase, which is defined as those time periods between electrode advancements, both normal (e.g., end-plate noise when the recording electrode is near an end-plate) and abnormal activity may be observed. Abnormal activity, collectively termed spontaneous activity, includes fibrillation potentials, fasciculation potentials, complex repetitive discharges (CRDs), myotonic discharges, grouped repetitive discharges (GRDs), and cramp potentials. Of these, fibrillation potentials are the most common type encountered and often the only type observed with PNS injuries. Fibrillation potentials are spontaneous muscle fiber action potentials that repeat with metronomic regularity at 0.5 to 15 Hz, a reflection of autonomous ion channel changes producing spontaneous muscle fiber depolarizations. These fibrillation potentials are the sine qua non of motor axon loss and usually appear 3 or more weeks after a muscle fiber has lost its innervation. They cannot be volitionally produced or suppressed. Because of the high innervation ratio of most limb muscles, a large number of fibrillation potentials are generated for each disrupted motor axon. This magnification effect makes the EMG the most sensitive EDX indicator of motor axon loss. This degree of sensitivity far exceeds that of motor NCSs and clinical examination. Although fibrillation potentials are nonspecific, their distribution has a strong localizing role, and their size and density provide information regarding lesion duration and severity. Fasciculation potentials are irregular and represent spontaneous firings of motor units or portions of motor units. They signify irritability, rather than denervation. They are of little importance when present in isolation. They are seen with axon loss lesions (typically in association with fibrillation potentials), chronic demyelinating processes (e.g., radiation plexopathy), and thyrotoxicosis. CRDs are nonspecific discharges that derive from the near synchronous firing of multiple muscle fibers, with one fiber ephaptically pacing the others. They typically are seen with lesions of at least 6 months' duration. They are much less common acutely. Myotonic discharges also are muscle fiber action potentials. They typically are associated with disorders of the muscle membrane. GRDs derive from the near synchronous firing of multiple motor nerve fibers, with one fiber ephaptically pacing the others. When two or more GRDs fire concurrently, the term myokymia is employed; this is seen with radiation-induced brachial plexopathy. Cramp potentials have a strong association

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with fasciculation potentials and, like them, reflect irritability. Unlike the temporal and spatial recruitment observed during muscle activation, cramps are associated with synchronous motor unit activation, with firing frequencies typically exceeding 40 Hz. This accounts for the accompanying pain, which is probably an ischemic manifestation.

3.4.15 Activation Phase This phase of the EMG reflects the electrical potentials of individual motor units. The CNS activates the muscle fibers of an individual motor unit by activating an individual lower motor neuron. The activated lower motor neuron activates all of the muscle fibers in its domain via a single motor nerve fiber action potential. The summation of the muscle fiber action potentials so generated is termed a motor unit action potential (MUAP) and is recorded by the needle electrode. These potentials are generated by asking the patient to voluntarily contract the muscle under study while the needle electrode is held stationary. During this phase, the recruitment, firing pattern, and morphology of the recruited MUAPs are analyzed. With light contraction, one or two MUAPs fire repetitively in a semiregular fashion at their basal rate of 5 to 10 Hz. With increasing effort, an increasing number of MUAPs (spatial recruitment) appear, and the previously recruited MUAPs begin to fire at faster frequencies (temporal recruitment), up to 40 Hz. As spatial recruitment increases further, individual MUAPs become indiscernible. This pattern of MUAP firing is referred to as a full interference pattern. It is estimated that full temporal recruitment increases muscle contraction force threefold or more above that obtainable by full spatial recruitment. Recruitment is abnormal when it is reduced or early. Early recruitment is observed with myopathies and NMJ disorders, whereas reduced recruitment is seen when action potential propagation is blocked along motor nerve fibers, such as with axon loss and demyelinating conduction block lesions. In this setting, fewer motor units are available (i.e., decreased spatial recruitment) for muscle contraction force generation. The unaffected ones are recruited normally in both the spatial and temporal dimensions. Thus, fewer MUAPs (i.e., reduced spatial MUAP recruitment) firing at a faster rate (i.e., the upper frequencies of temporal recruitment that are normally not discernible) are observed, and the interference pattern is said to be discrete, rather than full. This pattern of discordance between spatial and temporal recruitment is pathologic and is termed neurogenic recruitment. A discrete interference pattern is also observed with poor effort, pain on activation, hysteria/conversion reaction, malingering, and upper motor neuron disease. In these settings, however, spatial and temporal recruitment patterns are concordant. The morphology of the observed MUAPs is described in terms of its external (duration and amplitude) and internal (phases and turns) configuration, as well as its stability. Following muscle fiber denervation, reinnervation may occur via collateral sprouting, a process in which the motor axons of unaffected motor units sprout collateral branches that grow outward and adopt the denervated muscle fibers (Sunderland II and III degree injuries).23,24 This recaptures the lost muscle contraction force. Thus, with collateral sprouting, the innervation ratio of the adopting lower motor neuron increases. On EMG, this is reflected as an increase in MUAP duration (and less frequently by

The Electrodiagnostic Examination with Peripheral Nerve Injuries increases in MUAP amplitude). These changes, which persist indefinitely, are termed chronic neurogenic changes and are indicative of remote motor axon loss. By increasing the number of phases (directional changes with baseline crossings) and turns (directional changes without baseline crossings), collateral sprouting also affects the internal configuration of the MUAP. When neurogenic recruitment is due to demyelinating conduction block, the external and internal configurations of the MUAP are unaffected because the motor axons remain in continuity with their muscle fibers; thus, collateral sprouting does not occur. When demyelinating conduction block affects the terminal nerve branches distal to the motor axon, however, the number of phases and turns may increase. Collateral sprouting cannot occur in the setting of complete motor axon loss lesions (Sunderland IV and V degree injuries) because there are no unaffected motor nerve fibers from which to sprout. 23,24 In this scenario, reinnervation can only occur via axonal regrowth from the site of axon disruption. External and internal configuration changes also occur with this form of reinnervation. Initially, a MUAP of very low amplitude and extreme polyphasicity (i.e., more than four phases) is observed to fire at a slow to moderate rate in an unsustained manner. With remodeling, the duration and phase count decreases, and the amplitude increases. With reinnervation via axonal regrowth, the affected MUAPs may ultimately regain their normal appearance. 9,13,25,26

3.5 Important Limitations of the Electrodiagnostic Examination Seven inherent limitations of the EDX examination of patients with PNS injuries must be appreciated. First, patients with nerve injuries restricted to lightly myelinated and unmyelinated nerve fibers cannot be identified by EDX testing because standard NCSs only assess the larger, more heavily myelinated fibers, such as those conveying vibratory, position, and light touch sensation. Patients with loss of small fiber modalities (i.e., pain and temperature) have normal EDX studies.9,25 Second, pain and intermittent paresthesias do not have EDX correlates. Thus, patients with isolated paresthesias have normal EDX examinations. Microneurography can detect abnormalities associated with paresthesias, but it is a specialized procedure that is performed in only a few centers.27,28 Third, some nerve injuries are not assessable by EDX examination. Because NCSs best assess lesions involving nerve segments that permit stimulation to be applied both proximally and distally, lesions located at the proximal and distal extremes of the PNS are not well assessed. On EMG, only muscles accessible to the needle electrode can be studied. For these reasons, nerve injuries located at the proximal or distal extremes of a nerve or involving muscles that cannot be assessed by EMG are not assessable by EDX examination (e.g., ilioinguinal nerve injuries). Fourth, a number of confounding factors may compromise or inhibit EDX examination of a nerve injury, including (1) the presence of two or more separate lesions situated along the same nerve fibers, with the more proximal one being axon loss in type and more severe in degree; (2) the presence of an underlying generalized PNS disorder (e.g., polyneuropathy, especially when it is axon loss in type and severe in degree); (3) the presence of an unrelated PNS disorder located in the distribution of a lesser injury located more proximally (e.g., severe

CTS and a mild lateral cord or upper trunk lesion); and (4) the unavailability of stimulating or recording sites for NCSs or muscle access sites for EMG due to a variety of reasons (e.g., casts, bandages, intravenous lines, metal hardware stabilizing bones or joints, and denuded areas of skin). Fifth, EDX studies cannot discriminate between Sunderland II and V degrees of nerve injury until collateral sprouting (MUAPs) occurs in secondand third-degree injuries at 8 to 12 weeks (▶ Table 3.1).23,24 Sixth, although the clinical manifestations of nerve injuries typically are maximal at onset, most of the EDX manifestations are not. Instead, they appear over a 2- to 3-week period and, in general, require 3 to 5 weeks for full development. Seventh, reparative processes, which begin almost at the moment of injury, mask the EDX manifestations associated with these lesions.

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3.6 The Electrodiagnostic Manifestations of Peripheral Nerve Injuries 3.6.1 Axon Loss Axon loss is the most common type of nerve fiber pathology encountered in the EDX laboratory because the majority of acute and chronic nerve lesions are either exclusively or predominantly axon loss. The EDX abnormalities observed with this type of pathology depend on the severity of the lesion and its age. Regarding lesion severity, the EDX abnormalities associated with mild axon loss are confined to the EMG: only a small number of fibrillation potentials are observed. With greater degrees of axon loss, the number of fibrillation potentials increases, and the SNAP amplitudes begin to decrease. With even greater degrees of axon loss, the CMAP amplitudes also become affected. As the CMAP amplitudes are declining, neurogenic MUAP recruitment appears. When the axon loss lesion is total or near total, the SNAPs and CMAPs are unelicitable, fibrillation potentials are abundant, and the MUAP firing pattern is either absent (no MUAPs firing) or discrete (only a few MUAPs firing at faster than their basal rates). 9,13 The EDX manifestations of nerve injuries described above do not develop simultaneously but, rather, over predictable time intervals. In the setting of significant, but incomplete, axon loss lesions, the first EDX abnormalities appear on the EMG. At the moment of axon disruption, the MUAPs show reduced spatial recruitment and a discrete firing pattern. Importantly with complete lesions (Sunderland IV and V), no MUAPs are observed. The CMAP amplitudes begin to decrease in size around day 2 or 3 and reach their nadir around day 7, whereas the SNAP amplitudes begin to diminish around day 6 or 7 and reach their nadir around day 10 or 11 (▶ Fig. 3.4; ▶ Fig. 3.5). The CMAPs, which also assess NMJ status, are affected earlier than the SNAPs because NMJ transmission failure occurs before nerve fiber conduction failure.2,16,29–34 During this time interval, when the CMAP and SNAP amplitudes are diminishing, although wallerian degeneration has begun, some of the disrupted nerve fibers transiently maintain their ability to conduct action potentials. Thus, stimuli applied distal to the lesion are propagated along some of the degenerating nerve fibers and, as a result, contribute to the recorded CMAPs and SNAPs, whereas stimulation applied proximal to the lesion does not because the action potentials cannot traverse the lesion site. This phenomenon, termed

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The Electrodiagnostic Examination with Peripheral Nerve Injuries

Fig. 3.4 The progressive changes in the amplitudes of the motor and sensory nerve conduction responses on stimulating proximal and distal to an early (< 10 days) total axon loss lesion while recording distal to it. (Used with permission from Wilbourn AJ. Common peroneal neuropathy at the fibular head. Muscle Nerve 1986;9:825–836.)

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Fig. 3.5 The two nerve conduction study patterns observed with axon loss—axon discontinuity conduction block and conduction failure—are illustrated using an ulnar motor conduction study, recording from the hypothenar eminence, with the lesion located at the elbow segment (star). Note that the distal latency and conduction velocity are essentially unchanged by this lesion type. (Copyright by The Cleveland Clinic; 2001. Used with permission.)

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The Electrodiagnostic Examination with Peripheral Nerve Injuries axon discontinuity conduction block, may persist for up to 7 days with motor axon loss and for up to 11 days with sensory axon loss. Like the conduction block pattern observed with demyelination, it has localizing value. The important point, clinically, is that conduction block is not synonymous with demyelination during this time period; therefore, any pathologic or pathophysiologic conclusions should be made after this period.9,13,14 Around day 14, insertional positive sharp waves appear in the denervated muscles on EMG. These potentials persist for ~ 7 days (i.e., around day 21) and are then replaced by fibrillation potentials. The latter are most abundant between weeks 3 and 5.9,13 Insertional positive sharp waves and fibrillation potentials appear somewhat sooner with shorter distal nerve stumps and somewhat later with longer ones.35 When the timing of these EDX changes is not considered, inaccurate conclusions may be drawn. We will generally wait to do the first EDX study at 4 to 6 weeks to allow fibrillation potentials (seen in Sunderland II, III, IV, and V) enough time to declare themselves. In some cases, however, it may be important to get early studies to document baseline preinjury function. Another important point is that the latency and CV values associated with axon loss lesions are usually normal, even when measured across the lesion site, because they reflect the surviving (i.e., normally conducting) fibers rather than the affected ones. They may be affected with severe lesions or following reinnervation, however. Still, even when all or most of the fastest conducting fibers are involved (i.e., with severe axon loss lesions) and the latency and CV values are abnormal, their degree of abnormality is not nearly as pronounced as that of the amplitude decrement. The new nerve fibers associated with reinnervation have smaller diameters (higher resistance) and thinner myelin sheaths (increased capacitance) and therefore conduct more slowly. Consequently, the latency and CV values recorded after reinnervation may be abnormal.

3.6.2 Focal Demyelination The EDX manifestations associated with lesions producing focal demyelination reflect its severity. Action potential propagation along normally myelinated nerves occurs at the nodal regions and is referred to as saltatory (leaping) conduction, as it conducts from node to node (i.e., it “leaps” over the internodal regions). The sodium channel density of internodal axolemma is about one-tenth that of nodal axolemma.36 Consequently, as demyelination exposes the internodal axolemma, the rate of action potential propagation is slowed due to the smaller number of sodium channels. This type of pathophysiology is termed demyelinating conduction slowing. As more internodal axolemma is exposed, conduction ceases and the pathophysiologic term demyelinating conduction block is applied. Thus, milder lesions are associated with conduction slowing and more severe ones with conduction block. Neither type produces secondary changes away from the lesion site. These lesions are truly focal and can be recognized on NCSs when the recording and stimulating sites are on opposite sides of the lesion. With demyelinating conduction slowing, the action potentials traverse the lesion site at slower rates but ultimately reach their targets. Demyelinating conduction slowing can be divided into two types: uniform and differential. Uniform (synchronized) slowing occurs when the action potentials of the affected

nerve fibers are slowed to equal degrees; differential (unsynchronized) slowing occurs when the action potentials are slowed to differing degrees. With incomplete lesions involving the fastest conducting fibers, uniform slowing produces prolonged latencies and slowed CVs. It may produce temporal dispersion. With differential slowing, all three findings are expected. With temporal dispersion, the duration is increased, while the amplitude and area are relatively preserved (some amplitude and area are lost to phase cancellation) (▶ Fig. 3.6; ▶ Fig. 3.7). With demyelinating conduction slowing, there are no EMG abnormalities (i.e., insertional activity is normal, abnormal spontaneous activity is absent, and the configuration and firing pattern of the MUAPs are normal). With demyelinating conduction block, action potentials do not traverse the lesion site. In this setting, the responses recorded are smaller when the stimulating and recording electrodes are on opposite sides of the lesion. This is true for both SNAPs and CMAPs. In addition, because motor NCSs are performed at two sites along the motor nerve fibers under study, three patterns may be observed, depending on the location of the demyelinating conduction block lesion in relation to the stimulating and recording electrodes. When the lesion lies between the proximal and distal stimulation sites, a conduction block pattern is observed: the proximal CMAP is substantially smaller (or absent with complete lesions) than the distal CMAP because the action potentials cannot traverse the lesion site (▶ Fig. 3.8). When both stimulation sites are distal to the lesion, however, an amplitude discrepancy is not observed because only the normally conducting distal segment is being assessed. Thus, the two responses are normal in their appearance. When both stimulation sites are located proximal to the lesion, a conduction failure pattern is observed (i.e., the two responses are equally reduced in amplitude or, with complete lesions, unelicitable) because both sites require the propagating action potentials to traverse the lesion site. With significant lesions, these changes typically are apparent immediately after the injury. The EMG abnormalities associated with demyelinating conduction block lesions of at least moderate severity resemble axon loss—neurogenic recruitment and fibrillation potentials. Fibrillation potentials are seen because most symptomatic demyelinating conduction block lesions are associated with at least a few disrupted motor axons. Due to the high innervation ratio of most skeletal muscles, these few disruptions may be associated with a large number of fibrillation potentials and mislead the examiner into believing that a severe axon loss lesion is present. Because the number of disrupted motor axons is minimal, chronic neurogenic MUAP changes do not follow.9,13

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3.7 Electrodiagnostic–Clinical Correlations With axon loss lesions, the affected nerve fibers are incapable of conducting action potentials. As a result, negative clinical manifestations appear. Motor nerve fiber involvement produces weakness and muscle atrophy, while sensory nerve fiber involvement produces impairment of both large diameter (i.e., vibration, proprioception, and light touch) and small diameter (i.e., pain and temperature) sensory modalities. With demyelinating conduction block lesions, similar clinical manifestations

67

The Electrodiagnostic Examination with Peripheral Nerve Injuries

Fig. 3.6 The nerve conduction pattern seen when focal demyelination causes uniform slowing along (a) the ulnar motor nerve fibers at the wrist, producing a prolonged distal latency, and (b) at the elbow, producing a slowed conduction velocity. Lesion locations are marked with stars. The prolonged distal latency demonstrated in (a) is solely for illustration purposes because prolonged motor distal latencies rarely are seen with ulnar neuropathies at the wrist; instead, most lesions at this location cause conduction failure or conduction block, not conduction slowing. (Copyright by The Cleveland Clinic; 2001. Used with permission.)

3

Fig. 3.7 The nerve conduction pattern seen when focal demyelination causes differential slowing along a nerve. The lesion location along the ulnar nerve at the elbow is marked with a star. (Copyright by The Cleveland Clinic; 2001. Used with permission.)

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The Electrodiagnostic Examination with Peripheral Nerve Injuries

Fig. 3.8 The nerve conduction pattern seen when focal demyelination causes conduction block along some or all of the motor nerve fibers of a nerve. The lesion location along the ulnar nerve at the elbow is marked with a star. (Copyright by The Cleveland Clinic; 2001. Used with permission.)

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result, with two exceptions. First, the small fiber sensory modalities (i.e., pain and temperature perception) are spared because these fibers are small-diameter fibers that are unmyelinated or only thinly myelinated and tend to be less affected by lesions producing demyelinating conduction block. Second, because the affected motor axons remain in continuity with the muscle fibers, muscle atrophy does not develop. Over time, if remyelination does not occur, disuse atrophy may appear. With demyelinating conduction slowing, weakness does not occur because all of the motor nerve fiber action potentials traverse the lesion site to reach their muscle fiber targets. Because the action potentials generated at the sensory receptor level also traverse the lesion site, sensory symptoms are unexpected. However, with differential slowing, the sensory nerve fiber action potential volleys are less synchronized. Thus, vibratory perception and muscle stretch reflexes, both of which depend on the synchronous arrival of action potentials, may be impaired. These two abnormalities do not appear with uniform slowing because the action potential volleys maintain their synchronicity. Focal slowing, both differential and uniform, may produce positive symptoms (e.g., paresthesias).14

3.8 The Differences between Lesions of Varying Onset and Severity The type of pathophysiology occurring with nerve injuries reflects not only the severity of the lesion, but also its acuteness (▶ Table 3.2).

With abrupt onset lesions, the majority of which are traumatic, the pathophysiology generally is axon loss, demyelinating conduction block, or a combination of the two. Of these possibilities, isolated axon loss is the most common, especially when the lesion is severe in degree. With gradual onset lesions (e.g., chronic entrapment) of moderate or lesser severity, the associated pathophysiology is axon loss, demyelinating conduction slowing, or both. Of these, isolated axon loss again predominates. When acute disorders produce focal demyelination, conduction block typically results (termed neurapraxia or Sunderland I degree injury, clinically), whereas the demyelination associated with chronic or slowly progressive disorders is usually associated with conduction slowing. With CTS (a slowly progressive, chronic entrapment disorder), essentially all patients manifest focal demyelinating conduction slowing that typically is uniform in type. These patients do not demonstrate significant axon loss until the process is quite advanced. With chronic ulnar neuropathies at the elbow segment, about half of the patients show focal demyelinating conduction slowing that typically is differential in nature. Demyelinating conduction slowing also occurs with peroneal neuropathies at the fibular head. Otherwise, demyelinating conduction slowing is rarely observed with focal neuropathies, especially if they are abrupt in onset. An example of how the abruptness of onset affects the pathophysiology of the nerve lesion, and hence its EDX manifestations, follows. With mild to moderate median neuropathies due to CTS, the underlying etiology is chronic entrapment of the median nerve within the carpal tunnel. Its pathology is demyelination, and its pathophysiology, at least initially, is uniform conduction slowing. The EDX examination typically discloses

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The Electrodiagnostic Examination with Peripheral Nerve Injuries Table 3.2 Types of Pathophysiology Seen with Lesions of Various Nerves

3

Nerve Lesion

Most Common Pathophysiology

Less Common Pathophysiology

Acute nerve injuries

Axon loss

Demyelinating conduction block

Carpal tunnel syndrome

Focal demyelinating conduction slowing

Axon loss (late in course)

Ulnar neuropathy at the elbow

Axon loss

Demyelinating conduction slowing, demyelinating conduction block

Ulnar neuropathy at the wrist

Axon loss

Demyelinating conduction block

Radial neuropathy at the spiral groove

Axon loss

Demyelinating conduction block

Posterior interosseous neuropathy

Axon loss

Anterior interosseous neuropathy

Axon loss

Peroneal neuropathy at the fibular head

Axon loss

Demyelinating conduction block

Source: Used with permission from Wilbourn AJ. The electrodiagnostic examination with peripheral nerve injuries. In: Mackinnon SE, ed. Clinics in Plastic Surgery: Peripheral Nerve Surgery. Philadelphia, PA: WB Saunders; 2003:139-154.

prolonged latencies, normal amplitudes, and a normal EMG. Clinically, most patients complain of intermittent paresthesias in the median nerve innervated digits that are worse at night.37 Conversely, with acute median neuropathies occurring within the carpal tunnel, the cause is usually an abrupt injury, the pathology is primarily axon loss (less commonly demyelination), and the pathophysiology is more often conduction failure (less frequently conduction block). NCS responses usually are unelicitable, or, less commonly, low-amplitude responses with normal latencies are observed. On EMG, neurogenic or absent MUAP recruitment and abundant fibrillation potentials (if the lesion is more than 21 days old) are observed. Clinically, the patient complains of marked weakness and sensory loss in the median nerve distribution.

3.8.1 The Proper Application of Electrodiagnostic Studies The EDX examination plays a major role in the evaluation of patients with suspected neuropathies, and all of its primary components—sensory NCS, motor NCS, and EMG—are useful. Only the sensory NCSs assess the sensory nerve fibers, and these studies are not only sensitive to axon loss, but are quite useful in lesion localization. Abnormal SNAPs indicate that the lesion lies at or distal to the DRG, and, in the setting of brachial plexus lesions, SNAP abnormalities typically can localize the lesion to a specific brachial plexus element before any other component of the EDX study is performed.17 By assessing the motor nerve fibers at multiple points along their course, motor NCSs localize focal demyelinating lesions; in the acute setting, they can provide semiquantitative assessments of lesion severity (axon loss and demyelinating conduction block). The EMG is the most sensitive component of the EDX study for the detection of motor axon loss, provided enough time has elapsed for denervation potentials to appear. When present, reinnervational MUAP changes identify the chronicity of the lesion. In addition, the relationship between the acute and chronic EMG abnormalities provides an indication of the rate of progression of the process. Moreover, EMG permits a wider sampling of the PNS because far more muscles can be assessed than nerves.9

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Again, the timing of the EDX examination in relation to the onset of the lesion is crucial. In general, the best time to perform an EDX examination is 3 to 6 weeks after the nerve injury. Prior to that time, the information gleaned is more limited but may still be of value in certain situations. First, when the presence of preexisting abnormalities is a concern, the study could be performed on the days of the injury (e.g., when a patient complains of hand numbness postoperatively and a preoperative neuropathy is suspected as a potential predisposition). Except for abnormalities of spatial recruitment, which are apparent immediately after nerve injuries that produce significant axon loss or demyelinating conduction block, all other abnormalities reflect preexisting disease. Second, with sharp nerve lacerations, immediate surgical repair typically is indicated. In some cases, such as for delayed presentations, EDX testing may be useful to determine completeness of the lesion. In this setting, the presence of volitional MUAPs in muscles innervated by the affected nerve indicates an incomplete lesion. Third, because lesions producing axon discontinuity conduction block are localizable prior to their conversion to conduction failure, and because they give estimations of the completeness of the lesion, motor NCSs performed during the first several days may be helpful. For example, should a patient awaken from hip surgery with an ipsilateral foot drop, the clinical question of whether the foot drop reflects a sciatic neuropathy at the surgical site or compression at the fibular head could be answered by performing a peroneal CMAP, recording from the tibialis anterior muscle, while stimulating above and below the fibular head. If conduction block is identified, its severity can be determined by the difference between the two responses, and its pathophysiology can be determined by repeating the study after the first week. If a conduction block is not identified with stimulation above the fibular head, then the lesion lies proximally. In this case, a sciatic neuropathy at the surgical site would be more likely. If the lesion were due to axon loss, and the study had been deferred until the second week, then the motor NCSs would not be of localizing value (conduction failure would be present), and it would be too soon to perform an EMG. EDX examinations are usually ordered on patients with known sensorimotor deficits confined to a single limb for lesion

The Electrodiagnostic Examination with Peripheral Nerve Injuries characterization (i.e., localization, underlying pathophysiology, severity, duration, and rate of progression). Its utility for lesion localization reflects the location (e.g., preganglionic vs. postganglionic), severity, and pathophysiology of the lesion, as well as the type of axons injured (motor, sensory, or mixed). The age of an axon loss lesion can be estimated, as well as its rate of progression. With neuropathies, EDX testing can localize the lesion to a particular nerve point (with NCSs) or segment (NCSs and EMG).14 Point localization requires that the lesion produce focal conduction slowing or block and be situated at a site where recording and stimulating electrodes can bracket it (e.g., at the fibular head). It is the most accurate degree of electrical localization possible and is only possible with NCSs. Segmental localization places the lesion somewhere between the motor branches innervating the most distal normal muscle and the most proximal abnormal muscle. This degree of accuracy is best achieved by EMG and requires knowledge of the branching order of the muscles under study. It is the EDX equivalent of clinical localization by muscle strength assessment. Its precision reflects the site of the lesion, the number and takeoff sites of the motor branches of the affected nerve, and the accessibility of the muscle domain of the affected nerve to EMG. The ideal nerve for localization by this technique is the radial nerve and its motor continuation, the posterior interosseous nerve, because a large number of motor branches arise from these two nerves, and most of the neuropathies affecting them are situated between the origins of two of these branches. In contrast, the median and ulnar nerves are less amenable to this form of localization because they contain long segments of nerve from which no motor branches arise (i.e., axillary, arm, and forearm segments). Individual variability in the branching order and the number of branches going to each muscle, as well as the particular nerve innervating the muscle under study, may impair this approach. Fascicular sparing may also interfere with localization by this method. For example, when partial ulnar neuropathies at the elbow spare the ulnar-innervated forearm muscles, the lesion may be mislocalized to the distal forearm or wrist. Lesion severity and duration must also be considered. Mild and remote lesions both tend to harbor more EMG abnormalities in the more distal muscles and thus are associated with distal mislocalizations.14 Two examples of deductive localization follow. First, with SNAP abnormalities, the responsible lesion lies at or distal to the DRG. Pairing is another form of deductive localization. With this technique, abnormal NCS responses are localized by performing other NCSs that assess some, but not all, of the PNS elements assessed by the abnormal one. For example, in the setting of an absent ulnar SNAP, the presence of absent median and ulnar CMAPs and a normal median SNAP indicates that the lesion lies proximal to the ulnar nerve (e.g., medial cord or lower trunk). Less commonly, EDX studies are performed to verify the existence of a nerve lesion, such as when the possibility of a CNS process or a nonorganic disorder (e.g., hysteria/conversion or malingering) is being considered. In general, EDX studies easily discriminate between nonorganic and organic causes of weakness because substantial muscle weakness is always accompanied by prominent EDX abnormalities. With nonorganic lesions, the recorded CMAPs are normal, fibrillation potentials are absent, and there usually is a considerable reduction in MUAP recruitment related to poor effort. With organic lesions involving

the PNS, the recorded CMAPs are low in amplitude or unelicitable whenever the underlying pathophysiology is axon loss. With demyelinating conduction block, however, motor NCSs only disclose its presence when the stimulating and recording electrodes can be positioned on opposite sides of the lesion. When a demyelinating conduction block lesion is situated proximal to the midtrunk level of the brachial plexus (i.e., the most proximal site at which upper extremity nerves can be stimulated), its presence may be inferred when discordant information is obtained from the motor NCSs and the EMG (i.e., when the CMAP recorded from a muscle is normal or near-normal, but EMG of that same muscle shows a neurogenic MUAP firing pattern). On EMG, reductions in spatial recruitment are prominent with both axon loss and demyelinating conduction block. With axon loss lesions, depending on lesion chronicity and severity, fibrillation potentials and neurogenic MUAP changes also may be observed. The presence of isolated fibrillation potentials does not necessarily indicate that the lesion is predominantly axon loss because predominantly demyelinating lesions often show abundant fibrillation potentials. EDX studies are useful for differentiating pathologic atrophy from disuse atrophy, as disuse atrophy (e.g., marked quadriceps wasting following cast removal) does not produce EDX abnormalities.9 EDX testing can identify mechanical causes of weakness (e.g., tendon rupture). In this setting, although the action of the muscle with the ruptured tendon is not observed, EMG of that muscle shows normal MUAP recruitment and a full interference pattern.9

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3.9 Prognosis Traumatic lesions producing focal demyelination (neurapraxia) have an excellent prognosis because no or very few axons undergo wallerian degeneration, and remyelination usually occurs within a few weeks to a few months. Although the new internodes are shorter in length and have thinner myelin coatings, both of which produce slower conduction rates, there are no clinical correlates (i.e., patients are asymptomatic). With axon loss lesions, the completeness of the lesion and the distance between the lesion and the denervated muscle fibers are important for initial prognostication and for the planning of subsequent studies. The completeness of the lesion is estimated by motor NCSs, prior to reinnervation, by comparing the distal CMAP amplitudes recorded from the two sides. The distance between the lesion and the denervated muscle fibers is determined by measurement, assuming the lesion is localizable. Reinnervation occurs via two mechanisms: collateral sprouting and axonal regrowth. Collateral sprouting occurs quicker, as the unaffected motor nerve fibers simply have to sprout collateral branches to the neighboring denervated muscle fibers. Collateral sprouting, like remyelination, occurs early (within 3 to four months), as exemplified by the case shown in ▶ Table 3.3. This mechanism necessitates that the injury be incomplete because it requires unaffected motor nerve fibers. With axonal regrowth, the nerve fibers sprout from the proximal axon stump and grow toward the muscle fibers at a rate of just over 1 inch per month.38 This form of reinnervation has the best outcome when the distance between the injury site and the denervated muscle fibers is short because muscle fibers degenerate when they remain denervated for a prolonged period of time.

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The Electrodiagnostic Examination with Peripheral Nerve Injuries Table 3.3 An electromyogram from a patient with a closed brachial plexus injury secondary to a motor vehicle accident. This study, which was performed 4 months postinjury, reveals denervation (fibrillations) in multiple muscles throughout the upper extremity. The infraspinatus, deltoid, flexor carpi ulnaris, and first dorsal interosseous muscles show evidence of recovery secondary to collateral sprouting because early motor unit action potentials (MUAPs) are present. The nerves innervating these 4 muscles therefore have a Sunderland II or III injury, and a good prognosis for spontaneous recovery. On the other hand, the biceps, triceps, pronator teres, brachioradialis, extensor digitorum communis, and abductor pollicis brevis muscles demonstrate no MUAPs at 4 months, indicating a more severe nerve injury (Sunderland IV or V) that is not likely to recover spontaneously; surgical intervention is therefore warranted. Muscle

Spontaneous Activity

Volitional MUAPs

Fibs

+ Wave

Fasc

Duration

Amplitude

Polyphasis

Increased

2+

2+

None

Increased

Decreased

Few

Biceps brachii (long head) Increased

3+

3+

None

Triceps brachii (long head) Increased

2+

2+

Pronator teres

Increased

3+

3+

None

No MUAPs

Brachioradialis

Increased

2+

2+

None

No MUAPs

Extensor digitorum communis

Increased

4+

4+

None

No MUAPs

Flexor carpi ulnaris

Increased

1+

1+

None

Increased

Increased

Few

FDI

Normal

1+

1+

None

Increased

Decreased

Many

APB

Increased

3+

3+

None

Supraspinatus

Normal

None

None

None

Normal

Normal

None

Normal

Reduced

Infraspinatus

Increased

1+

None

None

Gradual increase

Decreased

Many

Normal

Reduced

Generic muscle

Normal

None

None

None

Normal

Normal

Few

Normal

Reduced

3 Deltoid

Insertional Activity

Configuration Recruitment Reduced No MUAPs No MUAPs

Normal Normal

Reduced No MUAPs

Abbreviations: APB = abductor pollicis brevis; Fasc = fasciculations; Fibs = fibrillation potentials; FDI = first dorsal interosseous; MUAPs = motor unit action potentials.

Thus, the worst prognosis is associated with complete lesions that are located far from the denervated muscle fibers, and the best prognosis occurs with incomplete lesions located near the denervated muscle fibers. With second-degree lesions, the prognosis is usually excellent because intact endoneurial tubes permit unobstructed axonal regrowth. With third-degree lesions, the prognosis depends on the ability of the sprouting axons to grow across the lesion and enter the proper endoneurial tubes. This depends on the degree of connective tissue proliferation (scarring) along their path but usually results in useful recovery. With fourth-degree lesions, there is marked internal disorganization of the connective tissue elements, and the prognosis for recovery by axonal regrowth is poor. In general, fourth- and fifth-degree lesions require surgical intervention for maximal improvement. This can be direct (i.e., reapproximation of the ends), indirect (i.e., nerve grafting), or via nerve transfer. In cases in which it is impossible to determine the degree of nerve injury, surgical exploration with intraoperative recording may be necessary. Whenever the EMG study shows a lack of fibrillation potentials (i.e., a lack of denervated muscle fibers), then further functional motor recovery is unlikely, given that there are no denervated muscle fibers to reinnervate. Thus in this setting, the denervated muscle fibers have either been reinnervated or have been replaced by fibrofatty tissue (i.e., have degenerated). However, when a lack of fibrillation potentials is observed in the setting of chronic changes, there are two possibilities: a

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remote process for which reinnervation is complete or a slowly progressing process in which reinnervation is keeping pace with denervation (as is seen with spondylosis). These concepts are exemplified by the case depicted in ▶ Table 3.4.

3.10 Clinical Comments Electrodiagnostic testing is a useful adjunct in peripheral nerve disorders. However, EDX does not replace the value of a thorough history and physical examination, which are invaluable in the diagnosis and localization of nerve injury or compression. CTS in particular is a clinical diagnosis and many advocate that EDX studies are not warranted in the setting of classic carpal tunnel symptoms.39 Furthermore, 11% of patients with CTS can have normal EDX studies. This finding should not preclude appropriate treatment when clinical findings are strongly suggestive of CTS.40 An often unrecognized advantage of preoperative EDX testing in the setting of classic carpal tunnel symptoms is when the patient complains that they are worse following a release procedure. Typically, this reflects nerve fiber recovery with resultant transition from numbness to tingling. In this setting, repeat testing shows improvement of the previously abnormal values, thereby verifying that the procedure was successful. Return to normal values may not be observed because remyelination produces thinner and shorter internodes.

The Electrodiagnostic Examination with Peripheral Nerve Injuries Table 3.4 An electromyogram from a 73-year-old patient presenting with symptoms of left cubital tunnel syndrome. This EMG demonstrates chronic changes (no fibrillations, abnormal motor unit action potentials) in the first dorsal interosseous, triceps, and flexor carpi radialis muscles, as well as active denervation (positive fibrillations) of the flexor carpi ulnaris and abductor pollicis brevis muscles. Taken together with the nerve conduction studies (not shown), this EDX study showed evidence of left cubital tunnel syndrome, chronic C7 radiculopathy, and possible C8–T1 radiculopathy. Muscle

Insertional Activity Spontaneous Activity

Volitional MUAPs

Fibs/PSW Fasc

Other

Duration

Amplitude

Polyphasicity Recruitment

FDI

Normal

None

None

None

S1 increased

S1 increased

Normal

Sev red

APB

Normal

1+

1+

None

Moderate increase

Moderate increase

Normal

Moderate reduction

Flexor pollicis longus

Normal

None

None

None

Normal

Normal

Normal

Normal

Flexor carpi ulnaris

S1 increased

None

2+

None

Gradual increase Moderate increase

Normal

Sev red

Extensor carpi ulnaria

Normal

None

None

None

Normal

Normal

Normal

Normal

Flexor carpi radialis

Normal

None

None

None

S1 increased

S1 increased

Normal

Mild reduction

Triceps brachii (lateral head)

Normal

None

None

None

S1 increased

S1 increased

Normal

Mild reduction

Deltoid (middle)

Normal

None

None

None

Normal

Normal

Normal

Normal

3

Abbreviations: APB = abductor pollicis brevis; Fasc = fasciculations; Fibs = fibrillation potentials; FDI = first dorsal interosseous; MUAPs = motor unit action potentials; PSW = positive sharp waves.

EDX studies can be difficult to interpret by the surgeon treating the patient. As with all other areas of medicine, there is also considerable variability in the quality of EDX studies among electrodiagnosticians, and results may vary, as indicated in this chapter, with a number of physical and nonphysical factors. The surgeon should not be afraid to discuss the results of a study with the electrodiagnostician to clarify areas that are inconsistent with the clinical exam or to clarify the examiner‘s thoughts on the study findings. In important situations where the EDX findings may determine the need for surgical intervention (e.g., no evidence of recovery at 3 months following a brachial plexus injury), we have found that obtaining EDX examinations from skilled neurologists who see a high volume of peripheral nerve disorders is invaluable. The relationship of the Sunderland degrees of nerve injury to EDX findings is shown in the leftmost column of ▶ Table 3.1. Fibrillations appear at approximately 3 to 6 weeks and are seen in Sunderland II injuries and above. MUAPs are also a key finding on EDX examination because they indicate recovery and portend a good prognosis without surgical intervention (e.g., Sunderland II and III injury vs. IV and V). Over time, we have come to understand that there are several types of MUAPs. The MUAPs seen at 8 to 12 weeks following injury represent collateral sprouting from neighboring uninjured axons, whereas nascent MUAPs are seen later and represent actual regeneration of the injured axons to the target end plates. In chronic axonal injury, fibrillations disappear, and MUAPs with a different configuration than that seen in normal muscle are seen, which we refer to as “chronic MUAPs.” Intraoperative electrical stimulation can also help differentiate between an ischemic conduction block, focal demyelination (Sunderland I, neurapraxia), and axonal loss (Sunderland II/III) in the setting of an entrapment neuropathy. In both a demyelinating and ischemic block (Sunderland I), nerve stimulation distal to the site of entrapment will produce more vigorous muscle contractions than stimulation proximal to the compres-

sion site. When the compression site is released, stimulation proximal to the compression site will improve the muscle response almost immediately if the conduction block is due to ischemia, the differentially poorer stimulation response will persist if focal demyelination is present. Neurapraxia may take up to 3 months to completely resolve. In contrast, axonal injury (Sunderland II, III) will yield uniformly weak or no muscle response irrespective of whether one is proximal or distal to the entrapment point. When axonal injury is present, complete (Sunderland II) or incomplete (Sunderland III) recovery can be expected to occur over a period of several months.

3.11 Conclusion The indications for and limitations of the EDX examination of peripheral nerve injuries have been reviewed. Although it is an extension of the clinical examination, it can yield information not apparent by any other means, including the clinical examination. It not only confirms and localizes the lesion, but by demonstrating its pathophysiology and severity, it provides information useful for clinical management and prognostication. The EDX examination should never be curtailed, and its findings must always be considered in regard to the age of the lesion.

3.12 References [1] Thomas PK. Differential diagnosis of peripheral neuropathies. In: Refsum S, Bolis CL, Portera-Sanchez A, eds. International Conference on Peripheral Neuropathies. Amsterdam, Netherlands: Excerpta Medica; 1982:82 [2] Robinson LR. Traumatic injury to peripheral nerves. Muscle Nerve 2000;23:863–873 [3] Seddon HJ. Surgical Disorders of the Peripheral Nerves. 2nd ed. New York, NY: Churchill Livingstone; 1975 [4] Owens BD, Kragh JF, Wenke JC, Macaitis J, Wade CE, Holcomb JB. Combat wounds in Operation Iraqi Freedom and Operation Enduring Freedom. J Trauma 2008;64:295–299

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The Electrodiagnostic Examination with Peripheral Nerve Injuries [5] Defense. Department of Defense Casualty Reports. 2012 [updated February 2, 2012]. http://www.defense.gov/news/casualty.pdf [6] Kelsey J, Praemer A, Nelson L, Felberg A, Rice D. Upper Extremity Disorders: Frequency, Impact and Cost. New York, NY: Churchill Livingstone, 1997 [7] Kouyoumdjian JA. Peripheral nerve injuries: a retrospective survey of 456 cases. Muscle Nerve 2006;34:785–788 [8] Noble J, Munro CA, Prasad VS, Midha R. Analysis of upper and lower extremity peripheral nerve injuries in a population of patients with multiple injuries. J Trauma 1998;45:116–122 [9] Wilbourn AJ, Ferrante MA. Clinical electromyographyo. In: Joynt RJ, Griggs RC, eds. Baker’s Clinical Neurology [book on CD-ROM]. Philadelphia, PA: WB Saunders; 2000:record 7592–8248 [10] Lundborg G. Structure and function of the intraneural microvessels as related to trauma, edema formation, and nerve function. J Bone Joint Surg Am 1975;57:938–948 [11] Dahlin LB, Rydevik B, McLean WG, Sjöstrand J. Changes in fast axonal transport during experimental nerve compression at low pressures. Exp Neurol 1984;84:29–36 [12] Lundborg G, Dahlin LB. Pathophysiology of peripheral nerve trauma, In: Omer Jr GE, Spinner M, Van Beek AL, eds. Management of Peripheral Nerve Problems. 2nd ed. Philadelphia, PA: WB Saunders; 1998:353–363 [13] Ferrante MA, Wilbourn AJ. Basic principles and practice of electromyography. In: Younger DS, ed. Motor Disorders. Philadelphia, PA: Lippincott Williams & Wilkins; 1999:19–44 [14] Wilbourn AJ. Nerve conduction studies: types, components, abnormalities, and value in localization. Neurol Clin 2002;20:305–338, v [15] Waller A. Experiments on the section of the glossopharyngeal and hypoglossal nerves of the frog and observations of the alterations produced thereby in the structure of their primitive fibres. Phil Trans R 1850;140:423–429 [16] Dumitru D. Electrodiagnostic Medicine. Philadelphia, PA: Hanley & Belfus; 1995:341–384 [17] Ferrante MA, Wilbourn AJ. The utility of various sensory nerve conduction responses in assessing brachial plexopathies. Muscle Nerve 1995;18:879–889 [18] Lederman RJ. Nerve conduction studies. In: Levin KH, Luders HO, eds. Comprehensive Clinical Neurophysiology. Philadelphia, PA: WB Saunders; 2002:89–111 [19] Kimura J, Machida M, Ishida T, et al. Relation between size of compound sensory or muscle action potentials, and length of nerve segment. Neurology 1986;36:647–652 [20] Wilbourn AJ. Sensory nerve conduction studies. J Clin Neurophysiol 1994;11:584–601 [21] Lambert EH. Diagnostic value of electrical stimulation of motor nerves. EEG J 1962 (Suppl 22):9–16 [22] Wilbourn AJ. An unreported, distinctive type of increased insertional activity. Muscle Nerve 1982;5 9S:S101–S105 [23] Seddon HJ. Three types of nerve injury. Brain 1943;66:237–288

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[24] Sunderland S. A classification of peripheral nerve injuries producing loss of function. Brain 1951;74:491–516 [25] Kimura J. Electrodiagnosis in Diseases of Nerve and Muscle. 3rd ed. New York, NY: Oxford University Press; 2001 [26] Doherty TJ, Ming Chan K, Brown WF. Motor neurons, motor units, and motor unit recruitment. In: Brown WF, Bolton CF, Aminoff MJ, eds. Neuromuscular Function and Disease. Philadelphia, PA: WB Saunders; 2002:247–273 [27] Seivak M, Ochoa J, Fernandez JM. Positive manifestations of nerve fiber dysfunction: clinical, electrophysiologic, and pathologic correlates. In: Brown WF, Bolton CF, eds. Clinical Electromyography. 2nd ed. Boston, MA: Butterworth-Heinemann; 1993:117–147 [28] Chavin JM, Brown WF. Negative signs and symptoms of peripheral nerve and muscle disease. In: Brown WF, Bolton CF, Aminoff MJ, eds. Neuromuscular Function and Disease. Philadelphia, PA: WB Saunders; 2002:369–385 [29] Lissak K, Dempsey EW, Rosenblueth A. The failure of transmission of motor nerve impulses in the course of Wallerian degeneration. Am J Physiol 1939;128:45–56 [30] Gutmann E, Holubar J. Failure of transmission of motor and sensory nerve impulses after nerve section. Nature 1949;163:328–329 [31] Gilliatt RW, Taylor JC. Electrical changes following section of the facial nerve. Proc R Soc Med 1959;52:1080–1083 [32] Birks R, Katz B, Miledi R. Physiological and structural changes at the amphibian myoneural junction, in the course of nerve degeneration. J Physiol 1960;150:145–168 [33] Gilliatt RW, Hjorth RJ. Nerve conduction during Wallerian degeneration in the baloon. J Neurol Neurosurg Psychiatry 1972;35:335–341 [34] Griffin JW, George EB, Chaudry V. Wallerian degeneration in peripheral nerve disease. In: Harting HP, ed. Bailliere’s Clinical Neurology: Peripheral Neuropathies: Part 2. 1996;5:65–75 [35] Thesleff S. Trophic functions of the neuron. II. Denervation and regulation of muscle. Physiological effects of denervation of muscle. Ann N Y Acad Sci 1974;228:89–104 [36] Dodge FA, Cooley JW. Action potential of the motor neuron. IBM J Res Develop 1973;17:219–229 [37] Holmlund T, Wilbourn AJ. Acute median neuropathy at the wrist is not carpal tunnel syndrome. Muscle Nerve 1993;16:1099 [38] Buchthal F, Kühl V. Nerve conduction, tactile sensibility, and the electromyogram after suture or compression of peripheral nerve: a longitudinal study in man. J Neurol Neurosurg Psychiatry 1979;42:436–451 [39] Jablecki CK, Andary MT, So YT, Wilkins DE, Williams FH, AAEM Quality Assurance Committee. Literature review of the usefulness of nerve conduction studies and electromyography for the evaluation of patients with carpal tunnel syndrome. Muscle Nerve 1993;16:1392–1414 [40] Grundberg AB. Carpal tunnel decompression in spite of normal electromyography. J Hand Surg Am 1983;8:348–349

Nerve Repair and Grafting

4 Nerve Repair and Grafting Kirsty U. Boyd and Ida K. Fox

4.1 Introduction The last two decades have seen a shift from nerve repair or nerve grafts in proximal injuries toward nerve transfer. In distal nerve injuries, however, nerve repair or nerve grafts are usually more appropriate. Patient outcome and recovery are directly linked to the method and timing of nerve repair. Primary endto-end nerve repair remains the gold standard; however, advances in the understanding of internal neural topography, tension at nerve repair sites, timing of denervation, and surgical techniques to replace or augment primary nerve repair have had an impact on our approach to nerve repair and, even more so, on nerve grafting.1,2 This chapter reviews the principles of nerve repair and grafting and highlights some of the recent advances that have contributed to improved success in debilitating nerve injuries.

4.2 Nerve Injuries 4.2.1 Degree of Nerve Injury An understanding of the degree of nerve injury is critical in the management of traumatic peripheral nerve injuries, as it guides treatment and provides information about prognosis (▶ Table 4.1).1 In 1943 Sir Herbert Seddon described three histologic categories based on the degree of nerve injury.3 Neurapraxia involves a local conduction block along a discrete distance of the nerve. This could be a result of ischemia or anesthetic block with no histologic changes seen or as a result of demyelination of the axon. The axon itself is not damaged, and the potential for full spontaneous recovery is excellent in the acute situation. However, in a situation of chronic, not acute, compression, a permanent conduction block can exist. Thus, you will read later in this chapter that even though normal recovery can be anticipated with a neurapraxia, if it localizes to a known area of nerve compression where superimposed chronic compression

can be a factor (e.g., with associated swelling from the injury), then surgical decompression is recommended. Axonotmesis involves direct injury, resulting in wallerian degeneration, which occurs distal to the site of injury and results in permanent damage to the nerve. Seddon noted that axonotmetic injuries can be associated with varying degrees of internal neural fibrosis or scarring; furthermore, while spontaneous recovery will occur, the degree of recovery is directly related to the presence of fibrosis and can be complete or partial, depending on the degree of scarring and the potential for misdirection of sensory/motor regeneration.3 Neurotmetic injuries, by contrast, are more severe. Seddon described these injuries either as scarring “in continuity,” with complete scarring with total axonal discontinuity, or as a total nerve disruption.3 In 1951 Sunderland reclassified the types of injuries that Seddon had originally described and emphasized five degrees of nerve injury.4 Sunderland I injury, which was equivalent to Seddon’s neurapraxia, was associated with complete recovery over a period of days to weeks. Sunderland II injuries were equivalent to axonotmesis and associated with complete recovery following wallerian degeneration and axonal regeneration at a rate of 1 mm/day. Sunderland III injuries were described by Seddon under axonotmesis and have disruption of both the axons and the endoneurial sheaths, resulting in varying degrees of scarring. Although spontaneous recovery is expected, the pattern of recovery is mixed or incomplete. The majority of thirddegree injuries do not require surgical intervention. Even proximal axonotmetic injuries, far from the target, can recover normal function because some uninjured axons will collaterally sprout motor unit action potentials (MUAPs) to “babysit” and protect the muscle until the injuried axons eventually regenerate to the target nascent units. Sunderland IV and V injuries were equivalent to Seddon’s neurotmetic injuries. Sunderland IV injuries are associated with complete scarring and fibrosis at the site of the nerve injury due to

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Table 4.1 Degrees of Nerve Injury Degree of Nerve Injury

Recovery Classification

Recovery

Seddon classification* Sunderland classification**

Nerve Conduction Studies Fibrillations

MUAPs

Neurapraxia

I

Favorable

Spontaneous, fast, complete

None

Normal

Axonotmesis

II

Favorable

Spontaneous, slow, complete

Present

Present

III

Favorable

Spontaneous, slow, incomplete

Present

Present

IV

Unfavorable

No recovery

Present

Absent

V

Unfavorable

No recovery

Present

Absent

VI (mixed injury)***

Mixed

Variable

Neurotmesis

Abbreviation: MUAPs, motor unit action potentials. * Data from Seddon HJ. Three types of nerve injury. Brain 1943;66(4):237–288. ** Data from Sunderland S. A classification of peripheral nerve injuries producing loss of function. Brain 1951;74(4):491–516. *** Data from Mackinnon SE, Dellon AL, eds. Surgery of the Peripheral Nerve. Thieme, 1988.

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Nerve Repair and Grafting injury to the axon, endoneurium, perineurium, and epineurium, which prohibits regenerating axons from traversing the injury. These injuries do not recover spontaneously and will require surgical intervention. Sunderland V injuries involve a complete transection of the nerve requiring surgical intervention to reestablish continuity. 4 Mackinnon emphasized a sixth-degree injury, commonly referred to as a mixed injury.5 The sixth-degree injury combines various degrees of injury and even normal fascicles and has variable recovery unique to each fascicular injury (▶ Table 4.1). This injury is the surgeon’s dilemma, because some of the fascicles may have injury with recovery anticipated, and others have more significant injury requiring surgical intervention. It is interesting that Seddon did articulate all the five degrees in his original description but included second- and third-degree in his term axonotmesis and fourth- and fifth-degree injuries in his term neurotmesis. As well, Sunderland did note that his five degrees could be combined but did not emphasize a mixed-degree injury. Given that it stands as the most surgically challenging injury, because of the potential to downgrade normal or recovering injuries, we believe it indeed deserves status as a sixth-degree injury. Simplistic as it sounds, one might consider the classification of nerve injuries as being “favorable, recoverable” (Sunderland I, II, III) or “nonfavorable, nonrecoverable” (IV, V). To distinguish between the varying degrees of injury in the early period following wallerian degeneration but preceding axonal regeneration, the use of electrodiagnostic studies is critical. The presence of fibrillations will distinguish a neurapraxia (or first-degree injury) from the more significant damage associated with second- to fifth-degree injuries. MUAPs signify collateral sprouting and will be present in second- and third-degree injuries as early as 12 weeks postinjury but absent in fourth- and fifth-degree injuries. For the purpose of prognosis, first-, second-, and third-degree injuries will recover with nonoperative management unless the injury site localizes to a known area of nerve compression that needs to be surgically released or if regeneration slows at more distal areas of known nerve compression. Sunderland IV and V injuries will always require surgical intervention. More information regarding the role and interpretation of electrodiagnostic studies is given in Chapter 3.

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4.2.2 Mechanism of Nerve Injury Nerve injuries may also be classified by the mechanism of injury, specifically into blunt (or closed) and penetrating (or open) injuries (▶ Fig. 4.1). This classification is particularly useful, as it helps to guide early management and can assist the clinician in determining prognosis.1,2 Penetrating (or open) injuries can be further subdivided into sharp injuries or gunshot wounds. Sharp lacerations, such as those inflicted with a knife or glass, necessitate prompt surgical exploration in the setting of a focal neural deficit (▶ Fig. 4.1c,d). There is a high probability of partial or complete transection. Though not necessarily emergent, evaluation within 72 hours will allow for electrical nerve stimulation of the distal nerve, facilitating realignment for motor repair. If the patient has suffered concomitant vascular injuries, we advocate for prompt primary nerve repair following exploration and

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repair of vascular structures. These lacerations are generally associated with minimal zone of injury, and therefore can frequently be primarily coapted without tension (▶ Fig. 4.2). It is critical that if a primary repair is performed, it is done outside the zone of injury (▶ Fig. 4.3). In penetrating trauma associated with significant injury to adjacent structures, nerve injury can be overlooked in the initial examination. When a focal neural deficit is first noticed postoperatively following vascular repair or fracture fixation, the etiology of the nerve injury remains unclear. Injury secondary to the original trauma, hematoma or edema, or iatrogenic injury must be included in the differential. This complicates surgical management. Thus, we advocate for careful clinical examination of the patient prior to any surgical intervention wherever possible. Unlike sharp, penetrating injuries, gunshot wounds do not necessitate immediate exploration (▶ Fig. 4.4). In the majority of cases, the nerve is not physically transected; however, contusive and stretching forces can contribute to a neuroma-in-continuity.6 For more extensive wounds explored immediately due to concomitant vascular injury, nerve ends can be located and tagged; however, it can be difficult to determine the extent of injury, and primary repair may lead to inadequate resection of the damaged nerve (▶ Fig. 4.5).7 It is prudent to delay repair for 2 to 3 weeks when “bread loafing” the nerve will reveal the extent of scar damage (▶ Fig. 4.6). To determine where the healthy fascicles are, a combination of direct visualization under magnification and evidence of a noxious response, when trimming the proximal end, is used. To assess for this noxious response, the anesthetic is lightened as the nerve is bread-loafed proximally until the patient’s heart rate or blood pressure increases. A nerve stimulator can also be used to directly stimulate the surface of the proximal nerve looking for a similar noxious response. Stimulation of the distal nerve will not produce that response. The distance of proximal nerve resection can be used to determine the length distally to resect, with the goal in mind of being outside the zone of injury. When managed nonoperatively, the majority of upper extremity peripheral nerve gunshot wound injuries spontaneously recover, most between 3 and 6 months.8,9 Clinical examination or electrical studies will assist in clinical decision making regarding surgery. Blunt injuries can be further subdivided into crush injuries or avulsion or stretch injuries. Crush injuries comprise the most common peripheral nerve injuries and may be related to increased pressure caused by hematoma, edema, or fracture. These injuries can range from temporary neurapraxia to more significant injuries. Although the majority of these injuries can initially be managed nonoperatively, in the setting of compartment syndrome, prompt surgical exploration and release are necessary. For the majority of injuries, serial clinical examination and electrodiagnostic testing will dictate the need to progress to surgery. Stretch (or traction) injuries occur when the strain on the nerve exceeds a maximum threshold for stretch and thus damages the internal structure of the nerve. In avulsion brachial plexus injuries, this stretch causes further damage, leading to separation of the nerve from the spinal cord. This mechanism of injury is often associated with high-velocity or high-impact trauma, such as motor vehicle and motorcycle accidents. Avulsions typically occur in areas where the nerves are tethered,

Nerve Repair and Grafting

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Fig. 4.1 Closed and open sharp laceration nerve injuries. Management of nerve injuries depends on the mechanism of injury. Two major categories of nerve injury are closed and open. (a,b) Closed nerve injuries are managed conservatively for spontaneous recovery. Reconstructive options may proceed if conservative management fails. This patient encountered a stretch injury to the long thoracic nerve during an athletic event. The injury involved the right arm and is apparent with scapular winging. Physical therapy was elected to prevent further muscle lengthening of the serratus anterior. If spontaneous recovery failed within the time window of muscle reinnervation, surgical management to reconstruct the long thoracic nerve function could have proceeded. (c,d) Open sharp laceration nerve injuries are surgically managed promptly. Traumatic open injuries that involve a stretch or crush component are delayed in surgical management to allow the zone of injury to declare itself. This patient had a sharp lacerating injury to the forearm that involved the ulnar nerve. Due to the level of injury, the ulnar nerve injury was resected and grafted.

such as bony foramina or from the spinal cord. The peroneal nerve as it curves around the fibular head can be avulsed from the proximal nerve in high-velocity knee injuries. Separation from the distal end, at the neuromuscular junction, can also occur, such as when a nerve gets caught up in a drill bit and pulled out of the muscle. Avulsion injuries are difficult to treat because coaptation between two nerve ends is not feasible, and options such as neurotization provide less satisfactory results.10,11

4.2.3 Level of Nerve Injury A major contributor in patient recovery following peripheral nerve damage is the level of injury. The distance from the motor end plates directly influences time to recovery, with fibrosis, scarring, and fatty infiltration of the muscle occurring in denervated muscle at ~12 months.2,12,13 Thus, proximal nerve injuries located at a site remote from the muscle end plate have further distance to regenerate and are ultimately associated with worse outcomes than more distal injuries.14 We advocate nerve transfer techniques whenever possible in proximal injuries.

4.2.4 Patient Factors Affecting Outcomes Outcomes following nerve surgery are significantly affected by a variety of patient factors. The age of the patient dramatically affects peripheral nerve recovery. Younger patients tend to do better following nerve injury; specifically, children can make remarkable recoveries following devastating injuries. Several studies have investigated the role of aging in recovery following nerve injury. In a rat model, younger animals were found to have a more robust regenerative response following crush injury15 and end-to-side nerve repair.16 Most likely the superior cortical plasticity seen in children plays a major role in functional recovery. Smoking has been associated with slower functional recovery of peripheral nerve injury in a rat model, although in an experimental model of compression neuropathy and smoking, we did not see any effect.17 Medical comorbidities, such as diabetes, hypothyroidism, and peripheral vascular disease, can also affect nerve regeneration.2,13

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Fig. 4.2 Primary nerve repair of a sharp lacerating nerve injury. Nerve injuries that are sharp and lacerating induce a small zone of injury, which can allow for a tension-free primary repair. (a) This patient had a sharp lacerating injury to the right palm, which involved the digital nerves and tendons of the flexor digitorum superficialis and profundus. These tendons were repaired in zone 3. (b) Digital nerves of the median nerve were transected. (c) The proximal and distal ends of the digital nerves were trimmed by evenly transecting the ends for healthy nerve fibers. Primary repairs were performed without tension in all range of motion of the fingers, wrist, and hand.

4.3 Evaluation of Nerve Injury Evaluation of a patient with a nerve injury is covered in detail in Chapter 2. In patients with traumatic nerve injuries requiring repair or grafting, there are several crucial components to evaluation that bear mentioning in this chapter. As previously mentioned, patients with concomitant orthopedic or vascular injuries should be thoroughly examined for sensory, motor, or reflex deficits prior to operative intervention wherever possible, to avoid confusion regarding potential sharp iatrogenic injuries if a deficit is noticed postoperatively. This exam can be conducted quickly so as to avoid delay in transfer to the operating room. Sensory deficits may be determined using the Ten Test, which, while less sensitive than two-point discrimination, provides an excellent cursory evaluation of sensation in major nerve distributions or dermatomes.18 Motor examination should proceed from proximal to distal to identify any major deficits.

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For sharp, penetrating injuries, early surgical exploration is warranted. For blunt injuries and gunshot wounds, however, serial physical examinations and electrodiagnostic studies are indicated to assess for spontaneous recovery. Patients should be reassessed monthly with comparison to prior evaluations for evidence of recovery. Both sensation and motor function should be quantitatively documented at each visit to facilitate comparison. The use of imaging adjuncts such as ultrasound, computed tomography (CT), and magnetic resonance imaging (MRI) is not specifically helpful, and the clinical examination and electrodiagnostic studies are key.

4.4 Nerve Repair 4.4.1 Timing of Nerve Repair Sharp penetrating injuries, or injuries where there is a high index of suspicion for nerve transection, warrant early

Nerve Repair and Grafting

Fig. 4.3 Zone of injury within a nerve. The zone of injury depends on the mechanism of injury. A sharp lacerating injury will have a small zone of injury, whereas blunt, stretch, gunshot, and traumatic injuries will have large zones of injury. It is important to excise the injured nerve outside the zone of injury (dotted lines) to allow proximal nerve fibers to regenerate distally without inhibition from scar formation. Histologic section of proximal nerve exhibits normal nerve fibers. Histologic section of neuroma exhibits disorganized patterns of fibers in a dense stroma of scar tissue. Histologic section of distal nerve, distal to the injury, exhibits degenerating nerve fibers. Magnification: 400x, Toluidine blue.

4

Fig. 4.4 Gunshot wounds and nerve injuries. Gunshot injuries cause contusive and stretching forces that can contribute to a neuroma-incontinuity. Nerve transections by gunshot are in the minority of cases. Due to these injury mechanics, it is important to delay nerve repair to determine the extent of nerve injury. This patient had a shotgun injury to the forearm where the exit wound (b) was more devastating than the entry wound (a). Nerve repair was delayed to determine the extent of injury and whether spontaneous recovery occurred.

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Nerve Repair and Grafting

Fig. 4.5 Nerve tagging during surgical exploration and débridement. Tagging nerves during initial surgical exploration and débridement following a traumatic injury allows for easier identification through scar tissue in the subsequent operation for nerve reconstruction. Additionally, motor nerves respond to intraoperative stimulation up to 72 hours postinjury.

4

Fig. 4.6 The “bread-loafing” technique is used to determine the zone of injury (a). Bread loafing is used both proximal and distal to the site of injury until clean fascicles are visualized. Cross-section of neuroma (b) and cross-section of fascicles (c). Simultaneous assessment of the patient response (increase in heart rate and/or blood pressure under lightened anesthetic) to the painful stimulus of proximal bread loafing can be helpful in confirming the zone of injury. (Courtesy of Dr. Allen L. Van Beek.)

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Nerve Repair and Grafting

4

Fig. 4.7 Epineurial and fascicular nerve repair. (a) Epineurial nerve repair. (b) Fascicular nerve repair.

Fig. 4.8 Bad examples of epineurial and fascicular nerve repair. Poor clinical results can be expected with overlapping epineurial or fascicular nerve repairs due to the misalignment of motor and sensory fibers. When performing an epineural repair, the sutures are placed in the epineurium. Surface landmarks, such as blood vessels, are used as anatomical markers to assist in aligning the appropriate fascicles.

Fig. 4.9 Failed nerve repair. (a) This patient was referred for an assessment of an ulnar injury in the proximal forearm. Upon exposure, the ulnar nerve was found with an inappropriate nerve repair with large sutures (3–0 black silk suture). (b) In addition to the poor nerve repair, the injured medial antebrachial cutaneous nerve (MABC) had been unrecognized and untreated. The MABC could have been used as a nerve graft to avoid tension. (Fig. 4.9a is used with permission from Mackinnon SE, Dellon AL, eds. Surgery of the Peripheral Nerve. New York, NY: Thieme; 1988:94.)

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Nerve Repair and Grafting

Fig. 4.10 Tension-free nerve repair. A nerve repair without tension is important for optimal recovery, as tension on the nerve repair will significantly downgrade the functional results. In addition, it is important to have redundancy at the coaptation sites. Tension is checked by performing range of movement on the extremity. (a) Nerve repair without tension at single coaptation site. (b) Nerve grafting without tension at two coaptation sites.

4

Fig. 4.11 Tension-free redundancy at nerve repair sites. This patient had a radial sensory neuroma that was grafted with a lateral antebrachial cutaneous nerve graft. The tension-free repair sites are noted below the blue backgrounds, with redundancy at both ends of the nerve graft.

reconstruction. Timing is variable and depends on a number of factors, including patient stability, associated injuries, medical comorbidities, level and degree of injury, and operative resources. Nerve repair can be categorized by timing of the repair. Nerves that are acutely repaired in the first 72 hours are considered primarily repaired. Delayed primary repair occurs between 72 hours and 1 week. Nerve repairs performed after 1 week are considered secondary repairs. 19 Ideally, nerves should be repaired during daytime hours, with regular nursing staff, a well-rested surgeon, and optimal operating room resources. Within the first 72 hours, stimulation of the distal aspect of the motor nerve is still possible and thus can help to facilitate appropriate nerve alignment. In addition, nerve injuries explored early are less likely to be affected by nerve end retraction, scarring, and tension. Once the motor transmitters are gone from the distal stump, the distal nerve end can no longer be stimulated, and one must rely on knowledge of nerve topography for reconstruction.

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In patients with avulsion, crush, and blunt injuries and gunshot wounds, it is prudent to delay surgical intervention in favor of monitoring the patient for signs of spontaneous recovery. Electrodiagnostic studies are warranted at 8 to 12 weeks postinjury, and often electromyogram (EMG) changes will precede clinical evidence of returning muscle function. Specifically MUAPs will signify nerve recovery through collateral sprouting of an intact axon. Recovery should proceed at a pace consistent with the distance from the injury to the next motor branch and can be predicted based on an estimate of 1 mm/day. In general, for patients with no signs of recovery on serial clinical examination or on electrodiagnostic studies at 3 to 4 months postinjury, surgical intervention should be considered. Dr. Susan Mackinnon’s noted aphorism “Time is muscle” becomes important when deciding on the timing of surgical intervention. If muscles are not reinnervated within approximately one year, then (for most adults) it is unlikely that any motor recovery will occur. Muscle tissue is time sensitive: it will undergo fatty replacement and fibrosis with time. Sensory nerve

Nerve Repair and Grafting

Fig. 4.12 Types of nerve transfers. Primary nerve repairs and nerve grafting occur in a traditional end-to-end fashion with its native nerve. When a nerve is transposed to another nerve, it is described as a nerve transfer. Nerve transfers can have a coaptation of an end-to-end, end-to-side, or supercharge end-to-side fashion. Traditional nerve transfers occur from donor to recipient in an end-to-end fashion. In an end-to-side nerve transfer, the recipient nerve end is transferred to the side of the donor nerve. In a supercharge end-to-side nerve transfer, the donor nerve end is transferred to the side of a recipient nerve.

repair by contrast can be completed at any time post-injury. Historically, earlier nerve repairs have led to improved prognoses, most likely facilitated by primary nerve repair and appropriate nerve alignment.19 For a complete transection, best results occur if the repair is performed within 3 weeks of the injury, and a good prognosis can be expected with repairs performed in the first 6 months.19 The primary goal is to achieve motor axons reaching the target muscle end plate prior to muscle fibrosis and atrophy, which occurs at ~ 12 months.20 Thus, functional recovery is directly proportional to the number of axons reaching the target end plate and inversely proportional to the time of denervation.20

4.4.2 Type of Nerve Repair There has been much discussion in the literature regarding the type of nerve repair, specifically epineurial versus fascicular (▶ Fig. 4.7). Using the native artery or fascicular patterns to align the proximal and distal nerve ends, with no tension and minimal sutures, is our preferred method of repair with the use of an epineurial technique for small-diameter nerves, such as digital nerves. The disadvantage of fascicular repair is that the combination of more extensive dissection and intraneural stitches results in increased fibrosis, thus interfering with nerve healing.21,22 In the setting of larger peripheral nerves, we advocate fascicular repair to facilitate alignment of larger fascicular groups, especially when the motor/sensory topography is well known, such as the ulnar nerve in the forearm and hand. Both techniques have been determined to be effective as long as the nerve ends have been adequately trimmed back to normal nerve and fascicles are not overlapping within the repair (▶ Fig. 4.8; ▶ Fig. 4.9).22 The concept that, with a careful epineurial repair, misaligned nerves will reorient using neurotrophism and guided neurotropism, making this preferable to incorrectly oriented grouped fascicular repair, has been introduced.23 Through an undefined mechanism known as contact guidance, proximal nerve fibers will seek out the appropriate distal fascicles and preferentially align with them. This suggests that where anatomical land-

4

marks are lacking to assist with restoring appropriate alignment, an epineurial repair would be preferable. However, as we rapidly gain a better understanding of the specific motor/sensory topography of the peripheral nerve through experience with nerve transfers, this epineurial/fascicular repair debate becomes irrelevant. A microsurgical repair outside the zone of injury, with no tension, to allow early mobilization and appropriate motor/sensory alignment is key (▶ Fig. 4.10; ▶ Fig. 4.11). The majority of nerve repairs, both primary nerve repair and nerve grafting, are performed in an end-to-end fashion (▶ Fig. 4.10). End-to-side repair continues to be controversial, but it is being used with increasing frequency in the authors’ practice (▶ Fig. 4.12). There are two types of end-to-side repairs: traditional end-to-side nerve transfer and supercharge end-to-side nerve transfer. The traditional end-to-side procedure involves transferring the end of a recipient nerve to the side of a donor nerve. In a supercharge end-to-side nerve transfer, the end of a donor nerve is transferred to the side of a recipient nerve. The specifics of a supercharge end-to-side nerve transfer are described in Chapter 5. In traditional end-to-side repairs, collateral sprouting has been found to occur in sensory nerves, with or without an epineurial window; however motor neurons require a proximal axonotmetic injury in order for regenerative motor sprouting to occur (▶ Fig. 4.13).24 End-to-side repair is advocated for noncritical sensory nerves or the distal end of a donor sensory nerve, such as the dorsal cutaneous branch of the ulnar nerve, to recover more rapid sensation in the donor site. Recently, we advocated for restoring sensation to a donor defect by performing an end-to-side repair of the distal donor nerve to a sensory nerve in close proximity. For example, following harvest of the medial antebrachial cutaneous nerve, the distal end can be transferred end-to-side to the lateral (sensory) aspect of the median nerve. End-to-side nerve transfers are further discussed in Chapter 5. We have used a motor end-to-side from the accessory nerve to the suprascapular with a partial neurectomy to the accessory nerve, and a proximal axonotmetic injury to the accessory nerve to direct axons into the end-to-side transfer, but also back into the trapezius to decrease donor motor deficit. 25

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Fig. 4.13 Nerve regeneration in end-to-side nerve repairs. The two types of end-to-side nerve repairs or transfers are the traditional end-to-side and supercharge end-to-side. End-to-side nerve transfers have two sprouting mechanisms that are characteristic or either motor or sensory nerves. (a) Regenerative sprouting occurs in motor nerves in response to an injury. To elicit regenerative sprouting for a nerve transfer, a partial neurectomy and a proximal crush are required. The proximal crush causes a axonometric injury and creates a proximal regenerative front that would regenerate into the recipient nerve and back-fill the donor nerve. (b) Spontaneous collateral sprouting occurs in sensory nerves. Due to the spontaneous sprouting, no injury is required except for a perineurial window through which the nerve fibers can regenerate. (c) In supercharge end-to-side (SETS) nerve transfer, the donor nerve end is transferred into the side of a denervated recipient nerve. This allows nerve fibers to regenerate into the recipient nerve through a perineurial window. In effect, any donor nerve used in a traditional nerve transfer can be a donor for a SETS nerve transfer.

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4.4.3 Effect of Tension on Nerve Repair

4.4.4 Addressing a Nerve Gap

The optimal method of nerve repair is tension-free, primary end-to-end nerve repair (▶ Fig. 4.11).1 Animal studies have demonstrated that a percentage of nerve fibers are lost across each coaptation site, thus resulting in fewer nerve axons reaching the target motor end plate.13,26 Despite this, primary repair is not preferable in the setting of excessive tension. Reduction in microvascular flow occurs in a normal, uninjured nerve that is placed under only 15% strain. 27 A two-thirds delay in peak velocity persists for 1 hour after the strain has been removed. 27 Increased scarring associated with repair under tension contributes to impaired regeneration . Clinically, tension across nerve repair sites is fastidiously avoided. The two ends of a transected nerve are mobilized to facilitate reapproximation. Where possible, nerves may be transposed to gain some additional length, such as the ulnar nerve at the cubital tunnel. Although postural manipulation has been described to facilitate tension-free repair, we avoid this technique due to increased tension and scarring and the need for prolonged immobilization, resulting in increased scar around the nerve repair site.

When primary repair of a nerve is not possible, an alternative for bridging the nerve gap must be selected for reconstruction (▶ Fig. 4.14). Mobilization of the proximal and distal ends may overcome gaps < 5 mm because of the elastic properties of the nerve.28 If, however, there is any residual tension, two repair sites with a nerve graft are preferable to a single repair under tension.28,29 There are a variety of methods for addressing a nerve gap. The current gold standard remains autogenous nerve grafting; other options are allograft, acellularized allograft, nerve conduits, and nerve transfers. Each of these techniques is extensively addressed in subsequent chapters.

4.5 Nerve Conduits A nerve conduit is a hollow tube used to guide the regenerating nerve to its intended target. Originally, there were a number of biological options described, including vein, bone, artery, collagen, and small intestine submucosa.30 More recently, a number of synthetic conduits have been developed. In the authors’

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Fig. 4.14 Algorithm for sural alternatives. ANA, acellular nerve allograft; DCU, dorsal cutaneous branch of ulnar nerve; LABC, lateral antebrachial cutaneous nerve; MABC, medial antebrachial cutaneous nerve; PCM, palmar cutaneous branch of median nerve; TWM, Third webspace branch of median nerve.

practice, nerve conduits have largely fallen out of favor. Experimental and clinical studies support their use for small-diameter, noncritical sensory nerve defects < 3 cm. Even in this setting, however, they have been largely replaced by acellularized nerve allografts in our practice. Much of this dissatisfaction with nerve conduits stems from the lack of laminin scaffolding and Schwann cells, which are crucial to axonal regeneration. In 2009 Whitlock et al noted a significant decrease in the number of nerve fibers seen in a gap addressed with a conduit compared to nerve grafts. 31 Weber et al postulated that conduits permit regenerating axons to better align themselves via guided neurotropism.32 Restoration of good or excellent sensory function and functional recovery for larger mixed-nerve injuries in 75% of patients with a 1- to 4-cm gap has been described.33 However, these results are not duplicated in the literature, and the authors have not found similar success.34 The difficulties associated with nerve conduits in large-diameter nerve reconstruction were described by Moore et al, where the failure of these conduits was postulated to be related to decreased concentration of neurotrophic factors associated with larger diameter conduits and increased volume of these conduits.35 This finding is supported by Lloyd et al, who determined that minced nerve tissue placed within a nerve conduit significantly improved regeneration when compared to a saline-filled placebo.36 Even with minced nerve, isograft regeneration was superior to a nerve conduit.36

In the event that a nerve conduit is selected to bridge a nerve gap, care must be undertaken to ensure that a minimum of 5 mm of the nerve is inserted proximally and distally into the conduit to minimize the risk of the conduit coming dislodged. The nerve is inset using a buried horizontal mattress suture or secured with a sealant, such as fibrin glue. We advocate mincing a small portion of normal nerve and placing this within the conduit to provide a source of Schwann cells.

4.6 Nerve Grafting 4.6.1 Autograft Where a nerve gap exists, the gold standard for repair remains autografting. The advantages of using autografts include providing an immunogenically inert scaffold and a viable source of Schwann cells to facilitate axonal regeneration. 1,37,38 There is no consensus on the maximum gap that may be bridged by a nerve graft, and varying degrees of success have been reported in 20cm grafts.39,40 Our experience, however, is that nerve grafts of ≤ 6 cm are the most reliable. Small, thin grafts have improved functional outcomes due to easier revascularization. In 1976 Taylor and Ham introduced free vascularized nerve grafts to improve outcomes;41 however no significant difference in clinical outcome has been documented. Doi et al. recommend the use of a free vascularized graft for deficits larger than 6 cm or

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Fig. 4.15 Nerve regeneration through motor and sensory nerve grafts. Available nerve grafts for reconstruction exist in either a motor or sensory modality. Because of the donor muscle deficit following a nerve harvest, there are only a few available donors for motor nerve grafts compared to sensory nerve grafts. (a) Experimental animal studies concluded that regeneration is enhanced in motor compared to sensory grafts across a rat mixed tibial nerve. Clinically, motor grafts are reserved for isolated motor nerve injuries. However, sensory nerve grafts have been clinically proven to be an effective alternative for functional recovery. [15a used with permission from Brenner MJ, et al. Repair of motor nerve gaps with sensory nerve inhibits regeneration in rats. Laryngoscope 2006;116(9):1685–1692.] (b) When comparing motor and sensory nerve grafts, motor nerves have larger endoneurial tubes in comparison to sensory nerves. Modality graft matching is preferable. Magnification: 1,000x, Toluidine Blue.

Fig. 4.16 Sural nerve grafts. The sural nerve is currently the most commonly used donor nerve for grafting, due to the amount of attainable nerve material available during harvest. (a,b,c) An incision is made along the lateral/posterior aspect of the lower leg, and the sural nerve is identified and transected distally. (d) An additional incision is made proximally to acquire additional length of the sural nerve. In our clinical practice, sural nerves are used as graft material when there are no other immediate sensory nerves available for harvest in the vicinity of nerve reconstruction and in multiple nerve injury reconstruction.

associated soft tissue loss.42 In general, vascularization is critical for large diameter nerves to prevent central necrosis, but is not necessary for small diameter nerves. The major disadvantage to nerve autografts is the need for a second operative site, resulting in donor site morbidity, additional scarring, the potential for painful neuromas, and the added operative time for a graft harvest.19 In addition, there are limited donors available. Motor or mixed nerve grafts are preferable to sensory nerve donors, resulting in improved regeneration across the coaptation.43,44 We have done a series of experimental studies in the rat tibial nerve, which demonstrated significantly improved axonal regeneration across motor as compared to sensory nerve grafts. The tibial nerve is a mixed nerve, and when we repeated this study with pure motor nerves and pure sensory nerves, we did not see a difference in the quality of regeneration across the motor and sensory grafts. When we “minced” motor or sensory nerves and placed them in a conduit

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in a tibial nerve model where sensory and motor axons comingle, we did not see an improved regeneration pattern. We concluded from the series of studies that there is a hierarchy of factors that preferentially influence nerve regeneration. When the regenerating axons have no confusion as to target, such as in the pure sensory or pure motor situation, then they do not need the assistance of a motor graft. By contrast, in a mixed regeneration situation, such as the tibial nerve, the larger endoneurial tubes seen in the motor graft assist in regeneration that is superior to the regeneration seen in the sensory grafts that have smaller endoneurial tubes (▶ Fig. 4.15). The sural nerve continues to be the most commonly used donor nerve; however, it is associated with not insignificant donor morbidity and most often involves an unaffected extremity (▶ Fig. 4.16; ▶ Fig. 4.17). The authors’ preference is to use the ipsilateral medial antebrachial cutaneous nerve (MABC) as a donor nerve when possi-

Nerve Repair and Grafting

Fig. 4.17 Donor morbidity of the sural nerve harvest. Although the sural nerve is the most commonly used donor nerve for grafting, it can be associated with significant donor morbidity that often involves an unaffected extremity.

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Fig. 4.18 Incision for nerve graft harvest of the medial antebrachial cutaneous nerve (MABC). A longitudinal incision is made in the medial aspect of the arm with the patient supine.

ble (▶ Fig. 4.18; ▶ Fig. 4.19). This nerve is easily harvested, provides a generous donor, has anterior and posterior branches available, and leaves minimal sensory defect at the medial elbow and anterior forearm, especially if the distal end is transferred to the sensory median nerve in an end-to-side fashion (▶ Fig. 4.20). The lateral antebrachial cutaneous nerve (LABC) is used less frequently, but it is an available donor option for injuries to the superficial branch of the radial nerve (radial sensory nerve) (▶ Fig. 4.21). Injuries to the radial sensory nerve often include injury to the LABC, due to their close anatomical course in the forearm, making the LABC proximal to the injury suitable for graft material. The terminal sensory branch of the posterior interosseous nerve (PIN) is rarely used as a donor because the graft is too small and fibrotic (▶ Fig. 4.22). The radial sensory

nerve should be avoided as a potential donor, as neuropathic pain associated with injury to this nerve is extremely difficult to manage. An end-to-side transfer of the distal transected end of the radial sensory nerve to the side of the normal median nerve is also an option for recovery of function in the radial sensory nerve distribution. Potential motor donors include the distal anterior interosseous nerve (AIN) (▶ Fig. 4.23) and the nerve to the gracilis (Figs. 4.24-4.29). For critical motor deficits where a short graft is typically needed, such as the ulnar and accessory nerves, we use the nerve to the gracilis muscle, which may yield an 8- to 9-cm graft (▶ Fig. 4.30). Another excellent option for a nerve graft is the noncritical proximal segment of an injured nerve (▶ Fig. 4.31). Nerve mate-

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Fig. 4.19 Anatomy of the medial antebrachial cutaneous nerve during surgical exposure. The medial antebrachial cutaneous nerve is identified within the medial aspect of the arm. The MABC originates from the medial cord, courses distal, and branches into anterior and posterior segments. The basilic vein is an anatomical landmark used to identify the MABC. The anterior branch is found anterior and the posterior branch is found posterior to the basilic vein.

Fig. 4.20 Anterior branch of an MABC graft harvest. (A) The anterior branch of the MABC was exposed superior to the basilic vein and isolated in the medial aspect of the arm. The posterior branch of the MABC was also identified inferior to the basilic vein. (B) The anterior branch of the MABC was harvested. (C) To restore rudimentary sensation in the MABC anterior branch distribution, the distal end of the MABC anterior branch was transferred to the MABC posterior branch in an end-to-side fashion. Following the prioritized ulnar nerve reconstruction with the harvested MABC graft, the unused MABC graft material was used to bridge the end-to-side nerve transfer for a tension-free repair.

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Fig. 4.21 (a) Reconstruction of the radial sensory nerve with the lateral antebrachial cutaneous (LABC) nerve graft. Injuries to the radial sensory nerve in the forearm can include injury to the LABC nerve due to their close proximity in their anatomical course. This patient had a lacerating injury to the distal forearm. The lacerating injury transected the radial sensory nerve and included injury to the LABC nerve. (b) LABC nerve harvest. The LABC nerve branches from the musculocutaneous nerve and has a superficial anatomical course along the lateral aspect of the arm/ forearm. The LABC nerve was exposed proximally in the forearm for additional graft length. The LABC donor nerve was harvested as a nerve graft. (c) Radial sensory nerve reconstructed with an LABC nerve graft. The resultant radial sensory and LABC neuromas from the lacerating injury were resected. A gap distance of 5 cm was identified with the wrist in flexion and ulnar deviation. The radial sensory nerve gap was grafted with two cable LABC nerve grafts.

rial proximal to an injury indefinitely contains Schwann cells and is suitable for grafting, unlike the distal segment, which undergoes degeneration following a complete injury. An example of this scenario is a complete median nerve injury in the distal forearm, which requires grafting. The third web space nerve fascicles proximal to this injury are an available donor graft for the critical components of the median nerve (▶ Fig. 4.32). A distal end-to-side sensory nerve transfer (distal third web space fascicle to ulnar sensory component) is performed to restore rudimentary sensation to the third web space. Using a noncritical proximal segment of an injured nerve can prevent an additional exposure site and its associated donor site morbidity, depending on the length of graft material required. Knowledge of fascicular nerve anatomy is a prerequisite to this graft type, as intraoperative stimulation to confirm motor/sensory modality is not available due to the injury. An additional nerve graft option is the use of a noncritical distal segment of an injured nerve as a potential donor for critical parts of the injured nerve. This option is only available early after injury, however, as the distal segment undergoes degeneration with loss of Schwann cells after several months. Assessing

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the type/degree of proximal nerve injury and the period of time following injury will determine the integrity of a noncritical distal graft. An example of this type of graft is the dorsal cutaneous branch of the ulnar nerve (DCU) in an ulnar nerve injury. The DCU provides a donor of reasonable length when neurolysed proximally.

4.6.2 Allograft Given that autologous nerve donors are limited, another potential option for reconstruction is cadaver- or donor-related nerve allografting (▶ Fig. 4.33). These allografts act as a temporary scaffold, providing the substrate to permit host axonal regeneration.45 With systemic immunosuppression, the regeneration across fresh cadaver allograft is equal to that across a nerve autograft. Although the advantage of nerve allografts is that there is an unlimited, readily available supply with no additional donor site morbidity, the technique is not without significant drawbacks. Due to immunogenicity, nerve allografts require temporary systemic immunosuppression, potentially leaving recipients vulnerable to opportunistic infections or neoplastic processes.46 Immunosuppression can be discontinued 6 months

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Fig. 4.22 Terminal branch of a posterior interosseous nerve graft. The articular branch of the posterior interosseous nerve to the wrist is rarely used as a donor nerve for grafting, due to its small and fibrotic nature.

Fig. 4.23 Anterior interosseous motor nerve graft. (a) The anterior interosseous nerve (AIN) is an available motor nerve for grafting. This nerve is found deep to the flexor muscles to innervate the pronator quadratus and includes a sensory articular branch to the wrist. Although the AIN is expendable, it is also an available donor nerve for nerve transfers. (b) The AIN is dissected through the pronator quadratus until it branches. At this distal point, it is transected and harvested.

after axon regeneration has crossed the transplanted nerve (▶ Fig. 4.34). Because of these risks, nerve allografting should be reserved for unique patients with irreparable peripheral nerve injuries that, left untreated, would result in an essentially nonfunctional limb.

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Allografts are harvested from ABO blood-type–compatible individuals (cadaveric or, very rarely, living-related donors). To avoid central necrosis, nerves of small diameter are harvested, allowing for adequate revascularization. Nerves are stored at 4° C in University of Wisconsin solution and antibiotics for 7 days

Nerve Repair and Grafting

Fig. 4.24 This and the following five figures show surgical steps in a gracilis nerve branch harvest, which in this patient occurred on the medial side of the upper right leg. Incision for a gracilis nerve branch harvest. The nerve branch of the obturator nerve to the gracilis muscle is an available motor nerve for grafting. The patient is positioned with the hip abducted and knee flexed. The incision is made on the medial aspect of the thigh and medial to the topographical axis of the adductor longus muscle.

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Fig. 4.25 Exposure for a gracilis nerve branch harvest. Exposure reveals the adductor longus and gracilis muscles. Dissection is taken deep through the plane between these two muscles.

Fig. 4.26 Identification of the pedicle and nerve branch to the gracilis muscle. Within the plane between the adductor longus and gracilis muscles, the nerve branch to the gracilis is identified deep and superior to the pedicle of the gracilis.

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Fig. 4.27 Identification of the nerve branch to the gracilis muscle. Further dissection superior to the pedicle exposes the nerve branch to the gracilis muscle.

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Fig. 4.28 Proximal dissection for a gracilis nerve branch harvest. Proximal dissection is performed to attain additional graft length for harvesting. The nerve to the adductor longus is identified during the proximal exposure and is lateral to the gracilis nerve branch.

before use. In previous studies, use of FK506, and immunosuppressant, has demonstrated possible accelerated nerve regeneration and functional recovery; however, it is associated with both toxic and immunosuppressive properties that discourage long-term use. Recipients begin FK506 3 days preoperatively and then receive induction and standard immunotherapy postoperatively. The major complication of nerve allografting is rejection, which can be difficult to assess, given that there is no immediate functional end point to monitor, and the nerves are surgically buried. Use of a subcutaneous buried allograft to assess for rejection with erythema has been described. 47 Peripheral nerve

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allotransplantation is discussed further in Chapter 7. FK506 does appear to increase the rate of nerve regeneration 10 to 20% while it is being administered. We have not seen any side effects with its use in our allograft patients. Clinical trials with FK506 in patients not requiring nerve transplants but with significant nerve injuries are needed.

4.6.3 Acellularized Allograft An excellent alternative to nerve allograft for short gaps in noncritical sensory nerves is to process the donor allograft, thus rendering it acellular and nonimmunogenic.31 This

Nerve Repair and Grafting

Fig. 4.29 Gracilis nerve branch harvest.

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Fig. 4.30 A case of deep motor branch of ulnar nerve reconstruction with a gracilis motor nerve graft. Where there is an isolated critical motor deficit and a short graft is needed, the gracilis motor nerve branch is an available donor nerve for grafting. (a) This patient had an ulnar nerve motor loss following removal of a benign tumor in the motor fascicular group. He had normal ulnar nerve sensory findings. The neuroma was resected with a gap distance of 5 cm during wrist extension. (b) The gracilis motor nerve branch of the obturator nerve was harvested with a length of 8.5 cm. (c) The deep motor nerve branch was grafted with the gracilis motor nerve graft.

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Fig. 4.31 Noncritical nerve graft material from a proximal segment to an injured nerve. Noncritical nerve material proximal to a nerve injury is an available option for grafting. (a) The third web space is an excellent donor nerve for grafting in a case of distal median injuries. Injury to the median nerve at the wrist allows for the harvest of the proximal noncritical third web space nerve fascicles. The harvest of the third web space fascicles occurs on the medial aspect of the median nerve. (b) The third web space fascicles can be used as graft material for reconstructing critical components of a distal median nerve injury.

process involves a multistep detergent treatment to remove donor cellular material, such as Schwann cells and inhibitory chondroitin sulfate proteoglycans (CSPGs), but allowing the graft to retain its three-dimensional scaffolding, thus acting as a biological substrate for nerve regeneration. 31 The grafts are also sterilized with gamma irradiation before being stored at –80°C (–112°F). Prior to use, the grafts are thawed and rehydrated with normal saline for 10 minutes at room temperature. The effectiveness of acellularized nerve allografts has been investigated, and experimental studies have found it to be inferior to autograft but superior to an empty nerve conduit. 31, 48,49 Because it does not include viable Schwann cells, it can only be used for short gap reconstruction (≤ 3 cm). In sensory traumatic and postneuroma resection defects of the hand ranging from 0.5 to 3.0 cm, these processed nerve grafts were capable of restoring adequate sensation with no evidence of infection or rejection in experimental studies. 50 Acellularized allografts will support some regeneration to 3 but not 4 cm.51,52

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In the authors’ practice, the use of acellularized nerve grafts has largely replaced the use of nerve conduits. Current indications for use of these processed grafts include small-diameter, noncritical sensory nerve defects < 3 cm (▶ Fig. 4.35). Acellularized nerve grafts are also used as an “extender” to restore donor site sensation or prevent hyperalgesia following neuroma resection (▶ Fig. 4.36). Dorsi et al demonstrated that normal sensory nerves collaterally sprout into a previously denervated territory (▶ Fig. 4.37). In their tibial neuroma transposition model, this resulted in hyperalgesia.53 Using acellularized nerve allograft to extend the proximal nerve stump provides a scaffold to direct the regenerating axons away from the area of contact. These processed grafts have also been used in an end-to-side manner in sensory nerve transfers of the hand. Our contraindications to the use of processed allograft include motor nerve reconstruction, critical sensory reconstruction, large-diameter nerve reconstruction, and sensory gaps > 3 cm. In our practice, traditional autografting or nerve transfers would be indicated in these circumstances.

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Fig. 4.32 A case of median nerve reconstruction at the wrist with a third web space graft. This patient had a significant injury to the median nerve at the wrist that spared only the thenar and the digital nerves to the thumb. (a) The zone of injury was identified, and the neuroma was resected with proximal and distal median nerve components identified. The third web space was further neurolysed proximally to mobilize graft material. (b) The proximal end of the third web space fascicle was transected and used as a nerve graft to repair a portion of the median nerve. The proximal remainder of the third web space was transposed proximally to prevent a painful neuroma. The distal third web space was end-to-side transferred to the sensory component of the ulnar nerve to provide rudimentary sensation for donor deficit.

Fig. 4.33 Nerve allografts. The use of nerve allografts is reserved for patients with severe irreparable nerve injuries. Nerve allografts require the use of immunosuppression. It was found in experimental studies that regenerative outcomes of allografts are equal to those obtained using autografts with immunosuppression. In addition, a product of immunosuppression (FK506) has been consistently found to accelerate nerve regeneration in experimental studies.

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Fig. 4.34 Schwann cell migration in a nerve allograft. The role of Schwann cell migration and host cell infiltration dictates the timing of immunosuppression for nerve allograft reconstructions. (a) In nerve autografts, the graft is composed of native host cells, specifically, Schwann cells. (b) In nerve allografts, the graft is composed of donor Schwann cells and scaffolding. (c) During immunosuppression, the native host Schwan cells migrate into the graft from both proximal and distal ends. (d) Once the native host Schwann cells complete their migration and replace the donor cells, immunosuppression can be withdrawn. (e) Immunosuppression withdrawal occurs when native host cells have migrated into the donor graft, as axons regenerate from the proximal end.

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Fig. 4.35 Reconstruction of a noncritical sensory nerve with acellularized nerve allograft. This patient had a lacerating injury at the base of the long finger. (a) Upon exploration, the palmar digital artery was found to be transected. The palmar digital nerve to the radial aspect of the long finger was found to be intact but injured. (b) The digital nerve had been longitudinally injured by the sharp object. (c) The zone of injury was identified and resected until healthy nerve was seen at both proximal and distal ends. (d) A 2-cm acellularized allograft was used to bridge the nerve gap for a tension-free repair. The nerve repair was tested for tension by putting the long finger through full flexion and extension.

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Fig. 4.36 Acellularized nerve allograft as an extender from the sensory component of the ulnar nerve for intermuscular transposition. This patient had a distal ulnar nerve injury and required transposition of the sensory component of the ulnar nerve. (a) A 5.5-cm acellularized nerve allograft was used. (b) The acellularized nerve allograft was coaptated to the proximal end of the sensory component of the ulnar nerve, transposed proximally, and buried deep within the forearm musculature to prevent painful neuroma formation. At a distance of 5.5 cm with no distal “hook up,” our work suggests axonal regeneration will slow and dwindle.52

4.7 Specific Examples of Upper Extremity Nerve Repair and Grafting 4.7.1 High Ulnar Nerve Injury Following high ulnar nerve transection, the authors’ preferred recipe for nerve repair is based on whether the patient has neuropathic pain and whether or not a primary repair is possible. If the patient has no neuroma pain, then we would proceed with distal nerve and tendon transfers. If the patient has pain, then early exploration with repair or with MABC autograft to control neuroma formation would be considered. If the injury is near the medial epicondyle, then a transmuscular ulnar nerve transposition is done to decrease tension and/or graft length. If the MABC is uninjured (highly unlikely with an ulnar nerve transection), then rather than using the sural nerve as a graft, we would proximally transpose the ulnar nerve into the triceps/biceps muscular interval. We would “crush” the ulnar nerve with a hemostat for 10 to 15 seconds as proximally as possible to

create an axonotmetic injury so that there would be a delay (1 inch per month from the crush site) before the regenerating axons reached the end of the ulnar nerve. We would “cap” the ulnar nerve proximal stump with microbipolar cautery, and keep the ulnar nerve in its transposed location with 10 cc’s of fibrin glue. For distal reconstruction, we perform an accompanying distal anterior interosseous nerve (AIN)-to-ulnar end-toend transfer to facilitate intrinsic motor recovery and a third web median nerve sensory-to-sensory portion of the ulnar nerve transfer. A profundus tenodesis would also be performed (▶ Table 4.2). Nerve transfers are discussed in greater detail in Chapter 5.

4.7.2 High Median Nerve Injury Following high median nerve injury necessitating surgical repair, the authors’ preferred “recipe” for nerve repair would be early exploration with direct repair, if possible, otherwise an MABC autograft to avoid tension. Even with proximal repair, our choice for pronation recovery is an extensor carpi radialis brevis (ECRB) nerve transfer to the nerve to the pronator. This

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Fig. 4.37 Neuroma pain and hyperalgesia pain. (a) Pain from neuroma formation is well known; however, hyperalgesia pain is under-recognized and results from adjacent sensory territories collaterally sprouting into deinnervated territory. (b) Surgical management via nerve graft addresses both neuroma pain and hyperalgesia pain. (c) Surgical management via proximal transposition addresses neuroma pain, but does not address hyperalgesia pain from collateral sprouting of adjacent uninjured nerves. (d) Strategies for addressing hyperalgesia pain during a proximal transposition include end-to-side sensory nerve transfers, where the distal deinnervated end is transferred to the side of an adjacent functional sensory nerve.

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Table 4.2 “Recipes“ for high level nerve injuries as alternatives to sural graft Nerve Injury

Priorities

Reconstructive Technique

Median

AIN function thumb opposition pronation sensation

Motor nerve transfers:* ● ECRB to PT ● Brachialis or Supinator to AIN Sensory transfers: ● DCU to thumb and radial index sensory fascicles ETE ● TWM and distal DCU to ulnar sensory fascicles ETS Tendon transfers: ● Oppensplasty

Radial

wrist, finger, and thumb extension sensation

Ulnar

intrinsic function ring and small finger flexion sensation

Motor nerve transfers: FDS to ECRB ● FCR to PIN Sensory transfers: ● LABC to SBR ETE ● SBR to median ETS Tendon transfers: ● PT to ECRB for early wrist extension (optional) ●

Motor nerve transfers: AIN to ulnar motor Sensory transfers: ● TWM to ulnar sensory fascicles ETE ● PCM to DCU ETE or DCU to median ETS Tendon transfers: ● Tenodesis of FTP tendons ●

*All motor transfers are end-to-end ETE, end-to-end; ETS, end-to-side; PCM, palmar cutaneous branch of median; SBR, radial sensory nerve; TWM, third webspace branch of median nerve

is such an excellent transfer that we do not want to risk the possibility of not recovering pronation, as there are no good options for tendon transfer to recover pronation if the direct repair or graft of the median nerve proximal injury fails. The

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transfer is done in the forearm and close to target. For restoration of AIN function, distal nerve transfers from the radial nerve (the nerve to the supinator) can be performed in an end-to-end fashion. If it is possible to do a primary median nerve repair,

Nerve Repair and Grafting then that is performed. If the mechanism of injury is traumatic (i.e., a chainsaw injury), and the patient has no pain, then we would do forearm and hand nerve and tendon transfers rather than direct exploration at the injury site. If the patient had significant pain, then we would graft or proximally transpose the median nerve as described above for the ulnar nerve. The sensory component of the median nerve comes from the lateral cord and is located on the lateral half of the median nerve. Knowledge of the nerve topography allows the sensory component to be neurolysed separately from the motor component of the median nerve. Short grafting will allow for motor-to-motor direct reconstruction, which is preferable. A profundus tenodesis is also performed for “quick” recovery of index profundus function. Potential tendon transfer donors for opponensplasty include the extensor indices proprius (EIP), extensor digiti quinti, or abductor digiti quinti (Huber). The sensory portion could be transferred proximally to control neuroma pain, and a distal DCU-to-sensory median nerve transfer can be done distally in the forearm. These nerve transfers are described in more detail in Chapter 5.

4.7.3 Radial Nerve Injury Following high radial nerve injury necessitating surgical repair, the authors’ preference for repair includes early exploration and MABC grafting to avoid tension if the injury is close to motor targets. Given the distance from the injury to the distal motor end plates, a tendon transfer to restore wrist extension is suggested at the time of the original surgery. Our preference is to use pronator teres to ECRB. If tendon transfer is not performed, for example, because of hand stiffness, the use of a wrist cock-up splint is imperative to maintain appropriate extensor muscle length. Median-to-radial nerve transfers can also be performed and are discussed in more detail in Chapter 5. A sensory nerve transfer from the LABC to the radial sensory may be performed to restore sensation to the dorsum of the hand. The radial sensory nerve can also be transferred end-to-side to the median nerve to restore some sensation. These transfers are also discussed in Chapter 5. We no longer do sural nerve grafting of long, proximal defects of the radial nerve, but rather offer tendon or nerve transfers distally.

4.8 Postoperative Rehabilitation Following any nerve repair, early rehabilitation to promote nerve gliding and reduce scarring is desired. Due to the lack of tension with either primary nerve repair or nerve grafting, adjacent joint range of motion is not contraindicated. Patients are splinted for a maximum of 7 days; then the splints are removed, and patients are allowed gentle range of motion. Most patients begin protected range of motion at 2 or 3 days postoperatively. Where associated tendon transfers are performed, immobilization is longer to protect the tendon repair. If a bony injury accompanies the original nerve injury, rehabilitation is guided by bony fixation. Everyone deals with some scar formation, but early range of movement ensures that the scar which does form is “long” and will allow neural gliding. Neuropathic pain is managed with nortriptyline, pregabalin, lidoderm patches, and hand therapy. We have not found gaba-

pentin to be nearly as effective as pregabalin. Narcotics are avoided whenever possible. Cymbalta and baclofen are also useful, but they are ordered by our pain management service. Early intervention with a pain specialist is advocated, and our “pain” patients see pain management prior to their surgery. Physical and occupational therapy sessions are essential components of the postoperative process, allowing for splint modification, desensitization, reeducation, range of motion, and eventual strengthening. Our patients have a full preoperative consultation with our hand therapists and the patient’s own therapist (if they are from out of town) whenever possible. Patients are followed with serial clinical examination, monitoring return of function or sensation and advancing Tinel sign. Repeat postoperative electrodiagnostic studies are rarely performed as they do not alter patient management.

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4.9 Conclusion Nerve injuries often have devastating consequences and can significantly affect patient function, sensation, and pain. A thorough understanding of the different degrees of nerve injuries and their anticipated patterns of recovery will assist the nerve surgeon in treating these injuries. Primary neurorrhaphy remains the gold standard for nerve repair whenever possible with a tension-free, early repair in a healthy wound bed. Where a gap exists, nerve autografting is preferred and confers superior results, despite the presence of additional coaptations. As improved knowledge of nerve topography, microsurgical techniques, and the biology of nerve regeneration is gained, results following upper extremity nerve injury are improving. With the addition of acellularized allografts and nerve transfers, options for addressing these devastating injuries have significantly improved.

4.10 References [1] Ray WZ, Mackinnon SE. Management of nerve gaps: autografts, allografts, nerve transfers, and end-to-side neurorrhaphy. Exp Neurol 2010;223:77–85 [2] Hentz VR, Narakas A. The results of microneurosurgical reconstruction in complete brachial plexus palsy: assessing outcome and predicting results. Orthop Clin North Am 1988;19:107–114 [3] Seddon HJ. Three types of nerve injury. Brain 1943;66:237–288 [4] Sunderland S. A classification of peripheral nerve injuries producing loss of function. Brain 1951;74:491–516 [5] Mackinnon SD, Dellon AL, eds. Surgery of the Peripheral Nerve. New York, NY: Thieme;1988 [6] Kline DH, Hudson AR. Nerve Injuries: Operative Results for Major Nerve Injuries, Entrapments, and Tumors. 2nd ed. Philadelphia, PA: WB Saunders; 1995 [7] Nanobashvili J, Kopadze T, Tvaladze M, Buachidze T, Nazvlishvili G. War injuries of major extremity arteries. World J Surg 2003;27:134–139 [8] Omer GE. Injuries to nerves of the upper extremity. J Bone Joint Surg Am 1974;56:1615–1624 [9] Brien WW, Kuschner SH, Brien EW, Wiss DA. The management of gunshot wounds to the femur. Orthop Clin North Am 1995;26:133–138 [10] Becker M, Lassner F, Fansa H, Mawrin C, Pallua N. Refinements in nerve to muscle neurotization. Muscle Nerve 2002;26:362–366 [11] Bielecki M, Skowroński R, Skowroński J. A comparative morphological study of direct nerve implantation and neuromuscular pedicle methods in cross reinnervation of the rat skeletal muscle. Rocz Akad Med Bialymst 2004;49:10–17 [12] Weber RV, Mackinnon S. Nerve transfers in the upper extremity. J Am Soc Surg Hand 2004;4:200–213 [13] Myckatyn TM, Mackinnon SE. A review of research endeavors to optimize peripheral nerve reconstruction. Neurol Res 2004;26:124–138

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Nerve Repair and Grafting [14] Nath RK, Mackinnon SE. Nerve transfers in the upper extremity. Hand Clin 2000;16:131–139, ixix. [15] Belin BM, Ball DJ, Langer JC, Bridge PM, Hagberg PK, Mackinnon SE. The effect of age on peripheral motor nerve function after crush injury in the rat. J Trauma 1996;40:775–777 [16] Hess JR, Brenner MJ, Myckatyn TM, Hunter DA, Mackinnon SE. Influence of aging on regeneration in end-to-side neurorrhaphy. Ann Plast Surg 2006;57:217–222 [17] Rinker B, Fink BF, Barry NG, et al. The effect of cigarette smoking on functional recovery following peripheral nerve ischemia/reperfusion injury. Microsurgery 2011;31:59–65 [18] Strauch B, Lang A, Ferder M, Keyes-Ford M, Freeman K, Newstein D. The ten test. Plast Reconstr Surg 1997;99:1074–1078 [19] Weber RV, Boyd KU, Mackinnon SE. Repair and Grafting of Peripheral Nerves In: Plastic Surgery. Edited by Neligan P, vol. 1, Third Edition. Maryland Heights, MO: Elsevier; 2011 [20] Tung TH, Mackinnon SEM. Nerve transfers: indications, techniques, and outcomes. J Hand Surg Am 2010;35:332–341 [21] Cabaud HE, Rodkey WG, McCarroll HR, Mutz SB, Niebauer JJ. Epineurial and perineurial fascicular nerve repairs: a critical comparison. J Hand Surg Am 1976;1:131–137 [22] Zhao Q, Dahlin LB, Kanje M, Lundborg G. Specificity of muscle reinnervation following repair of the transected sciatic nerve. A comparative study of different repair techniques in the rat. J Hand Surg [Br] 1992;17:257–261 [23] Evans PJ, Bain JR, Mackinnon SE, Makino AP, Hunter DA. Selective reinnervation: a comparison of recovery following microsuture and conduit nerve repair. Brain Res 1991;559:315–321 [24] Pannucci C, Myckatyn TM, Mackinnon SE, Hayashi A. End-to-side nerve repair: review of the literature. Restor Neurol Neurosci 2007;25:45–63 [25] Ray WZ, Kasukurthi R, Yee A, Mackinnon SE. Functional recovery following an end to side neurorrhaphy of the accessory nerve to the suprascapular nerve: case report. Hand (NY) 2010;5:313–317 [26] Trumble TA, Archibald S, Allan CH. Bioengineering for nerve repair in the future. J Am Soc Surg Hand 2004;4:134–142 [27] Driscoll PJ, Glasby MA, Lawson GM. An in vivo study of peripheral nerves in continuity: biomechanical and physiological responses to elongation. J Orthop Res 2002;20:370–375 [28] Millesi H. The nerve gap: theory and clinical practice. Hand Clin 1986;2:651– 663 [29] Seddon HJ. Surgical Disorders of Peripheral Nerves. Edinburgh, Scotland: Churchill Livingstone; 1975 [30] Meek MF, Coert JH. Clinical use of nerve conduits in peripheral-nerve repair: review of the literature. J Reconstr Microsurg 2002;18:97–109 [31] Whitlock EL, Tuffaha SH, Luciano JP, et al. Processed allografts and type I collagen conduits for repair of peripheral nerve gaps. Muscle Nerve 2009;39:787–799 [32] Weber RA, Breidenbach WC, Brown RE, Jabaley ME, Mass DP. A randomized prospective study of polyglycolic acid conduits for digital nerve reconstruction in humans. Plast Reconstr Surg 2000;106:1036–1045, discussion 1046– 1048 [33] Agnew SP, Dumanian GA. Technical use of synthetic conduits for nerve repair. J Hand Surg Am 2010;35:838–841

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[34] Mackinnon S. Letter to the editor. Response to: Agnew SP, Dumanian GA. Technical Use of Synthetic Conduits for Nerve Repair. J Hand Surg [Br] 2010;35:838–841 [35] Moore AM, Kasukurthi R, Magill CK, Farhadi HF, Borschel GH, Mackinnon SE. Limitations of conduits in peripheral nerve repairs. Hand (NY) 2009;4:180– 186 [36] Lloyd BMB, Luginbuhl RD, Brenner MJ, et al. Use of motor nerve material in peripheral nerve repair with conduits. Microsurgery 2007;27:138–145 [37] Flores AJ, Lavernia CJ, Owens PW. Anatomy and physiology of peripheral nerve injury and repair. Am J Orthop 2000;29:167–173 [38] Siemionow M, Brzezicki G. Current techniques and concepts in peripheral nerve repair. Int Rev Neurobiol 2009;87:141–172 [39] Lenoble E, Sokolow C, Ebelin M, et al. Results of the primary repair of 28 isolated median nerve injuries in the wrist Ann Chir Main 1989;8:347–351 [40] Indication MH. technique and results of nerve grafting. Handchirurgie 1977;2 Suppl:1–24 [41] Taylor GI, Ham FJ. The free vascularized nerve graft. A further experimental and clinical application of microvascular techniques. Plast Reconstr Surg 1976;57:413–426 [42] Doi K, Tamaru K, Sakai K, Kuwata N, Kurafuji Y, Kawai S. A comparison of vascularized and conventional sural nerve grafts. J Hand Surg Am 1992;17:670– 676 [43] Brushart TM. Preferential reinnervation of motor nerves by regenerating motor axons. J Neurosci 1988;8:1026–1031 [44] Moradzadeh A, Borschel GH, Luciano JP, et al. The impact of motor and sensory nerve architecture on nerve regeneration. Exp Neurol 2008;212:370– 376 [45] Krarup C, Archibald SJ, Madison RD. Factors that influence peripheral nerve regeneration: an electrophysiological study of the monkey median nerve. Ann Neurol 2002;51:69–81 [46] Mackinnon SE, Doolabh VB, Novak CB, Trulock EP. Clinical outcome following nerve allograft transplantation. Plast Reconstr Surg 2001;107:1419–1429 [47] Feng FY, Ogden MA, Myckatyn TM, et al. FK506 rescues peripheral nerve allografts in acute rejection. J Neurotrauma 2001;18:217–229 [48] Moore AM, Ray WZ, Chenard KE, Tung T, Mackinnon SE. Nerve allotransplantation as it pertains to composite tissue transplantation. Hand (NY) 2009;4:239–244 [49] Hudson TW, Zawko S, Deister C, et al. Optimized acellular nerve graft is immunologically tolerated and supports regeneration. Tissue Eng 2004;10:1641–1651 [50] Karabekmez FE, Duymaz A, Moran SL. Early clinical outcomes with the use of decellularized nerve allograft for repair of sensory defects within the hand. Hand (NY) 2009;4:245–249 [51] Brown JM, Yee A, Mackinnon SE. Distal median to ulnar nerve transfers to restore ulnar motor and sensory function within the hand: technical nuances. Neurosurgery 2009;65:966–977, discussion 977–978 [52] Saheb-Al-Zamani M, Yan Y, Farber SJ, et al. Limited regeneration in long acellular nerve allografts is associated with increased Schwann cell senescence. Exp Neurol. 2013 Sept;247:165–177 [53] Dorsi MJ, Chen L, Murinson BB, Pogatzki-Zahn EM, Meyer RA, Belzberg AJ. The tibial neuroma transposition (TNT) model of neuroma pain and hyperalgesia. Pain 2008;134:320–334

Nerve Transfer for the Forearm and Hand

5 Nerve Transfer for the Forearm and Hand Renata V. Weber and Kristen M. Davidge

5.1 Introduction Nerve injuries affecting hand function may occur anywhere along the length of the nerve from where it exits the spinal canal to the distal tip of the finger. Proximal injuries typically affect several muscle groups and sensory dermatomes, whereas more distal injuries tend to affect the motor and sensory endorgans of that particular peripheral nerve. Most typical peripheral nerve injuries in the extremities are penetrating injuries, including gunshot injuries, due to transection of the nerve; stretch injuries from traction to the extremity; and contusion or crush injuries from external or internal compressive forces. Less common causes of nerve injury to the extremities include thermal injuries; electrical injuries, which cause a local thermal injury but often a more devastating long-term sequela of dysesthesia and/or allodynia; radiation injuries; and iatrogenic injuries, such as injection injuries and those resulting from surgical procedures.1 Brachial plexus neuritis, also known as Parsonage Turner syndrome, is usually a self-limiting condition; however, in up to 20% of patients, some permanent neuropathy will persist.2 The disability may range from diffuse paralysis of the shoulder girdle and upper arm to discrete deficits within the forearm and hand.3 Regardless of the inciting factor, any injury that does not or cannot recover spontaneously in an appropriate time period will require surgical intervention. Primary repair of peripheral nerve injuries remains the gold standard by which all other repairs are compared. In situations where traditional nerve repair offers little hope of useful neurologic recovery, nerve transfers have become increasingly useful and often the procedure of choice.4–6 These alternative strategies were created in response to delayed presentation following injury; proximal injures with poor outcomes, such as root avulsion and high median and ulnar nerve injuries; and in cases of significant tissue loss or large neuromas-in-continuity.4,7 In addition, injuries with excessive scarring at the primary site (exploration of which may endanger surrounding structures), in which the site of injury is unclear or the injury is at the level of the cell body (as in an idiopathic neuritis or radiation injury), and injuries that involve multiple levels of the nerve present similar challenges to the classic approach.8,9 Functional restoration should be the focus of nerve reconstruction rather than anatomical repair, as it provides the optimum outcome results in nerve injuries with discrete motor or sensory deficits.10–13 In the first half of the 20th century, tendon transfers and sensory flaps were created largely in response to the types of injuries that soldiers in the First and Second World Wars were sustaining and surviving.14,15 The tendon transfers created to restore hand function were especially effective and continue to be used, especially in the chronically denervated limb. Toward the end of the 20th century, advances in understanding of peripheral nerve topography and the redundancy of innervation within mixed nerves, coupled with the reintroduction of nerve transfer for elbow reanimation in 1993,16 sparked new interest in providing reanimation to the limb distal to the elbow. Over the last decade, our understanding of the brain plasticity and its

potential for sensory and motor reeducation has allowed for the development of nerve transfers into the more distal aspects of the forearm, hand, and fingers.4,17,18 Experience with severe brachial plexus injuries was a stimulus to explore alternate options to long nerve grafts. Additionally, knowledge regarding tendon transfers led to the consideration that the “nerve” rather than the muscle tendon unit could be transferred, thus eliminating the disruption in critical normal biomechanics of the muscle unit that occurs with tendon transfers. Interest in creating motor and sensory nerve transfers in the forearm and hand stemmed from the superior results witnessed with upper arm transfers for shoulder and elbow reanimation. Despite the excitement over the results in upper arm reanimation, the conventional wisdom was that little could be done to restore function to the hand, especially in high median and high ulnar nerve injuries or complete and lower brachial plexus injuries. The unsatisfactory results with tendon transfers and lasso procedures for ulnar nerve clawing led to the idea of transferring the terminal branch of the anterior interosseous nerve (AIN) to the deep motor branch of the ulnar nerve, which we first performed in April 1991. 19 Despite this being an antagonistic transfer and a donor-recipient mismatch, the transfer provides enough power to limit clawing and has rarely needed to be supplemented with additional tendon transfers. Satisfactory results from this transfer provided the stimulus for other transfers, including reconstruction of the radial nerve from expendable branches of the median nerve, as well as reconstruction of pronation from redundant ulnar, radial, or median nerve transfers.13,20,21 Our patients have always served as a stimulus to the continued growth and development of these nerve transfers. The first brachialis nerve branch-to-median-nerve transfer included a long sural nerve graft and was done in combination with a pronator-to-extensor digitorum communis (EDC) tendon transfer for a complex partial median and radial nerve injury. Since then, the surgical technique has undergone a metamorphosis into the transfer that is presented in this chapter. The brachialis nerve branch transferred to the AIN portion of the median nerve is done completely in the arm without the need to enter the forearm; this was not possible only a decade ago. The gold standard by which all other techniques are judged is a direct repair. The authors predict, however, that nerve transfers will become the surgical technique of choice for reconstruction in any nerve injury that cannot be repaired primarily and when significant gaps repaired with nerve grafts consistently produce poor results. In the previous centuries, the results of nerve repair in the upper extremity and especially of the brachial plexus were viewed with pessimism. Major advances in nerve suturing and neurotization techniques during the middle of the 20th century set the stage for the reintroduction of nerve transfers in the 1990s. The peripheral nerve surgery community was initially stunned, but its leaders were inspired to explore beyond the established current boundaries of nerve reconstruction. Today, the seemingly insurmountable barrier of hand reanimation in lower brachial plexus injuries has been challenged.

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5.2 Nerve Transfers of the Forearm Complex upper extremity nerve injuries are a challenging problem for the reconstructive hand surgeon and can have devastating consequences to the patient. Complete brachial plexus injuries is dealt with in Chapter 14, as the priority of functions to be restored when a limited number of donor nerves are available present a difficult choice in and of itself. Isolated nerve injuries to the radial, median, and ulnar nerves will be presented in this chapter, along with the procedures that have consistently given superior results and that we currently advocate.

5.2.1 Principles and Indications for Nerve Transfers

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Most of the motor nerve transfers are modeled after the tendon transfers they replace; thus similar principles hold true for nerve transfers as for tendon transfers. The donor nerve must be expendable or redundant. Choosing a terminal branch is fairly straightforward; however, when a fascicle of a mixed nerve in the midarm is the necessary donor nerve, the intricate intraneural anatomy will influence the choice and position of the transfer because of the variety in fascicle length and diameter.22,23 Unlike a tendon transfer, a nerve transfer does not rely on amplitude and excursion of the tendon muscle unit, nor is it limited to the one tendon/one function and the straight line of pull principles. With tendon transfers, the type of muscle fiber unit and the insertion of the tendon will influence the ultimate effectiveness of that muscle’s contraction in its new position. 24, 25 The major advantages of a nerve transfer are that (1) a nerve transfer offers the capacity for restoring sensibility in addition to motor function; (2) multiple muscle groups can be restored with a single nerve transfer; (3) the insertion and attachments of the muscle(s) in question are not disrupted, so that the original muscle function and tension are maintained; (4) transferring to a specific distal target ensures that any worthwhile function traversing the anatomical area of injury is not downgraded; and (5) cell body injuries where a proximal healthy nerve is not available (i.e., neuritis) and dorsal root injuries (e.g., failed disc surgery) can be reconstructed.8,26

Criteria for motor nerve transfer: 1. Donor nerve is near motor end plates of target muscle (shortest distance = shortest time for reinnervation; “time is muscle”). 2. Donor motor nerve is expendable or redundant. 3. Donor nerve has “pure” motor nerve fibers. 4. Donor motor nerve has a large number of motor axons. 5. Donor nerve innervates a muscle that is synergistic to the target muscle (preferred but not required) to facilitate reeducation. 6. Motor reeducation improves functional recovery.

The donor nerves are selected based on proximity to the motor end plates, and the repair is done without tension. Nerve grafts

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are not needed, as the goal of the transfer is to eliminate the need for two neurorrhaphy sites. Nerve transfers for both motor and sensory nerves have similar criteria and are listed in the boxes Criteria for motor nerve transfer (p. 102) and Criteria for sensory nerve transfer (p. 102), below.6,27

Criteria for sensory nerve transfer: 1. Donor sensory nerve is near the target sensory nerve (“time is not sensation”). 2. Donor sensory nerve is expendable (noncritical sensory distribution). 3. Denervated distal end of the donor nerve is repaired endto-side to adjacent normal sensory nerve or a sensory nerve that will be innervated. 4. Sensory reeducation improves functional recovery.

In all motor nerve transfers, we use an end-to-end coaptation. In some of the sensory nerve transfers in noncritical distribution, an end-to-side coaptation may be used. In Chapter 1 of this book, end-to-side repair is discussed in detail; suffice to say here that sensory nerves will sprout in an endto-side fashion to a limited degree only. By contrast, in order to ensure any motor axonal sprouting, the donor motor axon must be injured. A motor axon will not sprout without an injury, unlike sensory axons, which will spontaneously, unilaterally sprout. 28 We have used a motor end-to-side with a direct neurotomy made in the donor nerve in hypoglossal-to-facial nerve transfers, spinal accessory-to-suprascapular nerve transfers, and AIN-to-deep motor branch ulnar nerve transfers. In these cases, a direct injury is made to the donor nerve to allow motor axonal regeneration into the attached respective recipient nerve. The AIN-to-ulnar end-to-side transfer is used in proximal second- and third-degree axonotmetic injuries of the ulnar nerve (i.e., severe cubital tunnel syndrome) to “supercharge” recovery of the ulnar intrinsic muscles, as well as following repair of complete injuries of the proximal ulnar nerve to preserve, or “babysit,” the motor end plates in the ulnar intrinsics while the proximal nerve regenerates slowly over time. This is technically a reverse end-to-side, which we term supercharge or SETS. This supercharge AIN-to-ulnar nerve transfer is discussed in more detail in Chapter 10. We also use sensory endto-side coaptations to restore sensation to the “distal” cut end of any sensory nerves to prevent painful hypersensitivity in the denervated distal territory of that sensory nerve, in cases such as after harvesting a nerve for grafting.29 One way to look at nerve coaptation is by relating it rather simplistically to an electrical circuit. We know that for a given voltage, resistors hooked up in series have the same current through each resistor. When the resistors are connected in parallel, the current is shared between the parallel resistors. If we think of nerves as resistors, and the voltage is set by the spinal cord neuron body, then it makes sense that an end-to-end coaptation (series) provides the same current in the donor and recipient nerve, which in humans translates to strong muscle contraction and good sensory input. When nerves are connected end-to-side (parallel), the current will be shared between the nerves, which clinically translates to protective sensation and some occasional reports of successful motor reinnervation.30–32

Nerve Transfer for the Forearm and Hand With transgenic rodent models, we have been able to show experimentally that only sensory nerves will sprout consistently by collateral sprouting.33,34 Thus, we reserve end-to-side techniques only for sensory nerve transfers in noncritical territories where only protective sensation is required. In areas of critical sensation or for motor recovery, we advocate end-to-end transfer. The SETS procedure is the reverse of the traditional ETS, and is discussed in detail in Chapter 10. When more than one nerve is available for a motor transfer, a nerve that innervates a synergistic muscle group is preferred over one that is antagonistic. As in tendon transfers, a nerve that innervates a synergistic muscle group will give a better result because less motor retraining in the postoperative period is needed. Although we used to think that an antagonistic muscle group would require more retraining, this has not always been the case, especially evident with the anterior interosseous-todeep ulnar motor nerve transfer, which will be described later in this chapter. The surgical indications for nerve transfers have expanded as our comfort with the technique has evolved. The box Indications for nerve transfer (p. 103), below, includes the most common reasons for using a nerve transfer over other techniques of repair. As in any complex reconstruction, the nerve transfer can often be in conjunction with tendon transfers and other procedures and customized to the particular patient’s needs.

Indications for nerve transfer: 1. Brachial plexus root avulsion injuries 2. High proximal injuries that require a long distance for regeneration 3. Major limb trauma with segmental loss of nerve tissue 4. Severe injuries in locations where avoidance of these scarred areas is recommended to avoid potential greater injury to critical structures 5. Nerve injuries where no proximal nerve is available for grafting 6. As an alternative to nerve grafting when time from injury to reconstruction is prolonged 7. Partial nerve injuries with a defined functional loss 8. Nerve injuries where the level of injury is uncertain, such as with idiopathic neuritides or radiation trauma

Recovery of motor function depends on a critical number of motor axons reaching the target muscle and reinnervating muscle fibers within a critical time period. The limitation of a nerve transfer at present is governed by the constraints of distance and time. The absolute time for denervation after which reinnervation is not possible is unknown, but our experience is that in many patients, nerves denervated 12 months or more will usually show fatty infiltration and not be receptive to reinnervation. We have seen excellent recovery of function with nerve transfers done by 9 to 12 months following injury. For best results, however, we still encourage decision making around 3 to 4 months after injury. Nerve growth in the clinical setting at present is limited to 1 inch per month or 1.0 to 1.5 mm per day.35 A nerve transfer closer to the motor end plate can significantly affect the distal component of an injury. The use of nerve transfers has considerably altered our concept of

an absolute “window” of opportunity for reinnervation. This means that even late reconstructions (8 to 10 months) of high nerve injuries have the potential for successful reinnervation.

5.2.2 Perioperative Assessment and Pearls Most patients are referred from another consultant or from their primary physician 2 to 4 months after sustaining an injury to the upper arm with neurologic deficit that has not resolved spontaneously. Ideally, we prefer to evaluate these patients as close to the time of injury as possible in order to better follow the recovery process. Occasionally, the patients are first evaluated at 6 to 9 months after injury, at which point the urgency for repair becomes more immediate. Typically, if there is no evidence of nerve regeneration by 3 to 4 months, electrodiagnostic testing is used to determine if spontaneous recovery is likely. Electromyographic (EMG) studies performed within 6 weeks of injury may not be useful to predict recovery, as it typically takes 8 to 12 weeks for voluntary motor unit action potentials (MUAPs) to appear. Sunderland I nerve injuries will recover spontaneously within 4 months. The reason for the EMG is to evaluate the extent or likelihood of recovery in more significant injuries (II, III, and IV nerve injuries) in order to elucidate the damaged nerves and begin a reconstructive plan. Initially, fibrillation potentials will be seen on EMGs around 6 weeks. As muscle recovery progresses, the number of fibrillation potentials will decrease, and MUAPs will appear and increase.36,37 The demonstration of MUAPs indicates a favorable prognosis for functional recovery and first occurs approximately 8 to 12 weeks post-injury. MUAPs suggest collateral sprouting from an adjacent uninjured axon, whereas nascent units represent end plate reinnervation from a regenerating injured axon and thus will occur later than MUAPs. If present by 3 to 4 months, either predicts spontaneous recovery of function. During this time physical therapy to maintain joint movement is critical for optimal recovery. We typically do not use computed tomography (CT) scanning or magnetic resonance imaging (MRI) to assess the injury. MRI can visualize all portions of the brachial plexus, whereas CT/ myelography will only evaluate possible root avulsion. The MRI can be advantageous for imaging the distal brachial plexus because of its multiplanar capability.38 Muscle, nerve, and vascular structures can be readily distinguished from each other, and pathologic lesions may be accurately localized in relation to surrounding structures. Recently we have used ultrasound (performed by a skilled neurologist) and found it useful.39 During the surgery, the anesthesiologist should use short, active depolarizing agents during induction, so that the handheld nerve stimulator can be used to locate and verify the donor nerves prior to transfer. Intraoperative electrical stimulation is critical in the procedure, so a surgeon performing a nerve transfer for the first few times and unfamiliar with the dissection may choose to not use a tourniquet, as the compression may cause a neurapraxia. Intraoperative monitoring is used occasionally if there is continuity within a portion of the nerve that has potential for further recovery. Most often, this is seen in large mixed nerves that have sustained a Sunderland VI injury.

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Nerve Transfer for the Forearm and Hand Only rarely can a tourniquet be used in nerve transfers of the arm and shoulder area, because of the location of the incisions. However, for most forearm nerve transfers, a tourniquet is useful to expose the nerves more rapidly in a bloodless field. Both the donor and recipient nerves should be exposed and electrically mapped within 30 to 40 minutes to ensure that the donor nerve does not become refractory to stimulation because of neurapraxia induced by the tourniquet. Alternatively, infiltration of the skin with epinephrine is acceptable, and careful dissection without a tourniquet is possible with minimal bleeding. Care should be taken to avoid infiltrating with local anesthetic to prevent conduction block of the nerves. The entire limb is prepped into the field. Even when transfers are performed for the elbow and shoulder in the upper arm, this allows better evaluation of the fascicles during the intrafascicular dissection. When the fascicle from the donor nerve is stimulated, wrist and finger movement can be visualized so that there is less likelihood of taking a critical function rather than a redundant one for the transfer. When getting ready to transect the donor and recipient nerves, always think “cut distal” on the donor nerve to provide more length and “cut proximal” on the recipient nerve; otherwise, there may be tension at the repair site. “Donor distal, recipient proximal” is our mantra, and we repeat this every transfer. Postoperative splinting is usually for comfort, as the transfers are done without any tension. Each of the repairs in this chapter will detail any specific immobilization performed that is unique to that transfer. Otherwise, we routinely splint or place in a sling for (maximum) 7 days, with protected movement allowed. If tendon transfers are performed at the same setting, then the splinting and rehabilitation protocols related to the tendon transfer will take precedence.

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5.3 Motor and Sensory Transfers for Isolated Nerve Injuries in the Forearm 5.3.1 Radial Nerve Injury: Lack of Wrist and Finger Extension Radial nerve injury results in the loss of wrist and finger extension (▶ Fig. 5.1). Lack of radial nerve function creates a major disability. Finger flexion strength is diminished because the wrist cannot be extended for more forceful grip, and the inability to extend the fingers prevents the patient from releasing objects from the palm. Because the radial nerve receives contributions from the entire brachial plexus via the posterior cord, isolated injuries are most often from direct trauma distal to the brachial plexus.40 Radial nerve palsies are typically reconstructed with direct nerve repair, nerve grafts, or tendon transfers. For a high radial nerve injury, an “internal splint” is usually performed by transferring the pronator teres (PT) to the extensor carpi radialis brevis (ECRB) to provide early wrist extension while the nerve is regenerating.41 Although the standard set of tendon transfers for radial palsy are some of the most reliable in existence, they may produce some unnatural ergonomics and a lack of power grip.42,43 In a review of 49 cases by Dunnet et al, > 80% of

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Fig. 5.1 Radial nerve injuries. (a) Injury to the radial nerve results in the loss of wrist and finger extension, known as wrist drop. (b) Another example of wrist drop during an attempt at wrist and finger extension.

patients reported a loss of endurance, and > 66% reported impaired coordination and dexterity.44 Wrist extension is provided by the extensor carpi radialis longus (ECRL) and ECRB. The ECRL nerve begins more proximal than the ECRB, and it splits from the radial nerve usually in the distal upper arm proximal to the elbow. Because ECRB alone provides good wrist extension, and the nerve branch to this muscle comes from the radial nerve proper before it becomes the posterior interosseous nerve (PIN), these are the two branches that are the primary targets for restoration of function in lower radial nerve injuries. In patients who have an intact median nerve, the two available flexor digitorum superficialis (FDS) branches and the branches to the flexor carpi radialis (FCR) and palmaris longus (PL) are available for transfer (▶ Fig. 5.2).20 During the early development of this transfer, it was suggested that the more powerful wrist flexor should be rerouted to restore wrist extension (FCR nerve branch to ECRB nerve branch). Although this did provide strong extension, which is essential for forcible grip, it proved to be significantly more difficult to retrain the patient, as it was not a synergistic transfer. We quickly returned to our preference of transferring the FDS nerve branches to the ECRB nerve branch, and FCR to PIN (▶ Fig. 5.3). The synergy of this transfer facilitates postoperative rehabilitation, because, via the tenodesis effect, wrist extension augments finger flexion.21,45 It becomes intuitive for the patient to begin flexing the digits (FDS) and then learn to extend the wrist (ECRB) as the nerve transfer begins to function. Similarly, pairing wrist flexion (FCR) with finger extension by innervating the

Nerve Transfer for the Forearm and Hand

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Fig. 5.2 Radial, median, and ulnar nerve anatomy in the proximal forearm. At this location, the radial nerve has three primary nerve branches: superficial sensory, extensor carpi radialis brevis, and posterior interosseous nerve (PIN). The supinator branch is located deep to the PIN and courses deep into the supinator for innervation. The median nerve has several nerve branches: the pronator teres, flexor carpi radialis/palmaris longus, anterior interosseous, and two flexor digitorum superficialis branches. (Note that the more proximal and medial branch to the pronator is not portrayed in this figure.) The ulnar nerve can have multiple branches to the flexor carpi ulnaris distal to the cubital tunnel. Note that the flexor digitorum profundus branch from the ulnar nerve is not portrayed.

Fig. 5.3 Illustration of median-to-radial nerve transfer. Two nerve transfers occur in the median-to-radial nerve transfer for restoration of wrist/finger extension. The donors (green) and recipients (red) occur in the following specific sets for optimal results with postoperative rehabilitation: (1) flexor carpi radialis to posterior interosseous (PIN) and (2) flexor digitorum superficialis (FDS) to extensor carpi radialis brevis. PIN and FDS are antagonistic.

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Fig. 5.4 Identifying the tendon of the superficial head of the pronator teres (PT). This identification is used for either the PT-to-extensor carpi radialis brevis (ECRB) tendon transfer or step-lengthening of the PT for median nerve exposure. The periosteal extension of the tendon is marked in purple to mobilize and release it from the radius for the PT-to-ECRB tendon transfer.

extensor digitorum communis (EDC) and extensor pollicis longus (EPL) via the PIN, a synergistic effect assists with reeducation. The PL fascicle can be neurolysed separately from the FCR fascicle to be used as a “fallback” for tendon transfer for the EPL, if necessary. In addition, to restore sensation, the radial sensory branch can be coapted end-to-side to the median nerve at a location distal enough to prevent tension to the transfer. Alternatively, the radial sensory nerve may be coapted end-to-end to the lateral antebrachial cutaneous (LABC) nerve. If the median nerve is not available, one of the branches to the flexor carpi ulnaris (FCU) of the ulnar nerve may be used via a separate incision to transfer to the PIN.46,47 Pairing the FCU with the PIN has a similar complementary effect as pairing the FCR with the PIN. The transfer should be equally easy to reeducate postoperatively, as, again, the wrist flexor naturally assists in finger extension. Wrist extension is provided by the PT tendon transfer to the ECRB tendon, if available (▶ Figs. 5.4–5.9).8 This “internal splint” provides the patients with the benefit of the immediate effect of the tendon transfer while they wait for the nerve transfer to reinnervate the fingers. A recent study suggests that this procedure may limit effective active pronation of the extremity,48 but we have not encountered this problem; also, we find this tendon transfer a useful addition to the nerve transfer in the appropriate patient with a supple hand and accepting of the longer scar. The LABC and radial sensory nerves share a similar sensory distribution over the distal dorsal radial side of the hand and

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thumb; thus the LABC becomes an excellent donor nerve for restoration of sensation to the dorsum of the hand. At the level of the proximal forearm, these two nerves run essentially parallel, are similar in size, and are easily coapted. Alternatively, an endto-side coaptation of the radial sensory branch to the median nerve proper distal to the takeoff of the AIN will only provide protective sensation.

5.3.2 Median-to-Radial Nerve Transfer: Technique With the patient under general anesthesia, with or without the tourniquet inflated, the radial and median nerves are exposed through a single volar incision in the proximal to mid-forearm level. A lazy-S incision is started in the proximal forearm at the lateral edge of the antecubital fossa and traced distally to the midvolar forearm (▶ Fig. 5.10). It may be extended to the distal third by returning to the radial side of the forearm at the mid to distal third of the forearm. Care is taken to avoid the branches of the LABC, which accompanies the cephalic or accessory cephalic vein (▶ Fig. 5.11). The lacertus fibrosus is identified and incised. The fascia is incised in order to expose the radial vascular bundle running between the PT and brachioradialis. By retracting the brachioradialis laterally and the radial vessels medially, in the distal portion of the incision, the superficial head of

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Fig. 5.5 Releasing and mobilizing the pronator teres (PT) tendon for tendon transfer to the extensor carpi radialis brevis (ECRB). The PT tendon is released from its insertion point to the radius and mobilized for the PT-to-ECRB tendon transfer. Note that the tendon is extended by the periosteum for reliability of the tendon transfer.

Fig. 5.6 Identifying the extensor carpi radialis brevis (ECRB) inferior to the extensor carpi radialis longus (ECRL). The ECRB is located below the ECRL. Their function can be confirmed by pulling the respective tendon proximally and observing the actions of the hand. ECRL inserts at the base of the second metacarpal, producing wrist extension with radial deviation, while the ECRB inserts at the base of the third metacarpal, producing neutral wrist extension.

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Fig. 5.7 Identifying the recipient extensor carpi radialis brevis (ECRB) muscle for tendon transfer. The recipient tendon transfer is located below the extensor carpi radialis longus (ECRL). By retracting ECRL, the ECRB tendon is observed.

Fig. 5.8 Weaving the donor pronator teres (PT) tendon into the recipient extensor carpi radialis brevis (ECRB) tendon for transfer with the tourniquet deflated. After identifying the ECRB tendon, weaving forceps are used to pierce the ECRB tendon to grasp the PT tendon. This first weave sets the tension for the tendon transfer, followed by a series of weaves distally.

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Fig. 5.9 Pronator teres (PT)-to-extensor carpi radialis brevis (ECRB) tendon transfer. Immediately following the first weave, the ECRB and PT tendon are sutured to set the tension. Afterward, a series of PT and ECRB weaves occur distally and sutured.

Fig. 5.10 Orientation and incision for median-toradial nerve transfer. A lazy-S incision occurs over the proximal volar forearm, starting in the antecubital fossa and extending half of the distance toward the wrist crease over the medial border of the brachioradialis. The incision is lengthened distally to mobilize the pronator teres tendon for transfer to the extensor carpi radialis tendon. (a) Orientation image and dotted markings for an unused incision. (b) Actual incision is visualized.

the PT can be identified (▶ Fig. 5.12). A step-lengthening of the PT tendon is performed to release the superficial head (▶ Fig. 5.13). Moving proximally, the median nerve is exposed deep, and ulnar to the radial vessels (▶ Fig. 5.14; ▶ Fig. 5.15). If a PT tendon transfer is performed at the same time, the step-lengthening is not performed in order to preserve the continuity of the

tendon transfer. Instead, the distal radial attachment is elevated along with an extension of periosteum and reflected proximally to expose the median nerve. The median nerve is traced distally by dividing the deep head of the PT tendon. Additionally, the tendinous arch of the FDS is released in a similar fashion as when decompressing the median nerve for PT syndrome (▶ Fig. 5.16). This allows enough of the median

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Fig. 5.11 Exposure and identification of the lateral antebrachial cutaneous (LABC) nerve. Upon exposure, the LABC is identified to accompany the cephalic or accessory cephalic vein. These structures are protected as dissection continues through the antebrachial fascia.

Fig. 5.12 Landmarks for identifying the tendon of the superficial head of the pronator teres (PT). The tendon of the superficial head of the PT lies between the radial vessels and the radial sensory nerve.

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5 Fig. 5.13 Step-lengthening the pronator teres (PT) for exposure of the median nerve proximally. For adequate exposure of the median nerve in the proximal forearm, the step-lengthening of the superficial head of the PT provides effective release of this muscle. (a) Anatomical schematic of the right forearm. (b) The PT tendon is step-lengthened for exposure of the median nerve. dPT, deep head of the PT; MN, median nerve; RV, radial vessels, (Used with permission from Brown JM, Mackinnon SE. Nerve transfers in the forearm and hand. Hand Clin 2008;24(4):319–340.)

Fig. 5.14 Identifying the deep head of the pronator teres (PT) for exposure of the median nerve. The deep head of the PT is identified radial to the median nerve. The deep head has a deep origin that is superficial to the median nerve. The deep head of the PT is divided to expose the median nerve. The deep head is small and its compressive tendon is typically below a small muscle belly. The pick-up forceps hold the proximal portion of the deep pronator.

nerve to be exposed in order to identify the major branches necessary for the transfer (▶ Fig. 5.17). The branch to the PT is the most proximal and superficial below the antecubital fossa and is present on the superficial surface of the median nerve. It quickly divides into two distinct branches before entering the muscle. Above the elbow is a second pronator branch, located on the ulnar side of the median

nerve. The branches to the FCR and PL are encountered on the deep ulnar side of the nerve. The branches to the FDS are distal to the FCR branch. A detailed internal neurolysis is not needed, as the branches of the median nerve are distinct from the median nerve proper.13 At this level, the larger-caliber AIN begins to separate from the radial aspect of the median nerve. Electrical stimulation with a handheld stimulation device is used to

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Fig. 5.15 Release of the deep head of the pronator teres (PT). By releasing the deep head of the PT, the median nerve is identified. The respective donor nerves for the median-to-radial nerve transfer are located on the medial aspect of the median nerve. The anterior interosseous nerve can be used as a landmark to gauge where the donor nerves branch from the median nerve. The deep pronator is retracted by the pick-up forceps.

Fig. 5.16 Identifying and releasing the tendinous arch of the flexor digitorum superficialis (FDS). The next structure that is released to further expose the median nerve is the tendinous arch of the FDS. The tendinous arch is seen with a sharp border.

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Fig. 5.17 Exposure of the median nerve and its donor branches. Following the release of the tendinous arch of the flexor digitorum superficialis (FDS), the median nerve and its donor branches are identified. The donor flexor carpi radialis (FCR) nerve branch is identified proximally with the palmaris longus nerve branch. Distally, the FDS nerve branch is identified. In most cases, there is an additional FDS nerve branch distal to this branch point. This can be confirmed by electrically stimulating the medial aspect of the median nerve. The AIN is the only branch that exists radially from the median nerve.

confirm the identity of the branches as they are tagged with vessel loops for later use. If a PT tendon transfer is performed at the same time as the median nerve transfer, the surgeon must “move along” at a fairly quick pace if a tourniquet is used. Both donor and recipient nerves need to be exposed and electrically mapped in 30 to 40 minutes to ensure that the median nerve does not become refractory to stimulation because of neurapraxia induced by the tourniquet. The radial nerve is identified by finding first the radial sensory directly under the brachioradialis muscle (▶ Fig. 5.18). The muscle is retracted laterally and the nerve traced proximally to the main trunk of the PIN. The crossing vessels making up part of the leash of Henry need to be divided to expose the PIN and branch to the ECRB, both of which will be radial to the sensory branch (▶ Fig. 5.19). The PIN is followed distally and decompressed by incising the leading edge of the supinator. The mobilization of the PIN allows for a tension-free repair without the need for nerve grafts and releases a secondary compression point that could impede regeneration.49,50 The PIN and ECRB nerves need to be divided well proximally, above the elbow crease, using retractors to allow access to the lateral elbow and distal upper arm without the need for extension of the incision. The mantra “Donor distal, recipient proximal” is key to a satisfactory result. The

coaptation neither requires a nerve graft nor is repaired under tension. The “overlap” between the donor and distal nerves is typically 6 to 8 cm. Dissection and exclusion of the branch to the supinator allow for more aggressive mobilization of the PIN without tension (▶ Fig. 5.20). The biceps provide effective supination so that patients do not have disability from its loss and, when functioning, can be used as an expendable donor for situations of median nerve loss. Internal neurolysis of the supinator nerve branch allows all transferred axons to be directed to finger and wrist extension (▶ Fig. 5.20).4 With the recipient nerves transected proximally, mobilized, and transposed, the donor nerves that had been previously dissected and tagged with vessel loops are traced distally into the muscle bellies and transected distally to allow as much usable length as possible (▶ Fig. 5.21). The FDS and FCR branches are coapted to the ECRB and PIN using 9-0 nylon sutures (▶ Fig. 5.22). The tourniquet is deflated prior to the transfer. All bleeding is controlled before performing the coaptation. Prior to the repair, the arm is moved in full pronation, supination, flexion, and extension to assess for tension. The wound is closed in layers, usually with a pain pump and drain. The patient is placed in a posterior splint with the elbow at 90 degrees, the shoulder and wrist in neutral, the forearm in pronation, and the fingers free. The splint, drain, and pump

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Fig. 5.18 Exposure of the radial nerve by releasing the tendinous portion of the extensor carpi radialis brevis (ECRB) and supinator. The superficial branch of the radial nerve is identified. Lateral to this nerve are the recipients: the posterior interosseous nerve and the ECRB nerve.

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Fig. 5.19 Exposure of the radial nerve and its recipient branches. Following the release of the tendinous portion of the ECRB and supinator, the radial nerve and its recipient branches are exposed. Lateral to the superficial branch of the radial nerve is the nerve to the ECRB. The posterior interosseous nerve (PIN) is the second recipient nerve and is identified lateral to the ECRB nerve. Two supinator nerves are seen to branch from the deep aspect of the PIN. The supinator nerve is not included in the median-to-radial nerve transfer.

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Fig. 5.20 Neurolyzing the recipient PIN with exclusion of the supinator nerve. The PIN is divided proximally with the supinator branch. The supinator branch is then neurolysed from the PIN, as it is not included in the reconstruction. Supination function is present from the biceps muscle.

Fig. 5.21 Transecting the donor median and recipient radial nerves for nerve transfer. To acquire sufficient length for nerve transfer, the donor median nerves, flexor carpi radialis (FCR) and flexor digitorum superficialis (FDS), are transected distally, and the recipient radial nerves, posterior interosseous nerve (PIN) and extensor carpi radialis brevis (ECRB), are transected proximally. Note the long distance between the donor distal (median) and recipient proximal (radial) branches on the blue backgrounds.

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Fig. 5.22 The median-to-radial nerve transfer comprises two transfers: The donor FCR nerve is transferred to the recipient PIN. The donor FDS nerve is transferred to the recipient ECRB nerve.

are removed at the first postoperative visit on day 2, and the patient is placed in a custom splint or sling, depending on whether or not a tendon transfer is also performed.

5.3.3 Sensory Restoration in the Radial Nerve Distribution: Technique The LABC is our preferred donor nerve for restoration of sensation to the dorsum of the hand because of the overlap in sensory distribution between these two nerves. At the level of the mid-forearm, these two nerves run essentially parallel. The radial sensory nerve courses under the brachioradialis, and the LABC runs with the cephalic vein. The size match is excellent for a direct end-to-end repair, which restores a broad area of sensation to the dorsum of the hand at the expense of the less critical distal LABC distribution (▶ Fig. 5.23). Preoperatively, it is wise to assess sensation in the radial sensory distribution to ensure that there is poor sensibility. We use the Ten Test to assess.51,52 Because the dorsum of the hand is not a critical surface, or when the LABC is not available, the radial sensory nerve can be coapted end-to-side to the median nerve proper distal to the takeoff of the AIN. An epineurial window is made in the median nerve, and the perineurium of the median nerve is incised longitudinally to stimulate sprouting of sensory nerves. The epineurium of the radial sensory nerve is sewn to the side of the median nerve using 9-0 nylon sutures. The radial side of the

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nerve should be avoided to minimize entering the median motor fascicle. This technique, however, will provide protective sensation only. We reserve end-to-side techniques only for sensory nerve transfers in noncritical territories where only protective sensation is required. In areas of critical sensation, we advocate end-to-end transfer. Distal sensory nerve transfers are appropriate in high proximal injuries that will require years for recovery. However, when the distal nerve transfer is performed, the surgeon must consider the possibility that if some sensation does regenerate from the proximal repair or spontaneously in partial nerve injuries in one or two years, then it will develop a painful neuroma at the level of the transection. At the time of the transfer, we turn that proximal nerve end into innervated muscle as a preventive measure.

5.3.4 Median Nerve Injury: Lack of Forearm Pronation, Thumb Opposition, and Finger Flexion The median nerve carries the majority of sensation to the hand that is important for fine manipulation (▶ Fig. 5.24) and innervates a significant portion of the muscles that control wrist and finger flexion, a major component of thumb opposition, as well as the ability to pronate the forearm.16,22,53 In the forearm, once the median nerve divides into its motor branches, the median nerve is composed predominantly of sen-

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Fig. 5.23 Lateral antebrachial cutaneous (LABC)-to-superficial branch of radial (radial sensory) nerve transfer. (a) The donor LABC nerve is identified superficially. The recipient radial sensory nerve is identified deep by retracting the brachioradialis. (b) Donor (green) and recipient (red) anatomy for nerve transfer is shown. (c) The donor LABC nerve is end-to-end transferred to the recipient radial sensory nerve.

Fig. 5.24 Injury to the left median nerve presents with loss of pronation, wrist/finger flexion, and thenar function. (a,b) Patient demonstrates inability to pronate the left hand. (c) The inability to make a fist due to loss of finger flexion. (d) The patient is unable to flex the IP joint of the thumb. (Used with permission from Tung TH, Mackinnon SE. Flexor digitorum superficialis nerve transfer to restore pronation: two case reports and anatomic study. J Hand Surg Am 2001;26(6):1065–1072.)

sory fibers except for the recurrent median motor branch, which divides in the carpal tunnel to power the thenar muscles of the thumb and radial two lumbricals. 54 Injury to the median nerve proximal to the motor divisions will result in problems with pronation and weakness in grip strength. 55 With injuries directly in the forearm, direct repair will restore both sensory and motor function, although care to identify the critical AIN and pronator motor branches is imperative. Recovery takes at least 1 year, and patients require extensive occupational therapy for up to 2 years. In cases where primary repair is not possible, a few specific transfers have been developed that are exceedingly useful, but they are very often used in conjunction with tendon transfers, much more so than in other aspects of reanimation in the upper arm.

5.3.5 Thumb Opposition Median nerve injuries occurring anywhere along the nerve from where it emerges from the brachial plexus to the carpal tunnel may result in thenar atrophy. In rare instances where there is a Marinacci communication in the forearm or a RicheCannieu communication in the hand, for median fibers to be carried by the ulnar nerve and the median nerve injury is distal to that crossover anomaly, the median innervated thenar muscles of the hand may be spared.53 This is the opposite of the more common Martin-Gruber crossover. Acute injuries in the forearm are treated with extensive mobilization of the nerve and primary repair with careful attention paid to lining up the motor fascicles. If primary repair is not possible, nerve grafting is usually the second choice for injuries distal to the

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Nerve Transfer for the Forearm and Hand mid-forearm. The more proximal injuries have resulted in poorer outcomes because the topography between sensory and motor fascicles is less easily identified. Despite attention to detail, aberrant regeneration of sensory fibers into motor pathways results in no thenar functional recovery.46,56,57 Tendon transfers for opposition are well established and extremely effective. They continue to be used in conjunction with carpal tunnel surgery associated with thenar wasting; however, they do require postoperative immobilization and may produce unusual ergonomics. A nerve transfer from the terminal AIN, which is well established for intrinsic reanimation in ulnar nerve injuries, is an equally good donor nerve for median-sided intrinsic reanimation, although recovery takes much longer.56 The distal AIN to the pronator quadratus and the recurrent motor branch of the median nerve have a comparable number of motor axons, with the former containing ~ 900 motor axons, and the latter with ~ 1,050 motor axons. Ten to 15% of axons are lost because an interposition graft is usually necessary for the transfer; however, in both experimental and clinic studies, this transfer has been shown to be useful. 4,31 The donor site morbidity is minimal compared to tendon transfers. 4,56

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5.3.6 Terminal Anterior Interosseous Nerve-to-Median Recurrent Motor Branch Nerve Transfer: Technique With the patient under general anesthesia and the tourniquet inflated, the surgeon uses an extended carpal tunnel incision with a zig-zag incision to cross the wrist crease into the distal third of the volar forearm. The nonfunctioning motor thenar nerve is identified within the carpal tunnel. Once identified, the branch is neurolysed from the remainder of the median nerve progressing as far proximally as possible or until the injury is encountered.4 This neurolysis can easily extend as high as 9 to 10 cm proximal to the wrist crease. We do this not physically with microscissors, but rather by visualizing the recurrent motor fascicles distally and following them proximally with our eyes, with magnification, and with micro instrumentation. This speeds up the dissection and is not traumatic. Once the proximal extent of the dissection is reached, the motor branch is neurolysed separate from the sensory component of the median nerve to allow for transfer of the terminal AIN branch. In the forearm, the median nerve, the superficial and deep forearm finger flexors, and the FCU are all retracted radially with a Weitlander or self-retraining retractor. At the proximal edge of the pronator quadratus muscle, the anterior interosseous neurovascular bundle will be lying radial to the AIN. The nerve can be traced into the midpoint of the muscle by dividing it in order to gain an additional 0.7 to 1.5 cm before branching occurs. The AIN is transposed over the pronator quadratus muscle. The proximal end of the recurrent motor branch is transected as far proximally as possible. Typically, an interposition graft is necessary to bridge the gap between the two ends, depending on the level of the median nerve injury. A medial antebrachial cutaneous (MABC) or LABC nerve may be used as the graft. The wrist should then be flexed and extended in both pronation

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and supination before the graft is trimmed so that a tensionfree coaptation will be performed (▶ Fig. 5.25).9 Prior to the repair, the tourniquet is deflated and the wound accessed for evidence of bleeding. Once completed, the repair is again set through a complete range of motion to confirm a tension-free repair. The surgeon closes the skin in layers in the forearm and with simple sutures in the palm. The patient is placed in a volar wrist splint with the wrist in neutral and the elbow and fingers free. Once the operative dressing is removed 2 to 3 days postoperatively, the patient is kept in a wrist splint for a total of 7 to 10 days. Once the splint is removed, active and passive range of motion exercises under the direction of a hand therapist may begin, and digital movement can commence immediately postoperatively. In a high median nerve injury, the AIN is not an available donor nerve. Alternative nerve transfers have been described, such as an ulnar-to-median nerve transfer in the hand using the third lumbrical motor branch58 and a radial-to-median nerve transfer using the PIN branches to the extensor digiti quinti (EDQ) and extensor carpi ulnaris (ECU) via an interposition nerve graft. However, in this situation, we prefer to use standard tendon transfers to restore opposition, along with the sensory nerve transfer described next.

5.3.7 Median Nerve Sensory Restoration Loss of sensation to the hand is a tremendous functional deficit. Proprioception is important for pinch and fine motor tasks. 34 Many surgeons believe that the success of motor function restoration is largely determined by the quality of hand sensation. 53 Additionally, some have proposed that restoring sensation is a prerequisite to restoring motor function.40 The radial side of the index finger and the ulnar side of the thumb are by far the most important sensory distributions to restore, with the remaining finger surfaces less critical.56 As mentioned previously for motor injuries, primary repair of the median nerve in the forearm aligning sensory and motor fascicles to minimize loss of target-specific reinnervation is the gold standard, with nerve grafting the next option when extensive mobilization still does not bridge the neural gap. In cases of a primary repair of the median nerve, 31% of patients achieved S3 or better sensory recovery.59 The outcome data for nerve grafts in upper extremity injuries come from the trauma and amputation literature, and the consensus is that short grafts < 6 cm in length have better motor and sensory recovery than grafts ≥ 20 cm. Nerve grafts between 6 and 20 cm have too much variability in results, so that no conclusive recommendation can be made. Even in short grafts with optimal conditions, the sensory recovery in the median nerve varies from 36%60 to as high as 63%61 for low median nerve injuries. Because both motor and sensory recovery rates are generally poor with long grafts, vascularized nerve grafts have been proposed for defects > 20 cm;62 yet, despite the use of vascularized nerve grafts, the static two-point discrimination ranges from 10 to 20 mm. In our experience, nerve recovery after sensory nerve transfers in the hand provides protective sensation but poor measurable sensation by two-point moving and static discrimination sensation, comparable to data published by Brunelli.63 Because

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Fig. 5.25 Illustration of anterior interosseous (AIN)-to-recurrent thenar nerve transfer with interpositional nerve graft. (a) To restore thenar function following median nerve injury in the distal forearm, the AIN is an available donor nerve for transfer. (b) To facilitate this transfer, an interpositional nerve graft is required to bridge the distance. (c) The recurrent thenar fascicle is located from the radial aspect of the median nerve.

outcome studies in cases of grafts > 5 cm are for the most part consistently worse than our results with sensory nerve transfers, we advocate considering using a sensory nerve transfer if a primary repair or a graft < 5 to 10 cm cannot be performed. 64 Local donor nerves include the common digital nerve to the third web space, the common digital nerve to the fourth web space, and the dorsal cutaneous branch of the ulnar (DCU) nerve.7,40,41 Although the common digital nerve to the third web space is innervated by the median nerve and would not be available in lower median nerve injuries, it is preserved in upper trunk brachial plexus injuries and is thus a donor for this transfer. The common digital nerve to the third web space is transferred to the first web space nerves in a direct end-to-end manner to provide the optimal restoration of sensation to the most critical surfaces. The common digital nerves to the second web space and the terminal end of the third web space nerves are transferred end-to-side to either the ulnar digital nerve of the small finger or the common digital nerve to the fourth web space to restore protective sensation in the less critical area. Alternatively, if available as in C5-C6 plexus injuries, the third web space-to-first web space nerve transfer can be done in the very distal forearm, which allows for less dissection than when the same transfer is done in the palm (▶ Fig. 5.26; ▶ Fig. 5.27). The carpal tunnel is released, and the interfascicular dissection is continued to ~ 6 cm proximal to the wrist. Using microforceps, the surgeon “taps” along the surface of the median

nerve. The forceps will “fall into” the natural cleavage plane between the third web space component of the median nerve and the remainder of the nerve. The recurrent motor branch is identified as previously described in the terminal AIN-to-recurrent median motor branch transfer. The remaining “excluded” fibers represent the first and second web space branches. The third web space branch is then transferred to the radial side of the remaining sensory component of the median nerve in the distal forearm. The distal component of the third web space nerve is turned end-to-side to the ulnar or median nerve. In the latter situation, collateral sprouting will occur from the “reinnervated” median nerve once regeneration into that nerve has occurred. In the case of a median nerve injury with an intact ulnar nerve, the common digital nerve to the fourth web space may be used. The common digital nerve from the fourth web space is transferred to the first web space nerves in a direct end-toend fashion; the common digital nerves to the second and third web spaces are transferred end-to-side to the ulnar digital nerve of the small finger to restore protective sensation in the less critical distributions, while the fourth web space distribution remains denervated (▶ Fig. 5.28). If enough length is preserved to the donor nerve remnant in the fourth web space, the distal end may also be transferred end-to-side to the ulnar digital nerve of the small finger. These sensory transfers are a derivative of the Littler island flap.

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Fig. 5.26 Illustration of third web space of median-to-first web space of median nerve transfer for C5, C6 palsies. (a) C5, C6 palsies include deficits in the median nerve sensory distribution. The thenar nerve branch is intact in these palsies. (b) Surgical strategy is to reinnervate critical sensation, which includes the first web space. (c) Critical sensation end-to-end nerve transfer is the donor third web space fascicle of the median nerve to the recipient first web space fascicle of the median nerve. Noncritical sensation end-to-side nerve transfer is the donor sensory component of the ulnar nerve to the recipient distal third web space fascicle of the median nerve. (d) Fascicular donor and recipient anatomy for restoration of critical sensation using endto-end nerve transfer. (e) Fascicular donor and recipient anatomy for restoration of noncritical sensation using end-to-side nerve transfer.

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Fig. 5.27 Third web space of median-to-first web space of median nerve transfer for C5, C6 palsies. (a) The median nerve donor and recipient fascicles are identified. For critical sensation, the donor third web space fascicle is identified on the medial aspect of the median nerve, and the recipient first web space fascicle is identified on the lateral aspect of the median nerve. The fourth web space branch of the ulnar nerve is a donor nerve for noncritical sensation in an end-to-side fashion. (b) The donor third web space fascicle is coapted to the recipient first web space fascicle of the median nerve in an end-to-end fashion for critical sensation. The recipient distal third web space fascicle of the median nerve is coapted to the donor fourth web space branch of the ulnar nerve in an end-to-side fashion for noncritical sensation. Arrows show the direction of nerve regeneration.

Though mostly now of historical importance, the Littler island flap for sensory restoration is still useful in the rare instance of a soft tissue defect to either digit.65,66 A less used alternative to the ulnar sensory nerves in the hand is the dorsal sensory branch of the ulnar nerve, which is transferred in the distal forearm just proximal to the wrist to the median nerve.

5.3.8 Ulnar Sensory Nerve Transfer for Median Sensory Deficits: Technique We use a carpal tunnel incision with release of the carpal ligament, which is extended distally using a Brunner-type zig-zag incision toward the first and fourth web spaces (▶ Fig. 5.29). Surgeons who are extremely comfortable operating on sensory nerves in the hand may use a more limited incision in the palm distal to the carpal tunnel (▶ Fig. 5.28). The superficial palmar arch and common digital arteries will be juxtaposed to the common digital nerves and overlying the lumbricals, with the digital arteries palmar to the associated digital nerves at the level of the metacarpal shaft.67 At the metacarpal heads, the positions reverse, so that in the digits, the nerves are more superficial or volar than the arteries. The donor nerve in the fourth web space should be dissected and transected at the level of the metacarpal head. The branch to the radial side of the index is usually found first. In the process of tracing this nerve proximally toward the carpal tunnel, the ulnar digital nerve of the thumb is encountered. The two branches are usually neurolysed to allow better mobilization to the ulnar side of the hand. If the donor nerve can be transected closer to the base of the metacarpal level, then the distal fourth

web space nerve is coapted end-to-side to the ulnar digital nerve of the small finger, along with the second and third web space nerves. If the entire length of the fourth web space nerve is needed to reach the nerves of the first web space for a primary repair, then the ulnar side of the long finger and the radial side of the ring finger will not be specifically reinervated. The proximal half of the common digital nerve to the fourth web space is coapted to the digital nerves in the first web space endto-end using 9-0 nylon sutures. We also try to include the radial digital nerve to the thumb in the reconstruction, although predominantly directing the repair to the ulnar digital nerve of the thumb and the radial side of the index finger. The common digital nerves to the second and third web spaces are mobilized in a similar manner as the common digital nerve to the fourth web space; these two nerves are transected as far proximally as needed to reach the ulnar digital nerve. An epineurial window is created and the perineurium opened longitudinally to stimulate collateral sprouting of sensory nerves. Recipient nerves are transferred to the ulnar digital nerve of the small finger using 9-0 nylon sutures. The size discrepancy is quite large (▶ Fig. 5.29); however, because the recipient nerves are being sutured end-to-side, that difference is not problematic. Care should be taken to avoid making all the epineurial windows in the same plane along the long axis of the nerve, so that sprouting to the recipient nerves comes from different areas of the nerve. The surgeon can also suture the distal portion of the third web space nerve end-to-side to the “reinnervated” portion of the median nerve, knowing that over time, collateral sprouting will occur from the reinnervated nerve. An additional nerve transfer to restore median nerve sensation includes the DCU-to-the sensory component of the median

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Fig. 5.28 Sensory nerve transfer for median nerve injury. Nerve transfer within the hand for median nerve sensation. (a) Schematic of a fourth web space nerve transferred to the first web space nerves in a direct end-to-end fashion. (b) Schematic of the second and third web spaces transferred endto-side to the ulnar digital nerve of the small finger. The fourth web space distribution remains dennervated. (c) Clinical example of the end-to-side transfer of the fourth web space nerve to the first web space nerves in the midpalm, with a close-up view (d). (Used with permission from Colbert SH, Mackinnon SE. Nerve transfers in the hand and upper extremity. Tech Hand Up Extrem Surg 2008;12:20–33.)

nerve transfer (▶ Fig. 5.30; ▶ Fig. 5.31). This technique is performed in the distal forearm, and knowledge of interfascicular anatomy is critical to the success of this procedure. As previously stated, sensory transfers in the distal forearm rather than the hand involve less dissection but more familiarity with the internal fascicular anatomy. The technique involves a carpal tunnel incision with a Brunner-type zig-zag proximally across the wrist, followed by a lazy-S incision proximally into the distal forearm. In the hand incision, a carpal tunnel release can be performed to release any possible site of compression and slowing of nerve regeneration. In the distal forearm incision, the dissection proceeds deep to the flexor muscle bundle to identify the median nerve medially and the ulnar nerve ulnarly. The median nerve is neurolysed to isolate and identify the recipient sensory components and the motor recurrent thenar fascicle. The recurrent thenar fascicle is identified and protected. Electrical stimulation can be used to confirm its function. However, if the nerve lesion

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compromises the function of the recurrent thenar fascicle and disallows the use of electrical stimulation, the fascicle can be followed proximally from its branch point in the hand by either neurolysis or (in Dr. Susan Mackinnon’s term) “visual neurolysis.” This technique can be performed on any fascicle, depending on how comfortable the surgeon is with his or her knowledge of the interfascicular nerve anatomy. The third web space fascicle is then neurolysed from the ulnar aspect of the median nerve to be used as a noncritical recipient in the sensory end-to-side nerve transfer. The remaining median nerve constitutes the fascicles that innervate the radial aspect of thumb and the first and second web spaces, which are used as the critical recipients in the sensory end-to-end nerve transfer. Once the recipient median nerve components are identified, the dissection progresses to the exposure of the ulnar nerve to isolate the donor DCU. The dissection occurs ~ 15 cm proximal from the wrist crease where the DCU is known to branch from the ulnar aspect of the ulnar nerve about

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Fig. 5.29 Exposure for sensory nerve transfers in the hand. Bruner zig-zag extensions of the carpal tunnel incision provide exposure of digital nerves within the hand for nerve transfer. In this case, the entire median nerve was harvested instead of the palmaris longus tendon. (Used with permission from Brown JM, Mackinnon SE. Nerve transfers in the forearm and hand. Hand Clin 2008;24(4):319–340.)

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10 cm proximal to the wrist crease. This donor nerve is followed as distally as possible to acquire sufficient length for a tensionless end-to-end repair. Once the donor nerve is isolated, the donor DCU is transected distally, and the recipient sensory component of the median nerve is transected proximally. The donor and recipient nerves are coapted in an end-to-end fashion to restore critical sensation. To restore rudimentary sensation to the donor nerve territory, the distal end of the DCU is coapted to the sensory component of the ulnar nerve on its radial aspect. As described, the sensory component is located on the radial aspect of the ulnar nerve, while the motor component to the deep motor branch is located on the medial aspect of the ulnar nerve, distal to the branch point of the dorsal cutaneous branch. To restore rudimentary sensation to the noncritical third web space territory, the third web space fascicle is transected proximally and endto-side transferred to the sensory component of the ulnar nerve on its radial aspect. Prior to repair, the tourniquet should be released and any bleeding controlled. Care should be taken to ensure there is no tension at the neurorrhaphy. The surgeon closes the skin with interrupted simple sutures, horizontal mattress sutures, or surgeon’s choice for palmar incision. Like motor transfers for opposition, the hand is placed in a volar splint for 7 to 10 days mostly for comfort, after which therapy is begun to prevent joint stiffness. The sensory reeducation will enhance the cortical remapping.

5.3.9 Upper Plexus Median Nerve Sensory Restoration In upper trunk plexus injuries, because the C7 is spared, some sensation to the third web space is preserved and available as a donor nerve. Unlike the ulnar sensory-to-median sensory nerve transfer, the selected median-to-median sensory nerve transfer may be accomplished in the distal forearm, in large part because a distinct fascicle provides sensation to this web space, which can be reliably neurolysed in the distal forearm for a long distance without plexus formation (▶ Fig. 5.32).68 Extensive scars to the palm are avoided by using an extended carpal tunnel incision. A larger territory of the thumb sensory distribution can be restored. The repair is simpler and faster to perform as long as the surgeon is comfortable with the internal anatomy of the median nerve. By Ten Test criteria, most patients will recover 6 out of 10 sensibility.51,52

5.3.10 Intramedian Sensory Nerve Transfer for Partial Median Sensory Deficits in Upper Plexus Injuries: Technique Releasing the carpal tunnel removes the secondary compression site for the recovering nerve.13,69 In addition, for the less experienced surgeon, it allows for visualization of the median nerve and its branches within the carpal tunnel. The nerve

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Fig. 5.30 Illustration of dorsal cutaneous branch of the ulnar (DCU)-to-the sensory component of the median nerve transfer for median nerve sensory deficits. (a) Median nerve sensory deficits in red. (b) Surgical strategy is to reinnervate critical sensation, which includes the first web space/radial aspect of the thumb and the second web space. (c) Critical sensation end-to-end nerve transfer is the donor DCU to the recipient first web space/radial aspect of the thumb and the second web space fascicles. Noncritical sensation end-to-side nerve transfers are the donor sensory component of the ulnar nerve to the recipient distal DCU and the donor sensory component of the ulnar nerve to the recipient distal third web space fascicle of the median nerve. (d) Fascicular donor and recipient anatomy for restoration of critical sensation using end-to-end nerve transfer. (e) Fascicular donor and recipient anatomy for restoration of noncritical sensation using end-to-side nerve transfers.

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Fig. 5.31 Dorsal cutaneous branch of the ulnar (DCU)-to-the sensory component of the median nerve transfer for median nerve sensory deficits. (a) The donor ulnar and recipient median nerve fascicular components are identified. To identify the sensory components of the median nerve, the thenar fascicle was neurolysed away and protected. Additionally, the third web space fascicle was neurolysed, leaving the sensory component of the median nerve to the radial aspect of the thumb, first web space, and second web space. (b) The donor DCU is coapted to the recipient sensory component of the median nerve in an end-to-end fashion for critical sensation. The recipient distal DCU and recipient distal third web space fascicle are coapted to the donor main sensory component of the ulnar nerve in an end-to-side fashion for rudimentary sensation. Arrows show the direction of nerve regeneration. Compare this figure with the drawings of ▶ Fig. 5.30.

begins to divide into its common digital branches at the distal aspect of the carpal tunnel, and their destination can be presumed according to the lateral-to-medial orientation of the fascicles, corresponding to their numbered web spaces.40 The fascicles can be either physically dissected or visually neurolysed proximally into the distal forearm. We prefer the latter once the surgeon gains comfort with the anatomy and dissection. The fascicles to the first through third web spaces should be distinct up to 13 mm above the radial styloid and in some cases may extend even more proximally.68 The recurrent motor branch, which can be reanimated during the same operative procedure, is isolated and addressed as previously described. Within the wrist, the fascicle to the third web space is neurolysed from the rest of the nerve using microforceps to “tap” along the surface of the median nerve. The cleavage plane between the third web space branch and the remaining median nerve should be easily identified. A loop is placed around the donor nerve (third web space fascicle). The first and second web space fascicles are indistinct at this level; however, the first web space fascicles are on the radial side of the remaining nerve, once the motor branch is likewise excluded. The donor fascicle (third web space fascicle) should be transected distally; the radial half of the “excluded” median nerve is then incised proximally to allow an end-to-end coaptation (▶ Fig. 5.26; ▶ Fig. 5.27). Recent cadaver dissections have revealed that there is in fact more “separation” between median fascicular groups than was realized in the early 1990s, when the third web space distinction was first recognized. Also, the plexus formation between

Fig. 5.32 Third web space fascicular anatomy in the median nerve and plexi formation. The third web space fascicle has been neurolysed from the median nerve to reveal reliable locations of plexus formation between the third web space fascicle and the median nerve. This understanding enables the use of the third web space fascicle in several sensory nerve transfers at the level of the wrist. (The asterisk denotes the branch point of the anterior interosseous nerve.) (Used with permission from Ross D, et al. Intraneural anatomy of the median nerve provides “third web space” donor nerve graft. J Reconstr Microsurg 1992;8(3):225–232.)

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Fig. 5.33 Extensor carpi radialis brevis (ECRB)-to-pronator teres (PT) nerve transfer in the left forearm. (a,b) Proximal forearm exposure of the left hand is used to identify donor ECRB (green) and recipient PT (red) nerves for transfer. (c,d) The donor ECRB nerve is mobilized distally, and the recipient PT nerve is mobilized proximally for nerve transfer and coapted in an end-to-end fashion. MN, median nerve; RN, radial nerve.

fascicular groups is largely “pseudo” plexus formation, and can be carefully neurolysed back to join their primary fascicular group. Performing the transfer in the forearm as opposed to the palm provides sensation to both sides of the thumb rather than just the ulnar side and restores sensation to the radial side of the index finger. It does leave the second and third web spaces numb, although the distal component of the third web space nerve may be turned end-to-side to the ulnar or median nerves. Frequently, the second web space nerve can also be included as a recipient in the transfer; however, the radial side of the median nerve is preferentially reinnervated, and the motor fascicle is excluded. Prior to repair, as in all cases, the tourniquet should be released and bleeding controlled. Closure of the skin and splinting are similar to previously described transfers in this region. The sensory reeducation begins once some light touch perception is noted.

Forearm Pronation and Wrist/Finger Flexion In high median nerve injuries, where extrinsic finger and wrist flexion, as well as pronation, is affected, several nerve transfers

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have been established to restore these functions. In the case of the injury occurring distal to the brachial plexus to the median nerve in the upper arm and elbow areas, a primary neurorrhaphy or graft may result in a good result. If a repair is not possible, finger flexion can be reconstructed with side-to-side tenodesis of the flexor digitorum profundus (FDP) tendons of the index and long finger to the conjoint tendons of the ulnar-innervated ring and small fingers in association with an ECRL or brachioradialis tendon transfer.23 Pronation is not so easily restored with tendon transfer, and we use an ECRB nerve branch-to-pronator nerve branch transfer with uniformly excellent results (▶ Fig. 5.33). In the case where the nerve cannot be repaired, nerve transfers offer an alternative to tendon transfers. Branches of the radial nerve, the brachialis branch of the musculocutaneous nerve, and branches of the ulnar nerve have all been used to restore essential median nerve function.70 The ECRB branch of the radial nerve (with or without its contribution to the supinator) can be used to reinnervate the AIN directly without a graft in a tension-free manner (▶ Fig. 5.34).71 This allows for the independent flexion of the thumb and improves the strength to finger flexion by reinnervating the FDP of the index and long fingers.

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Fig. 5.34 Illustration of extensor carpi radialis brevis (ECRB)-to-pronator teres (PT) nerve transfer in the right forearm. The ECRB nerve branch is identified branching from the radial nerve lateral and distal to the superficial radial sensory nerve branch. The ECRB nerve branch (green) is transferred to the PT nerve branch (red) in an end-to-end fashion to restore pronation function.

A nerve stimulator is used to verify lack of response to stimulation, and the PT branches are divided as far proximally as possible before the nerve divides from the median nerve proper. Interestingly, the pronator fascicles can be “neurolysed visually” all the way to the mid-arm. In some patients there will be some functioning expendable median branches to use to reinnervate the pronator nerve. The FDS or FCR ± PL nerve branches are the preferred donor nerves to transfer to the nonfunctioning PT branches, and these branches are dissected as far distally as possible into the muscle (▶ Fig. 5.35; ▶ Fig. 5.36). The FCU nerve branch is an available donor to innervate a nonfunctioning PT nerve branch. Several nerve branches to the FCU from the ulnar nerve can be isolated just distal to the cubital tunnel (▶ Fig. 5.37). Even with excellent recovery of finger function, simple hand functions such as writing, typing, and throwing are difficult without active pronation. We have seen isolated injuries in which only pronation fails to recover after a traction injury at the root level.47 Because of the location of the fibers that contribute to the pronator branch within the C6 and C7 spinal roots, despite plexus formation distal to the injury, pronation is lost, whereas the remainder of the median nerve function recovers to a large extent. Other injuries that can cause a similar scenario are lower brachial plexus injuries, very high median nerve injuries, and neuritis-induced neuropathy. Successful nerve transfers to restore this function are similar to those for AIN reinnervation.56,72 The brachialis branch of the musculocutaneous nerve can be easily mobilized, making it a relatively easy transfer (▶ Fig. 5.38).47 We moved cautiously toward using the brachialis nerve as a donor because of its importance as a strong elbow flexor.

Recent studies have concluded, however, that it is not worth reinnervating even in a patient with complete musculocutaneous nerve palsy.73–75 The logical conclusion is that the brachialis nerve in patients with normal biceps is a completely expendable nerve donor. The brachialis motor branch usually carries 3,500 axons; however, with normal biceps muscle function, loss of this muscle is inconsequential.48 It is also possible to use just one fascicle of the brachialis nerve branch; however, if biceps function is normal, taking the entire brachialis branch for the transfer does not diminish elbow flexion strength. This may appear contradictory to our recommendation of reinnervating both biceps and brachialis branches when the musculocutaneous nerve or upper plexus is injured in order to provide optimal elbow flexion. Because a reinnervated muscle generates less power than its normal counterpart, we feel that it is only acceptable to use the brachialis branch when the biceps muscle function is normal, and the musculocutaneous nerve has never been injured. Many actions, such as turning a doorknob, require the simultaneous use of wrist extension and forearm pronation. Therefore, using the ECRB branch of the radial nerve is associated with slightly more intuitive retraining, and we prefer transfer to restore pronation. We have started using the brachialis branch in lower plexus injuries for the restoration of the median and even ulnar nerves. The FDS, FCR, or PL branches may also be used in isolated injuries of the median nerve (▶ Fig. 5.39). If the entire median nerve is nonfunctional, then donor branches from the radial and ulnar nerve can be used. In the radial nerve, the ECRB and supinator are available donor nerves to innervate AIN function (▶ Fig. 5.40).

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Fig. 5.35 Illustration of flexor digitorum superficialis (FDS)-to-pronator teres (PT) nerve transfer. The FDS nerve branch is identified on the medial aspect of the median nerve and branches distal to the flexor carpi radialis/palmaris longus nerve branch and adjacent to the anterior interosseous nerve. A second FDS nerve branch can be found farther distal on the median nerve; however, the proximal branch is used as the donor nerve. The FDS nerve branch (green) is transferred to the PT nerve branch (red) in an end-to-end fashion to restore pronation function.

In complete median nerve injuries, the two donors can be used in combination to restore AIN function and pronation, that is, supinator-to-AIN and ECRB-to-PT nerve transfers (▶ Fig. 5.41). In the ulnar nerve, a redundant branch to the FCU can be used to reinnervate the AIN. In the case of combined lower ulnar and median nerve palsy with intact shoulder and elbow function, such as in C8-T1 avulsions, we transfer the brachialis branch of the musculocutaneous nerve to the proximal AIN to restore some finger flexor function. The brachioradialis branch of the radial nerve, sometimes with either an MABC or medial brachial cutaneous interpositional nerve graft, is a second choice.

5.3.11 Restoration of Anterior Interosseous Nerve Function (Extensor Carpi Radialis Brevis/Supinator or Flexor Digitorum Superficialis-to-Anterior Interosseous Nerve Transfer): Technique Using the same incision as for a median-to-radial motor nerve transfer (▶ Fig. 5.10), both the median and radial nerves in the proximal forearm are identified. Care is taken to avoid the branches of the LABC, which accompanies the cephalic or accessory cephalic vein, and the lacertus fibrosus is once again identified and incised. The radial neurovascular bundle is used as a landmark to find the superficial head of the PT, which is released using a step-lengthening technique moving proximally. Reflect the divided muscle medially to expose the median

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nerve, which is deep and ulnar to the radial vessels. The median nerve is traced distally by dividing the deep head of the PT tendon. On one occasion we inadvertently divided and subsequently repaired the distal biceps tendon, which was small and mistaken for the deep head of the pronator muscle tendon in a young adolescent. Additionally, the tendinous arch of the FDS is released as when decompressing the median nerve for PT syndrome (▶ Fig. 5.16). The AIN is identified as it deviates from the radial side of the main trunk of the median nerve (▶ Fig. 5.42). If the AIN is not readily discernible as a distinct fascicle, then a longitudinally oriented prominent vessel commonly marks the cleavage plane between the AIN and the remainder of the median nerve.4 Gently tapping with the tips of the micro-forceps across the transverse diameter of the median nerve demonstrates this cleavage plane as it dips into this interval (▶ Fig. 5.17). Neurolysis of the nerve allows the AIN to be separated from the median nerve easily to the level of the antecubital fossa and in fact into the mid-arm. Once the AIN is identified, separated, and looped, the radial nerve is exposed. As described previously, the radial sensory nerve is identified under the brachioradialis and is followed a few centimeters proximally toward the antecubital fossa until the PIN and branch to the ERCB are visualized. The radial recurrent vessels making up part of the leash of Henry are divided, and the ECRB branch will be found radial to the sensory branch (▶ Fig. 5.43). These nerves are then traced distally into the ECRB muscle. The branch to the ERCB continues past the supinator muscle, parallel to but separate from the radial sensory

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Fig. 5.36 Flexor digitorum superficialis (FDS)-to-pronator teres (PT) nerve transfer. (a) The recipient PT nerve branch is found on the anterior aspect of the median nerve in the proximal forearm. Two branches can be identified to innervate the PT. The donor FDS is found on the medial aspect of the median nerve adjacent to the anterior interosseous nerve. (b) The donor nerve is transected distally, and the recipient nerve is transected proximally. (c) The donor FDS nerve and recipient PT nerves are coapted to restore pronation function. (Used with permission from Tung TH, Mackinnon SE. Flexor digitorum superficialis nerve transfer to restore pronation: two case reports and anatomic study. J Hand Surg Am 2001;26(6):1065–1072.)

branch. This branch should be followed as far distally as possible. Several centimeters of the nerve are obtainable. If possible, the nerve is transected at the interface with the ERCB muscle belly (▶ Fig. 5.44). The supinator branch can be included to increase the donor motor nerve axonal count (▶ Fig. 5.18). To include this branch, the arcade of Frohse must be in released. The PIN is neurolysed so that the supinator branch may be transected where it enters the muscle. The supinator nerve is

found on the posterior aspect of the PIN.9 There are two supinator branches that proximally come together as one branch. Once mobilized, the donor nerve is sutured end-to-end to the AIN using 9-0 nylon (▶ Fig. 5.45). In cases of an isolated AIN palsy, an intramedian nerve transfer is easily performed by using redundant branches of the FDS or PL/FCR to restore motor function to this vital median component (▶ Fig. 5.46). The FDS has two branches. These are transected distally where they enter the muscle (▶ Fig. 5.47).

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Fig. 5.37 Illustration of flexor carpi ulnaris (FCU)-to-pronator teres (PT) nerve transfer. The FCU nerve branch is identified branching from the ulnar nerve just distal to the elbow. Several branches to the FCU can be identified at this location. The FCU nerve branch (green) is transferred to the PT nerve branch (red) in an end-to-end fashion to restore pronation function.

Because of its proximity to the AIN, there is very little mobilization needed. It is repaired end-to-end to the AIN (▶ Fig. 5.48). However, it can and must be neurolysed from the main median nerve to allow a tension-free transfer. The wound is closed in layers over a drain, occasionally with a pain pump. The patient is placed in a posterior splint with the elbow at 90 degrees, the forearm pronated, the wrist neutral, and the shoulder and fingers free. The splint, drain, and pump are removed at the first postoperative check on day 2, and the patient placed in a sling for 7 additional days. Longer splinting is used if tendon transfers are performed at the same time. Many patients with neuritis of the AIN recover FDP but not FPL function. In these patients, it is possible to selectively innervate the FPL and protect the portion of the AIN to the FDP. The more radial half of the AIN innervates the FPL and can be neurolysed from the functioning ulnar half of the AIN that innervates the FDP to the index finger. A nearby FDS branch is an ideal transfer to the denervated FPL (▶ Fig. 5.49). In patients with FPL palsies, the FPL tendon will tend to stretch out because of overpull of the EPL tendon. The relative lengthening of the FPL will result in less force generated (as per the tendon force length curve) once reinnervation occurs unless the joint is protected during the postoperative period. 76 An extension blocking splint at the interphalangeal (IP) joint of the thumb is recommended in patients with AIN palsies or isolated FPL palsies. This is similar to splinting patients with radial nerve palsies with wrist splints and dynamic finger extension splints.

5.3.12 Restoration of Pronator Teres Function (Extensor Carpi Radialis Brevis-to-Pronator Teres Nerve Transfer): Technique As the median nerve enters the forearm, it gives off three distinct groups of branches (▶ Fig. 5.2). The first group

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innervates the PT, is found along the superficial or volar aspect of the median nerve, runs along the top of the nerve as it crosses the antecubital fossa, and divides to innervate the superficial and deep heads of the PT along its deep surfaces. If the pronator nerve is dissected more proximally, then a second branch is identified medially and deep that joins this branch. Distal to this branch is the nerve that innervates the PL and FCR and is found along the ulnar side of the median nerve and deep. The last group innervates the FDS, is found distal to the second group still on the ulnar side of the medial nerve and more distally. There are two FDS branches. The larger fascicular group on the radial side of the median nerve that continues distally before branching is the AIN. To facilitate exposure to the PT branch, the previously described skin incision is extended proximally along the radial side of the antecubital fossa. The PT superficial head is divided with a step-lengthening incision and retracted radially as described previously. The median nerve is identified proximally between the vessels laterally and the flexor pronator muscle medially. The pronator branch is looped, and the ECRB branch is isolated, as previously described. As in all nerve transfer cases, the recipient nerve (pronator branch) is transected as proximally as possible, whereas the donor nerve (ECRB branch) is transected as far distally as possible. The two are coapted in and end-toend manner with 9–0 nylon (▶ Fig. 5.34). Although we prefer the ECRB branch over other nerve branches as the donor nerve for restoring pronation because of easier postoperative motor reeducation, the brachialis branch of the musculocutaneous nerve, FCR with or without PL branches of the median nerve, FDS of the median nerve (▶ Fig. 5.35; ▶ Fig. 5.36), and redundant FCU branch of the ulnar nerve (▶ Fig. 5.37) all give excellent results. As previously noted, meticulous care is taken with closure of the wounds, and splinting is usually based on associated tendon transfers.

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Fig. 5.38 Relevant nerve anatomy for brachialis-to-anterior Interosseous nerve (AIN) transfer. (a) The donor brachialis nerve branches from the medial aspect of the musculocutaneous nerve, from which the musculocutaneous nerve becomes the lateral antebrachial cutaneous (LABC) nerve. The recipient AIN branches from the lateral aspect of the median nerve in the forearm, distal to the palmaris longus (PL) and flexor carpi radialis (FCR) nerve branch and proximal to the flexor digitorum superficialis (FDS) nerve branch. (b) To mobilize the AIN for transfer, the AIN is visually neurolysed proximally from its branch point until enough transposable length is determined for a tension-free repair. The AIN fascicle is then neurolysed from the median nerve and proximally transected for transfer. (c) Intrafascicular anatomy of the median nerve at this level reveals the AIN fascicle in its posterior/medial portion. Adjacent to the AIN fascicle are the PL/FCR and sensory fascicles. The pronator teres fascicle is found on the anterior portion of the median nerve.

5.3.13 Restoration of the Median Nerve in a Lower Plexus Injury (Brachialis-toAnterior Interosseous Nerve Transfer): Technique With the patient under general anesthesia and a sterile tourniquet on the upper part of the arm, a curvilinear incision is made in the midline volar forearm 4 to 5 cm distal to the elbow crease. Proximally, the incision borders the medial side of the antecubital fossa, continuing centrally and proximally into the biceps–triceps groove in the distal third of the upper arm (▶ Fig. 5.50). The LABC nerve is used to assist in finding the bra-

chialis nerve by following it proximally in the arm. The brachialis branch is more medial than the LABC and found 12 to 13 cm proximal to the lateral epicondyle. It travels deep into the muscle, while the LABC continues distally. Gently “tugging” on the LABC will produce traction of the skin, allowing it to be identified easily. After incising the forearm fascia, the lacertus fibrosus and the PT superficial head are divided as in previous exposures of the median nerve. The nerve, its three major groups, and the AIN branch should be easily identified (▶ Fig. 5.51). In the proximal region of the incision, the brachial fascia is opened widely and extended to meet the opening in the lacertus fibrosus.

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Fig. 5.39 Illustration of flexor digitorum superficialis (FDS)-to-anterior interosseous nerve (AIN) transfer. The redundant FDS nerve branch is an available donor for transfer to restore AIN function in isolated AIN injuries. A secondary FDS branch is preserved as it branches distal in the forearm. The donor FDS branch is identified adjacent to the AIN branch and is seen on the medial aspect of the median nerve; the AIN is identified on the lateral/posterior aspect of the median nerve. The donor FDS branch (green) is transferred to the recipient AIN (red) in an endto-end fashion.

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Fig. 5.40 Illustration of extensor carpi radialis brevis (ECRB)-to-anterior interosseous nerve (AIN) transfer. The ECRB nerve branch is an available donor for transfer to restore AIN function in complete median nerve injuries. The donor ECRB branch is identified between the superficial branch and the posterior interosseous nerve. The recipient AIN is seen branching from the lateral/posterior aspect of the median nerve. The donor ECRB branch (green) is transferred to the recipient AIN (red) in an end-to-end fashion.

As the dissection proceeds into the distal upper arm, the median nerve is identified. Just lateral to the median nerve is the interval between the biceps and brachialis muscles. By opening this potential space, the brachialis branch and LABC is identified. The biceps branch takes off more proximally at the level of the midarm and may not be visualized through this incision. The brachialis branch can be mobilized several centimeters from the main musculocutaneous nerve. Once intraoperative

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stimulation with a handheld nerve stimulator verifies the correct donor nerve, the brachialis branch is looped and set aside for transfer. In the distal portion of the incision, the AIN may be dissected from the main median nerve to the mid distal arm until interplexus formations prevent the easy separation of the fascicles. The AIN and the branch to the PT fascicular group are separated by the FCR/FDS group.13 The two nerves can meet end-to-end in the distal third of the arm for a direct, tension-

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Fig. 5.41 Illustration of supinator-to-anterior interosseous (AIN) and extensor carpi radialis brevis (ECRB)-to-pronator teres (PT) nerve transfers. The supinator and ECRB nerve branches are available donors for transfer to restore AIN and PT function in complete median nerve injuries. The donor supinator branch (green) is identified deep to the posterior interosseous nerve (PIN) and is transferred to the recipient AIN (red) to restore AIN function. For pronation, the donor ECRB branch (green) is identified between the superficial branch and PIN and is transferred to the recipient PT branch (red).

Fig. 5.42 Identification of median nerve branches and the recipient anterior interosseous nerve (AIN). The median nerve is decompressed and exposed in the forearm by releasing the superficial head of the pronator teres and the tendinous arch of the flexor digitorum superficialis. The recipient AIN is identified branching from the median nerve’s lateral aspect.

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Fig. 5.43 Identification of radial nerve branches and the donor extensor carpi radialis brevis (ECRB) nerve branch. The radial nerve is exposed by retracting the brachioradialis muscle laterally. The donor ECRB nerve branch is identified branching from the lateral aspect of the radial nerve proximal to the deep branch of the radial nerve (PIN) and distal to the superficial branch of the radial nerve.

Fig. 5.44 Isolating the donor and recipient nerve for extensor carpi radialis brevis (ECRB)-to-anterior interosseous nerve (AIN) transfer. The donor ECRB nerve is isolated by transecting the nerve distally. The recipient AIN is isolated by transecting the nerve proximally. The donor distal and recipient proximal transections will allow for a tension-free repair. Note the extensive overlap between the donor (ECRB) and recipient (AIN) nerves.

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Fig. 5.45 Extensor carpi radialis brevis (ECRB)-to-anterior interosseous nerve (AIN) transfer. The ECRB is transferred to the AIN for a tension-free repair. This transfer is used to reinnervate AIN function, specifically the flexor digitorum profundus III and IV, flexor pollicis longus, and pronator quadratus.

Fig. 5.46 Exposure and identification of the median nerve and donor flexor digitorum superficial (FDS) nerve branch and recipient anterior interosseous nerve (AIN). The median nerve is exposed by step-lengthening the superficial head of the pronator teres (PT), releasing the deep head of the PT, and releasing the arch of the proximal FDS. In this particular patient, there was a small tendinous attachment for the deep head of the PT. The recipient AIN is identified on the radial aspect of the median nerve. The nerve to the FDS is seen branching from the ulnar aspect of the median nerve.

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Fig. 5.47 Mobilizations of the flexor digitorum superficialis (FDS) nerve and anterior interosseous nerve (AIN) for transfer. The donor FDS nerve is transected distally to transpose for the nerve transfer. The AIN is transected proximally to transpose for the nerve transfer.

Fig. 5.48 Flexor digitorum superficialis (FDS)-to-anterior interosseous nerve (AIN) transfer. The FDS nerve branch was transferred to the AIN to restore AIN function. This nerve transfer is used for isolated AIN palsy.

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Fig. 5.49 Flexor digitorum superficialis (FDS)-to-flexor pollicis longus (FPL) nerve transfer. For isolated FPL nerve injuries, FDS is an available donor to reinnervate FPL. (a) The donor FDS nerve branch is identified adjacent to the anterior interosseous nerve (AIN) branch. (b) The recipient FPL nerve fascicle is identified within the AIN on its lateral aspect following neurolysis. (c) The donor FDS branch is transected distally, and the recipient FPL fascicle is transected proximally from the AIN. (d) The donor FDS branch is transferred to the recipient FPL fascicle to restore FPL function.

free coaptation (▶ Fig. 5.19). It is important to note that the motor component of the median nerve is located on the medial aspect of the median nerve in the arm. Thus, the brachialis branch-to-AIN transfer occurs on the medial side of the median nerve in the distal arm, with the AIN group located medial and posterior. The lateral portion of the median nerve in the distal upper arm is sensory. Within the median nerve, the AIN fascicles move from medial and posterior in the arm to lateral as it crosses the elbow and into the proximal forearm. In our initial uses of this transfer, the brachialis branch was transferred to the AIN with an interposition nerve graft in an end-to-end manner. Knowledge about the topography of the median nerve in the distal forearm stems from our experience with the double fascicular transfer for elbow reanimation discussed in Chapter 14. More recently, we have started visually neurolyzing the AIN and pronator branches without actually dissecting it free from the median nerve (▶ Fig. 5.39; ▶ Fig. 5.52). This allows for quicker dissection. The median nerve contains sensory fascicles in the distal arm on the lateral

side. The portion of the nerve that predominantly will go to form the AIN with some innervation of the FCR, PL, and FDS is on the medial side.9 We prefer to perform the transfer in the mid-arm. The brachialis nerve branch can be transferred in this fashion in the distal to midarm to both the AIN and the pronator branches (▶ Fig. 5.50). These two fascicular groups (AIN and PT) are separable to a very proximal level in the arm. The pronator group fascicle lies on the anterior surface of the median nerve in the arm and the AIN medially in the arm. Since the repair is within the same location and does not cross the elbow, we usually only use an elbow sling postoperatively for 7 to 10 days.

5.3.14 Ulnar Nerve Injury: Intrinsic Muscle Function and Ulnar Sensory Loss Injury to the ulnar nerve results in significant pinch and grip weakness, and often clawing of the ring and small fingers

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Fig. 5.50 Median and musculocutaneous nerve anatomy for brachialis-to-anterior interosseous nerve (AIN) and pronator teres (PT) nerve transfer. (a) This case (October 2007) was one of the first brachialis-to-AIN transfers that involved a large exposure and dissection to identify the appropriate components for transfer. The recipient AIN and pronator nerve branches were visually neurolysed from the distal branch point proximally, then neurolysed proximally from the median nerve. The PT nerve branch has two distinct branches that innervate the PT. The donor brachialis is seen branching from the medial aspect of the musculocutaneous nerve. (b) The donor brachialis branch is transferred to the AIN and PT branches in an endto-end fashion to restore median nerve function. (c) Interfascicular anatomy of the median nerve identifies the PT fascicle on the anterior aspect of the median nerve and the AIN fascicle on the medial/posterior aspect of the median nerve.

(▶ Fig. 5.53).77 A review of the literature by Post et al noted that intrinsic recovery following repair of high sharp lacerations of the ulnar nerve was poor; they suggested that distal nerve transfers may offer an improved strategy for function.78 With injuries directly in the forearm, direct repair will restore both sensory and motor function. It takes at least 1 year to recover, and the patients need extensive occupational therapy for up to 2 years; however, excellent results have been achieved, especially in younger patients.79 In above-elbow injuries, sensory recovery usually returns eventually; however, the recovery of intrinsic muscle function is unlikely, even with early repair.80,81 Some hand surgeons recommend performing distal tendon transfers for intrinsic function at the time of the proximal nerve repair. Tendon transfers results are limited, will relax with time, and should be considered as secondary procedures to supplement a failed or weak nerve transfer. In our experience, in isolated ulnar nerve injuries with an intact median nerve, the distal branch of the AIN leading to the pronator quadratus is a very good donor nerve for transfer to the deep motor branch of the ulnar nerve.19,82 The motor branch of the ulnar nerve can be neurolysed 10 cm proximal to the wrist, allowing for a primary neurorrhaphy in the distal forearm to be performed (▶ Fig. 5.54).

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The disadvantage of this transfer includes an antagonistic transfer and a mismatch in donor and recipient size. The terminal AIN contains ~ 900 axons, some being afferents from the wrist joint. The ulnar nerve to the intrinsics contains more than 1,200 motor axons, resulting in an axon count discrepancy. However, there are few good long-term reconstructive options even with tendon transfers. We feel this particular nerve transfer offers the best method for prevention of clawing and improvement of pinch strength.5 Distal radial to ulnar nerve transfer has also been described when AIN is unavailable.83 We have noticed that most patients do well with postoperative reeducation and have no clawing; in younger patients, the results have been even more substantial.84 Patients are offered an EDQ-to-EDC tendon transfer for persistent small finger abduction (Wartenberg sign).76 We further improve finger flexion by “tenodesing” the FDP tendons of the ring and small fingers side-to-side to the FDP tendons of the long finger. We recommend this nerve transfer in a timely presentation of a high ulnar nerve injury in patients without a Martin-Gruber anastomosis.5 An extensor indicis proprius-to-adductor tendon transfer passed through the second metacarpal space can also provide increased pinch strength if desired. Sensory reinnervation is performed at the same time in most cases by using the

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Fig. 5.51 Brachialis-to-anterior interosseous nerve (AIN) transfer. (a,b) Prior to the nerve transfer, the lateral antebrachial cutaneous (LABC) nerve and the donor brachialis nerve were identified. The median nerve and its branches were also identified. The AIN branch was found on the lateral aspect of the median nerve in the forearm. The AIN fascicle was neurolysed proximally in segments to confirm its innervation without disrupting the median nerve. (c,d) The donor brachialis nerve (green) was transected distally and the recipient AIN fascicle (red) transected proximally to mobilize for an endto-end nerve transfer.

median nerve. The transfers are done at the level of the distal forearm, avoiding scars in the palm of the hand. When performing a distal sensory nerve transfer, it is important to consider the possibility that one or two years later partial sensory regeneration may occur in the case of a more proximal nerve repair or may occur spontaneously in partial injuries. A painful neuroma may develop at the level of the transection for the nerve transfer. At the time of the transfer, the surgeon should turn that proximal nerve end into innervated muscle for the prevention of a potential painful neuroma if sensory recovery does eventually occur. In the case of isolated ulnar nerve palsy, our donor nerve of choice is the third web space fascicle of the median nerve, which is transected and coapted to the sensory fascicle of the ulnar nerve in the distal forearm at the time of the motor transfer (▶ Fig. 5.55). The third web space sensation is somewhat restored by reimplanting the divided distal stump in an end-toside manner into an epineurial window of the remaining median nerve. The perineurium is opened, creating a limited and recoverable demyelination of the donor nerve and allowing for increased sprouting from the sensory donor nerve.85 Alternatively, the palmar cutaneous branch of the median nerve, which branches from the median nerve ~ 8 cm proximal

to the radial styloid, can be used instead of the third web space fascicle of the median nerve for the direct end-to-end coaptation to the fourth web space fascicle of the ulnar nerve. If the median nerve is not available, the LABC is a good donor nerve (▶ Fig. 5.56).84,86 This necessitates a much larger incision in order to dissect the nerve, but rarely is a nerve graft needed. Alternatively, the LABC or MABC terminal branches can be used. However these donor nerves are smaller than the recipient, with less axon potential, and only protective sensation can be achieved.

5.3.15 Anterior Interosseous Nerve-toMotor Component of the Ulnar Nerve Transfer: Technique With the patient under general anesthesia and the tourniquet inflated, the ulnar and median nerves are exposed through an extended carpal tunnel incision. A zig-zag incision is used to cross the wrist crease and proceed proximally to include the distal third of the volar forearm in the midline. In this case, the nonfunctioning ulnar nerve is identified before the donor median nerve by opening Guyon canal and retracting the ulnar

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Fig. 5.52 Brachialis-to-anterior interosseous nerve (AIN) transfer in a reduced exposure. Further experience with this nerve transfer can allow for an exposure that is significantly smaller with the understanding of interfascicular anatomy of the median nerve. (a) The recipient AIN fascicle is identified and neurolysed from the medial/posterior aspect of the median nerve. (b) The donor brachialis nerve branch is identified with several branches into the brachialis muscle. (c) The donor brachialis branch is transected distally. (d) The donor brachialis branch is transferred to the recipient AIN fascicle in an end-to-end fashion to restore AIN function. Until the surgeon is familiar with this complicated but reliable intrafascicular anatomy, a long exposure should be used.

neurovascular bundle ulnarly. The origin of the hypothenar muscles is noted adjacent to the hook of the hamate. The deep motor branch of the ulnar nerve will be dividing from the radial and deep surface of the ulnar nerve, traversing under the leading edge of the hypothenar muscle group, which we incise to prevent a secondary compression site that could impede regeneration (▶ Fig. 5.57). The motor branch is then neurolysed from the rest of the ulnar nerve into the forearm. Often the motor branch can be identified and traced proximally without the need for an actual physical neurolysis by following the motor fascicles proximally under magnification.47 This visual neurolysis is possible because of the familiarity with the ulnar nerve topography. It is faster than a physical neurolysis, saving time in the operating room, and preserves the inherent vasculature of the nerve, thereby preventing disruption and additional scarring. The fascicles remain distinct for a long distance into the forearm with some inconsequential interplexus connections and pseudoplexus formation. It should be noted that the motor branch in the hand is radial to the sensory component. As you trace the nerve proximally, the sensory branch rotates superi-

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orly and radially, so that it shifts from lateral to the motor branch in the hand to radial to the motor branch in the forearm. The dorsal cutaneous branch joins the nerve on the ulnar side, placing the motor branch at this level in the middle (▶ Fig. 5.58). The limitations of dissection depend on how distal intraplexiform connections are found. The motor branch is marked with a vessel loop for later. The proximal end is usually mobilized 4 to 6 cm just proximal to the level of the proximal aspect of the pronator quadratus. Through the same volar incision, the surgeon retracts the median nerve and the superficial and deep forearm finger flexors radially with a Weitlander or self-retraining forceps. The pronator quadratus muscle can be found lying directly over the distal radioulnar joint. At the proximal edge of the muscle, the anterior interosseous neurovascular bundle will be lying radial to the AIN. The nerve can be traced into the muscle by dividing it to gain an additional 0.7 to 1.5 cm before branching occurs (▶ Fig. 5.59). Using a handheld nerve stimulator, the surgeon verifies and transects the AIN branch just as it begins to arborize.5

Nerve Transfer for the Forearm and Hand

5.3.16 Reverse End-to-Side Supercharge Transfer: Technique

Fig. 5.53 Ulnar nerve injuries. (a) Patients with ulnar nerve injuries present with clawing and loss of intrinsic muscle function, as demonstrated by the inability to abduct the digits. (b) A Froment sign is present in the left thumb with the patient’s attempt to pinch and hold the paper.

The AIN is transposed over the pronator quadratus muscle. The ulnar nerve is moved to lie adjacent to it to verify that enough nerve has been mobilized and that a direct end-toend coaptation will be possible. Remember, the donor (AIN) nerve is divided distally and the recipient (ulnar) nerve proximally (▶ Fig. 5.60). The surgeon should cut the donor nerve first, as the recipient nerve can always be neurolysed farther proximally in order to have a tension-free repair without the need for a nerve graft (▶ Fig. 5.61). A nerve graft should never be necessary. Alternatively, an end-to-side supercharge nerve transfer (SETS) can be used as a “babysitting” procedure while the ulnar nerve is recovering, if the high ulnar nerve injury is expected to recover (see discussion below). In some cases of both median and ulnar nerve palsy, standard tendon transfers may be helpful using the radial innervated muscles, such as the ECU and EDQ tendons, as tendon transfers.9 Prior to closure, the surgeon should view the repair with the arm in full pronation and supination to access for tension. The patient is placed in a volar wrist splint, with the wrist in neutral and the elbow and fingers free. Once the operative dressing is removed, the patient is kept in a splint for 7 days. If tendon transfers are necessary adjuncts at the time of the nerve transfer, the patient is placed in a dorsal or volar splint as appropriate for the tendon transfer and protected for 4 weeks before beginning passive and active assisted range of motion exercises under the direction of an occupational therapist.

An area that the authors are investigating clinically is the use of a “babysitting” procedure in ulnar motor nerve injuries similar to the accepted treatment of facial nerve palsy with cross-facial sural nerve grafts.87 In a high proximal ulnar nerve injury, there is no question that an AIN-to-deep motor transfer will be better than a proximal repair. There are many situations, however, where repairing the ulnar nerve may result in recovery. Similarly, in revision cubital tunnel surgery with preoperative ulnar intrinsic weakness, decompression surgery may result in ulnar intrinsic recovery. In these gray areas of possible ulnar intrinsic recovery, we share with you a technique that we use clinically and have studied in the laboratory. We “supercharge” the distal motor fascicular group of the ulnar nerve in the distal forearm with the distal AIN branch in an end-toside fashion.88 The AIN is prepared as previously described, and the distal portion is sutured end-to-side to the ulnar motor component of the ulnar nerve in the distal forearm (▶ Fig. 5.62; ▶ Fig. 5.63; ▶ Fig. 5.64). The branches of the AIN are “fanned out” to cover the two to three fascicles making up the motor ulnar group. The transfer from the AIN to the side of the ulnar nerve is done about 8 to 9 cm proximal to the wrist crease to avoid the need for an extension nerve graft. This transfer is also discussed in Chapter 9.

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5.3.17 Sensory Restoration in the Ulnar Nerve Distribution: Technique Nerve transfers to restore sensation to the ulnar side of the hand and fingers are usually performed in conjunction with the terminal AIN-to-ulnar deep motor nerve transfer described previously (see ▶ Fig. 5.61). Not infrequently, a proximal ulnar nerve repair will be done to restore extrinsic ulnar motor function and sensation, while the terminal AIN is transferred to the ulnar deep motor branch for intrinsic function. However, if sensation to the fingers cannot be achieved from a proximal repair, then sensory nerve transfers in the hand are performed. 89 After the deep motor branch has been neurolysed from the ulnar nerve, the remaining fascicles include the dorsal cutaneous sensory branch of the ulnar nerve and the main ulnar sensory nerve. The two sensory groups are separated from each other and then are tagged with a different colored vessel loop from that of the deep motor branch. The median nerve in the forearm is neurolysed to separate out several fascicles within the median nerve proper. The thenar motor branch at this level lies on the radial and deep portion of the median nerve, and the sensory branches compose the rest of the nerve in cross section. The ulnar-most fascicular group of the median nerve represents the third web space innervation. This particular fascicular group is neurolysed for a length of 4 cm. The main ulnar sensory branch providing sensation to the fourth web space and ulnar border of the small finger is transected as proximally as possible and coapted end-to-end to the proximal stump of the median nerve fascicle to the third web space (▶ Fig. 5.65; ▶ Fig. 5.66).

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Fig. 5.54 Intramuscular dissection for mobilizing the anterior interosseous nerve (AIN) for motor nerve transfer. (a) An intramuscular dissection through the pronator quadratus is undertaken to obtain the maximal length of the AIN. (b) The AIN is then cut at the midposition of the muscle where it begins to branch and transferred via the end-to-end strategy to the ulnar motor fascicle. (The asterisk indicates intramuscular dissection with associated nerve branching. Orientation: left hand, proximal (P) and distal (D). (Used with permission from Brown JM, et al. Distal median to ulnar nerve transfers to restore ulnar motor and sensory function within the hand: technical nuances. Neurosurgery 2009;65(5):966-977.)

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The distal end of the third web space fascicle, which was mobilized, is coapted end-to-side to the middle aspect of the median nerve via an epineurial window. Likewise, the dorsal sensory cutaneous branch of the ulnar nerve is coapted end-toside to the remaining median nerve via an epineurial window. The perineurium is incised longitudinally to stimulate sprouting of sensory nerves, and the epineurium of the branches is sewn to the perineurium of the median nerve using 9-0 nylon sutures. The palmar cutaneous median branch can also be transferred end-to-end to the DCU. This sensory transfer provides optimal sensation to the fourth web space and the ulnar side of the small finger, which are critical for grasping. It also offers protective sensation for the ulnar side of the forearm and the third web space. Extrinsic flexion

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of the ring and small fingers is managed via a side-to-side tenodesis of the FDP tendons to those of the index and long fingers (▶ Figs. 67–72).47 Nerve transfers for the restoration of wrist flexion are not required unless there is accompanying median nerve injury, as discussed previously. The third web space median nerve-to-main ulnar sensory nerve transfer is placed deep, just overlying the pronator quadratus and under the flexor muscles. This will ensure that there is no tension and no nerve graft needed. The ulnar motor nerve is divided more proximally than would be intuitive (~ 9 cm proximal to the wrist to avoid tension or a nerve graft). If the palmar cutaneous branch of the median nerve is used, the division from the median nerve occurs ~ 8 cm proximal to

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Fig. 5.55 After performing the priority nerve transfers (anterior interosseous to the deep motor branch of the ulnar and median third web space to the sensory component of the ulnar), epineurial windows are made on the ulnar side of the median nerve. This allows for the end-to-side reinnervation of the DCU and the median third web space sensory fascicle, restoring rudimentary protective sensation to these distributions. (Used with permission from Brown JM, et al. Distal median to ulnar nerve transfers to restore ulnar motor and sensory function within the hand: technical nuances. Neurosurgery 2009;65(5):966-977.)

Fig. 5.56 Lateral antebrachial cutaneous (LABC)-to-dorsal cutaneous branch of the ulnar (DCU) nerve transfer. The LABC-to-DCU sensory nerve transfer is an example of an alternative strategy for restoring sensation to the DCU territory. The DCU is neurolysed from its distal branch point proximally to mobilize for transfer. (Used with permission from Brown JM, Mackinnon SE. Nerve transfers in the forearm and hand. Hand Clin 2008;24 (4):319-40.)

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Fig. 5.57 Identification of the ulnar nerve after exposing Guyon canal. (a) The ulnar nerve is identified adjacent to its artery traversing distally through the canal to the ulnar border of the hamate, where the nerve separates into sensory and motor components. At this level, the deep motor branch descends under the hypothenar muscles and turns radially around the hook of the hamate. Note that visualization of this branch is often difficult until its decompression is completed. (b) Adhering to the five-step procedure for decompression of the deep motor branch, the palmaris brevis and fascial bands are released to expose the ulnar nerve and its associated vessels. (c) Following the release, the neurovascular bundle is medially retracted to provide further exposure, allowing the surgeon to orient himself or herself by palpating the hook of the hamate (purple). (d) Upon further retraction, the deep motor branch is identified ulnar to the hamate, where it disappears under the leading edge of the hypothenar fascia (scissors). (e) Decompression of this branch is achieved by opening this fascia until the flexor tendon of the fifth digit (small finger) is visualized. Although not shown here, note that the dissection must cross the wrist proximally in order to release the distal forearm fascia. Orientation: left hand, proximal (P) and distal (D). (Used with permission from Brown JM, et al. Distal median to ulnar nerve transfers to restore ulnar motor and sensory function within the hand: technical nuances. Neurosurgery 2009;65(5):966–977.)

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Fig. 5.58 Interfascicular anatomy of the ulnar nerve. At the location where the dorsal cutaneous nerve branches from the medial aspect of the ulnar nerve, the ulnar nerve is neurolysed to reveal its two components: motor (deep motor branch) and sensory (ulnar nerve sensory territory). The motor component is found between the sensory component and the dorsal cutaneous branch. The sensory component of the main ulnar nerve is found on the lateral aspect of the ulnar nerve.

Fig. 5.59 Identification of the donor anterior interosseous nerve (AIN) for transfer in the distal forearm. Deep to the flexor muscle bundle, the AIN is identified proximal to the pronator quadratus in the distal forearm adjacent to its respective vessels. The AIN is specifically the pronator quadratus nerve branch and the articular branch to the wrist joint. The donor pronator quadratus branch is divided through its muscle branches into the muscle and visualized at about midlevel of the muscle. This is the level of transection for mobilization for AIN-to-motor component of the ulnar nerve transfer.

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Fig. 5.60 Proximal transection of the recipient ulnar nerve. The recipient ulnar nerve is neurolysed to separate its motor and sensory components and transected proximally for anterior interosseous nerve-to-the motor component of the ulnar nerve transfer. The motor component is marked in purple. The motor component is one third of the cross-section of the main ulnar nerve, and the sensory is two thirds.

Fig. 5.61 Anterior interosseous nerve (AIN)-to-the motor component of the ulnar nerve transfer. The AIN, specifically, the pronator quadratus nerve branch, is transferred to the motor component of the ulnar nerve. Included in this transfer is the third web space of the median to sensory component of the ulnar nerve transfer for restoration of ulnar nerve sensation.

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Fig. 5.62 Identifying the ulnar nerve and determining the area of neurolysis. The ulnar nerve is identified with the dorsal cutaneous branch of the ulnar nerve. Be aware of the anatomy, as the dorsal cutaneous branch is ulnar to the ulnar nerve, and the ulnar artery is radial to the ulnar nerve. By isolating the anterior interosseous nerve, the surgeon can transpose this nerve to the ulnar nerve to determine the area of neurolysis for reverse end-to-side nerve transfer.

Fig. 5.63 Internal neurolysis of the ulnar nerve and identification of the recipient motor component. Internal neurolysis of the ulnar nerve reveals the motor and sensory components of the ulnar nerve. The motor component courses distally and becomes the deep motor branch innervating the intrinsic muscles of the hand. This recipient motor component is identified between the dorsal cutaneous branch (DCU) and the sensory component of the ulnar nerve, resulting in a sensory-motor-sensory topography. The dorsal cutaneous branch is ulnar to the main ulnar nerve, though here the main ulnar nerve is retracted and the DCU appears superior. The motor component is smaller compared to the sensory component and accounts for 40% of the ulnar nerve, and the sensory accounts for the other 60%.

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Fig. 5.64 Reverse end-to-side anterior interosseous nerve (AIN)-to-ulnar motor nerve transfer. The AIN is transferred to the motor component of the ulnar nerve through a reverse end-to-side perineural window coaptation. As the nerve gradually regenerates from a proximal injury to its target muscles, the reverse end-to-side nerve transfer can help preserve the distal target muscles in the interim by providing a closer source of nerve fibers.

the radial styloid. As with the third web space fascicle, the distal half of the palmar cutaneous nerve branch can be coapted end-to-side to the median nerve proper, while the proximal half is coapted end-to-end to the sensory portion of the ulnar nerve. When using the LABC, the volar incision should be extended proximally and laterally toward the lateral epicondyle or lateral border of the antecubital fossa. The LABC is fairly large at this level and can be found on the undersurface of the skin/fascial flap, rather than over the extensor muscles. It can be traced distally to the proximal mid-forearm for a length of 5 to 6 cm. A direct end-to-end repair is performed at this level. The ulnar nerve sensory branch and the ulnar cutaneous sensory nerve are traced more proximally, and, if necessary, tiny intrafascicular connections may be transected to maximize mobilization. Keeping the proximal ulnar nerve intact leads to poorer sensory recovery. A portion of axons will be “lost” into the dead-end motor fascicles, and the rest are required to cover a larger sensory distribution, diluting the sensitivity at the volar finger tips, which is where it is most critical. The postoperative management is the same as for the motor transfer. Sensory reeducation begins as soon as touch is noted.

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5.4 Postoperative Care In all nerve transfers, the wounds are closed in layers, usually with a drain and pain pump. The skin is closed in layers, and the dressing includes a splint. The dressings are removed 2 or 3 days after surgery. A splint is most often used when the transfers are near the wrist, and a sling is used for those near the elbow. Permanent sutures in the hand are removed at 2 weeks, although in the arm and forearm dissolvable sutures are more commonly used, along with a dermal sealant for dressing, such as Dermabond. The patient should be educated regarding the nerve transfer so that he or she will understand what actions will activate their reinnervated muscles. Once the postoperative discomfort has subsided, generally by 3 to 4 weeks, the patient begins daily contractions of the donor muscles, usually under the guidance of a hand therapist familiar with these procedures. Often the surgeon needs to spend time educating the patient’s therapist on these relatively new procedures and equate them to corresponding tendon transfers in order to maximize the therapy encounters and improve the patient’s reeducation. With a nerve transfer, a new nerve is now innervating the muscle. Because the cortical command required to initiate movement is different from that of the preinjured

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Fig. 5.65 Illustrative third web space of median-to-sensory component of the ulnar nerve transfer for ulnar nerve sensory deficits. (a) Ulnar nerve sensory deficits include sensory loss to the ulnar aspect of the hand. (b) Surgical strategy is to reinnervate critical sensation, which includes the sensory component of the ulnar nerve to the fourth web space and the ulnar aspect of the small finger territories. (c) Critical sensation end-to-end nerve transfer is the donor third web space fascicle of the median nerve to the recipient sensory component of the ulnar nerve. Noncritical sensation end-toside nerve transfers are (1) the recipient distal third web space fascicle of the median nerve to the sensory component of the median nerve and (2) the distal dorsal cutaneous branch of the ulnar nerve to the sensory component of the median nerve. (d) Fascicular donor and recipient anatomy for restoration of critical sensation using end-to-end nerve transfer. (e) Fascicular donor and recipient anatomy for restoration of noncritical sensation using end-to-side nerve transfers.

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Fig. 5.66 Third web space of the median to sensory component of the ulnar nerve transfer for ulnar nerve sensory deficits. (a) The donor third web space fascicle is identified on the medial aspect of the median nerve and is neurolysed. (b) The donor third web space fascicle is transected, and its distal end is end-to-side transferred to the recipient sensory component of the median nerve to provide rudimentary sensation to the donor territory. (c) The recipient sensory component of the ulnar nerve is identified on the lateral aspect of the ulnar nerve and is neurolysed. (d) For critical sensation, the donor proximal third web space is end-to-end transferred to the recipient distal sensory component of the ulnar nerve. For noncritical sensation, the recipient distal dorsal cutaneous branch of the ulnar nerve is end-to-side transferred to the donor proximal third web space fascicle of the median nerve. The arrows show the direction of nerve regeneration.

Fig. 5.67 Orientation and incision for median-toulnar nerve transfer with flexor digitorum profundus (FDP) tenodesis. The FDP tenodesis was performed in addition to the median-to-ulnar nerve transfer and Guyon canal release, which describes the elongated incision. The gray box denotes the location of the FDP tenodesis. This FDP tenodesis is specific for an ulnar nerve injury and paralysis of the ulnar-innervated FDP.

150

Nerve Transfer for the Forearm and Hand

5

Fig. 5.68 Exposure and identification of the flexor digitorum profundus (FDP) tendons. By retracting the flexor digitorum superficialis laterally, the FDP and its tendons are identified. An independent FDP tendon to the index finger exists and is not included in the tenodesis. The respective median- and ulnar-innervated FDP tendons to the long, ring, and little fingers are identified and confirmed by pulling on the tendon.

Fig. 5.69 Identifying the division between the median- and ulnar-innervated flexor digitorum profundus (FDP) tendons. Forceps are used in this image to visualize the division between the median- and ulnar-innervated FDP tendons. The ulnar-innervated FDP tendons are sutured to the medianinnervated FDP tendons to complete the FDP tenodesis in an ulnar nerve injury.

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Nerve Transfer for the Forearm and Hand

5

Fig. 5.70 Establishing the appropriate tension on the ulnar-innervated flexor digitorum profundus and insertion of the first suture. The ulnarinnervated FDP tendons are retracted proximally ~ 6 to 7 mm for tension (arrow) and to improve the effectiveness of the FDP tenodesis. The insertion of the first suture is important, as it sets the tension. The suture is inserted in the ulnar-innervated FDP tendons, and the tension is set. The suture is then inserted into the median-innervated FDP (specifically, the FDP tendon to the long finger) and tied off.

Fig. 5.71 The first suture for the flexor digitorum profundus (FDP) tenodesis. The insertion of the first suture is important, as it sets the tension. The following sutures insert easily.

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Nerve Transfer for the Forearm and Hand

5

Fig. 5.72 Flexor digitorum profundus (FDP) tenodesis. The FDP tenodesis is completed with three sutures, the first suture being the one that sets the tension on the ulnar-innervated FDP tendons. The second and third sutures follow easily. The independent FDP tendon to the long finger, which is not included in this tenodesis, is what drives the function of the ulnar-innervated FDP tendons for ulnar nerve injuries.

period, cortical remapping plays a critical role in final functional outcome.90 The patient “relearns” motor control of the new muscle by trying to contract the donor muscle and the reinnervated muscle at the same time.46 The sensory component is likewise stimulated prior to any outward sign of reinnervation. Cortical remapping occurs from continued sensory input from the newly innervated areas. Once there is evidence of motor and sensory regeneration in the new target areas, therapy continues to be essential for strengthening and improving proprioception.

5.5 Conclusion Nerve transfers within the forearm and hand have been used to restore function in numerous neurologic deficits when primary repair or nerve grafting is either not possible or will result in poor outcomes. Many of these transfers are performed in conjunction with the more popular tendon transfers and are tailored to the individual situation. Surgeons intending to perform these procedures must understand the indications, timing, and expected results of anatomical nerve repair, local nerve transfer, and functional tendon transfer to select the best reconstruction for a given clinical scenario. The forearm presents a unique anatomical substrate in which intimate understanding of the mi-

croneuroanatomy can allow for creative reconstitution options. Even within the same nerve, there is the ability to reroute “live” fascicles to nonfunctioning “dead” ones to restore critical function or sensation at the expense of a less important one. Close proximity, redundant fascicular patterns, and even cross-innervation allow for numerous donor-recipient combinations that are not possible in other areas of the body. The most common combinations are listed in ▶ Table 5.1. The understanding of the fascicular structure of nerves, the number and location of contributions to each muscle group, and the consequences of discrete denervations has grown rapidly. Nerve transfers allow us to reduce donor deficits and improve outcomes in a more timely fashion. The sensory nerve transfer that we described in this chapter include end-to-end repair for critical sensation and end-to-side for non-critical sensation and for recovery of some sensation in the distal nerve distribution of donor nerves. We bring the color drawings shown in ▶ Fig. 5.26, ▶ Fig. 5.30, and ▶ Fig. 5.66 into the operating room to help keep all these transfers straight. Innovation in this area of peripheral nerve surgery initially grew out of the dissatisfaction of a few pioneers with the status quo. With motivated patients, attention to outcomes, and collaboration with colleagues from various training backgrounds, the evolution of this specialty will continue to expand.

153

Nerve Transfer for the Forearm and Hand Table 5.1 Common Donor–Recipient Nerve Combinations for Motor and Sensory Transfers Injured Nerve

Possible Donor Nerves

Recipient Nerves

Function Restored

Radial nerve (motor)

FDS (median nerve)

ECRB

Wrist extension

FCR (median nerve)

Posterior interosseus

Finger extension

ECRB (radial nerve) BR (radial nerve) Supinator (radial nerve)

Pronator teres

Pronation

Brachialis (MC nerve) FDS (median nerve) FCR, PL* (median nerve)

Anterior interosseus

Finger flexion

Terminal AIN (median nerve)

Recurrent motor

Thumb opposition

Ulnar nerve (motor)

Terminal AIN (median nerve)

Deep motor

Hand intrinsics

Radial nerve (sensory)

LABC, median nerve†

Radial sensory

Sensation to dorsum of hand

3rd web space 4th web space Dorsal ulnar sensory

1st web space

Sensation to key pinch area

Ulnar digital small finger† LABC

2nd and 3rd web spaces

Protective sensation to noncritical median nerve

3rd web space Radial sensory LABC/MABC/PCM

4th web space Small finger ulnar digital

Sensation to 4th and 5th digits

Main median†

Dorsal ulnar sensory

Sensation to ulnar border of hand

Median nerve (motor)

5

Median nerve (sensory)

Ulnar nerve (sensory)

* If available. † End-to-side. Abbreviations: AIN, anterior interosseous nerve; BR, brachioradialis; ECRB, extensor carpi radialis brevis; FCR, flexor carpi radialis; FCU, flexor carpi ulnaris; FDS, flexor digitorum superficialis; LABC, lateral antibrachial cutaneous; MABC, medial antibrachial cutaneous; MC, musculocutaneous; PCM, palmar cutaneous median; PL, palmaris longus.

5.6 References [1] Kline DG, Hudson AR. Mechanisms and pathology of injury. In: Kline DG, Hudson AR, eds. Nerve Injuries. Philadelphia, PA: WB Saunders; 1995. p. 29 [2] Conway RR. Neuralgic amyotrophy: uncommon but not rare. Mo Med 2008;105:168–169 [3] van Alfen N, van Engelen BG. The clinical spectrum of neuralgic amyotrophy in 246 cases. Brain 2006;129:438–450 [4] Brown JM, Mackinnon SE. Nerve transfers in the forearm and hand. Hand Clin 2008;24:319–340, v [5] Tung TH, Weber RV, Mackinnon SE. Nerve transfers for the upper and lower extremities. Oper Tech Orthop 2004;14:213–222 [6] Mackinnon SE, Novak CB. Nerve transfers: new options for reconstruction following nerve injury. Hand Clin 1999;15:643–666, ix [7] Humphreys DB, Mackinnon SE. Nerve transfers. Oper Tech Plast Reconstr Surg 2002;9:89–99 [8] Weber RV, Mackinnon SE. Nerve transfers in the upper extremity. J Am Soc Surg Hand 2004;4:200–213 [9] Mackinnon SE, Colbert SH. Nerve transfers in the hand and upper extremity surgery. Tech Hand Up Extrem Surg 2008;12:20–33 [10] Lewis RC, Tenny J, Irvine D. The restoration of sensibility by nerve translocation. Bull Hosp Jt Dis Orthop Inst 1984;44:288–296 [11] Nath RK, Mackinnon SE, Shenaq SM. New nerve transfers following peripheral nerve injuries. Oper Tech Plast Reconstr Sur 1997;4:2–11 [12] Stocks GW, Cobb T, Lewis RC. Transfer of sensibility in the hand: a new method to restore sensibility in ulnar nerve palsy with use of microsurgical digital nerve translocation. J Hand Surg Am 1991;16:219–226 [13] Tung TH, Mackinnon SE. Flexor digitorum superficialis nerve transfer to restore pronation: two case reports and anatomic study. J Hand Surg Am 2001;26:1065–1072

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[14] Hovius SE. Musculo-tendinous transfers of the hand and forearm. Clin Neurol Neurosurg 1993;95 Suppl:S92–S94 [15] Littler JW. Neurovascular pedicle transfer of tissue in reconstructive surgery of the hand[abstract]. J Bone Joint Surg 1956;38a:917 [16] Brandt KE, Mackinnon SE. A technique for maximizing biceps recovery in brachial plexus reconstruction. J Hand Surg Am 1993;18:726–733 [17] Babiloni C, Vecchio F, Babiloni F, et al. Coupling between “hand” primary sensorimotor cortex and lower limb muscles after ulnar nerve surgical transfer in paraplegia. Behav Neurosci 2004;118:214–222 [18] Brown JM, Shah MN, Mackinnon SE. Distal nerve transfers: a biology-based rationale. Neurosurg Focus 2009;26:E12 [19] Novak CB, Mackinnon SE. Distal anterior interosseous nerve transfer to the deep motor branch of the ulnar nerve for reconstruction of high ulnar nerve injuries. J Reconstr Microsurg 2002;18:459–464 [20] Lowe JB, Tung TR, Mackinnon SE. New surgical option for radial nerve paralysis. Plast Reconstr Surg 2002;110:836–843 [21] Mackinnon SE, Roque B, Tung TH. Median to radial nerve transfer for treatment of radial nerve palsy: case report. J Neurosurg 2007;107:666–671 [22] Jabaley ME, Wallace WH, Heckler FR. Internal topography of major nerves of the forearm and hand: a current view. J Hand Surg Am 1980;5:1–18 [23] Watchmaker GP, Gumucio CA, Crandall RE, Vannier MA, Weeks PM. Fascicular topography of the median nerve: a computer-based study to identify branching patterns. J Hand Surg Am 1991;16:53–59 [24] Guelinckx PJ, Faulkner JA. Parallel-fibered muscles transplanted with neurovascular repair into bipennate muscle sites in rabbits. Plast Reconstr Surg 1992;89:290–298 [25] Guelinckx PJ, Carlson BM, Faulkner JA. Morphologic characteristics of muscles grafted in rabbits with neurovascular repair. J Reconstr Microsurg 1992;8:481–489 [26] Tung TH, Mackinnon SE. Nerve transfers: indications, techniques, and outcomes. J Hand Surg Am 2010;35:332–341

Nerve Transfer for the Forearm and Hand [27] Dvali L, Mackinnon S. Nerve repair, grafting, and nerve transfers. Clin Plast Surg 2003;30:203–221 [28] Hayashi A, Pannucci C, Moradzadeh A, et al. Axotomy or compression is required for axonal sprouting following end-to-side neurorrhaphy. Exp Neurol 2008;211:539–550 [29] Dorsi MJ, Chen L, Murinson BB, Pogatzki-Zahn EM, Meyer RA, Belzberg AJ. The tibial neuroma transposition (TNT) model of neuroma pain and hyperalgesia. Pain 2008;134:320–334 [30] Amr SM, Moharram AN. Repair of brachial plexus lesions by end-to-side sideto-side grafting neurorrhaphy: experience based on 11 cases. Microsurgery 2005;25:126–146 [31] Mennen U. End-to-side nerve suture in clinical practice. Hand Surg 2003;8:33–42 [32] Pienaar C, Swan MC, De Jager W, Solomons M. Clinical experience with endto-side nerve transfer. J Hand Surg [Br] 2004;29:438–443 [33] Brenner MJ, Dvali L, Hunter DA, Myckatyn TM, Mackinnon SE. Motor neuron regeneration through end-to-side repairs is a function of donor nerve axotomy. Plast Reconstr Surg 2007;120:215–223 [34] Tarasidis G, Watanabe O, Mackinnon SE, Strasberg SR, Haughey BH, Hunter DA. End-to-side neurorraphy: a long-term study of neural regeneration in a rat model. Otolaryngol Head Neck Surg 1998;119:337–341 [35] Seddon HJ, Medawar PB, Smith H. Rate of regeneration of peripheral nerves in man. J Physiol 1943;102:191–215 [36] Leffert RD. Clinical diagnosis, testing, and electromyographic study in brachial plexus traction injuries. Clin Orthop Relat Res 1988;237:24–31 [37] Parry CBW. Thoughts on the rehabilitation of patients with brachial plexus lesions. Hand Clin 1995;11:657–675 [38] Panasci DJ, Holliday RA, Shpizner B. Advanced imaging techniques of the brachial plexus. Hand Clin 1995;11:545–553 [39] Zaidman CM, Seelig MJ, Baker JC, Mackinnon SE, Pestronk A. Detection of peripheral nerve pathology: comparison of ultrasound and MRI. Neurology 2013;80:1634–1640 [40] Kim DH, Kam AC, Chandika P, Tiel RL, Kline DG. Surgical management and outcome in patients with radial nerve lesions. J Neurosurg 2001;95:573–583 [41] Green DP. Radial nerve palsy. In: Green DP, Hotchkiss RN, Pederson WC, et al, eds. Green’s Operative Hand Surgery., Vol. 2. Philadelphia, PA: Elsevier; 2005:113 [42] Bowden RE, Napier EJ. The assessment of hand function after peripheral nerve injury. J Bone Joint Surg Br 1961;43:481–492 [43] Lowe JB, Sen SK, Mackinnon SE. Current approach to radial nerve paralysis. Plast Reconstr Surg 2002;110:1099–1113 [44] Dunnet WJ, Housden PL, Birch R. Flexor to extensor tendon transfers in the hand. J Hand Surg [Br] 1995;20:26–28 [45] Ray WZ, Mackinnon SE. Clinical outcomes following median to radial nerve transfers. J Hand Surg Am 2011;36:201–208 [46] Berger A, Brenner P. Secondary surgery following brachial plexus injuries. Microsurgery 1995;16:43–47 [47] Weber RV, Mackinnon SE. Upper extremity nerve transfers. In: Slutsky DJ, Hentz VR, eds. Peripheral Nerve Surgery: Practical Applications in the Upper Extremity. Philadelphia, PA: Churchill Livingstone Elsevier; 2006:89 [48] Skie MC, Parent TE, Mudge KM, Wood VE. Functional deficit after transfer of the pronator teres for acquired radial nerve palsy. J Hand Surg Am 2007;32:526–530 [49] Johnston RB, Zachary L, Dellon AL, Mackinnon SE, Gottlieb L. The effect of a distal site of compression on neural regeneration. J Reconstr Microsurg 1993;9:271–274, discussion 274–275 [50] Schoeller T, Otto A, Wechselberger G, Pommer B, Papp C. Distal nerve entrapment following nerve repair. Br J Plast Surg 1998;51:227–229, discussion 230 [51] Strauch B, Lang A, Ferder M, Keyes-Ford M, Freeman K, Newstein D. The ten test. Plast Reconstr Surg 1997;99:1074–1078 [52] Strauch B, Lang A. The ten test revisited. Plast Reconstr Surg 2003;112:593– 594 [53] Davis TRC. Median nerve palsy. In: Green DP. Hotchkiss RN, Pederson WC, et al, eds. Green’s Operative Hand Surgery. Vol. 1. 5th ed. Philadelphia, PA: Elsevier; 2005:1131 [54] Haase SC, Chung KC. Anterior interosseous nerve transfer to the motor branch of the ulnar nerve for high ulnar nerve injuries. Ann Plast Surg 2002;49:285– 290 [55] Tse R, Hentz VR, Yao J. Late reconstruction for ulnar nerve palsy. Hand Clin 2007;23:373–392, vii [56] Robotti E, Longhi P, Verna G, Bocchiotti G. Brachial plexus surgery: an historical perspective. Hand Clin 1995;11:517–533

[57] Vernadakis AJ, Humphreys DB, Mackinnon SE. Distal anterior interosseous nerve in the recurrent motor branch graft for reconstruction of a median nerve neuroma-in-continuity. J Reconstr Microsurg 2004;20:7–11 [58] Schultz RJ, Aiache A. An operation to restore opposition of the thumb by nerve transfer. Arch Surg 1972;105:777–779 [59] Chassard M, Pham E, Comtet JJ. Two-point discrimination tests versus functional sensory recovery in both median and ulnar nerve complete transections. J Hand Surg [Br] 1993;18:790–796 [60] Singh R, Mechelse K, Hop WC, Braakman R. Long-term results of transplantations to repair median, ulnar, and radial nerve lesions by a microsurgical interfascicular autogenous cable graft technique. Surg Neurol 1992;37:425–431 [61] Haase J, Bjerre P, Simesen K. Median and ulnar nerve transections treated with microsurgical interfascicular cable grafting with autogenous sural nerve. J Neurosurg 1980;53:73–84 [62] Doi K, Kuwata N, Kawakami F, Tamaru K, Kawai S. The free vascularized sural nerve graft. Microsurgery 1984;5:175–184 [63] Brunelli GA. Sensory nerves transfers. J Hand Surg [Br] 2004;29:557–562 [64] Weber RV, Mackinnon SE. Median nerve mistaken for palmaris longus tendon: restoration of function with sensory nerve transfers. Hand (NY) 2007; 2:1–4 [65] Oka Y. Sensory function of the neurovascular island flap in thumb reconstruction: comparison of original and modified procedures. J Hand Surg Am 2000;25:637–643 [66] Teoh LC, Tay SC, Yong FC, Tan SH, Khoo DB. Heterodigital arterialized flaps for large finger wounds: results and indications. Plast Reconstr Surg 2003;111: 1905–1913 [67] Botte MJ. Vascular system. In: Botte MJ, Krames C, eds. Surgical Anatomy of the Hand and Upper Extremity. Philadelphia, PA: Lippincott Williams & Wilkins; 2002:261 [68] Ross D, Mackinnon SE, Chang YL. Intraneural anatomy of the median nerve provides “third web space” donor nerve graft. J Reconstr Microsurg 1992;8: 225–232 [69] Merle M, Becker C, Pankovic C, Bagot d’Arc M. Microsurgical repair of peripheral nerves and vessels using Tissucol: clinical and experimental study Rev Laryngol Otol Rhinol (Bord) 1987;108:13–14 [70] Boutros S, Nath RK, Yüksel E, Weinfeld AB, Mackinnon SE. Transfer of flexor carpi ulnaris branch of the ulnar nerve to the pronator teres nerve: histomorphometric analysis. J Reconstr Microsurg 1999;15:119–122 [71] Laugier. Note on the suture of the median nerve [French]. Paris Gazette Hop 1864;75:297 [72] Platt H. On the result of bridging gaps in injured nerve trunks by autogenous facial tubulization and autogenous nerve grafts. Br J Surg 1919;7: 384–389 [73] Martins RS, Siqueira MG, Heise CO, Foroni L, Teixeira MJ. A prospective study comparing single and double fascicular transfer to restore elbow flexion after brachial plexus injury. Neurosurgery 2013;72:709–714, discussion 714–715, quiz 715 [74] Ladak A, Spinner RJ. Double fascicular nerve transfer for elbow flexion: is 2 better than 1? Neurosurgery 2013;72:1055–1056 [75] Carlsen BT, Kircher MF, Spinner RJ, Bishop AT, Shin AY. Comparison of single versus double nerve transfers for elbow flexion after brachial plexus injury. Plast Reconstr Surg 2011;127:269–276 [76] Lieber RL, Jacobson MD, Fazeli BM, Abrams RA, Botte MJ. Architecture of selected muscles of the arm and forearm: anatomy and implications for tendon transfer. J Hand Surg Am 1992;17:787–798 [77] Tse R, Hentz VR, Yao J. Late reconstruction for ulnar nerve palsy. Hand Clin 2007;23:373–392, vii [78] Post R, de Boer KS, Malessy MJ. Outcome following nerve repair of high isolated clean sharp injuries of the ulnar nerve. PLoS ONE 2012;7:e47928 [79] Anderson GA. Ulnar nerve palsy. In: Green DP, Hotchkiss RN, Pederson WC, eds. Green’s Operative Hand Surgery. Vol. 1. 5th ed. Philadelphia, PA: Elsvier; 2005:1162 [80] Stuebe AM, Novak CB, Mackinnon SE. Recovery of ulnar nerve innervated intrinsic muscles following anterior transposition of the ulnar nerve. Ca J Plast Surg. 2001;9:25–28 [81] Lester RL, Smith PJ, Mott G, McAllister RM. Intrinsic reinnervation—myth or reality? J Hand Surg [Br] 1993;18:454–460 [82] Wang Y, Zhu S. Transfer of a branch of the anterior interosseus nerve to the motor branch of the median nerve and ulnar nerve. Chin Med J (Engl) 1997;110:216–219

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Nerve Transfer Procedures for Tetraplegia

6 Nerve Transfer Procedures for Tetraplegia Kristen M. Davidge and Ida K. Fox

6.1 Introduction Recent reports of the use of nerve transfers to improve upper extremity function in patients with a cervical-level spinal cord injury (SCI) or tetraplegia1–7 represent an exciting new development for the field of peripheral nerve surgery. The expansion of this innovative reconstructive surgery—peripheral nerve transfer—to treat a novel and often poorly served patient population is important to include in this textbook on peripheral nerve surgery because it exploits a unique feature of the peripheral nervous system (the ability to regenerate) to treat what is currently an untreatable central nervous system (CNS) disorder. At present there are over a quarter million individuals living with SCI in the United States, and over half of these injuries are at the cervical level.8 The motor nerves originating from spinal levels C5 through T1 comprise the brachial plexus and control upper extremity function. Shoulder, elbow, and hand function are instrumental to basic activities of daily living (ADLs) and critically influence the level of independence in tetraplegia. 8,9 Patients with a cervical SCI have said that hand function is more important to them than other activities, such as walking and sexual performance.9 Restoration of hand function is therefore of primary concern in the reconstructive hierarchy for cervical SCI and calls upon the expertise and skill set of the hand and upper extremity surgeon.10 The traditional approach to surgical reconstruction of the hand in tetraplegia employs principles of tendon transfer and tenodesis to restore critical movements, which include wrist extension, wrist flexion, key pinch, grasp, and release.11–13 Unfortunately, options for reconstruction of hand function can be limited in mid and high cervical SCI. This and other limitations, such as the required non-weight-bearing extremity use during the recovery period, have made adaptation and use of these techniques relatively uncommon.10,14 Nerve transfers, by contrast, may offer several potential advantages over tendon transfers and have become the reconstructive method of choice in brachial plexus and peripheral nerve injuries.15–20 Recent reports1–7 of the expanded application of nerve transfer techniques to patients with tetraplegia are promising and may be particularly well suited for use with patients with SCI for a variety of reasons (▶ Fig. 6.1). In this chapter we introduce the concept of using nerve transfers in SCI to highlight the pathophysiology of spinal cord versus peripheral nervous system injury patterns, discuss preliminary information on this exciting new application of peripheral nerve transfer surgery, and suggest areas for future work and improvement.

6.2 Historical Perspective Hand surgeons bring specific expertise to the management of patients with tetraplegia that has facilitated important advances in functional reconstruction of the upper limb. The first surgical approach to the restoration of hand function in this population was described by Bunnell in 1948. Using principles

of tenodesis and tendon transfer, he outlined the surgical reconstruction of wrist extension and rudimentary grasp in patients with C6–C7 tetraplegia.21 Wilson22 and Street and Stambaugh23 further detailed flexor tenodesis procedures for reestablishing grasp function, while Lipscomb et al24 described the first two-stage “grasp and release” reconstruction in patients with preserved wrist extension. In the latter half of the 20th century, Erik Moberg and Douglas Lamb made significant advances to the classification, surgical planning, and reconstructive techniques for patients with varying levels of spinal cord injury.12,25–27 Moberg emphasized the importance of elbow extension and key pinch in maximizing function in tetraplegia. Lamb convened the First International Conference on Surgical Rehabilitation of the Upper Limb in Tetraplegia in Edinburgh in 1978, which established a universal classification system based on residual sensory and motor function of the upper limb.28 This was later modified in 1984 to incorporate function of the extensor carpi radialis brevis (ECRB) muscle29 and has continued as an important tool to direct surgical treatment options in tetraplegia (▶ Table 6.1). Lamb et al also contributed many of the principles of tendon transfer in this population and demonstrated early results of these transfers.25–27 Traditional reconstructive goals for patients with higher-level cervical SCI (C5), where little to no function is preserved below the elbow, are to restore active elbow extension using deltoidto-triceps or biceps-to-triceps tendon transfers (groups 0,1) and active wrist extension using the brachioradialis-to-ECRB tendon transfer (group 1).10–13,30–32 Rudimentary pinch and grasp are achieved via the tenodesis effect.12 In midlevel cervical SCI (C6, C7), elbow and wrist extension are preserved, and the focus shifts to reconstruction of active pinch and grasp, via transfer of the brachioradialis, extensor carpi radialis longus (ECRL), and/or pronator teres (PT) tendons.10,13,33,34 Wrist flexion is achieved by gravity, or it can be dynamically reconstructed, such as with a PT-to-flexor carpi radialis (FCR) transfer (group 4).10,13,32,34 Finger and thumb extension is restored via tenodesis or, less commonly, tendon transfer.10,13,33–35 In lowlevel cervical tetraplegia (C8), the upper extremity functions at a relatively high level, with only intrinsic muscle function lacking. Tendon transfers for thumb opposition and static or dynamic anticlawing procedures may be performed to optimize hand function.10,13,36,37 For all levels of cervical SCI, joint fusions and the Zancolli anticlaw lasso can be used to augment stability in pinching and grasping activities.10,12,13,36–38 Until very recently, the above-listed procedures were state of the art in upper extremity reconstruction in tetraplegia. Although studies have documented generally favorable outcomes following tendon transfers in this population,39–41 adaptation and use of these techniques has been limited.10,14 Indeed, tendon transfers have several biomechanical limitations, including the “one tendon/one function” principle (each transferred musculotendinous unit can successfully power a single motion), inability to restore independent finger motion owing to the aforementioned principle and lack of available donors, and inability to restore full range of motion owing to differential

6

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Nerve Transfer Procedures for Tetraplegia

6

Fig. 6.1 A nerve transfer procedure can be used to rewire the system to make some muscles work again following a spinal cord injury (SCI). We can use the nerve transfer (which is done in the arm and not at the level of the spinal cord) to bypass the damaged area and to deliver a signal from the brain to a muscle that became disconnected following the injury. A donor nerve is taken from another muscle whose use is not essential and then transferred to help in providing a more critical function. The illustration shows a specific example of a brachialis-to-anterior interosseous nerve (AIN) transfer. This is a surgical technique used to restore the lost ability to pinch or grasp small objects between the fingers, which occurs in many patients with cervical SCI. In this surgery we use a donor nerve that is attached to the brachialis muscle. This nerve is functioning normally to help flex the elbow. It can be sacrificed because the biceps muscle is also working to flex the elbow. The donor nerve is cut and reattached to the nerve going to muscles in the forearm that provide pinch by bending the tips of the thumb and index finger.

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Nerve Transfer Procedures for Tetraplegia Table 6.1 International Classification for Surgery of the Hand in Tetraplegia Group

Motor Characteristics

0

No muscle below the elbow suitable for transfer Flexion and supination of the elbow

Description of Function

1

BR

2

ECRL

Extension of the wrist (weak or strong)

3

ECRB

Extension of the wrist

4

PT

Extension and pronation of the wrist

5

FCR

Flexion of the wrist

6

Finger extensors

Extrinsic extension of the fingers (partial or complete)

7

Thumb extensor

Extrinsic extension of the thumb

8

Partial digital flexors

Extrinsic flexion of the fingers (weak)

9

Lacks only intrinsics

Extrinsic flexion of the fingers

X

Exceptions

6

Abbreviations: BR, brachioradialis; ECRB, extensor carpi radialis brevis; ECRL, extensor carpi radialis longus; FCR, flexor carpi radialis; PT, pronator teres.

excursion of donor and recipient muscles. Furthermore, limited availability of transferable muscles in tetraplegia may mean that one hand function is sacrificed at the expense of reconstructing a more critical hand function. Also of specific concern to patients with SCI are the weeks of immobilization and months of non-weight-bearing activity required following tendon transfer surgery.10,26,42 Finally, and perhaps most importantly, tendon transfers do not provide volitional prehension, which is essential for active hand function. Nerve transfers offer several potential advantages over tendon transfers and have become the reconstructive method of choice in brachial plexus and peripheral nerve injuries. 15–20 A nerve transfer takes an expendable, innervated donor nerve and coapts it to a nonfunctional recipient nerve to return motor function. Because a nerve transfer aims to reinnervate the musculotendinous unit(s) responsible for the absent but desired function(s), it does not have the biomechanical limitations of tendon transfers. Along the same lines, a single nerve transfer can reconstruct multiple functions. For example, transfer of the FCR motor branch of the median nerve to the posterior interosseous nerve (PIN) has been shown to restore both thumb and independent finger extension in isolated radial nerve palsy. 43 Moreover, expendable muscles that are less suitable for tendon transfer, such as the brachialis, can be effectively used as donors in nerve transfer procedures. Considering that multiple motor nerve branches innervate each muscle, the potential to leave some nerve branches intact may assist in minimizing donor morbidity when necessary. Additionally, nerve transfers do not require prolonged periods of postoperative immobilization; rather, early range of motion is encouraged. Recent work has focused on extrapolation of these well-established nerve transfer procedures for use in tetraplegia.1–7,44 A unique situation exists in SCI, whereby lower motor neurons (LMNs) below the level of the cord injury remain in continuity with their cell bodies and are otherwise intact unless a concomitant peripheral nerve injury exists.45,46 The muscles innervated by these intact peripheral nerves are paralyzed due to the disruption of CNS input and become flaccid and atrophic due to disuse rather than denervation. This is an important point, as it

means that there is no time limitation to the utility of nerve transfers following an SCI as is seen following a peripheral nerve injury.6 A nerve transfer in a patient with SCI therefore entails transferring an uninjured LMN with intact CNS input (i.e., a nerve that innervates a muscle under the patient’s volitional control) to an uninjured LMN without CNS control (i.e., a nerve that innervates a paralyzed muscle). In so doing, a peripheral nerve injury is intentionally created to restore volitional control to otherwise nonfunctional musculotendinous units. This procedure exploits the regenerative capacity of peripheral nerves and comprises a novel approach to restoring upper extremity function in tetraplegia. There are historic reports describing nerve transfers in SCI. Benassy47 and Kiwerski48 describe transfer of the musculocutaneous to the median nerve, but those results were likely variable due to more limited understanding of the complicated but reproducible internal topography of the median nerve in the arm. In these reports, the entire distal musculocutaneous nerve (of note, the motor component at this level is mainly composed of the brachialis muscle branches, which has 3,500 motor fibers) was transferred to the entire distal median nerve (this mixed nerve has 40,000 nerve fibers at this level). An intraneural dissection to eliminate inadvertent injury to functioning (pronator teres, FCR, etc.) or non-essential (sensory or thenar muscle) elements of the median nerve was not done likely due to the limited knowledge of the internal fascicular anatomy available at that time. With the knowledge gained from the vast experience of nerve transfer to treat peripheral nerve injury in the last few decades, nerve transfers in this uniquely vulnerable and routinely underserved patient population becomes more compelling. Recent case reports have supported the safety, feasibility, and preliminary success of upper limb nerve transfers in cervical SCI. In 2010 Bertelli et al reported restoration of finger and thumb extension in a patient with C6-level tetraplegia using a supinator-to-PIN transfer.3 The same group also demonstrated successful reinnervation of the triceps brachii for elbow extension using the teres minor motor branch in a patient with C6 SCI1 and of the flexor pollicis longus (FPL) for thumb flexion

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Nerve Transfer Procedures for Tetraplegia using the ECRB motor branch in a patient with C7 SCI.2 In all three cases, minimal to no donor site morbidity was observed. 3, 5,6 In a case of C5 tetraplegia, Friden and Gohritz reported restoration of Medical Research Council (MRC) grade 3 wrist extension at 5 months postoperatively via a brachialis-to-ECRL nerve transfer.5 In 1982, Kiwerski reported successful transfer of the musculocutaneous nerve to the median nerve to restore basic hand function in 20 patients with C6 or C7 SCI. 48 This was after Benassy’s initial case report of the same procedure in 1965. 49 Our center subsequently reported the more specific brachialisto-anterior interosseous nerve transfer for reconstruction of prehension in a patient with C7 tetraplegia.6 The concept that the nerve to the brachialis is an expendable donor arose from the traumatic brachial plexus literature, where reinnervation of biceps brachii alone has demonstrated satisfactory restoration of elbow flexion.50,51 Our initial experience with the brachialis-to-AIN transfer in the setting of a peripheral nerve injury was positive. In five patients with this type of transfer, MRC grade 3 or 4 recipient muscle strength and no deficit in elbow flexion strength were seen. 52 In our patient with C7 tetraplegia, bilateral brachialis-to-AIN nerve transfers were performed, and MRC grade 3 strength in the FPL and flexor digitorum profundus (FDP) was achieved bilaterally at 2 years’ follow-up.6 Functionally, the patient is now able to feed himself and perform rudimentary writing activities. Once again, no deficits in elbow flexion related to harvest of the entire brachialis nerve were observed,6 and further reports have corroborated this.53

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6.3 Pathophysiology Neurologic impairment following injury to the cervical spinal cord is a result of both direct physical damage and indirect factors, such as edema, vascular compromise, and free radicals that are sequelae of the original insult. 45,46 These mechanisms result in a variable zone of cord injury, termed the injured metamere. LMN cell bodies within the injured metamere are damaged, and denervation of target muscles ensues. Depending on the severity of the injury, a certain amount of functional recovery, whether complete or incomplete, can be expected. Variability in both the size of the injured metamere and the extent of the recovery explains the comparable variability in residual upper extremity function among patients with the same cervical level of cord injury.45 The injured metamere defines three groups of neuromuscular function.45,46 LMNs above the injured metamere are intact and therefore normal, and volitional control of corresponding muscles is preserved. Traditionally, these functioning muscles have served as donors for tendon transfers to restore grasp and pinch. Muscles innervated by LMNs within the injured metamere are flaccid and atrophic. Because these axons have been disrupted from their cell bodies within the anterior cord, these LMNs cannot be stimulated. Below the injured metamere, LMNs are in continuity, yet they lack descending control from upper motor neurons (UMNs). The corresponding muscles are usually flaccid but may occasionally be spastic due to the loss of UMN input. Though hypotonic, these muscles are not denervated, and stimulation of the corresponding distal peripheral nerve axons will produce muscle contraction even months to years following the original injury.54 This is an important point when

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considering nerve transfers to restore function in tetraplegia, as the normal time constraints to nerve repair dictated by irreversible downregulation of motor end plates in the setting of a denervating peripheral nerve injury are absent until the intraoperative, iatrogenic peripheral nerve injury is deliberately created in the course of performing the nerve transfer. Nerve transfers are a novel approach to restoring upper extremity function in tetraplegia. Essentially, a nerve transfer in a patient with an SCI aims to transfer an uninjured peripheral nerve with intact UMN input (above the injured metamere) to an uninjured LMN without UMN control (below the injured metamere). In other words, a peripheral nerve injury is intentionally created to treat a CNS problem and restore volitional control to otherwise nonfunctional musculotendinous units. Nerve transfers exploit the regenerative capacity of peripheral nerves and offer several advantages over traditional tendon transfers, including the ability to restore more than one function with each transfer and the capacity to restore independent finger motion using a single donor nerve transfer. As compared to a peripheral nerve injury, determining the eligible donor and recipient nerves for a nerve transfer procedure in the SCI population is much more complex. As noted, the mechanism of injury to the cervical spinal cord is a result of direct physical and indirect factors.45,46 These mechanisms result in the injured metamere and a combined UMN and LMN insult.45,46 Above the injured metamere, both UMNs and LMNs are intact and therefore normal, volitional control of corresponding muscles is preserved, and standard physical examination and electrodiagnostic testing may be used to evaluate the donor muscle. Below the injured metamere, UMNs are injured, but LMNs remain in continuity. The corresponding muscles are paralyzed due to a lack of cortical input but remain innervated and are viable nerve transfer recipients. However, within the injured metamere, LMNs are damaged, target muscles are denervated, and, typically, nerve transfers cannot be used to improve function. Clinically, it can be challenging to determine which muscles are atrophic due to denervation versus disuse, and corroborative information from electrodiagnostic testing and intraoperative nerve stimulation may be useful.45 By contrast, intraoperative dissection and interfascicular separation of the nerve fibers of interest are somewhat simplified (compared to that in peripheral nerve injury patterns) due to the ability to perform intraoperative nerve stimulation. In SCI, even the “nonfunctional” (not under volitional control) nerve fibers will, when activated by intraoperative nerve stimulation, produce a muscle contraction. In these surgeries, unlike traditional peripheral nerve surgery, it is critical to document and categorize preoperatively what is and is not under the patient’s volitional control in order to delineate putative donor and recipient fascicles.

6.4 Surgical Anatomy As with all nerve transfer procedures, an understanding of the gross and internal topographical anatomy of the peripheral nerves is critical to the success of these surgeries. A unique feature of patients with isolated SCI is that the individual nerve branches of the recipient nerve can also be stimulated. The LMN, neuromuscular junction, and muscle are functioning and can be activated through use of a standard handheld nerve

Nerve Transfer Procedures for Tetraplegia stimulator. This allows for confirmation of expected topographical anatomy and more precise inclusion and exclusion of the pertinent nerve fascicles. Despite this unique feature, detailed knowledge of the relevant anatomy remains pertinent and will allow safer, more expeditious, and successful patient treatment. In the following, the anatomy relevant to nerve transfers in SCI will be discussed with emphasis on the differences that are most pertinent to this specific patient population. The two transfers that have been described that seem most useful to this patient population5,6 involve use of the nerve branches to the brachialis muscle as the donor. Depending on the level of injury, the recipient can be the AIN to restore volitional prehension or the nerve to the ECRL to restore volitional wrist extension and secondary finger motion through tenodesis.

6.4.1 Nerve to the Brachialis Muscle Anatomy The brachialis muscle is innervated by nerve fibers that originate from the fifth and sixth cervical roots. These fibers travel through the brachial plexus to make up the musculocutaneous nerve. The musculocutaneous nerve provides innervation to the coracobrachialis, biceps, and brachialis muscles before it terminates as the lateral antebrachial cutaneous (LABC) sensory nerve. The musculocutaneous nerve comes off the lateral cord of the brachial plexus and passes through the coracobrachialis muscle to then travel to the medial aspect of the arm. The biceps branch of the musculocutaneous nerve comes off in the proximal half of the arm. More distally, the brachialis branch comes off the nerve in the distal half of the arm. There is usually a single main branch of the nerve that then subdivides prior to innervating the brachialis muscles. Less frequently, there may be two separate branches off the musculocutaneous nerve proper that innervate the brachialis muscle.55–57 Finally, the LABC nerve continues distally and laterally to terminate at its sensory territory.

6.4.2 Anterior Interosseous Nerve Anatomy Nerve fibers from the sixth, seventh, and eighth cervical roots, as well as the first thoracic root, travel through the brachial plexus to make up the median nerve. The AIN is the largest branch of the median nerve and provides motor innervation to the FDP to the index and (sometimes) the long finger, the FPL, and the pronator quadratus muscles. It then terminates as sensory nerve branches to the wrist joint. Although the AIN naturally branches off the median nerve proper distal to the elbow, it can easily be separated by internal neurolysis well proximal to the antecubital fossa in the distal half of the arm. Ultimately, the AIN will branch off the median nerve proper at the radial aspect of the median nerve in the forearm. However, in the arm, the nerve is typically located on the underside, or deepest, surface of the median nerve. Other motor branches to the PT, FCR, palmaris longus, and flexor digitorum superficialis muscles are located at the superficial aspect of the median nerve at this level. The sensory component of the median nerve, as well as the thenar musculature (median nerve intrinsic hand muscle contribution), can also be separated from the adjoining AIN at this level.58

6.4.3 Nerve to the Extensor Carpi Radialis Longus Muscle Anatomy The ECRL muscle is innervated by nerve fibers that originate from the sixth and seventh cervical roots (with variable contribution from the fifth and eighth). These fibers traverse the brachial plexus to travel within the radial nerve. The radial nerve gives off branches to the triceps, anconeus, brachioradialis, and ECRL muscles in the arm. Of note, there is a variable contribution from the radial nerve to the brachialis muscle; however, as stated above, the main innervation for the brachialis muscle is from the musculocutaneous nerve. The ECRB and supinator muscle branches come off more distal to the elbow and just before or at the point where the radial nerve divides and terminates into the posterior interosseous and radial sensory nerves. The natural separation of the ECRL branch from the radial nerve proper occurs just proximal to the elbow at the lateral aspect of the arm. It usually comes off distal to the branch to the brachioradialis, but in some cases there is a single branch to both the brachioradialis and the ECRL that later subdivides.59,60 Either way, the ECRL branch can be separated from the radial nerve proper by internal neurolysis to gain additional proximal length on this nerve branch for use in transfer.

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6.5 Evaluation and Management of Patients 6.5.1 History A routine history will include eliciting biomedical information about the SCI and the patient‘s coexisting and secondary diseases. The following psychosocial aspects of the history are also incredibly important to obtain: the patient’s mental readiness for surgery and realistic expectations, support system for perioperative activity limitations, and ability to obtain the necessary postoperative therapy. The history of the original SCI, including the level of injury, degree of recovery obtained (for the right and left upper extremities separately), and any relevant spine stabilization or upper extremity functional procedures, should be noted. Many patients have very different levels of function for the right versus left side, and information about the use of which hand for what activity may inform the order and type of surgery to be done. In addition, patients will often recover significant amounts of function in the first 6 to 12 months after the initial SCI due to both direct biologic factors (e.g., resolution of localized edema) and rehabilitation with strengthening and retraining. Patients who continue to experience improvement in function should be observed closely to maximize spontaneous recovery prior to considering nerve transfer or other surgical intervention. In contrast, the presence of a spinal cord syrinx, which may expand and further downgrade existing function, may be a contraindication to nerve transfer. The management of the patient’s injury-associated conditions, including degree of spasticity (presence of baclofen indwelling pump, use of Botox injections, etc.), frequency of autonomic dysreflexia, bowel and bladder care regimens, integumentary system status (pressure sores, contractures, etc.), and infectious history (upper respiratory and urinary), should

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Nerve Transfer Procedures for Tetraplegia be considered. Other pre- and postinjury medical and surgical conditions should be noted. Functional needs, including hand dominance (before SCI and current status), employment, and hand-specific hobbies, are important. Asking patients with spasm and/or contractures about how they exploit these secondary conditions for functional use is critical, as taking away or changing these use patterns may or may not be helpful. Also, asking patients about how they do transfers from a manual or power wheelchair, if they use one, as well as how they feed themselves, write or type, and do other things, is useful. Pain, though somewhat less common than that seen in patients with peripheral nerve injury, can significantly affect evaluation and subsequent management of these patients.

6.5.2 Physical Exam The physical exam of patients with SCI is complicated by truncal instability, and patients often require stabilization in the wheelchair or by an assistant to allow for a complete upper extremity motor exam. Evaluation of the right and left sides separately is critical, as patients often have significant asymmetry. Motor testing, sensory examination, and observation of how patients use their hands to do specific tasks, as well as assessment of contracture and spasticity, are important for determining which type of surgery is appropriate. Other exam components, such as a patient’s overall physical status (presence of tracheotomy, ability to move about a room using a wheelchair, presence of pressure sores), may influence suitability for general anesthesia and an invasive surgical procedure. We perform manual muscle testing of the right and left upper extremity with attention paid to assessing the strength of putative donor muscles, including the brachialis and brachioradialis. For most patients considering nerve transfer, we prefer to use the brachialis in the first stage and save the brachioradialis, if present, for salvage or additional procedures. The strength of the biceps (which will remain as the main elbow flexor after a brachialis transfer) should be carefully assessed. Checking elbow flexion with the forearm in pronation and supination allows for individualized assessment of the brachialis and biceps, respectively. Assessment of potential recipient function, including wrist extension and thumb and finger flexion, is important. Sometimes figuring out what is truly antigravity volitional function, as opposed to a patient’s clever adaptive strategies using gravity and/or spasm, can be challenging and demands repeated exams and careful communication with the patient, who is often able to differentiate between volitional and spasm-induced movement. Noting the presence or absence of other volitional function, such as PT or FCR muscle function, is also important. This is because, intraoperatively, if there are extra branches of donor nerve available, it may be possible to innervate these muscles as well. However, unlike in peripheral nerve surgery where the putative recipient muscles do not respond to intraoperative nerve stimulation, in an SCI, documenting muscles under volitional control is critical, as almost all the muscles will stimulate intraoperatively.

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6.5.3 Electrodiagnostic Testing and Imaging The exact role of electrodiagnostic testing and imaging is unclear at this time, but both may be helpful. Many of the initial high-velocity injury mechanisms that caused the SCI can in turn cause formal peripheral nerve injury, such as brachial plexus injury, as well. In addition, the extent of SCI is often unclear—patients may have an extensive zone of injured metamere, syrinx, or central cord syndrome and may not be candidates for nerve transfer. Electromyography may help in preoperative evaluation and diagnosis of these more complex pictures and may allow for better determination of operative suitability. Nerve conduction studies of the median and ulnar nerve provide estimates of the degree of C8/T1 motor unit loss. Adjunctive ultrasonography may provide information on the degree of muscle atrophy and/or fatty replacement that may preclude reinnervation. The extent of this may not be dependent on time since injury, as spasm may in fact work to preserve muscle bulk in some patients even if they are years since injury. Both forms of testing are also helpful for confirming physical exam findings regarding donor redundant muscle function.

6.5.4 Perioperative and Anesthetic Considerations Autonomic dysreflexia is a condition of significant sympathetic nervous system discharge in response to sensory stimuli, including bowel or bladder issues (e.g., full bladder due to a kinked Foley catheter), tight dressings, or other noxious stimuli below the level of the SCI. Hypertension ensues, and this can be life-threatening. To avoid this intraoperatively, deep anesthetic should be induced prior to placement of a Foley catheter. Postoperative strategies to avoid this include use of noncircumferential dressings, rapid resumption of routine bowel and bladder care regimens, and meticulous postoperative exam (to check for hematoma or other wound complications) and pain management. Other perioperative management concerns are the avoidance of pressure sores and lack of thermoregulatory control. Patients should be maintained on a low air loss or other specialty bed, undergo frequent position changes pre- and postoperatively, and be appropriately positioned and padded throughout the surgical procedure. A warming blanket in preoperative holding is helpful to avoid starting the surgery with a hypothermic patient, and temperatures should be carefully watched and regulated throughout the hospital stay. Use of short-acting paralytics for induction of anesthesia is important for allowing intraoperative nerve stimulation to aid in the interfascicular dissection required of these nerve transfers. Because of the proximal nature of the dissection, a tourniquet is not used; however, intradermal injection of 1:1 million epinephrine solution can be helpful for controlling skin bleeding. Bipolar cautery is used throughout as well. Placement of an indwelling pain pump for management of postoperative pain is helpful, but patients should be warned that this may exacerbate or create a temporary motor neurapraxia of another nerve in the area.

Nerve Transfer Procedures for Tetraplegia Table 6.2 Traditional Reconstructive Options for Tetraplegia by Level of Spinal Cord Injury SCI Level

Missing Function

Reconstructive Options

High(C5)

Elbow extension

1. Deltoid-to-triceps tendon transfer 2. Biceps-to-triceps tendon transfer

Wrist extension

BR-to-ECRB or -ECRL tendon transfer

Pinch

1. FPL tenodesis to distal radius 2. Thumb IPJ fusion

Pinch

Thumb: 1. BR-to-FPL tendon transfer 2. PT-to-FPL tendon transfer 3. FPL tenodesis 4. Thumb fusion

Mid(C6–C7)

Index finger: ECRL-to-FDP index tendon transfer

Low (C8)

Grasp

ECRL-to-FDP of all digits tendon transfer

Wrist flexion

1. Gravity 2. PT-to-FCR tendon transfer

Finger extension

1. EDC tenodesis to radius 2. BR-to-EDC tendon transfer

Thumb extension

1. EPL tenodesis to radius 2. Side-to-side transfer of EPL to EDC

Intrinsics

Zancolli anticlaw lasso

Intrinsics

1. Opponensplasty 2. Zancolli anticlaw lasso

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Abbreviations: BR, brachioradialis; ECRB, extensor carpi radialis brevis; ECRL, extensor carpi radialis longus; EDC, extensor digitorum communis; EPL, extensor pollicis longus; FCR, flexor carpi radialis; FDP, flexor digitorum profundus; FPL, flexor pollicis longus; IPJ, interphalangeal joint; PT, pronator teres; SCI, spinal cord injury.

6.5.5 Options for Novel Nerve Transfer Treatment Many patients with cervical spine injuries will have preserved volitional elbow flexion through biceps, brachialis, and possibly brachioradialis muscles. The brachialis is relatively expendable, and because the nerve to the brachialis comes off in the distal half of the arm, it is close to putative recipients to restore prehension (through transfer to the AIN)6 or wrist extension and the resultant hand function through tenodesis (through transfer to the ECRL).5 Other options have been proposed and may prove useful in the future as well, but will not be covered in detail in the next sections.1–4,7,61 These include use of supinator to improve wrist extension by transfer to the extensor carpi ulnaris or to restore finger/thumb extension by transfer to the posterior interosseous nerve. Transfers of teres or deltoid branches of the axillary nerve to the triceps branches of the radial nerve may restore elbow extension, but this is complicated for a number of reasons.62 Significant further work must be done to determine eligibility and timing of surgery, particularly with respect to the deltoid-to-triceps nerve transfer.

6.6 Surgical Techniques 6.6.1 General Principles and Positioning A clear understanding of the intraneural topography is critical to successful nerve transfer surgery. However, in patients with

SCI, that knowledge can be confirmed by direct intraoperative nerve stimulation. In SCI, the LMN is entirely intact; therefore, a handheld nerve stimulator can be used to confirm fascicles. There are some caveats to depending solely on intraoperative stimulation. First, long-acting paralytics cannot be used for anesthetic, as this would preclude stimulation. Second, the nerve will fatigue, and there are limits on the amount of neurotransmitter available intraoperatively, so stimulation should be done sparingly. Finally, because the issue is volitional control and not inability to stimulate, the surgical mindset needs to be radically different from that for treatment of a peripheral nerve injury. In SCI, nearly everything (unless there is an additional brachial plexus or other peripheral-level injury) will stimulate using a handheld nerve stimulator. Therefore, the surgeon must have a very clear operative plan with an understanding of which muscles are under volitional control and are truly functioning for the patient to use (not muscles that are just working through tenodesis or that because of spasm appear to be working) and which muscles intraoperatively stimulate (but are not under volitional control) and would be appropriate as nerve transfer recipients. ▶ Table 6.2 summarizes traditional reconstructive options for tetraplegia by SCI level. General anesthesia without long-acting muscle paralysis is required. The arm is abducted at the shoulder and rests on an arm table. The surgeon sits in the axilla, facing the medial aspect of the arm. Standard sterile prep and drape of the arm from axilla to fingertips facilitates exposure for intraoperative nerve stimulation. A tourniquet is generally not used because of

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Nerve Transfer Procedures for Tetraplegia

Fig. 6.2 Note incision at medial arm directly overlying intermuscular septum. This more limited incision is appropriate for these patients with who have an intact neuromuscular connection below the level of the SCI that can respond to intraoperative stimulation.

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the proximal nature of the dissection and the need to avoid a temporary neurapraxia that would interfere with intraoperative nerve branch stimulation. Loupe magnification at 3.8x or 4.5x is used for initial dissection and isolation of the main nerve trunks. Loupe or operating microscope dissection is used to perform the internal neurolysis. A two-person approach for the neurolysis is helpful, with the assistant gently holding the nerve proximal and distal to the site of desired internal neurolysis using Ragnell retractors or micro-jeweler’s forceps. The surgeon removes the perineurium and performs the internal neurolysis along the natural cleavage planes. Vessel loops are helpful for tagging and separating the fascicles and can also be used to provide gentle traction. The ends of the vessel loops can be clipped with a hemoclip or knotted to themselves to keep them in place. Stimulation will assist in identifying the proper branches. The internal neurolysis of the donor nerve (e.g., the brachialis branch of the musculocutaneous nerve) is straightforward at this level. The other branches can easily be separated off the pertinent donor nerve fascicle to allow for easy transposition to the recipient fascicle. The donor nerve should be dissected and transected as distally as possible as it contains live axons under volitional control. By contrast, the internal neurolysis of the recipient nerve (e.g., the AIN branch of the median nerve) will be more challenging. At the desired level of coaptation, this fascicle is more intimately associated with other branches that must be deliberately excluded to avoid reinnervating muscles that are already under volitional control (e.g., the PT is intact in some patients) or are not the target of choice (e.g., sensory branch or branches to the FCR, FDS, or thenar muscles). Microsurgical instruments and 8–0 or 9–0 nylon epineurial sutures are used to perform the nerve repair. Fibrin glue is placed after suture repair to reinforce and stabilize the nerve repair (▶ Figs. 6.2–6.5).

6.6.2 Brachialis Nerve Dissection To gain access to the nerve to the brachialis muscle, a longitudinal incision is made at the medial aspect of the arm at the intermuscular groove between the biceps and triceps muscles. The brachial artery can be palpated here as well, and the incision

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can be made just superior and parallel to this landmark. Dissection begins through the subcutaneous tissue. To find the musculocutaneous nerve, the fascia overlying the biceps muscle is incised, and the muscle is rolled superolaterally away from the triceps muscle, which is located medially and inferiorly. The LABC nerve is seen continuing distally toward the antecubital fossa, and its function can be confirmed by gently applying traction to the nerve and palpating the resulting skin retraction in the sensory territory supplied by that nerve (tug test). The branches to the brachialis muscle come off the main musculocutaneous nerve proximal to the elbow. There are one or two separate branches to the muscle available for use as donor nerve material. The donor branches should be sharply transected as far distally as possible, where the nerves enter the muscle, to gain as much length as possible but prior to terminal branching, which makes the coaptation more technically challenging. We do not routinely isolate and stimulate the biceps muscle nerve, as the physical exam can usually provide unequivocal confirmation of normal biceps function. In mixed patterns of injury or where preoperative exam is confusing, stimulation of both the biceps and brachialis muscle nerves may be helpful to confirm that one can be sacrificed. In this case, we use a disposable handheld nerve stimulator (Vari-stim, Medtronic Xomed Inc., Jacksonville, FL) set at 2 mA or lower to confirm function of both prior to transecting the brachialis muscle nerve branches.

6.6.3 Anterior Interosseous Nerve Dissection Although we commonly think of the anterior nerve branch in its location in the forearm, it can be separated from the median nerve proper at the level of the arm in order to perform a brachialis-to-AIN transfer procedure. The median nerve is accessed through the same longitudinal arm incision as the musculocutaneous nerve. After locating the musculocutaneous nerve and its brachialis branches, the segment of median nerve suitable for internal neurolysis is chosen. It is important to carefully determine where the AIN recipient nerve should be transected. If the recipient nerve is transected too distally, there will be insufficient length to perform a tension-free nerve repair to the brachialis donor branches. If too

Nerve Transfer Procedures for Tetraplegia

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Fig. 6.3 Initial dissection reveals the medial antebrachial nerve, vascular structures and median nerve. Dissection with separation of the biceps muscle from the underlying brachialis muscle will reveal the musculocutaneous nerve terminal branches to the brachialis muscle and the lateral antebrachial cutaneous nerve. Distal dissection to gain length of donor brachialis nerve branches is completed.

Fig. 6.4 Intraneural dissection of the median nerve to separate branches under volitional control (in this case the branch to pronator teres), sensory branches, and the AIN recipient is possible to do at this level using loup magnification and microsurgical instruments. Deliberate exclusion of these as well as thenar muscle and flexor digitorum superficialis (FDS) branches is completed to avoid loss of critical donor fibers to targets that are too distal to reinnervate or less critical, respectively. If small branches to FDS or flexor carpi radialis are not easily separable they can be included with the main AIN recipient.

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Nerve Transfer Procedures for Tetraplegia

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Fig. 6.5 Tension free coaptation of the donor brachialis to AIN and FCR median recipient branches. In this case, two brachialis nerve branches were identified and transferred individually into the AIN and FCR median percipient branches.

proximal a transection is performed, then redundancy in the repair will increase the time to reinnervation. Therefore, we will deliberately transect the recipient AIN at a level proximal to the site of the neuromuscular junction of the donor brachialis nerve branches. To isolate the AIN at this level in the median nerve, a meticulous internal neurolysis must be performed. The AIN in the forearm is located at the lateral aspect of the median nerve; more proximally above the elbow, it is found more medially and on the underside of the median nerve. In patients with intact volitional PT or FCR function, it is vital to separate these intact functional fascicles and protect them. Downgrading any function in this particular patient population is simply unforgivable. Sensory fascicles should also be carefully separated and excluded to avoid wasting motor fibers in these targets. Also, the thenar musculature component of the median nerve should be excluded, as this also would be a waste of nerve fibers. This is because the nerve transfer site is so proximal that attempts to regenerate these very distal thenar motor fibers is futile—the motor end plates will be unresponsive by the time these nerve fibers reach the intrinsic muscles of the hand.

6.6.4 Extensor Carpi Radialis Longus Dissection The radial nerve can be accessed just proximal to the elbow in the groove between the biceps muscle medially and the brachioradialis and ECRL muscles laterally. Although a single incision that crosses the elbow may be used, two separate smaller incisions at the medial and lateral arm with tunneling of the nerve ends for coaptation may avoid crossing a joint and any associated wound healing complications from that.

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This site of dissection should be done at a level proximal to the brachial nerve branches of the neuromuscular junction, as the radial nerve branch to the ECRL recipient should be transected to gain length for a tension-free nerve repair. The brachioradialis branch comes off proximally, and the next branch of the radial nerve proximal to the elbow goes to the ECRL. Distal to the elbow, the branches to the ECRB, radial sensory nerve, supinator, and posterior interosseous nerve are found, but access to these branches is unnecessary for the purposes of this transfer. Internal neurolysis of the ECRL branch should be performed proximally to allow for redundant length on the nerve so that a tension-free coaptation to the brachialis nerve can be performed at the lateral aspect of the arm. The brachialis nerve branch should be followed as distally as possible and tunneled under the biceps. If the brachialis cannot reach, the coaptation can be done at the medial aspect of the arm but this will increase the time required for recovery of function.

6.6.5 Postoperative Care Patients are admitted overnight to monitor carefully for any perioperative hemodynamic instability and ensure safety for discharge. Patients should be limited to non-weight-bearing activities on the operative arm for 2 to 4 weeks or until stable wound healing is visible and edema resolves. The operative arm, however, may be used as an assist for other ADLs as tolerated. Once complete healing occurs, patients may resume weight bearing and begin therapy with attention focusing on strengthening the donor muscle function (elbow flexion); this may begin preoperatively. Also, therapy to maintain passive range of

Nerve Transfer Procedures for Tetraplegia motion, along with edema and scar management, is instituted as needed. At approximately 6 months posttransfer, reinnervation may begin. Co-contracture exercises with elbow flexion and passive and/or active assisted thumb and finger flexion or wrist extension begin with strengthening over time. As hand function improves, overall arm function may improve with added use of the extremity for ADLs, strengthening, and improved ability to participate in other therapy and exercise modalities.

[8] [9] [10] [11]

[12]

6.7 Conclusion Results of brachialis-to-AIN nerve transfer in patients with brachial plexus and peripheral nerve injuries are promising 52 and may be extrapolated to the SCI patient population. This has been corroborated in the single case report (of bilateral brachialis-to-AIN transfer) in a 71-year-old male with a C7 motor level injury who was 22 months post-SCI.6 He gained useful hand function for holding small objects (food, pen) with the fingers and thumb without the use of tenodesis. His hand function continued to improve over the 2 years postsurgery, as did his overall upper extremity function. The overall extremity function improvement was due to increased use and resulting improvement of overall extremity strength by virtue of the improved hand function. Results of the brachialis-to-ECRL transfer in a single case report (of unilateral surgery) in a 36-year-old male with a C5 level injury who was 12 months post-SCI showed M3 wrist extension at 5 months postsurgery.5 This also led to improved hand function due to tenodesis. Overall, nerve transfers to restore function in SCI make sense from a physiologic and biomechanical standpoint, have a wellestablished track record in the brachial plexus and peripheral nerve injury patient population, and now show preliminary promise in patients with SCI.61 Further work to determine the optimal indications, limitation, and utility is required to avoid any downgrading of function in a patient population with no capacity to tolerate further loss of limited upper extremity use.

[13] [14]

[15] [16] [17]

[18]

[19]

[20] [21] [22] [23] [24]

[25] [26] [27] [28]

6.8 References [1] Bertelli JA, Ghizoni MF, Tacca CP. Transfer of the teres minor motor branch for triceps reinnervation in tetraplegia. J Neurosurg 2011;114:1457–1460 [2] Bertelli JA, Mendes Lehm VL, Tacca CP, Winkelmann Duarte EC, Ghizoni MF, Duarte H. Transfer of the distal terminal motor branch of the extensor carpi radialis brevis to the nerve of the flexor pollicis longus: an anatomic study and clinical application in a tetraplegic patient. Neurosurgery 2012;70:1011– 1016, discussion 1016 [3] Bertelli JA, Tacca CP, Ghizoni MF, Kechele PR, Santos MA. Transfer of supinator motor branches to the posterior interosseous nerve to reconstruct thumb and finger extension in tetraplegia: case report. J Hand Surg Am 2010;35:1647–1651 [4] Bertelli JA, Tacca CP, Winkelmann Duarte EC, Ghizoni MF, Duarte H. Transfer of axillary nerve branches to reconstruct elbow extension in tetraplegics: a laboratory investigation of surgical feasibility. Microsurgery 2011;31:376– 381 [5] Fridén J, Gohritz A. Brachialis-to-extensor carpi radialis longus selective nerve transfer to restore wrist extension in tetraplegia: case report. J Hand Surg Am 2012;37:1606–1608 [6] Mackinnon SE, Yee A, Ray WZ. Nerve transfers for the restoration of hand function after spinal cord injury. J Neurosurg 2012;117:176–185 [7] Oppenheim JS, Spitzer DE, Winfree CJ. Spinal cord bypass surgery using peripheral nerve transfers: review of translational studies and a case report on

[29]

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[33]

[34] [35]

[36]

[37]

its use following complete spinal cord injury in a human. Experimental article. Neurosurg Focus 2009;26:E6 Ackery A, Tator C, Krassioukov A. A global perspective on spinal cord injury epidemiology. J Neurotrauma 2004;21:1355–1370 Landi A, Mulcahey MJ, Caserta G, Della Rosa N. Tetraplegia: update on assessment. Hand Clin 2002;18:377–389 Zlotolow DA. The role of the upper extremity surgeon in the management of tetraplegia. J Hand Surg Am 2011;36:929–935, quiz 935 Freehafer AA, Mast WA. Transfer of the brachioradialis to improve wrist extension in high spinal-cord injury. J Bone Joint Surg Am 1967;49:648– 652 Moberg E. Surgical treatment for absent single-hand grip and elbow extension in quadriplegia: principles and preliminary experience. J Bone Joint Surg Am 1975;57:196–206 Revol M, Cormerais A, Laffont I, Pedelucq JP, Dizien O, Servant JM. Tendon transfers as applied to tetraplegia. Hand Clin 2002;18:423–439 Curtin CM, Hayward RA, Kim HM, Gater DR, Chung KC. Physician perceptions of upper extremity reconstruction for the person with tetraplegia. J Hand Surg Am 2005;30:87–93 Boyd KU, Nimigan AS, Mackinnon SE. Nerve reconstruction in the hand and upper extremity. Clin Plast Surg 2011;38:643–660 Brown JM, Shah MN, Mackinnon SE. Distal nerve transfers: a biology-based rationale. Neurosurg Focus 2009;26:E12 Fox IK, Mackinnon SE. Adult peripheral nerve disorders: nerve entrapment, repair, transfer, and brachial plexus disorders. Plast Reconstr Surg 2011;127:105e–118e Mackinnon SE, Novak CB, Myckatyn TM, Tung TH. Results of reinnervation of the biceps and brachialis muscles with a double fascicular transfer for elbow flexion. J Hand Surg Am 2005;30:978–985 Ray WZ, Pet MA, Yee A, Mackinnon SE. Double fascicular nerve transfer to the biceps and brachialis muscles after brachial plexus injury: clinical outcomes in a series of 29 cases. J Neurosurg 2011;114:1520–1528 Tung TH, Mackinnon SE. Nerve transfers: indications, techniques, and outcomes. J Hand Surg Am 2010;35:332–341 Bunnel S. Surgery of the Hand. 2nd ed. Philadelphia, PA: Lippincott; 1948 Wilson JN. Providing automatic grasp by flexor tenodesis. J Bone Joint Surg Am 1956;38-A:1019–1024 Street DM, Stambaugh HD. Finger flexor tendodesis. Clin Orthop Relat Res 1959;13:155–163 Lipscomb PR, Elkins EC, Henderson ED. Tendon transfers to restore function of hands in tetraplegia, especially after fracture-dislocation of the sixth cervical vertebra on the seventh. J Bone Joint Surg Am 1958;40-A:1071–1080 Lamb DW, Landry R. The hand in quadriplegia. Hand 1971;3:31–37 Lamb DW, Chan KM. Surgical reconstruction of the upper limb in traumatic tetraplegia: a review of 41 patients. J Bone Joint Surg Br 1983;65:291–298 Lamb DW. Upper limb surgery in tetraplegia. J Hand Surg [Br] 1989;14:143–144 McDowell CL, Moberg EA, Smith AG. International conference on surgical rehabilitation of the upper limb in tetraplegia. J Hand Surg Am 1979;4:387–390 McDowell CL, Moberg EA, House JH. The second international conference on surgical rehabilitation of the upper limb in tetraplegia (quadriplegia). J Hand Surg Am 1986;11:604–608 Hentz VR, Ladd AL. Functional Reconstruction of the Upper Extremity in Tetraplegia. Vol 1. New York: McGraw-Hill; 1996 Revol M, Briand E, Servant JM. Biceps-to-triceps transfer in tetraplegia: the medial route. J Hand Surg [Br] 1999;24:235–237 Zancolli EA, Zancolli ER. Surgical reconstruction of the upper limb in middle level tetraplegia. In: Tubiana R, ed. The Hand. Philadelphia, PA: WB Saunders; 1991 House JH, Walsh T. Two-stage reconstruction of the tetraplegia hand. In: Master Techniques in Orthopedic Surgery. Philadelphia, PA: Lippincott-Raven; 1998 Zancolli E. Surgery for the quadriplegic hand with active, strong wrist extension preserved: a study of 97 cases. Clin Orthop Relat Res 1975:101–113 House JH, Gwathmey FW, Lundsgaard DK. Restoration of strong grasp and lateral pinch in tetraplegia due to cervical spinal cord injury. J Hand Surg Am 1976;1:152–159 McCarthy CK, House JH, Van Heest A, Kawiecki JA, Dahl A, Hanson D. Intrinsic balancing in reconstruction of the tetraplegic hand. J Hand Surg Am 1997;22:596–604 Zancolli EA. Structural and Dynamic Basis of Hand Surgery. 2nd ed. Philadelphia, PA: Lippincott; 1979

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Nerve Transfer Procedures for Tetraplegia [38] House JH, Comadoll J, Dahl AL. One-stage key pinch and release with thumb carpal-metacarpal fusion in tetraplegia. J Hand Surg Am 1992;17:530–538 [39] Meiners T, Abel R, Lindel K, Mesecke U. Improvements in activities of daily living following functional hand surgery for treatment of lesions to the cervical spinal cord: self-assessment by patients. Spinal Cord 2002;40:574–580 [40] Rothwell AG, Sinnott KA, Mohammed KD, Dunn JA, Sinclair SW. Upper limb surgery for tetraplegia: a 10-year re-review of hand function. J Hand Surg Am 2003;28:489–497 [41] Wangdell J, Fridén J. Satisfaction and performance in patient selected goals after grip reconstruction in tetraplegia. J Hand Surg Eur Vol 2010;35:563–568 [42] Gross DP, Battié MC, Asante AK. The Patient-Specific Functional Scale: validity in workers’ compensation claimants. Arch Phys Med Rehabil 2008;89:1294– 1299 [43] Ray WZ, Mackinnon SE. Clinical outcomes following median to radial nerve transfers. J Hand Surg Am 2011;36:201–208 [44] Louie G, Mackinnon SE, Dellon AL, Patterson GA, Hunter DA. Medial antebrachial cutaneous—lateral femoral cutaneous neurotization in restoration of sensation to pressure-bearing areas in a paraplegic: a four-year follow-up. Ann Plast Surg 1987;19:572–576 [45] Coulet B, Allieu Y, Chammas M. Injured metamere and functional surgery of the tetraplegic upper limb. Hand Clin 2002;18:399–412, vivi. [46] Van Heest A. Tetraplegia. In: Wolfe SW, Hotchkiss RN, Pederson WC, Kozin SH, eds. Green’s Operative Hand Surgery. 5th ed. Philadelphia, PA: Elsevier Churchill Livingstone; 2005:1271–1295 [47] Benassy J. Transposition of the musculo-cutaneous nerve upon the median nerve. Case report Med Serv J Can 1966;22:695–697 [48] Kiwerski J. Recovery of simple hand function in tetraplegia patients following transfer of the musculo-cutaneous nerve into the median nerve Paraplegia 1982;20:242–247 [49] Benassy J. A case of transposition of the musculo-cutaneous nerve upon the median nerve Paraplegia 1965;3:199–202 [50] Carlsen BT, Kircher MF, Spinner RJ, Bishop AT, Shin AY. Comparison of single versus double nerve transfers for elbow flexion after brachial plexus injury. Plast Reconstr Surg 2011;127:269–276 [51] Oberlin C, Ameur NE, Teboul F, Beaulieu JY, Vacher C. Restoration of elbow flexion in brachial plexus injury by transfer of ulnar nerve fascicles to the nerve to the biceps muscle. Tech Hand Up Extrem Surg 2002;6:86–90 [52] Ray WZ, Yarbrough CK, Yee A, Mackinnon SE. Clinical outcomes following brachialis to anterior interosseous nerve transfers. J Neurosurg 2012;117: 604–609

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[53] Davidge KM, Novak CB, Kahn LC, Mackinnon SE, Fox IK. Use of peripheral nerve transfers in tetraplegia: case series and preliminary results. Paper presented at: American Society for Surgery of the Hand 68th Annual Meeting; October 4, 2013; San Francisco, CA [54] Davidge KM, Kahn LC, Novak CB, Juknis N, Ruvinskaya R, Fox IK. Restoring prehension/wrist flexion and decreasing spasticity 11 years following spinal cord injury: A case study of the use of the brachialis nerve transfer. Paper Presented at: American Society for Peripheral Nerve/ American Society for Reconstructive Microsurgery Combined Scientific Paper Session at the Annual Meeting; January 12, 2014; Kaua, Hawaii. [55] Pacha Vicente D, Forcada Calvet P, Carrera Burgaya A, Llusá Pérez M. Innervation of biceps brachii and brachialis: anatomical and surgical approach. Clin Anat 2005;18:186–194 [56] Chiarapattanakom P, Leechavengvongs S, Witoonchart K, Uerpairojkit C, Thuvasethakul P. Anatomy and internal topography of the musculocutaneous nerve: the nerves to the biceps and brachialis muscle. J Hand Surg Am 1998;23:250–255 [57] Yang ZX, Pho RW, Kour AK, Pereira BP. The musculocutaneous nerve and its branches to the biceps and brachialis muscles. J Hand Surg Am 1995;20:671– 675 [58] Boyd KU, Dhaliwal G, Yee A, Mackinnon SE. Brachialis to anterior interosseous nerve transfer: an anatomic study (abstract presentation). Paper presented at: Annual Meeting of the American Society for Peripheral Nerve Annual Meeting; January 13, 2012; Las Vegas, Nevada [59] Branovacki G, Hanson M, Cash R, Gonzalez M. The innervation pattern of the radial nerve at the elbow and in the forearm. J Hand Surg [Br] 1998;23:167– 169 PubMed [60] Abrams RA, Ziets RJ, Lieber RL, Botte MJ. Anatomy of the radial nerve motor branches in the forearm. J Hand Surg Am 1997;22:232–237 PubMed [61] Fox IK, Davidge KM, Novak CB, Kahn LC, Juknis N, Ruvinskaya R, Mackinnon SE. Nerve transfer surgery to improve hand function in spinal cord injury: Multiplidisciplinary evaluation and management. Paper Presented at: Paralyzed Veterans of America 2013 Summit and Expo; August 29, 2013; Orlando, Florida [62] Davidge KM, Kahn LC, Juknis N, Ruvinskaya R, Novak CB, Fox IK. The deltoid to tricept nerve transfer: A novel approach to early salvage of elbow extension in cervical spinal cord injury. Electronic poster presented at: American Society for Peripheral Nerve Annual Meeting; January 10–12, 2014; Kauai, Hawaii

Nerve Autograft Substitutes: Conduits and Processed Allografts

7 Nerve Autograft Substitutes: Conduits and Processed Allografts Amy M. Moore, Wilson Z. Ray, and Philip J. Johnson

7.1 Introduction The gold standard of nerve grafting remains the autologous nerve graft, as it promotes axonal regeneration through the provision of both Schwann cells and an extracellular scaffold of endoneurial tubes. Autografting can have significant associated morbidity, however, including loss of donor nerve function, additional incisions, scarring, and potential painful neuroma formation.1–3 Furthermore, there is a limited supply of expendable donor nerves, and the harvesting of these nerves adds to the overall operative time for the patient. There are also situations where harvest of a nerve autograft is counterintuitive; sacrificing one noncritical small diameter nerve to fix another noncritical small diameter nerve is an example. Another example is autograft harvest in a patient with an established pain syndrome where pain at a nerve donor site is more likely to occur. If the reconstructed nerve is noncritical, more harm may be done with the autograft harvest than good. In clinical situations such as these, or when donor autografts are unavailable or insufficient, “off-the-shelf” autograft substitutes may assist in providing a temporary framework to support axonal regeneration. The use of tubular structures to repair nerve injuries dates back as early as 1891, when Büngner reported successful nerve regeneration through an arterial graft.4 Since that time, two

major categories of autograft substitutes have arisen—nerve conduits and nerve allografts. Experimental interest in and clinical use of conduits, both synthetic and nonsynthetic, began in the 1980s. At least seven synthetic nerve conduits and four synthetic nerve wraps have since been approved by the US Food and Drug Administration (FDA) for clinical use in peripheral nerve reconstruction (▶ Table 7.1).5 The earliest report of clinical nerve allografting dates back to 1876, when Eduard Albert repaired a median nerve defect with a tibial nerve taken from the freshly amputated leg of another patient.6 It was not until the advent of microsurgical techniques in the 1970s and adequate immunosuppressive regimens in the 1980s, however, that cadaveric nerve allografts became a feasible clinical alternative to autografts for devastating cases of peripheral nerve injury.7 Because of the antigenic nature of fresh cadaveric allografts, with donor Schwann cells being their most antigenic component, various strategies have been developed to decellularize the grafts, rendering them nonimmunogenic while maintaining their endoneurial architecture. There is currently one acellularized nerve allograft (ANA) available for clinical use that is FDA approved (▶ Table 7.1). In this chapter we review both the experimental and the clinical evidence for the use of conduits and ANAs. We also discuss the future of these autograft alternatives and the

7

Table 7.1 FDA-Approved Guidance Conduits and Wraps for Peripheral Nerve Injury FDA Approval

Company

Product

Material

Diameter

Length

Absorbable Nerve Conduits 1995, 1999

Synovis Micro Companies Alliance Inc.

Neurotube

Polyglycolic acid

2.3–8.0 mm

2–4 cm

2001

Integra Life Sciences Corp.

NeuraGen

Type I collagen

1.5–7.0 mm

2–3 cm

2001

Collagen Matrix Inc.

Neuroflex

Type I collagen

2–6 mm

2.5 cm

2001

Collagen Matrix Inc.

NeuroMatrix

Type I collagen

2–6 mm

2.5 cm

2003

Cook Biotech Products

AxoGuard Nerve Connector

Porcine small intestinal submucosa

1.5–7.0 mm

10 mm

2003, 2005

Polyganics B.V.

Neurolac

Poly(DL-lactide-ε-caprolactone)

1.5–10.0 mm

3 cm

2010

Salumedica L.C.C.

SaluTunnel Nerve Protector

Polyvinyl alcohol

2–10 mm

6.35 cm

Absorbable Nerve Cuffs/Wraps 2000, 2001

Salumedica L.C.C.

Salubridge

Polyvinyl alcohol

2–10 mm

6.35 cm

2003

Cook Biotech Products

AxoGuard Nerve Protector

Porcine small intestinal submucosa

2–10 mm

2–4 cm

2004

Integra Life Sciences Corp.

NeuraWrap

Type I collagen

3–10 mm

2–4 cm

2006

Collagen Matrix Inc.

NeuroMend

Type I collagen

4–12 mm

2.5–5.0 cm

Avance

Human acellularized nerve

1–5 mm

1.5–5.0 cm *

Acellular Nerve Allografts 2007

AxoGen. Inc

* Available in lengths up to 7 cm by special order. Adapted with permission from Kehoe S, Zhang XF, Boyd D. FDA-approved guidance conduits and wraps for peripheral nerve injury: a review of materials and efficacy. Injury;2012;43:553–572.

169

Nerve Autograft Substitutes: Conduits and Processed Allografts possible modifications that may help them become equivalent or even superior to nerve autografts. The challenge in the next several years will be to determine appropriate limits for the use of conduits and ANAs in patients with nerve injuries.

7.2 Nerve Conduits: Ideal Characteristics and Physiology Nerve conduits are appealing because they provide a means for bridging a nerve gap and can be quickly taken “off the shelf” as needed. Hypothetically, conduits promote regeneration by (1) removing suture line tension from the repair; (2) preventing scar tissue infiltration into the nerve from the surrounding tissue; (3) preventing axonal escape from the suture sites; (4) allowing for the accumulation of neurotrophic factors that are secreted from the divided nerve endings, creating a suitable environment for regeneration; (5) providing a tubular structure to guide axonal regeneration and allow Schwann cell migration; and (6) potentially allowing the microenvironment of the regenerating nerve to be manipulated by controlling biochemical and physical contents, such as adding neurotrophic factors or a fibrin matrix into the conduit lumen. 3,8–11 A conduit should possess certain characteristics to be clinically applicable. The ideal conduit should (1) be tubular in structure to encompass both the proximal and distal nerve ends and mechanically support the regenerating nerve across the gap; (2) be available in a variety of lengths and internal diameters, such that the conduit diameter is slightly larger than the grafted nerve to prevent constriction but not so large that it allows efflux of neurotrophic substances or ingrowth of fibrous scar; (3) be biodegradable yet last at least until axons regenerate into the distal stump; (4) elicit a minimal inflammatory response; (5) be noncarcinogenic; (6) be able to withstand sterilization; and (7) consist of a sturdy but flexible material that is able to resist external compression or collapse during movement and allow sutures to be passed easily during implantation. 3,11,12 Finally, to be clinically feasible, the conduit should be individually packaged and readily available for use. Predictable physiologic changes occur within the conduit after implantation. In 1983, using a rat sciatic nerve model, Williams et al examined the spatial and temporal progression of nerve regeneration across a 10-mm silicone conduit.13 Their results demonstrated that, within 24 hours, the conduit is filled with fluid containing neurotrophic nutrients, such as proteins, clotting factors, and soluble factors.11 Within the first week, an acellular fibrin matrix extends between the proximal and distal nerve ends in the center of the conduit. This matrix provides the scaffold for Schwann cells, fibroblasts, and endothelial cells that migrate inward from the proximal and distal nerve ends. These cells enter the conduit 7 days postimplantation. 13 Within 2 weeks, axons appear, lagging behind the migrating Schwann cells and fibroblasts. This is followed by the entrance of capillaries and vessels. Axon myelination occurs 3 to 5 days after axonal elongation.13 Upon reaching the distal nerve stump, axons proceed down the preserved endoneurial tubes of the intact distal nerve.11

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170

7.3 Nerve Conduits: Experimental and Clinical Evidence A significant amount of research has been invested in the development of biologic and synthetic nerve conduits. A variety of materials have been used, including biologic tissues such as arteries, veins, and muscle, as well as synthetic polymers of both nonbiodegradable (“biodurable”) and biodegradable (“absorbable”) types.14–25 Whereas research in the 1980s focused mostly on biologic tissues and nonbiodegradable polymers such as silicone, more recent experimental research has shifted the focus to biodegradable conduits and strategies to enhance them, including the addition of nerve-stimulating factors or matrix structure.3,11,26 Several FDA-approved nerve conduits are on the market, and many have good scientific support for their use (▶ Table 7.2 and ▶ Table 7.3). A brief review of the most popular conduits follows.5,27

7.3.1 Polyglycolic Acid (PGA) Conduit Also known as the GEM Neurotube (Synovis Micro Companies Alliance Inc., Birmingham, AL), the PGA conduit has been the most extensively studied synthetic biodegradable conduit both experimentally and clinically. It is a porous synthetic aliphatic polyester made of polyglycolic acid.15 Animal studies date back to the early 1980s,51–53 and clinical use of a PGA conduit was first described by Mackinnon and Dellon in 1990.28 Rosen et al51 and Seckel et al52,53 first used PGA tubes in rat short nerve gap models to demonstrate the effectiveness of regeneration through these devices. In 1988 Dellon and Mackinnon demonstrated neural regeneration across PGA conduits to be equal to the classical interfascicular interpositional sural nerve graft for a 3-cm gap in a subhuman primate model. 54 These findings were the basis for translating the use of PGA conduits to the clinical realm. In 1990 Mackinnon and Dellon published their results on the use of PGA conduits in 15 patients with digital nerve gaps ranging from 5 to 30 mm. They reported excellent functional sensation in 33%, good functional sensation in 53%, and poor functional sensation in 14% of the nerve reconstructions. These results were comparable to those found with the classical nerve graft technique.28 In the 1980s, however, Mackinnon used tubed PGA sheets (rather than the corrugated conduits that are now available) in a series of patients for large-diameter nerve reconstructions without success (personal communication). Therefore, in her clinical practice, she restricted their use to small-diameter, noncritical sensory nerves with gap distances ≤ 30 mm. In 2000 Weber et al reported the results of the first randomized, prospective, multicenter evaluation comparing autografts and PGA conduits for the repair of digital nerve gaps.20 PGA tubes produced good to excellent functional sensation in 100% of patients with nerve gaps < 4 mm, 83% of patients with nerve gaps 5 to 7 mm, and 71% of patients with nerve gaps > 8 mm. Compared to standard autografting, PGA conduits provided statistically better sensory return in gap lengths > 5 mm. In 2005 Battiston et al reported another clinical series of 19 patients in which PGA conduits were used for digital nerve repairs. They reported 76.5% of patients had “very good” results

Nerve Autograft Substitutes: Conduits and Processed Allografts Table 7.2 Clinical Data on FDA-Approved Absorbable Nerve Conduit and ANA Use for Small-Caliber Nerve Repair Conduit/ANA length (cm)

Follow-up Outcome

1.7 ± 0.6 ~ 2 (range 0.5–3)

Gap + 0.5 overlap/end

22.4 mo (range 11–32 mo)

Sensory: 33% excellent, 53% good, 7% poor, 7% none

2.5

2

Gap + 0.5 overlap/end

2y

Sensory: excellent

62, 74 controls 36 ± 14 Digital (98)

0.7 ± 0.56

Not given

Gap + 0.5 overlap/end

9.4 ± 4.4 mo (range up to 12 mo)

Sensory: 44% excellent, 30% good, 26% poor

1 (1)

11

Medial plantar

2

Not given

Gap + 0.5 overlap/end

10 mo

Sensory: excellent

Battiston et al, Series 20059

19, 13 muscle–vein (30)

40 (range 15–67)

Digital

2 (range 1–4)

Not given

Not given

Sensory: 30 mo (range 6– 10% excellent, 58% 74 mo) good, 16% poor, 16% none

PGA

Ducic et al, 200531

Report

1 (1)

63

Spinal accessory

2.5

Not given

2.5

4 mo

Motor: full (M5) shoulder abduction

PGA

Dellon, 200632 Report

3 (1)

40

Radial sen- Radial sory, digital 2.5, digital 3.0 in toe-tothumb

2.3

Radial 3.5, digital 4.0

30 mo

Sensory: excellent

Collagen

Lohmeyer, 200733*

Report

12 (11)

Range 12–66

Digital

Range 0.6–1.8

2

Not given

12 mo

Sensory: 66% excellent, 17% poor, 17% none

Collagen

Bushnell, 200834

Series

12 (12)

33 (range 18–50)

Digital

≤2

2–4

≤2

15 mo (12–22 mo)

Sensory: 44% excellent, 44% good, 12% fair

Collagen

Taras and Jacoby, 200835

Technique

2 (2)

22, 23

Digital, ra- 2, 1.5 dial sensory

Not given

Not given

8 mo, 6 mo

Sensory: excellent, not given

Collagen

Lohmeyer et al, 200936*

Series

15 (14)

38 (range 12–66)

Digital

1.27 ± 0.37 (range 0.6–1.8)

2

Gap + 0.2 overlap/end

12 mo

Sensory: 33% excellent, 42% good, 8% poor, 17% none

Collagen

Thomsen et al, Series 201037

11 (10)

30

Digital

1.13 (range 0.5–2)

2–4

2–3

11.8 mo (6–17 mo)

Sensory: 36% excellent, 9% good, 46% fair, 9% poor

PLC

Bertleff et al, 200538

21, 13 controls 40 (30)

Digital

0.6–2

Not given

Gap + 0.4–0.5 overlap/end

12 mo

Sensory: good, no difference from controls

Material

Study and Year

Study Type

Conduit/ANA repairs (total no. of patients)

Age (y) Nerve

Gap size (cm)

PGA

Mackinnon and Dellon, 199028

Series

16 (15)

30.5 ± 7.6

Digital

PGA

Crawley and Report Dellon, 199229

1 (1)

51

Inferior alveolar

PGA

Weber et al, 200020

RCMT

PGA

Kim and Dellon, 200130

Report

PGA

RCMT

Conduit/ANA diameter (mm)

7

171

Nerve Autograft Substitutes: Conduits and Processed Allografts Table 7.2 continued Conduit/ANA length (cm)

Follow-up Outcome

Not given

Gap + 0.4–0.5 overlap/end

14 mo

Sensory: poor

Not given

7 mo

Sensory: poor

2.23 (range 0.5–3.0)

9 (range 5–12)

Sensory: 50% excellent, 50% good

Not given

5 mo

Sensory: fair

Study and Year

Study Type

Conduit/ANA repairs (total no. of patients)

Age (y) Nerve

PLC

Meek, 200639

Report

1 (1)

20

Plantar dig- 2 ital

PLC

HernandezLetter Cortes, 201040

1 (1)

17

Digital

Not given Not given

Avance

Karabekmez et Series al, 200941

10 (7)

44 (range 23–65)

Digital

2.23 (range 0.5–3.0)

Avance

Shanti and Ziccardi, 201142

1 (1)

62

Inferior alveolar

Not given 3–4

Report

Gap size (cm)

Conduit/ANA diameter (mm)

Material

Not given

* These publications represent data from same cohort at different time points. Abbreviations: ANA, acellularized nerve allograft; FDA, US Food and Drug Administration; PGA, polyglycolic acid; PLC, poly(DL-lactide-ε-caprolactone); RCMT, randomized controlled multicenter trial.

7

(defined as static two-point discrimination [s2PD] < 15 mm), and 17.7% had “good” results (s2PD > 15 mm but some superficial pain and tactile sensation present).9 PGA conduit use has also been described in a variety of nondigital nerve gap defects. Successful regeneration has been reported in short gap (≤ 3 cm) defects of the inferior alveolar nerve,29 medial plantar nerve,30 terminal branches of the facial nerve,43 spinal accessory nerve,31 plantar digital nerves,15 and median nerve.44 PGA conduits have been used to bridge nerve gap defects (both sensory and motor), as well as to assist with the prevention of neuroma formation by rerouting painful sensory nerves to more appropriate end targets.29,30 They have also recently been shown to be effective when multiple tubes are bundled together to repair a larger diameter median nerve defect.44

7.3.2 Poly(DL-lactide-ε-caprolactone) Conduit Commercially known as the Neurolac nerve guide (Polyganics B.V., Groningen, the Netherlands), this conduit is absorbable and made of poly(DL-lactide-ε-caprolactone). In the late 1990s, Den Dunnen and Meek performed multiple studies evaluating the characteristics and efficacy of Neurolac tubes.55–58 These studies demonstrated that the Neurolac tube could be used effectively for nerve regeneration. The biomaterial maintains its mechanical strength and flexibility for up to 10 weeks. 59 These conduits have the benefit of being transparent, allowing direct visualization to ensure correct position of the nerve stumps. Furthermore, degradation products are thought to be less acidic than PGA tubes, which may translate into less environmental damage.38 In 2005 Bertleff et al reported their results of a blinded, randomized, multicenter clinical investigation that used the Neurolac conduit to repair sensory nerve defects < 2 cm

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in length. They found sensory recovery with the conduit to be comparable to direct coaptation repairs. However, they reported significantly more wound-healing problems in the Neurolac group, and subgroup analysis was not provided. 38 Recently, other reports have been published presenting concerns regarding this conduit. Two studies in rats have shown that the conduits exhibit slower degradation, with small fragments associated with chronic foreign body tissue reaction being found at 16 and 24 months after implantation.60,61 It is unknown how this reaction affects long-term functional outcomes. Also, Meek and Coert reported further difficulties with clinical use, such as conduit collapse and the need for soaking in warm saline prior to use to allow flexibility and softness for suture placement.62

7.3.3 Collagen Conduits Collagen is the most abundant protein in the human body and is involved in extracellular matrices and connective tissues. There are more than 15 types of collagen. Type I collagen is most common, comprising ~ 90% of total collagen in the body. It is a key structural component in bones, tendons, and ligaments.63,64 Up to 50% of nerve protein is made from types I and III collagen.15 Because of its strength, fibrous structure, and bioabsorbable properties, collagen represents a good biomaterial for nerve conduits. Numerous collagen-based conduits and nerve wraps are commercially available. These include NeuraGen and NeuraWrap (Integra Life Sciences Corp., Plainsboro, NJ), and NeuroFlex, NeuroMatrix, and NeuroMend (Collagen Matrix, Inc., Franklin Lakes, NJ). These products are made from purified type I collagen, derived from bovine deep flexor tendon. Fabricated from porcine types I and III collagen, RevolNerv (Orthomed S.A., Saint-Jeannet, France) is another collagen nerve conduit that has recently become available.

Nerve Autograft Substitutes: Conduits and Processed Allografts Table 7.3 Clinical Data on FDA-Approved Absorbable Nerve Conduit and Acellular Nerve Allograft Use for Large-Caliber Nerve Repair Material

Study and Year Study Type

Conduit/ANA Age repairs (total no. of patients)

Nerve

Gap size (cm)

PGA

Navissano et al, 200543

Series

7 (7)

26

Facial

PGA

Donoghoe et al, 200744

Series

2 (2)

40, 61

Median (forearm)

PGA

Rosson, 200945*

Series

4 (3)

A: 9; B: 53; C: 51

A: ulnar (fore- A: 2.7; B: 3.0, 1.5; arm); B: meC: 4.0 dian, ulnar (midbrachium); C: ulnar (midbrachium)

Conduit/ANA diameter (mm)

Conduit/ANA Followlength, cm up

Outcome

Range 1– Not given 3

Not given

Range 7–12 mo

Motor: 14% very good, 57% good, 29% fair

3

2.3 (4 conduits/ repair)

4

5y

Motor: APB function; sensory: good to excellent

A: not given; B: not given (4 conduits/median, 3 conduits/ulnar); C: 8 mm

A: not given; B: not given; C: 4 (two stretched 2 cm end-toend with sliced nerve interposed)

A: 2.5 y; B: 5.5 y; C: 14 mo

A: motor: excellent; B: motor: reinnervation of forearm median/ulnar muscles; no intrinsic reinnervation; C: reinnervation of forearm ulnar muscles and FDI

PGA

Hung and Del- Report lon, 200846

1 (1)

4

Median (carpal 4 tunnel)

4

2y 5 (two stretched 2 cm end-toend with sliced nerve interposed)

Motor: APB function; sensory: good

PGA

Dellon, 200847 Letter

1 (1)

4.2

Ulnar (proximal arm)

8

18 mo 5 (two stretched 2 cm end-toend with sliced nerve interposed)

Sensory: progression of Tinel to midforearm; motor: EMG evidence of reinnervation to RF/SF FDP

Collagen

Ashley, 200648 Series

11 (5)

≤2

Brachial plexus ≤ 2

5–7

≤2

23.3 ± 4 Motor: 60% mo excellent, 20% good, 20% poor; sensory: 45%

Collagen

Wangensteen Series and Kalliainen, 201049

126 (96)

2–7 Varied: 82 dig- 1.3 1.3 (range ital, 23 other (range 0.25–2.0) 0.25–2) small caliber, 21 large caliber

Not given

256 days

Qualitative improvement, 24% 2PD improvement; not stratified for nerve type/ size

Collagen

Boeckstyns, et series al, 201350

32 (31)

36 (21– median 66)

24 mo

Equivalent to direct suture at this short gap ≤ 0.6 cm

4.2

≤ 0.6

Not given

7

* This publication includes data presented in two previous papers; duplicate data are excluded from the table. Abbreviations: 2PD, two-point discrimination; ANA, acellularized nerve allograft; APB, abductor pollicis brevis; EMG, electromyography; FDI, first dorsal interosseous; FDP, flexor digitorum profundus; PGA, polyglycolic acid; RF, ring finger; SF, small finger.

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Nerve Autograft Substitutes: Conduits and Processed Allografts Collagen conduits are effective in promoting and supporting nerve regeneration across short nerve gaps.18,19,65–67 In 1991 Archibald et al published the first study using type I collagen conduits in both rat and monkey nerve repairs. Using electrophysiological assessments, they showed that entubulation repair with a collagen-based conduit over a 4-mm distance was as effective in supporting nerve regeneration as an isograft. 19 (Because isografts between major histocompatibility complex II–compatible animals require no immunosuppression and serve as autograft equivalents, we will use the “autograft” substitution in the remainder of this chapter for clarity.) Collagen conduits were also similar to autografts in the repair of 5-mm median nerve defects in the monkey model, and both the conduit and autograft were comparable to direct suture repair. 18 In one study, Kemp et al examined the interaction between regenerating axons, Schwann cells, and neovascularization in nonpermeable (silicone) versus semipermeable conduits (type I collagen). Using a rat sciatic nerve model with 5- and 10-mm nerve gaps, they found that the collagen-based conduits demonstrated enhanced axonal regeneration and neovascularization in both nerve gap lengths compared to silicone conduits.67 Alluin et al demonstrated that the type I and III collagen tubes (RevolNerv) also supported nerve regeneration comparable to an autograft in a 10-mm nerve gap defect in a rat peroneal nerve model.65 Clinically, there have been reports of successful use of the NeuraGen conduit in repairing small nerve gap defects. In two articles, Taras et al reported the successful clinical use of NeuraGen conduits in 75 peripheral nerves, which included the median, ulnar, radial, posterior interosseous, common digital, proper digital, and superficial radial sensory.11,35 However, outcome data and the specifics of each case were not provided. Taras and colleagues did report that their repairs had no conduit rejection and that there were two cases of scar sensitivity. Currently, they are conducting a human clinical trial. In 2008 Farole and Jamal published results using the NeuraGen conduit as a nerve cuff (not conduit) for the repair of lingual and inferior alveolar nerve injuries.68 They found that eight of nine nerve repairs showed improved sensory function, which suggests a favorable role for the NeuraGen conduit as a cuff to protect the nerve at the injury site. Lohmeyer et al published a prospective cohort study involving 12 cases of NeuraGen conduit use to repair digital nerve defects with gap distances of 12.5 mm ± 3.7 mm.36 One year postoperatively, four patients demonstrated excellent sensation (s2PD < 7 mm), five good sensibility (s2PD < 15 mm), one poor (s2PD > 15 mm), and two with no return of protective sensation. Thomsen et al also found RevolNerv conduits to be effective in digital nerve repair.37 In 11 secondary nerve graft procedures following resection of posttraumatic digital neuromas with gap distances ranging from 5 to 20 mm, 4 demonstrated excellent sensation (s2PD < 6 mm), 1 good (s2PD 6–10 mm), 5 fair (s2PD 11–15 mm), and 1 poor (s2PD > 15 mm). Finally, Wangensteen and Kalliainen published a large retrospective case series evaluating NeuraGen conduit repair of a variety of nerves, including 82 digital nerves, 23 nondigital small-caliber (2–4 mm diameter) nerves, and 21 large-caliber (≥ 5 mm diameter) nerves.49 Because of the retrospective nature of the study, the defect

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length was recorded in only 26 of the cases (mean 13 mm, range 2.5–20.0 mm), and only 26 of the cases involved in the study had quantitative testing of nerve recovery documented in their charts. Of these, Semmes-Weinstein monofilament testing was performed on 6, and 67% demonstrated improvement; two-point sensory examination was performed on 17, with 24% improvement; and electromyography was performed on 3, with 33% improvement. Unfortunately, the results did not distinguish between digital, small-, and large-caliber nerves, so whether the NeuraGen conduits were successful in permitting regeneration of large-diameter, mixed composition nerves is unclear. Biodegradable conduits have pushed forward as the leader in conduit nerve repairs, because, unlike nonabsorbable materials such as silicone, they allow greater interaction with the surrounding environment and reduce axonal compression.17,62 More importantly, studies using silicone conduits have reported a high rate of reoperation to remove the foreign body secondary to nerve compression and irritation.69–71 Biologic and biodegradable conduits avoid this complication.

7.4 Direct Comparisons of Conduits To date, there have been no clinical reports directly comparing commercially available nerve conduits. However, there have been a few animal studies. As mentioned above, Kemp et al compared the use of silicone conduits versus type I collagen conduits in the repair of rat sciatic nerves. They found the semipermeable collagen conduit to enhance peripheral nerve regeneration in comparison to the nonpermeable silicone conduit. 67 Another comparative study has been published by Waitayawinyu et al, which compared type I collagen conduits to PGA conduits using a rat sciatic nerve with a 10-mm gap defect.72 They reported that type I collagen conduits yielded statistically greater isometric muscle contraction force, axonal counts, and wet muscle weights in comparison to the PGA conduit group. They also concluded that the collagen conduits are not statistically different from autograft (positive) controls. More recently, a study comparing commercially available conduits was performed. Using isometric motor testing of the tibialis anterior muscle, Shin et al compared the results of three commercially available nerve conduits used to repair a 10-mm defect in a rat sciatic nerve model.73 They had four experimental groups: autograft (positive control), poly(DL-lactide-ε-caprolactone) tube (Neurolac, Ascension Orthopedics Inc., Austin, TX), type 1 collagen tube (NeuraGen, Integra Life Sciences), and PGA tube (GEM Neurotube, Synovis Micro Companies Alliance) groups. At 12 weeks following repair, muscle force testing was performed. Shin et al found that the Neurolac tube was not significantly different from the autograft control group and that both of these groups were significantly superior to the NeuraGen and Neurotube groups. They also reported that the Neurotube demonstrated the worst motor recovery, yet the significance was not discussed with regard to its comparison with the NeuraGen group.

Nerve Autograft Substitutes: Conduits and Processed Allografts Although the results of the studies by Waitayawinyu et al 72 and Shin et al73 appear to show a hierarchy in the efficacy of commercially available conduits, it is important to acknowledge some concerns with the given data. First, both studies used different size conduit diameters between groups. NeuraGen and Neuralac conduits are available in smaller diameters more appropriate for a rat sciatic nerve repair, such as 1.5-mm inner diameter, whereas the smallest available inner diameter of the PGA nerve conduit is 2.3 mm. This volume discrepancy is critical and readily explains the inferior results of the Neurotube group (see Expanding the Indications of Nerve Substitute Use section for further discussion of conduit volume). Second, the studies lacked a negative control group. Ideally, to prove significance and to make clinical applications, studies should contain both positive and negative control groups. A third confounder jeopardizing the validity of the Waitayawinyu et al study is that they examined their histologic outcome measure at the late time point of 15 weeks. Because of the superlative regenerative power of the rat, in order to recognize true differences among experimental groups, the timing of outcome measurements is critical.74 Clinical correlation can only be made with earlier time points when both positive and negative control groups are still significantly different. Evaluating histology at late time points may show experimental groups to be equivalent due to the “blow-through” effect, in which the superlative rodent regenerative capacity masks true differences among groups.74 Although we are criticizing these studies for inappropriate timing, careful selection of time points is a new paradigm shift. We can also criticize many of our own early studies for inaccurate timing. Previously, it had been thought that the longer the follow-up, the better. However, this simply is not the case when extrapolating rodent data for clinical use using histomorphometry as the outcome measurement. Functional walking track measurement, such as the sciatic function index, however, never recovers to normal in the rodent model following neurotmetic (transection repair or graft) injury. Going forward, we must recognize that future studies need to be performed with strict timing methodology to truly determine the hierarchy of available conduits. Only then can the findings in animal studies be accurately translated to clinical use.

7.5 Acellularized Nerve Allografts ANAs are a promising substitute for nerve autografts, as they are available in great abundance and offer the potential for size/ length and motor/sensory specificity. They were developed out of a desire to take advantage of the regenerative successes of allogeneic nerve tissue (allografts) while preventing the negative effects of the grafts’ inherent immunogenicity. Freshly transplanted nerve allografts have been shown to be as effective as autologous nerve grafts,7,75–77 as they contain both viable donor Schwann cells and endoneurial microstructure that provides the same level of regenerative support. 7,74,76–79 Fresh allografts are complicated by the need for systemic immunosuppression during the period of host axonal regeneration and is typically administered until 6 months after nerve regeneration distal to the interposed graft is observed.7 Unfortunately, immunosup-

pression predisposes graft recipients to opportunistic infections, neoplasia, and toxicity-induced side effects. 80,81 Decellularization techniques were developed to allow the allografts to retain their extracellular matrix components while removing their immunogenic cellular components, especially the highly antigenic Schwann cells. Several techniques exist, including detergent processing, radiation, freeze-thawing, and extended storage in cold University of Wisconsin solution (cold preservation).82–91 ANAs may offer several advantages over hollow, synthetic nerve conduits.41 First, they preserve the three-dimensional scaffolding and endoneurial architecture present within native nerve;87,92,93 this three-dimensional architecture promotes cell migration and nerve fiber elongation but is absent within hollow conduits. Second, ANAs maintain collagen and laminin within their extracellular matrix. These components of the neural basal lamina play an important role in axonal outgrowth. 94 Third, removal of chondroitin sulfate proteoglycans (CSPGs) during processing may promote accelerated regeneration, as CSPGs have been shown to inhibit axonal growth and to be initially upregulated following peripheral nerve injury.95–97 The only FDA-approved, clinically available ANA is the Avance nerve graft by Axogen, Inc. (Alachua, FL). The Avance ANA is produced through a proprietary protocol for processing cadaveric nerve involving a combination of detergent decellularization, chondroitinase CSPG degradation, and gamma-irradiation sterilization. In a rat sciatic nerve gap model, Whitlock et al compared the effectiveness of the Avance ANA (using rat-derived nerve processed via Axogen’s Avance proprietary protocol to avoid the confounder of xenografting) with the Integra NeuraGen collagen conduit for promoting regeneration across 14and 28-mm nerve gaps (▶ Fig. 7.1).98 Avance ANAs were superior to NeuraGen conduits but inferior to autograft controls in the 14-mm gap evaluated 6 weeks postoperatively (▶ Fig. 7.1a). At this shorter gap length, Avance ANAs resulted in more consistent regeneration into the midgraft (7/8 animals versus 4/10 animals in the conduit group) and approximately 20 times more myelinated fibers present in the nerve distal to the graft. At the longer 28-mm gap length, autografts were again superior to Avance ANAs, which were superior to NeuraGen conduits (▶ Fig. 7.1c,d). Although Avance ANAs resulted in only onequarter of the regeneration seen in autografts, they were far superior to NeuraGen conduits, resulting in 26 times more myelinated nerve fibers distal to the graft. Of note, the differences between groups became less apparent when the 14-mm short gap model was followed out to 12 weeks. At the longer 28 mm length, significant differences persisted even at 22 weeks (▶ Fig. 7.1b). A recent rat hind limb study by Moore et al99 compared three established models of acellularized nerve grafts (cold preservation, detergent processed, and Avance processed nerve grafts) to silicone nerve conduits using histomorphometry and functional muscle testing.99 Silicone conduits were used, because collagen conduits were no longer available to our lab. Silicone conduits longer than 10 mm have been demonstrated to prevent nerve regeneration and therefore were used as a strong negative control.

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175

Nerve Autograft Substitutes: Conduits and Processed Allografts

7

Fig. 7.1 Histomorphometric findings of processed allografts and collagen conduits for repair of peripheral nerve gaps in a rat model. (a,b) The experimental model of this study assessed nerve regeneration for 14-mm graft at 6 and 12 weeks, (c,d) while a 28-mm graft was assessed at 6 and 22 weeks. Levels of significance: * p < 0.05, ** p < 0.01, *** p < 0.001, NS, not significant (p > 0.05), according to Tukey’s or Mann–Whitney rank sum tests, as described in the text. Error bars represent standard deviation for the group. (Adapted with permission from Whitlock EL, Tuffaha SH, Luciano JP, et al. Processed allografts and type I collagen conduits for repair of peripheral nerve gaps. Muscle Nerve 2009;39(6):787–799.)

The detergent-processed allografts were equivalent to autografts in support of axonal regeneration across a 14-mm nerve gap at 6 weeks postoperatively, while the Avance processed and cold-preserved allografts supported significantly fewer regenerating nerve fibers. All acellular grafts had superior regeneration in comparison to silicone nerve conduits, the negative control (▶ Fig. 7.2). Measurement of muscle force confirmed that detergent-processed allografts promoted autograft-equivalent levels of motor recovery 16 weeks postoperatively. Avance processed and cold-preserved allografts promoted less motor recovery compared to autografts but significantly greater recovery than silicone conduits (▶ Fig. 7.3). Thus, they concluded that a hierarchy of ANAs exists, but ANAs are significantly more effective in promoting nerve regeneration and functional recovery than silicone conduits. This study gives evidence for the effective use of ANAs in short nerve gap injuries. For use in humans, Avance grafts are available in diameters between 1 and 5 mm and lengths between 15 and 50 mm, or up to 70 mm by special order. There are only a few published

176

reports assessing Avance ANAs in human nerve repair.27,100 The results from the ongoing clinical trial based on the RANGER (Registry of Avance Nerve Graft Evaluating utilization and outcomes for the Reconstruction of peripheral nerve discontinuities) registry, show significant functional return on par with autograft repairs. This study is the first multicenter clinical evaluation of processed nerve allografts. In the most recent published update of the trial, 71 cases of nerve repair with Avance nerve graft were reported: mean nerve injury gap length was 23 ± 12 mm and the majority of repairs were to digital nerves (48/71) and the next most common injured nerve was the median nerve (10/71). Meaningful recovery, defined as S3–4 and/or M3-M5 was achieved in 87% of cases. As the gap length increased, the percentage achieving meaningful recovery decreased. Karabekmez et al evaluated early clinical outcomes following Avance graft repair of 10 sensory nerve gaps in the hands of 7 patients.41 The mean graft length was 2.23 cm (range 0.5–3.0 cm) in eight digital and two dorsal sensory nerves. Five repairs achieved excellent function (s2PD ≤ 6 mm or m2PD [moving

Nerve Autograft Substitutes: Conduits and Processed Allografts

7

Fig. 7.2 Histomorphometric analysis of axonal regeneration for different types of processing of acellularized nerve allografts. Fiber counts demonstrate significantly greater numbers of nerve fibers distal to implanted isografts and detergent-processed allografts than AxoGen-processed and cold-preserved allografts. Representative histologic sections demonstrate populations of axons successfully regenerating through fresh nerve isografts, processed nerve allografts, and nerve guidance conduits 6 weeks postoperatively. Sections acquired 3 to 5 mm distal to implanted nerve isografts and detergent-processed allografts show numerous myelinated axons loosely organized into regenerating units. Sections acquired distal to AxoGen-processed nerve allografts and cold-preserved nerve allografts show few myelinated axons successfully innervating the host nerve distal to the repair site. Host nerve tissue distal to implanted nerve guidance conduits demonstrates no healthy, myelinated axons. (Adapted with permission from Moore AM, et al. Acellular nerve allografts in peripheral nerve regeneration: a comparative study. Muscle Nerve 2011;44(2):221-234.)

two-point discrimination] ≤ 3 mm), five good function (s2PD 7– 15 mm or m2PD 4–7 mm), and none poor function (absence of either stating or moving discrimination). By the end of study (mean follow-up time 9 months), the average s2PD was 5.5 mm and m2PD, 4.4 mm. This was the first study to demonstrate clinical efficacy in humans for ANA repair of sensory nerve gaps up to 3 cm in the hand.

Recently, Shanti and Ziccardi published a case report describing the use of an Avance ANA to repair a gap in the inferior alveolar nerve.42 The patient had developed numbness of the left lip and chin after undergoing extraction of the left mandibular first molar and immediate allogeneic bone grafting for socket preservation. Upon exploration 8 months postinjury, the inferior alveolar nerve was found to be transected with its proximal

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Nerve Autograft Substitutes: Conduits and Processed Allografts

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Fig. 7.3 Muscle force testing of axonal regeneration through different types of processing of acelluarlized nerve allografts. Evoked muscle force measurements reveal differential motor recovery in distal musculature 16 weeks after implantation of fresh nerve isografts, processed nerve allografts, and nerve guidance conduits. (a) Measurements of maximum isometric force production in EDL muscle innervated by repaired sciatic nerve demonstrate the AxoGen-processed nerve allografts and cold-preserved nerve allografts support significantly lower degrees of motor recovery compared to fresh nerve isografts. In comparison, silicone nerve guidance conduits did not support any functional motor recovery in distal musculature. (b) Assessment of EDL muscle mass shows that muscles innervated by sciatic nerves repaired with either processed nerve allografts experienced similar degrees of atrophy. EDL muscles innervated by sciatic nerves repaired with AxoGen-processed nerve allografts did exhibit greater degrees of atrophy, though results were not statistically significant. (c) Calculation of maximum specific force production in reinnervated EDL muscle reveals that, upon correction for differences in muscle atrophy, AxoGen-processed nerve allografts and cold-preserved nerve allografts still support significantly lower degrees of motor recovery compared to fresh nerve isografts. Data represent the mean ± standard deviation; * indicates statistical significance (p < 0.05) compared to nerve isograft. (Adapted with permission from Moore AM, et al. Acellular nerve allografts in peripheral nerve regeneration: a comparative study. Muscle Nerve 2011;44(2):221-234.)

and distal ends retracted, preventing primary repair. A 3- to 4mm diameter Avance graft was used to bridge the nerve gap. By 5 months postoperatively, the patient reported tingling and itching in the affected chin and had improvement in her sensory exam (to an S3 + level of the British Medical Research Council Nerve Injury Committee Classification Scheme—superficial cutaneous pain, tactile sensibility, and some 2PD). Although this study does not provide long-term results or comparison to patients undergoing autograft or conduit repair, it does provide an example of the recently expanded use of ANAs in nerve reconstruction. Certainly, additional studies, both clinical and experimental, are needed to delineate the indications for and limitations to the use of ANAs for nerve gap repair. We expect that, like conduits, there will be a limit (i.e., a finite graft length) to the ability of ANAs to support regeneration. Although ANAs have endoneurial architecture that hollow conduits lack, they do not

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contain the Schwann cells and endogenous growth factors present in autografts. Therefore, until further studies demonstrate the equivalency of ANAs for the repair of longer gaps or of defects in critical nerves, we feel it is prudent to continue to use the gold standard nerve autograft for repair of critical nerves and to use ANAs for defects in noncritical sensory nerves up to 3 cm.41 To begin the address of inconsistent regenerative outcomes between long ANAs and autografts, Saheb-Al-Zamani et al 101 generated a rat model with nerve defects up to 60 mm in the rat sciatic nerve repaired with long nerve grafts (both isografts and ANAs) (▶ Fig. 7.4a). Evaluation of regeneration using these long nerve grafts revealed diminishing nerve regeneration as the length of the nerve graft increased. Isografts consistently demonstrated axonal regeneration into the distal nerve stump by 10 and 20 weeks while the ANAs demonstrated decreased regeneration as a function of increasing graft length (▶ Fig. 7.4b,c).

Nerve Autograft Substitutes: Conduits and Processed Allografts

7

Fig. 7.4 Images of long gap peripheral nerve injury model in the rat. (a) Two 30-mm sciatic nerve grafts are sutured end-to-end to create a 60-mm graft (P, proximal; D, distal). The two nerve pieces were coapted together in a proximal-distal end to end fashion to form a graft of up to 60 mm. The coapted donor was then trimmed to the desired length and implanted under the skin. Arrows indicate suture lines. (b) Histomorphometric analysis of regenerating nerve fibers demonstrated decreased axonal regeneration with increased graft lengths in both graft groups. The total number of myelinated nerve fibers was quantified at 10 weeks (b) and 20 weeks (c) after reconstruction. At both time points, isografts (ISO) demonstrated superior regeneration in comparison to ANAs at all lengths. (Error bars are standard deviation, * indicated p < 0.05 vs. isograft). (Adapted with permission from Saheb-Al-Zamani M, Yan Y, Farber SJ, et al. Limited regeneration in long acellular nerve allografts is associated with increased Schwann cell senescence. Experimental Neurology 2013;247:165-77.)

Functional recovery of the EDL muscle (innervated by the common peroneal branch of the sciatic) was consistent with the histological data with measurable recovery in all of the isograft groups and no recovery in the 60-mm ANA. Further investigation into the regenerative results of these variable length grafts revealed that isografts consistently promoted axonal regeneration into the distal nerve while ANA had unpredictable results. Although the number of regenerating axons decreased with graft length, all animals treated with isografts supported axonal regeneration into the distal nerve stump at all graft lengths. In contrast, the ANA failed to consistently support axonal regeneration through graft lengths beyond 20 mm. Of the sixteen animals provided 40 mm ANAs, four animals (25%) demonstrated no axonal regeneration (regenerative failure) into the distal stump. Of the fourteen animals provided 60 mm ANAs, thirteen animals (> 90%) demonstrated no axonal regeneration in the distal stump. These results suggest a regenerative limit to ANAs between 40 and 60 mm in length and overall inconsistent regeneration results for ANAs.

Using the Thy1-GFP transgenic rat (neurons and their axons express GFP), Saheb-Al-Zamani et al101 also evaluated the differential progress of axonal regeneration in ANAs and isografts of variable lengths (▶ Fig. 7.5). Isografts showed substantial regeneration of GFP + axons beyond the distal coaptation for 20- and 40-mm grafts. The 60mm isograft showed diminished axonal regeneration across the graft and up to the point of distal coaptation with limited growth into the distal nerve. In contrast to the isograft, only the 20-mm ANA demonstrated substantial axonal regeneration up to and into the distal nerve. The 40-mm ANA demonstrated regeneration to the middle of the graft (~ 20 mm of growth) but in the 60-mm ANA, regenerating axons only regenerated ~ 10 mm into the graft. These qualitative results suggests that regenerative failure in long grafts is more than an issue of chronic denervation developed in the grafts, as axons failed to extend to similar distances as graft length increased. To begin to understand a mechanism that may cause this axonal arrest, these graft tissues were harvested after the 10 weeks

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Nerve Autograft Substitutes: Conduits and Processed Allografts

7

Fig. 7.5 Images of nerve regeneration visualized in the Thy1-GFP rat reveal axonal arrest within the ANA when nerve regeneration fails. (a) Thy1-GFP rats express green fluorescent protein (GFP) in their axons allowing for visualization of the regenerated axons in grafts after 10 weeks. A strong inverse relationship between the axonal regeneration and the length of ANA was observed. Both 20-mm isografts (b) and ANAs (e) were able to support axonal regeneration through the length of the graft. When the graft length was increased to 40 mm, axonal regeneration was hindered in ANAs (f) but not isografts (c); this difference in extent of regeneration was even more pronounced at 60 mm (d,g). Of note, the axons regenerated a shorter distance in the 60-mm ANA (g) than in the 40-mm ANA (f). (Adapted with permission from Saheb-Al-Zamani M, Yan Y, Farber SJ, et al. Limited regeneration in long acellular nerve allografts is associated with increased Schwann cell senescence. Experimental Neurology 2013;247:165-77.)

of potential regeneration and probed for molecular markers of apoptosis and cellular senescence. 101 Axonal arrest within ANAs corresponded with a unique expression of cellular senescence markers (SA-βgal, p16INK4A, and IL-6) within the grafts including SCs. As nerve regeneration is dependent on SCs creating a positive regenerative environment, an accumulation of senescent SCs has intriguing implications. Senescent cells commonly develop a unique profile of protein expression, the senescent associated-secretory profile or phenotype (SASP), which affects inflammatory and regenerative processes.102,103 One hypothesis could be that senescent SCs develop a SASP that alters the regenerative environment reducing pro-regenerative or increasing inhibitory axonal growth cues. Further research with regard to this area would be of fundamental importance toward understanding the mechanisms of regenerative failure in long or large ANAs and developing therapies.

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7.6 Expanding the Indications of Nerve Substitute Use Because of the success of conduit repairs of short gap lengths in small-diameter nerves, particularly digital nerves (diameter ~ 1 mm), clinicians are beginning to push the limits of conduit use to include the repairs of larger caliber nerve gap lengths in more critical nerves, such as the median and ulnar nerves (diameter ~ 4–7 mm). Unfortunately, clinical failures from expanding the indications for conduit use are now beginning to arise. Moore et al published a clinical series of four patients who had conduit failures.104 One patient had a lacerated median nerve repaired with a NeuraGen conduit (7 mm [diameter] × 2 cm [length]) (▶ Fig. 7.6). Two children with obstetric brachial plexus palsy were repaired with NeuraGen tubes. One child’s C5–C6 roots were coapted using the type I collagen conduit

Nerve Autograft Substitutes: Conduits and Processed Allografts

7 Fig. 7.6 The patient presented 4 years after right median nerve repair with a failed collagen conduit. Histology of the surgical specimen reveals dense fibrinous scar tissue and lack of nerve structures in the section of the distal conduit. The middle conduit shows significant disorganized architecture with no axonal organization, consistent with neuroma. The proximal nerve shows normal architecture. (Adapted with permission from Moore AM, Kasukurthi R, Magill CK, Farhadi HF, Borschel GH, Mackinnon SE. Limitations of conduits in peripheral nerve repairs. Hand (NY) 2009;4(2):180–186.)

(7 mm × 3 cm). In the other child, two conduits (4 mm × 3 cm) were used from the C5 root to the upper and lower trunks, and another (4 mm × 3 cm) was used from the C6 root to the lower trunk. A fourth patient had his ulnar nerve repaired with a GEM Neurotube (4 mm × 2 cm) (▶ Fig. 7.7). All four of these patients required further interventions for poor outcomes, although one child’s parents chose to not have further surgery. Six other patients with conduit and wrap failures have approached our practice following the clinical series by Moore et al. One patient had a complete ulnar nerve laceration at the elbow that was repaired with two 6-mm-in-length collagen conduits (▶ Fig. 7.8). The second patient had an ulnar nerve laceration at the wrist that was repaired with a collagen wrap (7 mm [diameter] × 2 cm [length]) (▶ Fig. 7.9). The third patient had a granular cell tumor removed from the ulnar nerve, specifically, the deep motor branch, and was repaired with a nerve wrap (▶ Fig. 7.10). The fourth patient had a lacerating injury to the ulnar nerve that was repaired with a collagen conduit (▶ Fig. 7.11). The fifth patient had a gunshot injury to the median nerve that was repaired with a nerve wrap (▶ Fig. 7.12). The sixth patient had an iatrogenic injury to the sensory component of the median nerve following a carpal tunnel release. This was wrapped with a NeuraWrap (▶ Fig. 7.13). All six patients required further interventions for poor outcomes. Not surprisingly, these cases have sparked interest in why these conduit and wrap repairs failed and have led to reevaluating the clinical indications for them. The conduit failures in these patients could have been the result of technical factors, such as failure to properly secure the conduits and the lack of full resection of damaged nerve prior to conduit placement. However, these conduits failed most

likely because they were used in large diameter nerves over excessively long distances. These defects exceeded the critical volume of regeneration capable for a nerve conduit. Although further studies are needed to establish the critical volume of regeneration, the basic equation for volume of a cylinder, V = πr2L, where V= volume, r = radius, and L = length, dictates that if the radius is doubled (i.e., increased diameter of the nerve), the overall volume is quadrupled (▶ Fig. 7.14). Volume becomes important when considering neurotropism. Neurotropism is the concept that the proximal sprouting axons regenerate along a concentration gradient of neurotrophic factors released into the gap by the distal stump. As the volume of a conduit becomes larger, there may be an associated decrease in or dilution of the concentration of neurotrophic factors. Thus, the regenerating axons have less tropic and trophic support to reach the distal nerve stump. Although the concept of volume-limiting nerve regeneration is not novel, it is also not widely recognized. Conduit volume and length were first described as influential factors in nerve regeneration by Lundborg et al in 1982, when they determined the critical gap length of regeneration across a silicone conduit in a rat.16 They found that the distal stump contribution to regeneration was limited by the length (or volume) of the chamber, suggesting that humoral factors from the distal stump were critical. It was later established that the fluid secreted by the nerve stumps into the conduit promoted neurite outgrowth. 13, 105 Because critical gap lengths and volumes of empty conduits are known to exist in rat models, it would make sense that limitations of conduit volumes exist in humans as well. Further studies are needed to determine the exact numbers of these critical parameters. Unfortunately, this is hard to accomplish in animal models because, with the exception of the rarely

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Fig. 7.7 The patient presented 9 months after right ulnar nerve repair with a failed polyglycolic acid (PGA) conduit (2 cm length, 0.7 cm diameter). Histology of the surgical specimen reveals dense fibrinous scar tissue and lack of nerve structures in the section of the distal conduit. The proximal conduit section shows significant disorganized architecture with no axonal organization, consistent with neuroma. No regeneration was seen through the conduit. Proximally, normal nerve architecture is demonstrated. (Adapted with permission from Moore AM, Kasukurthi R, Magill CK, Farhadi HF, Borschel GH, Mackinnon SE. Limitations of conduits in peripheral nerve repairs. Hand (NY) 2009;4(2):180–186.)

used porcine sciatic nerve model, it is difficult to simulate the large diameter of human nerves even in “large” animal models. The concept of Schwann cell senescence also would be relevant with large volume ANAs as discussed by SahebAl-Zamani.101 Although not common, a few clinical cases reporting the successful use of conduits in large-diameter nerves exist. Lundborg et al reported successful median and ulnar nerve repairs over short distances (2–3 mm) with silicone conduits.69,71 At 5 years’ follow-up, they concluded that conduit repair of the median and ulnar nerves resulted in functional outcomes similar to direct suture repair and that the patients treated with tubular repair actually had less cold intolerance. Of note, 8 of the 17 silicone tubes were subsequently removed due to “slight local problems”; upon reexposure, the nerves showed no external or microscopic signs of nerve compression or inflammation. 71 In 2007 Donoghoe et al published two cases in which they repaired the median nerve with 3-cm GEM Neurotube conduits, using four separate 2.3-mm-diameter conduits in cable formation. 44 Both patients recovered s2PD < 6 mm and abductor pollicus brevis function. More commonly, manipulations of conduits have been performed to achieve successful results in larger diameter or longer gap nerve repairs. For example, Hung and Dellon reported the successful repair of a 4-cm human median nerve defect with the use of the GEM Neurotube conduit. The authors augmented the long repair by including a slice of autogenous nerve within the conduit.46 Previous studies have shown that the addition of nerve tissue can enhance nerve regeneration in rodent models over greater distances.106,107 This phenomenon has also been reported to enhance vein conduits in the repairs of longer gaps

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and in larger nerve diameters.108–110 However, the functional results of these vein conduit studies can be criticized as less than adequate,108–111 likely due to the thin-walled nature of veins that are subject to collapse from surrounding tissue. Because of the lack of clinical and experimental evidence of conduit use in large-diameter nerve defects, further research is needed.

7.7 Future Directions There is considerable interest in expanding conduit “indications” to enhance regeneration across longer nerve gap distances and to improve functional outcomes of larger, more critical motor nerves. In the past decade, beyond the study of different conduit materials, basic science research has investigated the addition of neurotrophic factors, Schwann cells, and other matrix molecules to conduits to enhance nerve regeneration. 10,112 Despite the investment in enhancing conduits to the level of autografts, these engineering strategies have yet to be used clinically. Future advances in nerve conduits to treat larger nerve gaps will likely involve the incorporation of Schwann cells. A major breakthrough in peripheral nerve research would be the creation of a completely nonimmunogenic “off the shelf” nerve substitute containing not only three-dimensional internal architecture, but also Schwann cell and growth factor support; this substitute would theoretically provide regenerative capacity equal to that of an autograft. In the native nerve, Schwann cells replicate after nerve injury and form longitudinally oriented strands called bands of Büngner to assist and direct axonal regeneration.14,113,114 Leitz et al showed that

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Fig. 7.8 Failed nerve conduit case: the patient presented with a 5-year-old ulnar nerve laceration at the right elbow that was repaired with two collagen conduits. (a) At our institution’s revision surgery, the ulnar nerve was noted in the transposed position with a large green suture. A neuroma of the medial antebrachial cutaneous nerve is apparent. (b) There was little continuity between the proximal and distal ends of the injured ulnar nerve. (c) Histologic assessment revealed scarce and almost no nerve fibers within the ulnar nerve distal to the conduit. (d) Within the conduit, scarce nerve and almost no nerve fibers were seen. (e) Proximal to the conduit, normal nerve fibers were found. Original magnification: 400x. (f,g) Reconstruction of failed ulnar nerve repair for pain included distal sensory nerve transfers, specifically the third web space fascicle-to-sensory component of the ulnar nerve transfer for critical sensation. Noncritical sensation was restored via end-to-side nerve transfer, which included the distal third web space fascicle and dorsal cutaneous branch of the ulnar nerve. (h) The injured segment of the ulnar nerve was removed. The distal end of the proximal ulnar nerve was cauterized, proximally crushed several times, and transposed intermuscularly.

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Fig. 7.9 Failed nerve wrap case: the patient presented with left ulnar nerve laceration repair with collagen wrap 5 months postoperatively. (a) Upon exposure, the ulnar nerve was incorporated in the nerve repair, while the deep motor branch was not included in the repair. (b) No regeneration was expected in the histology of the deep motor branch. Magnification: 400x. (c) The divided distal segment of the nerve wrap revealed scarce, small unmyelinated nerve fibers (sensory fibers). (d) The middle segment revealed nerve fibers sprouting in various directions, giving an uneven appearance to the section. In addition, dense scar formation was seen. (e) The proximal segment revealed healthy nerve fibers. Magnification: 250x. (f) The nerve wrap and the zone of injury were resected to reveal the distal deep motor branch and the sensory branches of the ulnar nerve. Proximally, the sensory component and the motor component were topographically mapped. Note the persistent presence of the wrap around the nerve. (g) The motor component of the ulnar nerve was grafted to the deep motor branch with one medial antebrachial cutaneous (MABC) graft. The sensory component of the ulnar nerve was grafted to the two sensory branches with two MABC nerve grafts. Three 6-cm MABC nerve grafts were used in total.

Schwann cells can be induced to form bands of Büngner for axonal regeneration, if seeded onto resorbable polymer filaments that have longitudinal grooves a few micrometers in width.14,115 Furthermore, recent studies have examined the manipulation of Schwann cells to enhance their contribution to nerve regeneration, such as genetically modifying Schwann

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cells to increase their motility116 or overproduce specific neurotrophic factors.117 Animal studies have shown that the addition of Schwann cells enhances nerve regeneration through nerve conduits.112,118–123 Some animal studies have demonstrated that the addition of cultured autologous Schwann cells enhanced

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Fig. 7.10 Failed nerve wrap case: the patient presented with right ulnar motor nerve repair with a nerve wrap following granular cell tumor removal 2 months postoperatively. (a) Upon exposure, the motor component of the ulnar nerve was identified and involved in the previous repair. The sensory component of the ulnar nerve was protected. (b) The distal segment of the nerve wrap revealed scarce, small unmyelinated nerve fibers (sensory fibers). (c) The middle segment revealed nerve fibers sprouting in various directions, giving an uneven appearance to the section. In addition, dense scar formation was seen. (d) The proximal segment revealed healthy nerve fibers. Magnification: 250x. (e) Following resection of the motor component of the ulnar nerve, the gracilis branch of the obturator nerve was harvested as a motor graft. (f) The motor autograft was used to reconstruct the motor component of the ulnar nerve.

regeneration through ANAs, even to a level approaching that of autografts.124,125 In the clinical realm, the ability to harvest human Schwann cells from biopsies and expand them in vitro has already been established, but it has not yet been put into practice.126 This is likely due to the difficulty of isolation, expansion, and purification of primary Schwann

cells. Additionally, the harvest of autologous Schwann cells requires nerve biopsy, risking permanent numbness, neuroma formation, and/or intractable pain. The focus of recent research, therefore, seems to be shifting toward the substitution of Schwann cell–like cells for autologous primary Schwann cells.

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Fig. 7.11 Failed nerve conduit case: the patient presented with right ulnar nerve repair with a collagen conduit 6 months postoperatively. (a) The ulnar nerve was identified and decompressed through the Guyon canal. (b) Proximally, the previous repair was identified. (c) Histologic evaluation revealed no nerve fibers distal to the nerve conduit. (d) In the middle of the conduit, histologic assessment revealed no regenerative nerve fibers. (e) Proximal to the nerve conduit, many myelinated nerve fibers were visible. (f) The area of injury and previous reconstruction were identified and resected. (g) Three cables of the medial antebrachial cutaneous nerve (MABC), each 5 cm in length, were used to bridge the nerve gap. (h) The MABC cable graft was inset with care to make sure that the proximal motor fascicular group was grafted to the distal motor fascicular group, and the proximal sensory fascicular group was grafted to the distal sensory fascicular group.

Bone marrow stromal cells,127–129 skin-derived precursor cells,130 and adipose-derived stem cells131,132 have all shown the ability to be induced into a Schwann cell–like phenotype in culture and to improve regeneration through ANAs. A compre-

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hensive comparison of the Schwann cell-like cells from these three different sources, against each other and against primary Schwann cells, has yet to be performed but would be useful in determining a front-runner for future studies. Of course, the

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Fig. 7.12 Failed nerve wrap case: the patient presented with left median nerve repair with a nerve wrap 1 year postoperatively. (a) The median nerve was exposed, and a tight wrap was identified surrounding the nerve. (b) The wrap was divided and note it is still present or, at least, a connective “shell” or “rind” is still present at one year. (c) The ulnar nerve was identified to have been previously repaired with apparent sutures. (d) Histologic evaluation revealed healthy nerve fibers in the proximal segment. (e) In the middle segment, the nerve fibers were seen sprouting in various directions, giving an uneven appearance in the section. (f) The distal segment revealed scarce nerve fibers. (g) Reconstruction included resection of the neuroma and identification of the appropriate fascicular motor and sensory components in the median nerve. (h) The gap was reconstructed with three cable grafts originating from the third web space fascicle of the median nerve. (i) Distally, an end-to-side transfer was performed to restore rudimentary sensation to the third web space.

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Fig. 7.13 Failed nerve wrap case: the patient presented with a right median nerve injury following a carpal tunnel release that repaired with a nerve wrap 2 years postoperatively. The sensory component of the median nerve was injured and repaired with a nerve wrap. (a) Upon exposure, the median nerve was identified with a large neuroma. (b) Histologic evaluation revealed scarce nerve fibers in the distal segment. (c) The middle segment displayed significant disorganized architecture with no axonal organization, consistent with neuroma. (d) The proximal segment revealed healthy nerve fibers. (e) The neuroma was resected, and the motor and sensory components of the median nerve were identified. (f) The gap was reconstructed with several medial antebrachial cutaneous nerve cable grafts with an individual graft for repair of the motor component.

morbidity of harvest would need to be considered in the clinical setting, as bone marrow harvest is a more complicated and morbid procedure than skin biopsy or small-volume liposuction. A final consideration in advancing this field will be optimizing and standardizing the cell-seeding technique as well.133 In the future we may see conduits of ANAs being used clinically with the addition of autologous cultured Schwann cells or Schwann cell–like cells, perhaps finally achieving an autograft equivalent.

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7.8 Conclusion: Recommendations for Conduit and ANA Use Clinical and basic science research has established the indications for conduit and ANA use in peripheral nerve repairs, and successful regeneration through these autograft alternatives is achievable. However, we strongly feel that, until a larger body of data exists regarding expanding their use, conduits and

Nerve Autograft Substitutes: Conduits and Processed Allografts

Fig. 7.14 The importance of conduit volume for repair of various large-diameter nerves. The figure illustrates the importance of diameter in determining the overall volume of a nerve gap. Conduits A and B are of equal volume. Doubling the radius in conduit B gives a total volume equal to that of conduit A with only one-fourth the length, according to the equation V = πr2L. (Used with permission from Moore AM, Kasukurthi R, Magill CK, Farhadi HF, Borschel GH, Mackinnon SE. Limitations of conduits in peripheral nerve repairs. Hand (NY) 2009;4(2):180–186.)

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Fig. 7.15 Differences exist in the internal architecture of motor and sensory nerves. The endoneurial tubes of a motor nerve (a) and larger compared to a sensory nerve (b). Flourescent laminin stain, 60x magnification, 10 μm bar.

ANAs should be used only to bridge gaps < 3 cm in small, noncritical sensory nerves and that autografts should be used for anything larger, longer, or critical in nature. It is perhaps telling that a recent article comparing nerve repair to conduit repair used very short (≤ 0.6 cm) collagen conduits and reported satisfactory results at this very short length for forearm nerve reconstruction.50 When provided equal access to motor and sensory pathways, injured motor neurons preferentially regenerate down motor pathways—a phenomenon termed preferential motor reinnervation.134 Our laboratory has shown that motor nerve grafts, with their larger endoneurial tubes, enhance axonal regeneration compared to the sensory grafts for grafting of peripheral mixed nerves.107,135–138 Although a single short communication recently failed to show this regenerative advantage,139 we still would preferentially use ANAs derived from motor nerves if available (although they currently are not) for grafting mixed nerve gaps when autografts are not a feasible option (▶ Fig. 7.15).

Furthermore, experimental studies have shown conclusively that the addition of a small piece of nerve or minced nerve into an empty conduit enhances nerve regeneration; therefore, we recommend this technique whenever a nerve conduit is used.106,107,140 The proximal portion of the nerve will contain healthy viable Schwann cells, whereas the distal portion of the nerve has gradual loss of Schwann cells when axotomized following injury. After the surgeon has “freshened up” the proximal and distal nerve ends, we recommend using another sliver of nerve from the proximal end, mincing this into tiny particles containing viable Schwann cells, and adding the minced nerve to the conduit. Finally, care should be taken to make sure there is no blood or blood products within the conduit, as this will inhibit nerve regeneration.

7.9 References [1] Millesi H. Bridging defects: autologous nerve grafts. Acta Neurochir Suppl (Wien) 2007;100:37–38

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[28] Mackinnon SE, Dellon AL. Clinical nerve reconstruction with a bioabsorbable polyglycolic acid tube. Plast Reconstr Surg 1990;85:419–424 [29] Crawley WA, Dellon AL. Inferior alveolar nerve reconstruction with a polyglycolic acid bioabsorbable nerve conduit. Plast Reconstr Surg 1992;90:300–302 [30] Kim J, Dellon AL. Reconstruction of a painful post-traumatic medial plantar neuroma with a bioabsorbable nerve conduit: a case report. J Foot Ankle Surg 2001;40:318–323 [31] Ducic I, Maloney CT, Dellon AL. Reconstruction of the spinal accessory nerve with autograft or neurotube? Two case reports. J Reconstr Microsurg 2005;21:29–33, discussion 34 [32] Dellon AL, Maloney CT Jr. Salvage of Sensation in a Hallux-to-Thumb Transfer by Nerve Tube Reconstruction. The Journal of Hand Surgery, 2006. 31 (9):1495-1498. [33] Lohmeyer J, Zimmermann S, Sommer B, Machens HG, Lange T, Mailänder P. Bridging peripheral nerve defects by means of nerve conduits. Chirurg. 2007 Feb;78(2):142-147. [34] Bushnell, B.D., et al., Early clinical experience with collagen nerve tubes in digital nerve repair. J Hand Surg Am, 2008;33(7):1081-1087. [35] Taras JS, Jacoby SM. Repair of lacerated peripheral nerves with nerve conduits. Tech Hand Up Extrem Surg 2008;12:100–106 [36] Lohmeyer JA, Siemers F, Machens HG, Mailänder P. The clinical use of artificial nerve conduits for digital nerve repair: a prospective cohort study and literature review. J Reconstr Microsurg 2009;25:55–61 [37] Thomsen L, Bellemere P, Loubersac T, Gaisne E, Poirier P, Chaise F. Treatment by collagen conduit of painful post-traumatic neuromas of the sensitive digital nerve: a retrospective study of 10 cases. Chir Main 2010;29:255–262 [38] Bertleff MJ, Meek MF, Nicolai JP. A prospective clinical evaluation of biodegradable neurolac nerve guides for sensory nerve repair in the hand. J Hand Surg Am 2005;30:513–518 [39] Meek MF, Nicolai JP, Robinson PH. Secondary digital nerve repair in the foot with resorbable p(DLLA-epsilon-CL) nerve conduits. J Reconstr Microsurg. 2006 Apr;22(3):149-151. [40] Hernandez-Cortes P, Garrido J. Failed digital nerve reconstruction by foreign body reaction to neurolac nerve conduit. Microsurgery. 2010;30:414-416. [41] Karabekmez FE, Duymaz A, Moran SL. Early clinical outcomes with the use of decellularized nerve allograft for repair of sensory defects within the hand. Hand (NY) 2009;4:245–249 [42] Shanti RM, Ziccardi VB. Use of decellularized nerve allograft for inferior alveolar nerve reconstruction: a case report. J Oral Maxillofac Surg 2011;69:550–553 [43] Navissano M, Malan F, Carnino R, Battiston B. Neurotube for facial nerve repair. Microsurgery 2005;25:268–271 [44] Donoghoe N, Rosson GD, Dellon AL. Reconstruction of the human median nerve in the forearm with the Neurotube. Microsurgery 2007;27:595–600 [45] Rosson GD, Williams EH, Dellon AL. Motor nerve regeneration across a conduit. Microsurgery. 2009;29(2):107-114. [46] Hung V, Dellon AL. Reconstruction of a 4-cm human median nerve gap by including an autogenous nerve slice in a bioabsorbable nerve conduit: case report. J Hand Surg Am 2008;33(3):313 -315 [47] Dellon AL. Letters to the Editor: In Reply. Journal of Hand Surgery-American Volume, 2008;33(8):1442-1443. [48] Ashley WW Jr, Weatherly T, Park TS. Collagen nerve guides for surgical repair of brachial plexus birth injury. J Neurosurg, 2006;105(6 Suppl):452-456 [49] Wangensteen KJ, Kalliainen LK. Collagen tube conduits in peripheral nerve repair: a retrospective analysis. Hand (NY) 2010;5:273–277 [50] Boecksyns ME, Sørensen AI, Viñeta JF, et al. Collagen conduit verses microsurgical neurorrhaphy: 2-year follow-up of a prospective, blinded clinical and electrophysiological multicenter randomized, controlled trial. J Hand Surg Am. 2013;28(12):2405–2411 [51] Rosen JM, Hentz VR, Kaplan EN. Fascicular tubulization: a cellular approach to peripheral nerve repair. Ann Plast Surg 1983;11:397–411 [52] Seckel BR, Chiu TH, Nyilas E, Sidman RL. Nerve regeneration through synthetic biodegradable nerve guides: regulation by the target organ. Plast Reconstr Surg 1984;74:173–181 [53] Seckel BR, Ryan SE, Gagne RG, Chiu TH, Watkins E. Target-specific nerve regeneration through a nerve guide in the rat. Plast Reconstr Surg 1986;78: 793–800 [54] Dellon AL, Mackinnon SE. An alternative to the classical nerve graft for the management of the short nerve gap. Plast Reconstr Surg 1988;82:849–856 [55] den Dunnen WF, van der Lei B, Schakenraad JM, et al. Poly(DL-lactide-epsilon-caprolactone) nerve guides perform better than autologous nerve grafts. Microsurgery 1996;17:348–357

Nerve Autograft Substitutes: Conduits and Processed Allografts [56] den Dunnen WF, Stokroos I, Blaauw EH, et al. Light-microscopic and electronmicroscopic evaluation of short-term nerve regeneration using a biodegradable poly(DL-lactide-epsilon-caprolacton) nerve guide. J Biomed Mater Res 1996;31:105–115 [57] den Dunnen WF, Meek MF, Robinson PH, Schakernraad JM. Peripheral nerve regeneration through P(DLLA-epsilon-CL) nerve guides. J Mater Sci Mater Med 1998;9:811–814 [58] Meek MF, den Dunnen WF, Schakenraad JM, Robinson PH. Evaluation of functional nerve recovery after reconstruction with a poly (DL-lactide-epsiloncaprolactone) nerve guide, filled with modified denatured muscle tissue. Microsurgery 1996;17:555–561 [59] Meek MF, Jansen K, Steendam R, van Oeveren W, van Wachem PB, van Luyn MJ. In vitro degradation and biocompatibility of poly(DL-lactide-epsilon-caprolactone) nerve guides. J Biomed Mater Res A 2004;68:43–51 [60] Jansen K, Meek MF, van der Werff JF, van Wachem PB, van Luyn MJ. Longterm regeneration of the rat sciatic nerve through a biodegradable poly(DLlactide-epsilon-caprolactone) nerve guide: tissue reactions with focus on collagen III/IV reformation. J Biomed Mater Res A 2004;69:334–341 [61] Meek MF, Jansen K. Two years after in vivo implantation of poly(DL-lactideepsilon-caprolactone) nerve guides: has the material finally resorbed? J Biomed Mater Res A 2008 [62] Meek MF, Coert JH. US Food and Drug Administration /Conformit Europe- approved absorbable nerve conduits for clinical repair of peripheral and cranial nerves. Ann Plast Surg 2008;60:466–472 [63] Di Lullo GA, Sweeney SM, Korkko J, Ala-Kokko L, San Antonio JD. Mapping the ligand-binding sites and disease-associated mutations on the most abundant protein in the human, type I collagen. J Biol Chem 2002;277:4223–4231 [64] Lodish H, Berk A, Zipansky L, Matsudaira P, Baltimore D, Darnell J. Collagen: the fibrous proteins of the matrix. In: Molecular Cell Biology. 4th ed. New York: WH Freeman; 2000 [65] Alluin O, Wittmann C, Marqueste T, et al. Functional recovery after peripheral nerve injury and implantation of a collagen guide. Biomaterials 2009;30: 363–373 [66] Eppley BL, Delfino JJ. Collagen tube repair of the mandibular nerve: a preliminary investigation in the rat. J Oral Maxillofac Surg 1988;46:41–47 [67] Kemp SW, Syed S, Walsh W, Zochodne DW, Midha R. Collagen nerve conduits promote enhanced axonal regeneration, Schwann cell association, and neovascularization compared to silicone conduits. Tissue Eng Part A 2009;15: 1975–1988 [68] Farole A, Jamal BT. A bioabsorbable collagen nerve cuff (NeuraGen) for repair of lingual and inferior alveolar nerve injuries: a case series. J Oral Maxillofac Surg 2008;66:2058–2062 [69] Lundborg G, Dahlin LB, Danielsen N. Ulnar nerve repair by the silicone chamber technique: case report. Scand J Plast Reconstr Surg Hand Surg 1991;25:79–82 [70] Lundborg G, Rosén B, Abrahamson SO, Dahlin L, Danielsen N. Tubular repair of the median nerve in the human forearm: preliminary findings. J Hand Surg [Br] 1994;19:273–276 [71] Lundborg G, Rosén B, Dahlin L, Holmberg J, Rosén I. Tubular repair of the median or ulnar nerve in the human forearm: a 5-year follow-up. J Hand Surg [Br] 2004;29:100–107 [72] Waitayawinyu T, Parisi DM, Miller B, et al. A comparison of polyglycolic acid versus type 1 collagen bioabsorbable nerve conduits in a rat model: an alternative to autografting. J Hand Surg Am 2007;32:1521–1529 [73] Shin AY, Shin RH, Vathana T, Friedrich P, Bishop AT. Motor outcomes of segmental nerve defect in the rat using bioabsorbable synthetic nerve conduits: a comparison of commercially available conduits. Paper presented at: Annual meeting of the American Society for Surgery of the Hand; 2008; Chicago, IL [74] Brenner MJ, Moradzadeh A, Myckatyn TM, et al. Role of timing in assessment of nerve regeneration. Microsurgery 2008;28:265–272 [75] Bain JR, Mackinnon SE, Hudson AR, et al. Preliminary report of peripheral nerve allografting in primates immunosuppressed with cyclosporin A. Transplant Proc 1989;21:3176–3177 [76] Strasberg SR, Hertl MC, Mackinnon SE, et al. Peripheral nerve allograft preservation improves regeneration and decreases systemic cyclosporin A requirements. Exp Neurol 1996;139:306–316 [77] Midha R, Mackinnon SE, Evans PJ, et al. Comparison of regeneration across nerve allografts with temporary or continuous cyclosporin A immunosuppression. J Neurosurg 1993;78:90–100 [78] Bain JR, Mackinnon SE, Hudson AR, Falk RE, Falk JA, Hunter DA. The peripheral nerve allograft: an assessment of regeneration across nerve allografts in

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[124] Hess JR, Brenner MJ, Fox IK, et al. Use of cold-preserved allografts seeded with autologous Schwann cells in the treatment of a long-gap peripheral nerve injury. Plast Reconstr Surg 2007;119:246–259 [125] Sun XH, Che YQ, Tong XJ, et al. Improving nerve regeneration of acellular nerve allografts seeded with SCs bridging the sciatic nerve defects of rat. Cell Mol Neurobiol 2009;29:347–353 [126] Casella GT, Bunge RP, Wood PM. Improved method for harvesting human Schwann cells from mature peripheral nerve and expansion in vitro. Glia 1996;17:327–338 [127] Hu J, Zhu QT, Liu XL, Xu YB, Zhu JK. Repair of extended peripheral nerve lesions in rhesus monkeys using acellular allogenic nerve grafts implanted with autologous mesenchymal stem cells. Exp Neurol 2007;204:658–666 [128] Wang D, Liu XL, Zhu JK, et al. Repairing large radial nerve defects by acellular nerve allografts seeded with autologous bone marrow stromal cells in a monkey model. J Neurotrauma 2010;27:1935–1943 [129] Wang D, Liu XL, Zhu JK, et al. Bridging small-gap peripheral nerve defects using acellular nerve allograft implanted with autologous bone marrow stromal cells in primates. Brain Res 2008;1188:44–53 [130] Walsh S, Biernaskie J, Kemp SW, Midha R. Supplementation of acellular nerve grafts with skin derived precursor cells promotes peripheral nerve regeneration. Neuroscience 2009;164:1097–1107 [131] Kingham PJ, Kalbermatten DF, Mahay D, Armstrong SJ, Wiberg M, Terenghi G. Adipose-derived stem cells differentiate into a Schwann cell phenotype and promote neurite outgrowth in vitro. Exp Neurol 2007;207:267–274 [132] Zhang Y, Luo H, Zhang Z, et al. A nerve graft constructed with xenogeneic acellular nerve matrix and autologous adipose-derived mesenchymal stem cells. Biomaterials 2010;31:5312–5324 [133] Jesuraj NJ, Santosa KB, Newton P, et al. A systematic evaluation of Schwann cell injection into acellular cold-preserved nerve grafts. J Neurosci Methods 2011;197:209–215Corrected Proof. [134] Brushart TM. Preferential reinnervation of motor nerves by regenerating motor axons. J Neurosci 1988;8:1026–1031 [135] Aberg M, Ljungberg C, Edin E, et al. Considerations in evaluating new treatment alternatives following peripheral nerve injuries: a prospective clinical study of methods used to investigate sensory, motor and functional recovery. J Plast Reconstr Aesthet Surg 2007;60:103–113 [136] Brenner MJ, Hess JR, Myckatyn TM, Hayashi A, Hunter DA, Mackinnon SE. Repair of motor nerve gaps with sensory nerve inhibits regeneration in rats. Laryngoscope 2006;116:1685–1692 [137] Moradzadeh A, Borschel GH, Luciano JP, et al. The impact of motor and sensory nerve architecture on nerve regeneration. Exp Neurol 2008;212:370– 376 [138] Nichols CM, Brenner MJ, Fox IK, et al. Effects of motor versus sensory nerve grafts on peripheral nerve regeneration. Exp Neurol 2004;190:347–355 [139] Neubauer D, Graham JB, Muir D. Nerve grafts with various sensory and motor fiber compositions are equally effective for the repair of a mixed nerve defect. Exp Neurol 2010;223:203–206 [140] Maeda T, Mackinnon SE, Best TJ, Evans PJ, Hunter DA, Midha RT. Regeneration across “stepping-stone” nerve grafts. Brain Res 1993;618(2):196–202

Peripheral Nerve Allotransplantation

8 Peripheral Nerve Allotransplantation Amy M. Moore, Wilson Z. Ray, and Philip J. Johnson

8.1 Introduction The traditional repair of large, segmental or complex nerve injuries requires equally long autologous nerve grafts. When nerve continuity cannot be restored by a tension free coaptation and donor autografts are insufficient, cadaveric nerve allografts provide a readily accessible alternative. Transplanted nerve allografts act as a temporary conduit, providing the substrate to permit host axonal regeneration. They also avoid graft site morbidity associated with nerve autografting, such as sensory loss, scarring, and neuroma formation. The results of experimental studies on rodent, large animal, nonhuman primates, as well as our own clinical experience, have demonstrated that, in the presence of immunosuppression, nerve allografts provide equal regeneration and function to that of an autograft. Due to the morbidity of systemic immunosuppression, nerve allotransplantation must be approached with caution, and careful patient selection is essential. In contrast to the allotransplantation of solid organs, nerve allografts require only temporary systemic immunosuppression.1 Once axon regeneration has crossed the transplanted nerve allograft, systemic immunosuppression can be withdrawn.1–3 Recent work has advanced our understanding of the involved immunology and the basis of nerve allotransplant rejection. Clinical and laboratory investigations are under way, investigating how to further diminish donor alloantigenicity and mechanisms to modify host response without the toxicity of systemic immunosuppression. This chapter will focus on our experience with peripheral nerve allotransplantation.

8.2 Regeneration of Peripheral Nerves Following peripheral nerve injury, a very regulated and sophisticated sequence of events occurs and is described in detail in Chapter 1. Depending on the severity of the injury, ranging from a transient neurapraxia to a mixed neurotmesis, nerve recovery follows a variable course. Assuming the injury causes significant disruption in functional continuity, in addition to distal wallerian degeneration, an orchestrated and complex interaction occurs. Early events revolve around the removal of cellular debris by local macrophages and Schwann cells. 4–7 This is followed by a cascade of degenerative processes, all of which ultimately prime the nerve for axonal regeneration. 5 Only after this degenerative process has completed can reinnervation occur. Axons from the site of injury produce regenerating units. Unmyelinated fibers from the regenerating units sprout from the proximal stump. Guided by neurotrophic factors released by the distal stump,8–11 the sprouting axons attempt to reestablish nerve continuity. In addition to neurotrophic factors, columns of Schwann cells (bands of Büngner) provide a supportive role to regenerating axons acting as a potential guide. The gold standard for repair of segmental peripheral nerve injuries traditionally has relied on interposed autologous

nerve grafts. Nerve grafts serve as a bridge or a structural framework to overcome irreducible nerve gaps created by injury and subsequent wallerian degeneration. Nerve grafts themselves will undergo degeneration when removed from their local environment, yet provide the necessary matrix for the regenerating axons.12 Although the sural nerve is the most commonly used autograft,13,14 there are many other suitable nerves that can be utilized as interposition grafts, including the medial and lateral cutaneous nerves of the forearm, the dorsal cutaneous branch of the ulnar nerve, the superficial and deep peroneal nerves, the intercostal nerves, the greater auricular nerve, and the posterior and lateral cutaneous nerves of the thigh.15 Donor grafts are chosen based on the caliber of graft required, the total length of nerve gap, and donor site morbidity. In addition to nerve grafts, considerable experimental and clinical work has been done investigating synthetic nerve conduits.16–23 with current trends focused on the local delivery of neurotrophic factors and cultivation of donor Schwann cells. 24– 31 No doubt continued investigation into this work will eventually augment the currently available alternatives for bridging a nerve gap. Interest in nerve allografts as a source of repair dates back to the 1880s.32 The lack of immunosuppressive agents prohibited any meaningful functional recovery. Exploration of various decellularization techniques (cold storage, radiation, and freezedrying) aimed at minimizing allograft antigenicity have also been reported.33–43 Despite these attempts to minimize host immune response, all have failed to produce consistent results equivalent to autologous nerve grafts. The application and success of immunosuppressive therapy in nerve allotransplantation revived clinical interest.44–46 In 1992 we reported the successful restoration of sensation in an 8-year-old boy, using donor allograft with 2 years of systemic immunosuppressive therapy.47 Several subsequent reports have since followed, using donor nerve allografts.1,3,48,49

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8.3 Schwann Cell Migration in Peripheral Nerve Allografts As previously discussed, following nerve injury Schwann cells serve to provide neurotrophic factors and structural support to the injured axons. The injury of axons itself causes the release of multiple mitogenic cytokines, inducing a proliferative Schwann cell phenotype.5,50,51 A predictable sequence of events occurs following severe nerve injury. Host Schwann cells play a vital role in preparing the nerves for regeneration. In conjunction with macrophages, Schwann cells work to clear debris and degenerating axons.4–7,52 They are further stimulated by mitogenic factors released from infiltrating macrophages to form columns of cells along the basement membrane of the endoneurial tube called bands of Büngner.53–56 These bands serve to help guide the sprouting axons. When repair of a nerve injury requires the use of nerve grafts, the presence of viable Schwann cells is essential for axonal regrowth. Autografts rely upon the presence of viable

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Peripheral Nerve Allotransplantation

Fig. 8.1 Schwann cell migration in nerve allografts. (a) Nerve autografts are composed of native cells and include Schwann cells that help support nerve regeneration. (b) Nerve allografts include donor Schwann cells that support graft survival under immunosuppression. (c) Host Schwann cell migration occurs from both proximal and distal ends into the donor graft and coexist with donor Schwann cells. These cells support axonal regeneration from proximal to distal. (d) At a certain point, host Schwann cells populate the entire donor graft. (e) After this, immunosuppression can be withdrawn, with the donor graft being accepted by the host.

8

resident Schwann cells (▶ Fig. 8.1a), making host Schwann cell migration less critical for axonal regeneration and subsequent remyelination.57–59 In acellular nerve grafts, axonal regeneration is dependent on host Schwann cells migration, creating a finite upper limit for regenerative capacity.60,61 In allotransplanted nerve grafts, both donor and host Schwann cells proliferate and contribute to axonal regeneration, as long as immunosuppression is present (▶ Fig. 8.1b). However, eventually donor Schwann cells are lost despite adequate immunosuppression through an unknown mechanism that may involve chronic rejection. Host Schwann cell migration is important in the process of nerve allograft remyelination and axonal regeneration. 62 It has been demonstrated that host Schwann cells migrate into the nerve allograft from both proximal and distal recipient nerve stumps (▶ Fig. 8.1c,d).63–66 Jensen et al63 reported their observations of in vivo imaging, which demonstrated a greater proportion of migration from the distal host nerve. Host Schwann cells repopulated an acellularized nerve graft proximally and distally very early (within 10 days), whereas axonal regeneration lagged behind Schwann cell migration by 10 to 15 days.63 Our laboratory has further explored Schwann cell migration into a nerve allograft. We demonstrated that, under adequate immunosuppression, there is a delay in host Schwann cell migration into the allograft. During this delay, the donor Schwann cells appear to assist axonal regeneration across the allograft. 67 Eventually, host Schwann cells migrate into the graft, and what is observed is the coexistence of both host and donor cells. The movement of host Schwann cells across the allograft may be related to episodes of subclinical rejection. In this study, once immunosuppression was stopped after axonal regeneration

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through the graft was complete (▶ Fig. 8.1e), host Schwann cell migration into the graft occurred immediately to fill in the gaps left by the loss of remaining donor Schwann cells.67 Schwann cells are known to play a key role in eliciting nerve allograft rejection. All Schwann cells express major histocompatibility complex (MHC) I. Transplanted Schwann cells can be induced to express MHC II molecules, acting as facultative antigen-presenting cells (APCs).68–74 As such, they are recognized as a prime target of the host alloimmune response; thus, donor Schwann cells are the most antigenic component of the nerve allograft.68–75 In nerve allotransplantation, immunosuppression cannot be safely withdrawn until the entire length of the graft has become populated with host Schwann cells. Should large portions of the graft remain populated by donor Schwann cells, the removal of immunosuppression and the resultant loss of donor Schwann cells could result in a devastating conduction block (▶ Fig. 8.2).1,75

8.4 Immunosuppression/Graft Pretreatment 8.4.1 Cold Preservation A method used to reduce the allogenicity of nerve allografts is cold preservation. Previous studies have demonstrated a timedependent reduction of immune response following cold preservation.76–79 The expression of MHC class II molecules is decreased proportional to the storage time. These studies have also shown that, in addition to a time-dependent reduction of allogenicity, there is a time-dependent decrease in axonal

Peripheral Nerve Allotransplantation

Fig. 8.2 The effects of early immunosuppression withdrawal in nerve allografts. (a) Nerve autografts are composed of native cells and include Schwann cells that help support nerve generation. (b, c) Host Schwann cell migration occurs from both proximal and distal ends into the donor graft. (d) If immunosuppression is withdrawn early, donor cells are rejected, leaving segments of unmyelinated nerve fibers. (e) A conduction block occurs as a result.

regeneration with increasing cold preservation. With more than 6 weeks of cold preservation, the graft is acellular and completely nonantigenic. At 1 week of cold preservation, there is a reduction in the expression of MHC class II molecules but not a reduction in the number of viable Schwann cells.43,78,80–82 Our current clinical protocol involves 7 days of cold preservation at 4 to 5°C in University of Wisconsin solution, prior to implantation.

8.4.2 FK-506 Several studies have investigated immunology of nerve allograft transplantation.68,72,80,83–85 The majority of this work has focused on ways to minimize the negative effects of systemic immunosuppression, while maximizing regenerative potential. It is well established in both animal and clinical models that peripheral nerve allograft transplantation induces both a humoral and a cell-mediated immune response.73,86–89 In contrast to solid organ transplant, in nerve allotransplantation Schwann cells represent the main immunogenic target for acute and chronic rejection, eliciting host rejection through expression of both MHC I and II molecules.70–74 In the late 1970s our laboratory began investigating the effects of immunosuppression on nerve regeneration and the use of nerve allografts.90 Early work focused on the use of cyclosporine, but later the focus was shifted to the more potent calcineurin phosphatase inhibitor, FK-506. FK-506, also known as tacrolimus, ultimately inhibits the activation of T-cell proliferation.91 In 1995 Gold et al first described the augmented neuroregeneration provided by FK-506 in a rat peripheral nerve model.92 Since that time FK-506 has been shown to be effective in the enhancement of peripheral nerve regeneration in multiple models, including transection,93 crush,94,95 chronic axo-

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tomy,96 isograft,97 and allograft1,98 models. In addition, FK506 has been shown to accelerate the functional recovery in both small and large animal models.63,93 Previous studies suggest that the immunosuppressive mechanism of FK-506 is mediated through calcineurin inhibition 99,100 and that a neuroprotective effect is provided by blocking neuronal apoptosis. 101, 102 Although several calcineurin-independent pathways have been implicated (FKBP-52, GAP43, heat shock proteins, and cytoskeletal dynamics), the exact mechanism of enhanced nerve regeneration remains unclear.103–105 FK-506 has been shown to increase the number of regenerated myelinated and unmyelinated nerve fibers106 and to stimulate even chronically axotomized motoneurons.96 Furthermore, our laboratory and clinical investigations have demonstrated that further augmentation of nerve regeneration can be obtained with low-dose FK-506 in combination with other immunosuppressive regimes (anti-CD-40 ligand/co-stimulatory blockade and cold preservation in University of Wisconsin solution).107,108 In contrast, immunosuppressive doses of FK-506 with therapeutic doses of anti-CD-40 ligand/co-stimulatory blockade abrogates the beneficial effects of FK-506 on nerve regeneration.107 Although not specifically studied, we suspect the decreased regenerative enhancement by FK-506 results from interference of each other’s mechanism of action (costimulatory blockade vs calcineurin inhibition), making both drugs less effective. For example, alloantigen needs to be recognized by host T cells to allow co-stimulation to be effective. Further studies are needed to elucidate the specifics behind this phenomenon. Our clinical and research experience has demonstrated that FK-506 should be administered preoperatively for a greater effect on nerve regeneration and functional recovery. In 2006 we demonstrated that preloading FK-506 3 days before surgery

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Peripheral Nerve Allotransplantation Table 8.1 Patient Treatment Patient No.

8

Age/Gender

Allograft Total Length (cm)

Allograft Total Gap Autograft Total (cm) Length (cm)

Autograft Total Gap Surgery Date (mo/y)

1

8/M

230

Sciatic (23)

9/1988

2

12/M

160

Posterior tibial (20)

9/1993

3

15/F

178

Median (27) Ulnar (15)

59

Median (29) Ulnar (15)

9/1994

4

3/F

72

Ulnar (12) SBR (12) PIN (12)

24

PIN (12)

9/1995

5

26/F

226

Radial (20) Ulnar (15) Median (22)

44

Radial (22)

9/1996

6

16/M

350

Median (23) Ulnar (18) Radial (27)

63

Ulnar (18) Radial (27)

9/1996

7

24/M

140

Posterior tibial (14)

28

Posterior tibial (14)

6/1998

8

35/M

198

Median (24) Radial (21) Ulnar (18)

48

Median (24)

2/2000

9

15/M

228

Posterior tibial (20) Peroneal (11)

51

Posterior tibial (20) Peroneal (11)

7/2000

10

19/M

~ 100 (living donor + allograft)

Radial (20)

74

Median (8) Ulnar (10)

7/2005

11

21/M

~ 200 (living donor + allograft)

Median (19) Radial (18)

129

Median (19) Ulnar (18)

2/2006

12

57/M

2 × 48 cm

N/A

N/A

N/A

10/2011

Abbreviations: SBR, Superficial branch of radial nerve; PIN, Posterior interosseous nerve.

enhanced the neuroregenerative effects of the drug.109 We have recently shown that presurgical treatment with FK-506 enhances nerve regeneration by 15 to 20% for the duration of the FK506 treatment.110–114 Taken together this suggests that for severe nerve injuries, even when allografts are not required for reconstruction, low or therapeutic doses of FK-506 could be considered to enhance nerve regeneration. There are many examples of successful clinical use of FK-506 in non-transplantation diseases such as rheumatoid arthritis, inflammatory bowel disease, and myasthenia gravis. 115–145 We further demonstrated that if immunosuppression drops below therapeutic levels and rejection is suspected, the allograft can be rescued by providing immunosuppressive doses of FK-506 but only within 7 days of the start of rejection. 98 These observations have been translated to Mackinnon’s current clinical practice.

8.5 Experience with Allotransplantation Mackinnon has significant clinical experience with nerve allotransplantation. The results of the first seven cases have been reported previously.1 Since that time five further patients have undergone reconstruction with nerve allografts. All cases are reviewed and summarized in ▶ Table 8.1.

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8.5.1 Patient 1 The patient, an 8-year-old boy, suffered complete motor and sensory loss in his left leg. Three months later he underwent sciatic nerve reconstruction using 230 cm of nerve allograft. The patient was treated with 26 months of oral cyclosporine beginning the day of transplantation. He regained protective sensation on the plantar aspect of his foot but did not regain any motor function distal to his knee.

8.5.2 Patient 2 A 12-year old male patient sustained total posterior tibial nerve motor and sensory loss in his right leg. Four months later he underwent reconstruction using 160 cm of nerve allograft. Notably, the allograft had undergone 1 week of cold preservation, and the patient was started on immunosuppressive therapy 4 days prior to surgery. He was maintained on cyclosporine for 19 months. The patient regained 8 of 10 sensations in his lower extremity on the Ten Test.

8.5.3 Patient 3 A 15-year-old female patient sustained a right brachial plexus injury that left her with complete loss of radial, median, and ulnar nerve function. Eight months later the patient underwent

Peripheral Nerve Allotransplantation reconstruction using both 178 cm of allograft and 59 cm of autograft. She was also treated with cyclosporine therapy for 12 months. She had excellent reinnervation of the extrinsic ulnar and median muscles with good recovery of light-touch sensation.

injury with loss of function in the median, ulnar, and radial nerve distributions. The patient underwent reconstruction using 48 cm of autograft and 198 cm of allograft. He was maintained on FK-506 for 32 months. He had a good recovery of protective sensation to the distal extremity with good proximal function.

8.5.4 Patient 4

8.5.9 Patient 9

A 3-year-old girl sustained a significant left upper extremity injury, resulting in no radial or ulnar nerve function. Five months after the injury, the child underwent reconstruction of the radial and ulnar nerves using 72 cm of allograft and 24 cm of autograft. The patient received cyclosporine immunosuppression therapy for 18 months. At follow-up she had good sensory return with motor function in the flexor digitorum superficialis and ulnar distribution.

A 15-year-old male patient suffered a gunshot wound to his right lower extremity with no neurologic function below his knee. Four months after the injury, he underwent reconstruction of the posterior tibial nerve and peroneal nerve using 51 cm of autograft and 228 cm of allograft. He was maintained on FK-506 for 24 months. The patient had return of protective sensation to the distal dorsum and sole of his foot.

8.5.5 Patient 5 A 26-year-old female patient sustained a left upper extremity injury with complete loss of sensory and motor function of the radial, median, and ulnar nerves. Three months after the initial injury, she underwent multiple nerve transfers and grafting using 44 cm of autograft and 226 cm of allograft. The patient was treated with FK-506 immunosuppression for 17 months. She had good sensory recovery in the median nerve distribution but not the ulnar or radial nerve distribution. She had motor recovery of the flexor carpi ulnaris, ulnar flexor digitorum profundus, and thenar muscle group.

8.5.6 Patient 6 A 16-year-old male patient sustained a left upper extremity injury with loss of all motor and sensory function in the radial, median, and ulnar nerves. Three months after the injury, he underwent reconstruction using 63 cm of autograft and 350 cm of allograft. The patient was treated with cyclosporine immunosuppression, but 3 weeks after surgery, he presented with upper extremity erythema and edema. The patient’s immunosuppression was subtherapeutic, cyclosporine doses were increased, and he was treated with a course of antibiotics. Reexamination 2 weeks later revealed thickening of the radial nerve with rejection of the allografts. A suitable donor was not found with the acceptable denervation interval, and immunosuppression was stopped.

8.5.7 Patient 7 A 24-year-old male patient suffered a left lower extremity injury. He had no sensation on the sole of his foot and no posterior tibial nerve function distal to the midcalf. Five months after the injury, the patient underwent reconstruction of the posterior tibial nerve using 28 cm of autograft and 112 cm of allograft. The patient was maintained on FK-506 for 19 months. He had good recovery of sensory function to the sole of his foot.

8.5.8 Patient 8 A 35-year-old male patient sustained a large animal bite to his right upper extremity. He presented several months after the

8.5.10 Patient 10 The patient, a 19-year-old male, sustained a circular saw injury to his right axilla that led to complete loss of function in his right upper extremity. Six weeks after the injury, he underwent exploration of the brachial plexus and reconstruction of the median, ulnar, and radial nerves using 74 cm of autograft and 100 cm of allograft from both living donor and cadaveric sources. He was maintained on FK-506 for 18 months. The patient had excellent return of function of the median and ulnar nerves to the level of the intrinsic hand musculature.

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8.5.11 Patient 11 A 21-year-old male patient was involved in a motorcycle accident (▶ Fig. 8.3). He suffered near amputation of his right upper arm with complete loss of median, ulnar, and radial nerve function. Nine months after the injury, he underwent exploration and reconstruction of the median, ulnar, and radial nerves using 129 cm of autograft and 200 cm of allograft from both living donor and cadaveric sources. The patient was maintained on FK-506 for 18 months. He made good functional recovery in the ulnar and median distribution but ultimately required tendon transfers for the radial distribution.

8.5.12 Patient 12 The patient, a 54-year-old man, had severe right intercostal neuralgia following a complicated history that involved two thoracic operations of a right upper lobe resection and a pleura leak repair. The patient reported postthoracotomy intercostal pain following the second operation of the pleura repair. He was referred 8 years following this incident and underwent reconstruction of the T5–T8 intercostal neuromas with two cadaveric 48-cm nerve allografts. The two nerve allografts were looped between T5–T6 and T7–T8 intercostal nerves proximal to the neuroma at the nerve root level. Surgical management of postthoracotomy intercostal pain was published in an article by Guelinckx et al, who looped the proximal intercostal nerves with a graft.110 In our case, long nerve allografts were used to allow the regeneration of the intercostal nerves to taper off, thereby preventing neuroma pain. The patient was maintained on immunosuppression (FK506) for 13 months. The intercostal neuralgia diminished significantly by 7 months following

197

Peripheral Nerve Allotransplantation

8

Fig. 8.3 Case study: Patient 11. (a) Presentation. The patient, a 21-year-old male, was involved in a motorcycle accident and suffered a near amputation of his right upper arm with complete loss of radial, median, and ulnar nerve function. (b) Nerve autografts and allografts used for reconstruction. Nerve grafts were harvested from the patient, a living donor, and cadaveric sources, which totaled an allograft length of ~ 200 cm. The cadaveric allografts are seen as white due to processing. (c) Reconstruction of radial, median, and ulnar nerves with autografts and allografts. Nine months after the injury, the patient underwent reconstruction of the radial, median, and ulnar nerves with autografts and allografts.

198

Peripheral Nerve Allotransplantation

8

Fig. 8.4 This and the following five figures illustrate the case study of Patient 12, a 54-year-old man who had right intercostal neuralgia following a thoracotomy. X-rays portray the location of the thoracotomy and the area of intercostal nerve injuries. The examination determined the intercostal nerves (T5–T8) were injured.

reconstruction. At 2.5 years postoperative, the patient denies pain of chest wall but has continued discomfort with a Visual Analog Score of 3 at the nerve root exposure site at the spine. The patient’s pain is controlled with Lidoderm patches and avoidance of heavy activity. The intercostal neuralgia pain abated 7 months following reconstruction (▶ Figs. 8.4–8.9). The current clinical regimen involves the initial use of all suitable donor autografts and use of allografts taken from ABO blood type–matched donors harvested within 24 hours of death. Recently, living related donors have been used in addition to cadaveric sources. To reduce allogenicity, the nerves are stored in University of Wisconsin cold storage solution at 4°C for 7 days prior to implantation.77,110 Because small-diameter allografts revascularize more consistently, multiple small-diameter cables are used. Preoperatively, FK-506 is given to the patient 3 days prior to surgery for induction and to maximize the regenerative effects of the drug. Our current immunosuppressive protocol is detailed in ▶ Table 8.2.

8.6 Future Directions: Vascularized Composite Allotransplantation As the field of vascularized composite tissue allotransplantation (VCA) continues to advance, the role of nerve regeneration

within the composite tissue allograft will have increased significance in the justification of elective reconstructive transplantation. The long-term functional outcome in patients undergoing either hand or face transplantation ultimately depends on the quality of nerve regeneration and targeted muscle reinnervation. There are two critical differences between nerve regeneration in an allograft model and that of VCA (▶ Fig. 8.10). First, in a nerve allograft, successful regeneration and ultimate function seem largely dependent upon both proximal and distal Schwann cell migration into the allograft.63,67,112 In VCA, distal host Schwann cells do not exist because the entire distal neuromuscular unit is composed of donor tissue. Repopulation of the donor nerve with host Schwann cells in VCA depends on host Schwann cell proliferation and migration proximally through the transplanted nerves. It is unknown if there is a limit to the distance over which host Schwann cells are able (or stimulated) to migrate.75,112,115[149] The second difference between nerve regeneration in a nerve allograft and in a vascularized composite tissue allograft involves the impetus of Schwann cell migration. In nerve allografts, multiple subclinical rejection episodes resulting in loss of donor Schwann cells are likely the cue for host Schwann cell migration into the graft to replace the lost Schwann cells.67 In VCA, skin and muscle have greater antigenicity than Schwann cells and thus require more stringent

199

Peripheral Nerve Allotransplantation

Fig. 8.5 Decompression and exposure of intercostal nerves (T5–T8). The decompression and exposure of the right intercostal nerves (T5–T8) occurred proximal and posterior to the injury. Following decompression, the intercostal nerves were transected to reveal the proximal ends for nerve looping. Orientation: patient prone, head to the left, feet to the right.

8

Fig. 8.6 Cadaveric nerve allografts for reconstruction. Two 48-cm nerve allografts were harvested from a cadaver for reconstruction. Each allograft was used as a bridge loop between two intercostal nerves.

immunosuppression.84 It is unknown to what extent host Schwann cell migration will be stimulated in the presence of this stringent immunosuppression without subclinical episodes of rejection.

200

The answers to the behavior and fate of host and donor Schwann cells in VCA have not yet been fully elucidated. From our current understanding of nerve allotransplantation, we believe that the nerves in composite tissue allotransplants need

Peripheral Nerve Allotransplantation

8 Fig. 8.7 Nerve loops for reconstruction of postthoracotomy intercostal pain. The two nerve allografts were looped between the proximal ends of T5– T8 intercostal nerves.

Fig. 8.8 Nerve loops for reconstruction of postthoracotomy intercostal pain. After reconstruction, the loops were mobilized into the exposure site.

201

Peripheral Nerve Allotransplantation

8

Fig. 8.9 Pre- and postoperative pain evaluation. The patient reported severe pain along the territory of the right intercostal nerves preoperatively. Seven months following surgery, the patient’s pain had abated.

Table 8.2 Nerve Allotransplantation Patient Protocol Preoperative Preparation

Intraoperative Details

Postoperative Care

Assess patient suitability: ● Medical comorbidities ● Infection/malignancy ● Psychosocial fitness

Resect patient’s injured nerve to healthy proximal and distal stumps

Induction immunotherapy (dose 2): ● Basiliximab 20 mg IV (postoperative day 4)

Laboratory tests: ABO blood type ● CBC, CMP ● HIV/hepatitis

Use patient’s autografts in addition to cadaveric Standard immunotherapy: ● Continue FK-506 (goal level 5–8 ng/mL) allografts, donor related or donor unrelated ● Azathioprine 1.0–1.5 mg/kg/day allografts

●

Insert extra allograft subcutaneously for rejection Antibiotic: Nerve allografts: ● Sulfamethoxazole-trimethoprim 3 times weekly monitoring Consider related donor ● Harvest small-diameter grafts ● Cold preservation (4°C): University of Wisconsin solution, 7 days ●

Immunotherapy: FK-506 (tacrolimus) 1–2 mg by mouth bid (start 3 days preoperatively) ● Induction immunotherapy (dose 1): basiliximab 20 mg IV (immediately preoperatively) ●

Stop immunotherapy 6 months after Tinel sign crosses distal repair site

Abbreviations: bid, twice daily; CBC, complete blood count; CMP, comprehensive metabolic panel; HIV, human immunodeficiency virus; IV, intravenously. Adapted with permission from Fox IK, Mackinnon SE. Experience with nerve allograft transplantation. Semin Plast Surg. 2007;21(4):242–249.

202

Peripheral Nerve Allotransplantation

Fig. 8.10 Schwann cell migration in composite tissue allografts. (a) In a scenario of vascularized composite tissue autografts, the nerves are composed of native Schwann cells that support axonal regeneration. (b) Vascularized composite tissue allografts include donor Schwann cells that are transplanted into the host. (c) Host Schwann cell migration occurs from only the proximal end in comparison to nerve allografting. (d) In an ideal situation, migration of host Schwann cells must traverse the entire distance to the muscle before a possible rejection episode occurs.

8

Fig. 8.11 The effects of rejection on the nerve in vascularized composite tissue allografts. (a) Vascularized composite tissue allografts include donor Schwann cells that are transplanted into the host. (b) Early acute rejection can be abated, which allows nerve regeneration to continue to the target. (c) No rejection allows for the innervation of the target with support from both the host and donor Schwann cells. (d) However, if a significant rejection episode occurs affecting the donor Schwann cells, a large segment of nerve is left without Schwann cells. (e) This results in a devastating conduction block and permanent functional deficit.

203

Peripheral Nerve Allotransplantation perfect Schwann cell support for regeneration. This may require that there be no lapses in therapeutic immunosuppression to prevent even minor episodes of acute rejection and subsequent early loss of the donor Schwann cells.[149] Donor Schwann cells are no different from host Schwann cells in their ability to support nerve regeneration.75 If, however, a significant rejection episode occurs affecting the donor Schwann cells, then a large segment of nerve may be left unsupported, resulting in a devastating conduction block and permanent functional deficit (▶ Fig. 8.11). Until immunosuppressive strategies are developed that consistently induce tolerance of all donor tissue, the late loss of donor Schwann cells due to unexpected episodes of rejection is a significant concern. Strategies to enhance nerve regeneration in VCA must consider the delicate balance and interplay between donor and host cells. Ideally, strategies should include promoting eventual complete repopulation of donor nerve by host Schwann cells, keeping donor Schwann cells alive to support axonal regeneration until the host Schwann cells arrive, and avoiding rejection until these objectives are accomplished. It is only then that the ultimate function of the VCA can be protected during episodes of rejection that are likely to occur over the lifetime of the patient.

8

8.7 Conclusion Nerve allotransplantation provides an alternative strategy to manage severe, long gap or segmental nerve injuries, but the potential morbidity associated with systemic immunosuppression has limited its utilization. We reserve this procedure for patients with devastating injuries not amenable to other surgical options. Research directed toward inducing tolerance to donor tissue without the need for chronic immunosuppression is currently underway. If successful, the indications for nerve allotransplantation will expand and our ability to treat devastating nerve injuries will improve.

8.8 References [1] Mackinnon SE, Doolabh VB, Novak CB, Trulock EP. Clinical outcome following nerve allograft transplantation. Plast Reconstr Surg 2001;107:1419–1429 [2] Hayashi A, Koob JW, Liu DZ, et al. A double-transgenic mouse used to track migrating Schwann cells and regenerating axons following engraftment of injured nerves. Exp Neurol 2007;207:128–138 [3] Elkwood AI, Holland NR, Arbes SM, et al. Nerve allograft transplantation for functional restoration of the upper extremity: case series. J Spinal Cord Med 2011;34:241–247 [4] Burnett MG, Zager EL. Pathophysiology of peripheral nerve injury: a brief review. Neurosurg Focus 2004;16:E1 [5] Fu SY, Gordon T. The cellular and molecular basis of peripheral nerve regeneration. Mol Neurobiol 1997;14:67–116 [6] Stoll G, Jander S. The role of microglia and macrophages in the pathophysiology of the CNS. Prog Neurobiol 1999;58:233–247 [7] Bigbee JW, Yoshino JE, DeVries GH. Morphological and proliferative responses of cultured Schwann cells following rapid phagocytosis of a myelin-enriched fraction. J Neurocytol 1987;16:487–496 [8] Morris JH, Hudson AR, Weddell G. A study of degeneration and regeneration in the divided rat sciatic nerve based on electron microscopy: 3. Changes in the axons of the proximal stump. Z Zellforsch Mikrosk Anat 1972;124:131–164 [9] Mackinnon SE, Dellon AL, Lundborg G, Hudson AR, Hunter DA. A study of neurotrophism in a primate model. J Hand Surg Am 1986;11:888–894

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[10] Lundborg G, Dahlin LB, Danielsen N, Nachemson AK. Tissue specificity in nerve regeneration. Scand J Plast Reconstr Surg 1986;20:279–283 [11] Brushart TM, Seiler WA, IV. Selective reinnervation of distal motor stumps by peripheral motor axons. Exp Neurol 1987;97:289–300 [12] Matsuyama T, Mackay M, Midha R. Peripheral nerve repair and grafting techniques: a review. Neurol Med Chir (Tokyo) 2000;40:187–199 [13] Midha R. Sural nerve injury and neuroma. In: Midha R, Zager EL, eds. Surgery of Peripheral Nerves: A Case-Based Approach. New York, NY: Thieme; 2008:207–210 [14] Schlosshauer B, Dreesmann L, Schaller HE, Sinis N. Synthetic nerve guide implants in humans: a comprehensive survey. Neurosurgery 2006;59:740–747, discussion 747–748 [15] Norkus T, Norkus M, Ramanauskas T. Donor, recipient and nerve grafts in brachial plexus reconstruction: anatomical and technical features for facilitating the exposure. Surg Radiol Anat 2005;27:524–530 [16] Xie F, Li QF, Gu B, Liu K, Shen GX. In vitro and in vivo evaluation of a biodegradable chitosan-PLA composite peripheral nerve guide conduit material. Microsurgery 2008;28:471–479 [17] Liu BS. Fabrication and evaluation of a biodegradable proanthocyanidincross-linked gelatin conduit in peripheral nerve repair. J Biomed Mater Res A 2008;87:1092–1102 [18] Hung V, Dellon AL. Reconstruction of a 4-cm human median nerve gap by including an autogenous nerve slice in a bioabsorbable nerve conduit: case report. J Hand Surg Am 2008;33:313–315 [19] Oh SH, Kim JH, Song KS, et al. Peripheral nerve regeneration within an asymmetrically porous PLGA/pluronic F127 nerve guide conduit. Biomaterials 2008;29:1601–1609 [20] Chang JY, Lin JH, Yao CH, Chen JH, Lai TY, Chen YS. In vivo evaluation of a biodegradable EDC/NHS-cross-linked gelatin peripheral nerve guide conduit material. Macromol Biosci 2007;7:500–507 [21] Chiu DT, Strauch B. A prospective clinical evaluation of autogenous vein grafts used as a nerve conduit for distal sensory nerve defects of 3 cm or less. Plast Reconstr Surg 1990;86:928–934 [22] Chen YS, Chang JY, Cheng CY, Tsai FJ, Yao CH, Liu BS. An in vivo evaluation of a biodegradable genipin-cross-linked gelatin peripheral nerve guide conduit material. Biomaterials 2005;26:3911–3918 [23] Merrell JC, Russell RC, Zook EG. Polyglycolic acid tubing as a conduit for nerve regeneration. Ann Plast Surg 1986;17:49–58 [24] Hedayatpour A, Sobhani A, Bayati V, Abdolvahhabi MA, Shokrgozar MA, Barbarestani M. A method for isolation and cultivation of adult Schwann cells for nerve conduit. Arch Iran Med 2007;10:474–480 [25] Kim SM, Lee SK, Lee JH. Peripheral nerve regeneration using a three dimensionally cultured schwann cell conduit. J Craniofac Surg 2007;18:475–488 [26] Li Q, Ping P, Jiang H, Liu K. Nerve conduit filled with GDNF gene-modified Schwann cells enhances regeneration of the peripheral nerve. Microsurgery 2006;26:116–121 [27] Hadlock T, Sundback C, Koka R, Hunter D, Cheney M, Vacanti J. A novel, biodegradable polymer conduit delivers neurotrophins and promotes nerve regeneration. Laryngoscope 1999;109:1412–1416 [28] Fansa H, Keilhoff G, Förster G, Seidel B, Wolf G, Schneider W. Acellular muscle with Schwann-cell implantation: an alternative biologic nerve conduit. J Reconstr Microsurg 1999;15:531–537 [29] Mohammad JA, Warnke PH, Pan YC, Shenaq S. Increased axonal regeneration through a biodegradable amnionic tube nerve conduit: effect of local delivery and incorporation of nerve growth factor/hyaluronic acid media. Ann Plast Surg 2000;44:59–64 [30] Jesuraj NJ, Santosa KB, Newton P, et al. A systematic evaluation of Schwann cell injection into acellular cold-preserved nerve grafts. J Neurosci Methods 2011;197:209–215 [31] Moore AM, Wood MD, Chenard K, et al. Controlled delivery of glial cell linederived neurotrophic factor enhances motor nerve regeneration. J Hand Surg Am 2010;35:2008–2017 [32] Albert E. Einige Operationen an Nerven. Wien Med Presse 1885;26:1285– 1288 [33] Marmor L. The repair of peripheral nerves by irradiated homografts. Clin Orthop Relat Res 1964;34:161–169 [34] Campbell JB, Bassett AL, Boehler J. Frozen-irradiated homografts shielded with microfilter sheaths in peripheral nerve surgery. J Trauma 1963;3:303– 311 [35] Hiles RW. Freeze dried irradiated nerve homograft: a preliminary report. Hand 1972;4:79–84

Peripheral Nerve Allotransplantation [36] Anderson PN, Turmaine M. Peripheral nerve regeneration through grafts of living and freeze-dried CNS tissue. Neuropathol Appl Neurobiol 1986;12: 389–399 [37] Wilhelm K, Ross A. [Homeoplastic nerve transplantation with lyophilized nerve] Arch Orthop Unfallchir 1972;72:156–167 [38] Wilhelm K. [Briding of nerve defects using lyophilized homologous grafts] Handchirurgie 1972;4:25–30 [39] Singh R, Lange SA. Experience with homologous lyophilised nerve grafts in the treatment of peripheral nerve injuries. Acta Neurochir (Wien) 1975;32:125–130 [40] Martini AK. [The lyophilized homologous nerve graft for the prevention of neuroma formation (animal experiment study)] Handchir Mikrochir Plast Chir 1985;17:266–269 [41] Evans PJ, Mackinnon SE, Best TJ, et al. Regeneration across preserved peripheral nerve grafts. Muscle Nerve 1995;18:1128–1138 [42] Lawson GM, Glasby MA. A comparison of immediate and delayed nerve repair using autologous freeze-thawed muscle grafts in a large animal model: the simple injury. J Hand Surg [Br] 1995;20:663–700 [43] Ray WZ, Kale SS, Kasukurthi R, et al. Effect of cold nerve allograft preservation on antigen presentation and rejection. J Neurosurg 2011;114:256– 262 [44] Pollard JD, Fitzpatrick L. A comparison of the effects of irradiation and immunosuppressive agents on regeneration through peripheral nerve allografts: an ultrastructural study. Acta Neuropathol 1973;23:166–180 [45] Pollard JD, McLeod JG, Gye RS. Regeneration through peripheral nerve allografts: an electrophysiological and histological study following the use of immunosuppressive therapy. Arch Neurol 1973;28:31–37 [46] Gye RS, Hargrave JC, Loewenthal J, McLeod JG, Pollard JD, Booth GC. Use of immunosuppressive agents in human nerve grafting. Lancet 1972;1: 647–650 [47] Mackinnon SE, Hudson AR. Clinical application of peripheral nerve transplantation. Plast Reconstr Surg 1992;90:695–699 [48] Gruber SA, Mancias P, Swinford RD, Prashner HR, Clifton J, Henry MH. Livingdonor nerve transplantation for global obstetric brachial plexus palsy. J Reconstr Microsurg 2006;22:245–254 [49] Mackinnon SE. Nerve allotransplantation following severe tibial nerve injury: case report. J Neurosurg 1996;84:671–676 [50] Rogister B, Delrée P, Leprince P, et al. Transforming growth factor beta as a neuronoglial signal during peripheral nervous system response to injury. J Neurosci Res 1993;34:32–43 [51] Mews M, Meyer M. Modulation of Schwann cell phenotype by TGF-beta 1: inhibition of P0 mRNA expression and downregulation of the low affinity NGF receptor. Glia 1993;8:208–217 [52] Perry VH, Brown MC. Role of macrophages in peripheral nerve degeneration and repair. Bioessays 1992;14:401–406 [53] Bunge MB, Johnson MI, Ard MD, Kleitman N. Factors influencing the growth of regenerating nerve fibers in culture. Prog Brain Res 1987;71:61–74 [54] Baichwal RR, Bigbee JW, DeVries GH. Macrophage-mediated myelin-related mitogenic factor for cultured Schwann cells. Proc Natl Acad Sci U S A 1988;85:1701–1705 [55] Ridley AJ, Davis JB, Stroobant P, Land H. Transforming growth factors-beta 1 and beta 2 are mitogens for rat Schwann cells. J Cell Biol 1989;109:3419– 3424 [56] Chandross KJ, Chanson M, Spray DC, Kessler JA. Transforming growth factorbeta 1 and forskolin modulate gap junctional communication and cellular phenotype of cultured Schwann cells. J Neurosci 1995;15:262–273 [57] Romine JS, Aguayo AJ, Bray GM. Absence of Schwann cell migration along regenerating unmyelinated nerves. Brain Res 1975;98:601–606 [58] Aguayo AJ, David S, Bray GM. Influences of the glial environment on the elongation of axons after injury: transplantation studies in adult rodents. J Exp Biol 1981;95:231–240 [59] Aguayo AJ, Kasarjian J, Skamene E, Kongshavn P, Bray GM. Myelination of mouse axons by Schwann cells transplanted from normal and abnormal human nerves. Nature 1977;268:753–755 [60] Sjöberg J, Kanje M, Edström A. Influence of non-neuronal cells on regeneration of the rat sciatic nerve. Brain Res 1988;453:221–226 [61] Nadim W, Anderson PN, Turmaine M. The role of Schwann cells and basal lamina tubes in the regeneration of axons through long lengths of freezekilled nerve grafts. Neuropathol Appl Neurobiol 1990;16:411–421 [62] Hayashi A, Moradzadeh A, Tong A, et al. Treatment modality affects allograftderived Schwann cell phenotype and myelinating capacity. Exp Neurol 2008;212:324–336

[63] Jensen JN, Brenner MJ, Tung TH, Hunter DA, Mackinnon SE. Effect of FK-506 on peripheral nerve regeneration through long grafts in inbred swine. Ann Plast Surg 2005;54:420–427 [64] Fornaro M, Tos P, Geuna S, Giacobini-Robecchi MG, Battiston B. Confocal imaging of Schwann-cell migration along muscle-vein combined grafts used to bridge nerve defects in the rat. Microsurgery 2001;21:153–155 [65] Tseng CY, Hu G, Ambron RT, Chiu DT. Histologic analysis of Schwann cell migration and peripheral nerve regeneration in the autogenous venous nerve conduit (AVNC). J Reconstr Microsurg 2003;19:331–340 [66] Fukaya K, Hasegawa M, Mashitani T, et al. Oxidized galectin-1 stimulates the migration of Schwann cells from both proximal and distal stumps of transected nerves and promotes axonal regeneration after peripheral nerve injury. J Neuropathol Exp Neurol 2003;62:162–172 [67] Whitlock EL, Myckatyn TM, Tong AY, et al. Dynamic quantification of host Schwann cell migration into peripheral nerve allografts. Exp Neurol 2010;225:310–319 [68] Gulati AK. Immune response and neurotrophic factor interactions in peripheral nerve transplants. Acta Haematol 1998;99:171–174 [69] Gulati AK, Cole GP. Nerve graft immunogenicity as a factor determining axonal regeneration in the rat. J Neurosurg 1990;72:114–122 [70] Pollard JD, Gye RS, McLeod JG. An assessment of immunosuppressive agents in experimental peripheral nerve transplantation. Surg Gynecol Obstet 1971;132:839–845 [71] Trumble TE, Shon FG. The physiology of nerve transplantation. Hand Clin 2000;16:105–122 [72] Lassner F, Schaller E, Steinhoff G, Wonigeit K, Walter GF, Berger A. Cellular mechanisms of rejection and regeneration in peripheral nerve allografts. Transplantation 1989;48:386–392 [73] Mackinnon S, Hudson A, Falk R, Bilbao J, Kline D, Hunter D. Nerve allograft response: a quantitative immunological study. Neurosurgery 1982;10:61–69 [74] Yu LT, Rostami A, Silvers WK, Larossa D, Hickey WF. Expression of major histocompatibility complex antigens on inflammatory peripheral nerve lesions. J Neuroimmunol 1990;30:121–128 [75] Glaus SW, Johnson PJ, Mackinnon SE. Clinical strategies to enhance nerve regeneration in composite tissue allotransplantation. Hand Clin 2011;27:495– 509, ixix. [76] Fox IK, Schwetye KE, Keune JD, et al. Schwann-cell injection of cold-preserved nerve allografts. Microsurgery 2005;25:502–507 [77] Evans PJ, MacKinnon SE, Midha R, et al. Regeneration across cold preserved peripheral nerve allografts. Microsurgery 1999;19:115–127 [78] Evans PJ, Mackinnon SE, Levi AD, et al. Cold preserved nerve allografts: changes in basement membrane, viability, immunogenicity, and regeneration. Muscle Nerve 1998;21:1507–1522 [79] Hare GM, Evans PJ, Mackinnon SE, Wade JA, Young AJ, Hay JB. Phenotypic analysis of migrant, efferent lymphocytes after implantation of cold preserved, peripheral nerve allografts. J Neuroimmunol 1995;56:9–16 [80] Atchabahian A, Mackinnon SE, Hunter DA. Cold preservation of nerve grafts decreases expression of ICAM-1 and class II MHC antigens. J Reconstr Microsurg 1999;15:307–311 [81] Levi AD, Evans PJ, Mackinnon SE, Bunge RP. Cold storage of peripheral nerves: an in vitro assay of cell viability and function. Glia 1994;10:121–131 [82] Strasberg SR, Mackinnon SE, Hare GM, Narini PP, Hertl C, Hay JB. Reduction in peripheral nerve allograft antigenicity with warm and cold temperature preservation. Plast Reconstr Surg 1996;97:152–160 [83] Siemionow M, Sonmez E. Nerve allograft transplantation: a review. J Reconstr Microsurg 2007;23:511–520 [84] Hettiaratchy S, Melendy E, Randolph MA, et al. Tolerance to composite tissue allografts across a major histocompatibility barrier in miniature swine. Transplantation 2004;77:514–521 [85] Argall KG, Armati PJ, Pollard JD, Watson E, Bonner J. Interactions between CD4 + T-cells and rat Schwann cells in vitro: 1. Antigen presentation by Lewis rat Schwann cells to P2-specific CD4 + T-cell lines. J Neuroimmunol 1992;40: 1–18 [86] Trumble T, Gunlikson R, Parvin D. A comparison of immune response to nerve and skin allografts. J Reconstr Microsurg 1993;9:367–372 [87] Trumble TE, Gunlikson R, Parvin D. Systemic immune response to peripheral nerve transplants across major histocompatibility class-I and class-II barriers. J Orthop Res 1994;12:844–852 [88] Ishida O, Ochi M, Ikuta Y, Akiyama M. Peripheral nerve allograft: cellular and humoral immune responses of mice. J Surg Res 1990;49:233–238 [89] Fox IK, Mackinnon SE. Experience with nerve allograft transplantation. Semin Plast Surg 2007;21:242–249

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Peripheral Nerve Allotransplantation [90] Strasberg SR, Hertl MC, Mackinnon SE, et al. Peripheral nerve allograft preservation improves regeneration and decreases systemic cyclosporin A requirements. Exp Neurol 1996;139:306–316 [91] Wang MS, Zeleny-Pooley M, Gold BG. Comparative dose-dependence study of FK506 and cyclosporin A on the rate of axonal regeneration in the rat sciatic nerve. J Pharmacol Exp Ther 1997;282:1084–1093 [92] Gold BG, Katoh K, Storm-Dickerson T. The immunosuppressant FK506 increases the rate of axonal regeneration in rat sciatic nerve. J Neurosci 1995;15:7509–7516 [93] Jost SC, Doolabh VB, Mackinnon SE, Lee M, Hunter D. Acceleration of peripheral nerve regeneration following FK506 administration. Restor Neurol Neurosci 2000;17:39–44 [94] Lee M, Doolabh VB, Mackinnon SE, Jost S. FK506 promotes functional recovery in crushed rat sciatic nerve. Muscle Nerve 2000;23:633–640 [95] Udina E, Ceballos D, Gold BG, Navarro X. FK506 enhances reinnervation by regeneration and by collateral sprouting of peripheral nerve fibers. Exp Neurol 2003;183:220–231 [96] Sulaiman OA, Voda J, Gold BG, Gordon T. FK506 increases peripheral nerve regeneration after chronic axotomy but not after chronic schwann cell denervation. Exp Neurol 2002;175:127–137 [97] Doolabh VB, Mackinnon SE. FK506 accelerates functional recovery following nerve grafting in a rat model. Plast Reconstr Surg 1999;103:1928–1936 [98] Feng FY, Ogden MA, Myckatyn TM, et al. FK506 rescues peripheral nerve allografts in acute rejection. J Neurotrauma 2001;18:217–229 [99] Liu J, Farmer JD, Jr, Lane WS, Friedman J, Weissman I, Schreiber SL. Calcineurin is a common target of cyclophilin-cyclosporin A and FKBP-FK506 complexes. Cell 1991;66:807–815 [100] Clipstone NA, Crabtree GR. Calcineurin is a key signaling enzyme in T lymphocyte activation and the target of the immunosuppressive drugs cyclosporin A and FK506. Ann N Y Acad Sci 1993;696:20–30 [101] Dawson TM, Steiner JP, Dawson VL, Dinerman JL, Uhl GR, Snyder SH. Immunosuppressant FK506 enhances phosphorylation of nitric oxide synthase and protects against glutamate neurotoxicity. Proc Natl Acad Sci U S A 1993;90:9808–9812 [102] Yardin C, Terro F, Lesort M, Esclaire F, Hugon J. FK506 antagonizes apoptosis and c-jun protein expression in neuronal cultures. Neuroreport 1998;9: 2077–2080 [103] Gold BG, Zeleny-Pooley M, Wang MS, Chaturvedi P, Armistead DM. A nonimmunosuppressant FKBP-12 ligand increases nerve regeneration. Exp Neurol 1997;147:269–278

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[104] Klettner A, Baumgrass R, Zhang Y, et al. The neuroprotective actions of FK506 binding protein ligands: neuronal survival is triggered by de novo RNA synthesis, but is independent of inhibition of JNK and calcineurin. Brain Res Mol Brain Res 2001;97:21–31 [105] Tanaka K, Fujita N, Higashi Y, Ogawa N. Neuroprotective and antioxidant properties of FKBP-binding immunophilin ligands are independent on the FKBP12 pathway in human cells. Neurosci Lett 2002;330:147–150 [106] Udina E, Ceballos D, Verdú E, Gold BG, Navarro X. Bimodal dose-dependence of FK506 on the rate of axonal regeneration in mouse peripheral nerve. Muscle Nerve 2002;26:348–355 [107] Brenner MJ, Mackinnon SE, Rickman SR, et al. FK506 and anti-CD40 ligand in peripheral nerve allotransplantation. Restor Neurol Neurosci 2005;23:237– 249 [108] Grand AG, Myckatyn TM, Mackinnon SE, Hunter DA. Axonal regeneration after cold preservation of nerve allografts and immunosuppression with tacrolimus in mice. J Neurosurg 2002;96:924–932 [109] Snyder AK, Fox IK, Nichols CM, et al. Neuroregenerative effects of preinjury FK-506 administration. Plast Reconstr Surg 2006;118:360–367 [110] Yan Y, Johnson PJ, Glaus SW, Hunter DA, Mackinnon SE, Tung TH. A novel model for evaluating nerve regeneration in the composite tissue transplant: the murine heterotopic limb transplant. Hand (NY) 2011;6:304–312 [111] Yan Y, Sun HH, Mackinnon SE, Johnson PJ. Evaluation of peripheral nerve regeneration via in vivo serial transcutaneous imaging using transgenic Thy1YFP mice. Exp Neurol 2011;232:7–14 [112] Yan Y, Sun HH, Hunter DA, Mackinnon SE, Johnson PJ. Efficacy of short-term FK506 administration on accelerating nerve regeneration. Neurorehabil Neural Repair 2012;26:570–580 [113] Sun HH, Saheb-Al-Zamani M, Yan Y, Hunter DA, Mackinnon SE, Johnson PJ. Geldanamycin accelerated peripheral nerve regeneration in comparison to FK-506 in vivo. Neuroscience 2012;223:114–123 [114] Yan Y, MacEwan MR, Hunter DA, et al. Nerve regeneration in rat limb allografts: evaluation of acute rejection rescue. Plast Reconstr Surg 2013;131: 499e–511e [115] Moore AM, Ray WZ, Chenard KE, Tung T, Mackinnon SE. Nerve allotransplantation as it pertains to composite tissue transplantation. Hand (NY) 2009;4: 239–244 [116] Glaus SW, Johnson PJ, Mackinnon SE. Clinical strategies to enhance nerve regeneration in composite tissue allotransplantation. Hand Clin 2011;27:495– 509, ix

Median Nerve Entrapment and Injury

9 Median Nerve Entrapment and Injury Kristen M. Davidge and Douglas M. Sammer

9.1 Introduction The median nerve is susceptible to compression at multiple sites in the upper extremity and is vulnerable to mononeuritis as well. Because of these and other factors, the median nerve develops neuropathy more often than other nerves in the upper

extremity. In fact, compression neuropathy of the median nerve at the wrist, or carpal tunnel syndrome (CTS), is one of the most common disorders affecting the hand. Furthermore, as the population ages and as obesity becomes more widespread, the incidence of median neuropathies is likely to rise.

Fig. 9.1 Median nerve anatomy in the upper extremity. This illustration depicts the median nerve throughout the upper extremity originating from the spinal cord to innervating its respective motor and sensory targets.

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9 Fig. 9.2 Internal topographical anatomy of the median nerve. Proximal forearm: The median nerve is composed of several motor and sensory fascicles. In the proximal forearm of the median nerve, the pronator teres fascicle is on the most anterior aspect, followed medially by the flexor carpi radialis (FCR) and palmaris longus (PL) fascicles. Further medially, the flexor digitorum superficialis (FDS) fascicular group is identified. This fascicular group includes two fascicles that correspond to two branch points to the FDS. The anterior interosseous fascicle is on the posterior aspect of the ulnar nerve and continues distal to become lateral before its branch point. This fascicle includes a small sensory articular component to the wrist joint. It is important to acknowledge a thenar motor component within the main sensory component. Distal forearm: The anterior interosseous nerve includes three fascicles: flexor pollicis longus (FPL), flexor digitorum profundus (FDP), and pronator quadratus (PQ)/articular. The FPL and FDP fascicles are large compared to the PQ fascicle and have an anterior orientation. The median nerve includes a recurrent thenar fascicle that is found posterior and lateral. As the median nerve courses distal, the sensory fascicles are revealed to have three major groups: first web space and radial aspect of thumb, second web space, and third web space. These groups have a lateral, middle, and medial orientation, respectively. The palmar cutaneous nerve branches from the anterior and lateral aspect of the median nerve. Hand: The recurrent thenar nerve branches from the lateral aspect of the median nerve to innervate the thenar musculature. The three sensory fascicular groups branch from the median nerve to innervate their appropriate sensory territories. The lateral branch includes the first web space and radial aspect of the thumb fascicles before its respective branch point.

Despite the apparent “commonplace” nature of CTS, its diagnosis and treatment are not always straightforward. Other upper extremity neurologic conditions, including radiculopathy, brachial plexus neuritis, thoracic outlet syndrome, and other less common median neuropathies, can cloud or mimic the diagnosis of CTS. It is therefore important that the surgeon be familiar with the diagnosis and treatment of these other conditions. Some basic questions regarding CTS remain unanswered. The etiology of CTS, for example, is still not fully understood, and its relationship to work-related activities remains somewhat controversial. Recent clinical and laboratory studies have helped to shed light on these issues.

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9.2 Anatomy of the Median Nerve The median nerve arises from the lateral and medial cords of the brachial plexus (▶ Fig. 9.1). The sensory portion comes from the lateral cord, and the medial cord predominantly supplies the motor component (except for C7 pronator and flexor carpi radialis [FCR]). It then crosses anteriorly over the brachial artery and runs along its medial aspect, between the brachialis muscle and the medial intermuscular septum. In < 5% of the population, a supracondylar process is present 3 to 6 cm above the medial epicondyle, which may be up to 2 cm in length.1–3 In addition, a fibrous ligament (ligament of Struthers) may span between the supracondylar process and

Median Nerve Entrapment and Injury

9 Fig. 9.3 Brachialis and median nerve anatomy in the arm and forearm. This illustration describes the branching pattern and direction that is anatomically relevant for both nerves. Fascicular anatomy of the median nerve is also present. Important anatomical landmarks (shown in bold) include the (1) distance between the brachialis nerve “terminus” and medial epicondyle at 7.7 ± 1.9 cm and (2) maximum neurolyzable distance of the proximal anterior interosseous nerve (AIN) fascicle to the medial epicondyle. Histologies were taken from the brachialis nerve branches (*), anterior interosseous fascicle (**), and AIN branch (***).

the medial epicondyle.1 When these structures are present, the median nerve separates from the brachial vessels and passes posterior to the supracondylar process or the ligament of Struthers as it approaches the elbow.4,5 At the elbow, the median nerve courses under the lacertus fibrosus (bicipital aponeurosis), which fans out ulnarly across the antecubital fossa.6,7 The median nerve then passes through the pronator teres muscle, usually between the superficial (humeral) and deep (ulnar) heads. In some instances it passes deep to both heads, and rarely the median nerve will course through the substance of the superficial head.8 After emerging from the distal edge of the pronator teres, it passes behind (dorsal to) the fibrous edge of the flexor digitorum superficialis (FDS), traveling between the FDS and the flexor digitorum profundus (FDP) before becoming more superficial in the distal forearm. There are four branches or groups of branches that arise from the median nerve at the level of the elbow and proximal forearm (▶ Fig. 9.2).9,10 The most proximal group consists of two branches to the pronator teres. This usually arises as a single branch off the anterior surface of the median nerve that

subsequently bifurcates, forming a ‘Y’ shape, with the branches of the Y distal. The pronator branch is superficial, whereas the subsequent branches to the FCR, palmaris longus (PL), and FDS arise from the ulnar side of the median nerve and are deep. Distal to the pronator branches are branches to the FCR, PL, and then most distal the FDS. In addition, there is usually a more distal branch to the FDS (dual branches in 94% of cases). It should be noted that the order of branching of the nerves to the FCR, PL, and FDS can be variable, but they are usually in the order described above. The anterior interosseous nerve (AIN) arises an average of 3 cm distal to the intercondylar line9 and is located on the radial side of the median nerve (▶ Fig. 9.3). It innervates the FDP to the index and long fingers, the flexor pollicis longus (FPL), and the pronator quadratus. The fibers to the FPL are on the radial side of the AIN, and the fibers to the FDP are on the ulnar side. The AIN fascicular group itself is easily separable and can be neurolyzed for a long distance proximal to its physical separation from the median nerve. Small vessels mark the cleavage plane between the AIN and the sensory component of the

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9 Fig. 9.4 Martin-Gruber anastomosis. This illustration details the Martin-Gruber anastomosis (MGA) where the median nerve provides innervation to the ulnar nerve. There are two patterns of the anastomosis that are common, #1 and #3. The anastomosis originates either from the proximal median nerve distal to the elbow or from the proximal anterior interosseous nerve. Occasionally, the MGA can have two branches to innervate the ulnar nerve (#2, #4). Rarely, there will be an MGA where the flexor digitorum profundus is innervated by contributing branches from the median and ulnar nerve (#5, #6).

median nerve. It should be noted that the AIN will move from its radial location within the median nerve in the proximal forearm to an ulnar location within the median nerve in the arm. An understanding of this topography is important for nerve transfer. Martin-Gruber anastomosis is an anomalous median-to-ulnar connection in the proximal forearm (▶ Fig. 9.4). It has been identified in ~ 10 to 25% of extremities in cadaveric studies, and 15 to 40% of patients in nerve conduction studies. A recent cadaveric study showed a bilateral incidence of 15%.11 The “anastomotic” nerve branch may arise from the median nerve proper or from the AIN. In addition, a branch to the FDP may arise from the “anastomotic” branch. The Martin-Gruber anastomosis is particularly important in patients with a high ulnar nerve injury. If the ulnar nerve is injured proximal to the Martin-Gruber anastomosis, some ulnar nerve function in the hand will be preserved. In the distal forearm, the palmar cutaneous branch of the median nerve (PCM) arises from the volar-radial aspect of the median nerve 5 cm proximal to the wrist flexion crease

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(▶ Fig. 9.5). It courses distally between the FCR and PL tendons and penetrates the antebrachial fascia 2 cm proximal to the wrist flexion crease.12 The PCM travels through a specific tunnel at this point, ranging in length from 3 mm to 2 cm. The tunnel may pass through the thickened antebrachial fascia or through the flexor retinaculum itself.13,14 The PCM usually crosses the wrist as a single branch, dividing into three or more branches in the palm, superficial to the palmar fascia.15 A cadaveric study by Watchmaker et al demonstrated that the PCM may lie as much as 6 mm ulnar to the thenar crease.16 Anatomical variations in the course of the PCM have been reported, including branching through the substance of the FCR tendon or PL tendon,17 and the presence of duplicate branches.15 At the wrist the median nerve enters the carpal tunnel (▶ Fig. 9.6). The carpal tunnel is formed by an osseous canal bordered by the carpus dorsally, the hamate and triquetrum ulnarly, and the scaphoid, trapezium, and FCR sheath radially. The volar roof of the carpal tunnel is formed by the antebrachial fascia proximally, the flexor retinaculum or transverse carpal ligament (TCL), and the aponeurosis of the thenar and

Median Nerve Entrapment and Injury

9

Fig. 9.5 Palmar cutaneous branches of the median and ulnar nerve. The palmar cutaneous branch of the median nerve consistently branches from the anterior/lateral aspect of the median nerve. The palmar cutaneous branch of the ulnar nerve is variable in branch pattern. A transverse palmar cutaneous branch of the ulnar nerve is observed branching from the lateral aspect of the superficial sensory branch. This transverse branch can be encountered during our incision (purple) for a carpal tunnel or Guyon canal release, but unlike the PCM in the palm, it is large enough to be protected.

hypothenar muscles distally. Nine tendons—four FDS, four FDP, and the FPL—pass through the carpal tunnel along with the median nerve. The median nerve lies in the volar-radial quadrant of the carpal tunnel, just deep to the flexor retinaculum. At the distal border of the carpal tunnel, the median nerve divides into multiple branches, including the proper digital nerves to the thumb and radial border of the index finger, as well as the second and third common digital nerves. The recurrent motor branch typically arises from the radial border of the median nerve just distal to the flexor retinaculum, turning back to innervate the abductor pollicis brevis (APB), opponens pollicis, and superficial head of the flexor pollicis brevis (FPB). While there is some small plexus formation between the group sensory fascicles, it is minimal. Lanz described four categories of anatomical variation of the median nerve.18 Category I consists of variations in the recurrent motor branch. Although an extraligamentous and recurrent motor branch is considered normal, its incidence in various

studies ranges from 46 to 98%.19–21 The motor branch may arise while still subligamentous, it may take a transligamentous course, or it may arise from the ulnar border of the median nerve. Category II includes an accessory median nerve branch that arises distal to the carpal tunnel. Category III includes a bifid or duplicated median nerve, which may be separated by a persistent median artery or anomalous muscle. Amadio described a bifid median nerve in which the radial half of the nerve traveled in a separate compartment within the carpal canal.22 Category IV consists of an accessory median nerve branch that arises proximal to the carpal tunnel. The accessory branch may travel with the median nerve in the carpal tunnel, or it can perforate and lie volar to portions of the flexor retinaculum. The surgeon must be aware of these variations when performing carpal tunnel release (CTR). The Riche-Cannieu motor anastomosis is an ulnar-to-median nerve connection in the palm that can result in preservation of thenar function in the setting of severe CTS or median nerve

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Fig. 9.6 Transverse illustration of the carpal tunnel of the left hand. Our preferred carpal tunnel release of the transverse carpal ligament occurs superficial to the tendons of the flexor digitorum superficialis. This prevents any scarring from healing to occur over the median nerve and recurrent symptoms.

injury.23 The presence of the Riche-Cannieu anastomosis varies by ethnicity24 and may have a hereditary basis.25 A study by Kimura et al. found that the Riche-Cannieu anastomosis may be present in > 80% of hands and on average contributes 28% of the motor innervation to the APB.24 The Berrettini branch is a common sensory connection between the common digital nerves to the third (median) and fourth (ulnar) web spaces.26

9.3 Carpal Tunnel Syndrome 9.3.1 Introduction Paget provided one of the first descriptions of CTS secondary to trauma in 1854.27 Almost 60 years later, the first histologic evaluation of CTS was performed. In this study, median nerve specimens obtained in an autopsy of a person with thenar wasting demonstrated demyelination of the median nerve within the carpal tunnel.28 Interestingly, the authors suggested that release of the TCL could be performed to treat this disorder. One of the

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first documented CTRs in a patient without a wrist fracture was performed by Drs. Galloway and MacKinnon in 1924 in Winnipeg, Manitoba. Unfortunately, this early CTR was complicated by postoperative pain. Upon reoperation the PCM was found to be entrapped in scar tissue and was excised.29 In1966 Phalen presented the first large series of CTRs and gave an excellent description of the presentation and examination of CTS.30 CTS has an annual incidence of 0.5 to 5.1 per 1000 and an estimated cumulative incidence of 8%.31,32 It occurs more often in women than men and most commonly presents in the fourth or fifth decades of life. It is more common in working populations.33 CTR is one of the most frequently performed hand operations (up to 1.5 per 1000 population annually).34,35

9.3.2 Clinical Presentation and Diagnosis CTS classically presents with pain and paresthesias in the sensory distribution of the median nerve, including the volar

Median Nerve Entrapment and Injury

9 Fig. 9.7 Median nerve innervation. The median nerve innervates the lateral/radial aspect of the anterior hand. Exclusive area of the median nerve to test for sensation is located on the distal aspect of the index finger.

Fig. 9.8 Thenar wasting following prolonged median nerve injury. Thenar wasting was apparent with the patient’s inability to abduct the thumb in the left hand following a median nerve injury.

Fig. 9.9 Effects of proximal compression due to abnormal posture. (a) Normal positioning and posture. (b) Abnormal posture was seen in this patient with forward flexion of the shoulders and neck. Fig. 9.9a is modified from Kendall FP, McCreary EK, Provance PG, Rodgers MM, Romani WA. Muscles: Testing and Function with Posture and Pain (5th ed). Baltimore, Maryland: Lippincott Williams & Wilkins; 2005.

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9 Fig. 9.10 Pain evaluation of carpal tunnel syndrome (CTS) with other extremity pathologies. (a) Patients with CTS may present with a simple pain evaluation with a sensory deficit in the median nerve territory in the hand. (b) However, a significant number of patients with CTS have other extremity pathologies. In this complex case, the patient presented with bilateral carpal tunnel and cubital tunnel and right shoulder imbalance.

aspect of the thumb, index, long, and radial border of the ring fingers (▶ Fig. 9.7). Because the PCM lies volar to the TCL, sensibility over the thenar area is preserved, and patients do not experience symptoms in the PCM sensory distribution. Symptoms may be more severe or occur only at night, often awakening the patient. Symptoms are often exacerbated by gripping and by certain wrist or finger positions. With severe or long-standing compression, thenar weakness and atrophy may be present (▶ Fig. 9.8). It is not uncommon for pain to radiate proximally into the forearm or even the shoulder. However, this proximal pain may be related to cervical disk disease, and the patient should be carefully evaluated for more proximal compression (▶ Fig. 9.9). We evaluated the pain drawings of patients with CTS to see whether they drew symptoms outside the territory of the median nerve and found that there is a significant percentage involving proximal extremity issues (▶ Fig. 9.10). Examination should include the entire extremity and the cervical spine to evaluate the possibility of more proximal pathology. Sensory changes can be quantified with two-point discrimination testing or Semmes-Weinstein monofilament testing. Two-point discrimination changes are a late finding and suggest diminished innervation density of sensory receptors secondary to severe or prolonged nerve compression. Pressure threshold (Semmes-Weinstein monofilament) or vibratory threshold test-

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ing is more sensitive in evaluating sensory changes in CTS and is measured by our hand therapists, but it is not routinely done in the clinic.36 Additionally, the Ten Test can be used to evaluate subtle changes in sensibility.37 First, the examiner lightly strokes a normal digit in the same or contralateral hand. Normal sensibility is assigned a value of 10. The examiner then simultaneously lightly strokes the normal digit and an affected digit, and the patient is asked to rank the sensibility in the abnormal digit on a scale of 1 to 10, with 1 representing absent sensibility. The Ten Test will not be useful with the presence of diffuse bilateral sensory neuropathy. Thenar motor strength and the presence of thenar atrophy should be evaluated. Provocative tests should be performed, including the Tinel test, Phalen test, median nerve compression test, and fist (lumbrical) test. The Tinel test is performed by percussing over the median nerve at the wrist; it is positive when paresthesias occur in the median nerve distribution. The reported sensitivity of the Tinel test ranges from 14 to 65%, and false-positives are common (45 to 65%).38 The Phalen test involves having the patient flex the wrist to ~ 90 degrees for up to 60 seconds; it is positive when paresthesias occur in the median nerve distribution. The Phalen test may have a higher sensitivity and specificity than the Tinel test, 38 although reported sensitivity and specificity vary greatly. The median nerve compression test consists of the application of pressure

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Fig. 9.11 Rate of recovery expectation of patients with various degrees of nerve injury. (a,b) Patients with dynamic ischemic injury can expect immediate return of function as blood flow returns following decompression. (c,d) Patients with demyelination injury (first-degree injury) can expect return of function after a period of time during remyelination of the axons (typically 3 months). (e,f) Patients with axonal injury (second- or third-degree injury) can expect progressive return of function over time (rate of 1 inch/ month). The degree of function is greater in a second-degree compared to a third-degree injury. (g,h) In a mixed injury scenario, the patient can have a combination of immediate and progressive return of function, depending on what components of the nerve are injured and to what degree. (Figs. 9.12a and 9.12c are used with permission from Mackinnon SE, Dellon AL, eds. Surgery of the Peripheral Nerve. New York, NY: Thieme;1988:141,158.)

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to the median nerve at the wrist, usually with the examiner’s thumb. This test is positive if paresthesias occur in the median nerve distribution. Like the other provocative tests, the reported sensitivity and specificity of the carpal tunnel compression test vary greatly (23–100% and 29–100%, respectively).39,40 It should be noted that if the Phalen test and the carpal tunnel compression test are performed simultaneously

as a combined provocative maneuver, symptoms are elicited more quickly. The fist or lumbrical test involves gently flexing the fingers into the palm, without forming a tight fist. This can be accomplished by having the patient loosely grip a pen in the palm. The test is positive when paresthesias occur in a median nerve distribution. A positive test suggests incursion of space-occupying lumbricals into the carpal tunnel with

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Fig. 9.12 Thickening of synovial tissue in the carpal tunnel in a case of recurrent carpal tunnel. A revision carpal tunnel release was performed, and a thickening of the synovial tissue was observed. (a) The dotted incision marks the original incision. The new incision begins proximal to the original incision. (b) Thickened synovial tissues are noted, with the median nerve adherent to the undersurface of the flexor retinaculum.

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Fig. 9.13 This patient presented at our institution 2 years after a complex history that included bilateral endoscopic carpal tunnel releases (ECTRs) by an outside institution. It was noted at the time of the right ECTR that the majority of the median nerve had been lacerated. The lacerated median nerve was immediately primarily repaired. After 6 months without resolution of median nerve pain, stem cells from the patient’s hip were injected into her wrist without relief of pain. During examination at our institution, the patient had good thenar motor function in the right hand and thumb sensation but otherwise no median nerve sensation in the hand except for severe pain.

finger flexion. Recently, the scratch-collapse test was described, and its use as a diagnostic tool in CTS was evaluated. It was found to have a sensitivity of 64%, higher than that of the Tinel test or the wrist flexion/compression test. The specificity of the scratch-collapse test was also high (99%), similar to that of the Tinel test and the wrist flexion/compression test in this study.41

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Although CTS is a clinical, not “electrical,” diagnosis, electrodiagnostic studies provide a useful adjunct to the clinical diagnosis of CTS.42 However, they should be interpreted with an awareness of their limitations. Nerve conduction studies only evaluate large myelinated nerve fibers. Because nerve compression first affects small unmyelinated fibers, nerve conduction studies may initially be negative in the presence of CTS.43 In fact, the false-negative rate of nerve conduction studies is ~ 11%

Median Nerve Entrapment and Injury

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Fig. 9.14 Exposure of the median nerve and internal neurolysis. (a) The median nerve was identified proximal and distal to the zone of injury. It was found to have a course within dense scar tissue. (b) The median nerve was isolated from the scar tissue, and distal neurolysis revealed the sensory branches of the median nerve. The intact thenar motor branch and sensory fascicles to the thumb were protected. Suture material was found within the remainder of the injured median nerve. (c) Proximal neurolysis revealed the fascicular anatomy of the median nerve. The third web space is neurolyzed proximally so that it can be used as graft material.

in patients with clinical CTS.44 False-negative tests presumably occur in patients with early or mild disease who have not yet developed demyelination of large nerve fibers. As demyelination progresses, a focal conduction block occurs, resulting in increased latency and decreased conduction velocity on nerve conduction studies. Although specific diagnostic values vary somewhat between institutions, a distal median nerve sensory latency > 3.5 ms or a distal median nerve motor latency > 4.5 ms is considered positive for CTS. A decrease in amplitude may be seen as well, suggesting axonal loss. Electromyography (EMG) may also show evidence of denervation of the thenar musculature in long-standing or severe cases. There is no diagnostic gold standard, but a combination of “characteristic” symptoms and a positive electrodiagnostic study has the best predictive value for CTS.45 However, because a negative electrodiagnostic study does not preclude the diagnosis of CTS, it is generally accepted that CTS is a clinical diagnosis. We obtain electrodiagnostic studies in all patients who are going to undergo CTR to

“stage” the degree of compression and help to predict the rate of postoperative recovery (▶ Fig. 9.11).

9.3.3 Etiology The etiology of idiopathic CTS is not fully understood. However, the final common pathway is likely compression of the median nerve resulting in impaired microcirculation. A breakdown in the blood–nerve barrier produces subperineurial edema and eventually fibrosis. Demyelination occurs, which is at first localized, then more diffuse, followed by axonal degeneration. Any condition that reduces the volume of the carpal canal or increases the volume of its contents can initiate this process. Several systemic factors have been proposed as risk factors for the development of CTS. Wieslander et al documented the following odds ratios (ORs) for systemic conditions among patients with CTS versus those without diabetes (OR 1.4), thyroid disease (OR 4.6), rheumatoid arthritis (OR 2.3), obesity (OR 2.0),

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Fig. 9.15 Neuroma resection and first web space grafted with a third web space graft. (a) The zone of injury was identified, and the neuroma was resected with proximal and distal median nerve components identified. The third web space was further neurolyzed proximally to mobilize graft material. (b) The proximal end of the third web space fascicle was transected and used as a nerve graft to repair a portion of the median nerve. The proximal remainder of the third web space was transposed proximally to prevent a painful neuroma. The distal third web space was end-to-side transferred to the sensory component of the ulnar nerve to provide rudimentary sensation for donor deficit.

and smoking (OR 1.5).46 This study was limited, however, by small sample size. More recent studies have provided stronger support for the relationship between gender, diabetes, obesity, and CTS. In a large case-control study by Becker et al., ORs for diabetes, obesity, and female gender were 1.8, 2.9, and 3.7, respectively.47 In addition to age, all three factors were significant independent risk factors for CTS in multivariable analyses.47 A recent 17-year longitudinal cohort study similarly found female gender and increasing body mass index to be the most significant personal factors associated with development of CTS. 48 This is consistent with findings of several other authors. 49–52 There is substantial evidence to support an association between certain work activities and CTS. A study by Latko et al. evaluated the relationship between repetitive hand work and CTS.53 The study involved 352 factory workers. Each worker’s job was categorized on a 10-point scale for severity of repetition and hand exertion. All workers underwent screening for CTS by physicians, including history, physical exam, and elec-

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trodiagnostic studies. A clear association was found between repetitive hand use and the diagnosis of CTS. There is also evidence of a strong association between exposure to vibration and CTS. In a study by Wieslander et al, men who underwent CTR had an OR of occupational exposure to vibrating hand tools of 4.3 when compared to randomly selected population referents.46 Furthermore, the OR > 20 years of occupational exposure to vibrating hand tools was 16.0 in men who underwent CTR compared to the general population.46 These associations between CTS and repetition, force, and vibration have been supported by many other authors.54–60 It follows that specific occupations have been recognized as higher risk for development of CTS owing to their repetitive, strenuous nature and repeated wrist flexion posturing. Such industries include manufacturing,58,61 construction,62 meat and poultry processing,59,61,63–65 and dairy farming.66 CTS has also been extensively studied in dental hygienists; in this population, the prevalence of CTS is 6 to 8%,67 with a relative risk of

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Fig. 9.16 Second web space grafted with a medial antebrachial cutaneous nerve (MABC) graft. (a) The MABC was isolated within the arm for donor material. (b) The MABC was then transected with the distal end transferred to the sensory component of the median nerve through an end-to-side epineural window fashion. The sensory component of the median nerve is located on the superior aspect of the median nerve. Note that, in this image, the median nerve has been rotated so that it appears to be on the inferior portion. (c) The MABC graft was used to repair the remaining portion of the median nerve. The thenar branch and remaining sensory branches to the thumb were protected and were found to be not injured.

~ 5.2,68 making dental hygienist one of the highest risk occupations for CTS.69 Duration of occupation is a significant factor in the development of CTS in dental hygienists.68,70 The wrist flexion and/or extension posture adopted during typing has also been related to median nerve compression neuropathy, 71 and significant efforts have been made toward better ergonomic designs in the workplace to reduce CTS symptomatology.72 However, both de Krom et al and Andersen et al. found no statistically significant association between keyboarding and CTS, although the latter authors did identify a possible relationship between use of a mouse for more than 20 hours per week and CTS.49,73 Amadio et al. investigated the role of subsynovial connective tissue and shear injury in the etiology of CTS (▶ Fig. 9.12). They hypothesized that CTS is the result of shear injury to the subsynovial connective tissue, leading to fibrosis that subsequently results in compression and ischemia of the nerve.74

The common patient report of achieving nocturnal relief of symptoms by shaking the hands is pathognomonic of CTS and may relate to the nerve/synovial relationship. We have found personally that nocturnal CTS symptoms can be quickly relieved with placement of the wrist in neutral, finger extension, and movement of the FDP (but not the FPL) tendons, suggesting that wrist positioning, lumbrical muscle pressure, and tenosynovial issues may all be factors in the etiology of CTS. Indeed, McCabe et al suggested that positioning of the wrist in flexion or extension during sleep in a lateral position may present a common causal pathway for many risk factors associated with CTS, including age, gender, obesity, and pregnancy.75 A specific anatomical cause of CTS is identified in only a minority of cases. Often this is a space-occupying lesion, such as a tumor, bone spur, or inflammatory synovitis. Another identifiable anatomical cause of CTS in some patients is lumbrical incursion into the carpal tunnel. Because the lumbricals originate

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Fig. 9.17 Pre- and postoperative pain diagrams. (a) Preoperative pain diagram demonstrates pain upon presentation 2 years after a right hand ECTR, failed primary median nerve repair, and stem cell injection into the wrist. (b) Postoperative pain diagram. Following the revision reconstruction by our institution, pain was reduced significantly.

from the FDP tendons, their origin in relation to the carpal tunnel varies with finger position. With the fingers extended, their origin is distal to the carpal tunnel. However, when the fingers are flexed, the lumbricals are drawn into the carpal tunnel by the proximal excursion of the FDP tendons. In most people this does not cause a problem. However, in heavy laborers with hypertrophic lumbricals, this may lead to compression of the median nerve.76,77

9.3.4 Nonsurgical Treatment Conservative initial treatment is appropriate for mild CTS. Commonly recommended nonoperative treatments include activity modification, neutral wrist splinting, nonsteroidal antiinflammatory drugs (NSAIDs), and corticosteroid injection. Many other treatments have also been used with varying reported success, including vitamin B6, diuretics, laser acupuncture, magnets, and chiropractic therapy. A Cochrane review of nonoperative modalities failed to demonstrate any benefit over placebo of vitamin B6, diuretics, NSAIDs, magnets, laser acupuncture, or chiropractic treatment.78 Splinting is often effective at improving or eliminating mild or nocturnal CTS symptoms.79,80 Off-the-shelf wrist cock-up splints are often used and are readily available. However, these splints immobilize the wrist in 20 to 30 degrees of extension. Multiple studies have demonstrated that carpal canal pressure

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Fig. 9.18 Steps in the carpal tunnel release procedure. Incision for carpal tunnel release: an incision is made ulnar to the thenar crease between the palmar sensory territories of the median and ulnar nerve. In addition, this approach allows for the division of the transverse carpal ligament (TCL) well away from the median nerve.

is increased with wrist flexion or extension and that carpal canal pressure is lowest with the wrist in a neutral position. 81–84 Therefore, splints should be modified to maintain the wrist in neutral flexion-extension (this can often be accomplished by “stepping on” the splint). We recommend that the patient wear

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Fig. 9.19 Identification of the TCL. The distal aspect of the dissection continues until the tendinous V intersection of the thenar and hypothenar muscles is identified. The division of this ligament occurs longitudinally (dotted line) from this tendinous V over the tendons of the flexor digitorum superficialis (FDS). The V is the distal landmark for release.

the splint at night only. A study by Walker et al demonstrated that there was no significant difference between nocturnal use alone and full-time splinting in terms of symptom improvement.79,80 Furthermore, if neutral splints are worn during the day, patients tend to alter their elbow and shoulder positions, resulting in pain in these areas secondary to abnormal posture. We have found that custom-made splints to (1) keep the wrist in neutral; (2) keep the metacarpal-phalangeal (MCP) joints extended; and (3) leaving the interphalangeal joints free are more successful. Blocking the MCPs prevents the lumbricals from gliding into the carpal tunnel. It also prevents “fisting” and pressure on the median nerve in the forearm by the flexor/pronator muscles. Injection of corticosteroid into the carpal tunnel is often effective at relieving CTS symptoms temporarily.85 Most studies show that the results of steroid injection are short-lived,85 although one study demonstrated sustained improvement in symptoms in 50% of patients at 1 year after injection. 86 A positive response to steroid injection is believed to be a good prog-

nostic indicator for success after CTR, although a negative response to steroid injection does not mean that CTR will fail. Steroid injection is also used as a diagnostic tool in patients with a questionable diagnosis or in patients with recurrent symptoms after CTR. However, we reserve steroid injections for the rare patients with CTS who require short-term relief (e.g., pregnancy-related CTS). Carpal tunnel steroid injection should be performed using a 25-gauge needle. The needle is inserted through the skin 1 cm proximal to the wrist flexion crease and ulnar to the PL tendon. It is advanced at a 45-degree angle into the carpal tunnel. Once the needle is in the carpal tunnel, the steroid can be injected without resistance. If the patient experiences paresthesias or pain in the fingers during needle insertion or injection, the needle should be withdrawn and the injection aborted to prevent a nerve injection injury. It should be noted that in an animal model, the only steroid that does not cause nerve injury when injected directly into a nerve is dexamethasone.87

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Fig. 9.20 Division of the TCL. Dividing the TCL reveals the tendons of the FDS. As the lateral half of the ligament is elevated, the median nerve is revealed posteriorly. This “ulnar” division of the ligament prevents any scarring from healing over the median nerve to the divided carpal ligament.

9.3.5 Open versus Endoscopic Carpal Tunnel Release Endoscopic carpal tunnel release (ECTR) was first performed over 20 years ago.88,89 Even though two decades have passed, the safety and efficacy of ECTR are still debated. Multiple randomized, controlled trials have been performed that compare open CTR (OCTR) to ECTR. 90–102 None of these demonstrate a significant difference in short- or long-term symptomatic outcomes. Furthermore, none of these studies demonstrate a significant difference in complication rates (▶ Figs. 9.14–9.18). In a case series by Hankins et al., 14,722 patients were treated with ECTR, with one reported iatrogenic injury.103 The two primary advantages of ECTR are that the incision is probably less painful in the short term and that patients may be able to return to work more quickly. A 2002 study by Trumble et al.

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showed quantitatively less scar tenderness after surgery in the ECTR group, persisting up to 3 months postoperatively. 102 In the same study, return to work was 20 days earlier in the ECTR group compared to the OCTR group.102 A 2007 meta-analysis of the literature concluded that ECTR resulted in an earlier return to work and activities of daily living (ADLs) by an average of 6 days when compared to OCTR.104 In summary, ECTR can be as safe and effective as OCTR when performed by an appropriately trained and experienced surgeon. It may result in less pain early after surgery, and may allow an earlier return to work. However, we prefer OCTR and do not advocate ECTR. OCTR is a reliable and time-tested operation with a low complication rate. Our preference is influenced by the substantial number of complications following ECTR that are referred to our center. Even a small injury to the median nerve can be life-altering for the patient and his or her family (▶ Fig. 9.14). Although median nerve injury is a known complication of both open and endoscopic

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Fig. 9.21 Proximal dissection and antebrachial fascia. Once the TCL is completely divided, the dissection is taken proximally through the antebrachial fascia to ensure complete release of the carpal tunnel. The surgeon moves to the end of the table to directly visualize this release; it is not done blindly.

techniques, we believe that most surgeons would regret not having used an open technique if the median nerve becomes injured during ECTR.

9.3.6 The Advantages of Open Carpal Tunnel Release In 1973 Taleisnik described the “standard” CTR incision, which involved a long curvilinear incision in the palm that extended into the distal one-third of the forearm.12 The standard OCTR incision is now usually confined to the palm and measures 2 to 3 cm in length.105 Based on the findings of an anatomical study

by Watchmaker et al, we recommend making the incision 5 mm ulnar to the interthenar depression to avoid injury to the PCM (▶ Fig. 9.5).16 This also allows division of the TCL at its ulnar aspect, preventing scar formation directly over the median nerve (▶ Fig. 9.6). A Bier block or local anesthetic with sedation is sufficient. The skin is incised with a knife, and dissection is thus carried through the subcutaneous fat to the palmar aponeurosis (▶ Figs. 9.19–9.22). The palmar aponeurosis is divided longitudinally with a knife, and dissection continues until the transverse fibers of the TCL are identified. At least 20% of the time an ulnar cutaneous branch is seen in the distal one-third of the incision and is easily protected (▶ Fig. 9.5; ▶ Fig. 9.22).

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Fig. 9.22 Transverse palmar cutaneous branch of the ulnar nerve. A transverse palmar cutaneous branch of the ulnar nerve can be encountered in the distal third during exposure for a carpal tunnel and/or Guyon canal release. It is usually seen crossing the incision between 2.0 and 3.5 cm distal to the wrist crease.

The transverse carpal ligament is divided sharply along its ulnar aspect with a knife (▶ Fig. 9.19; ▶ Fig. 9.20). The distal- and proximal-most extent may be completed with tenotomy scissors under direct visualization. The distal extent of the release is the V between the hypothenar and thenar muscles/fascia. If marked thenar atrophy is present, the recurrent motor branch may be released and specifically decompressed through this incision. If a tight band of antebrachial fascia is identified, it can be divided with scissors under direct visualization (▶ Fig. 9.21). Capacious release is confirmed by visual inspection or Freer elevator to probe the proximal and distal extents of the carpal canal. The tourniquet is deflated, hemostasis is achieved, the wound is irrigated, and the skin is closed with simple interrupted sutures. A well-padded wrist splint is applied for comfort and is removed in 2 or 3 days. Finger motion and light hand

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use are encouraged immediately. Sutures are removed 14 days postoperatively. Patients wear a wrist splint at night for 2 to 3 weeks after surgery to prevent bowstringing of the flexor tendons. A gradual return to full activity is permitted 5 to 6 weeks after surgery. Neurolysis should not be performed routinely. Multiple studies have demonstrated no difference in postoperative symptoms when comparing OCTR with and without internal neurolysis.106–108 Routine epineurotomy and routine tenolysis are also unnecessary.109,110 Smaller, “limited open” incisions have been described, with and without the use of specialized instruments.111–113 There is no strong evidence that these techniques have an advantage over standard OCTR.104 In obese patients, we use a slightly modified technique (▶ Fig. 9.23). A forearm tourniquet is used to prevent a venous-only tourniquet effect. In addition, a longer incision is used, including a zigzag

Median Nerve Entrapment and Injury

Fig. 9.23 Forearm tourniquet and extended incision for carpal tunnel release in obese patients. (a) In obese patients, a forearm tourniquet can be used for visualization during exposure. (b) The incision is extended across the wrist in a zigzag fashion for complete safe visualization.

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extension proximal to the wrist flexion crease for complete visualization. With an increasing incidence of obesity in our patient population, our incisions are becoming longer, not shorter.

9.3.7 Outcomes In appropriately selected patients, CTR results in consistent improvement in symptoms and patient satisfaction, ranging from > 80% to as high as 98%.30,114–117 After CTR, nocturnal and intermittent symptoms tend to improve rapidly. Residual symptoms are slower to improve (▶ Fig. 9.11). Two-point discrimination changes or thenar weakness indicates a more severe injury and may take a year to improve.118,119 Higgs et al demonstrated that even in patients with excellent or good outcomes, half of patients reported some degree of residual CTS symptoms.120 In spite of this, the reoperation rate for recurrent or persistent symptoms is low, usually < 5%.115,121,122 We believe that the degree and rapidity of recovery after CTR depend on the type and severity of nerve injury (▶ Fig. 9.11).

Patients with nocturnal paresthesias and only intermittent symptoms likely have only dynamic ischemia of the nerve. Certain wrist positions or hand activities will result in decreased perfusion of the nerve, with symptoms that resolve quickly once blood flow is restored. We believe that patients with only dynamic ischemia will have very rapid, almost immediate relief of symptoms after CTR. Prolonged compression, however, will lead to demyelination. Symptoms become persistent, and threshold tests will be positive. In addition, electrodiagnostic studies will show increased sensory latencies. In this scenario, we expect symptoms to take up to 3 or 4 months to resolve, as remyelination occurs (▶ Fig. 9.4). Patients with long-standing or severe compression will develop axonal loss. Symptoms are constant, and two-point discrimination changes or thenar atrophy will be present. Electrodiagnostic studies show diminished amplitude, reflecting axonal loss. EMG may show fibrillation potentials, incomplete motor unit recruitment, and abnormal insertional activity. Recovery is slow, with nerve regeneration occurring at ~ 1 mm per day. Finally, many patients will have

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Fig. 9.24 (a) Iatrogenic injury of the palmar cutaneous branch of the median nerve (PCM) during carpal tunnel release (CTR). This patient had significant pain in the distribution of the PCM following CTR. The original incision and the area of the patient’s maximum pain are noted with the dotted line. The new incision is ulnar to the original incision and begins proximally. (b) Exposure and identification of the injured PCM. The median nerve and the PCM are identified proximally and followed into the area of the previous surgery. Scar formation is noted all around the palmar cutaneous branch. Rather than just neurolyze the palmar cutaneous branch, we elected to excise this neuromatous tissue and proximally transpose the PCM. (c) Surgical pain management for the injured PCM. The most proximal portion of the PCM is clamped with a hemostat prior to cauterizing the distal end of the median nerve. The cauterizing “caps” the PCM. The hemostatic compression of the PCM produces a second-degree injury, which essentially moves the front of regenerating axons several centimeters more proximal to the distal end of the nerve. The nerve is then transposed proximally to lie between the superficialis and the profundus muscles in a proximal direction. It is held in this position with several cc’s of fibrin glue.

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Median Nerve Entrapment and Injury Table 9.1 Baseline Demographics and Intraoperative Findings for Patients Undergoing Revision Carpal Tunnel Surgery Patient Profile

Persistent (N = 34)

Recurrent (N = 17)

New (N = 34)

Age (y) (mean ± SD)

51.1 ± 14.5

55.7 ± 10.9

47.2 ± 10.9

Gender was Male

9 (26.5%)

8 (47.1%)

15 (44.1%)

Smokers

11 (32.4%)

9 (52.9%)

16 (47.1%)

BMI (mean ± SD)

31.4 ± 6.5

28.3 ± 6.1

28.9 ± 5.8

Take pain medication

11 (32.4%)

5 (29.4%)

13 (38.2%)

Receive workers’ compensation

14 (41.2%)

7 (41.2%)

22 (64.7%)

Number of prior releases 1

28 (82.4%)

15 (88.3%)

28 (82.3%)

2

5 (14.7%)

2 (11.8%)

5 (14.7%)

3

1 (2.9%)

0

1 (2.9%)

Prior endoscopic release

3 (8.8%)

4 (23.5%)

8 (23.5%)

Time from first release to final release (mo) (mean ± SD)

31.7 ± 44.0

131.0 ± 83.9

28.4 ± 41.5

Numbness

24 (70.6%)

12 (70.6%)

23 (67.6%)

Pain

28 (82.4%)

10 (58.8%)

29 (85.3%)

Weakness

8 (23.5%)

4 (23.5%)

8 (23.5%)

Paresthesia

12 (35.3%)

10 (58.8%)

14 (41.2%)

Median 2-pd (mm, (mean ± SD)

5±2

4±1

5±2

Pinch strength (lbs.) (mean ± SD)

9.2 ± 6.6

12.6 ± 5.92

9.7 ± 6.4

Grip strength (lbs), mean ± SD

31.5 ± 27.8

47.8 ± 27.0

35.9 ± 30.8

Average pain (VAS) mean ± SD

6.23 ± 2.31

6.54 ± 1.85

6.44 ± 2.42

Worst pain (VAS) mean ± SD

7.04 ± 2.28

6.70 ± 1.92

6.78 ± 2.52

Adherence of nerve to Skin Scar Flexor retinaculum

3 (7.1%) 10 (23.8%) 36 (85.7%)

6 (31.6%) 4 (21.1%) 13 (68.4%)

3 (8.6%) 9 (25.7%) 26 (74.3%)

Incomplete release: Proximal Distal Proximal and distal

17(40.5%)

6 (31.6%)

7 (20.0%)

12 (28.6%)

7 (36.8%)

8 (22.9%)

9 (21.4%)

1 (5.3%)

1 (2.9%)

Median nerve injury/transection

2 (4.8%)

2 (10.5%)

17 (48.6%)

Compression palmar cutaneous branch

0

0

3 (8.6%)

Presenting symptoms

9

Intraoperative findings

Abbreviations: 2-pd, two-point discrimination; BMI, body mass index; SD, standard deviation; VAS, visual analogue scale.

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Fig. 9.25 Pre- and postoperative pinch/grip strength and pain levels for revision carpal tunnel release. Change in mean physical exam and pain scores before and after revision carpal tunnel surgery. Error bars signify standard error. Average follow-up times were 3.5 ± 2.4, 4.1 ± 3.7, and 4.7 ± 3.3 months for the persistent, recurrent, and new subgroups, respectively.

Fig. 9.26 Revision carpal tunnel release (CTR) following a failed CTR. This patient had previous carpal tunnel surgery with initial relief of symptoms, then recurrence of symptoms several years later. The original incision is noted. The new proposed incision is ulnar to the original incision and begins much more proximal to the incision in normal tissue.

more than one component of median nerve injury. These patients often experience stages of improvement as the complex nerve injury resolves. Multiple factors, including duration of symptoms, severity of electrodiagnostic study results, patient age, and workers’ compensation status, have been thought to influence the outcome of CTR. Cseuz et al. demonstrated that outcomes were better in patients who underwent CTR within 1 year of developing CTS,123 and DeStefano et al. noted better results when CTR was

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performed within 3 years of developing CTS.124 However, not all studies support a correlation between duration of symptoms and outcomes.125 Furthermore, a number of studies have shown that electrodiagnostic results are not predictive of outcomes after CTR.44,125–127 There is some concern that elderly patients have poor outcomes after CTR, because they tend to present with more advanced disease and may have a diminished capacity for nerve regeneration and decreased central plasticity. However, Weber et al demonstrated no correlation between

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Fig. 9.27 Proximal exposure and identification of the median nerve. A vessel loop is placed around the median nerve.

patient age and symptom relief in an elderly population, who showed a high satisfaction rate after CTR.128 A consistent improvement in symptoms and high satisfaction rates after CTR in the elderly have also been demonstrated in other studies.129,130 One group that has been reported to have comparatively inferior results after CTR are patients receiving workers’ compensation.118 However, our results with patients receiving workers’ compensation generally have been excellent.

9.3.8 Complications Severe complications after CTR are rare but can be devastating. An injury to the median nerve or the PCM can irreparably alter a patient’s life (▶ Fig. 9.24). Lacerations or transections of the median nerve or its branches, the ulnar nerve, tendons, and blood vessels have been reported.27 Complex regional pain syndrome is another rare but serious complication of CTR.102,131 Problems with wound healing or infection can occur but are uncommon.110 Pillar pain is a complication unique to CTR. It is defined as postoperative pain located in the thenar or hypothenar areas and is distinct from incisional pain. The etiology is not well understood, but it may be due to alterations in the carpal arch after division of the TCL or to a

change in the position and stability of the origin of the thenar and hypothenar muscles.132 Another posssibility is an edematous or neurologic origin.133 Pillar pain has been documented after both OCTR and ECTR.134 Regardless of etiology, it can take many months to improve.135 In our experience using the ulnarbased incision described above, we do not see pillar pain and thus believe that it may be related to microneuromas of small cutaneous branches (▶ Fig. 9.5; ▶ Fig. 9.18). We believe that these are less common with a more ulnar incision.

9.3.9 Revision Surgery It is important to distinguish between patients who have had no improvement in symptoms after surgery (persistent), those with a recurrence of the same symptoms after initial improvement (recurrent), and those with new or different symptoms (new). Patients who experienced no improvement likely have an incompletely divided TCL, particularly if ECTR was performed or in obese patients where proximal and distal releases are more difficult.136 The possibility of an incorrect initial diagnosis or symptoms from a concomitant process should also be considered in these patients. Patients with recurrence after initial improvement or resolution of symptoms are more likely

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Fig. 9.28 Identifying the distal V intersection between the thenar and hypothenar muscles. The median nerve is then followed distally into the area of previous surgery, where dense scar tissue is encountered. Next, the Guyon canal is opened. This allows identification of the distal V, which marks the intersection of the thenar and hypothenar muscles.

to have intraneural scarring or median nerve adhesions to the underside of the TCL or the overlying scar. When the nerve is scarred to the TCL, the patient may experience pain or paresthesias with wrist extension due to traction on the nerve. The possibility of more proximal nerve compression at the forearm, elbow, or cervical spine should be evaluated, and the patient should be questioned and examined for evidence of peripheral neuropathy. Finally, in patients with new and different nerve symptoms (usually pain) after surgery, one must consider the possibility of an iatrogenic nerve injury. Patients with new symptoms often complain of neuropathic pain in the distribution of the median nerve. The portion of the median nerve that innervates the third web space is most at risk with CTR. When an injury to this portion of the median nerve occurs, patients will report relief of symptoms in the thumb and index finger, but they will complain of burning pain on the ulnar side of the long finger and the radial side of the ring finger and will have a

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painful Tinel sign at the site of the injury. An injury to the PCM results in pain at the incision, as well as burning and hypersensitivity in the proximal palm over the thenar area (▶ Fig. 9.24). Rarely, patients may have complete transection of the median nerve with complaints and findings across the entire median nerve sensory distribution. Even more rare are problems with the ulnar nerve. Patients who present with an iatrogenic nerve injury require a detailed sensory and motor examination of the hand in order to localize the injury. The Strauch Ten Test can be used to quickly evaluate sensibility in the hand, followed by static two-point discrimination testing (Disk-Criminator, North Coast Medical Inc., Gilroy, CA). Moving two-point discrimination is also measured, with > 8 mm being considered nonfunctional. Because the Tinel test can be exquisitely painful in the area of injury, we prefer to use the “proximal” Tinel sign to help determine what portion of the nerve has been injured. The examiner starts percussion over the median nerve well proximal

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9

Fig. 9.29 Distal exposure and identification of the median nerve. The flexor retinaculum is released on the ulnar side of the flexor retinaculum, with the distal dissection ending once the distal V has been reached. There still is dense scarring around the median nerve.

to the site of injury. This will elicit pain in the sensory distribution of the injured portion of the nerve. This proximal Tinel sign represents nerve fibers that have regenerated proximally up the nerve along the basal lamina. We have also found the scratch-collapse test to be useful in these patients. The initial treatment of recurrent or persistent CTS should be conservative, consisting of splinting and occupational therapy. Reoperation should be considered only after conservative management fails and should be reserved for patients with a clearly established diagnosis in whom other sources of symptoms have been ruled out. Electrodiagnostic studies can be helpful in some cases, but these will usually remain positive even after successful CTR. Sometimes the neurologist will be able to determine a change between the pre- and postoperative studies. Unfortunately, electrodiagnostic studies poorly evaluate

postoperative changes and may not be helpful in decision making. As opposed to patients with persistent or recurrent symptoms, patients who present with new symptoms secondary to iatrogenic nerve injury are often in extreme distress. Splinting and neuropathic medications such as Lyrica or Lidoderm patches may be used to provide comfort, but a neurotmetic injury needs to be treated surgically. We reviewed the demographics, intraoperative findings, and outcome data on 85 consecutive patients (95 hands) undergoing revision carpal tunnel surgery between January 2001 and March 2012 (▶ Table 9.1).137 Patients were classified according to whether they had persistent, recurrent, or new symptoms. Significant postoperative improvements in grip and pinch strength were seen in the persistent and new groups (▶ Fig. 9.25). Mean pain scores significantly decreased in all

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Fig. 9.30 Division of the transverse carpal ligament ulnar to the median nerve. Once the entire flexor retinaculum has been divided, the median nerve is seen to be adherent to the underside of the flexor retinaculum, tethered up to the area of the previous surgical incision.

three groups following revision surgery; however, patients with recurrent symptoms demonstrated the most substantial improvement in pain overall.

9.3.10 Operative Procedure We use an extended incision well ulnar to the thenar crease and ignore the previous incision, which is usually more radial (and may be in part responsible for the recurrence of symptoms) (▶ Figs. 9.27–9.40). We have found that it is safe to do so and have had no problems with the vascularity of the skin bridge. Dissection should begin proximal to the previous surgical field and should proceed distally through the operated area and into healthy tissue. Internal neurolysis is necessary, and we consider this

232

to be a graded procedure. Initially, the median nerve is freed from the overlying attachment to the flexor retinaculum. Longitudinal and circumferential epineurotomies are performed, and neurolysis is performed until bands of Fontana are noted (▶ Fig. 9.40).105 These bands represent redundancy of nerve fibers. Their presence suggests that there is no more compression. In situations in which an injury to the median nerve is suspected, the median nerve and its branches should be evaluated for evidence of injury. We begin our neurolysis in the healthy proximal portion of the median nerve and dissect to the portion of the nerve that we know to be injured based on the patient’s preoperative examination. The portion of the nerve that is injured is excised and reconstructed with autologous tissue whenever possible (▶ Fig. 9.13).

Median Nerve Entrapment and Injury

9

Fig. 9.31 Exposure of the median nerve. Using blunt tenotomy scissors, the median nerve is separated from its attachment to the overlying transverse carpal ligament.

The terminal portion of the AIN to the pronator quadratus is an excellent donor for small defects because it is in the field of dissection, and its harvest results in no sensory deficit. If a larger injury has occurred involving the entire median nerve or the critical thumb/index portion of the nerve, then a longer autograft should be used. In these situations, the medial antebrachial cutaneous (MABC) nerve is our donor of choice, as all the reconstruction is limited to one extremity (▶ Fig. 9.16). An incision from the axilla to the elbow may be needed to harvest adequate MABC donor graft. This nerve is located adjacent to the basilic vein and has two branches, anterior and posterior. If only

one is needed, the anterior branch has less of a donor deficit. To avoid persistent numbness in the donor territory, the distal divided end of the donor nerve is sewn end to side to any adjacent normal sensory nerve. A recent animal model neuroma study by Dorsi et al demonstrates that the hyperalgesia that can occur in an area of denervated skin is a result of a pathway that is independent from the proximal end of the cut nerve.138 It may be that this hyperalgesia is due to aberrant reinnervation of the denervated skin by surrounding intact sensory nerves. The goal of performing an end-to-side transfer of the distal cut end of a donor nerve after nerve harvest is to recover sensation

233

Median Nerve Entrapment and Injury

9

Fig. 9.32 Longitudinal neurolysis of the median nerve. At this point, microscissors are used to open up the external epineurium longitudinally. A marking pen has been used to “ink” the area of the proposed transverse neurolysis of the external epineurium.

and also to prevent aberrant reinnervation and subsequent pain in the denervated donor distribution (▶ Fig. 9.6). The third web space portion of the median nerve is also a suitable donor in some situations (▶ Fig. 9.15). If the third web portion of the median nerve is already injured focally, the remaining healthy portions to the third web space proximal to the site of injury can be harvested and used as donor graft.139 The technique to identify this fascicular group is described in Chapter 5. Briefly, this involves tapping lightly on the volar surface of the nerve with microforceps, moving from the radial side toward the ulnar side, and identifying a cleavage plane or longitudinal depression between the portion to the third web space and the remainder of the nerve. If this part of the median nerve is harvested for nerve grafting, we perform an end-toside transfer of the distal divided portion to the third web space

234

to the ulnar nerve or to the remainder of the median nerve to restore some sensibility in the third web space distribution and to prevent painful aberrant reinnervation. If the gap is less than 3 cm, an acellularized allograft may be used for noncritical sensation. We prefer allografts over empty nerve conduits because allografts retain the basal lamina, which is important in nerve regeneration. If a nerve conduit is used, we recommend taking a small portion of the proximal healthy nerve, mincing it, and placing it in the conduit to provide Schwann cells and trophic factors. After neurolysis and reconstruction, the median nerve should lie in healthy tissue free from scar. If this cannot be achieved, soft tissue flap coverage is required. Many options for coverage have been described, including the hypothenar fat pad,140,141

Median Nerve Entrapment and Injury

9

Fig. 9.33 Transverse neurolysis of the median nerve. The epineurium has now been released transversely as well as longitudinally. Compare the spacing of the blue ink marks here with ▶ Fig. 9.32 to note how much release has been achieved with the transverse neurolysis

palmaris brevis,142,143 abductor digiti minimi,144 and vein wrapping.145,146 We favor the hypothenar fat flap or Seprafilm. Outcomes after revision CTR are not as consistent as after primary CTR, with success rates ranging from 50 to 75% in some studies.121,147,148 Cobb and Amadio noted that, although most patients experience some symptomatic improvement, persistent symptoms are more common than after primary surgery.121 They identified active workers’ compensation and negative EMG findings to be predictors of poor results.121 Jones et al noted symptomatic improvement following revision surgery with rates of 76% (primary endoscopic release) and 90% (primary open release) and complete relief of symptoms with rates of 56% (primary endoscopic release) and 57% (primary open release).149 We have also recently reported our results (▶ Table 9.1; ▶ Fig. 9.25).137

9.4 Pronator Syndrome Pronator syndrome is much less common than CTS. It is more common in women and usually presents in the fifth decade.150 It may also be more common in patients who perform repetitive upper extremity activities.7 Individuals who maintain significant forearm pronation during work or other activities may develop a short, tight pronator teres and are at risk for nerve compression at this level. Sleeping with “fisting” and fingers “gripped” may also develop this entrapment. Symptoms include pain in the volar forearm, exacerbated by pronation against resistance reproduced with supination and pressure over the median nerve at the leading edge of the pronator. In addition, median nerve distribution paresthesias or sensory changes may be present. Unlike CTS, symptoms and findings may involve the

235

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Fig. 9.34 Revision carpal tunnel release (CTR) following open reduction and internal fixation (ORIF) of a wrist facture and failed CTR. (a) This patient had an ORIF of a wrist fracture with a CTR at the same time. The two incisions for the CTR and the ORIF are noted. The planned new incision is well ulnar to the previous surgeries and begins more proximal to those surgeries.

9

Fig. 9.35 Proximal exposure and identification of the median nerve. The median nerve is first identified proximally and then carefully followed distally into the region of the carpal tunnel.

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Median Nerve Entrapment and Injury

Fig. 9.36 Distal exposure and identification of the median nerve. Guyon canal is opened in order to clearly identify the V between the thenar and hypothenar muscles. The V is marked by a circle. The flexor retinaculum can then be released heading toward the V.

9

Fig. 9.37 Division of transverse carpal ligament (TCL). The flexor retinaculum has been completely released.

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Fig. 9.38 Identification of the median nerve through subsynovial tissue attached to the TCL. The median nerve is clearly seen adherent to the undersurface of the flexor retinaculum exactly along the course of the previous, more radial division of the flexor retinaculum.

9

Fig. 9.39 Longitudinal and transverse neurolysis of the median nerve. The nerve is bluntly freed from its attachment to the overlying flexor retinaculum with tenotomy scissors; then neurolysis is performed both longitudinally and transversely.

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Median Nerve Entrapment and Injury

Fig. 9.40 Longitudinal and transverse neurolysis of the median nerve. (a) A longitudinal neurolysis on a recurrent carpal tunnel is performed to open up the thickened epineurium. (b) Ink marks are then noted on the thickened epineurium. The transverse neurolysis and epineurotomy are performed along this ink mark. (c) Once the transverse neurolysis has been performed, the distance gained in this transverse release is apparent and is between 1 and 2 cm. The distance of release is noted by the separation of the ink marks.

Fig. 9.41 Steps in pronator teres syndrome surgery. Incision for median nerve decompression: a lazy-S incision is made in the proximal left forearm. The surgeon will operate from the ulnar side of the extremity.

9

Fig. 9.42 Identification and protection of the antebrachial cutaneous nerve branches. Any crossing cutaneous branches, either from the medial or lateral antebrachial cutaneous nerves, are protected throughout.

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Fig. 9.43 Identifying the radial vessels and superficial branch of the radial nerve as a landmark to locate the tendon of the superficial head of the pronator teres. The first step in median nerve release in the forearm is to identify the radial vessels and the radial sensory nerve. The tendon of the superficial head of the pronator teres will be found between these two structures.

9

Fig. 9.44 Identifying the tendon of the superficial head of the pronator teres. The tendon of the superficial head of the pronator teres is easily identified between the radial sensory nerve and the radial vessels.

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Median Nerve Entrapment and Injury

Fig. 9.45 Step lengthening of the superficial head of the pronator teres. A step-lengthening tenotomy in the pronator teres tendon is performed. The deeper step in the tenotomy is made proximally where it is easier to visualize. The more superficial step is made more distally.

9

Fig. 9.46 Once the step lengthening is made in the tendon, a significant release on the whole pronator muscle will be achieved. In this figure, the length obtained by this tenotomy is easily seen as between 1 and 2 cm.

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Median Nerve Entrapment and Injury

Fig. 9.47 Proximal dissection and exposure of the median nerve. The next step in the release will be to move proximally to identify the median nerve. It will be located between the flexor pronator muscle and the radial vessels. The trick in finding the median nerve proximally is to stay ulnar to the vessels.

9

Fig. 9.48 Deep head of the pronator teres. The median nerve is noted deep and intimate with the flexor pronator muscle. It can also be seen to be well ulnar to the radial vessels.

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Median Nerve Entrapment and Injury

Fig. 9.49 Once the median nerve is identified, the next step will be to move distally to identify the deep head of the pronator teres, which will wrap on the radial side of the median nerve and can be just visualized wrapping around the median nerve on the radial side. Frequently, this will have a fair amount of muscle superiorly, and the tendinous fascia will be deep. Once the muscle is released, there is a tendinous band.

9

Fig. 9.50 Remnant tendinous fascia of the deep head of the pronator teres. Once this muscle tendon is removed, there is frequently thin fascial tissue, which will kink and compress the nerve. This needs to be released as well.

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Median Nerve Entrapment and Injury

Fig. 9.51 Tendinous arch of the flexor digitorum superficialis (FDS). After the release of the deep head of the pronator teres and any distal fascial tissue, the tendinous arch of the FDS is identified for release. In this case, a very thin but tight remnant of the tendinous arch was found.

9

Fig. 9.52 Arch of the FDS. After the release of the tendinous arch, any additional arch of the FDS that is found compressing the median nerve is released. In this case, the FDS arch has an attachment superficial to the median nerve.

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Median Nerve Entrapment and Injury

Fig. 9.53 Median nerve release in the forearm. After the deep head of the pronator has been removed, the tendinous leading edge of the superficialis frequently will be seen compressing the median nerve.

PCM distribution. Patients may also experience weakness or difficulty with small object manipulation. On examination, pain is reproduced by digital pressure over the median nerve in the proximal forearm. A Tinel sign may be present at this level as well, and the pronator teres may be tender.151,152 Weakness may be present in median nerve innervated muscles.7 There are multiple potential sites of compression, including a supracondylar process or ligament of Struthers, the pronator teres, the bicipital aponeurosis (lacertus fibrosus), and the fibrous edge of the FDS. Other, less common causes of compression have been described, including an anomalous head of the pronator teres, a snapping brachialis muscle, Gantzer muscle (accessory FPL), and an anomalous palmaris profundus or FCR brevis.105,153,154 Provocative maneuvers used to evaluate the common sites of compression are resisted forearm pronation (pronator teres), resisted elbow flexion with the forearm supinated (lacertus fibrosus), and resisted long finger proximal interphalangeal flexion (FDS). Passive supination with pressure placed over the median nerve at the leading edge of the pronator teres will reproduce symptoms. In addition, the scratch-collapse test is frequently positive. This test is performed by firmly pressing over the median nerve to elicit a response due to the nerve’s being deep, rather than a scratch of the skin superficial to the nerve. Occasionally, a ligament of Struthers may be palpated.151 Electrodiagnostic studies are helpful in confirming the clinical diagnosis when positive,2 but negative studies more are common.6, 155 Radiographs should be obtained to identify a supracondylar process.156 Recently, there has been a move by a workers’ compensation carrier to require positive electrodiagnostic studies

9

prior to surgery. A draft of the guidelines requires positive electrodiagnostic findings that localize the median nerve compression to the forearm, stating that electrodiagnostic studies are the gold standard in diagnosing proximal median nerve entrapment. Given the high incidence of negative studies in patients with proximal median nerve entrapment, our opinion is that these requirements are inappropriate and may result in denial of medically necessary treatment. For example, if a patient’s symptoms are pain (mediated by C and A delta fibers) or intermittent and not constant pain (ischemia), then the electrodiagnostic studies will by definition be normal. Initial treatment of pronator syndrome consists of stretching of the pronator teres and forearm flexors. Activity modification, splinting, and NSAIDs may also be helpful. Surgery is indicated when conservative measures fail. A longitudinal S-shaped incision is made in the proximal one-third of the volar forearm, with the proximal extent in the antecubital fossa (▶ Fig. 9.41). Dissection is carried down to the lacertus fibrosus, which is divided sharply and cutaneous nerves protected (▶ Fig. 9.42). The tendon of the superficial head of the pronator teres is identified just radial to the radial artery and is lengthened in a step-cut fashion (▶ Figs. 9.44–9.47). Next, the median nerve is identified proximally, medial to the brachial vessels (▶ Fig. 9.47). It is followed distally until the deep head of the pronator teres is encountered, where it originates from the ulna along with the ulnar portion of the FDS (▶ Fig. 9.48; ▶ Fig. 9.49; ▶ Fig. 9.50). The tendinous portion of the deep head of the pronator teres is resected, and the tendi-

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Fig. 9.54 Flexor digitorum superficialis (FDS)-to-anterior interosseous (AIN) nerve transfer. The redundant FDS nerve branch is an available donor for transfer to restore AIN function in isolated AIN injuries. A secondary FDS branch is preserved as it branches distal in the forearm. The donor FDS branch is identified adjacent to the AIN branch and on the medial aspect of the median nerve; the AIN is identified on the lateral/posterior aspect of the median nerve. The donor FDS branch (green) is transferred to the recipient AIN (red) in an end-to-end fashion.

nous leading edge of the FDS, also known as the arch of the FDS, is divided (▶ Fig. 9.51; ▶ Fig. 9.52). Any crossing vessels that compress the median nerve should be ligated and divided. These steps will expose the median nerve and its branches in the proximal forearm, in particular the anterior interosseous nerve can be identified on the radial side (▶ Fig. 9.53). If not identified preoperatively, an attempt should be made to palpate a supracondylar process or ligament of Struthers through the proximal aspect of the exposure. The surgeon should be able to easily run a finger proximally along the median nerve. If any compression is felt, the incision should be extended proximally, allowing resection of the ligament or supracondylar process. After hemostasis and layered closure, a sterile dressing and a well-padded splint keeping the elbow in slight flexion are applied. The splint is removed within a few days, and the patient is instructed in range of motion exercises, including elbow extension with forearm supination.105

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9.5 Anterior Interosseous Nerve Palsy AIN palsy results in weakness of the FDP to the index finger (occasionally the long finger), the FPL, and the pronator quadratus (although pronator quadratus weakness is not clinically detectable when the pronator teres is functional).157 There is no sensory loss or paresthesias, and pain usually is not present. The syndrome occurs spontaneously, usually without inciting event. However, in some cases AIN palsy may result from local trauma or compression by a tumor or by fibrous bands of the pronator teres or FDS. Most cases are not due to mechanical compression, but rather neuritis and will recover spontaneously. We have been referred several cases following surgery for completely unrelated issues. Parsonage-Turner syndrome should be considered in the setting of a prior viral syndrome, especially if there is pain associated with the palsy. If diagnosed

Median Nerve Entrapment and Injury early (within 72 hours), medical consultation with a neurologist is crucial, because patients may respond to antiviral medications or systemic corticosteroids. In general, AIN palsy should be considered nonoperative, and patients are given 7 to 9 months to show evidence of clinical or electrical recovery (motor unit action potentials or nascent units).158 However, we have had patients with delayed improvement where release of the median nerve through the pronator teres at 4 to 6 months has hastened recovery. In some cases, recovery may be spotty (e.g., the FDP recovers, but the FPL does not). In these circumstances, intramedian nerve transfers (e.g., FDS to FPL) may be performed to restore function (▶ Fig. 9.54). The radial side of the AIN innervates the FPL, and the ulnar side, the FDP. These fascicles are isolated and neurotized for specific reinnervation. An isolated AIN palsy rarely occurs after other surgical procedures and does not imply negligence. It may be viral in origin, with the stress of surgery eliciting the palsy. When it occurs in the same upper extremity as the surgery, it is particularly dismaying. Cases following median nerve decompression have been reported and are likely secondary to neuritis and not direct mechanical injury.159

9.6 Conclusion Median neuropathy most commonly occurs due to compression at the carpal tunnel. When conservative treatment fails, open carpal tunnel release safely and reliably improves symptoms in most patients, including the elderly and those with workers’ compensation claims. Complications after CTR are rare but can be devastating, and the utmost care should be taken to avoid injury to the median nerve and its branches. More proximal sites of median nerve compression are less common, but they should be considered in every patient who presents with median nerve symptoms. Initial treatment for pronator syndrome is conservative, and surgery should be reserved for patients who fail nonoperative management. AIN palsy is a purely motor mononeuropathy, without pain or sensory deficit. It is usually due to neuritis and should be treated conservatively. If symptoms do not resolve within 5 to 7 months, then surgical decompression may be considered.

9.7 Acknowledgment The authors thank John C. Koshy, MD for his assistance with the portion of this chapter that relates to recovery after carpal tunnel release.

9.8 References [1] Laha RK, Dujovny M, DeCastro SC. Entrapment of median nerve by supracondylar process of the humerus: case report. J Neurosurg 1977;46:252–255 [2] Gessini L, Jandolo B, Pietrangeli A. Entrapment neuropathies of the median nerve at and above the elbow. Surg Neurol 1983;19:112–116 [3] Terry RJ. A study of the supracondyloid process in the living. Am J Phys Anthropol 1921;4:129–139 [4] Crotti FM, Mangiagalli EP, Rampini P. Supracondyloid process and anomalous insertion of pronator teres as sources of median nerve neuralgia. J Neurosurg Sci 1981;25:41–44 [5] Suranyi L. Median nerve compression by Struthers ligament. J Neurol Neurosurg Psychiatry 1983;46:1047–1049

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Ulnar Nerve Entrapment and Injury

10 Ulnar Nerve Entrapment and Injury Kristen M. Davidge and Kirsty U. Boyd

10.1 Introduction Compression neuropathy is commonly found to affect the ulnar nerve and can occur at many potential sites along the course of the nerve from the brachial plexus to the wrist. Cubital tunnel is the second most common compression neuropathy in the upper extremity, and the surgical technique for the management of this diagnosis remains controversial.1 Guyon canal is another site of frequent compression, with a variety of potential etiologies contributing to symptoms in this region. Similarly, given its superficial location around the elbow and its course through the forearm and wrist, the ulnar nerve is susceptible to injury from direct trauma. Because of the longer distance to the motor end plates associated with ulnar nerve recovery and the complexity of intrinsic motor function, outcomes following injury have been notoriously poor. With the recent shift to the use of distal nerve transfers in peripheral nerve surgery, the recovery of intrinsic hand function has been significantly improved. This chapter highlights the anatomy of the ulnar nerve, the common etiologies of ulnar neuropathy, and the various options for management for compression neuropathies of the ulnar nerve. It also discusses the approach to failed decompression and revision surgery.

10.2 Ulnar Nerve Anatomy 10.2.1 Course and Internal Topography Upper Arm The ulnar nerve is formed from the C8 and T1 nerve roots and comprises the terminal branch of the medial cord of the brachial plexus (▶ Fig. 10.1). At its origin in the axilla, it lies medial to the axillary artery and travels distally anterior to the triceps brachii muscle. In the middle third of the arm, the ulnar nerve pierces the medial intermuscular septum and travels between this septum and the medial head of the triceps. The ulnar nerve gives off no branches proximal to the elbow apart from an infrequent articular branch. Topographically, the motor fascicles to the flexor carpi ulnaris (FCU) are located on the lateral side of the ulnar nerve in the upper arm, which is important for nerve transfers.2

Elbow At the elbow, the ulnar nerve enters a fibro-osseous tunnel between the medial epicondyle of the humerus and the olecranon (▶ Fig. 10.2). Commonly referred to as the cubital tunnel, this space is bounded superficially by a fascial bridge spanning the olecranon and medial epicondyle, which can be thickened at its most distal part between the two heads of the FCU. This distal thickening, called Osborne band, was first described in 1957 3 and has been found in 77% of cadaveric dissections.4 On its deep surface, the fibro-osseous tunnel is formed by the ulnar groove of the medial epicondyle proximally, as well as the joint capsule and medial collateral ligament distally.5

The fascicular anatomy of the ulnar nerve is variable at the elbow. At the level of the medial epicondyle, Sunderland found that the motor fibers to the intrinsics and sensory fibers to the hand were more superficial than the motor fibers to the FCU and flexor digitorum profundus (FDP).6 This finding may explain the relative sparing of FCU and FDP function in compression of the ulnar nerve at the elbow.7 We have not determined a specific topography of the ulnar nerve at the elbow. The increased number of fascicles and increased connective tissue around the nerve at this level render this challenging.

Forearm Distal to the cubital tunnel, the ulnar nerve enters the forearm between the two heads of the FCU and travels medial to the ulnar artery between the FCU and the FDP muscles. The most proximal motor branch to the FCU arises ~ 1.6 cm distal to the medial epicondyle.8 Subsequent branches to the FCU and two ulnar FDP muscles originate from both the radial and ulnar sides of the nerve in the proximal and midforearm, respectively.8 The remaining three fascicular groups of the ulnar nerve in the forearm comprise the following: the dorsal sensory branch to the ulnar hand, ring, and small fingers (ulnar group); the motor branch to the intrinsic muscles (central group); and the sensory branch to the volar aspect of the small finger and ulnar half of the ring finger (radial group) (▶ Fig. 10.3). The dorsal cutaneous branch of the ulnar hand (DCU) exits the main nerve ~ 9 cm proximal to the wrist crease, leaving the motor fascicular group in the ulnarmost position of the ulnar nerve as it approaches the Guyon canal. The DCU, however, is “neurolyzable” to a distance almost 18 cm proximal to the wrist crease. This is an important point if the DCU is to be used as a donor graft to reconstruct distal ulnar nerve transection injuries and when proximal transposition of this nerve is performed for the management of DCU neuromas.

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Wrist and Hand Since its first description by Jean Casimir Feliz Guyon in 1861, 9 the anatomy of the ulnar nerve at the wrist has been studied in detail by several authors.10–13 Gross and Gelberman divided this area into three zones according to the internal topography of the ulnar nerve.13 At the entrance to zone 1 proximally, the ulnar nerve and artery lie radial to the FCU tendon and pisiform bone, superficial to the transverse carpal ligament (inserting onto the pisiform), and deep to the antebrachial fascia. Distally, the antebrachial fascia blends with the volar carpal ligament and may be reinforced by the palmaris brevis muscle to form the roof of the Guyon canal. Just distal to the pisiform, the motor nerve fascicles transition to the deep surface of the ulnar nerve and diverge from the more superficial sensory fascicles. Along with the deep branch of the ulnar artery, the motor branch courses deep to the leading edge of the flexor digiti minimi muscle, over the pisohamate ligament, and radially around the hook of the hamate (zone 2). At this level, the floor of the canal is formed by opponens digiti minimi and the medial wall

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Fig. 10.1 Ulnar nerve anatomy. The ulnar nerve originates from the C8,T1 roots and extends throughout the upper extremity to innervate its respective motor and sensory targets.

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Fig. 10.2 Compression points of the ulnar nerve. In the upper extremity, compression of the ulnar nerve can exist at any of the following sites: arcade of Struthers, medial intermuscular septum, cubital tunnel, Osborne ligament, deep flexor-pronator aponeurosis, antebrachial fascia, Guyon canal, and deep motor branch at leading edge of hypothenar muscles. Provocative tests can help diagnose the site of compression (red). Specifically, the scratchcollapse test with ethyl chloride hierarchy test, which involves palpating these areas, is a useful tool.

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Fig. 10.3 Internal topographical anatomy of the ulnar nerve. The ulnar nerve has a distinct fascicular pattern as it courses distally from the forearm into the hand. The motor component of the ulnar nerve is found between the sensory component and the dorsal cutaneous fascicles. Distal to the dorsal cutaneous nerve branch point, the motor component is identified on the medial aspect of the ulnar nerve. This motor component branches from the ulnar nerve on its medial/ulnar aspect to become the deep motor branch and then dives deep to the leading edge of the hypothenar muscles to course around the hook of the hamate and innervate the intrinsic muscles. The sensory component of the ulnar nerve is a larger fascicular group compared to the motor component (with a 2/3:1/3 ratio) and innervates the ulnar aspect of the ring finger, the small finger, and the fourth web space.

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Ulnar Nerve Entrapment and Injury by abductor digiti minimi. As it courses distally, the sensory branch sits superficial to the hypothenar musculature, with the superficial branch of the ulnar artery (zone 3). The ulnar artery and its tributaries remain radial and superficial to the ulnar nerve as it travels distally into the wrist and palm. Specific release of the ulnar nerve through the Guyon canal is a challenging procedure, as the leading edge of the hypothenar fascia is released prior to actually visualizing the deep motor branch of the ulnar nerve. Review of the accompanying surgical video is recommended.

10.2.2 Blood Supply The extrinsic vascular supply to the ulnar nerve arises from the axillary artery, superior and inferior ulnar collateral arteries, posterior ulnar recurrent artery (PURA), and the ulnar artery. 14 The superior ulnar collateral artery (SUCA) branches from the brachial artery at the midhumeral level, then pierces the medial intermuscular septum to course with the ulnar nerve on its posterior surface.15 It travels with the ulnar nerve for a variable distance (4 to 15 cm), passing through the cubital tunnel and terminating deep to the FCU by anastomosing with the PURA. The SUCA forms the basis for vascularized ulnar nerve grafts used occasionally in brachial plexus reconstruction. The PURA arises from the ulnar artery near its origin and supplies the ulnar nerve in the forearm. The inferior ulnar collateral artery makes a minor contribution to blood supply to the ulnar nerve at the elbow.14 The extrinsic vascular supply of the ulnar nerve anastomoses with the intrinsic vessels within the epineurial and endoneurial sheaths (▶ Fig. 10.4). If the extrinsic system is disrupted, nerves can survive over long distances based on their intrinsic vasculature. In fact, Maki et al demonstrated that blood flow paradoxically increases in nerve segments where only the proximal and distal intrinsic vasculature remains intact. 16 These authors also found that blood flow within a nerve is maintained over a diameter-to-length ratio of 1:63 when only proximal intrinsic blood flow is intact and 1:45 when only one extrinsic vessel remains intact.16 These important findings provide justification for the safety and feasibility of mobilization and anterior transposition of the ulnar nerve in the surgical treatment of cubital tunnel syndrome. Similarly, a recent clinical study of ulnar nerve transposition with and without preservation of vascular pedicles showed no difference in sensory or motor function.17

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10.2.3 Anatomical Variations Martin-Gruber anastomoses are anomalous motor connections between the median and ulnar nerves in the proximal forearm (see Chapter 9). Four types have been described: type 1 (60%), in which motor branches from the median nerve travel with the ulnar nerve to innervate “median” muscles; type 2 (35%), in which motor branches from the median nerve travel with the ulnar nerve to innervate “ulnar” muscles; type 3 (3%), in which motor fibers from the ulnar nerve travel with the median nerve to innervate “median” muscles; and type 4 (1%), in which motor fibers from the ulnar nerve travel with the median nerve to innervate “ulnar” muscles.18 Types 3 and 4 anomalous ulnar-tomedian connections have also been referred to as the Marinacci anomaly.19

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Martin-Gruber anastomoses have been identified in ~ 10 to 25% of extremities in cadaveric studies and 15 to 40% of patients in nerve conduction studies. A more recent cadaveric study showed a bilateral incidence of 15%.20 The “anastomotic” nerve branch may arise from the median nerve proper or from the anterior interosseous nerve (AIN). In addition, a branch to the FDP may arise from this anastomotic branch. The MartinGruber anastomosis is particularly important in patients with a high ulnar nerve injury. If the ulnar nerve is injured proximal to this anomalous connection, some ulnar nerve function in the hand will be preserved. The Riche-Cannieu anastomosis is an anomalous ulnar-tomedian motor connection in the palm, between the deep motor branch of the ulnar nerve and the recurrent branch of the median nerve. The Berrettini branch is a common sensory connection between the common digital nerves to the third (median) and fourth (ulnar) web spaces.21

10.3 Etiology and Pathophysiology of Ulnar Nerve Compression 10.3.1 Ulnar Nerve Compression Proximal to the Elbow The arcade of Struthers is a thick fascial connection between the medial head of the triceps and the medial intermuscular septum located ~ 10 cm proximal to the medial epicondyle. It is a potential site of proximal nerve compression especially after nerve transposition. In a series of more than 500 ulnar nerve explorations, Mackinnon and Dellon failed to find an arcade at this level and therefore concluded that this was an iatrogenic compression band due to incomplete release of the medial intermuscular septum in a transposition procedure.22 The editor of this book now believes the arcade was not recognized and has publicly and personally apologized to Robert Spinner, Morton Spinner’s son for what she believes was an error. With its relationship to both the septum and the ulnar nerve and the triceps muscles, the arcade of Struthers can set up a dynamic relationship resulting in medial arm pain and after transposition surgery, compression on the ulnar nerve. As we have moved toward using sterile tourniquets in cubital tunnel surgery, we have definitely been impressed by the arcade of Struthers as a proximal compressive structure and take care to evaluate this as a potential problem after anterior transposition of the nerve.23 A rare additional cause of proximal ulnar compression is an anomalous chondroepitrochlearis muscle, which arises from the sixth and seventh ribs and inserts on the medial epicondyle.24

10.3.2 Cubital Tunnel Syndrome Potential etiologies for ulnar nerve compression at the elbow are multiple and can include trauma (fractures, dislocations, and direct soft tissue trauma), arthritis, heterotopic ossification, soft tissue masses, metabolic conditions predisposing to neuropathy, such as diabetes and alcoholism, external compression, and occupations that require repetitive or persistent elbow flexion. Importantly, elbow flexion is a common posture as-

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Fig. 10.4 Impact of intrinsic blood flow during mobilization in a nerve. (a) A nerve is supplied with blood from both extrinsic and intrinsic sources. (b) When the nerve is mobilized and its extrinsic vessels are divided, the intrinsic flow increases from both proximal and distal ends and is supplied by the endoneurial vessels. This scenario mimics a transposition of a nerve, specifically, an ulnar nerve transposition. (c) When the nerve is mobilized and is transected distally, intrinsic flow increases from the proximal end and is maintained up to a diameter-to-length ratio of 1:63 in a rabbit sciatic nerve model. This scenario mimics a nerve transfer when the donor distal end and recipient proximal end are mobilized for transfer. (Modified from Maki Y, Firrell JC, Breidenbach WC. Blood flow in mobilized nerves: results in a rabbit sciatic nerve model. Plast Reconstr Surg 1997; 100: 627-633, discussion 634-635)

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sumed by many during sleep that can result in recurrent and potentially prolonged periods of increased pressure and tension on the ulnar nerve. Over time, this may lead to a symptomatic compression neuropathy at the elbow. Congenital variations, such as cubitus valgus, an anconeous epitrochlearis muscle (present in 11% of cadaveric specimens 4), a low-lying or prominent medial triceps muscle, and a thick Osborne band, may also contribute to the development of cubital tunnel syndrome. Hypoplasia of the fascial roof of the cubital tunnel has been related to increased risk of ulnar nerve subluxation and nerve dysfunction.25 There has been much interest in the dynamic anatomy of the ulnar nerve at the elbow, which has been studied with increasing sophistication over time. This research has led to several

theories regarding the pathophysiology of cubital tunnel syndrome. Feindel and Stratford were among the first to note that the cubital tunnel narrows during elbow flexion.26 Subsequent cadaveric studies have documented a decrease in cross-sectional area by 30 to 45% and a change in morphology of the cubital tunnel from triangular to elliptical as the elbow progresses from extension to flexion.7,27–29 Other findings with increasing elbow flexion have included decreased cross-sectional area of the ulnar nerve,28 increased intra- and extraneural pressures within the cubital tunnel,28,30–32 increased strain on the ulnar nerve,33,34 and elongation and excursion of the ulnar nerve.7,29,33,35 A recent study by Novak et al, however, suggested that significant excursion of the ulnar nerve occurs proximal to the cubital tunnel but not within the tunnel itself (▶ Fig. 10.5).36 Furthermore, they

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Fig. 10.5 Excursion of the ulnar nerve. Elbow flexion will exert increased tension on the ulnar nerve, specifically at the cubital tunnel. Tension is further increased with the shoulder elevated as the brachial plexus courses anterior to the shoulder. An ulnar nerve transposition can significantly relieve tension when it is mobilized anterior to the medial epicondyle.

found no stretching of the ulnar nerve, but rather a slack region proximal to the elbow that is taken up with flexion.36 A major limitation of the above studies is their examination of cadaveric specimens with supposedly normal ulnar nerves. Four studies have evaluated extraneural pressures in patients undergoing surgical treatment for cubital tunnel syndrome and have supported the idea that pressures in the cubital tunnel are maximal in full flexion.37–40 However, studies have failed to show significant reductions in pressures following decompression of this region.28,30,41 Mechanisms other than dynamic compression, such as traction, ischemic changes, and extraneural scar, have therefore been proposed as additional contributing factors to symptomatology with elbow flexion in cubital tunnel syndrome.28,33,35,37,42,43 Furthermore, recurrent subluxation of the ulnar nerve has been hypothesized to contribute to mechanical irritation and compression neuropathy at the elbow (▶ Fig. 10.6). Subluxation has been reported in 7 to 16% of ulnar nerves in healthy volunteers. 44,45 Recently, Calfee et al documented hypermobility of the ulnar nerve in one-third of 400 elbows but found no relationship between hypermobility and ulnar nerve dysfunction. 46

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10.3.3 Ulnar Nerve Compression at the Forearm and Wrist Ulnar nerve compression in the forearm and wrist are mostly due to extrinsic forces (▶ Fig. 10.2). In the forearm, compression may occur where the nerve exits the FCU47 and by fibrovascular bands coursing over the nerve from the ulnar artery to the distal FCU.48

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Compression of the ulnar nerve at the wrist was first described by Jay Ramsey Hunt in 1908.10 Although compression at the level of the wrist is the second most common site of ulnar nerve impingement, it occurs only one-twentieth as commonly as cubital tunnel syndrome.49 Compression at this level can have a variety of etiologies, but it is not infrequently linked to trauma. Specifically, hypothenar hammer syndrome,50 fractures of the hook of the hamate,47–53 and fractures of the distal radius or carpal dislocations51,54–57 have all been associated with low ulnar neuropathy. Perhaps more commonly, Guyon canal syndrome has been linked to compression by extra-anatomical structures such as ganglion cysts,58,59 giant cell tumors,60 lipomas,61 tortuous vascular leashes or vascular malformations,62,63 schwannomas, and anomalous musculature.64–66 With our increasing familiarity with the scratch-collapse test and the use of ethyl chloride to “freeze out” areas that have elicited a positive scratch collapse, we have been impressed by an association between compression of the ulnar nerve at the tendinous leading edge of the hypothenar musculature and by the thickened distal antebrachial fascia. This has been especially observed in patients with intrinsic muscle atrophy and likely represents a form of “double crush,” as described by Upton and McComas.67

10.4 Evaluation of a Patient with Ulnar Nerve Compression 10.4.1 History A thorough history will often delineate the site of ulnar nerve compression. Patients will complain of pain, paresthesias, or

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Fig. 10.6 Subluxation of the ulnar nerve. A subluxing ulnar nerve occurs during elbow flexion and onto the medial epicondyle. This is an indication for transposition to relieve tension and the repetitive strain of the ulnar nerve subluxing. This specific case was a revision ulnar nerve procedure, denoted by the extended incision, when a simple decompression failed and produced painful subluxation.

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Fig. 10.7 Ulnar nerve sensory innervation. The ulnar nerve innervates the ulnar aspect of the anterior/posterior hand. The exclusive area of the ulnar nerve to test for sensation is located on the distal aspect of the little finger.

diminished sensation in the ulnar nerve distribution, specifically, in the small finger and the ulnar half of the ring finger (▶ Fig. 10.7). Patients may associate these symptoms with accompanying weakness of the intrinsic muscles of the hand, often alluding to being “clumsy,” cramping, or dropping things (▶ Fig. 10.8). Difficulty with manipulating door handles, shirt buttons, and keys and opening jars are frequent complaints. Patients with distal compression at the wrist will often complain of worse hand function than those with cubital tunnel alone. Symptoms are often related to elbow positioning and are frequently worse with prolonged elbow flexion. Many patients awaken at night with increased pain and paresthesias related to a natural tendency to flex the elbows during sleep. Symptoms tend to progress slowly over many years, and although patients may notice a gradual loss of muscle bulk in the hand, they have often learned to accommodate for their hand weakness over time.

10.4.2 Pain Questionnaire In our institution, all patients are asked to complete the Pain Questionnaire with each visit. This document is valuable for several reasons: It helps to qualify and characterize the patient’s symptoms and allows the examiner to determine the impact of the compression neuropathy on the patient’s quality

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of life. Asking patients to document their symptoms on an anatomical illustration can help to elucidate multiple sites of compression and other contributing etiologies (▶ Fig. 10.2; ▶ Fig. 10.9). The questionnaire can also be useful to document postoperative progress following surgey.

10.4.3 Physical Examination Physical examination of the ulnar nerve starts distally and works proximally; it includes a comparison of the affected extremity and the contralateral side. Motor and sensory deficits are also compared and expected to be generally similar. If sensory loss is much worse than motor loss, a systemic sensory neuropathy is considered. If motor deficits are substantially more severe than sensory deficits, cervical compression of the C8–T1 nerve roots or a systemic motor neuropathy should be excluded. A diagnosis of cervical radiculopathy should also be considered when both thenar atrophy and ulnar intrinsic wasting are present. Motor examination starts with inspection for wasting of the first dorsal interossei dorsally, hypothenar eminence volarly, and forearm musculature (▶ Fig. 10.8). Intrinsic muscle weakness may also manifest as clawing of the ring and little fingers (Duchenne sign) due to unopposed action of the long extensors at the metacarpophalangeal joints and long flexors at the inter-

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Fig. 10.8 Presentation of ulnar nerve injury. Examination techniques to test for motor deficits include finger abduction/adduction, attempting to cross the middle over the index finger, and lateral pinch. Signs of ulnar nerve deficit are clawing, Wartenburg sign, hypothenar wasting, Froment sign, and first dorsal interosseous wasting during pinch. We recognize a “pseudo” Froment’s sign where there is a definite difference in IP joint flexion between sides but not apparent without a comparison to the normal side. This is especially seen in patients who normally hyperextend the IP joint.

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10 Fig. 10.9 Pain evaluation of simple and complex ulnar neuropathy. (a) Patients with ulnar neuropathy may present with a simple pain evaluation that includes a sensory deficient in the ulnar nerve territory. (b) The pain evaluation is an important tool to determine whether an additional upper extremity component is involved that is contributing to the ulnar neuropathy. In this specific case, the patient is also describing shoulder pain and diffuse forearm pain.

phalangeal (IP) joints and/or an abducted posture of the little finger (Wartenburg sign) due to unopposed action of extensor digiti minimi (▶ Fig. 10.10).68 Strength of the intrinsic muscles is assessed first, followed by the extrinsic muscles. Intrinsic muscle strength is tested by examining index and small finger abduction against resistance, as well as by the patient’s ability to cross his or her index and middle fingers (▶ Fig. 10.8).69 Froment sign is another method used to evaluate weakness of the first dorsal interosseous and thumb adductor muscles (▶ Fig. 10.11).68 The patient is asked to hold a piece of paper in his or her first web space bilaterally. As the examiner gently pulls away the paper, patients with intrinsic weakness will attempt to maintain their pinch using the flexor pollicis longus, thereby flexing their thumb on the affected side. Although a positive Froment sign entails overt flexion of the thumb IP joint, we consider any difference in thumb IP joint flexion between the two hands to be important and have termed this a “pseudoFroment” sign (▶ Fig. 10.12). Proximal ulnar nerve compression may result in weakness of the FCU and ulnar-innervated FDP muscles. FCU function is testing by looking for radial

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deviation with wrist flexion, and ulnar wrist flexion against resistance. Flexion of distal IP joints of the ring and small fingers against resistance tests ulnar-innervated FDP extrinsic ulnar function. Sensation in the ulnar nerve distribution (small and ulnar half of the ring fingers) can be evaluated using the Ten Test, 70 as well as static and moving two-point discrimination (Disk-Criminator, North Coast Medical Inc., Gilroy, CA). Specific testing of sensation in the DCU distribution as compared to volar-ulnar sensation helps to determine relative compression of the ulnar nerve at the elbow (DCU sensation decreased) versus Guyon’s canal (DCU sensation spared).

10.4.4 Provocative Testing Provocative testing of the ulnar nerve involves assessing for a Tinel sign at multiple potential sites of compression, specifically, the elbow for cubital tunnel syndrome and the wrist for compression at the Guyon canal (▶ Fig. 10.2). Pressure over potential compression sites, especially in areas where the ulnar nerve lies more superficially, can also elicit symptoms.

Ulnar Nerve Entrapment and Injury

Fig. 10.10 Clawing and Wartenburg sign. (a) Intrinsic muscle weakness can manifest as clawing (Duchenne sign) of the ring and little fingers due to an unopposed action of the long extensors at the metacarpophalangeal joints and long flexors at the interphalangeal joints. (b) Wartenburg sign is the abducted posture of the little finger due to unopposed action of the extensor digiti minimi.

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Fig. 10.11 Right hand Froment sign. A way to evaluate weakness of the first dorsal interosseous and thumb adductor muscles is to have the patient pinch. A positive Froment sign is the overt flexion of the thumb interphalangeal joint associated with this weakness. Having the patient hold a piece of paper during pinch, then having the examiner pull the paper away, will help elicit this sign.

Recently, the authors described another provocative test, the use of a hierarchical scratch-collapse test as an adjunct to physical examination for the diagnosis of ulnar compression neuropathy. The scratch-collapse test involves having the patient seated facing the examiner with the shoulders relaxed, the arms adducted, the elbows flexed to 90 degrees, and the wrists neutral. The patient is then asked to externally rotate his or her shoulders against light forearm resistance from the examiner. The examiner then stimulates the nerve at a potential site of compression and asks the patient to repeat the external rotation. If the patient has nerve compression at that site, there will be a transient loss of strength on the ipsilateral side, and it will be impossible for the patient to maintain external rotation. The arm will simply “collapse” internally. Using a topical anes-

Fig. 10.12 Pseudo-Froment sign. A patient with ulnar neuropathy can exhibit a negative Froment sign but have differences in the interphalangeal joint of the thumb. This is called a pseudo-Froment sign. This patient exhibited right ulnar neuropathy, with the right thumb having less hyperextension (i.e., relatively more flexion) compared to the other hand. First dorsal interosseous wasting is evident in the right hand.

thetic, such as ethyl chloride, allows the test to be performed in a hierarchical manner. This topical spray can be used to “freeze out” an area that has caused a positive scratch collapse. Repeating the test will no longer result in the arm’s collapse. Other potential sites of compression may then be tested. Patients who have compression at multiple sites will collapse at a new secondary point once the original compression site has been negated by the ethyl chloride. The scratch-collapse test was found to predict compression at Osborne band and to correlate well with electrodiagnostic studies and intraoperative findings in patients undergoing anterior submuscular transposition for cubital tunnel syndrome.71 It is also specific enough to distinguish compression of the ulnar nerve at the proximal edge of the Guyon

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Ulnar Nerve Entrapment and Injury canal versus compression of the deep motor branch distally under the fascial leading edge of the hypothenar musculature. It does take significant practice to develop expertise and if the most problematic site is not tested then the SCT may be “negative.” It takes practice to perfect this test but if the surgeon has a challenging, difficult patient practice it is worth the effort. If the surgeon has a simpler, straightforward patient population then it is not necessary to learn the SCT nuances.

10.4.5 Electrodiagnostic Studies Nerve conduction and electromyographic (EMG) studies are useful adjuncts in the diagnosis of ulnar neuropathy, especially at the level of the elbow.72 Specifically, they can help to localize a lesion or site of compression, exclude alternate diagnoses, and assess the severity and progression of ulnar neuropathy. 73 Nerve conduction studies can be used to document conduction blocks at the elbow or wrist and can localize the level of compression. Short-segment incremental study has been demonstrated as a sensitive technique for detecting ulnar neuropathy at the wrist, specifically, in the presence of a compressive lesion such as a ganglion cyst.74,75 The majority of patients will also show an amplitude drop of the compound muscle fiber action potential (CMAP).76 However, with established cubital tunnel syndrome, it becomes more difficult to determine an associated distal ulnar nerve compression at the Guyon canal. A neurologist skilled in EMG is needed to make this distinction. EMG studies illustrate axonal injury and can be used to diagnose the degree of injury by the presence of fibrillations, positive sharp waves, motor unit action potentials (MUAPs), and compound muscle action potentials. Such electrodiagnostic studies can also be useful prognosticators of ulnar neuropathy at the elbow.77 They are not always correct, however, and can yield false-negative results.1 The electrodiagnostic sensitivity for ulnar nerve entrapment at the elbow ranges from 80 to 96%.78 At the wrist, there is less in the literature about the correlation between electrodiagnostic studies and intraoperative findings.79 It is possible, though, to include electrical stimulation of the nerve at the palm, which can be useful in demonstrating a conduction abnormality in the distal nerve.80

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10.4.6 Imaging The use of imaging for ulnar neuropathy is not typical but has certainly been described. Ultrasonography has been used to evaluate the cross-sectional area of the ulnar nerve, and this has proven to be diagnostic for compression neuropathy.1,81,82 The cross-sectional areas were found to vary with different grades of severity of ulnar neuropathy at the elbow. 82 This difference in cross-sectional area was found to highly correlate with the severity score obtained by electrodiagnostic studies. 81 Ultrasound has reasonable sensitivity and specificity as an imaging adjunct for ulnar compression neuropathy.82 Additionally, high-resolution ultrasound has proven useful for the diagnosis of peripheral nerve lesions.83 Magnetic resonance imaging (MRI) has also been shown to be useful for the diagnosis of ulnar neuropathy at the elbow. 82 Particularly, targeting hyperintensity of the ulnar nerve resulted in greatest sensitivity (90%) and specificity (80%). 82

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10.5 Management of Cubital Tunnel Syndrome 10.5.1 Nonoperative Management All patients presenting with cubital tunnel syndrome should be educated on avoiding postures that aggravate ulnar nerve compression at the elbow. Maintaining the elbow in an extended position at night and as much as possible during daytime activities should be encouraged. A soft elbow pad is useful for avoiding direct nerve compression and, at night, can be turned 180 degrees so that the padding rests in the antecubital fossa and resists elbow flexion. Rigid elbow splints are often ineffective because of patient discomfort and noncompliance. Work-related modifications, such as using a headset rather than holding a phone to the ear, and lowering a keyboard to allow minimal elbow flexion while typing, are also important aspects of nonoperative treatment. Cortisone injections are not recommended due to the risk of intraneural injection or subcutaneous placement. All patients with mild to moderate symptoms and with motor conduction velocities > 40 m/s across the elbow are given a trial of 2 to 4 months of conservative management. In our experience, many patients with mild cubital tunnel syndrome can be successfully managed without surgery. Padua et al similarly reported that 50% of their patient cohort symptomatically and electrophysiologically improved with activity modification at 1year follow-up.84 Failure to improve with conservative management and advanced motor involvement at presentation (conduction velocities < 40 m/s, fibrillations, or abnormal MUAPs) are among the indications for operative management.85

10.5.2 Operative Management Multiple surgical techniques have been described for the treatment of cubital tunnel syndrome, including simple decompression, medial epicondylectomy, and anterior transposition in a subcutaneous, transmuscular, intramuscular, and submuscular position with and without lengthening of the flexor/pronator tendon unit. There remains ongoing controversy regarding the ideal technique, and comparative studies of this literature have reached different conclusions.86 Transposing the nerve anterior to the medial epicondyle is advocated by many for reasons that include reduced tension and compression forces on the ulnar nerve during elbow flexion, definitive treatment of nerve subluxation, and provision of a well-vascularized bed for the nerve.85 Our preferred technique is an anterior transposition of the nerve with release of the flexor/pronator origin and positioning in a transmuscular location. This transposition places no tension on the nerve, minimizes excursion of the nerve during full range of motion (ROM) activities at the elbow, and requires less muscle dissection than submuscular techniques. Additionally, release of the flexor/pronator origin addresses any associated medial epicondylitis.85

Anterior Transmuscular Transposition The anterior transmuscular transposition procedure (the authors’ preferred technique) is performed under regional or

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Fig. 10.13 Incision and orientation for a transmuscular ulnar nerve transposition. Incision is placed behind the medial epicondyle along the course of the nerve. The dotted line denotes the course of the medial antebrachial cutaneous (MABC) branch across the incision and is found ~ 3.5 cm distal to the medial epicondyle.

general anesthesia, with the patient positioned supine and arm abducted. The entire extremity is prepped and draped, and a sterile tourniquet is positioned high on the arm. An incision is designed posterior to and centered at the medial epicondyle (▶ Fig. 10.13). Dissection is carried through the subcutaneous tissue, taking care to avoid injury to the medial antebrachial cutaneous (MABC) nerve (▶ Fig. 10.14). The ulnar nerve is identified below the medial intermuscular septum proximally (▶ Fig. 10.15), and a long length of the septum is excised (▶ Fig. 10.16). Palpation of the interval between the biceps and triceps proximally is then performed to ensure no residual fascial shelf. The ulnar nerve is released in a proximal to distal direction, with release of the cubital tunnel and Osborne band (▶ Fig. 10.17). The nerve is followed distally between the two heads of the FCU, while preserving motor branches to the FCU and FDP. Almost mirroring the proximal medial intermuscular septum is a distal fascial septum, which runs between the ulnar-innervated FCU and the median-innervated flexor/pronator muscles (▶ Fig. 10.18; ▶ Fig. 10.19; ▶ Fig. 10.20). We carefully remove this septum as it kinks the nerve when it is transposed. Of note, good retraction and some effort are necessary to visualize and excise this distal fascia, especially at its most distal extent (▶ Fig. 10.21). The soft tissue above the flexor/pronator muscle origin is elevated, and a step-cut incision in the flexor/pronator origin is marked (▶ Fig. 10.17). The proximally based fascial flap elevates easily with some muscle attached, and dissection is carried down to the brachialis muscle. The distally based fascial flap

must be elevated with sharp dissection. The muscle is then dissected close to the medial epicondyle so that it remains innervated (▶ Fig. 10.22). The extent of the distal muscle dissection will vary from patient to patient depending on the muscle thickness, but it is important to release enough muscle distally so that it does not kink the ulnar nerve when the nerve is transposed anteriorly. Distal kinking of the ulnar nerve is the greatest error made in transposition surgery. Intermuscular fascia must also be excised where the nerve is to lie to avoid compression. We call this the T fascia, and it is best appreciated in the accompanying surgical video (▶ Fig. 10.23; ▶ Fig. 10.24). The primary goal is to ensure that the ulnar nerve runs in a relaxed straight line in front of the medial epicondyle, through the flexor/pronator muscle with no tension, compression, or kinks (▶ Fig. 10.25). Under loupe magnification, motor branches to the FCU or FDP that inhibit tension-free transposition of the ulnar nerve should be neurolyzed proximally (▶ Fig. 10.26). The nerve is then transposed anterior to the medial epicondyle, and the fascial flaps are closed loosely over the nerve with two nonabsorbable sutures (▶ Fig. 10.27). At least one finger should be able to be easily passed between the fascial flaps and the ulnar nerve to avoid iatrogenic compression of the nerve in its new position. The entire course of the nerve is reevaluated to ensure it lies in a straight line with no further proximal or distal sites of compression. The tourniquet is then released, and meticulous hemostasis is achieved with bipolar cautery. With the tourniquet deflated, we then palpate proximally along the ulnar nerve to assess for an arcade of Struthers and will make a second incision to

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Fig. 10.14 Exposure and MABC nerves. Upon exposure, the MABC nerves are identified and protected. The main branch is identified 3.5 cm distal to the medial epicondyle. Several smaller branches are identified. It is important to protect these branches carefully, as injury to these branches will result in neuroma pain.

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Fig. 10.15 Medial intermuscular septum. The dissection is carried proximally to expose the medial intermuscular septum. Note the sharp edges of this septum as it rests on the ulnar nerve and is resected.

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Fig. 10.16 Resection of the medial intermuscular septum. Following resection of the medial intermuscular septum, vessels are seen deep to this septum and lateral to the ulnar nerve. It is important to note these vessels to prevent bleeding in this area when the septum is resected.

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Fig. 10.17 Cubital tunnel. The ulnar nerve is exposed by dissecting through the fascia superficial to the ulnar nerve in the cubital tunnel. Osborne ligament and the medial intermuscular septum are identified. Fascia is elevated from the medial epicondyle to expose the pronator/flexor muscle origin. A step-cut incision is marked on this origin (dotted lines).

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Fig. 10.18 Distal intermuscular septum. The dissection is carried distally to expose the distal intermuscular septum between the flexor carpi ulnaris (FCU) and flexor/pronator muscle group. This septum is resected. It is important to note crossing nerve branches that innervate these muscles when dividing this septum.

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Fig. 10.19 Aponeurosis of the FCU. Dissection is carried further distal along the ulnar nerve to prevent any kinks when the ulnar nerve is transposed. The aponeurosis of the FCR is divided to prevent kinking during transposition.

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Fig. 10.20 Deep flexor/pronator aponeurosis. Dissection is again carried further distal along the ulnar nerve. A deep flexor/pronator aponeurosis is identified as being a tight band of fascia. This aponeurosis is divided to prevent kinking during transposition.

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Fig. 10.21 Distal intermuscular septum. It is important to check distally that there are no further kink points. A distal intermuscular septum is identified further distal and has a sharp edge. This septum is divided to prevent kinking during transposition.

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Fig. 10.22 Muscle bed for the ulnar nerve following transposition. The pronator/flexor muscles are transmuscularly divided close to the medial epicondyle so that it remains innervated while creating a bed for the ulnar nerve. An intermuscular septum is divided to provide a smooth bed for the nerve. Note that the flexor pronator and FCU muscles are “slid” or advanced distally for a distance of about 3 cm. so the nerve does not “kink” on them when transposed.

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Fig. 10.23 Elevation of fascial flaps and resection of the fascial septum. A step-cut incision is made on the pronator/flexor muscle origin. The medialdistal fascial flap is elevated with sharp dissection, and the lateral-proximal flap is elevated with ease. A fascial septum T is identified between the pronator teres and flexor carpi radialis (FCR) and is elevated for excision. It is important to ensure the ulnar nerve runs in a relaxed straight line through the pronator/flexor muscle.

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Fig. 10.24 Resection of the fascial septum. Once the fascial septum is excised, the pronator/flexor muscles are identified. An intermuscular septum is also identified and is divided to ensure a soft canal for the ulnar nerve.

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Fig. 10.25 Ulnar nerve transposition. The ulnar nerve is transposed above the medial epicondyle following release of the proximal and distal kink points and providing a pronator/flexor muscle bed. The FCU branch is identified for proximal neurolysis.

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Fig. 10.26 FCU neurolysis. To provide additional excursion length on the ulnar nerve, the FCU is neurolyzed proximally from the ulnar nerve.

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Fig. 10.27 Fascial flaps for ulnar nerve transposition. The fascial flaps are sutured together to prevent the ulnar nerve from returning to the cubital tunnel. It is important that these flaps are loose to prevent compression on the ulnar nerve in its transposed location. Two fingers are easily passed under this flap. Note how far distally the distal muscle has been released.

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Ulnar Nerve Entrapment and Injury release this if necessary. The MABC branches are then inspected. If inadvertent avulsion or injury has occurred, the distal end of the injured branch should be cauterized and transposed proximally away from the incision. Furthermore, we suggest “clamping” the injured MABC fascicle as proximally as possible to create an axonotmetic injury that allows regeneration for a distance prior to reaching the neurotmetic site. Bupivacaine is placed along the incision, and a continuous infusion pump is positioned to assist with postoperative pain control. A Jackson-Pratt drain is also used. The incision is then closed in two layers with 3–0 absorbable subcutaneous and 4–0 monofilament intradermal sutures. Steri-Strips and a padded dressing are placed. The arm is immobilized with 4-inch Orthoglass to position the wrist in neutral, forearm pronated, and the elbow flexed at 45 to 60 degrees. The dressing, infusion pump, and drain are removed 2 or 3 days after surgery. ROM exercises are initiated for all joints in the affected extremity, and heavy lifting is restricted during the first postoperative month. Progressive strengthening is initiated at 4 weeks, and return to full activities is permitted at 8 weeks.

Alternative Techniques for Anterior Transposition Other techniques for anterior transposition of the ulnar nerve follow the same principles of exposure and transposition, as described above, but place the transposed ulnar nerve in varying planes relative to the flexor/pronator mass.

Subcutaneous Transposition The nerve is placed in a subcutaneous position anterior to the medial epicondyle. This position can be maintained by suturing subcutaneous tissue in the anterior skin flap to the fascia of the medial epicondyle, or by suturing a small fascial flap elevated off of the flexor/pronator mass to the overlying dermis on the medial aspect of the transposed nerve.87 Subcutaneous transposition avoids dissection of the flexor/ pronator mass. We have not observed motor weakness with our transmuscular transposition procedure. This may be explained by the fact that the motor end plates are located distal to the medial epicondyle in the midportion of the flexor/pronator mass and are likely not injured during muscle flap elevation. A disadvantage of the subcutaneous transposition is the extensive mobilization of the ulnar nerve required to avoid proximal or distal kinking, given the natural submuscular position of the nerve above and especially below the cubital tunnel.85

Intramuscular Transposition Intramuscular transposition was described by Adson88 and later adopted by Kleinman.89,90 A groove is dissected in the flexor/ pronator mass in line with the transposed position of the ulnar nerve, taking care to excise any fibrous septa that may compress the nerve. Similar to subcutaneous transposition, a soft tissue or fascial sling is created to maintain the nerve in its anterior position. Postoperatively, 3 weeks of immobilization is advocated.89,90

Cited benefits of this technique relative to subcutaneous transposition are the more protected position of the nerve and the straighter axis of the transposed nerve.89–91 Additionally, this technique requires less dissection than submuscular transposition. However, potential scarring from intramuscular dissection and iatrogenic compression remain concerns.

Submuscular Transposition Originally described by Learmonth,92 anterior submuscular transposition has been advocated as the “definitive” procedure for cubital tunnel syndrome and the procedure of choice in revision surgery.93,94 Disadvantages include a longer incision (15 to 20 cm), more extensive dissection of the flexor/pronator mass, heterotopic bone formation, and the potential for new compression of the ulnar nerve in its submuscular position.85,93,95 In this technique, the flexor/pronator mass is incised 1 to 2 cm distal to the medial epicondyle, and the muscle mass is reflected distally. The lacertus fibrosus is divided, and the ulnar nerve is transposed adjacent and parallel to the median nerve. The flexor/pronator mass is directly reattached, or it can be lengthened in a step-cut fashion to minimize compression on the transposed ulnar nerve.85 Postoperatively, the elbow is immobilized in 90 degrees of flexion, and ROM exercises should be initiated at 5 to 10 days. A recent study by Zimmerman et al reported 89% success rate with no reoperations and a minimum 6 year follow up with this technique.96

In situ Decompression /Medial Epicondylectomy

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In situ decompression involves release of all relevant compression points without disturbing the ulnar nerve from its bed. Traditional exposure involves a 6- to 10-cm incision, as described above, but more recently, endoscopic and limited incision techniques have been used. Neurolysis of the ulnar nerve is not recommended in primary cases. Following decompression, it is important to assess for nerve subluxation over the medial epicondyle and, if present, give consideration to medial epicondylectomy or anterior transposition. The former entails a subperiosteal exposure of the medial epicondyle, leaving the flexor/pronator origin in continuity with the periosteal sleeve. O’Driscoll et al demonstrated that only ~ 20% of the epicondyle can be removed without injuring the medial collateral ligament or entering the elbow joint.5 The safe plane of resection of the epicondyle is therefore between the sagittal and coronal planes of the humerus. The raw bone edges are rasped smooth, and the periosteal flaps with attached flexor/pronator origin are imbricated with a buried 3–0 nonabsorbable suture. Proponents of in situ decompression cite the risks associated with anterior transposition, which include increased technical complexity, higher complication rates, and risk of nerve devascularization.95,97 The major criticisms of this technique are the failure to adequately address nerve subluxation and tension on the nerve during elbow flexion and the higher risk of recurrence. Without transposition, we believe that continued tension and traction on the nerve during elbow flexion will, over time,

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Fig. 10.28 Injury to the medial antebrachial cutaneous (MABC) nerve following ulnar nerve decompression and transposition. The MABC nerve is prone to injury during an ulnar nerve procedure. It is important to identify and protect these branches, as injury to these nerves will result in neuroma pain. These patients were referred with significant elbow pain following their ulnar nerve procedure. Neuromas of the MABC nerve were found. Surgical management of the neuromas included neuroma resection, cautery cap, proximal crush, and proximal intermuscular transposition.

result in a late recurrence of cubital tunnel symptoms years later. Goldfarb et al showed a recurrence rate of 7% following simple decompression, with a mean follow-up of 49 months. 97 This follow-up is longer than in most studies of cubital tunnel syndrome, although we still lack good data on the incidence of later recurrence with this and other techniques. Endoscopic and minimal access incisions also carry the increased risk of hematoma, nerve injury, and inadequate release of nerve compression.93,98 Decompression with medial epicondylectomy addresses the issue of subluxation but has important risks, such as pain, weakness, and instability of the elbow joint. Moreover, it maintains the nerve in a superficial subcutaneous position, where it is vulnerable to injury.95

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10.5.3 Complications General complications, such as infection, delayed wound healing, and hematoma, can occur as with any procedure. Injury to the MABC nerve is a specific and common complication of surgical treatment for cubital tunnel syndrome and can result in neuroma formation, hyperalgesia in the forearm, and a painful scar (▶ Fig. 10.28).99,100 Injury to the ulnar nerve itself has been rarely reported but is a greater risk during revision surgery or in the context of significant scarring. All surgical techniques can also be complicated by damage to the muscular branches to the FCU and FDP, resulting in postoperative weakness, and failure to release all compression points on the ulnar nerve, leading to persistent symptoms postoperatively. Transposition procedures may result in iatrogenic compression points on the ulnar nerve from inadequate proximal or distal dissection. 86,99,100 Simple decompression can lead to early or late ulnar nerve subluxation, and medial epicondylectomy can be complicated by pain and injury to the elbow joint. 85 Chronic regional pain syndrome is a very rare complication of cubital tunnel surgery.

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10.5.4 Outcomes and Comparative Studies Reported outcomes following cubital tunnel surgery are highly variable. In a systematic review of 42 studies (1977–2007), good and excellent results ranged from 35 to 96% and patient satisfaction from 65 to 92%.101 A prior meta-analysis reported excellent outcomes in only 25 to 45% of 3024 patients surgically treated for cubital tunnel syndrome between 1970 and 1997. 102 In a third systematic review, Mowlavi et al similarly found outcomes to vary widely according to surgical procedure and severity of presentation.103 Although numerous studies have been published on the surgical management of cubital tunnel syndrome, our understanding of treatment outcomes in this population has been hampered by largely retrospective research with poor methodologic quality, small sample sizes, and use of nonvalidated and study-specific outcome measures.101,104,105 The ongoing debate regarding the optimal surgical procedure for cubital tunnel syndrome has been fueled by the limitations of existing research. Indeed, comparative studies of decompression and transposition techniques have continued to reach conflicting conclusions.86,104 The best evidence to date comes from randomized, controlled trials that, while insufficiently powered, have shown no difference in outcomes between simple decompression and anterior transposition in a subcutaneous 106 or submuscular plane107,108 in patients without prior injury to the elbow. Two recent meta-analyses also demonstrated no difference between decompression and anterior transposition, 109,110 although Macadam et al110 found a trend in the odds ratios favoring transposition. Comparisons of subcutaneous and submuscular transpositions in small, retrospective series have also been equivocal.111–113 With the increasing use of minimal access approaches to the cubital tunnel, Watts and Bain114 compared outcomes between endoscopic and open decompression of the ulnar nerve and reported higher patient satisfaction and

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Fig. 10.29 Guyon canal release. (a) The ulnar nerve is identified adjacent to its artery traversing distally through the canal to the ulnar border of the hamate, where the nerve separates into sensory and motor components. At this level, the deep motor branch descends under the hypothenar muscles and turns radially around the hook of the hamate. Note that visualization of this branch is often difficult until its decompression is completed. (b) The palmaris brevis and fascial bands are released to expose the ulnar nerve and its associated vessels. (c) Following the release, the neurovascular bundle is medially retracted to provide further exposure allowing the surgeon to orient himself or herself by palpating the hook of the hamate (purple). (d) Upon further retraction, the deep motor branch is identified ulnar to the hamate, where it disappears under the leading edge of the hypothenar fascia (scissors). (e) Decompression of this branch is achieved by opening this fascia until the flexor tendon of the fifth digit (small finger) is visualized. Note the last step of extending the incision proximal to the wrist to release the distal antebachial fascia is not illustrated in the photographs. Orientation, left hand: proximal (P) and distal (D). (Used with permission from Brown JM, Yee A, Mackinnon SE. Distal median to ulnar nerve transfers to restore ulnar motor and sensory function within the hand: technical nuances. Neurosurgery 2009;65(5):966–977.)

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Ulnar Nerve Entrapment and Injury fewer complications with the endoscopic approach. However, the safety and long-term results of endoscopic approaches require further evaluation. Based on our experience with revision cubital tunnel surgery, it is our belief that the type of surgical procedure matters less than the intraoperative technique and postoperative management, which should include early active mobilization. Successful outcomes are more likely when the surgeon is careful to release all potential compression points and avoids causing iatrogenic nerve compression or “kinking” of the nerve during transposition, destabilizing the nerve following in situ decompression, or injuring the MABC nerve in any technique (▶ Fig. 10.2).86 Closer attention to these factors in future studies will likely improve surgeon and patient satisfaction with cubital tunnel surgery. Furthermore, predictors of patient outcomes other than management of the ulnar nerve at the elbow need to be evaluated. Factors such as patient age, symptom severity, duration of symptoms, and workers’ compensation status have been variably correlated with outcomes.105 We believe that the rate of recovery following cubital tunnel surgery, as with carpal tunnel release, will depend largely on the type and severity of nerve injury. Patients with intermittent symptoms (dynamic ischemia) will have rapid symptomatic relief following decompression of the ulnar nerve, whereas patients with prolonged compression and persistent symptoms (axonal demyelination) will require 3 to 4 months prior to symptomatic resolution to account for remyelination. Patients with severe ulnar nerve compression and axonal loss will experience a slow recovery as the nerve regenerates, and patients with mixed injury will demonstrate a staged improvement.

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10.6 Management of Compression at the Guyon Canal 10.6.1 Nonoperative Management The management of ulnar nerve impingement at the wrist is typically surgical. Although splinting, hand therapy, and activity modification may improve symptoms transiently, there is no good evidence supporting this as a mainstay of treatment. In fact, the majority of patients noted no influence from nonoperative management.115

10.6.2 Operative Management The authors’ preferred technique for surgical decompression of the ulnar nerve at the level of the Guyon canal focuses on release of the deep motor branch and involves six discrete steps. Step 1 involves opening the Guyon canal (▶ Fig. 10.29). This is approached through a Taleisnik incision, made ~ 1 cm ulnar to the thenar crease and crossing the wrist in a zigzag fashion (▶ Fig. 10.30). The palmaris brevis is often visible and is divided using micro bipolar electrocautery (▶ Fig. 10.31). Caution is taken to preserve the cutaneous branch that often sits at the juncture of the proximal two-thirds and distal one-third of the palmar incision (▶ Fig. 10.32). Step 2 involves retracting the ulnar neurovascular bundle medially to provide exposure. Step 3 is to palpate the hook of the hamate, which will help to orient

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Fig. 10.30 Steps in the surgical decompression of the ulnar nerve at the level of the Guyon canal. (a) Incision for the Guyon canal. Incision is made ulnar to the thenar crease and taken proximally across the wrist in a Brunner fashion.

the surgeon and identify the tendinous leading edge of the hypothenar muscles. At this location, just deep to this tendinous leading edge, the deep motor branch curves radially around the hamate deep to the hypothenar muscles. Step 4 involves identifying and releasing the tendinous leading edge (▶ Fig. 10.33). It is important to note that the deep motor branch will not be visible at this point of the dissection, and thus confidence in correctly identifying the landmarks is critical to this release. Once the tendinous leading edge has been divided 2 to 3 mm, the deep motor branch will be easily visualized (▶ Fig. 10.34). Step 5 involves decompressing the deep motor branch by releasing the tendinous leading edge around the hook of the hamate to the small finger flexor tendons. In step 6, the antebrachial fascia proximal to the wrist crease is divided, and the nerve is inspected proximally and distally to ensure there are no further sites of compression (▶ Fig. 10.35). This dissection is performed in the main operating room, under tourniquet control and loupe magnification to facilitate visualization of both the deep motor and superficial sensory branches.116

10.6.3 Complications Given the abundant blood supply to the hand, infections and wound healing problems are rare. Scarring is not significantly different than an open carpal tunnel release. Injury to the nerve, though possible, is minimized by fastidious hemostasis, excellent visualization, and a thorough knowledge of the anatomy of the ulnar nerve at the wrist.

10.6.4 Outcomes and Comparative Studies Using clinical and electrodiagnostic assessment, Kaiser et al noted significant improvement in all parameters following decompression of the Guyon canal. They noted improved outcomes when the procedure was performed earlier in the course of the compression.117 Following excision of space-occupying lesions, results have been excellent.59,79,118 Of note, following carpal tunnel release, patients with ulnar neuropathy have found

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Fig. 10.31 Initial exposure for the Guyon canal. Upon initial exposure, the palmaris brevis is identified. In some cases, a crossing cutaneous palmar branch of the ulnar nerve is identified and protected in the distal third of the incision.

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Fig. 10.32 Identification of the hypothenar muscles for orientation. By sweeping the ulnar nerve and vessels medially, the hypothenar muscles are identified medial to the marked hook of the hamate (purple). The deep motor branch of the ulnar nerve courses deep to this muscle. The palmar cutaneous branch of the ulnar nerve is identified and protected through this exposure.

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Fig. 10.33 Identification of the tendinous leading edge of the hypothenar muscles. The tendinous leading edge of the hypothenar muscles can compress the deep motor branch of the ulnar nerve. This tendon was exposed by partially dividing the muscular tissue superficial to the tendon. The deep motor branch cannot be visualized until this tendon structure is divided.

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symptomatic relief. Release of the transverse carpal ligament resulted in diminished pressures both in the carpal tunnel and in the Guyon canal, which may explain this phenomenon.119

10.7 Ulnar Nerve Compression at Multiple Sites Although compression of the ulnar nerve at the level of the elbow is common, and compression at the level of the wrist is certainly well described, there is very little in the literature that discusses compression at multiple sites. Thus, the prevalence of compressive ulnar neuropathy at both the elbow and the wrist remains unknown. In our experience, compression at both sites, or potentially even at more sites, is not uncommon, truly a “double crush” phenomenon. We have recently presented our experience with concomitant release of the Guyon canal and ulnar nerve transposition at the elbow. Over a 10-year period from 2002 to 2012, the frequency of concomitant release has fluctuated, however currently just over one half of our patients receive release at both sites (▶ Fig. 10.36). In examining our indications to perform a concomitant release at the wrist, we have determined that the presence of intrinsic wasting, the inability to perform an index crossover, and a positive Froment or pseudo-Froment sign are significantly more likely to result in release at both sites. In our study, electrodiagnostic studies did not significantly affect surgical

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decision making for concomitant Guyon canal release, but it did influence our decision to perform an additional “supercharged” end-to-side nerve transfer (see Chapter 5). However, we have recently started using the hierarchical scratch-collapse test, as described above, as an adjunct to physical examination. Further study in this area would be beneficial to determine the utility and indications for release at multiple sites.

10.8 Failed Decompression Despite well-described and routine procedures to decompress and manage ulnar compressive neuropathies, a subset of patients will experience a failed decompression. As with carpal tunnel syndrome, failure of ulnar nerve decompression can be subdivided into three categories: failure to alleviate patient symptoms (persistent), recurrence of symptoms after a period of symptomatic release (recurrent), and development of new symptoms following surgery (new).

10.8.1 Recurrent Cubital Tunnel Syndrome Etiology and Prevention Surgical failures are more common following cubital tunnel syndrome than carpal tunnel syndrome and have been reported

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Fig. 10.34 Decompression of the deep motor branch of the ulnar nerve. The deep motor branch of the ulnar nerve is decompressed by dividing the tendinous leading edge of the hypothenar muscles.

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Fig. 10.35 Decompression of the ulnar nerve through the Guyon canal. The ulnar nerve is decompressed through the Guyon canal, and any antebrachial fascia is released. In this case, an aberrant abductor digiti minimi muscle was identified and divided.

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Fig. 10.36 Concomitant releases of the Guyon canal and ulnar nerve transposition. Over a 10-year period, the frequency of concomitant release of the Guyon canal with an ulnar nerve transposition has fluctuated. However, in our practice, over half of patients have received releases at both sites. The indications for concomitant releases include determining the presence of intrinsic wasting, inability to cross fingers, and positive Froment sign. These signs are significantly more likely to result in release at both sites. Dark bars represent ulnar nerve transposition only and light bars represent transposition and Guyon’s (partial data for 2011) dark bar-ulnar nerve transposition alone; light bar-both procedures.

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Fig. 10.37 Revision surgery following failed decompression of the ulnar nerve. Incision for revision transmuscular ulnar nerve transposition. Note the original incision from an ulnar nerve transposition (solid line). For revision operations, the incision is extended in order to identify the ulnar nerve outside scar tissue.

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Fig. 10.38 Proximal exposure of the ulnar nerve. The ulnar nerve is exposed proximal to the original operation and the associated scar tissue. The medial intermuscular septum is also identified intact.

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Fig. 10.39 Distal exposure of the ulnar nerve. The dissection is carried distally to expose the ulnar nerve outside scar tissue. By having the ulnar nerve identified distally, a good estimate of the course of the ulnar nerve through scar tissue can be determined. The distal exposure requires retracting the flexor carpi ulnaris (FCU). We look for the ulnar nerve distally just posterior to the distal intermuscular septum in normal tissue.

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Fig. 10.40 Medial intermuscular septum. The proximal and distal exposures are checked for additional kink points by intermuscular septa. These septa are divided to prevent kinking from a transmuscular transposition. The ulnar nerve is elevated from the medial epicondyle with scar tissue. The medial intermuscular septum is identified and noted for resection.

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Fig. 10.41 Medial intermuscular septum resected. The medial intermuscular septum is identified and resected to prevent kinking of the ulnar nerve during transposition.

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Fig. 10.42 Fascial flap incision. After the ulnar nerve has been elevated and both proximal and distal exposures checked for kinking, the pronator/ flexor origin is exposed. At this point, the operation returns to the standard transmuscular ulnar nerve transposition. A step-cut incision is marked on the tendinous fascia. The step-cut is reversed from its usual orientation with the proximally-oriented flap now placed on the lateral side, to accommodate the previous FCR release.

as high as 25%.99 However, follow-up times for most studies of cubital tunnel syndrome are short, and the true recurrence rate is unknown but likely higher. Persistent symptoms following cubital tunnel surgery may be due to technical factors, such as incomplete release of all compression points,120 incorrect diagnosis, or additional sites of proximal or distal ulnar nerve compression, such as cervical disk disease and Guyon canal syndrome. A thorough history and physical examination, electrodiagnostic testing, and imaging are critical in assessing alternate and associated diagnoses at the initial evaluation. Furthermore, as discussed previously, meticulous attention to intraoperative technique will help to avoid incomplete release or iatrogenic compression of the ulnar nerve resulting in persistent symptoms postoperatively. Finally, appropriate informed consent is important to set realistic expectations for patients and to avoid patient dissatisfaction postoperatively. Recurrent symptoms following cubital tunnel surgery are most often attributed to perineural scarring.99,100 Excessive scarring may be exacerbated by prolonged immobilization after the primary surgery. We therefore encourage early postoperative mobilization at 2 to 3 days and nerve-gliding exercises to prevent this complication. Furthermore, we believe that anterior transposition of the nerve has the ability to reduce tension and traction on the ulnar nerve in the long term.

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The development of new symptoms postoperatively is almost always due to technical error, most commonly injury to the MABC. When reviewing 100 patients requiring a secondary operation for cubital tunnel syndrome, 55 were found to have pain in the MABC distribution, and 73 had a neuroma intraoperatively.100 Injury to the ulnar nerve itself is uncommon but has been described.

Patient Evaluation Patients presenting with persistent, recurrent, or new symptoms necessitate a thorough history and physical examination. It is important to rule out missed proximal causes of ulnar neuropathy, such as degenerative disk disease, postural abnormalities, and muscle imbalance. Investing in preoperative physical therapy may address these issues and assist the patient in avoiding secondary surgery. Review of the patient’s pain questionnaire may prove useful in identifying alternate or associated diagnoses. Repeat sensory testing of all nerve territories and evaluation for a Tinel sign at the surgical site, proximally and distally, are beneficial. Electrodiagnostic testing and imaging are also useful in this patient population to confirm inadequate decompression of the ulnar nerve.121 Obtaining operative records of the initial surgery is imperative.

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Fig. 10.43 Muscle bed for the ulnar nerve following transposition. The pronator/flexor muscles are transmuscularly divided close to the medial epicondyle so that it remains innervated while creating a bed for the ulnar nerve. An intermuscular septum is divided to provide a smooth bed for the nerve. Scar tissue is also divided from the ulnar nerve.

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Indications for repeat surgical exploration include pain,100 paresthesias and numbness, and motor weakness following cubital tunnel surgery.121 Unremitting pain remains the primary reason for revision surgery.122

Revision Surgery It must be noted that revision surgery is not the same as primary surgery. Anatomical structures, especially in the setting of a nerve transposition, are altered. The presence of scarring makes dissection difficult, especially given that a thick white scar and fascia can mimic the appearance of nerve. Surgical landmarks related to surface anatomy can no longer be expected to be accurate. For this reason, it is advisable to extend the incision proximally and distally; such an incision will be very long, and patients need to be informed preoperatively (▶ Fig. 10.37). The ulnar nerve should be identified proximally and distally to the previous operative zone, then cautiously traced back into the previous incision (▶ Fig. 10.38; ▶ Fig. 10.39; ▶ Fig. 10.40). Close attention to the distalmost aspect of the incision may reveal kinking secondary to transposition with inadequate distal release. Consideration should be given to decompressing multiple sites, including the arcade of Struthers and the ulnar nerve at the wrist (▶ Fig. 10.41). Once the ulnar nerve has been identified both proximally and distally, the ulnar nerve is transposed transmuscularly in

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a similar fasion as a primary transmuscular ulnar nerve transposition (▶ Figs. 10.42–10.47). In our experience, the use of the hierarchal scratch-collapse test has proven very useful in evaluating and treating multiple compression sites in this population. Revision cubital tunnel surgery should be performed by experienced surgeons, in a controlled setting, with significant time allotted. Sterile tourniquet control, meticulous hemostasis, loupe or microscope magnification, and collaboration with anesthesia colleagues will facilitate successful outcomes. Of particular importance is the need to avoid paralytics with induction, so that the surgeon is able to visualize and stimulate the nerve. Constant attention should be paid to the hand to monitor for distal muscle contraction when working close to the ulnar nerve. Revision surgery has been found to be highly effective for treatment of intractable pain and paresthesias in the context of cubital tunnel syndrome.100,120,121 Recovery of intrinsic motor function and sensation is more variable and does not necessarily relate to the degree of compression, the timing since original surgery, or the original method of decompression.121

10.8.2 Recurrent Guyon Canal Release Patients presenting with persistent intrinsic muscle dysfunction and sensory abnormalities following decompression of the Guyon canal should be evaluated to rule out a proximal site of

Ulnar Nerve Entrapment and Injury

Fig. 10.44 Ulnar nerve transposition. The ulnar nerve is transposed above the medial epicondyle following release of proximal and distal kink points and providing a pronator/flexor muscle bed.

compression. Imaging may be useful to evaluate for ongoing or recurrent compression by a space-occupying lesion or vascular anomaly. If no other etiology is identified, reexploration should be considered. The most common site of incomplete release in our experience is where the deep motor branch of the ulnar nerve passes deep to the fascial leading edge of the hypothenar musculature.

10.9 Nerve Transfers to Supercharge Recovery Nerve transfers are covered in Chapter 5; however, mention of the supercharged end-to-side (SETS) procedure is relevant to this discussion of ulnar neuropathy because it has improved the treatment and prognosis of intrinsic muscle paralysis.116 First performed by Mackinnon in 2009, the SETS procedure involves transferring the terminal branch of the AIN to the deep motor branch of the ulnar nerve in an end-to-side fashion. By providing a source of motor axons in close proximity to the motor end plates of the intrinsic muscles, the SETS transfer aims to speed, or “supercharge,” spontaneous motor recovery (▶ Fig. 10.48). In the context of cubital tunnel syndrome, we used the SETS procedure in 70 patients with clinical wasting of the intrinsic muscles and fibrillations/MUAPs on EMG (i.e., a

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second- or third-degree injury pattern). In the authors’ experience, this nerve transfer has significantly improved hand function in this patient population and has resulted in no discernible donor deficit. Prior studies using rat models have demonstrated significant regeneration across the SETS coaptation.123 The technical nuances of the SETS transfer are published; 116 and, thorough decompression of the Guyon canal as described above is critical for success of this procedure. Ensuring knowledge of internal topography of the ulnar nerve at the wrist will facilitate a tension-free coaptation ~ 7 to 9 cm proximal to the wrist crease. Review of the accompanying video is recommended and it is also discussed in Chapter 5.

10.10 Conclusion Cubital tunnel syndrome is the most common compression neuropathy of the ulnar nerve. Although multiple etiologies exist, dynamic compression and traction forces on the nerve during elbow flexion play a significant role in the pathophysiology of this condition.36 When motor weakness is present or when conservative management fails, operative decompression is indicated. There remains ongoing debate regarding the “best” surgical management for cubital tunnel syndrome, whether that is simple decompression, medial epicondylectomy, or anterior transposition. Indeed, all procedures have strong propo-

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Fig. 10.45 FCU neurolysis. To provide additional excursion length on the ulnar nerve, the FCU is neurolyzed proximally from the ulnar nerve.

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Fig. 10.46 Medial antebrachial cutaneous nerve (MABC). After completing the transposition, the MABC nerve is identified to determine whether it was injured from the original operation. In this case, the nerve was not injured.

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Fig. 10.47 Fascial flaps for ulnar nerve transposition. The fascial flaps are sutured together to prevent the ulnar nerve from returning to the cubital tunnel. It is important that these flaps are loose to prevent compression on the ulnar nerve in its transposed location.

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Fig. 10.48 (a) A supercharge nerve transfer involves coaptating the donor distal end to the side of the recipient nerve via a perineurial window. The recipient nerve is a recovering nerve and has a proximal regenerative front, while the donor nerve provides an additional regenerative front closer to the target muscle. (b) A supercharge nerve transfer for a recovering ulnar nerve from a proximal injury includes the anterior interosseous (AIN) to ulnar motor nerve transfer. Note the distal fascicles of the AIN are "fanned" to cover the fascicles of the ulnar motor.

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Ulnar Nerve Entrapment and Injury nents and can yield excellent results. Focusing on careful intraoperative technique is the best way to ensure good outcomes. This includes avoiding injury to the MABC nerve and ensuring that no new compression points or kinking of the ulnar nerve have been created. Overall, however, outcomes of cubital tunnel surgery remain less successful than carpal tunnel surgery, and future studies need to better evaluate predictors of surgical outcomes in this population. Distal ulnar nerve compression at the Guyon canal is usually related to extrinsic compression and often requires surgical intervention. A second point of entrapment at the Guyon canal should also be considered in every patient presenting with proximal ulnar nerve compression and intrinsic atrophy. In these instances, decompression of the Guyon canal may help facilitate sensory and motor recovery. Additionally, the SETS nerve transfer may speed motor recovery in patients presenting with advanced intrinsic muscle weakness associated with proximal ulnar nerve compression.124

10.11 References [1] Yoon JS, Walker FO, Cartwright MS. Ulnar neuropathy with normal electrodiagnosis and abnormal nerve ultrasound. Arch Phys Med Rehabil 2010;91:318–320 [2] Tung TH, Weber RV, Mackinnon SE. Nerve transfers for the upper and lower extremities. Oper Tech Orthop 2004;14:213–222 [3] Osborne GV. The surgical treatment of tardy ulnar neuritis. J Bone Joint Surg 1957;39B:782 [4] Dellon AL. Musculotendinous variations about the medial humeral epicondyle. J Hand Surg [Br] 1986;11:175–181 [5] O’Driscoll SW, Horii E, Carmichael SW, Morrey BF. The cubital tunnel and ulnar neuropathy. J Bone Joint Surg Br 1991;73:613–617 [6] Sunderland S. Nerves and Nerve injuries. Edinburgh, Scotland: E & S Livingstone; 1968:816–828 [7] Apfelberg DB, Larson SJ. Dynamic anatomy of the ulnar nerve at the elbow. Plast Reconstr Surg 1973;51:79–81 [8] Watchmaker GP, Lee G, Mackinnon SE. Intraneural topography of the ulnar nerve in the cubital tunnel facilitates anterior transposition. J Hand Surg Am 1994;19:915–922 [9] Guyon F. Note sur une disposition anatomique propre a la face anterieure de la region du poignet et non encore decrite par le docteur. Bull Soc Anat Paris 1861;6:184–186 [10] Hunt JR. Occupational neuritis of the deep palmar branch of the ulnar nerve. J Nerv Ment Dis 1908;35:673–689 [11] McFarlane RM, Mayer JR, Hugill JV. Further observations on the anatomy of the ulnar nerve at the wrist. Hand 1976;8:115–117 [12] Denman EE. The anatomy of the space of Guyon. Hand 1978;10:69–76 [13] Gross MS, Gelberman RH. The anatomy of the distal ulnar tunnel. Clin Orthop Relat Res 1985;196:238–247 [14] Hattori Y, Doi K. Vascularized ulnar nerve graft. Tech Hand Up Extrem Surg 2006;10:103–106 [15] Prevel CD, Matloub HS, Ye Z, Sanger JR, Yousif NJ. The extrinsic blood supply of the ulnar nerve at the elbow: an anatomic study. J Hand Surg Am 1993;18:433–438 [16] Maki Y, Firrell JC, Breidenbach WC. Blood flow in mobilized nerves: results in a rabbit sciatic nerve model. Plast Reconstr Surg 1997;100:627–633, discussion 634–635 [17] Nakkamura K, Uchiyama S, Ido Y, et al. The effects of vascular pedicle preservation on blood flow and clinical outcome following ulnar nerve transposition. J Hand Surg Am. 2014;39(2):291–302 [18] Anderson GA. Ulnar nerve palsy. In: Wolfe SW, Hotchkiss RN, Pederson WC, Kozin SH, eds. Green’s Operative Hand Surgery. 6th ed. Philadelphia, PA: Elsevier Churchill Livingstone; 2011:1164 [19] Marinacci AA. The problem of unusual anomalous innervation of hand muscles: the value of electrodiagnosis in its evaluation. Bull Los Angel Neuro Soc 1964;29:133–142 [20] Lee KS, Oh CS, Chung IH, Sunwoo IN. An anatomic study of the Martin-Gruber anastomosis: electrodiagnostic implications. Muscle Nerve 2005;31:95–97

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Ulnar Nerve Entrapment and Injury [49] Pearce C, Feinberg J, Wolfe SW. Ulnar neuropathy at the wrist. HSS J 2009;5:180–183, quiz 184–185 [50] Conn J, Bergan JJ, Bell JL. Hypothenar hammer syndrome: posttraumatic digital ischemia. Surgery 1970;68:1122–1128 [51] Howard FM. Ulnar-nerve palsy in wrist fractures. J Bone Joint Surg Am 1961;43-A:1197–1201 [52] Baird DB, Friedenberg ZB. Delayed ulnar-nerve palsy following a fracture of the hamate. J Bone Joint Surg Am 1968;50:570–572 [53] Foucher G, Schuind F, Merle M, Brunelli F. Fractures of the hook of the hamate. J Hand Surg [Br] 1985;10:205–210 [54] Shea JD, McClain EJ. Ulnar-nerve compression syndromes at and below the wrist. J Bone Joint Surg Am 1969;51:1095–1103 [55] Zoëga H. Fracture of the lower end of the radius with ulnar nerve palsy. J Bone Joint Surg Br 1966;48:514–516 [56] Vance RM, Gelberman RH. Acute ulnar neuropathy with fractures at the wrist. J Bone Joint Surg Am 1978;60:962–965 [57] McCarroll HR. Nerve injuries associated with wrist trauma. Orthop Clin North Am 1984;15:279–287 [58] Kwak KW, Kim MS, Chang CH, Kim SH. Ulnar nerve compression in Guyon’s canal by ganglion cyst. J Korean Neurosurg Soc 2011;49:139–141 [59] Inaparthy PK, Anwar F, Botchu R, Jähnich H, Katchburian MV. Compression of the deep branch of the ulnar nerve in Guyon’s canal by a ganglion: two cases. Arch Orthop Trauma Surg 2008;128:641–643 [60] Francisco BS, Agarwal JP. Giant cell tumor of tendon sheath in Guyon’s canal causing ulnar tunnel syndrome: a case report and review of the literature. Eplasty 2009;9:e8 [61] Ozdemir O, Calisaneller T, Gerilmez A, Gulsen S, Altinors N. Ulnar nerve entrapment in Guyon’s canal due to a lipoma. J Neurosurg Sci 2010;54:125–127 [62] Kim SS, Kim JH, Kang HI, Lee SJ. Ulnar nerve compression at Guyon’s canal by an arteriovenous malformation. J Korean Neurosurg Soc 2009;45:57–59 [63] Ozdemir O, Calisaneller T, Altinors N. Compression of the ulnar nerve in Guyon’s canal by an arteriovenous malformation. J Hand Surg Eur Vol 2007;32:600–601 [64] Guidicelli T, Londner J, Gonnelli D, Magalon G. Two anomalous muscles of a forearm revealed by ulnar nerve compressions, a Double Crush syndrome [inTK] Ann Chir Plast Esthet 2012 [65] Ogun TC, Karalezli N, Ogun CO. The concomitant presence of two anomalous muscles in the forearm. Hand (NY) 2007;2:120–122 [66] Dimitriou C, Natsis K. Accessory abductor digiti minimi muscle causing ulnar nerve entrapment at the Guyon’s canal: a case report. Clin Anat 2007;20:974–975 [67] Upton AR, McComas AJ. The double crush in nerve entrapment syndromes. Lancet 1973;2:359–362 [68] Dell PC, Sforzo CR. Ulnar intrinsic anatomy and dysfunction. J Hand Ther 2005;18:198–207 [69] Earle AS, Vlastou C. Crossed fingers and other tests of ulnar nerve motor function. J Hand Surg Am 1980;5:560–565 [70] Strauch B, Lang A, Ferder M, Keyes-Ford M, Freeman K, Newstein D. The ten test. Plast Reconstr Surg 1997;99:1074–1078 [71] Brown JM, Mokhtee D, Evangelista MS, Mackinnon SE. Scratch collapse test localizes Osborne’s band as the point of maximal nerve compression in cubital tunnel syndrome. Hand (NY) 2010;5:141–147 [72] Robertson C, Saratsiotis J. A review of compressive ulnar neuropathy at the elbow. J Manipulative Physiol Ther 2005;28:345 [73] Dimberg EL. Electrodiagnostic evaluation of ulnar neuropathy and other upper extremity mononeuropathies. Neurol Clin 2012;30:479–503 [74] Yalinay Dikmen P, Oge AE, Yazici J. Short segment incremental study in ulnar neuropathy at the wrist: report of three cases and review of the literature. Acta Neurol Belg 2010;110:78–83 [75] Visser LH, Beekman R, Franssen H. Short-segment nerve conduction studies in ulnar neuropathy at the elbow. Muscle Nerve 2005;31:331–338 [76] Yuksel G, Karlikaya G, Tutkavul K, Akpinar A, Orken C, Tireli H. Electrodiagnosis of ulnar nerve entrapment at the elbow. Neurosciences (Riyadh) 2009;14:249–253 [77] Friedrich JM, Robinson LR. Prognostic indicators from electrodiagnostic studies for ulnar neuropathy at the elbow. Muscle Nerve 2011;43:596–600 [78] Todnem K, Michler RP, Wader TE, Engstrøm M, Sand T. The impact of extended electrodiagnostic studies in ulnar neuropathy at the elbow. BMC Neurol 2009;9:52 [79] Papathanasiou ES, Loizides A, Panayiotou P, Papacostas SS, Kleopa KA. Ulnar neuropathy at Guyon’s canal: electrophysiological and surgical findings. Electromyogr Clin Neurophysiol 2005;45:87–92

[80] Wee AS. Ulnar nerve stimulation at the palm in diagnosing distal ulnar nerve entrapment. Electromyogr Clin Neurophysiol 2005;45:47–51 [81] Volpe A, Rossato G, Bottanelli M, et al. Ultrasound evaluation of ulnar neuropathy at the elbow: correlation with electrophysiological studies. Rheumatology (Oxford) 2009;48:1098–1101 [82] Ayromlou H, Tarzamni MK, Daghighi MH, et al. Diagnostic value of ultrasonography and magnetic resonance imaging in ulnar neuropathy at the elbow. ISRN Neurol 2012;2012:491892 [83] Lee FC, Singh H, Nazarian LN, Ratliff JK. High-resolution ultrasonography in the diagnosis and intraoperative management of peripheral nerve lesions. J Neurosurg 2011;114:206–211 [84] Padua L, Aprile I, Caliandro P, Foschini M, Mazza S, Tonali P. Natural history of ulnar entrapment at elbow. Clin Neurophysiol 2002;113:1980–1984 [85] Mackinnon SE, Novak CB. Compression neuropathies. In: Wolfe SW, Hotchkiss RN, Pederson WC, Kozin SH, eds. Green’s Operative Hand Surgery. 6th ed. Philadelphia, PA: Elsevier Churchill Livingstone; 2011:977– 1014 [86] Mackinnon SE. Comparative clinical outcomes of submuscular and subcutaneous transposition of the ulnar nerve for cubital tunnel syndrome. J Hand Surg Am 2009;34:1574–1575, author reply 1575 [87] Eaton RG, Crowe JF, Parkes JC. Anterior transposition of the ulnar nerve using a non-compressing fasciodermal sling. J Bone Joint Surg Am 1980;62:820– 825 [88] Adson AW. The surgical treatment of progressive ulnar paralysis. Minn Med 1918;1:455–460 [89] Kleinman WB, Bishop AT. Anterior intramuscular transposition of the ulnar nerve. J Hand Surg Am 1989;14:972–979 [90] Plancher KD, McGillicuddy JO, Kleinman WB. Anterior intramuscular transposition of the ulnar nerve. Hand Clin 1996;12:435–444 [91] Henry M. Modified intramuscular transposition of the ulnar nerve. J Hand Surg Am 2006;31:1535–1542 [92] Learmonth JR. A technique for transplanting the ulnar nerve. Surg Gynecol Obstet 1942;75:792–793 [93] Palmer BA, Hughes TB. Cubital tunnel syndrome. J Hand Surg Am 2010;35:153–163 [94] Ehsan A, Hanel DP. Recurrent or persistent cubital tunnel syndrome. J Hand Surg Am 2012;37:1910–1912 [95] Heithoff SJ. Cubital tunnel syndrome does not require transposition of the ulnar nerve. J Hand Surg Am 1999;24:898–905 [96] Zimmerman R, Jupiter J, González del Pino J. Minimum 6-year follow-up after decompression and submuscluar transposition for primary entrapment. J Hand Surg Am. 2013;38(12):2398–2404 [97] Goldfarb CA, Sutter MM, Martins EJ, Manske PR. Incidence of reoperation and subjective outcome following in situ decompression of the ulnar nerve at the cubital tunnel. J Hand Surg [Br] 2009;34B:379–383 [98] Cobb TK. Endoscopic cubital tunnel release. J Hand Surg Am 2010;35:1690– 1697 [99] Lowe JB, Mackinnon SE. Management of secondary cubital tunnel syndrome. Plast Reconstr Surg 2004;113:E1–E16 [100] Mackinnon SE, Novak CB. Operative findings in reoperation of patients with cubital tunnel syndrome. Hand (NY) 2007;2:137–143 [101] Macadam SA, Bezuhly M, Lefaivre KA. Outcomes measures used to assess results after surgery for cubital tunnel syndrome: a systematic review of the literature. J Hand Surg Am 2009;34:1482–1491, e5 [102] Bartels RH, Menovsky T, Van Overbeeke JJ, Verhagen WI. Surgical management of ulnar nerve compression at the elbow: an analysis of the literature. J Neurosurg 1998;89:722–727 [103] Mowlavi A, Andrews K, Lille S, Verhulst S, Zook EG, Milner S. The management of cubital tunnel syndrome: a meta-analysis of clinical studies. Plast Reconstr Surg 2000;106:327–334 [104] Chung KC. Treatment of ulnar nerve compression at the elbow. J Hand Surg Am 2008;33:1625–1627 [105] Shi Q, MacDermid J, Grewal R, King GJ, Faber K, Miller TA. Predictors of functional outcome change 18 months after anterior ulnar nerve transposition. Arch Phys Med Rehabil 2012;93:307–312 [106] Nabhan A, Ahlhelm F, Kelm J, Reith W, Schwerdtfeger K, Steudel WI. Simple decompression or subcutaneous anterior transposition of the ulnar nerve for cubital tunnel syndrome. J Hand Surg [Br] 2005;30:521–524 [107] Gervasio O, Gambardella G, Zaccone C, Branca D. Simple decompression versus anterior submuscular transposition of the ulnar nerve in severe cubital tunnel syndrome: a prospective randomized study. Neurosurgery 2005;56: 108–117, discussion 117

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[116] Brown JM, Yee A, Mackinnon SE. Distal median to ulnar nerve transfers to restore ulnar motor and sensory function within the hand: technical nuances. Neurosurgery 2009;65:966–977, discussion 977–978 [117] Kaiser R, Houšťava L, Brzezny R, Haninec P. The results of ulnar nerve decompression in Guyon’s canal syndrome [in Czech] Acta Chir Orthop Traumatol Cech 2012;79:243–248 [118] Saint-Cyr M, Kleinert HE. Compression of the ulnar nerve and spasm of the ulnar artery in Guyon’s canal caused by a hypermobile pisiform bone. Scand J Plast Reconstr Surg Hand Surg 2008;42:215–217 [119] Ablove RH, Moy OJ, Peimer CA, Wheeler DR, Diao E. Pressure changes in Guyon’s canal after carpal tunnel release. J Hand Surg [Br] 1996;21:664–665 [120] Gabel GT, Amadio PC. Reoperation for failed decompression of the ulnar nerve in the region of the elbow. J Bone Joint Surg Am 1990;72:213–219 [121] Rogers MR, Bergfield TG, Aulicino PL. The failed ulnar nerve transposition: etiology and treatment. Clin Orthop Relat Res 1991;269:193–200 [122] Dorsi MJ, Chen L, Murinson BB, Pogatzki-Zahn EM, Meyer RA, Belzberg AJ. The tibial neuroma transposition (TNT) model of neuroma pain and hyperalgesia. Pain 2008;134:320–334 [123] Kale SS, Glaus SW, Yee A, et al. Reverse end-to-side nerve transfer: from animal model to clinical use. J Hand Surg Am 2011;36:1631–1639, e2 [124] Davidge KM, Moore AM, Yee A, Mackinnon SE. The supercharge end-to-side anterior interosseous to ulnar motor nerve transfer for restoring intrinsic unction: Clinical experience. Plastic and Reconstructive Surgery. 2015 [in press]

Radial Nerve Entrapment and Injury

11 Radial Nerve Entrapment and Injury Kirsty U. Boyd, Linda T. Dvali, J. Megan Patterson, Brendan M. Patterson, and Kristen M. Davidge

11.1 Introduction Radial neuropathy can result from direct trauma or compression anywhere along the course of the nerve, from the brachial plexus to the distal posterior interosseous nerve (PIN) and superficial sensory branch. Many consider the radial sensory branch to be the most unforgiving nerve in the body with respect to pain and impact on quality of life. Thorough knowledge of the anatomy of the radial nerve will facilitate understanding of the various levels of injury, especially following trauma. The shorter distance to motor end plates associated with radial nerve recovery tends to contribute to superior outcomes following injury when compared to the median and ulnar nerves; however, proximal injuries are still associated with a significant loss of function. This chapter illustrates the anatomy of the radial nerve, the various common etiologies of radial neuropathy, and the potential techniques for reconstruction. Results of surgical techniques are reviewed, as well as a detailed description of the authors’ preferred techniques.

11.2 Historical Perspective Clinical cases describing the finding of radial nerve palsy of various etiologies have been present in the literature since 1863, when Agnew reported complete recovery of the PIN after removing a mass that was compressing both the PIN and the median nerve.1 In 1905 repeated pronation and supination was the suspected etiology for radial nerve paralysis in a musical conductor.2 In 1931 Grigoresco and Iordanesco reported a case of a man who presented with a PIN palsy after sleeping with his head on his forearm after a minor injury.3 Numerous other authors have reported PIN and radial nerve paralysis of various etiologies.3–11

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11.3 Etiology of Radial Neuropathy 11.3.1 Orthopedic Injury Of all of the various etiologies, trauma has evolved as a particularly important cause of radial nerve injury. The radial nerve is injured through orthopedic injury more than any other major nerve,12,13 with ~12% of humeral shaft fractures being complicated by radial nerve paralysis.1,14,15 Although most cases involve simple traction injuries, in more severe cases the radial nerve can become entrapped in the bony fragments or fracture callus.12,15 Radial nerve entrapment after orthopedic trauma is most often associated with displaced spiral fractures of the distal shaft of the humerus, particularly when the displacement causes radial angulation (▶ Fig. 11.1).16 In some cases, transient radial nerve paralysis may result from traction within the supinator muscle associated with radial head dislocations.17 Although radial nerve injury associated with fractures of the humerus most often occurs because of the fracture itself,

Fig. 11.1 Prevalence of radial nerve injury with humeral fractures. The radial nerve is uniquely at risk with humeral fractures because of several anatomical predispositions. The nerve takes a spiral course around the humerus and is tethered both by the lateral septum in the arm and the tendinous leading edge of the supinator in the proximal forearm. Thus, it does not have the same kind of “give” as do the ulnar and median nerves. In addition, the trauma and edema associated with the fracture make the radial nerve “stickier” with excursion than normal. The swelling associated with the fracture also makes entrapment points along the course of the nerve in the arm and forearm “tighter.” All of these factors make it more at risk for both traction injury and superimposed compression injury especially if an open reduction and internal fixation procedure is necessary.

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Radial Nerve Entrapment and Injury the incidence of radial nerve injury following operative fixation of fractures of the humeral shaft has been reported to be between 1.9 and 3.3%.18–20 After fracture fixation or insertion of fixation devices along the middle and distal one-third of the humerus, injuries associated with interfragmentary entrapment and direct nerve injury have been reported.21,22 A common site for radial nerve injury resulting from operative fixation is at the location of the lateral intermuscular septum as the nerve passes from the posterior to the anterior compartment of the arm. 12–15 In addition, the radial nerve is at risk during humeral fracture and subsequent operative fixation along the posterior midshaft region at the distal aspect of the deltoid tuberosity. Another potential site of injury is along the lateral aspect of the humerus in its distal one-third proximal to the lateral epicondyle to the level of the proximal aspect of the metaphyseal flare.16 The radial nerve can also be injured during other orthopedic or vascular access procedures17,23 or traction injury or compressive neurapraxia after surgery.24,25 The vulnerability of the PIN during exploration of the elbow should also be considered. A Monteggia fracture involves dislocation of the radial head and an associated fracture of the ulna. If this injury is complicated by radial nerve palsy, this normally occurs at the level of the PIN.26–28 It is interesting to note that the two nerves most associated with iatrogenic orthopedic injuries are the radial and the peroneal. We hypothesize that this is in part due to the spiral path they both take as they transition down the extremities, making them relatively less tolerant to stretch or traction. The associated entrapment points at the fibular head and the arcade of Fröhse and lateral septum in the spiral groove add “tethering” points to compound the susceptibility of these two nerves to palsy.

11.3.2 Neoplasms

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Tumors have been reported to cause radial nerve compression. The most common tumors to result in compression of the radial nerve are lipomas.20,28,30,31,32 However, ganglia, other benign tumors, and inflammation causing radial nerve or PIN compression have been reported. Unless associated with significant compression, benign tumors rarely result in complete nerve paralysis.33 Cases of inflammation due to rheumatoid arthritis and injury have also been shown to produce radial nerve or PIN palsy.6,34–36

11.3.3 Gunshot Wounds Traumatic lacerations are less likely to injure the radial nerve due to the deep position of the motor portion of the nerve; 1 however, gunshot wounds have been reported as a common cause of radial nerve injury. The extent of nerve disruption is related to the nature of the missile. Nerve injuries of this nature, in general, have a favorable prognosis. A study by Omer found that 69% of 331 patients with gunshot wounds of low velocity and 69% of 264 patients with gunshot wounds of high velocity spontaneously recovered good clinical function after 4 to 7 and 3 to 6 months, respectively.37 A more recent study using electrodiagnostics to compare level of radial nerve injury, completeness of nerve injury, and associated nerve involvement

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in those with gunshot wounds versus those with blunt trauma reported no significant differences between the two.38 For this reason, most gunshot wounds are treated as “closed” injuries.

11.3.4 Injection Injury Although radial nerve injury can result from direct injectiontype injuries, the formation of scar tissue secondary to the drug can also cause entrapment.6,8,9 More specifically, repeated intramuscular injections of pentazocine to the deltoid region has resulted in fibrous myopathy in the triceps, causing radial nerve compression.39 The drugs track longitudinally along the nerve. Typically, nerve injection injuries are associated with severe pain and produce a Sunderland III or VI injury. They are difficult to treat except with medication and surgical release if localized to an area of known nerve entrapment. Neuritis of the radial nerve has also been described.40,41

11.3.5 Compression Neuropathy Numerous causes for compression of the radial nerve in the brachium have been described in detail. The traditional “Saturday night palsy,” seen when patients fall asleep on their arm and awake with a radial nerve palsy, as with many other transient compression neuropathies, tends to resolve without any intervention. Other potential transient compression neuropathies are crush; pressure against the humerus; compression of the nerve against the bone from leaning on a chair, operating room table, stretcher, or traction device; and compression of the nerve beneath a pneumatic tourniquet during surgery.10,11,18,37,42–44 Compression by anatomical structures is an important cause of radial nerve palsy in both the arm and the forearm. Proximally in the arm, compression has been reported as a result of a fibrous arch (lateral intermuscular septum) formed by the lateral head of the triceps.45,46 Physical activity involving traction on the upper arm where the radial nerve crosses the lateral intermuscular septum has also been reported to cause proximal radial nerve palsy.20 Generally, radial nerve palsies due to compression at high sites in the arm do not require surgical intervention, as they often resolve spontaneously. However, if the nerve is directly damaged by an injected substance, recovery may never occur due to damage to the nerve that will not respond to simple surgical exploration. Compression of the radial nerve in the arm can result from a number of direct and indirect causes, but radial nerve injury in the proximal forearm and elbow region is most commonly due to nerve compression at several well-described anatomical sites. Although lacerations, dislocations, and fractures of the radial head can damage the PIN, compression by known anatomical structures are by far the leading cause of pure motor paralysis due to PIN syndrome. The additional complaint of pain in the region without distal sensory loss is known as radial tunnel syndrome. True sensory complaints in the distribution of the radial sensory nerve compression resulting only in sensory symptoms is most likely due to entrapment in the distal third of the forearm (between the tendons of the brachioradialis and the extensor carpi radialis longus [ECRL]) known as Wartenberg syndrome.

Radial Nerve Entrapment and Injury

11.4 Surgical Anatomy The radial nerve is formed by the posterior cord of the brachial plexus with contributions from C5, C6, C7, C8, and T1 (▶ Fig. 11.2). Traveling dorsal to the axillary artery and vein, posterior and intimate to the humeral shaft, the radial nerve transits beneath the lateral head of the triceps, where it gives off motor branches to the triceps. Two sensory branches, the posterior cutaneous nerve of the arm and forearm, arise and continue in a subcutaneous plane. The radial nerve proper then continues deep, crossing the humerus and piercing the lateral intermuscular septum ~ 10 cm proximal to the lateral humeral epicondyle.16 From 2 to 3 cm proximal to the lateral epicondyle, the radial nerve lies between the brachialis muscle and the origin of the brachioradialis muscle. This relationship is useful in identifying the nerve during surgery. It is at this location that the radial nerve branches off to innervate the brachioradialis and ECRL muscles before finally bifurcating into the motor radial nerve component: the PIN and the superficial radial nerve (sensory component).13 The PIN transits over the radiohumeral joint and passes dorsolaterally around the radial head through the substance of the supinator muscle and along the dorsal surface of the interosseous membrane.47 It supplies the majority of the forearm and hand extensors, including the extensor carpi radialis brevis (ECRB), supinator, extensor digitorum communis (EDC), extensor digiti quinti (EDQ), extensor carpi ulnaris (ECU), abductor pollicis longus (APL), extensor pollicis longus (EPL) and brevis (EPB), and extensor indicis proprius (EIP). The supinator muscle is an area of anatomical importance. In 1908 Fröhse and Frankel described a fibrous arch from the lateral and medial edges of the lateral humeral epicondyle where the two heads of the supinator muscle arise.48 Morton Spinner recognized this area as an important source of compression and popularized the tendinous superficial head of the supinator of this muscle, the arcade of Fröhse47 (the also popularized the arcade of Struthers as an important compression point on the ulnar nerve, see Chapter 10). Once the PIN passes beneath the arcade of Fröhse, between the two heads of the supinator, the nerve divides into multiple branches.47 Additional potential sources of compression in this area are the vascular leash of Henry (the radial recurrent artery) and the tendinous margin of the ECRB.34 As the nerve divides, one major segment innervates the relatively superficial muscles, including the EDC, EDQ, and ECU, whereas a second segment innervates the deeper muscles, such as the APL, EPL, EPB, and EIP. The nerve supplying the ECRB always appears to lie superficial to the PIN proximal to the entrance of the PIN in the supinator muscle. The nerve to the ECRB is a distinctly separate nerve, originating more proximally on the radial nerve in the area of the motor/sensory bifurcation. In fact, it can appear to arise from the sensory portion of the nerve. It is important to recognize this motor branch and preserve it from injury during surgical dissection. It is also an excellent donor nerve to transfer to the median nerve for median palsy. The nerve to the supinator (C5) divides into 2 branches behind the PIN and also an excellent donor nerve for median nerve palsies (C7, C8) and for PIN function (C6, C7, C8). In 25% of patients, the radial nerve may pass over a seemingly bare area of the radius proximal to branching of the PIN and posterior to the bicipital tuberosity.17 In this region, the nerve is at risk of direct injury during fracture or by the placement of

plates to correct fractures. There can be additional, rare anatomical variations in this region. A study of 58 cadaver forearms found that in 4%, the PIN ran superficial to the supinator muscle and was covered only by a thin aponeurosis. In 5% of the forearms, the nerve ran deep to the supinator, in contact with the periosteum of the radius.49 Terminally, after innervating the extensor muscles, the PIN travels along the most radial side of the fourth extensor compartment to innervate the dorsal wrist capsule and intercarpal ligaments. If an extensor brevis manus muscle is present, it is supplied by a branch from the terminal portion of the PIN. 28 The PIN’s terminal branch may be blocked during diagnostic procedures for wrist pain as well as resected during a partial dorsal wrist denervation procedure for the treatment of wrist pain.24 Resection may also be helpful in managing radial sensory neuroma pain. Other anatomical anomalies have been reported to occur as variations in the muscles in the elbow and proximal forearm region. Occasionally, the medial portion of the lateral humeral epicondyle gives rise to a solitary muscular head, which results in the PIN’s traveling along the top of the supinator muscle rather than passing through it. Another variation affecting the PIN is the fusion (or failure of segmentation) of the brachioradialis and brachialis muscles, possibly resulting in compressive forces over the radial nerve at the proximal aspect of the radial tunnel.16 This may be one cause of radial tunnel syndrome.

11.5 Diagnosis and Physical Examination A complete patient history and careful physical examination are often all that are needed to determine the level of injury and suspected cause of radial nerve dysfunction. With a complete PIN lesion, the patient is unable to extend the metacarpophalangeal joints of any finger. However, the intrinsic muscles still function via the ulnar nerve, so the patient is still able to extend the interphalangeal (IP) joints. Similarly, although the EPL tendon is paralyzed, it does not prevent the IP joint of the thumb from being extended to at least a neutral position by the median and ulnar innervated thumb intrinsics. Nevertheless, hyperextension of the thumb at the IP joint is not possible, and the patient is unable to elevate the thumb off the table when resting flat. With PIN palsy, wrist extension is possible; it is associated with radial deviation due to the remaining innervation of the ECRL (a branch proximal to the PIN). The presence of sensory loss in the distribution of the radial sensory nerve and muscle paralysis of the brachioradialis, the ECRL, and the triceps muscles, in addition to those muscles innervated by the PIN, localize the level of the radial nerve injury to the proximal arm. If sensation is lost in the posterior aspect of the forearm and the posterolateral surface of the arm, it is likely that the posterior cutaneous nerves are also injured, localizing the radial nerve injury more proximally at the level of exit of this nerve from the axilla and its takeoff from the posterior cord of the brachial plexus. Even more proximally, a lesion in the posterior cord of the brachial plexus is accompanied by weakness in muscles innervated by the axillary nerve (deltoid) and in muscles innervated by the thoracodorsal nerves, such as the latissimus dorsi. Finally, with a C7 radiculopathy, both the

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Fig. 11.2 Anatomy of the radial nerve. The radial nerve, similar to the peroneal nerve, is at more risk for stretch and compression with extremity injuries because of its "spiral" course and multiple entrapment points. (* denotes dual innervation of the brachialis muscle by the musculocutaneous nerve and radial nerve that can occur in a small percentage of patients.)

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Radial Nerve Entrapment and Injury palmar and dorsal aspects of the middle finger are involved when determining the region of sensory loss. Additionally, a C7 root lesion can result in weakness in the muscles innervated by the median nerve (pronator teres, flexor carpi radialis [FCR]), as well as extensor muscle weakness. Electromyography will help to localize a cervical root issue. A final diagnostic dilemma may be the possibility of tendon ruptures, rather than nerve paralysis, to explain a loss of finger and thumb extension. In fact, it is common for an injury in the PIN with loss of extension of the fingers to be confused with the rupture of tendons of the fingers and thumb, as is commonly seen in rheumatoid arthritis.27 A simple test of a “tenodesis effect” can help clarify the diagnosis. If the tendons are intact, a flexed wrist will result in extended fingers, and an extended wrist will result in flexed fingers; that is, the tenodesis effect is still present with a PIN lesion and not present when the tendons are ruptured. For closed radial nerve injuries, serial clinical examination and repeat electrodiagnostic studies are essential to document spontaneous recovery and can be instrumental in surgical decision making for injuries that do not improve along the expected curve.

about these muscles.50 Nirschel and Pettrone confirmed this impression.51 It is now also considered a degenerative rather than an inflammatory process. The clinical diagnosis includes pain over the lateral epicondyle with resisted wrist extension and finger extension. Clinically, the surgeon is faced with the problem of distinguishing radial tunnel syndrome from lateral epicondylitis (tennis elbow). Provocative tests have been developed to aid with the diagnosis. One provocative test developed by Roles and Maudsley simulates radial tunnel syndrome by resisting the patient’s attempt to extend the middle finger.35 Lister has added that resisting middle finger extension causes more pain than resisting extension of the index, ring, or little fingers.52 Lister also reported that pain is referred to the mobile muscle and over the radial head in radial tunnel syndrome, whereas in lateral epicondylitis, pain is referred to the lateral epicondyle. In radial nerve compression, the radial nerve is tender to palpation in the region of this muscle mass. We find that the scratch-collapse test is also routinely positive in radial tunnel syndrome. However, because the nerve is deep, below the supinator, we use digital pressure as the stimulus for the test, not a superficial scratch.

11.6 Radial Tunnel Syndrome

11.8 Management of Radial Nerve Palsy

The radial tunnel begins distal to the motor branches to the brachioradialis and the ECRL. In the radial tunnel, the radial nerve is bordered medially by the brachialis muscle and the biceps tendon, laterally by the origin of the brachioradialis muscle, and posteriorly by the lateral humeral epicondyle at the entrance to this region. When traveling distally, the radial nerve is crossed by the ECRB, which may be large enough to compress the nerve against the underlying capitellum. Because the ECRL originates posterior to the nerve, it does not contribute to compression. However, the ECRB has a fibrous arch that compresses the radial nerve as it branches into the PIN against the arcade of Fröhse in the distal region of the radial tunnel. Another possible source of compression of the radial nerve in the radial tunnel is the point at which it crosses over the radial head, where it may pass through a region of fibrous adhesions. Although the anatomy that gives rise to radial tunnel syndrome overlaps that which gives rise to PIN syndrome in the arcade of Fröhse, the symptoms are not the same. Although this anatomical overlap between structures causing compression in both radial tunnel syndrome and PIN syndrome exists, patients with radial tunnel syndrome do not experience motor paralysis. Instead, they typically have aching pain in the proximal forearm that may worsen with use of the arm. No distal sensory changes are present in the radial sensory nerve.

11.7 Lateral Epicondylitis (Tennis Elbow) Goldie described lateral epicondylitis as an inflammation at the origin of the ECRB and EDC muscles from the lateral humeral epicondyle, resulting in granulation tissue forming

After diagnosing a radial nerve palsy, treatment options must be determined. For this purpose, an algorithm based on a concise and clinically relevant classification system has been developed. The general principles involved in the management of radial nerve injuries are well established.

11.8.1 Open Radial Nerve Injury

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Open injuries associated with radial nerve dysfunction should be explored promptly. Fractures or wounds requiring exploration allow the radial nerve to be examined intraoperatively. The radial nerve may be compressed by the humerus or divided by a fracture in this region. Early treatment of this injury may involve direct nerve repair for nerve transections.2 Stretch injuries are by far more common and should be managed as closed injuries. Barton reported that 16% of humeral shaft fractures were complicated by immediate radial nerve palsy, whereas only 1 case of radial nerve division out of 23 cases of radial nerve palsy was observed after immediate exploration. 42

11.8.2 Closed Radial Nerve Palsy A closed radial nerve palsy should be surgically explored immediately only if transection of the radial nerve is suspected despite a closed wound (as seen with significant fracture displacement and high-velocity injuries). Otherwise, the patient should be observed for 3 months. The patient should be provided with a wrist splint, and hand therapy is undertaken to maximize function and preserve passive range of motion of the affected joints. If no clinical or electrical evidence of reinnervation is detected at the 3-month observation period,

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Radial Nerve Entrapment and Injury surgical exploration is indicated. 53 Determining whether or not the nerve is regenerating appropriately is important. The order in which innervation is expected to recover is the same sequence in which the muscles are innervated proximal to the elbow by the radial nerve: the brachioradialis muscle, the ECRL, and the ECRB. The sequence of the remaining muscles to be reinnervated is the ECU, EDC, and EDQ. After innervating this group, the nerve travels proximally 4 cm to innervate the APL, EPB, EIP, and EPL. Closed radial nerve palsies that fail to demonstrate clinical or electrical evidence of radial nerve recovery after 3 months should be considered for surgical intervention. The options for surgical management include decompression/neurolysis, interpositional nerve grafting, distal nerve transfer, and tendon transfer. It should be noted that in patients who are recovering well and then suddenly stall in their progress, the nerve may be “held up” at a known site of compression. In these circumstances, a simple decompression can allow the stalled nerve to regenerate more quickly once the pressure is relieved. The scratch-collapse test is usually positive at the entrapment point at the lateral septum and/or the arcade of Fröhse.

11.9 Surgical Options 11.9.1 Primary Repair and/or Nerve Grafting Patients with low or intermediate radial nerve injuries have excellent results when, depending on the injury, they are repaired primarily, decompressed/neurolysed, or grafted at 3 to 4 months because the motor end plates are in relatively close proximity for regenerating axons.4

11.9.2 Tendon Transfers In contrast, high radial nerve injury results in a longer distance for axons to travel.53 Therefore, those injuries that fail to recover within 3 months may be more appropriately considered for distal nerve transfers or tendon transfers.53 Tendon transfers are the current treatment of choice for radial nerve palsies that fail to recover. They provide predictably good results in patients with radial nerve paralysis (see Chapter 17 for a detailed discussion of tendon transfers for restoration

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Fig. 11.3 Decompression at the right spiral groove. Exposure of the radial nerve in the spiral groove through the interval between the brachialis and brachioradialis. The radial nerve is identified under tourniquet control exactly in the interval between the brachioradialis muscle and the brachialis muscle, just proximal to the elbow. This is a very “slick” and simple fascial plane between these two muscles. If the surgeon is struggling to find the radial nerve, then he or she is not in the correct plane. Finding the cutaneous branch and then dissecting 2 cm distal to that is helpful in identifying the radial nerve. The patient is positioned supine, with the right upper extremity exposed in this case.

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Fig. 11.4 Lateral intermuscular septum. Once the radial nerve has been identified, the tourniquet is removed so that the decompression of the radial nerve through the spiral groove can be achieved. The radial nerve is identified with the posterior cutaneous nerve, just distal to the sharp and thickened edge of the lateral intermuscular septum.

11 of radial nerve function). The combination of tendon transfers used for the treatment of radial nerve paralysis depends on the level of injury, overall function, and anatomy. The most common tendon transfers for wrist extension use the pronator teres muscle to motor the ECRB, selected for its more central position inserting on the base of the long metacarpal. For finger extension, the EDC can be reconstructed using the FDS (III), the flexor carpi ulnaris [FCU], or the FCR tendons.53 The FCR is our tendon transfer of choice. For thumb extension, the EPL can be reconstructed using the palmaris longus or the FDS (IV). 53 Numerous authors have reported that early tendon transfer in radial nerve transection produces excellent results.53 A useful alternative to tendon transfer in patients with high proximal nerve injuries, situations of complete nerve function loss, or delayed presentation is distal nerve transfer. In general tendon transfers are used when the passive range of movement is good and a quick recovery is wanted, and the patient can tolerate a month of splinting and immobilization. A nerve transfer requires just a few days of immoblization and offers the possibility of independent finger extension, but requires postoperative reeducation and 10 to12 months before recovery. The tendon transfer is not time-dependent, and the nerve transfer should be done within several months.

11.9.3 Nerve Transfers Nerve transfer involves the recruitment of redundant nerve fascicles from a donor nerve to innervate critical motor or sensory nerves close to target end-organs. Although the technique was not favored until recently, the list of commonly used nerve transfer donors is rapidly expanding.54 First described in 1948 by Lurje as an alternative option for severe brachial plexus injuries when other treatments were not feasible, nerve transfer was overshadowed by the popularity of nerve grafting during the 1960s and 1970s.3,55 Historically, nerve transfers were limited to brachial plexus avulsion injuries where no proximal source of nerve is available.56,57 Today, they are being progressively used to reconstruct many proximal nerve injuries and often in preference to long nerve grafts whenever feasible.54 Transfers can be performed without the need for an interpositional nerve graft if the mantra “donor/distal, recipient/proximal;” is adhered to.54 It is clear that the use of nerve transfer in the treatment of radial nerve injuries has become more accepted; however, all the potential benefits of this technique have yet to be elucidated. 53 Distal nerve transfer should be considered as a surgical option if the radial nerve fails to recover following orthopedic trauma or in the case of a complete radial nerve lesion. It is a viable option for

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Fig. 11.5 Release of the lateral intermuscular septum. A score and release is made to the tendinous lateral intermuscular septum at several levels to completely decompress the radial nerve.

11 many clinical situations that previously had limited or no alternatives. Disappointing recovery following long nerve grafts in the case of acutely transected nerves with limited trauma has resulted in the need for another reconstructive option. Idiopathic nerve palsies or neuritis with the absence of an identifiable healthy proximal segment presents a similar situation.53 Current options for nerve transfers to reinnervate the PIN are redundant fascicles from the median nerve, such as the palmaris longus, FCR, and FDS. These are discussed in detail in Chapter 5.

11.10 Surgical Techniques for Decompression 11.10.1 Decompression at the Spiral Groove This is an uncommon decompression; thus we advise taking an excellent anatomy book into the operating room. We had good results in this release for pain relief in patients with associated failed clinical spine surgery and persistent pain in conjunction with PIN and radial sensory nerve release. If we are also releasing the radial tunnel simultaneously, then we release the

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radial tunnel first, as this helps to orient the surgeon for the location of the radial nerve proximally. A separate incision is made in the interval between the brachioradialis and the brachialis muscles (▶ Fig. 11.3). Dissection is carried down to the level of the radial nerve. The radial nerve is found between the muscle compartments, not within a muscle. We then slowly follow the radial nerve proximally until we reach the lateral intermuscular septum (▶ Fig. 11.4). This is ~ 12 cm proximal to the lateral epicondyle. It is very obvious, and the tendon septum is quite long, probably 3 cm, and is divided at several levels (▶ Fig. 11.5; ▶ Fig. 11.6). There are large vessels around the radial nerve at this level, so care must be taken not to injure them. Also, the posterior cutaneous branch from the radial nerve is in this region, and care must be taken taken to protect the nerve.

11.10.2 Posterior Interosseous Nerve/ Radial Tunnel Decompression Radial nerve compression in the proximal forearm is approached using a standard procedure during which all potential points of compression are released. The incision is marked by defining the interval between the ECRL and the brachioradialis muscles (▶ Fig. 11.7). Preoperatively, the patient is asked to flex

Radial Nerve Entrapment and Injury

Fig. 11.6 Complete release of the radial nerve in the spiral groove. Once that septum has been completely divided and released, the surgeon will be able to run a finger proximally along the course of the radial nerve. Be careful of thin walled vessels in this area.

11 Fig. 11.7 Radial nerve decompression in the proximal forearm. Incision for the posterior interosseous nerve (PIN) release. The most critical thing in a successful, “easy” decompression of the PIN through the arcade of Fröhse is marking preoperatively the exact interval between the brachioradialis and the extensor carpi radialis longus (ECRL). In patients with PIN palsy, the brachioradialis is functioning, and the posterior border of this muscle can be seen. It is imperative to make this mark preoperatively to facilitate dissection.

the elbow against resistance. The interval is easily seen with this maneuver. An incision is designed over this interval in the proximal forearm, exactly along the lateral or posterior border of the brachioradialis muscle. Marking this landmark prior to surgery is critical.

After the incision is completed, careful dissection is made through the subcutaneous tissues down to the fascia. At this point, important landmarks will guide the surgeon easily down to the radial nerve. First note the presence of the posterior cutaneous nerve of the forearm. This cutaneous nerve runs exactly longitudinally along the interval between the

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Fig. 11.8 (a) Posterior cutaneous branch of the radial nerve. Coming down through the soft tissue, the posterior cutaneous nerve of the forearm is identified and retracted and lying on the blue background. The posterior cutaneous nerve helps identify the interval between the brachioradialis muscle and the ECRL muscle. The fascia over the brachioradialis is slightly thinner than the ECRL, as the brachioradialis appears “redder” and the ECRL appears “lighter.” (b) Interval between the brachioradialis and ECRL. The interval between the “redder” brachioradialis and the “lighter” ECRL is marked.

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Fig. 11.9 Dissection between the brachioradialis and ECRL. Blunt finger dissection takes the surgeon down toward the arcade of Fröhse. If there is any difficulty dissecting between these two muscles, then the surgeon is not in the correct plane.

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Fig. 11.10 Exposing the radial nerve in the region of the arcade of Fröhse. Down curve retractors will identify the fat around the radial nerve and its branches in the region of the arcade of Frohse.

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Fig. 11.11 Superficial branch of the radial nerve. The radial sensory nerve is noted; just above this will be the smaller nerve to the extensor carpi radialis brevis (ECRB) muscle.

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Fig. 11.12 Recurrent radial vessels. The recurrent crossing radial vessels need to be divided in order to visualize and decompress the PIN.

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Radial Nerve Entrapment and Injury

Fig. 11.13 Identifying the components of the radial nerve. The radial sensory nerve is located medially, and the PIN is located laterally. The smaller ECRB nerve sits anatomically between these two nerves.

ECRL and the brachioradialis muscles. Additional confirmation of the appropriate interval is made by noting the slight color difference between these two muscles (▶ Fig. 11.8). The brachioradialis (BR) has a thinner fascial layer, making it appear more red, whereas the ECRL, encased in thicker fascia, appears lighter or white. We remember Red as in BR and Light as in ECRL. The posterior cutaneous nerve is then elevated and protected. The avascular plane between the two muscles is easily finger dissected (▶ Fig. 11.9). Deep retractors are then placed to expose the radial nerve (▶ Figs. 10–13). From volar to dorsal, three branches of the radial nerve can be identified. The robust radial sensory branch is the most volar, followed by the smaller diameter ECRB. The PIN is located most dorsally and is obliquely oriented as it dives under the superficial head of the supinator. The possible points of compression are the tendinous medial border of the ECRB, the radial fan of vessels overlying the nerve, and the leading fascial edge of the superficial head of the supinator muscle. Once the fascial edge of the ECRB is released, the supinator muscle is visualized (▶ Fig. 11.14). The fascial edge of the superficial head of the supinator is completely released (arcade of Fröhse), exposing the underlying PIN (▶ Fig. 11.15). In most cases, the entire superficial head of the supinator requires release to ensure adequate decompression (▶ Fig. 11.16). Take care not to injure the two veins on either side of the PIN. If the preoperative history and physical examination suggest radial nerve compression in the proximal radial tunnel (as indicated by aching pain over the radial nerve above the elbow), then two additional steps may be required. The first step is

more proximal dissection and release. The surgeon can accomplish this bluntly using a finger to dissect proximally toward the radial head. At the level of the radial head, the radial nerve is visualized proximal to where it divides into the sensory nerve and PIN. The surgeon guides a finger proximally along the course of the radial nerve about the humerus. In the most proximal region of the radial tunnel, conjoined fibers of the brachioradialis and the brachialis muscles may require release. Sometimes a second, proximal incision in the distal arm at the interval of the brachioradialis and brachialis facilitates a complete proximal release. If there is associated lateral epicondylitis, then a proximal tenotomy of the ECRB tendon is performed across the forearm to “disconnect” it from the lateral epicondyle (▶ Fig. 11.17). This tenotomy is performed through the PIN incision under the ECRB muscle leaving the muscle intact. Once the nerve is appropriately decompressed, consideration is made regarding intraneural neurolysis. Neurolysis should be considered in patients who present with significant motor weakness or paralysis in any of the muscles innervated by the PIN, particularly when the intraoperative findings demonstrate pseudoneuroma, as evidenced by firm areas of nerve that lack normal architecture. Neurolysis should progress until a good fascicular pattern and good perineurial markings, such as bands of Fontana, are evident.

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11.10.3 Decompression of the Radial Sensory Branch Compression of the radial sensory branch, or neuroma in this area can be exquisitely painful and life altering. It is important

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Fig. 11.14 (a) Tendinous border of the ECRB. The ECRB muscle is retracted to identify the tendinous component of the ECRB. This will be divided. In patients with associated lateral epicondylitis, this tendon is released all the way across the forearm to detach it from the lateral epicondyle. (b) Identifying the tendinous leading border of the superficial head of the supinator. The tendinous leading edge of the supinator is noted just below the tendon of the ECRB. The tendon of the ECRB will be divided all across the forearm.

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11

Fig. 11.15 (a) Tendinous medial border of the superficial head of the supinator. Once the tendon of the ECRB has been divided, the muscle can be retracted to identify the tendinous leading edge of the superficial head of the supinator (arcade of Fröhse). (b) Release of the tendinous medial border of the superficial head of the supinator. The muscle and the tendon of the superficial head of the supinator are divided to decompress the PIN.

303

Radial Nerve Entrapment and Injury

11

Fig. 11.16 (a) Distal border of the superficial head of the supinator. A very tendinous distal border within the superficial head of the supinator can be seen in this patient. These distal fascial edges are not always present. (b) PIN decompression. With the PIN decompressed, the nerve to the supinator muscle can be seen. It is located behind the PIN; usually a branch to the superficial and a second branch to the deep supinator muscles can be identified. Care is then taken to look proximally to ensure no other proximal compressive bands exist over the radial nerve.

304

Radial Nerve Entrapment and Injury

Fig. 11.17 Lateral epicondylitis and tenotomy of the extensor carpi radialis brevis (ECRB). If there is an associated lateral epicondylitis, a proximal tenotomy of the ECRB is performed.

11

Fig. 11.18 Decompression of the radial sensory branch. Superficial branch of the radial nerve as it courses superficially between the brachioradialis and extensor carpi radialis longus (ECRL). When the radial sensory nerve is located between the ECRL tendon and the brachioradialis tendon, it is maximally compressed when the forearm is pronated and the wrist is flexed with ulnar deviation.

305

Radial Nerve Entrapment and Injury

Fig. 11.19 Superficial branch of the radial nerve in the forearm. The radial nerve is seen to exit superficially between the brachioradialis and ECRL.

11 to document the distinction between radial sensory neuropathy and lateral antebrachial cutaneous neuropathy. The lateral antebrachial cutaneous (LABC) nerve runs in the forearm (at approximately the radial one-third/ulnar two-thirds junction) with the cephalic vein. This nerve can often be confused with the radial sensory nerve on history and physical examination. One excellent way to distinguish between the two nerves is to inject local anesthetic proximal forearm beside the cephalic vein to block the LABC but not the deeper radial sensory nerve. If the patient’s pain is relieved, that is pathognomonic. The radial sensory nerve can be decompressed in the forearm. The complex branching pattern and the diffuse sensory territory make this nerve notoriously easy to injure in a variety of common plastic surgery procedures (De Quervain tenosynovitis release, ligament reconstruction tendon interposition, carpometacarpal arthroplasty, thumb metacarpophalangeal joint arthrodesis, etc.). The patient in ▶ Figs. 18– 21 had a small but “bothersome” radial sensory nerve and in this case a full release of the radial sensory nerve in the forearm was successful in relieving pain. The tendon of the brachioradialis muscle was completely divided and the nerve neurolysed.

306

11.11 Surgical Techniques for Radial Nerve Repair 11.11.1 Primary Repair and Nerve Grafting If the radial nerve has been sharply transected, consideration should be made for immediate, primary repair. Outcomes after primary nerve repair are promising when the radial nerve is transected at a location that is fairly close to motor end plates.58 Consideration regarding the age, level of injury, length of defect, associated injuries, and interval to surgery should be made when considering the best surgical option for each particular injury. Excellent results have been reported after primary radial nerve repair in 78 to 90% of patients.58–60 In a sharp penetrating injury or iatrogenic injury, primary repair in a tension-free manner is the surgical procedure of choice. Loupe magnification to dissect distally and proximally helps identify the two cut ends. By a technique known as “bread loafing,” the two ends are cut back to healthy-looking fascicles with cleanly trimmed ends, remembering that it will take ~ 3 weeks for scar formation to occur. Using the microscope, epineurial sutures are used to approximate the two ends, and alignment is facilitated by

Radial Nerve Entrapment and Injury

Fig. 11.20 Tenotomy of the brachioradialis. Down curve retractors are used to expose the muscle tendon junction of the brachioradialis so that a step lengthening can be performed. The tendinous component of the brachioradialis is removed underneath the muscle.

the presence of longitudinal vessels that run along the surface of the nerve. A minimum of sutures required to approximate the two ends under no tension are used, and the final repair is often reinforced using fibrin glue. If there is any tension, an interpositional nerve graft is preferable. A nerve graft can also allow the surgeon to go extra-anatomical in the event of a diffuse zone of injury or an unfavorable wound bed. The authors’ first choice of donor nerve would be the ipsilateral medial antebrachial cutaneous (MABC) nerve, which can be harvested quickly from the same extremity. It provides an excellent diameter nerve graft and potentially multiple cables. If only a short graft is required, either the anterior or the posterior division of the MABC can be harvested. To minimize donor deficit, the distal aspect of the harvested MABC can be coapted in an end-to-side manner to the sensory aspect of the median nerve in the arm.

11.11.2 Tendon Transfers Radial nerve tendon transfers are well described in Chapter 17. Our preference would be to use the pronator teres to ECRB to restore wrist extension, FCU to EDC to restore finger extension, and palmaris longus to a rerouted EPL to restore thumb extension.

11

Tendon transfers can be performed in a delayed fashion, whereas with nerve transfers, the adage “Time is muscle” dictates timing for surgical intervention. In patients with delayed presentation, patients who are noncompliant, or patients desiring rapid recovery, tendon transfers for radial nerve injury are a good option. Median to radial nerve transfer takes longer to recover (10 to 12 months), but the results with independent finger and thumb extension can be spectacular. In addition, the authors will frequently perform a pronator teres-to-ECRB tendon transfer concomitant with nerve transfers to quickly restore wrist extension. This avoids the use of a wrist cock-up splint.

11.11.3 Nerve Transfers To reconstruct the PIN, the median nerve is an excellent donor because it has a limited number of anatomical variations and because of its proximity to the radial nerve, allowing end-toend nerve transfer without the need for an interpositional nerve graft. Potential donors from the median nerve include redundant branches to the FDS and palmaris longus and FCR. Intimate knowledge of the internal topography of the median nerve, combined with intraoperative nerve stimulation using a disposable nerve stimulator, facilitates identification of these

307

Radial Nerve Entrapment and Injury

Fig. 11.21 Decompression of the radial sensory nerve. The radial sensory nerve can be seen to be nicely decompressed along its entire length.

11 redundant fascicles. Internal neurolysis of the median nerve is not necessary because the median nerve has already branched at this level. The surgeon simply needs to expose the median nerve and identify the various branches. When choosing the median nerve donors, care should be taken to always avoid sacrificing the branches to the pronator teres or the anterior interosseous nerve (FPL, and profundus to index).61

11.12 Postoperative Care for Radial Nerve Decompression A dressing of gauze, a soft roll, and a posterior plaster splint are applied holding the elbow in 90-degree flexion with the forearm in neutral position and the wrist slightly extended. Immediate finger and shoulder movement is encouraged using the dressing as a limitation to the wrist and elbow. A sling is discontinued at 7 days. During the second week postoperatively, the patient will begin wrist movement and elbow flexion and extension exercises in order for the nerve to glide through the operative plane to prevent adhesion formation between the nerve and the tissues that have been extensively released. During the third week, gentle massage to the operative area is encouraged, and gentle resisted exercises of the thumb, fingers, wrist, and forearm are begun.

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11.13 Results 11.13.1 Decompression A review of the overall results of all the articles describing PIN syndrome has not been done. Of the 73 cases reported on radial tunnel syndrome,45,62 all but 6 patients achieved excellent results after decompression of the nerve. There were 92% good to excellent results.

11.13.2 Primary Repair Results of radial nerve repair in the brachium are generally discussed as being good, because it is a short distance to reinnervate the wrist extensors. Little reported information, however, is actually available. Sunderland lists three cases of repair to the radial nerve, two after laceration and one after a gunshot wound; one had a level of injury 12.5 cm above the lateral epicondyle and the other two with levels of repair at 4 to 5 cm proximally.63 All three patients recovered function in the EPL tendon by 40 to 45 weeks after the repair, but the strength of the muscle recovery and whether sensation recurred were not noted.

Radial Nerve Entrapment and Injury

11.13.3 Nerve Grafts The results of radial nerve repair using nerve grafts have been comparable to primary repairs. Millesi et al reported that 77% of patients with interfascicular radial nerve grafting achieved four out of five motor strength.64,65 Dolenc reported 14 cases of radial nerve transactions that required nerve grafts of varying lengths.66 He determined that the time from injury to surgery and the surgical condition were more important than the length of the nerve graft. In other studies, good results have been noted in 80% of patients who required radial nerve grafts.67,68 Unless the radial nerve injury is close to the elbow, we now would do a nerve transfer, not a long nerve graft.

11.13.4 Tendon Transfers Most authors agree that tendon transfers provide good results if nerve reconstruction fails in patients with radial nerve palsy. Sunderland recommended a tendon transfer if there were no signs of radial nerve recovery within 1 year.59,63 In the 1970s, Bevin advocated early tendon transfer in radial nerve transection. He reported an average recovery time from nerve repair to be 7.5 months, with 66 percent of patients achieving good or excellent function. In the tendon transfer group, all patients noted good to excellent results in 8 weeks.59 The pronator teres was transferred to the ECRL and ECRB, and the palmaris longus was transferred to the common digital extensors. When the palmaris longus was not present, the thumb extensors and abductor were motored by the FCU as well. However, it was difficult to fully determine from Bevin’s article the approximate level of the radial nerve injury in the patients reviewed. Burkhalter also advocated early tendon transfer because he believed the transfer acts both as a substitute during regrowth of the nerve or when lesions are irreparable and as a helper during reinnervation.58 Kruft et al maintained that irreversible radial nerve paralysis should be treated with early tendon transfer.69 They reported on 43 patients who underwent tendon transfer, with 38 patients ultimately returning to their original jobs. The authors qualified their results by stating that tendon transfers “never fully replace an intact radial nerve for the purpose of controlling the hand.” Elton and Omer observed that patients with radial nerve paralysis treated by tendon transfer often experienced extensor tightness, which prevented simultaneous flexion of the wrist and fingers.70 Barton described this as a “rather unnatural movement, seldom needed in ordinary life.”42 Several authors have commented that the greatest functional loss after radial nerve palsy was not the loss of finger extension, but instead the loss of power grip, which cannot be easily recreated with standard tendon transfers.58,70 As such, it is important to fully examine alternative approaches to treating radial nerve palsy to decrease the long-term morbidity associated with tendon transfers that clinically often appear “unnatural.”

11.13.5 Nerve Transfer In our experience, we have successfully transferred redundant branches of the median nerve to the PIN in the forearm of several radial nerve paralysis.61,72–75 Long-term results have been

excellent.75 It is critical to transfer synergetic nerves (FDS and ECRB and FCR to EDC). Functional recovery after nerve transfer is contingent upon a sufficient number of motor axons reinnervating muscle fibers during a specific time frame. Mackinnon and Novak have found that using nerve transfers to avoid long nerve grafts or to increase end-plate reinnervation after a delay in treatment in brachial plexus injuries has yielded superior clinical results.74 Potential recovery of motor function following nerve transfer compared with that of tendon transfer is potentially greater due to the preservation of muscle biomechanics and employs significantly less muscle dissection.53 Target muscle is most often undisturbed with minimal scarring or adhesion formation that could limit target muscle excursion.53 Moreover, the proximal forearm appears to be ideal for the technique of nerve transfer because of the availability of expendable donor nerve branches and the short distance required to reach the target motor end plates. Appropriate postoperative motor reeducation is key to an excellent result.

11.14 Conclusion There are many potential etiologies of radial nerve pathology, and radial sensory nerve injury is one of the most commonly injured and least forgiving nerves in the upper extremity (see Chapter 20). Compression neuropathies of the radial nerve exist, and surgical decompression can markedly improve symptoms. Advances in our knowledge of the anatomy, internal topography, and surgical technique have led to the possibility of new reconstructive options to improve outcomes and more closely parallel normal function.

11.15 References 11

[1] Agnew D. Bursal tumour producing loss of power of forearm. Am J Med Sci 1863;46:404–405 [2] Guillain G, Coutellemont R. L’action du musclecourt supinateur dans la paralysie du nerf radial. Presse Med 1905;10:50–52 [3] Grigoresco M. lordanesco C. Un cas rare de paralysie partielle du nerf radial. Rev Neurol (Paris) 1931;2:102–104 [4] Woltman HW, Learmonth JR. Progressive paralysis of the nervus interosseous dorsalis. Brain 1934;57:25 [5] Hobhouse NH. A case of posterior interosseous paralysis. BMJ 1936;1:841 [6] Otenasek FJ. Progressive paralysis of the nervus interosseus dorsalis; pathological findings in one case. Bull Johns Hopkins Hosp 1947;81:163–167 [7] Richmond DA. Lipoma causing a posterior interosseous nerve lesion. J Bone Joint Surg Br 1953;35-B:83 [8] Hustead AP, Mulder DW, MacCarty CS. Nontraumatic, progressive paralysis of the deep radial (posterior interosseous) nerve. AMA Arch Neurol Psychiatry 1958;79:269–274 [9] Kruse F. Paralysis of the dorsal interosseous nerve not due to direct trauma: a case showing spontaneous recovery. Neurology 1958;8:307–308 [10] Rousey G, Branche J. Deux cas de paralysies dissociees de la branche posterieure du radial, a type de pseudo-griffe cubitale. Rev Neurol (Paris) 1917;24:312 [11] Naylor A. Monteggia fractures. Br J Surg 1942;29:323 [12] Fleming P, Lenehan B, Sankar R, Folan-Curran J, Curtin W. One-third, twothirds: relationship of the radial nerve to the lateral intermuscular septum in the arm. Clin Anat 2004;17:26–29 [13] Uhl RL, Larosa JM, Sibeni T, Martino LJ. Posterior approaches to the humerus: when should you worry about the radial nerve? J Orthop Trauma 1996;10:338–340 [14] Bono CM, Grossman MG, Hochwald N, Tornetta P. Radial and axillary nerves: anatomic considerations for humeral fixation. Clin Orthop Relat Res 2000:259–264

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Radial Nerve Entrapment and Injury [15] Gerwin M, Hotchkiss RN, Weiland AJ. Alternative operative exposures of the posterior aspect of the humeral diaphysis with reference to the radial nerve. J Bone Joint Surg Am 1996;78:1690–1695 [16] Carlan D, Pratt J, Patterson JM, Weiland AJ, Boyer MI, Gelberman RH. The radial nerve in the brachium: an anatomic study in human cadavers. J Hand Surg Am 2007;32:1177–1182 [17] Van Geertruyden JP, Vico PG. Iatrogenic posterior interosseous nerve palsy following an elbow fracture. Acta Orthop Belg 1996;62:222–224 [18] Lin J, Shen PW, Hou SM. Complications of locked nailing in humeral shaft fractures. J Trauma 2003;54:943–949 [19] Chao TC, Chou WY, Chung JC, Hsu CJ. Humeral shaft fractures treated by dynamic compression plates: ender nails and interlocking nails. Int Orthop 2005;29:88–91 [20] Martínez AA, Cuenca J, Herrera A. Treatment of humeral shaft nonunions: nailing versus plating. Arch Orthop Trauma Surg 2004;124:92–95 [21] Yam A, Tan TC, Lim BH. Intraoperative interfragmentary radial nerve compression in a medially plated humeral shaft fracture: a case report. J Orthop Trauma 2005;19:491–493 [22] Cognet JM. Fabre T, Durandeau A. Paralysies radials persistantes apres fracture de la diaphyse humerale: origin, traitement et resultants. Rev Chir Orthop Repar Appar Mot 2002;88:655–662 [23] Mekhail AO, Ebraheim NA, Jackson WT, Yeasting RA. Vulnerability of the posterior interosseous nerve during proximal radius exposures. Clin Orthop Relat Res 1995:199–208 [24] Martin DF, Tolo VT, Sellers DS, Weiland AJ. Radial nerve laceration and retraction associated with a supracondylar fracture of the humerus. J Hand Surg Am 1989;14:542–545 [25] Panitz K, Neundorfer B, Piotrowski W. Prognosis of nerve injuries in humeral fractures. Chirurg 1975;46:392–394 [26] Stein F, Grabias SL, Deffer PA. Nerve injuries complicating Monteggia lesions. J Bone Joint Surg Am 1971;53:1432–1436 [27] Smith FM. Monteggia fractures: an analysis of 25 consecutive fresh injuries. Surg Gynecol Obstet 1947;85:630–640 [28] Spinner M, Freundlich BD, Teicher J. Posterior interosseous nerve palsy as a complication of Monteggia fractures in children. Clin Orthop Relat Res 1968;58:141–145 [29] Barber KW, Bianco AJ, Soule EH, MacCarty CS. Benign extraneural soft-tissue tumors of the extremities causing compression of nerves. J Bone Joint Surg Am 1962;44:98–104 [30] Eralp L, Ozger H, Ozkan K. Posterior interosseous nerve palsy due to lipoma [in TK] Acta Orthop Traumatol Turc 2006;40:252–254 [31] Ganapathy K, Winston T, Seshadri V. Posterior interosseous nerve palsy due to intermuscular lipoma. Surg Neurol 2006;65:495–496, discussion 496 [32] Fitzgerald A, Anderson W, Hooper G. Posterior interosseous nerve palsy due to parosteal lipoma. J Hand Surg [Br] 2002;27:535–537 [33] Marmor L, Lawrence JF, Dubois EL. Posterior interosseous nerve palsy due to rheumatoid arthritis. J Bone Joint Surg Am 1967;49:381–383 [34] Ritts GD, Wood MB, Linscheid RL. Radial tunnel syndrome: a ten-year surgical experience. Clin Orthop Relat Res 1987:201–205 [35] Roles NC, Maudsley RH. Radial tunnel syndrome: resistant tennis elbow as a nerve entrapment. J Bone Joint Surg Br 1972;54:499–508 [36] Ogawa BK, Kay RM, Choi PD, Stevanovic MV. Complete division of the radial nerve associated with a closed fracture of the humeral shaft in a child. J Bone Joint Surg Br 2007;89:821–824 [37] Omer GE. Results of untreated peripheral nerve injuries. Clin Orthop Relat Res 1982:15–19 [38] Guo Y, Chiou-Tan FY. Radial nerve injuries from gunshot wounds and other trauma: comparison of electrodiagnostic findings. Am J Phys Med Rehabil 2002;81:207–211 [39] Kim LY. Compression neuropathy of the radial nerve due to pentazocine-induced fibrous myopathy. Arch Phys Med Rehabil 1987;68:49–50 [40] Taras J, Donohue K. Radial nerve motor palsy following seasonal influenza vaccination: a case report. J Surg Orthop Adv. 2014;23(3):42–44 [41] Farber S, Saheb-Al-Zamani M, Zieske L, et al. Peripheral nerve injury after local anesthetic injection. Anesth Analg. 2013;117(3):731–739 [42] Barton NJ. Radial nerve lesions. Hand 1973;5:200–208 [43] Samardzić M, Grujicić D, Milinković ZB. Radial nerve lesions associated with fractures of the humeral shaft. Injury 1990;21:220–222 [44] Kettelkamp DB, Alexander H. Clinical review of radial nerve injury. J Trauma 1967;7:424–432

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[45] Lotem M, Fried A, Levy M, Solzi P, Najenson T, Nathan H. Radial palsy following muscular effort: a nerve compression syndrome possibly related to a fibrous arch of the lateral head of the triceps. J Bone Joint Surg Br 1971;53:500–506 [46] Manske PR. Compression of the radial nerve by the triceps muscle: a case report. J Bone Joint Surg Am 1977;59:835–836 [47] Spinner M. The arcade of Frohse and its relationship to posterior interosseous nerve paralysis. J Bone Joint Surg Br 1968;50:809–812 [48] Frohse FF. M. Die Muskein des Menschoichen Armes. Jena, Germany: Verlag Gustav Fischer; 1908:115–118 [49] Missankov AA, Sehgal AK, Mennen U. Variations of the posterior interosseous nerve. J Hand Surg [Br] 2000;25:281–282 [50] Goldie I. Epicondylitis lateralis humeri (epicondylalgia or tennis elbow): a pathogenetical study. Acta Chir Scand Suppl 1964;57:339 [51] Nirschl RP, Pettrone FA. Tennis elbow: the surgical treatment of lateral epicondylitis. J Bone Joint Surg Am 1979;61 6A:832–839 [52] Lister GD, Belsole RB, Kleinert HE. The radial tunnel syndrome. J Hand Surg Am 1979;4:52–59 [53] Lowe JB, Sen SK, Mackinnon SE. Current approach to radial nerve paralysis. Plast Reconstr Surg 2002;110:1099–1113 [54] Dvali L, Mackinnon S. The role of microsurgery in nerve repair and nerve grafting. Hand Clin 2007;23:73–81 [55] Lurje A. Concerning surgical treatment of traumatic injury to the upper division of the Brachial Plexus (Erb’s Type). Ann Surg 1948;127:317–326 [56] Brandt KE, Mackinnon SE. A technique for maximizing biceps recovery in brachial plexus reconstruction. J Hand Surg Am 1993;18:726–733 [57] Chuang DC, Yeh MC, Wei FC. Intercostal nerve transfer of the musculocutaneous nerve in avulsed brachial plexus injuries: evaluation of 66 patients. J Hand Surg Am 1992;17:822–828 [58] Burkhalter WE. Early tendon transfer in upper extremity peripheral nerve injury. Clin Orthop Relat Res 1974:68–79 [59] Bevin AG. Early tendon transfer for radial nerve transection. Hand 1976;8:134–136 [60] Lilla JA, Phelps DB, Boswick JA. Microsurgical repair of peripheral nerve injuries in the upper extremity. Ann Plast Surg 1979;2:24–31 [61] Brown JM, Tung TH, Mackinnon SE. Median to radial nerve transfer to restore wrist and finger extension: technical nuances. Neurosurgery 2010;66 Suppl Operative:75–83, discussion 83 [62] Darmoliński A, Buczek E, Gamrot J. Our experience with microsurgical methods of the treatment of injuries of the radial nerve caused by humeral fracture [in TK] Neurol Neurochir Pol 1992 Suppl 1:226–230 [63] Sunderland S. Observations on injuries of the radial nerve due to gunshot wounds and other causes. Aust N Z J Surg 1948;17:253–290 [64] Millesi HM, Meissl G, Berger A. Further experience with interfascicular grafting of the median, ulnar, and radial nerves. J Bone Joint Surg Am 1976;58:209–218 [65] Millesi H. Interfascicular grafts for repair of peripheral nerves of the upper extremity. Orthop Clin North Am 1977;8:387–404 [66] Dolenc V. Radial nerve lesions and their treatment. Acta Neurochir (Wien) 1976;34:235–240 [67] Kalomiri DE, Soucacos PN, Beris AE. Nerve grafting in peripheral nerve microsurgery of the upper extremity. Microsurgery 1994;15:506–511 [68] Frykman GG. Results of nerve grafting. In: Gelberman RH, ed. Operative Nerve Repair and Reconstruction. Philadelphia, PA: Lippincott; 1991 [69] Kruft S, von Heimburg D, Reill P. Treatment of irreversible lesion of the radial nerve by tendon transfer: indication and long-term results of the Merle d’Aubigné procedure. Plast Reconstr Surg 1997;100:610–616, discussion 617–618 [70] Elton R, Omer G. Tendon transfers for the nerve injured upper limb. J Bone Joint Surg Am 1972;54:1561 [71] Bowden R, Napier J. The assessment of hand function after peripheral nerve injury. J Bone Joint Surg Br 1961;43:481–492 [72] Tung TH, Mackinnon SE. Nerve transfers: indications, techniques, and outcomes. J Hand Surg Am 2010;35:332–341 [73] Mackinnon SE, Roque B, Tung TH. Median to radial nerve transfer for treatment of radial nerve palsy. Case report. J Neurosurg 2007;107:666–671 [74] Mackinnon SE, Novak CB. Nerve transfers: new options for reconstruction following nerve injury. Hand Clin 1999;15:643–666, ixix. [75] Ray WZ, Mackinnon SE. Clinical outcomes following median to radial nerve transfers. J Hand Surg Am 2011;36:201–208

Thoracic Outlet Syndrome

12 Thoracic Outlet Syndrome Stephen H. Colbert

12.1 Introduction Thoracic outlet syndrome (TOS) is a term that represents a collection of different physiologic pathologies that present with varying constellations of symptoms in the neck, shoulder, and upper extremity. Simply stated, it is the result of compression of one or more of the major neurovascular structures that traverse the upper border of the thorax in transit to or from the upper extremity. Its debated history, pathophysiology, and even existence make TOS perhaps the most controversial topic in peripheral nerve surgery. This lack of professional consensus, combined with wide variability in symptomatology and lack of a gold standard for diagnosis, explains how the diagnosis, and the patients with the condition, often may be overlooked. Having treated hundreds of patients with TOS, we have identified a philosophy of etiology and management. We believe that the paresthesias and numbness experienced in the hand with overhead activities relates to compression of the brachial plexus but that the frequently more concerning problem of pain in the scapular, neck, and shoulder area relates to muscle imbalance. It is our experience that the muscle imbalance can be treated successfully with very specific physical therapy and that surgical decompression of the brachial plexus is rarely needed (▶ Table 12.1).

12.2 History The relevant history of TOS begins as far back as Galen in the second century with recognition of a cervical rib, subsequently described by Vesalius in the 1500s.1 This and other landmarks throughout its early history relate to the recognition of the different anatomical structures involved. The association of the presence of a cervical rib with resultant symptoms was not described until 1742 by Hunauld,2 and the first cervical rib resection as treatment for these symptoms was performed by Coote in 1861.3 In 1920 Law described the role of fibrous ligaments running from the cervical rib to the first rib. 4 The cervical rib was thus the first recognized etiology of what today is called thoracic outlet syndrome and what, at the time, may have appropriately been called cervical rib syndrome. Thrombosis of the axillary or subclavian vein was recognized as another etiology of similar symptoms by Paget in 18755 and later by von

Schroetter in 18846 in a syndrome well recognized by their names, Paget-Schroetter syndrome, or as “effort-induced thrombosis.” In 1903 Bramwell7 elucidated the role of the first rib as a cause of symptoms, and Murphy performed the first resection of the first rib in 1910.8 Throughout the first half of the 20th century, further emphasis was placed on the importance of the role of the first rib in neurovascular compression.9–12 Halsted recognized the involvement of the subclavian artery in association with compressive bands and cervical ribs in 1916.13 Adson and Coffey were the first to recognize the benefit of sectioning the anterior scalene in 1927,14 although this was in the setting of patients with cervical ribs. A decade later, in 1938, Naffziger and Grant15 used the term scalenus syndrome, and they, along with Ochsner in 1935,16 presented the anterior scalene as a cause of symptoms separate from cervical ribs and popularized sectioning it as surgical treatment. Ochsner and colleagues used the terms scalenous anticus syndrome and Naffziger syndrome, with deference to Naffziger, although his article was published 3 years after Ochsner. The costoclavicular area, in particular, the costoclavicular membrane and the origin of pectoralis minor, were recognized as contributing factors by Falconer and Weddell in 194317 and Brintnall et al in 1956,18 and by Wright in 1945,19 respectively. Wright described “hyperabduction syndrome,” leading to the clinical test that bears his name still today. The term thoracic outlet syndrome was first used by Peet et al in 1956.20 Two years later, Rob and Standover21 proposed the term thoracic outlet compression syndrome. These terms, though perhaps less descriptive, reflect a better understanding of the varied nature of the syndrome and all of the anatomical structures involved. Clagett, in 1962,22 related such advanced understanding of the anatomy and pathophysiology of the syndrome and the relevance of the first rib as the backstop against which the neurovascular structures are most often compressed. The 1960s witnessed the development of multiple approaches to resection of the first rib following a period of popularity for scalenotomy that resulted in a relatively high recurrence rate. Clagett22 used a posterior thoracic approach, Falconer and Li23 used an anterior approach, and Roos24 was the first to employ a transaxillary approach. In the 1970s, Urschel et al25 promoted the benefits of reoperation for recurrent TOS, and in the 1990s Mackinnon26–28 emphasized the efficacy of appropriate physical therapy and the importance of relief of associated distal compression neuropathies in the management of TOS.

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Table 12.1 Neurogenic TOS

Arterial TOS

Venous TOS

Insidious or posttraumatic onset

Cold extremity

Edema

Pain (proximally)

Easy fatigue

Distended veins

Paresthesias (distally)

Raynaud syndrome

Achy pain

Symptoms follow activity

Symptoms with activity

Positional/intermittent Persistent with thrombosis

Abbreviation: TOS, thoracic outlet syndrome.

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Thoracic Outlet Syndrome

Fig. 12.1 Brachialis plexus and thoracic outlet anatomy. The brachial plexus has a course between the anterior and middle scalene and continues distal deep to the clavicle and superior to the first rib. This opening is referred to anatomically as the thoracic inlet and clinically as the thoracic outlet. 1 R, first rib; A, anterior scalene; BP, brachial plexus; C1–C7, cervical vertebrae; M, middle scalene; P, posterior scalene; ScA, subclavian artery; ScV, subclavian vein; T1, first thoracic vertebra.

12.3 Anatomy and Pathophysiology

12

Symptoms of TOS occur due to compression of the neurovascular structures in the cervicoaxillary canal (▶ Fig. 12.1). The three neurovascular elements are the subclavian vein, the subclavian artery, and the brachial plexus. This region at the apex of the thorax serves as an inlet for the subclavian vein, an outlet for the subclavian artery, and a transit for the brachial plexus. The cervicoaxillary canal may be conceptually divided into medial and lateral segments at the point where the first rib passes across its base. The medial or proximal segment is where the majority of neurovascular compression occurs. It comprises the costoclavicular space and the scalene triangle. The costoclavicular space is oriented along an anteromedial-to-posterolateral direction and is bounded by the first rib inferiorly, the clavicle superiorly, the costoclavicular ligament medially, the subclavius muscle and costocoracoid ligament anteriorly, the anterior scalene posteromedially, and the middle scalene posterolaterally. The subclavian vein passes through the space anterior to the anterior scalene muscle. The anterior scalene muscle originates from the anterior tubercles of the transverse proc-

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esses of the third through sixth cervical vertebrae and inserts onto the scalene tubercle of the first rib. The middle scalene originates from the posterior tubercles of the transverse processes of the second through seventh cervical vertebrae and inserts onto a more posterior portion of the first rib. The subclavian artery and brachial plexus pass through the space posterior to the anterior scalene called the scalene triangle or interscalene space. This space is bounded by the anterior scalene anteriorly, the middle scalene posteriorly, and the first rib inferiorly and thus has some overlap with the posterior aspect of the costoclavicular space. Because of the wide range of shoulder and upper extremity motion, the cervicoaxillary canal undergoes significant distortions during functional arm motion (▶ Fig. 12.2). As the arm is abducted, the clavicle rotates posteriorly toward the first rib and anterior scalene insertion. As the arm is continued into hyperabduction, the coracoid process of the scapula, which provides an insertion for the pectoralis minor tendon, rotates downward. At the same time, the neurovascular structures are stretched superiorly and axially around the tendon, coracoid process, and head of the humerus, which accentuates compression and tension on them. With shoulder movement in the opposite direction, depression, and internal rotation, such as with poor posture, the clavicle

Thoracic Outlet Syndrome

Fig. 12.2 Upper extremity movement affecting the cervicoaxillary canal. Note the arm elevation test increases tension on the brachial plexus nerves and not the distal potential entrapment points. For example, if the elbow is flexed this adds increased tension on the ulnar nerve at the cubital tunnel.

descends and may decrease the costoclavicular space.29 Similarly, this space is narrowed by elevation of the first rib, such as with emphysema or scalene muscle hypertrophy. As the scalene triangle permits passage of the brachial plexus and subclavian artery, these components become compressed when the triangle is narrowed. When the superior aspect of the triangle is narrowed, the upper components of the brachial plexus become compressed; when the floor of the triangle is elevated, the lower components of the brachial plexus and the subclavian artery become compressed.30 Thus, naturally, knowledge of the anatomy of the brachial plexus is a necessity not only for treating TOS surgically, but also for understanding its pathophysiology. Anatomical studies have pointed out that the relationships between the anterior and middle scalene muscles and the brachial plexus and subclavian artery are quite variable. As Atasoy points out,31 the insertions of the middle and anterior scalene muscles may overlap on the first rib, forming a ‘V’ or ‘U’ shape, which narrows the base of the scalene triangle and causes compression of the inferior components. Likewise, the superior aspects of these muscles may hypertrophy, overlap, or even be fused at the superior portion of the triangle and cause compression of the upper components. The origins of the scalene muscles may be variable,32 and ~ 40% of the time, the brachial plexus does not lie between the anterior and middle scalenes.33 In the most common variation, the C5 and C6 roots penetrate the anterior scalene.33 Finally, the scalenus minimus muscle may be present in 30 to 50% of people.33,34 This muscle runs from the transverse processes of the sixth and seventh cervical vertebrae between the subclavian artery and the most inferior (T1) root of the brachial plexus to insert onto the first rib and supporting fascia of the pleura, providing a potential compression point at the base of the triangle. With regard to the scalene muscles, the insertion of the anterior scalene may be relatively wide and anterior, extending toward the subcla-

vius muscle, which compresses the subclavian vein in the costoclavicular space. A cervical rib may be present in 0.5 to 1.0% of people,35–38 higher in some populations,39 the majority being bilateral and the incidence being twice as common in women as in men. The development of the rib may vary from a small exostosis from the seventh cervical vertebra to a complete rib attached anteriorly to the first rib. Such attachments may be fibrous, cartilaginous, or bony. This rib invades the scalene triangle and causes compression of the brachial plexus or the subclavian artery in 10 to 20% of cases.31 Subclavian artery compression may lead to stenosis and post-stenotic dilation. First rib and clavicle fractures resulting in significant callus or other deformity can narrow either the scalene triangle or the costoclavicular space, leading to compression of the inferior roots of the brachial plexus, the subclavian artery, or the subclavian vein. Several fascial bands have been described in the thoracic outlet and at the apex of the thoracic cavity. Sibson fascia, also known as the suprapleural membrane, extends from the transverse process of the seventh cervical vertebra to the deep surface of the first rib just over the pleura. Poitevin 40 described three fibrous thickenings in this area that may contribute to neurovascular compression, labeling them the vertebraseptocostal ligament, the transverse septocostal ligament, and the costoseptocostal ligament, as defined by their respective origins and insertions. In addition, Roos41 described nine different bands throughout the thoracic outlet that may lead to neurovascular compression. He subsequently expanded this classification to include 10 different structures that compress the lower plexus and 7 different structures that compress the upper and middle elements of the brachial plexus.42 Knowledge of extremity physiology has shown us that our joints do not function independently of one another. Motion or lack of motion at one joint will affect the function of

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Thoracic Outlet Syndrome sites of compression may indicate independently significant compression at the thoracic outlet.44 This multilevel nerve involvement may be a significant component of so-called cumulative trauma disorder, also known as repetitive stress disorder, or better, work-related upper extremity musculoskeletal disorder, as these patients will often have multiple levels of compression in both upper extremities (▶ Fig. 12.3). This is not an ideal term, as sleeping postures will also affect the propensity toward development of compression neuropathy. These sleep positions can also be propensiated if sleeping medicines are routinely used such that these postures are maintained for prolonged periods. These relationships make it important for physicians who are treating compression of the brachial plexus to be adept at evaluating the remainder of the upper extremities, and vice versa, for the hand surgeons who are treating carpal tunnel syndrome to be adept at evaluating the brachial plexus. Differences in individual anatomy and physiology thus create different causes of compression and account for the myriad of etiologies and associated pseudonyms for TOS. The distorted anatomical causes of compression may be congenital or acquired. It is estimated that up to 10% of patients have bony abnormalities, such as a cervical rib, first rib deformities, or clavicular deformities. Any or all of the three neurovascular structures may become compressed and lead to patient symptoms. The peripheral nerve surgeon should have a thorough understanding of the associated arterial and venous compressions. However, consistent with the subject of this book, this chapter will focus mainly on compression of the brachial plexus, or neurogenic TOS.

12.4 Diagnosis

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Fig. 12.3 Relationship between multilevel nerve compressions. Shoulder pathologies with abnormal shoulder kinetics may cause abnormal use of the hand, which can increase the prevalence of nerve compression at the wrist, specifically, carpal tunnel syndrome (red). The opposite is possible, with dysfunction in the hand causing compensatory use of the shoulder and thoracic outlet syndrome (red).

other joints, for example, leading to hip and knee pathology in a patient with an ankle abnormality. Likewise, the upper extremities tend to function as a unit such that elbow or shoulder pathology may occur in a patient with a fused wrist. This understanding that our dynamic musculoskeletal elements are intimately related can be discussed in context with the double crush theory proposed by Upton and McComas in 1973. 43 This theory hypothesizes that compression or injury of a nerve at one location makes it more susceptible to compression at another site. A degree of compression that typically may be subclinical in an otherwise normal nerve may be clinically significant in a nerve also compressed at a second site. Relief of compression at one site may alleviate symptoms at another site. Conversely, continued symptoms following release of distal

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TOS typically occurs in young and middle-aged adults and occurs in women 3 times more frequently than in men. Patient symptoms may differ depending on which structure is compressed. That is, symptoms of nerve compression are different from symptoms of arterial or venous compression. Neurogenic TOS is much more common than arterial or venous TOS, accounting for upwards of 98% of cases.42 Though more common, it is typically more difficult to diagnose because of greater variability in symptomatology (▶ Table 12.2).

12.4.1 Neurogenic Thoracic Outlet Syndrome Neurogenic TOS is thought to result from a combination of a congenital anatomical predisposition and trauma.43,45,46 The most common trauma is neck, and the most common mechanism is motor vehicle incidents.47,48 A second cause, and the most common in our practice, is poor posture of the neck, upper back, and shoulders (▶ Fig. 12.4).45 With the increasing prevalence of obesity and a propensity for increased forward flexion of the neck and shoulders to “work around” the obesity, this cause will likely increase in frequency. Such posture, either acute or repetitive, may lead to muscle spasm, or tightening, and swelling. Muscle swelling and the abnormal postures attained lead to compression of the nerves, which in turn causes nerve swelling and further compromise.

Thoracic Outlet Syndrome Table 12.2 Physical Examination Tests for Thoracic Outlet Syndrome Name

Description

Novak/Mackinnon/Patterson test

With elbows extended and wrists at neutral, hyperabduction of arms to 180 degrees, with or without digital compression at the brachial plexus, reproducing symptoms (▶ Fig. 12.2)

Wright hyperabduction

Hyperabduction of the arm reproducing symptoms and loss of radial pulse

Adson test (scalene test)

While seated, rest arms on knees, deep inhalation, extend neck, rotate head to affected side, results in loss of radial pulse

Halstead test (costoclavicular test)

Assume military posture, pull shoulders backward and downward, reproducing symptoms and loss of radial pulse

Roos test (elevated arm stress test) With arms abducted to 90 degrees and shoulders externally rotated, slowly open and close hands for 3 minutes, reproducing symptoms

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Fig. 12.4 Normal and abnormal posture. (a) Neutral, or straight spine position with normal posture. (b) Abnormal posture demonstrated with the head forward, excess curvature, and kyphosis of the thoracic and cervical spine.

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Thoracic Outlet Syndrome The poor posture is maintained to avoid stretch of the tightened muscles, and a muscle imbalance occurs.28,48 Scarring and fibrosis of the scalene muscles also occur,46,49 contributing to nerve compression and making postural correction more difficult. This tends to create a negative cycle that promotes the syndrome, and as will be discussed later, understanding of this cycle provides the rationale for appropriate physical therapy. Patients typically present with pain and paresthesias, and though presentations may be quite variable, the diagnosis is largely made clinically with a thorough history and physical examination.

History Onset of symptoms may be insidious or follow trauma. Achy neck and shoulder pain and stiffness may be early signs of muscle spasm and imbalance. The pain and paresthesias associated with nerve dysfunction, which are present in ~ 95% of cases, typically occur in a delayed fashion, weeks or months later, often after acute musculoskeletal symptoms have resolved. Numbness may be present with or without tingling, and symptoms may be exacerbated following strenuous physical activity or prolonged arm elevation. When separated in space, numbness tends to occur distally and pain proximally. The numbness is associated with brachial plexus nerve compression and the pain with muscle imbalance around the scapula. The occurrence of symptoms after activity helps distinguish TOS from primary shoulder or cervical spine pathology when symptoms tend to occur during activity. Although total plexus findings may occur, symptoms generally involve the lower plexus in TOS. When isolated upper plexus symptoms occur, cervical spine pathology is more often the causative agent. When the upper plexus is involved in TOS, symptoms occur in the neck, deltoid area, and lateral arm and may also radiate to the side of the face, the ear, the occiput, and in the median nerve distribution. We have seen a few patients whose sensory symptoms refer to the radial dorsal aspect of the hand and forearm relating to middle trunk compression with maximum compression at the C7, middle trunk. These patients often present with failed radial nerve releases at the forearm (arcade of Fröshe and Wartenberg sites) and or failed de Quervain releases. With the more common lower plexus involvement, symptoms involve the medial arm and hand, predominantly the ulnar innervated hand. Rarely (< 5% of the time), intrinsic hand muscle atrophy may be present and signify long-lasting or severe compression. Although isolated ulnar nerve symptoms below the elbow generally indicate cubital tunnel syndrome, the presence of symptoms at the shoulder and neck signals the possibility of proximal nerve compression at the thoracic outlet, and cubital tunnel syndrome and TOS frequently occur together. Symptoms may also radiate to the mastoid or occipital area in these cases and, as with upper plexus involvement, may be associated with headaches. Typically, pain originates proximally; and radiates distally, which may help distinguish TOS from distal compression syndromes that tend to radiate proximally, although, as stated previously, both distal and proximal compressions may coexist. It is important to distinguish between the more common cervical spine disease and TOS. Cervical spine disease may manifest as intervertebral disk herniation or spondylosis, each leading to nerve root compression. Cervical disk disease is asso-

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ciated with neck pain, stiffness, radiating paresthesias, and weakness. Generally, the C5–C6 or C6–C7 interval is involved, creating symptoms in the respective nerve root distribution. C5–C6 herniation causes sensory symptoms radiating to the thumb and motor weakness of elbow flexion and radial wrist extension. C6–C7 herniation causes sensory symptoms radiating to the index finger and motor weakness of elbow extension, ulnar wrist extension, and index finger flexion. Compression of the lower cervical or first thoracic nerve roots can more closely mimic TOS, with symptoms in an ulnar nerve distribution, but is much less common that compression of the fifth, sixth, or seventh roots. The typical patient with TOS has seen multiple physicians, and often other nonmedical providers, prior to seeing the peripheral nerve surgeon and is often confused about the diagnosis, which either has not been made clear or has been missed altogether. Urschel et al pointed out how TOS can be confused with coronary artery disease.50 In some cases, symptoms extend to the anterior chest wall and parascapular area. When combined with symptoms in the neck, this constellation may mimic angina pectoris and may become of greatest concern to the patient. Upper extremity complaints may be overshadowed in the pursuit to rule out coronary artery disease. Many of these patients will have negative cardiac evaluations and no explanation for their symptoms other than the label pseudoangina. The character, location, duration, and progression of symptoms and mitigating and alleviating factors should be thoroughly investigated and documented. A wise and efficient technique for accomplishing this involves a patient-completed symptom questionnaire that includes a body diagram and visual analogue scale for pain (see Chapter 20). Such a tool is helpful for both diagnosis and treatment monitoring.

Physical Examination Just as the history should be thorough and complete, so should the physical examination. As patients have often not been diagnosed or been diagnosed with problems other than TOS, the examination should be directed toward confirming the presence or absence of those other problems, as well as TOS itself. It is not uncommon for patients to have been told that their complaints are psychosomatic. Thus, often one of the most important aspects of the examination is to separate the true somatic problems from the psychosomatic ones. Along with a general examination and efforts to identify alternative causes or associated factors, a thorough upper extremity, neck, and shoulder examination will help identify neurogenic TOS as well as vascular causes of TOS. The blood pressure can be measured at both upper arms, and a difference of 20 mm Hg is considered significant and suggestive of arterial compromise. All aspects of the appearance of the upper extremities should be compared side to side. Strength, sensibility, and range of motion of the neck, shoulder, elbow, wrist, and fingers should be examined, also bilaterally, and signs of distal nerve compressions should be evaluated. The shoulder exam should include both active and passive motion to help elucidate neuromuscular weakness from rotator cuff pathology. Internal rotation of the shoulder and reaching of the hand up the patient’s back will often help the patient recognize the association of significant shoulder pathology. Muscles of the neck, upper

Thoracic Outlet Syndrome

Fig. 12.5 The Spurling test is used to identify cervical disk disease. It is performed by having the patient rotate his or her head to the side in question and extend their neck. The examiner proceeds with applying axial load on the head. A positive sign occurs with radicular pain and paresthesias on the ipsilateral side.

Fig. 12.6 Specific provocative test for thoracic outlet syndrome. This test was developed due to the lack of specificity and potential confounding presence of distal nerve compression with many other tests. The arms are hyperabducted to 180 degrees and held in position for 1 minute, taking care to keep the wrists and elbows straight to avoid eliciting symptoms of carpal tunnel or cubital tunnel syndrome.

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Fig. 12.7 Abnormal shoulder posture. (a) Poor posture is apparent with forward flexion of the shoulders and neck from a view of the patient from above. (b) Posture is corrected toward neutral positioning.

Fig. 12.8 Overuse of the upper trapezius muscle due to compensation. (a) Illustration shows proper scapula rotation with maximum humeral abduction. (b) The photo demonstrates abnormal scapular upper rotation of the patient’s left shoulder with it underrotated during maximum humeral abduction compared to the normal right shoulder. As result of the abnormal left shoulder pathology, the left upper trapezius is overused in an attempt to compensate for lack of scapular rotation.

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Thoracic Outlet Syndrome

Fig. 12.9 Long thoracic palsy. Long thoracic palsy results in the dysfunction of the serratus anterior muscle and manifests as scapular winging. Out of all the scapular kinematic pathologies, a long thoracic palsy is the most prominent (and the easiest to identify). The loss of scapular upward rotation and stabilization against the chest wall limits arm elevation greater than 90 degrees. In some patients with a well-developed trapezius muscle, the lower trapezius may provide adequate upward rotation and stability to allow full elevation and abduction. During examination, the shoulder may be depressed and the scapula is abducted and downwardly rotated. With shoulder flexion, scapular winging in the most prominent during the muscle's eccentric phase as the arm is lowered from flexion. Patients are typically unable to forward flex or abduct greater than 90 degrees (patient 1, patient 2). Some patients may acquire full range in the abduction plane by using strong compensatory muscle patterns. In these patients the trapezius and rhomboid muscles are often overdeveloped (patient 3, patient 4).

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back, shoulder girdle, and anterior chest should be examined for tension and tenderness. A Spurling test will help identify cervical disk disease. This is performed by having the patient rotate the head to the side in question and extend the neck. The examiner then applies axial load (▶ Fig. 12.5). A positive sign occurs with radicular pain and paresthesias on the ipsilateral side. Percussion of the brachial plexus producing a Tinel sign is indicative of nerve compression, as is reproduction of symptoms with digital compression of the brachial plexus. In addition to these more traditional examination techniques, a number of clinical maneuvers may be performed to evaluate for thoracic outlet compression. Wright described changes in the arm produced by hyperabduction of the arm, often called the Wright hyperabduction test.51 In particular, the radial pulse is diminished or obliterated as the neurovascular bundle is stretched around the downwardly rotated coracoid process, the pectoralis minor tendinous insertion, and the humeral head. Reproduction of symptoms should probably be considered the

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most reliable indicator with this test, as Wright himself pointed out that a small percentage of the normal or asymptomatic population will have a diminished pulse. The Adson test, or scalene test, was described in 1947.52 To decrease the interscalene space, the patient rests the arms on the knees while in a seated position, takes and holds a deep breath, extends the neck fully, and rotates the head to the affected side. A positive test occurs with obliteration of the radial pulse. Again, normal asymptomatic people will have a positive test frequently enough as to discredit its specificity and render it primarily of historical value. With the Halstead test, or costoclavicular test, the patient assumes a “military posture” by pulling the shoulder backward and downward, narrowing the costoclavicular space. A positive test is indicated by diminution of the radial pulse and reproduction of symptoms. The Roos test, or elevated arm stress test (EAST),24,42 involves the patient positioning the arms in line with the plane of the chest abducted to 90 degrees and the shoulder externally

Thoracic Outlet Syndrome

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Fig. 12.10 Spinal accessory palsy. Long thoracic palsy results in the dysfunction of the trapezius muscle and manifests as mild scapular winging, yet severe loss of shoulder function. During examination, the shoulder is depressed on the affected side, and shoulder abduction/adduction is the most difficult to perform compared to shoulder flexion. Patients 2 and 3 demonstrate full range of motion during flexion but are unable to abduct the shoulder past 90 degrees using compensatory muscles. Patients 1 and 4 are unable to flex the shoulder past 90 degrees.

rotated, then slowly opening and closing the hands for 3 minutes. Reproduction of symptoms throughout the entire upper extremity, beyond expected fatigue of the forearm and shoulder muscles, signifies a positive test. Because of the lack of specificity and potentially confounding presence of distal nerve compression symptomatology with many of these aforementioned tests, we prefer the following test described by Novak et al53: the arms are hyperabducted to 180 degrees and held in position for 1 minute, taking care to keep the wrists and elbows straight to avoid eliciting symptoms of carpal tunnel syndrome or cubital tunnel syndrome (▶ Fig. 12.6). Reproduction of symptoms indicates a positive test. The

onset of such symptoms may be accelerated with concomitant digital compression at the brachial plexus. A critical portion of the physical examination in patients with TOS is to evaluate for muscle imbalance. We like to position the patient standing in front of the examiner with a mirror located to the side or in front of the patient. This allows the examiner to see the facial expressions of pain or lack thereof during the examination of the shoulders. Resting or baseline posture is noted before and during the examination. The spine should be straight, and any kyphosis or scoliosis is noted (▶ Fig. 12.4). The examiner positions himself or herself behind the patient and looks for asymmetry in the location of the scapula. Is the

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Thoracic Outlet Syndrome

Fig. 12.11 Scratch-collapse locations for thoracic outlet and posture. For assessing the thoracic outlet and posture, multiple specific locations exist for the scratch-collapse test. (a) The initial provocative assessment involves touching the entire thoracic outlet to elicit a response. If positive, the examiner can carefully examine specific locations to distinguish the pathology. The anterior scalene is marked as a palpation reference; however, the primary scratch collapse is the brachial plexus found between the anterior and middle scalene. The next scratch-collapse point is the middle scalene and involves the long thoracic nerve due to its intermuscular course. Less frequent, the next scratch-collapse point is the upper trapezius and involves the spinal accessory nerve due to its intermuscular course. (b) For postural issues, the parascapular muscles can be palpated to elicit a response in the scratch-collapse test.

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Fig. 12.12 Scratch-collapse test for thoracic outlet and the use of posture correction. (a) This patient exhibited poor posture with mild scapular winging in the neutral position. The shoulder was more depressed on the right compared to the left. (b) It was evident that the patient had internally rotated shoulders and had a positive scratch-collapse test on the parascapular muscles on both sides. (c) With posture correction, by bringing back the shoulders for normal positioning, the parascapular muscles tested negative; however, the thoracic outlet became positive on the right only, for the scratch-collapse test.

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Thoracic Outlet Syndrome

Fig. 12.13 Ethyl chloride spray can be used to provoke a positive scratch-collapse test in a hierarchical fashion. Here is shown the scratch-collapse test for thoracic outlet and the use of ethyl chloride and posture correction. (a) This patient exhibited poor posture and depressed shoulders, more significant on the right compared to the left. (b) The scratch collapse tested positive on the parascapular muscles bilaterally and on the right thoracic outlet. Forward flexion of the neck was noted. With the use of ethyl chloride to numb sensation to the three locations of positive tests, the left thoracic outlet became positive. The use of ethyl chloride on this location, the left cubital tunnel, became positive. (c) With posture correction, by bringing back the shoulders for normal positioning, no provocation was elicited from any of the test locations.

scapula abducted off the midline? Is one scapula abducted more than another? Looking above the patient for positioning of the anterior aspect of the shoulders also helps to determine if there is asymmetry or marked forward flexion posture of the shoulders (▶ Fig. 12.7). As the patient goes through range of movement of the shoulders, overuse of the upper trapezius muscle can be observed (▶ Fig. 12.8). Does the scapula rotate smoothly with arm abduction, or does it just move up and down with overuse of the upper trapezius? Weakness in the serratus anterior muscle is evaluated with forward flexion of the arms (▶ Fig. 12.9). The elbows are kept straight, and the patient moves his or her arms slowly above the head in a forward direction and then slowly lowers the arms in front. It is as the patient lowers the arms that winging of the scapula can be noted if there is weakness of the serratus anterior muscle. If this maneuver is done a few times, the winging becomes more prominent. To test for weakness of the middle and lower trapezius muscles, the arms are abducted 90 degrees to the side (▶ Fig. 12.10). The patient then turns the palms up toward the ceiling and completes the rest of the range of movement exercise to bring the arms fully above the head, going through the abducted plane of movement. Once again the patient then slowly lowers the arms to the sides; it is as the arms are brought down to the side that winging will occur if there is weakness of the middle and lower trapezius muscles. In the last several years we have found that the scratch-collapse test is useful for distinguishing components of thoracic outlet nerve compression from muscle imbalance. The patient is positioned with the shoulders adducted to the sides, the elbows flexed to 90 degrees, the forearms in neutral rotation, and the wrists and fingers straight. Next, the patient gently resists internal shoulder rotation as the examiner puts inward pres-

sure on the outer aspects of the forearms. The examiner then touches, or “scratches,” the thoracic outlet area and immediately repeats the test (▶ Fig. 12.11). If there is significant thoracic outlet compression, the patient will not be able to resist the applied internal rotation force, and the arms will “collapse” inward. The examiner can repeat the test, touching along the medial border of the scapula. If there is significant muscle imbalance, then the scratch-collapse test will be positive with this maneuver. Interestingly, if the patient can “correct” the abducted scapular posture by contracting the parascapular muscles so that the clavicle is momentarily held in the proper position, the scratch-collapse test will become normal (▶ Fig. 12.12; ▶ Fig. 12.13; ▶ Fig. 12.14). Once the patient lets the scapula fall away, abducted to the patient’s typical abnormal postured position, the scratch-collapse test becomes abnormal again. This test allows the patient to see how the abnormal scapula posturing profoundly affects his or her neurologic system. Ethyl chloride cold spray can be used to prioritize the patient’s hierarchy of nerve compression and muscle imbalance (▶ Fig. 12.15). Once the examiner finds the area that provokes a positive scratch collapse, he or she can “freeze out” that area and identify the second area of collapse. The physical examination is not complete without a remaining thorough upper extremity evaluation with additional attention paid to the presence or absence of sites of nerve compression distal to the brachial plexus. In the same manner that percussion at the brachial plexus may elicit a Tinel sign, and the provocative tests reproducing symptoms may be indicative of TOS, similar tests at the elbow, forearm, and wrist may be indicative of more peripheral nerve compression. These provocative tests help identify subclinical compression in patients who do not have symptoms at rest.

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12 Fig. 12.14 Scratch-collapse test or distal nerve compression and the effects of posture correction. (a,c) This patient exhibited poor posture with internally rotated shoulders and forward flexion of the neck but had complaints of distal nerve compression on the left side. The scratch-collapse test was positive initially at the Guyon canal and the cubital tunnel. The use of ethyl chloride revealed the second location of the left thoracic outlet, and further use of ethyl chloride revealed the third location of the left parascapular muscles. (b,d) With posture correction, by bringing back the shoulders for normal positioning, no provocation was elicited from any of the test locations.

Ancillary Tests Imaging Plain radiographs of the chest and cervical spine assist in detecting cervical ribs and other bony abnormalities, such as prominent transverse processes, old rib or clavicle fractures, or findings of degenerative arthritis, such as osteophytes and intervertebral space narrowing. The latter findings are suggestive of cervical disk disease and may require computed tomography (CT) or magnetic resonance imaging (MRI) for confirmation and to evaluate for neural impingement. Although different studies have different specificities across different institutions, CT and MRI have generally replaced myelography in the evaluation of

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the cervical spine and brachial plexus. Generally, these studies are not necessary for patients with TOS; however, they may be useful in a select group of patients who are suspected to have tumors or other space-occupying soft tissue lesions. An example may be a patient who is suspected of having a Pancoast tumor. In addition, these studies may help rule out the presence of cervical disk disease, spinal stenosis, or nerve root impingement.54 As the resolution of these imaging modalities continues to improve, their utility in the diagnosis of TOS may be improving as well.55 Currently, both MRI and ultrasound seem to be most useful when performed with provocative maneuvers and detect vascular TOS to a greater degree than neurogenic TOS.56–59

Thoracic Outlet Syndrome

Fig. 12.15 Scratch-collapse test for thoracic outlet and postural issues. (a) This patient exhibited poor posture with a depressed left shoulder compared to the right. On examination, the scratch collapse test was positive at the left parascapular muscles. (b,c) However, observing the positioning of the shoulders, the right shoulder was further internally rotated compared to the left. With the use of ethyl chloride, the scratch-collapse test revealed the right thoracic outlet as the second provocation. With further use of ethyl chloride, the right carpal tunnel was revealed as the third provocation.

Fig. 12.16 Illustrative supraclavicular incision for thoracic outlet decompression. The patient is placed supine with an underlying shoulder bump to extend the neck and away from the side of surgery. A supraclavicular approach is used for ease of visualization of important neurovascular elements.

Neurodiagnostic Tests Electrodiagnostic studies typically are normal in patients with TOS unless there is associated cubital or, less commonly, carpal tunnel syndrome. The variable degree of nerve compression, its resultant neuropathophysiology, and patient symptomatology necessitate diagnostic tests of differing sensitivities to accurately estimate the degree of nerve dysfunction. Early in the course of disease, patients often have symptoms only with specific stressful activity, and abnormalities cannot be detected except by the most sensitive means. With progression of disease, tests with lesser degrees of sensitivity are required, and those with greater specificity become beneficial.

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Fig. 12.17 Supraclavicular incision for thoracic outlet decompression. An incision is made a fingerbreadth supraclavicular and ~ 8 cm in length. The arm tourniquet depicted here was unique to this case and not for the thoracic outlet decompression, but specific for an ulnar nerve transposition at the cubital tunnel.

Different elements of nerve function are affected by different degrees of compression or injury. Sensory function tends to be affected earlier than motor function. There are two components of sensation that are governed by receptors: threshold and discrimination. Threshold is defined as the minimum stimulus required for a neural response. Discrimination is the ability to detect two separate stimuli. Slowly adapting sensory receptors, the cutaneous Merkel receptors and the subcutaneous Ruffini corpuscles, tend to respond to static stimuli and can be assessed by measuring cutaneous pressure thresholds and static twopoint discrimination. In the 1890s, Max von Frey developed a reproducible method for testing cutaneous pressure thresholds with hair bristles of varying stiffness.60 Filaments were modified to modern versions made of nylon and glass fiber by Semmes and Weinstein in 196061 and Fruhstorfer in 2001, re-

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Thoracic Outlet Syndrome

Fig. 12.18 Illustrative initial exposure and identification of the supraclavicular nerves. Upon exposure, the supraclavicular nerves are identified and protected with vessel loops. The platysma is also identified and divided to reveal the underlying fascia.

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Fig. 12.19 Exposure and identification of the supraclavicular nerves. Upon exposure, the platysma is initially identified and divided. Beneath the platysma, the supraclavicular nerve and its branches are identified, carefully dissected both proximally and distally, and protected. The supraclavicular nerve branches originate from a proximal trunk noted with a vessel loop. Two vessel loops are used to protect and retract the supraclavicular nerves. In this case, the platysma was scarce.

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Fig. 12.20 Exposure and identification of the omohyoid. The sternocleidomastoid and external jugular vein are identified upon further exposure, and the dissection continues on a plane beneath the sternocleidomastoid. The omohyoid is identified through this plane and divided to expose the anterior scalene and brachial plexus. The supraclavicular nerve is protected and mobilized by two vessel loops.

spectively.60 Quickly adapting receptors, the cutaneous Meissner receptors and the subcutaneous Pacinian corpuscles, preferentially respond to moving stimuli and can be assessed by measuring vibratory thresholds and moving two-point discrimination. High-frequency vibratory sensation is the most sensitive to nerve compression and the most likely to be affected by early disease and thus presents a possible avenue for earlier detection of nerve compression, including neurogenic TOS. Instruments ranging from simple tuning forks to more complicated electromagnetic computerized vibration sensory analyzers have been developed to quantitatively test vibratory thresholds. The vibratory stimulus is placed against the skin, and the smallest perceived stimulus is recorded. Threshold testing can provide information about neuron conductivity that is affected by mild to moderate compression and represents demyelination. However, the most accessible, efficient, and utilized quantitative sensory tests involve assessing discrimination rather than thresholds. This is due to the ease of use and accessibility of testing instruments. Static two-point discrimination ≤ 6 mm is considered normal. Moving two-point discrimination can be rapidly assessed with a paper clip and ruler, calipers, or the precalibrated Disk-Criminator (North Coast Medical Inc., Gilroy, CA). The narrowest spacing at which two separate prongs are detected is recorded, which is normally 2 to 3 mm at the volar fingertips, with > 6 being abnormal and > 8 mm being inadequate for protection

from injury. This discrimination testing provides information about cutaneous innervation density, which tends to decrease with axonal loss resulting from severe compression. Thus, these tests tend to be less sensitive at identifying early disease than the provocative examination tests described above.53 Somatosensory evoked potentials (SSEPs) provide another means of testing for nerve dysfunction by measuring conduction latencies and amplitudes following peripheral sensory stimulation through the brachial plexus and spinal cord with more proximally placed recording electrodes. The transcutaneous nature of the test presents a promising way to circumvent the difficulty with direct access to the brachial plexus. Nevertheless, the value of the test remains controversial. Machleder et al62 and Yiannikas and Walsh63 have shown that SSEPs are abnormal in patients with TOS. However, Borg et al64 found that patients with SSEP findings have physical exam findings as well, thus questioning the value of SSEPs. The senior author (SEM) has studied SSEPs in patients with TOS versus controls and found changes in SSEPs to be related to provocative arm position, but not the presence of TOS.65 Yilmaz and colleagues66 and Rousseff et al67 performed the two largest comparative studies since and have also found no utility of SSEPs in diagnosing TOS. Nerve conduction studies (NCSs) and electromyography (EMG) are also controversial in diagnosing TOS, as noted above. They have great utility in identifying more peripheral nerve compression that may exist concomitant with TOS, however. Of

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Thoracic Outlet Syndrome

Fig. 12.21 Illustrative exposure of the critical structures for decompression of the thoracic outlet. The brachial plexus is identified between the anterior and middle scalene. The phrenic nerve has a course through or superficial to the anterior scalene. The long thoracic nerve has a course through or superficial to the middle scalene. The anterior scalene is divided with the phrenic nerve protected, and the middle scalene is divided with the long thoracic nerve protected.

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these two techniques, EMG findings tend to become positive only late in the course of pathology, detecting more advanced or severe disease. NCSs are suggested to be more useful in earlier detection, and ulnar nerve conduction velocities in particular are the most espoused by those who find them useful. 68,69 In our experience, however, they have not been useful in this patient population.

12.4.2 Vascular Thoracic Outlet Syndrome History Arterial and venous compressions occur at different anatomical locations as outlined above and produce different symptoms. Arterial compression will produce a cold, blanching, easily fatiguing, sometimes painful extremity occasionally with Raynaud

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phenomenon. These symptoms tend to occur with upper extremity activity, essentially representing claudication. If thrombosis is present, symptoms tend to be persistent and may progress to cyanosis, pallor, and, rarely, ulceration and gangrene, typically distally, at the fingers.68,70 Venous compression may lead to Paget-Schroetter syndrome, edema and discoloration of the upper extremity, distention of the superficial veins, and achy pain. Activity or efforts associated with venous thrombosis include strenuous arm activity, typically either in a sustained abducted position or with maximum or sudden downward and backward shoulder movement. Compression and venospasm may precede thrombosis. When thrombosis occurs, symptoms may resolve over the course of a number of days or a few weeks in concert with the development of collateral circulation. Collateral circulation is inferior to native circulation, and symptoms recur when activity places demands on the circulation greater than it can provide.29

Thoracic Outlet Syndrome

Fig. 12.22 Exposure and identification of the anterior scalene and phrenic nerve. Upon dividing the omohyoid and further dissection, the phrenic nerve is identified on the anterior surface of the anterior scalene. The nerve has a lateral to medial course to innervate the diaphragm. The phrenic nerve is isolated and protected by gentle retraction. Because of the sensitivity and critical function of this nerve, a vessel loop is not used to protect the nerve. The anterior scalene is identified deep to this nerve, and occasionally an accessory phrenic nerve is present and has a course through this muscle.

Physical Examination Vascular compression tends to create objective findings more readily than neural compression. The examination should be performed in the same fashion as outlined above. Blood pressure drop ≥ 20 mm Hg and diminution or obliteration of pulses with the Wright test, Adson test, or Halstead test suggest vascular compression. Findings of a blood pressure discrepancy, findings of thromboembolic disease, such as patchy digital ischemia or a thrill or bruit at the level of the subclavian artery, and findings of aneurysm, such as a palpable pulsatile mass in the supraclavicular fossa, warrant further study with arteriography.

Ancillary Tests Although the presence of vascular insufficiency may be more readily detected on physical examination than neurogenic TOS, angiography of the involved extremity is a prudent means of confirmation of the diagnosis and, as importantly, of disease localization and preoperative planning. Arteriography is particularly useful in cases of suspected subclavian or brachial artery pathology as suggested by certain physical exam findings, such as a supraclavicular pulsatile mass, a supraclavicular or infraclavicular bruit on auscultation, or absence of a palpable radial pulse at rest or with elevation of the extremity. Venogra-

phy is indicated when venous obstruction is suspected, such as in Paget-Schroetter syndrome. In certain institutions, CT angiography71 or ultrasound56,57 may provide sufficient information regarding the arterial and venous vasculature, respectively, and MRI with or without angiography55,56,58,59 may be beneficial in not only detecting physical compression of the brachial plexus but also identifying arterial abnormalities.

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12.5 Management Most patients with TOS are effectively managed with appropriate physiotherapy alone.68,72 Although a paucity of randomized, controlled clinical trials and meta-analyses exist,73 surprising given the controversy surrounding the diagnosis and treatment, estimates suggest that 5074 to 80% or more75 of patients will be successfully treated with physiotherapy and not require operative intervention. The basic principles of management include behavioral modification to limit work or recreational overhead activity, conservative relief of concomitant nerve compressions, such as carpal tunnel syndrome and cubital tunnel syndrome, relief of cervical positional aggravation with a soft cervical bolster or collar, weight loss for the obese population, and directed physical therapy. Concomitant peripheral nerve compressions that are resistant to conservative management may benefit

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Thoracic Outlet Syndrome

Fig. 12.23 Illustrative decompression of the brachial plexus by dividing the anterior scalene. The anterior scalene is divided to decompress the brachialis plexus. It is important to protect the phrenic nerve by gentle retraction to prevent injury to this critical nerve. A vessel loop is not used to protect this nerve.

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from surgical decompression, and surgical candidates for thoracic outlet decompression are prudently selected among those patients with a strong diagnosis who have failed nonoperative management.

12.5.1 Physical Therapy Novak and Mackinnon have published widely on their concepts of conservative management of TOS.72,76,77 Physical therapy is instituted early, upon diagnosis of TOS. Typically it takes 4 to 6 months of appropriate therapy to realize significant improvement. Most patients have had several previous failed therapy sessions. If they describe “corner stretches,” or weight exercises, then these are indications of inappropriate therapy. The main goal of physical therapy is to decrease external nerve compression resulting from muscle imbalance. This is achieved by restoring proper muscle balance in the cervical and thoracic regions via stretching, strengthening, and postural measures. The typical muscle imbalance occurs when neck and shoulder flexor muscles shorten and tighten and extensor muscles lengthen

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and weaken. A proximal crossed syndrome in the upper extremity of patients with TOS has been described by Janda consistent with the muscle imbalance concept.78 The pectoralis muscles, upper trapezius, scalene, and sternocleidomastoid muscles tighten, and the scapular stabilizers—the middle and lower trapezius, rhomboid, and serratus anterior muscles— weaken. Myofascial trigger points may be present, leading to referred pain, and cervicothoracic range of motion may be restricted. This pattern leads to the “head and shoulders forward,” or slumped, posture with loss of the more proper cervical lordosis.79 Exercises to lengthen and extend the neck, retropulse and lower the shoulders, stretch the cervical flexors, and restore cervical lordosis and proper shoulder posture are instituted. Scalene muscles are a well-recognized contributor to brachial plexus compression, as previously described. In addition to stretching and range of motion exercises, restoration of muscle balance and length may be assisted by chemoparesis of tight scalenes with botulinum toxin or block with local anesthetics.

Thoracic Outlet Syndrome

Fig. 12.24 Decompressing the brachial plexus by dividing the anterior scalene. The anterior scalene is divided with the phrenic nerve noted and protected by gentle retraction. Occasionally, an accessory phrenic nerve is present and has a course through the anterior scalene. If encountered during the division of the anterior scalene, it is protected. The phrenic nerve has been inked at the top of the incision. The upper and middle trunks are visualized following the division of the anterior scalene.

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Fig. 12.25 Exposure and identification of the middle scalene. To identify and divide the middle scalene, the surgical approach continues lateral to the brachial plexus. The middle scalene is identified lateral to the brachialis plexus. Typically, the long thoracic nerve has a course through this muscle or posterior to it. In this case, the long thoracic nerve was identified deep and lateral to the middle scalene.

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Thoracic Outlet Syndrome

Fig. 12.26 Illustrative decompression of the brachial plexus by dividing the middle scalene. The middle scalene is divided to decompress the brachial plexus. It is important to protect the spinal accessory nerve to prevent injury to this critical nerve. A vessel loop may be used to gently retract this nerve.

For the muscular elements involved, the implementation of these therapies begins with stretching and return of range of motion. During this process, pain control is critical to encourage progression. A slow progression is preferred with place, hold, and relaxation techniques to prevent reflex muscular contraction from overstretch. Once range of motion is achieved, strengthening is begun, also in a slow, progressive pattern, all the while maintaining pain control and range of motion. Early frequent exercise under the guidance of a trained physical therapist is combined with a daily home exercise program. Patient motivation and compliance with the home program is crucial to therapeutic efficacy; thus, patient education throughout the process cannot be overemphasized. Concurrent with restoration of muscular balance with these stretching and strengthening exercises is emphasis on correction of the abnormal posture. Such correction tends to be strongly fostered by this restoration of muscular balance, but open acknowledgment and education of the patient on postural correction can facilitate the process tremendously. External supports, such as the previously mentioned soft cervical spine supports or collars made from long tubes of stockinette stuffed

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with soft gauze or pillow filling, can prevent improper cervical posture nocturnally. If physiotherapy fails to alleviate symptoms of TOS, then we give preference to release of any concomitant persistent distal nerve compressions. If an anatomical element is present at the thoracic outlet that cannot be corrected with physiotherapy, such as a cervical rib, and symptoms persist following release of associated distal entrapments, then thoracic outlet decompression with cervical rib resection should be considered. Although the risk is quite minimal in skilled operative hands, given the significant morbidity of high nerve injury, considerable care is taken to ensure proper patient selection for surgical decompression. If no cervical rib exists, then consideration is given to scalenotomy with or without first rib resection. Generally, first rib resection is recommended when it is a significant compressive element.68 Management of vascular TOS involves additional attention to correction of vascular pathology. This is exemplified by the management of Paget-Schroetter syndrome, also known as effort thrombosis,5,6,80 exertional compression of the subclavian-axillary vein. Conservative treatment with arm elevation and anti-

Thoracic Outlet Syndrome

Fig. 12.27 Identification of the long thoracic nerve. In this case, the middle scalene was briefly divided to identify the long thoracic nerve. The long thoracic nerve had a course through the middle scalene and deep and lateral to the middle scalene. This nerve is isolated and protected. A vessel loop can be used, unlike the phrenic nerve.

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Fig. 12.28 Decompressing the brachial plexus by dividing the middle scalene. The brachial plexus is further decompressed by dividing the middle scalene on its lateral side. In this case, a tendinous band of the middle scalene was identified deep and was released. The lower trunk is identified following the division of the middle scalene. The long thoracic nerve is protected by retraction.

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Thoracic Outlet Syndrome

Fig. 12.29 Illustrative identification of the first rib for resection. The brachial plexus components that were decompressed, by dividing the anterior and middle scalene, are retracted laterally to expose part of the first rib. It is important to note the T1 root to the lower trunk is inferior to the first rib. The exposure of the first rib is taken farther anterior.

coagulation with warfarin has been reported by DeWeese et al81 and Adams and DeWeese.82 Findings included late swelling, pain, and superficial thrombophlebitis in 68%, venous distention in 18%, and pulmonary embolism in 12%. Patients failing these measures were treated with thrombectomy, resection of the anterior scalene muscle with or without first rib resection, and resection of any other compressive factors prior to the introduction of thrombolytic therapy with urokinase and streptokinase followed by tissue plasminogen activator. Intravascular stents have been used but have resulted in a much lower success rate than thrombolysis combined with decompression, as pointed out by Urschel and Patel.83,84 Multiple reports suggest that thrombolytic therapy combined with heparin and surgical decompression can reduce the need for thrombectomy, reducing the long-term morbidity and risk of recurrent thrombosis associated with thrombectomy.85–90 However, the most impressive of such reports comes from Urschel and Patel,84 who reported on a 50-year experience of surgical management of Paget-Schroetter syndrome, recognizing that the anatomical cause is an abnormal insertion of the constoclavicular ligament laterally on the first rib and concluding that thrombolysis and prompt surgical decompression with resection of the first rib is the ideal management.

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12.5.2 Surgical Treatment Varying approaches to surgical decompression of the thoracic outlet have been developed. As mentioned previously, the high posterior thoracoplasty approach was popularized by Clagett, 22 the anterior approach was used by Falconer and Li,23 and the transaxillary approach was developed by Roos.24 In 1991, in an excellent review of surgical management, Sanders reported that similar results are achieved with either the transaxillary or the supraclavicular approach to scalenotomy with or without first rib resection.91 In 1998 Urschel and Razzuk92 reported on superior long-term results with first rib resection combined with scalenotomy compared to scalenotomy alone. Scalenotomy alone is associated with a higher long-term recurrence rate, up to 65%. Urschel promotes a transaxillary approach for either upper or lower brachial plexus compression, without a need for a supraclavicular approach, because the majority of compressive factors insert on the first rib and are thus alleviated when the rib is resected through the transaxillary approach. The authors believe that the first rib should be resected in cases involving vascular compromise or pathology of the first rib, and a cervical rib should be resected if present. In cases involving normal skeletal anatomy without vascular compromise, it is our practice to perform a scalenotomy without rib resection.

Thoracic Outlet Syndrome

Fig. 12.30 Illustrative first rib resection. While the brachial plexus is protected, the first rib is resected by using a bone cutter.

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Fig. 12.31 Illustrative treatment of the first rib with a rongeur. The posterior segment is removed with a rongeur and by controlled avulsion of the posterior articular elements.

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Thoracic Outlet Syndrome

Fig. 12.32 Illustrative brachial plexus anatomy and the bony relationship. The brachial plexus is retracted and protected to expose the first rib for resection.

Authors’ Preferred Technique Recognizing that different surgical techniques may be favored by different surgeons, we prefer the direct supraclavicular approach for ease of visualization of the important neurovascular elements.93,94 The patient is placed supine with an underlying shoulder bump to extend the neck (▶ Fig. 12.16; ▶ Fig. 12.17). Plain epinephrine solution may be infiltrated for assistance in keeping a dry operative field, but local anesthetics should not be used so as not to paralyze nerves that will require activity for proper identification. Loupe magnification, bipolar electrocautery, and a portable nerve stimulator are utilized by the surgeon, and systemic paralytic agents are avoided to allow proper nerve identification and to avoid incidental nerve damage. Through an incision 2 cm above and paralleling the clavicle, the supraclavicular nerves are identified and protected deep to the platysma (▶ Fig. 12.18; ▶ Fig. 12.19). The dissection is carried deeper by division of the omohyoid muscle, elevation of the supraclavicular fat pad, and division of the lateral portion of the sternocleidomastoid muscle (▶ Fig. 12.20). The anterior scalene muscle is identified (▶ Fig. 12.21; ▶ Fig. 12.22) and divided, taking care not to injure the phrenic nerve (▶ Fig. 12.23; ▶ Fig. 12.24). Manipulation of the phrenic nerve is avoided as much as possible; specifically, we no longer place a vessel loop around the phrenic nerve.

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The trunks of the brachial plexus are mobilized, and the middle scalene is identified (▶ Fig. 12.25) and divided from its insertion on the first rib, taking care not to injure the long thoracic nerve (▶ Fig. 12.26; ▶ Fig. 12.27; ▶ Fig. 12.28). The long thoracic nerve may pass behind or through the middle scalene muscle. Thus great care is taken to ensure its identification with a nerve stimulator. The large vessels and nerves are protected (▶ Fig. 12.29; ▶ Fig. 12.30), and the first rib is encircled and divided with a bone cutter (▶ Fig. 12.31). The posterior segment is removed with a rongeur and by controlled avulsion of the posterior articular elements (▶ Fig. 12.32). This ensures complete removal of periosteal elements to prevent recurrent bone development, especially posteriorly, and return of symptoms. The anterior element of the first rib, cervical ribs, and prominent transverse processes are removed in a similar fashion. We have found that first rib resections are typically not necessary for satisfactory relief of symptoms. However, if there is any bony pathology or significant vascular complaints, we will then remove the rib. Relief of all compressive elements is confirmed by direct visualization as well as digital palpation (▶ Fig. 12.33; ▶ Fig. 12.34). The wound is irrigated, hemostasis is confirmed again with bipolar electrocautery, and a closed suction drain and indwelling pain pump with bupivacaine are placed. The wound is closed in layers, including reapproximation of the sternocleido-

Thoracic Outlet Syndrome

Fig. 12.33 Illustrative thoracic outlet decompression and relevant anatomy. Following the division of the anterior and middle scalene, the brachial plexus is decompressed, in addition to the phrenic nerve and the long thoracic nerve.

mastoid muscle, and a dressing is applied. Gentle range of motion is begun within 2 days of surgery, and formal physiotherapy is begun 2 weeks after surgery.

Recurrent Symptoms Persistent symptoms and recurrence are relatively uncommon. Both are generally felt to be due to incomplete resection of compressive elements, such as the first rib or an undiagnosed rudimentary cervical rib. Recurrence may be due to excessive scar formation. Diagnosis and treatment are similar to that of primary TOS, with recurrent decompression warranted in appropriately selected patients.95,96 An alternative approach, particularly the posterior thoracoplasty approach, is used to reduce dissection in a previously scarred bed and consequent risk of nerve or vessel injury. Neurolysis of the roots and trunks of the brachial plexus and dorsal sympathectomy of the upper three thoracic ganglia are additional elements of secondary thoracic outlet surgical decompression.

12.6 Conclusion TOS is an often overlooked condition more commonly resulting from compression of the trunks of the brachial plexus.

Symptoms of vascular compression may be associated or may be dominant, as may those of concomitant distal nerve entrapments. The diagnosis is made by careful history and physical exam and is supplemented by imaging and neurodiagnostic techniques. Most patients achieve relief with conservative management, the cornerstone of which is physiotherapy for restoration of proper muscle balance and posture. Surgical treatment involves resection of compressive elements, including the scalene muscles, first rib, and cervical rib as necessary, and is very effective when proper patient selection is emphasized.

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Fig. 12.34 Thoracic outlet decompression and relevant anatomy. Following the division of the anterior and middle scalene to decompress the brachial plexus, the anatomical structures are reviewed for their integrity. The phrenic nerve is identified as having a lateral-to-medial course to innervate the diaphragm. The long thoracic nerve is identified to innervate the serratus anterior. The supraclavicular nerves are protected by vessel loops. The upper, middle, and lower trunks are shown to be intact and decompressed. Electrical stimulation is used to test the motor nerve response.

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[22] Clagett OT. Research and prosearch. J Thorac Cardiovasc Surg 1962;44:153– 166 [23] Falconer MA, Li FWP. Resection of the first rib in costoclavicular compression of the brachial plexus. Lancet 1962;1:59–63 [24] Roos DB. Transaxillary approach for first rib resection to relieve thoracic outlet syndrome. Ann Surg 1966;163:354–358 [25] Urschel HC, Razzuk MA, Albers JE, Wood RE, Paulson DL. Reoperation for recurrent thoracic outlet syndrome. Ann Thorac Surg 1976;21:19–25 [26] Mackinnon SE, Novak CB. Clinical commentary: pathogenesis of cumulative trauma disorder. J Hand Surg Am 1994;19:873–883 [27] Mackinnon SE. Thoracic outlet syndrome: introduction. Semin Thorac Cardiovasc Surg 1996;8:175 [28] Mackinnon SE. Thoracic outlet syndrome. Chest Surg Clin N Am 1999;9:701 [29] Rosati LM, Lord JW. Neurovascular compression syndromes of the shoulder girdle. In: Modern Surgical Monographs. Orlando, FL: Grune& Stratton; 1961 [30] Swank WL, Simeone FA. The scalenusanticus syndrome. Arch Neurol Psychiatry 1944;51:432 [31] Atasoy E. Thoracic outlet syndrome: anatomy. Hand Clin 2004;20:7–14 [32] Rusnak-Smith S, Moffat M, Rosen E. Anatomical variations of the scalene triangle: dissection of 10 cadavers. J Orthop Sports Phys Ther 2001;31:70–80 [33] Harry WG, Bennett JD, Guha SC. Scalene muscles and the brachial plexus: anatomical variations and their clinical significance. Clin Anat 1997;10:250–252 [34] Kirgis HD, Reed AF. Significant anatomic relations in the syndrome of the scalene muscles. Ann Surg 1948;127:1182 [35] Guebert GM, Yochum TR, Rowe LJ. Congenital anomalies and normal skeletal variations. In: Yochum TR, Rowe LJ, eds. Essentials of Skeletal Radiology. 2nd ed. Vol 1. Baltimore, MD: Williams & Wilkins; 1996:197–306 [36] Brown SCW, Charlesworth D. Results of excision of a cervical rib in patients with the thoracic outlet syndrome. Br J Surg 1988;75:431–433 [37] Schein CJ, Haimovici H, Young H. Arterial thrombosis associated with cervical ribs—surgical considerations: report of a case and review of the literature. Surgery 1956;40:428–443

Thoracic Outlet Syndrome [38] McNally E, Sandin B, Wilkins RA. The ossification of the costal element of the seventh cervical vertebra with particular reference to cervical ribs. J Anat 1990;170:125–129 [39] Gulekon IN, Barut C, Turgut HB. The prevalance of cervical rib in Anatolian population. Gazi Medical Journal 1999;10:149–152 [40] Poitevin LA. Proximal compressions of the upper limb neurovascular bundle: an anatomic research study. Hand Clin 1988;4:575–584 [41] Roos DB. Congenital anomalies associated with thoracic outlet syndrome: anatomy, symptoms, diagnosis, and treatment. Am J Surg 1976;132:771–778 [42] Brantigan CO, Roos DB. Diagnosing thoracic outlet syndrome. Hand Clin 2004;20:27–36 [43] Brantigan CO, Roos DB. Etiology of neurogenic thoracic outlet syndrome. Hand Clin 2004;20:17–22 [44] Upton AR, McComas AJ. The double crush in nerve entrapment syndromes. Lancet 1973;2:359–362 [45] Sanders RJ, Hammond SL. Etiology and pathology. Hand Clin 2004;20:23–26 [46] Sanders RJ, Jackson CGR, Banchero N, Pearce WH. Scalene muscle abnormalities in traumatic thoracic outlet syndrome. Am J Surg 1990;159:231–236 [47] Kai Y, Oyama M, Kurose S, Inadome T, Oketani Y, Masuda Y. Neurogenic thoracic outlet syndrome in whiplash injury. J Spinal Disord 2001;14:487– 493 [48] Mackinnon SE. Thoracic outlet syndrome. Ann Thorac Surg 1994;58:287–289 [49] Machleder HI, Moll F, Verity MA. The anterior scalene muscle in thoracic outlet compression syndrome. Histochemical and morphometric studies. Arch Surg 1986;121:1141–1144 [50] Urschel HC, Razzuk MA, Hyland JW, et al. Thoraic outlet syndrome masquerading as coronary artery disease (pseudoangina). Ann Thorac Surg 1973;16:239–248 [51] Wright IS. The neurovascular syndrome produced by hyperabduction of the arms: the immediate changes produced in 15 normal controls, and the effects on some persons of prolonged hyperabduction of the arms, as in sleeping, and certain occupations. Am Heart J 1945;29:1 [52] Adson AW. Surgical treatment for symptoms produced by cervical ribs and the scalenus anticus muscle. Surg Gynecol Obstet 1947;85:687–700 [53] Novak CB, Mackinnon SE, Patterson GA. Evaluation of patients with thoracic outlet syndrome. J Hand Surg Am 1993;18:292–299 [54] Rapoport S, Blair DN, McCarthy SM, Desser TS, Hammers LW, Sostman HD. Brachial plexus: correlation of MR imaging with CT and pathologic findings. Radiology 1988;167:161–165 [55] Collins JD, Shaver ML, Disher AC, Miller TQ. Compromising abnormalities of the brachial plexus as displayed by magnetic resonance imaging. Clin Anat 1995;8:1–16 [56] Demondion X, Herbinet P, Van Sint Jan S, Boutry N, Chantelot C, Cotten A. Imaging assessment of thoracic outlet syndrome. Radiographics 2006;26:1735–1750 [57] Demondion X, Vidal C, Herbinet P, Gautier C, Duquesnoy B, Cotten A. Ultrasonographic assessment of arterial cross-sectional area in the thoracic outlet on postural maneuvers measured with power Doppler ultrasonography in both asymptomatic and symptomatic populations. J Ultrasound Med 2006;25:217–224 [58] Charon JP, Milne W, Sheppard DG, Houston JG. Evaluation of MR angiographic technique in the assessment of thoracic outlet syndrome. Clin Radiol 2004;59:588–595 [59] Demondion X, Bacqueville E, Paul C, Duquesnoy B, Hachulla E, Cotten A. Thoracic outlet: assessment with MR imaging in asymptomatic and symptomatic populations. Radiology 2003;227:461–468 [60] Fruhstorfer H, Gross W, Selbmann O. Von Frey hairs: new materials for a new design. Eur J Pain 2001;5:341–342 [61] Semmes J, Weinstein S, Ghent L, Teuber HL. Somatosensory Changes after Penetrating Brain Wounds in Man. Cambridge, MA: Harvard University Press; 1960 [62] Machleder HI, Moll F, Nuwer M, Jordan S. Somatosensory evoked potentials in the assessment of thoracic outlet compression syndrome. J Vasc Surg 1987;6:177–184 [63] Yiannikas C, Walsh JC. Somatosensory evoked responses in the diagnosis of thoracic outlet syndrome. J Neurol Neurosurg Psychiatry 1983;46:234–240 [64] Borg K, Persson HE, Lindblom U. Thoracic outlet syndrome: diagnostic value of sensibility testing, vibratory threshold and somatosensory evoked potentials at rest and during perturbation with abduction and external rotation of the arm. In: Proceedings oof the World Congress on Pain. Amsterdam; 1988 [65] Komanetsky RM, Novak CB, Mackinnon SE, Russo MH, Padberg AM, Louis S. Somatosensory evoked potentials fail to diagnose thoracic outlet syndrome. J Hand Surg Am 1996;21:662–666[Am]

[66] Yilmaz C, Kayahan IK, Avci S, Milcan A, Eskandari MM. [The reliability of somatosensory evoked potentials in the diagnosis of thoracic outlet syndrome] Acta Orthop Traumatol Turc 2003;37:150–153 [67] Rousseff R, Tzvetanov P, Valkov I. Utility (or futility?) of electrodiagnosis in thoracic outlet syndrome. Electromyogr Clin Neurophysiol 2005;45:131–133 [68] Urschel HC, Razzuk MA. Current management of thoracic outlet syndrome. N Engl J Med 1972;286:21 [69] Urschel HC, Kourlis H. Thoracic outlet syndrome: a 50-year experience at Baylor University Medical Center. Proc (Bayl Univ Med Cent) 2007;20:125–135 (BaylUniv Med Cent) [70] Urschel HC, Paulson DL, McNamara JJ. Thoracic outlet syndrome. Ann Thorac Surg 1968;6:1–10 [71] Hasanadka R, Towne JB, Seabrook GR, Brown KR, Lewis BD, Foley WD. Computed tomography angiography to evaluate thoracic outlet neurovascular compression. Vasc Endovascular Surg 2007;41:316–321 [72] Novak CB, Collins ED, Mackinnon SE. Outcome following conservative management of thoracic outlet syndrome. J Hand Surg Am 1995;20:542–548 [Am] [73] Vanti C, Natalini L, Romeo A, Tosarelli D, Pillastrini P. Conservative treatment of thoracic outlet syndrome: a review of the literature. Eura Medicophys 2007;43:55–70Review [74] Wehbé MA, Leinberry CF. Current trends in treatment of thoracic outlet syndrome. Hand Clin 2004;20:119–121 [75] Lindgren KA. Conservative treatment of thoracic outlet syndrome: a 2-year follow-up. Arch Phys Med Rehabil 1997;78:373–378 [76] Novak CB. Thoracic outlet syndrome. Clin Plast Surg 2003;30:175–188 [77] Novak CB. Conservative management of thoracic outlet syndrome. Semin Thorac Cardiovasc Surg 1996;8:201–207 [78] Janda V. Muscles and cervicogenic pain syndromes. In: Grant R, ed. Physical Therapy of the Cervical and Thoracic Spine. New York: Churchill Livingstone; 1988 [79] Mackenzie RA. Treat Your Own Neck. Waikanes, New Zealand: Spinal Publications; 1983 [80] Aziz K, Straenley CJ, Whelan TJ. Effort-related axilla-subclavian vein thrombosis. Am J Surg 1986;152:57 [81] DeWeese JA, Adams JT, Gaiser DL. Subclavian venous thrombectomy. Circulation 1970;41 Suppl:II158–II164 [82] Adams JT, DeWeese JA. “Effort” thrombosis of the axillary and subclavian veins. J Trauma 1971;11:923–930 [83] Urschel HC, Patel AN. Paget-Schroetter syndrome therapy: failure of intravenous stents. Ann Thorac Surg 2003;75:1693–1696, discussion 1696 [84] Urschel HC, Patel AN. Surgery remains the most effective treatment for PagetSchroetter syndrome: 50 years’ experience. Ann Thorac Surg 2008;86:254– 260, discussion 260 [85] Drapanas T, Curran WL. Thrombectomy in the treatment of “effort” thrombosis of the axillary and subclavian veins. J Trauma 1966;6:107–119 [86] Campbell CB, Chandler JG, Tegtmeyer CJ, Bernstein EF. Axillary, subclavian, and brachiocephalic vein obstruction. Surgery 1977;82:816–826 [87] Painter TD, Karpf M. Deep venous thrombosis of the upper extremity five years experience at a university hospital. Angiology 1984;35:743–749 [88] Schneider DB, Dimuzio PJ, Martin ND, et al. Combination treatment of venous thoracic outlet syndrome: open surgical decompression and intraoperative angioplasty. J Vasc Surg 2004;40:599–603 [89] Doyle A, Wolford HY, Davies MG, et al. Management of effort thrombosis of the subclavian vein: today’s treatment. Ann Vasc Surg 2007;21:723–729 [90] Smith RA, Dimitri SK. Diagnosis and management of subclavian vein thrombosis: three case reports and review of literature. Angiology 2008;59:100– 106Review [91] Sanders RJ. Thoracic Outlet Syndrome: A Common Sequela of Neck Injuries. Philadelphia, PA: Lippincott; 1991 [92] Urschel HC, Razzuk MA. Neurovascular compression in the thoracic outlet: changing management over 50 years. Ann Surg 1998;228:609–617 [93] Mackinnon SE, Patterson GA. Supraclavicular first rib resection. Semin Thorac Cardiovasc Surg 1996;8:208–213 [94] Mackinnon SE, Patterson GA, Colbert SH. Supraclavicular approach to first rib resection for thoracic outlet syndrome. Oper Tech Thorac Cardiovasc Surg 2005;10:318–328 [95] Urschel HC Jr. Reoperation for thoracic outlet syndrome. In: International Trends in General Thoracic Surgery. Vol 2. St. Louis, MO: CV Mosby; 1986 [96] Urschel HC, Razzuk MA. The failed operation for thoracic outlet syndrome: the difficulty of diagnosis and management. Ann Thorac Surg 1986;42:523–528

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13 Injury and Compression Neuropathy in the Lower Extremity Kirsty U. Boyd and Justin M. Brown

13.1 Introduction Lower extremity nerve entrapments and compressions have become increasingly well recognized in recent decades.1 A variety of contributing etiologies—acquired, traumatic, iatrogenic, neoplastic, vascular, and infectious—are potential causes of lower extremity neuropathies; however, the most common cause remains the presence of known entrapment points. As our understanding of the anatomy of these entrapment points continues to evolve, surgical decompression appears to be a valuable tool in the treatment of these entities. For example, imaging modalities and a better understanding of the pathogenesis of entrapment syndromes, what was once assumed to be spondylosis now has many other potential etiologies. In fact, lumbosacral radiculopathy is the most common presumptive diagnosis leading to referrals for electrodiagnostic studies.2 Spinal imaging has become sensitive for detecting such pathologies, but when imaging has failed to demonstrate stenosing degenerative disease, abscess, or tumor to account for patient symptoms, other etiologies must be considered. Lumbosacral plexopathies, though less common than brachial plexopathies, have become increasingly well recognized in recent years.

13.2 Historical Review Giulio Casserio was the Italian anatomist who in 1632 was the first to describe the lumbosacral plexus as an entity. 3 However, it was not until 1960 that an injury involving this structure was described.3 Involvement and injury to the lumbosacral plexus is likely far more common than was previously recognized.4 Traumatic injuries to the lumbosacral plexus are certainly not as common as those to the brachial plexus and are often associated with several spinal and pelvic fractures, making diagnosis of these lesions difficult.5 Surgery of the nerves in this region historically has been rarely performed.4 Functional outcome for very proximal injuries was considered hopeless and therefore infrequently attempted.5

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13.3 Surgical Anatomy of the Lumbosacral Plexus The lumbosacral plexus is less complex than its upper extremity counterpart, and its anatomy has been well described (▶ Fig. 13.1).4,6,17 Its primary subdivisions include roots, branches, divisions, and terminal nerves. The ventral primary rami of L1–S4 each contribute to the lumbosacral plexus, with variable input from T12. This entity can be subdivided into a lumbar plexus, formed from L1–L3 and part of L4, and a sacral plexus, formed from the remaining portion of L4 and L5–S4. The radicular composition is subject to pre- or postfixation, and the basic plan involves anterior fibers contributing more to flexion and posterior fibers more to extension.3

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The lumbar plexus is located deep in the superior and middle portions of the psoas major muscle, anterior to the bony transverse processes of the second through fifth lumbar vertebrae, with terminal branches emerging from the lateral border of the psoas. These terminal branches are deep to the ascending iliac veins, vena cava, aorta, and common iliac vessels on the right, and to the iliac arterial and venous plexuses on the left. After exiting the lumbar foramen, the roots of L1, L2, and L4 divide into upper and lower branches. The upper branch of L1 then divides again to become the iliohypogastric (occasionally with T12) and ilioinguinal nerves. The upper branch of T2 and the lower branch of T1 join to form the genitofemoral nerve. The lower branch of L2, all of L3, and the upper branch of L4 each divide into anterior and posterior divisions. The smaller anterior divisions fuse, forming the obturator nerve. Likewise, the larger posterior divisions join to become the femoral nerve. The posterior divisions of L2 and L3 also give rise to the lateral femoral cutaneous nerve. The sacral plexus lies deep within the true pelvis and upon the surface of the piriformis muscle at the sacroiliac junction. The hypogastric artery runs within the nerve trunks, and ascending veins overlie the plexus. After contributing to the lumbar plexus, the remaining L4 and L5 anterior rami fuse, forming the lumbosacral trunk or furcal nerve. These each divide into anterior and posterior divisions. The tibial nerve is formed from the coalescence of the anterior divisions, whereas the posterior contributions of L4–S2 produce the common peroneal nerve. These nerves merge into a common sheath forming the sciatic nerve. From the divisions of the sacral plexus arise three other important branches: posterior divisions of L4, L5, and S1 contribute to the superior gluteal nerve; posterior divisions of L5, S1, and A2 create the inferior gluteal nerve; and posterior divisions of S1 and A2 with anterior divisions of S1–S3 merge to form the posterior femoral cutaneous nerve. The iliohypogastric and ilioinguinal nerves proximally and the lateral femoral cutaneous nerve distally emerge from the lateral border of the psoas and run along the posterolateral muscular wall of the abdomen. The genitofemoral nerve emerges from the anterior surface of the psoas, running subfascially between the major and minor psoas muscles. The femoral nerve emerges from the lateral psoas border and then runs lateral to the external iliac artery within the groove between the psoas and iliacus muscles until it emerges from under the inguinal ligament. The obturator nerve and lumbosacral trunk emerge from the medial border of the psoas and initially run together. The lumbosacral trunk then passes behind the internal iliac vessels, where it joins the upper sacral roots on the ventral surface of the piriformis and exits the greater sciatic foramen with the sacral contributions as the sciatic nerve. The obturator nerve diverges to run behind the common iliac vessels along the sacral ala until it enters the leg through the obturator internus muscle. The inferior gluteal nerve exits the greater sciatic notch under the piriformis, just superior to the sciatic nerve, and immediately enters the gluteus maximus

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Fig. 13.1 Lumbosacral plexus anatomy. The lumbosacral plexus involves multiple components and further organized into the lumbar plexus (T12–L5) and the sacral plexus (L4–S5). Major components involve abdominal nerves (iliohypogastric, ilioinguinal, genitofemoral, and lateral femoral cutaneous), the femoral nerve, and the sciatic nerve.

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Fig. 13.3 Lasègue maneuver for assessing lumbar radiculopathy. By elevating the appropriate leg with the knee in extension, tension is put on the lumbosacral plexus, and patients will present with abrupt pain with a positive Lasègue sign.

13.4 Etiology of Lumbosacral Plexopathy Lumbosacral plexopathy presents with varying degrees of pain, sensory deficits, and weakness in the lower extremities, usually in an asymmetric fashion (▶ Fig. 13.2).7 The distribution of the deficit will often encompass multiple nerves originating from the pelvis.11 The diagnosis, etiology, and management are based on history, physical examination, imaging, and electrodiagnostic findings. Injury to the lumbosacral plexus can be broadly classified as inflammatory, infectious, vascular, neoplastic, and traumatic/iatrogenic. Whereas traumatic injury to the brachial plexus is relatively common, the lumbosacral plexus is well protected within the bony pelvis, lacking the anatomical narrowings and hypermobility of the upper extremity.3,10 Accordingly, the most common etiology of a lumbosacral plexopathy is nontraumatic, with neoplastic processes and diabetic amyotrophy being the most common.9 Fig. 13.2 Lower extremity injury to the lumbosacral plexus. Injury to the lumbosacral plexus presents with a range of various motor and/or sensory deficits, depending on the component injured. Specifically, injury to the femoral nerve results in muscle atrophy in the thigh following a long period of deinnervation.

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muscle. The superior gluteal nerve exits superior to the piriformis. The pudendal nerve exits the greater sciatic foramen under the piriformis and inferior to the sciatic nerve, adjacent to the ischial spine. It then reenters the pelvis through the lesser sciatic foramen. The lumbar plexus provides sensation to the skin overlying the pubic symphysis and part of the external genitalia, anterior and medial thigh, and anteromedial and medial leg. Muscular innervation includes iliacus, psoas, and anterior and medial thigh muscles. The sacral plexus provides sensibility to the gluteal region, remaining portions of the genitalia, and remaining portions of the lower extremity. Motor function includes the pelvic floor muscles, glutei, tensor fascia lata, hamstrings, and all of the muscles of the leg and foot.

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13.5 Nonsurgical Etiologies Lumbosacral radiculoplexus neuropathy (LRPN) affects both diabetic (diabetic amyotrophy) and nondiabetic patients alike. Most commonly, this disorder is found in men who have had long-standing type II diabetes.10 These disorders are considered to be immune-mediated diseases, which presumably cause ischemic nerve injury secondary to the development of a microvasculitis.10 Symptoms usually involve unilateral or bilateral back, buttock, or thigh pain with acute or subacute onset. Classic presentation involves severe thigh pain, which is followed shortly by weakness and wasting of thigh musculature. Accompanying sensory symptoms are usually mild.6,12 Radiation-induced lumbosacral plexopathies following treatment of gynecologic or urogenital cancers or lymphomas can develop from a few months to a few decades after radiotherapy.10 This entity is unique in its typical presentation of painless weakness that is frequently bilateral. Paresthesias may occur later, but bowel and bladder disturbances are rare. Pain certainly can occur with this mechanism, but it tends to be less

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Fig. 13.4 Injury to the left ilioinguinal and genitofemoral nerves. Neuropathic pain results following injury to the ilioinguinal and genitofemoral nerves. (a) ilioinguinal and genitofemoral nerves are identified. (b) The nerves are transected, cauterized, crushed, and proximally transposed. (c,d) Nerve stimulators were also used to treat neuropathic pain in this specific case.

13 dramatic than other lower extremity plexopathies. Etiology has been attributed to both vasculopathy and fibrosis-related vessel entrapment.13 Another relatively common source worth mentioning is intrapartum maternal lumbosacral plexopathy. Late in pregnancy, as an enlarged uterus begins to compress the pelvic structures, compression of the lumbosacral plexus may occur. Symptoms are often at their worst at the time of delivery. Pain may progress to weakness and, at times, complete foot drop. All symptoms usually resolve soon after delivery, and as the etiology is usually a neurapraxic injury, deficits generally recover in the following weeks.10

13.6 Vascular Etiologies The lumbosacral plexus is in close proximity to a number of important vascular structures. As such, pathology of these vessels

can present with neurologic sequelae. Compression can result from aneurysmal dilation of the distal aorta, iliac arteries, or their branches.14 These patients often present with abrupt sciatic pain with a positive Lasègue maneuver, mimicking a lumbar radiculopathy (▶ Fig. 13.3).8 The sequence of symptoms usually follows a pattern of pain, progressive unilateral paresthesias, sensory loss, and weakness. Incontinence does not commonly ensue.10,14 Associated nonneurologic symptoms include obstructive uropathy, lower extremity ischemia, edema, and deep vein thrombosis.14 Hypoperfusion of the plexus can also lead to plexopathy and even result in permanent deficits. 15 The vast majority of the vascular supply to the lumbosacral plexus arises from the internal iliac artery. Lateral sacral and iliolumbar branches enter the foramen and perfuse the cauda equina, whereas collaterals from the psoas muscle, within which it rests, supply the vasonervorum of the extraspinal plexus. Loss

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Fig. 13.5 Compression of the left lateral femoral cutaneous nerve. (a) The inguinal ligament can compress the lateral femoral cutaneous nerve resulting in sensory changes on the lateral aspect of the thigh. (b) Release of this ligament will decompress the lateral femoral cutaneous nerve. The vessel loop is around the nerve.

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Fig. 13.6 Anterior cutaneous branch of the femoral nerve and infrapatellar branch of the saphenous nerve. The anterior cutaneous branch of the femoral nerve innervates the anterior cutaneous aspect of the knee (purple), while the infrapatellar branch of the saphenous nerve is distal (green). The tug test helps delineate the sensory territories with movement of the skin. In this case, the anterior cutaneous branch of the femoral nerve was iatrogenically injured following placement of a portal for arthroscopy. Please note the yellow circle marked by patient preoperatively to denote worst area of pain just anterior to midincision.

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Fig. 13.7 Saphenous nerve within the Hunter canal. The saphenous nerve is identified within the Hunter canal deep to a tendinous aponeurosis through an exposure between the vastus medialis and sartorius.

of a single internal iliac artery is usually well compensated for by diffuse anastomoses to the contralateral supply. In elderly patients with advanced atherosclerotic disease, however, this compensation may be inadequate.16 Retroperitoneal hemorrhage can result in a plexopathy secondary to a compartment syndrome.10 Such bleeds are primarily spontaneous, most commonly occurring in the setting of anticoagulant therapy or congenital bleeding diatheses. Relatively small hematomas within the fascia of the iliacus muscle can result in isolated compression of the femoral nerve within the plexus.17 Alternatively, large hematomas can diffusely compress the lumbar plexus within the psoas muscle, leading to obturator weakness.8 These injuries tend to be unilateral with acute or subacute pain in the groin or lower abdomen that may radiate into the thigh or leg.

13.7 Neoplastic Processes Primary tumors are a significant cause of lumbosacral plexopathy, but metastases are the most frequent.10 Of these, 75%

invade the plexus by direct extension, most commonly originating from the gastrointestinal or genitourinary system. Sarcomas and lymphomas also occur with similar frequency. The remaining 25% reach the plexus via hematologic spread, in particular, breast and lung cancer. In fact, breast metastases are thought to be the most frequent source of a lumbosacral plexopathy. In the majority of these cases, the patient has been diagnosed prior to the onset of the plexopathy. Pain is usually the first symptom with neoplastic infiltration. The pain can involve the back, hip, thigh, leg, and foot, or all of these regions, depending on the extent of the involvement. Paresthesias and eventually weakness develop later. Associated signs include lower extremity edema and palpable masses on rectal examination. Among benign lesions, sacral sheath tumors can result in symptoms of lumbosacral plexopathy. The majority of these tumors are schwannomas, which may reach a large size before causing symptoms.18 In neurofibromatosis type 1, abdominopelvic lesions occur in as many as 40% of patients. 8

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Fig. 13.8 Release of the Hunter canal. The saphenous nerve is decompressed by releasing the Hunter canal and dividing the tendinous aponeurosis along the course of the nerve. The nerve to the vastus medialis is identified laterally.

Such retroperitoneal lesions frequently emanate from the lumbosacral plexus. These may be asymptomatic or result in slow, progressive neurologic deficit. Sacral giant cell tumors, sacrococcygeal teratomas, neuroblastomas, anterior sacral meningoceles, chondromas, and chordomas can all present similarly.19 Local pain is commonly followed by radicular pain within more than one root distribution. Sensory and motor deficits, which may include bowel and bladder dysfunction, then develop.

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13.8 Lumbosacral Trauma Traumatic closed injuries of the lumbosacral plexus are relatively rare. The incidence of lumbosacral plexus injury in general trauma has been estimated at 0.05 to 2.50%, but it has been suggested to be increasing11,20 and they often result in a severe neurologic deficit.10,11 In fact, these lesions may not be as rare as reported, as a number of issues confound the diagnosis,

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including the fact that most older series did not use electrodiagnostic studies to facilitate diagnosis.4,11 Additionally, there is a high mortality rate in this population, given the severity of injury and the associated major vascular trauma; those who survive are frequently incompletely worked up and are commonly assumed to have an inoperable entity.11 Most series that have looked at unstable pelvic fractures or displaced shear fractures have found an ~ 50% rate of associated neurologic injury. 11,21 Using electrodiagnostic evaluation, it has been found that most commonly three quadrants of the two lumbosacral plexus are affected, with bilateral injuries to the sacral components. Sacral-level injuries can result in loss of hip adduction and stability, loss of knee flexion, and loss of all function below the knee. Conversely, lumbar plexus injuries primarily compromise hip flexion and knee extension.22 In addition to stretch injury and rupture, lumbosacral root avulsions with associated pseudomeningoceles can occur.23,24 Persistent severe, shooting pain and burning dysesthesias indicate possible concomitant nerve rootlet ruptures within the cauda equina. These have usually

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Fig. 13.9 Decompression of the vastus medialis nerve. The nerve to the vastus medialis is decompressed by dividing the surrounding tissue along the course of the nerve, lateral to the saphenous nerve.

been associated with severe disruption of the pelvis or lower extremity and are most often unilateral.24 Associated vascular injury, including pseudoaneurysms and pelvic hematomas, can also play a part in the plexopathies encountered in pelvic trauma; however, this does not appear to be common within the pelvis.25 It has been suggested that the mechanism of injury is primarily traction, proposed to occur with hip flexion-abduction, posterior dislocation, and thigh hyperextension with external rotation of the disassociated pelvic fragment.22

13.9 The “Border Nerves”: Iliohypogastric, Ilioinguinal, and Genitofemoral 13.9.1 Historical Review Pain in the inguinal region and groin can result from a number of entities, from intra-abdominal disorders and genitourinary

abnormalities to lumbosacral spondylosis and hip joint disorders.26,27 Some authors cite adductor or rectus abdominis muscle strains, osteitis pubis, or disruption of the inguinal canal.28 More and more frequently, the contribution of neuropathies of the iliohypogastric, ilioinguinal or genitofemoral nerves, or some combination of these, is recognized.26,28,29 Although direct trauma or hypertrophy of the lower abdominal musculature from overtraining can entrap these nerves, symptoms most commonly arise following surgery in the inguinal region.26 Ruge, in 1893, coined the term Grenznerven, which was interpreted as “border nerves” by Bardeen and Elting in 1902, to describe the nerves innervating the region between the abdomen and thigh.30,31 In 1942 Magee described the syndrome of genitofemoral causalgia, and just a few years later, in 1945, Lyon suggested the term genitofemoral neuralgia.32 Groin pain that involves the medial thigh, in addition to the scrotum or testicle in men, or labia majora in women, should arouse suspicion of damage to one or more of these nerves, especially in the setting of athletics or following surgery in the region of the lower abdomen. Contact sports that result in trauma

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Fig. 13.10 Decompression of the left oburator nerve. The anterior branch of the obturator nerve is decompressed between the pectineus and adductor longus muscles and on the anterior surface of the adductor brevis within the medial aspect of the thigh.

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Fig. 13.11 Tension of the common peroneal nerve at different knee positions. (a) With the knee straight, the common peroneal nerve, as it courses around the fibular head distally, is in tension. (b) With the knee bent, the common peroneal nerve is in less tension.

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Fig. 13.12 Anatomical structures for release of the common peroneal nerve. (a) Proximal cross section of the leg depicts the position of the common peroneal nerve and the surrounding intermuscular septa. The posterior and anterior crural intermuscular septa, the intermuscular septum between the tibialis anterior and the extensor digitorum longus, and the deep tendinous fascia superficial to the soleus are released. (b) Longitudinal illustration of the common peroneal nerve and the surrounding muscles and intermuscular septa. In this illustration, the leg is flexed as depicted by the common peroneal nerve having a course around the head of the fibula.

to the iliac crest/lateral pelvis can result in injuries to these nerves. Entrapment neuropathies of the ilioinguinal nerve are described and are attributed to the region within which the nerve makes an abrupt turn at the anterosuperior iliac spine and pierces the transversalis muscle fascia.33 The main trunk of the iliohypogastric nerve is at risk during procedures such as nephrectomies, resulting in anesthesia in both lateral and anterior sensory branch distributions. The anterior branch is at risk during lower abdominal quadrant operations. Transection and neuroma formation, suture entrapment, fibrous adhesions, and excessive tension of associated fascia following surgery can all lead to pain.34 In fact, chronic pain following inguinal hernia repair is a relatively common complication, ranging in different series from 1 to 12% of cases.34,35 Symptoms typically include paresthesias, dysesthesias, or hypoesthesias within the inguinal region.36 Suture entrapments frequently present immediately postoperatively and may produce intense pain that is localized to the area of the stitch.37 Pulling and throbbing may be described even years after such an operation, and these symptoms are typically exacerbated by walking, stooping, or hyperextension of the hip.33,38 The pain will often have a burning quality, and shooting or lancinating symptoms are sometimes described.37 The mechanisms underlying neuropathic pain resulting from peripheral nerve injury as seen in these postoperative syndromes often involve both central and peripheral etiologies. Lo-

cal inflammation due to trauma is a known nociceptive cue and can occur with injuries that do not involve axotomy. In a complete injury, however, wallerian degeneration occurs. This process involves the release of inflammatory cytokines, including histamine and seratonin, as well as neurotrophic factors. Nerve sprouts from surrounding territories are drawn by the neurotrophins, while connective/scar tissue is laid down due to the fibroblastic response. Although this inflammatory period lasts only a few weeks, a more chronic syndrome may ensue due to ectopic activity of sensitized C fibers, abnormal spontaneous activity in regenerating nerve sprouts, and abnormal activity from haphazardly arranged nerve fibers.39 Regenerating nerve sprouts grow into surrounding scar tissue, forming a neuroma.40 Abnormal connections between A-beta and C fibers may be formed, producing spontaneous neuropathic signals. Local mechanical perturbation then tends to exacerbate these effects. Additionally, due to loss of the normal afferent input to the spinal cord from the sensory territory now denervated, central sensitization of neural structures involved in pain perception may occur, further amplifying this pain.40 Conservative measures to treat neuropathic pain should always be attempted prior to undertaking any surgical intervention. These include desensitization therapy, oral medications, transcutaneous stimulation, and local anesthetic blocks. Only when these have failed should neurolysis or neurectomy be considered.34

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Injury and Compression Neuropathy in the Lower Extremity

Fig. 13.13 Orientation, positioning, and incision for common peroneal nerve release. (a) The left leg is prepped. (b) The leg is positioned with the knee in slight flexion during this procedure. In this position, the common peroneal nerve is not under tension. (c) The fibular head is marked, and an incision is made just below the fibular head. The common peroneal has a course just below the fibular head. The most important step in this release is marking the incision correctly just below or distal to the fibular head. The tendency is to make the incision too proximally. A sand bag placed diagonally at the lateral edge of the foot helps secure the leg with the knee slightly flexed.

Fig. 13.14 Exposure and division of fascial layers superficial to the common peroneal nerve. Upon exposure, the division between the peroneus longus and the proximal-lateral connective tissue discerns the common peroneal nerve deep. The peroneal nerve can be palpated just below the fibular head. Two fascial layers are identified superficial to the nerve and require division to expose the common peroneal nerve.

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13.9.2 Surgical Anatomy The ilioinguinal nerve originates at the L1 root level with variable contribution from T12 and follows the abdominal wall, much like the intercostal nerves, passing through the psoas and

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then coursing along the surface of the lumborus quadratum muscle until it reaches the region just medial to the anterosuperior iliac spine.41 At this point, it gives off a recurrent sensory branch that innervates a small area over the iliac crest. It turns medially at this point to pierce the transversalis muscle/fascia,

Injury and Compression Neuropathy in the Lower Extremity

Fig. 13.15 Exposure and identification of the common peroneal nerve. Following the division of the superficial fascial layers, the common peroneal nerve is identified along its course around the fibular head and continues distal and deep to the peroneus longus.

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Fig. 13.16 Incision markings of the connective fascia superficial to the peroneus longus. The incision is marked on superficial muscle fascia in the direction of the nerve to expose the peroneus longus and compressive intermuscular septa.

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Injury and Compression Neuropathy in the Lower Extremity

Fig. 13.17 Incision of the connective fascia superficial to the muscles and identification of the intermuscular septa. Three intermuscular septums (arrowheads) of the peroneus longus are identified for release to decompress the peroneal nerve following the division of the superficial fascia. The proximal septum (posterior crural intermuscular septum) is the primary entrapment point with the tendinous leading edge of the peroneus longus. Distally, the anterior crural intermuscular septum and the less emphasized intermuscular septum are seen between the extensor digitorum longus and tibialis anterior.

then runs between this and the internal oblique muscles, often passing through the internal oblique to run between this and the external oblique, providing motor branches to both. After joining the spermatic cord, it passes through the inguinal canal. The terminal sensory branch passes on to innervate the base of the scrotum or labia and a small portion of the proximal inner thigh.30,42 The iliohypogastric nerve arises from the ventral rami of L1 and L2. This nerve passes through the psoas muscle and then curves downward, behind the lower pole of the kidney. Midway between the anterosuperior iliac spine (ASIS) and the apex of the iliac crest, this nerve pierces the abdominal wall, giving off muscular branches, and then follows the iliac crest. As it approaches the ASIS, it divides into two terminal branches, the lateral and anterior cutaneous branches. The lateral cutaneous branch crosses the iliac crest to innervate a small region of the upper buttock. The anterior branch courses with the ilioinguinal nerve. It pierces the transversalis muscle fascia and runs between this muscle and the external oblique muscle, providing motor branches to both. This nerve eventually terminates above the inguinal ligament to innervate a region of skin just above the pubis.41

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The genitofemoral nerve also originates from the L1 and L2 roots. It passes inferiorly and anteriorly through the psoas muscle to emerge on its surface, at the partition between the psoas major and minor muscles. It descends within this groove in the retroperitoneum until reaching the inguinal ligament, where it divides into its genital and femoral branches. The genital branch joins the ilioinguinal branch in the inguinal canal and passes on to innervate the mons pubis and scrotum or labium majora. Often branches of this nerve will anastomose with the terminal sensory region of the ilioinguinal nerve branches, making their final distributions difficult to distinguish.41 The femoral branches (or lumboinguinal nerves) most commonly consist of two branches, which pass under the inguinal ligament anywhere from 3 to 10 cm medial to the ASIS and innervate a small patch of skin on the anterior proximal thigh over the inguinal triangle.27,41 The genitofemoral nerve also gives off motor branches to the cremaster muscle.

13.9.3 Diagnosis Injuries to any of these nerves may result in thigh and groin pain. This pain may consist of dysesthesias, paresthesias, hypo-

Injury and Compression Neuropathy in the Lower Extremity

Fig. 13.18 Exposing the posterior crural intermuscular septum as the primary entrapment point. By retracting the peroneus longus muscle distally and off the posterior crural intermuscular septum, a dense and tight tendinous septum is revealed superficial to the common peroneal nerve. This septum is the primary entrapment point. Note that the retraction of the muscle allows for the identification of the septum facilitating its release.

esthesia, hyperalgesia, or any combination of these.34 Patients may describe dull aching or burning, or they may describe sharp, lancinating pains. Pain may be constant or intermittent. In more proximal injuries, observing for additional regions of pain or anesthesia can often help discriminate between the different nerves; for example, lateral buttock symptoms that begin at the pelvic rim, in addition to pain over the pubis, is more likely to be from the iliohypogastric nerve, whereas a stripe of pain along the pelvic rim that wraps dermatomally around and terminates in the groin is more likely to be the ilioinguinal nerve. When the terminal branches alone are affected, as can occur following procedures involving inferomedial groin incisions, the diagnosis can become more elusive. In pure entrapment syndromes, a Tinel sign can be useful if elicited at known sites of entrapment, such as where the ilioinguinal nerve pierces the transversalis fascia just medial to the ASIS. Electrodiagnostic studies are of limited value in these syndromes. In fact, eliciting responses from any of these nerves is technically challenging.6 Such studies, however, are of value in ruling out upper lumbar nerve root pathology as the source of the pain. Sensory nerve action potentials are not readily elicited for the ilioinguinal nerve, but needle electromyography may demonstrate denervation of the transversalis or internal oblique muscles in surgical transection injuries. In genitofemoral neuralgia, there are no useful electrodiagnostic tests.33,34

Nerve blocks are the mainstay of diagnostics (and therapeutics) for these entities. Infiltration at the medial border of the ASIS, which eliminates groin pain, implicates either the ilioinguinal or iliohypogastric and essentially rules out any contribution from the genitofemoral. A needle is inserted 2 to 3 cm medial and inferior to the ASIS and directed superolaterally to encounter the inner surface of the iliac bone. In an obese patient, this could require a needle up to 9 cm long. Infiltration of up to 10 mL of 1% lidocaine is performed as the needle is withdrawn. When the needle is subcutaneous once again, the needle is redirected more superiorly to pierce the external oblique, internal oblique, and transversalis fascia, where the injection is repeated. Nerve block of the genitofemoral is performed at the external inguinal ring, ~ 2 cm lateral to the pubic tubercle. Infiltration with 5 to 10 mL of 1% lidocaine in each direction in a fanlike distribution from lateral to superior to medial once the superficial fascia is penetrated is commenced. If this injection provides relief, whereas the other does not, it is likely a genitofemoral nerve injury. But consider that this block will also affect the distal ilioinguinal distribution, so beginning with this block may falsely identify a genitofemoral nerve when the ilioinguinal nerve is actually injured. Therefore, both injections should be performed.34 If confirmation of a genitofemoral neuralgia is required, a specific block of this nerve can be performed via a transpsoas approach.37

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Injury and Compression Neuropathy in the Lower Extremity

Fig. 13.19 Release of the posterior crural intermuscular septum and identification of the deep tendinous fascia. The posterior crural intermuscular septum is released distally along the common peroneal nerve. The length of this septum can vary from patient to patient. The surgeon must be sure to identify and release its most distal tendinous component. Afterward, the tendinous fascia is identified deep to the common peroneal nerve and is designated for division to create a soft canal for the nerve. A nerve branch from the peroneal nerve is an articular joint branch.

As with any nerve injury-related pain, aggressive medical management should be undertaken before considering surgery. This includes avoidance of exacerbating activities, topical anesthetics, desensitization therapy, application of a transcutaneous electrical nerve stimulation (TENS) unit, and administration of medications with proven efficacy in neuropathic conditions.34, 37,43 In patients with severe symptoms that persist for longer than 3 months, surgical intervention is recommended.

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13.9.4 Surgical Technique Our surgery is planned based on the results of the nerve blocks and in close consultation with the pain management physician who performed the blocks. Typically, the ilioinguinal and genitofemoral nerve are involved with pain following inguinal hernia repair; we address both through a retroperitonal approach if the pain management physician deems the patient a surgical candidate. We do not recommend the surgery that we describe here unless there has been an open injury. For example, we have not performed this surgery for blunt trauma. Exploration of the original surgical incision or laceration with attempts to excise and transpose a painful neuroma are rarely successful. We recommend a retroperitoneal approach

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to identify the involved nerves (typically, ilioinguinal, iliohypogastric, or genitofemoral) at the proximal location in the retroperitoneum.34 The best exposure can be achieved in a lateral extraperitoneal approach with the patient supine and the side of interest elevated. A transverse flank incision is used, beginning superolateral to the umbilicus and extending superolaterally to the anterior axillary line. After splitting the external and internal oblique muscles, the fibers of the transversus abdominis are split anatomically. Peritoneum and extraperitoneal fat are retracted medially, and the plane anterior to the quadratus lumborum is identified. After identifying and protecting the ureter and the femoral vessels, the psoas muscle is exposed, and the genitofemoral nerve coursing on its anterior surface is identified (▶ Fig. 13.4). We take a surgical atlas into the operating room to assist in identifying all the nerves in question. The genitofemoral nerve is identified on the psoas muscle, and care must be taken to follow the femoral branch of the genitofemoral nerve proximally in order to not miss the genital branch of the genitofemoral nerve, which runs medially and is easy to miss. Stimulation of the genitofemoral nerve will result in cremasteric muscle contraction.

Injury and Compression Neuropathy in the Lower Extremity

Fig. 13.20 Division of the deep tendinous fascia and the soleus muscle. Dividing the deep tendinous fascia to the common peroneal nerve and a portion of the soleus muscle along the course of the peroneal nerve creates a canal for the nerve. Specifically, this allows the nerve to lie flat with a smooth path around the lateral knee.

The next branch moving laterally is the lateral femoral cutaneous nerve. It will not result in any muscle contraction when stimulated, as it is a purely sensory nerve. Traction on the lateral femoral cutaneous nerve will result in a “pulling” or “indentation” of the skin of the lateral thigh, the so-called tug test of a cutaneous nerve. The ilioinguinal nerve is lateral and proximal to the lateral femoral cutaneous nerve, and the iliohypogastric nerve will often run with it. Stimulation of these nerves causes some anterior abdominal wall muscular contraction. If these nerves run intimately together, we treat them as one and do not try to separate them. Once we are certain of the line-up of these four nerves, we perform a neurectomy of the genitofemoral and ilioinguinal (iliohypogastric) (see ▶ Fig. 13.4). We first clamp the nerves proximally to make a second-degree (axonotmetic) injury, then we divide and cauterize the distal end and transpose proximally into the psoas muscle. On two occasions we have placed peripheral nerve stimulators on these nerves, as well as the manipulation described above. In one case, the patient described no pain relief and requested the stimulator be removed. The second case, done in 2000, had an excellent result. The patient has complete pain relief and underwent two battery changes successfully at 5 and 10 years postoperatively.

The peripheral nerve stimulators are tedious procedures to perform; therefore with such a small and inconsistent experience we are loath to suggest them in this patient population (▶ Fig. 13.4).

13.9.5 Results 13

Results for surgical treatment of border nerve injuries and neuromas generally have been reported as good; however, there is a lot of variability, and many studies are underpowered, simple case studies or have poor methodology. Kim et al described considerable pain relief in 90 to 91% of patients presenting with ilioinguinal and iliohypogastric lesions.44 Vuillemeyer and colleagues reported good outcomes with mesh removal and radical neurectomy following hernia repair.45 Starling and Harms achieved 89% relief of pain after resection of the involved segment of ilioinguinal nerve in patients presenting postinguinal herniorraphy.38 Stulz and Pfeiffer reported good results in only 69% of patients and noted that the remainder of patients suffered from residual chronic scar pain.46 Reviews of neuroma treatments in general are frequently less optimistic. The surgeon treating these injuries must be aware of factors that can affect outcomes, including whether the symptoms reside within a discrete nerve distribution or not, the duration of the symptoms,

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Injury and Compression Neuropathy in the Lower Extremity

Fig. 13.21 Release of the anterior crural intermuscular septum between the peroneus longus and extensor digitorum longus. The tendinous anterior crural intermuscular septum is released, and the vessels and small nerve branches can be identified within this plane. This septum is carefully released to avoid cautery of the vessels and possible injury of the surrounding small nerve branches.

the number of previous operations, and response to nerve block. Patients with chronic pain who do not respond well to a neurectomy operation may be candidates for postoperative desensitization therapy with reeducation of nonpainful stimuli or for a dorsal column stimulator.40 Our own results in patients who are carefully selected are only 50 to 60% successful, so we continue to do this procedure but with very careful patient selection.

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13.10 Meralgia Paresthetica 13.10.1 Historical Review Bernhardt-Roth syndrome, better known as meralgia paresthetica, was first described in 1878,47 and the first decompression operation was performed by Harvey Cushing in 1900.42 One of the earliest nerve entrapments described, this syndrome is the neuropathic consequence of entrapment of the lateral femoral cutaneous nerve as it exits the pelvis and pierces the inguinal ligament. This syndrome has been commonly described in those sustaining trauma to the region of the inguinal ligament, those assuming squatting postures for prolonged periods, and in those with leg-length discrepancies, the pelvic tilt resulting

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in stretching of the fascia lata and consequently the nerve against this entrapment point.26,27 Pregnancy and the presence of obesity-associated pannus are the most common scenarios, but tight clothing, belt holsters, iliac bone graft harvesting, and entrapment from surgical scarring have all been described. 47 Inguinal hernia repair can increase tension on the inguinal ligament leading to an entrapment. Compression syndromes have followed a Pfannenstiel incision and appear to be related to retractors compressing the nerve against the iliac crest. 48 In most cases, there is no identifiable cause for the onset of symptoms, but it is generally assumed that the nerve kinks as it passes under the inguinal ligament. Autopsies have demonstrated that compression-related changes in this nerve exist in about half of specimens.42

13.10.2 Surgical Anatomy After receiving contributions from the posterior divisions of the L2 and L3 nerve roots, the lateral femoral cutaneous (LFC) nerve traverses the psoas muscle and runs across the surface of the iliacus muscle. It pierces the fascia of this muscle just as it approaches the inguinal ligament.33 Classically, the nerve exits a

Injury and Compression Neuropathy in the Lower Extremity

Fig. 13.22 Identification of the distal intermuscular septum found between the extensor digitorum longus (EDL) and tibialis anterior. The distal intermuscular septum between the EDL and tibialis anterior is the third tendinous septum that is released. This is the third septum that is released during this procedure. This septum is carefully released to avoid cautery of the vessels and possible injury of the surrounding small nerve branches.

triangle made of the anterosuperior iliac spine externally, the inguinal ligament superiorly, and the fascia of the sartorius inferiorly, but it often exits the pelvis in a variable manner, with three primary configurations. In the type A configuration, it exits posterior to the ASIS and travels across the iliac crest. In type B, it emerges anterior to the ASIS and superficial to the sartorius muscle but within the substance of the inguinal ligament. In type C, it emerges medial to the ASIS, within the tendinous origin of the sartorius. It has also been noted that multiple branches may exist.47 After leaving the pelvis, the nerve then courses beneath the deep fascia of the upper thigh. It pierces this to reach its subcutaneous position, from which it provides sensation to the anterolateral thigh. Note should be made that the femoral branch of the genitofemoral nerve may at times overlap the distribution of the LFC and thereby confuse the diagnosis.47

13.10.3 Diagnosis Pain and paresthesias, which may progress to numbness of the upper lateral thigh, are the key features of neuropathy of this pure sensory nerve.33 Symptoms tend to be exacerbated by standing and walking and relieved by sitting. Pain and a Tinel sign frequently can be identified in the region of the ASIS and

radiating into the LFC nerve distribution. The scratch-collapse test is often positive at the exit point of the nerve just medial to the ASIS. Electrodiagnostic studies may identify attenuated sensory nerve action potentials or reduced sensory nerve conduction velocities.48 Although the specificity is as high as 98% in some series, specific findings have not been found to correlate with severity of symptoms or quality of recovery.48 Additionally, nerve block with local anesthetic being injected at the junction of the ASIS and the inguinal ligament can be used to confirm the diagnosis and rule out contribution of other nerve distributions, particularly in cases that are not clearly defined. As the vast majority of these cases may resolve with time, patients should be given a trial of conservative therapy. Conservative measures include weight loss, avoidance of clothing or accessories that may cause pressure to this region, nonsteroidal antiinflammatory drugs (NSAIDs), and potentially injection of local anesthetics and steroids.49 Severe symptoms that persist for several months in spite of this should undergo surgical decompression.

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13.10.4 Surgical Technique We will bring an anatomy text to the operating room for this procedure, as it is not a common operation. A 4-cm horizontal

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Injury and Compression Neuropathy in the Lower Extremity

Fig. 13.23 The lateral sural nerve is protected and occasionally has its own connective tissue compression point.

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Fig. 13.24 Orientation, positioning, and incision for superficial peroneal nerve release. (a) The left leg is prepped. (b) The leg is positioned with the knee extended during this procedure to allow exposure of the lateral compartment. (c) An incision is marked on the lateral-anterior aspect of the distal leg along the course of the superficial peroneal nerve, 3-4 cm lateral to the anterior edge of the tibia. The incision is marked 15 cm in length starting 10 cm proximal to the center of the lateral malleolus.

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Injury and Compression Neuropathy in the Lower Extremity

Fig. 13.25 Exposure and fascial landmarks for identifying the superficial peroneal nerve. Upon exposure, the superficial fascia is identified lateral to the fat streak. Two yellow longitudinal landmarks are visible through the superficial fascia. The anterior landmark is a layer of fat that divides the tibialis anterior and extensor digitorum longus. The superficial fascia is incised to reveal this fat landmark. Do not waste time looking for the nerve within the fat but instead move laterally. Posterior to this landmark is the second yellow/ white longitudinal landmark, which is the superficial peroneal nerve as it courses through the superficial fascia.

cutaneous incision is made just inferior to the ASIS in line with the inguinal ligament, dissection taken down to the fascia lata. The LFC nerve is carefully dissected from the sartorius muscle and decompressed distally by opening the fascia lata (repeated for each identifiable branch). It is then followed proximally, and a portion of the inguinal ligament is sectioned, including the tendinous arc from the iliac fascia (▶ Fig. 13.5).48,49 In patients who have refractory symptoms following a release, neurectomy can be performed, and some authors (not us) argue that it is the preferred primary operation. 48 In this case, the nerve can be exposed, released from under the inguinal ligament, and mobilized both proximally and distally. Once mobilized, the nerve is lifted and traction applied in line with its natural course within the pelvis. It is then cut as proximally as possible, allowing the free end to retract into the retroperitoneal space. Coagulating the free end prior to releasing the nerve may be advocated. This avoids the potential of the free end forming a neuroma near the incision site. It can also be clamped as far proximally as possible, cauterized, and divided distally, then transposed high into the retroperitoneal space. This would be our preferred approach. If this fails, the retroperitoneal approach as described above is performed.

13.10.5 Results Different series have reported a fairly wide range of results, indicating that patients experience partial or complete symptom resolution in 60 to 95% of cases. The most successful series tended to be more rigorous in their diagnosis of the disorder and focused more on the anatomical variability.47,49 Those patients expected to not do as well are those with long-standing neuropathies, those with more than one nerve involved or less clearly defined distributions, and the obese.47,49 Our results with surgical treatment of this nerve compression (unlike with ilioinguinal and genitofemoral nerves) are excellent.

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13.11 Femoral Nerve 13.11.1 Historical Review Although idiopathic entrapment of the femoral nerve remains a rare diagnosis, case series have emerged over the years.50,51 Regardless, diabetic amyotrophy remains the most common source of femoral neuropathy, and some authors argue that this accounts for the true etiology of some of the reported idiopathic entrapments.51 Enveloped within the iliac fascia,

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Injury and Compression Neuropathy in the Lower Extremity

Fig. 13.26 Exposing the superficial peroneal nerve. The superficial peroneal nerve is identified a couple of centimeters posterior to the fat landmark through the superficial fascia. Release of the superficial fascia over the nerve will expose it and its course. At this point, the nerve is often within a fibrous tunnel.

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compression of the femoral nerve secondary to hemorrhage has been described in the setting of bleeding disorders or anticoagulation. When this occurs, the usual sites of compression include the inguinal ligament, at the level of the lumbar roots, and in the cleft between the psoas and iliacus where the fascia is quite thick.52 Injuries during hip replacement (ranging from 0.1 to 2.3% of cases), femoral artery puncture procedures, gynecologic procedures (e.g., abdominal hysterectomy or those performed in the lithotomy position), urologic procedures, or as a result of pregnancy or prolonged labor have all been reported. Neuropathy from overstretching or compression in dancers and gymnasts has also been reported. Most entrapment neuropathies occur below the inguinal ligament, where the nerve lies in close proximity to the femoral head, the tendon insertion of the vastus intermedius, the psoas tendon, the hip, and the joint capsule. Additionally, neurovascular conflicts in which the femoral artery pulsating against the nerve results in microtrauma and neuropathy have also been reported.50 Muscular slips have been described, even actually dividing the nerve and thereby predisposing to a neuropathy.52

forming within the psoas muscles, these roots give off branches to the iliacus and psoas muscles. After these branches converge, this nerve emerges from the lateral border of the psoas and lies within the cleft between this muscle and the iliacus. Along with the external iliac artery, the iliac fascia binds the femoral nerve. The femoral nerve then courses toward the inguinal ligament, giving off additional small branches to the iliacus and the psoas. The nerve passes under the inguinal ligament, giving off a branch to the pectineus muscle, and enters the femoral triangle lateral to the femoral artery. Commonly ~ 4 cm distal to the inguinal ligament, the nerve divides into anterior and posterior divisions. The anterior division innervates the sartorius muscle and gives rise to the medial and intermediate femoral cutaneous nerves, which provide cutaneous sensation to the anterior thigh proximal to the knee. The posterior division gives rise to the saphenous nerve, which provides sensation to the anterior and medial aspect of the knee, as well as the medial aspect of the leg. In addition, the posterior division provides motor branches to the quadriceps, including the rectus femoris, vastus medialis, vastus intermedius, and vastus lateralis.

13.11.2 Surgical Anatomy

13.11.3 Diagnosis

The femoral nerve consists of contributions from the posterior divisions of L2, L3, and L4 and variably from L1 or L5. Prior to

Pain in the inguinal region that is exacerbated with hip extension and improved with hip flexion and external rotation,

Injury and Compression Neuropathy in the Lower Extremity

Fig. 13.27 Identifying the compression point by the transverse crural ligament. As the peroneal nerve courses distal and superficial, the nerve will exit the superficial fascia and the transverse crural ligament. This ligament is the main contributor to the compression of the superficial peroneal nerve, as seen in this image by its distal tendinous sharp edge (arrow). A Tinel sign or SCT can often be found at this location.

accompanied by dysesthesias of the anterior thigh and anteromedial leg, is the most common presentation of femoral neuropathy. These symptoms may progress to anesthesia in this region. Weakness may present as a limp with walking and progress to involuntary knee buckling under the patient’s weight. In severe cases, the patient may walk by keeping the leg hyperextended and depend on the contralateral leg to ascend stairs.51 A locking knee brace can be prescribed to help such a patient. Examination reveals weakness of knee extension and, if the lesion is proximal to the inguinal ligament, hip flexion. The patellar reflex is also impaired. Electrodiagnostic studies are useful in assessing this lesion. Conduction can be measured both above and below the inguinal ligament. Stimulation at the inguinal triangle can be recorded from surface disks placed over the vastus medialis. Saphenous sensory studies may also demonstrate reduced sensory nerve action potentials. Additional needle examination of the paraspinous muscles, psoas, and hip adductors can be undertaken to rule out a more diffuse plexus lesion. Compression or closed traction neuropathies usually are first-, second-, or third-degree injuries that recover well. Electromyography {EMG) at 3 to 4 months will show evidence of recovery (motor unit action potentials [MUAPs]). A surgical release at the ligament may hasten recovery if there are localizing provocative signs at the ligament (Tinel, scratch-collapse test, etc.).

13.11.4 Surgery In the case of femoral nerve entrapment at the inguinal ligament, exploration may be indicated. This usually involves a longitudinal incision from just proximal to the inguinal ligament extending over the femoral triangle with a lazy-S- or Z-incision across the crease. The incision is taken through the subcutaneous tissue until the nerve is identified surrounded by fat lateral to the femoral artery. The nerve is then followed proximally and under the inguinal ligament. A probe can be passed over the top of the nerve under the ligament to assess the constriction presented by this structure. The ligament is then divided and the nerve examined carefully. In a severe neuropathy, the nerve may require an internal neurolysis due to the progressive fibrosis over time. With transection injuries requiring a nerve graft ≤ 10 cm results are good if done in a timely fashion with a combined groin and retroperitoneal approach.

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13.11.5 Results Because few case reports are available, and numerous etiologies account for this nerve injury, little is known about the response of the femoral nerve to surgical intervention. Azuelos et al documented good results in all 30 cases, with the vascular compression situations responding the most dramatically.50 Direct

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Fig. 13.28 Release of the transverse crural ligament and characteristic of nerve compression. The superficial peroneal nerve is released distal through the superficial fascia and the transverse crural ligament until it exits. In this image, a subtle color change from yellow to white is observed as the nerve exits superficial (arrow). This observation is a characteristic of nerve compression. This compression point is typically 10 cm proximal to the lateral malleolus and the proximal fascial release continued for another 10 cm.

trauma to the femoral nerve can be successfully managed with a nerve graft with excellent results, as the majority of this nerve is motor, so topography matching is not an issue. Both a thigh and retroperitoneal dissection may be necessary to access healthy proximal and distal nerve stumps. There have been a few case reports of nerve transfers from the obturator nerve to the femoral nerve with some success, although the size match is obviously not ideal. Those nerve transfers would be appropriate if no healthy proximal stump was available.

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13.12 Saphenous Nerve 13.12.1 Historical Saphenous neuritis, also known as gonyalgia paresthetica or minor causalgia, results in pain within the medial thigh and knee, as well as paresthesias of the medial leg and foot. Although compression can occur anywhere along the adductor canal, the distal location where the nerve pierces the fascia just proximal to the knee has been most commonly implicated. 51 This nerve, though, may be entrapped anywhere along the adductor canal. Additionally, the femoral vessels or pes anserine

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bursitis may compress the nerve, or it may be injured by direct trauma or various operations, including varicose vein repairs and medial knee operations.51,53,54

13.12.2 Surgical Anatomy The saphenous nerve branches from the femoral nerve just distal to the inguinal ligament and courses within the quadriceps muscles in the subsartorial (Hunter) canal with the femoral artery. This fascial canal originates at the apex of the femoral triangle and runs distally to the adductor hiatus. The adductor magnus and longus muscles form the floor of this canal, and the vastus medialis forms the anterolateral border. The roof is formed by the fascia that runs between the vastus medialis, sartorius, and adductors.53 The nerve does not emerge from the adductor hiatus as the femoral artery and vein do. Instead, it passes between the sartorius and gracilis muscles, where it gives off an infrapatellar branch, which provides sensation to the anterior surface of the patella (▶ Fig. 13.6). It then passes through the fascia between the sartorius and gracilis muscles at ~ 10 cm above the knee. The nerve crosses the pes anserine bursa and descends along the medial aspect of the tibia. It runs with the saphenous vein in the medial calf and divides into two

Injury and Compression Neuropathy in the Lower Extremity

Fig. 13.29 Identifying the proximal superficial fascia to release. The superficial fascia is identified proximally and released to the point where the superficial peroneal nerve exits from deep between the fibularis longus and extensor digitorum longus. The compressive fascia is seen in this image and is shown partially released.

braches as it reaches the lower third of the leg. One branch continues straight to the ankle, while the other passes with the vein in front of the medial malleolus and often continues to the ball of the great toe.

13.12.3 Diagnosis Deep aching within the thigh, along with knee pain and paresthesias in the medial leg and foot, is a hallmark feature of this compression neuropathy. Palpation or percussion just proximal to the medial epicondyle of the femur, corresponding to its fascial foramen, may produce a Tinel sign or reproduce the symptoms. Nerve blocks at this location should eliminate the associated pain. Nerve conduction studies may be of use in thin patients. Because this is a purely sensory nerve, if any motor findings are present, a possible femoral neuropathy should be sought. Patients with open injuries, or after knee surgery, may develop neuromas, especially of the infrapatellar branch of the saphenous nerve (▶ Fig. 13.6). They typically have Tinel signs and positive scratch-collapse tests at the area of the neuromas. Care must be taken to ensure that there is not also a contribution from the terminal portion of a femoral cutaneous branch. Once again, an excellent anatomy book will help the examiner to map out what nerves are involved. A diagnostic nerve block can also be helpful.

13.12.4 Surgery As with other sensory neuropathies, surgical options include nerve decompression for entrapment and transposition for neuroma formation once conservative management has failed. For saphenous nerve compression, exploration is undertaken in the medial thigh. A longitudinal incision is made along the anterior aspect of the distal sartorius. This muscle is identified and followed distally until it becomes tendinous (▶ Fig. 13.7). At this level, the nerve should be found emerging from the medial fascia. This location is identified, and the fascia is split both proximally and distally, ensuring no remaining sites of constriction on the nerve. The saphenous nerve is decompressed at the entrapment point in the Hunter canal (▶ Fig. 13.8; ▶ Fig. 13.9). A finger is passed proximally under the sartorius to ensure no additional sites of entrapment are present. An anatomy atlas will be helpful, as this is an infrequent procedure. The patient’s own preoperative marking for neuromas is imperative for small neuromas. An incision is made longitudinally to identify the infrapatellar branch and the femoral cutaneous nerves. They are proximally clamped, distally cauterized, and then transposed (▶ Fig. 13.6). The saphenous nerve can also be injured at the ankle, for example, in tarsal tunnel surgery. In these cases, it is found anteri-

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Fig. 13.30 Release of the proximal superficial fascia as the peroneal nerve exits from deep. The superficial fascia is released to the point where the superficial peroneal nerve exists from deep between the fibularis longus and extensor digitorum longus. The exit point can be seen. The superficial fascia is further incised over the fat landmark to relieve longitudinal tensile force.

or to the medial malleolus and treated in a similar fashion with transposition.

13.12.5 Results Saphenous nerve decompression is described in the literature; however, these reports are in small series with limited followup. Several authors report starting with simple decompression with modest results, then progressing to neurectomy if decompression fails.55–57 We have had excellent results with the above treatment.

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13.13 Obturator Nerve 13.13.1 Historical Review Obturator neuropathy was first described as a syndrome of groin pain in athletes in 1997 by Bradshaw et al, who discussed a series of 32 patients with medial thigh pain with exercise-induced exacerbation and electrodiagnostic evidence of adductor muscle denervation.58 Successful symptom relief followed surgical release of the fascia overlying the adductor brevis. Outside of this scenario, the obturator nerve can be injured secondary to trauma, but it is rarely injured in isolation except in an iatro-

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genic situation. This nerve can be injured with pelvic trauma/ fractures or in childbirth as a result of compression between the head of the infant and the pelvic wall during prolonged labor. Stretch or compression during hip or pelvic surgery is another source of injury.51,59 The anterior branch of the obturator nerve may be entrapped in fascia as it passes over the adductor brevis, leading to a tethering of the nerve and making it more prone to injury due to traction. Retroperitoneal hemorrhage and pelvic tumors have both been reported to result in obturator neuropathies as well. When induced by exercise, the pain often begins in the adductor muscle origin and radiates distally into the medial thigh. The athlete may feel that the leg is not “propelling” appropriately during running, but anesthesia is uncommonly reported. For persistent neuropathies, sensory alteration of the medial thigh is the most common presenting symptom. Medial thigh and groin pain, however, is also frequently cited. Aching within the adductor region at the pubic bone, which extends down the medial thigh proximal to the knee, can occur as well. Maneuvers that tighten the fascia, including abduction or extension of the leg, tend to exacerbate symptoms. Weakness of adduction is also seen and can rarely progress to atrophy. Severe weakness of adduction and internal rotation can lead to a circumducting gait with an externally rotated and abducted leg.46

Injury and Compression Neuropathy in the Lower Extremity

Fig. 13.31 Care is taken not to injure any small distal nerve branches when releasing the transverse crural ligament. (a) Orientation and release of left superficial peroneal nerve. (b) A small branch of the superficial peroneal nerve is visualized deep to the transverse crural ligament (yellow arrows). (c) Release of the transverse crural ligament exposes this branch.

13.13.2 Surgical Anatomy

13.13.3 Diagnosis

After coalescence of the anterior branches of the anterior primary rami of L2, L3, and L4, the obturator takes form within the substance of the psoas and emerges from the medial border beneath the common iliac vessels at the level of the sacroiliac joint. It runs along the medial border of the psoas and over the pelvic brim, then courses along the lateral border of the lesser pelvis to enter the obturator foramen.60 This is a limited canal consisting of the bony foramen, the internal and external obturator muscles, and their membranes. At this level, the nerve divides into several branches: anterior, posterior, a branch that innervates the immediately adjacent external obturator muscle, and another articular branch. The anterior branch descends anterior to the external obturator muscle and adductor brevis and deep to the pectineus and adductor longus muscles. At this point, it gives off motor branches distal to the obturator foramen that supply the adductor brevis, longus, and gracilis muscles. The nerve terminates in the subsartorial plexus, where it coalesces with branches of the anterior femoral cutaneous and saphenous nerves. The posterior branch travels through the external obturator and innervates it during this course. It then runs between the adductor brevis and adductor magnus, innervating this muscle as well. The remaining portion of the nerve consists of a sensory branch, which terminates at the knee joint.

MRI may be useful in documenting the adductor atrophy, but it has not been found to be of value in identifying the entrapped nerve of the fibro-osseous tunnel. Electrodiagnostic studies are useful in this entity. Demonstration of denervation within the adductor muscles without similar effects in quadriceps or other adjacent muscles is pathognomonic. A nerve block can be applied to the obturator foramen using fluoroscopy. This can be useful both in confirming an electrodiagnostically silent lesion, by reproducing the paresthesias and ruling out other sources of groin pain. Additionally, a good response to such a nerve block is often indicative of a good response to surgery.61 Conservative therapy may include physical therapy to improve strength and preserve mobility, NSAIDs, rest, activity modification, massage, and nerve blocks. Those who presented with an acute onset of symptoms tend to respond well to conservative measures, whereas those with chronic symptoms fare less well. Surgery is indicated in those with pain and weakness that fails to respond to conservative measures.61

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13.13.4 Surgery To decompress the nerve, a 3-cm oblique incision is made over the lateral aspect of the adductor longus, parallel to the inguinal crease just distal to the pubic tubercle. Careful sub-

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Fig. 13.32 Markings for the horizontal release of the superficial fascia. The superficial fascia that was released along the fat landmark and the superficial peroneal nerve is horizontally marked in purple for release to relieve possible tensile force.

cutaneous dissection is undertaken, and the saphenous vein is identified, looped with a vessel loop, and retracted laterally. The fascia of the adductor and pectineal muscles is exposed. The fascia along the lateral border of the adductor is then opened, and the interval between this muscle and the pectineus is developed. Within this interval, on the surface of the adductor brevis, the anterior branch of the obturator nerve is seen within the thick fascia of this muscle (▶ Fig. 13.10). This fascia is then divided in line with the nerve. The branches are traced proximally under the pectineal muscle. Traversing vessels (usually branches of the medial circumflex femoral artery) should be coagulated and divided. At the level of the foramen, the surgeon carefully inserts a finger, being wary of rupturing vessels in this region. This is used to bluntly open the foramen. Once this is completed, hemostasis is obtained, and the incision is closed in the usual fashion. For iatrogenic injuries from pelvic surgery, we have nerve grafted from the proximal injury in the deep pelvis to the distal exposure in the medial thigh.

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13.13.5 Results Again, reports of surgical decompression of obturator compressive neuropathies are rare. Kitagawa et al reported relief of symptoms in six patients undergoing decompression, with im-

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provements in pain, paresthesia, and adductor strength.62 Good results, with return to competition, were achieved in athletes with surgical decompression of the obturator nerve.58

13.14 Common Peroneal Nerve 13.14.1 Historical Review The common peroneal nerve is particularly susceptible to injury due to its superficial location, as it lies subcutaneously over the fibular neck and is the most commonly injured peripheral nerve of the lower extremity.1,63 In its fixed location upon the hard surface of the fibula, it is particularly susceptible to direct trauma or laceration. Compression from simply crossing the legs or squatting or from surgical positioning is at times enough to result in an injury to this nerve. Known sources of foot drop have included plaster casts, leg braces, and tight bandages that compress the nerve at its superficial position over the fibular neck.64 Knee fractures, ligamentous knee injuries, and even surgical arthroplasty can all injure this nerve as a result of traction due to its relative immobility.63,65 Nontraumatic sources include masses such as ganglion cysts arising from the tibiofibular joint or even rarer lesions, such as nerve sheath tumors, lipomas osteomas, and bone calluses. It is associated with weight loss, prolonged hospital stay, and prolonged operative procedures.

Injury and Compression Neuropathy in the Lower Extremity

Fig. 13.33 Horizontal release of the superficial fascia. The superficial fascia is released horizontally to completely relieve possible compression.

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Fig. 13.34 Superficial peroneal nerve release. The superficial fascia posterior to the superficial peroneal nerve is also released to relieve compressive force to complete the decompression of the superficial peroneal nerve. The nerve distal has a course over the extensor digitorum longus.

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Fig. 13.35 This patient had pain following an inversion ankle sprain and developed severe neuropathic pain following ankle reconstruction. (a) Regions of different type of pain on the left ankle. (b) Surgical management included a common peroneal nerve release with exploration of the lateral sural nerve, superficial peroneal nerve, and sural nerve. (c) The involved superficial peroneal nerve was proximal transposed. (d) The involved sural nerve was proximal transposed. The proximal nerve is “crushed” with a hemostat to make an axonotemetic injury. Following this surgical management, the patient reported significant relief of neuropathic pain. Used with permission from Watson CP, Mackinnon SE. Nerve resection, crush and re-location relieve complex regional pain syndrome type II: a case report. Pain. 2014; 155(6):1168-1173.

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Given that it is a known area of nerve compression, it is seen with increasing frequency in surgical patients with subclinical predisposition to entrapment following lower extremity procedures, especially knee surgery. Also, patients with sciatic nerve traction or stretch following hip surgery may experience compression at the fibular head as the nerve regenerates distally. If patients demonstrate a positive Tinel sign or scratchcollapse test, they can often be helped with simple decompression at the fibular head.

13.14.2 Surgical Anatomy As discussed above, after contributing to the lumbar plexus, the remaining L4 and L5 anterior rami fuse, forming the lumbosacral trunk. These each divide into anterior and posterior divi-

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sions, and the posterior contributions of L4–S2 come together to form the common peroneal nerve. This nerve merges with the tibial nerve and travels together through the thigh, forming the sciatic nerve. Proximally, the sciatic nerve sends branches to the short head of the biceps femoris muscle. Just proximal to the popliteal fossa, the peroneal nerve again diverges from the tibial nerve. Following the course of the tendon of the biceps femoris, the nerve courses over the lateral head of the gastrocnemius and then dives under the edge of the peroneus longus muscle on the surface of the fibula. At this point, the nerve enters a tunnel formed by the two heads of the peroneus longus. The posterior edge of the peroneus longus, under which the nerve passes, can be thick and fibrous, resulting in a constriction point between this and the lateral edge of the fibula (▶ Fig. 13.11). We consider this tendinous leading edge, also

Injury and Compression Neuropathy in the Lower Extremity

Fig. 13.36 Deep peroneal nerve in relation to the extensor hallucis brevis (EHB). Over the juncture of the first and second metatarsals with the first and second cuneiform bones, the deep fascia is released, and crossing branches of the superficial peroneal nerve are preserved. The EHB tendon is excised. The fascia binding the sensory branch of the deep peroneal nerve to the bone is released and the nerve is decompressed proximally. (Used with permission from Mackinnon SE, Dellon AL, eds. Surgery of the Peripheral Nerve. New York, NY: Thieme; 1988:332.)

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known as the posterior crural intermuscular septum, to be the main entrapment point of the common peroneal nerve. Both Shizhen et al and Sunderland and Bradley note the distinct anatomical changes that take place within the nerve as it passes from the popliteal fossa to the edge of the fibular head.66,67 These changes include a dramatic increase in both the connective tissue component of the nerve (51 to 68%) and the corresponding number of fascicles.23,48,66,67 Similar changes are not demonstrated in the tibial nerve at this level. Conversely, the amount of strain the common peroneal nerve can withstand prior to rupture is less than the tibial nerve in this same region, making it more susceptible to injury.67 Intraoperatively, the predisposition at the knee to traction can be noted with in-

creased tension on the peroneal nerve with knee extension and decreased tension with knee flexion (▶ Fig. 13.11). After passing the leading edge of the peroneus longus, the next potential site of entrapment corresponds to the fascial septum between the peroneal and tibial anterior muscles known as the anterior crural intermuscular septum (▶ Fig. 13.12). As this nerve continues distally in the lateral compartment of the leg, it becomes superficial, piercing the crural fascia to become the dorsal cutaneous nerve at the distal third of the leg. Similarly, the deep peroneal nerve immediately gives off branches to the tibialis anterior after passing the fibrous edge of the peroneus longus. These branches keep the proximal aspect of this nerve branch tightly tethered in its position under the peroneus

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Injury and Compression Neuropathy in the Lower Extremity

Fig. 13.37 Deep peroneal nerve release in the foot. (a) The extensor hallucis brevis (EHB) can compress the deep peroneal nerve with its distal insertion. (b) Dividing the EHB will expose and decompress the deep peroneal nerve in the foot.

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Fig. 13.38 Identifying the tibial nerve in the lower leg. The tibial nerve is identified by dissecting between and retracting the lateral and medial heads of the gastrocnemius in the posterior and superior aspect of the lower leg. The tibial nerve courses deep to the soleus and its tendinous arch.

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Injury and Compression Neuropathy in the Lower Extremity

Fig. 13.39 Identifying the tendinous arch of the soleus. Further dissection, between the retracted lateral and medial heads of the gastrocnemius, reveals the tendinous arch of the soleus. The appearance of the tendinous arch describes its compressive nature with the sharp arch.

longus, as does its trajectory through the anterior intermuscular septum. This branch then continues distally in the anterior compartment of the leg, innervating the extensor hallucis longus, followed by the extensor digitorum longus (EDL) and the peroneus tertius. Although this is the most common anatomical orientation, numerous variations exist. For example, peroneus longus branches can originate from the common peroneal trunk, the deep peroneal branch, the superficial peroneal branch, the accessory deep peroneal branch, or all of these.68 Topography within the common peroneal nerve has been debated. Several centimeters proximal to the fibular neck, the common peroneal nerve can be dissected into an anterior and posterior component. The anterior group generally will become the deep peroneal nerve, while the posterior group becomes the superficial peroneal nerve. Our experience has been that as these fascicles approach the peroneus longus, the most superficial group of fascicles will remain anterior and will likely innervate the tibialis anterior as well as the joint. 1 Excellent anatomical work by Kudoh and Sakai followed the “streams” of functional fibers into the thigh.68 At the top of the popliteal fossa, the common peroneal stream could be reliably subdivided into deep peroneal, accessory deep peroneal and one or two sensory “streams.” In agreement with the discussion above, the most common scenario consisted of an anterior bundle corresponding to the deep peroneal nerve and a posterior bundle corre-

sponding to the remaining groups, the variant of this being that a sensory component occasionally accompanied the deep peroneal bundle. The accessory deep peroneal reliably innervates the peroneus brevis and provides sensation to the ankle. The superficial sensory branch of the peroneal nerve frequently has two branches, and the posterior branch is frequently missed. Both can travel in very long (up to 18 cm) fibrous tunnels. The deep peroneal nerve can be entrapped by the short extensor to the great toe.

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13.14.3 Diagnosis Manual testing of ankle dorsiflexion and eversion is the initial assessment for function in this territory. Patients with common peroneal nerve compression present with a drop foot, in most necessitating an ankle–foot orthotic. Additionally, patients may present with pain or a positive Tinel sign or scratch-collapse test at one of the compression points.69 Paresthesia on the lateral aspect of the leg and dorsum of the foot (superficial peroneal) or in the first web space (deep peroneal) may also be present. Like all chronic compression neuropathies, symptoms may slowly progress from subtle weakness with tripping and falls to complete foot drop. The pain associated with superficial and deep peroneal nerve entrapment can be severe. Lateral sural nerve compression can result in pain in lateral calf.

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Fig. 13.40 Decompression of the tibial nerve at the soleus. Decompression of the tibial nerve at the soleus at multiple locations along the arch occurs by releasing the tendinous arch of the soleus and performing a step-lengthening/tenotomy on the soleus tendon that is found compressing the tibial nerve.

Fig. 13.41 Foot posture and relevance to tarsal tunnel syndrome. (a,c) Patients with tarsal tunnel syndrome can exhibit abnormal foot posture with a pronated foot and flattened medial arch. Provocative tests such as the scratch-collapse will test positive at the tarsal tunnel. (b,d) Patients can induce a medial arch by slightly inverting the foot to normal aid flexing toes. This small change in foot posture will cause the scratch-collapse test to become negative. As results, patients undergo physical therapy to restore normal foot posture prior to the release of the tarsal tunnel.

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13.14.4 Surgical Technique

Fig. 13.42 Calcaneal branch patterns from posterior tibial nerve. Pattern of origin of medial calcaneal nerve from tibial nerve in 20 patients. (Used with permission from Dellon AL, Mackinnon SE. Tibial nerve branching in the tarsal tunnel. Arch Neurol. 1984;41:645-646.)

Decompression of the peroneal nerve can be performed under general anesthesia or epidural analgesia. We prefer exsanguination and tourniquet for optimal visualization. The patient is positioned in the supine position with the foot propped on a sand bag, keeping the knee bent (▶ Fig. 13.13). An oblique incision, just inferior to the fibular head and oriented from posterior-proximal to anterior-distal, is made along the course of the nerve. Marking the incision correctly is the most critical part of the procedure. Most surgeons inexperienced with this release tend to make the incision too proximal, or in the correct position inferior to the fibular head but too short. The incision needs to be extended more distally than most anticipate. Palpation of the fibular head prior to designing an incision immediately below it is paramount. Dissection is taken through the subcutaneous fat, and the underlying fascial expansion from the biceps tendon and iliotibial tract is divided, being careful to avoid the lateral cutaneous branch or peroneal contribution of the sural nerve (▶ Fig. 13.14). The common peroneal nerve is identified at the posterior edge of the peroneus longus, usually covered in a layer of yellow fat (▶ Fig. 13.15).

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Fig. 13.43 Anatomical landmarks for tarsal tunnel release. Sites of posterior tibial nerve compression extending from proximal to the medial malleolus onto the plantar aspect of the foot. Note the posterior tibial nerve entering the tarsal tunnel at its narrow proximal end, splitting into the medial and lateral plantar nerves, which then go through two separate tunnels. (a) Incision marking. Our approach is to use two incisions, leaving an intact short skin bridge. (b) Flexor retinaculum anatomical reference. (c) Abductor hallucis muscle anatomical reference. (Used with permission from Mackinnon SE, Dellon AL. Homologies between the tarsal and carpal tunnels: implications for surgical treatment in the tarsal tunnel syndrome. Contemp Orthop. 1987;14:75-78.)

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Fig. 13.44 Septum separating the medial and lateral plantar tunnels. Cross section through the distal portion of the tarsal tunnel demonstrating the separate tunnel for the medial and lateral plantar nerves. Note the roof of the tunnel composed of ligamentous origin from the calcaneus of the fascia giving rise to the abductor hallucis and that over the lateral plantar nerve continuing distally as the plantar aponeurosis. (Used with permission from Mackinnon SE, Dellon AL. Homologies between the tarsal and carpal tunnels: implications for surgical treatment in the tarsal tunnel syndrome. Contemp Orthop. 1987;14:75-78.)

Fig. 13.45 Provocative scratch-collapse test assessing the tarsal tunnel. (a) The patient resists internal rotation by the examiner with the arms by the patient’s side and elbows flexed at 90 degrees. (b) The examiner palpates the specific area of examination, the tarsal tunnel in this case. (c) With a positive scratch collapse, the patient will collapse at the same side of examination during an attempt to resist internal rotation following palpation. (d) Areas of palpation along the tarsal tunnel for the scratch collapse.

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The nerve can be palpated and rolled beneath the finger easily. Once identified, a cut in the superficial fascia of the peroneus longus directly over and in line with the trajectory of the nerve is undertaken for 1 to 2 cm (▶ Fig. 13.16; ▶ Fig. 13.17). Once this fascia is opened, the underlying muscle is retracted anteriorly with a small retractor, revealing the leading edge of the fascia and the deep fascia (▶ Fig. 13.18). With the muscle held in the retracted position, the surgeon carefully divides the posterior fascia of the peroneal longus, which is the tendinous leading edge most commonly implicated

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in common peroneal nerve compression (▶ Fig. 13.19). In patients with large soleus muscles, a trough can be cut in the muscle to allow the common peroneal nerve to lie flat and not be “tented” by the muscle (▶ Fig. 13.20). The incision should be extended to reveal the anterior tibial muscle, which can be assessed for viability and to rule out an associated compartment syndrome. Another potential source of compression is the intermuscular septum between the peroneus longus and EDL. Lifting this with forceps, the surgeon divides the fascia superficial to deep, being careful not to cut branches of the underlying nerve and injure accompanying small vessels, which would

Injury and Compression Neuropathy in the Lower Extremity

Fig. 13.46 Operative technique for release of tarsal tunnel. (a) Our approach for the tarsal tunnel release involves two incisions, leaving an intact short skin bridge (not depicted here). This single curved-S incision is our old approach. (b) Exposure through the superficial fascia allows the identification of the flexor retinaculum. (c) Transection of the flexor retinaculum release of the tibial nerve through the tarsal tunnel. (Used with permission from Mackinnon SE, Dellon AL, eds. Surgery of the Peripheral Nerve. New York, NY:Thieme;1988:311.)

require microbipolar cautery close to the small intermuscular nerve branches (▶ Fig. 13.21). There is an additional intermuscular septum that may compress the peroneal nerve distally. This intermuscular septum is located between the EDL and tibialis anterior (▶ Fig. 13.22). Although this septum is similar to the anterior crural intermuscular septum, it is often less tendinous in comparison and is released following the described format for the anterior crural intermuscular septum (▶ Fig. 13.23). Once released, the nerve can be lifted to reveal an underlying fascial band, which can be identified just proximal to the peroneus longus leading edge at the fibular head. With the nerve lifted, this too is incised and released. Once completely released, the distal portion will retract inferiorly, demonstrating the complete separation. The nerve is then followed under the peroneus longus until it divides into the deep and superficial branches. These are followed several centimeters into the extensor muscles to ensure that no additional fascial constraints are present.

13.14.5 Results We have been very happy with the results of decompression of the common peroneal nerve and perform this operation frequently.70 Others have also noted complete recovery in twothirds of patients with decompression alone; results improved with concomitant tibialis tendon transfer.71 However, surgical outcome was also dependent on the etiology of the nerve injury, with sharp injuries and knee dislocations showing improved results compared to crush injuries and gunshot wounds.71 Neurolysis has also been recommended, in addition to decompression, following knee dislocations.72 Our comment on neurolysis is that it is a technique that we routinely use when there is excessive scarring in the epineurium from previous surgery or trauma. In primary compression neuropathy, it is not necessary or advised. When there is scarring of the nerve, we do a graded neurolysis to allow us to see the bands of Fontana (see Chapter 1) implying redundancy of the nerve fibers.

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Fig. 13.47 Operative technique for release of the medal and lateral plantar tunnels. The release of the medial and lateral plantar tunnels involves dividing the tendinous fascia over the tunnels within the abductor hallucis muscle. A septum separates the two tunnels. (Used with permission from Mackinnon SE, Dellon AL, eds. Surgery of the Peripheral Nerve. New York, NY:Thieme 1988:312.)

13.15 Superficial Peroneal Entrapment 13.15.1 Historical Review

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Fig. 13.48 Incision and positioning. Our approach for the tarsal tunnel release involves two incisions. The first incision is on the posterior third of the medial aspect of the lower leg over the course of the tibial nerve. The second incision is at an angle on the foot over the course of the lateral planter branch of the tibial nerve. In our experience, the two linear incisions help promote healing following the release by leaving an intact short skin bridge.

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In 1960, Kopell and Thompson suggested that the site where the superficial peroneal nerve pierces the deep fascia in the distal leg, which had previously been assumed to be a source of painful muscular herniation, may actually result in pain due to compression of the emerging nerve rather than the muscle itself.57,73 In fact, athletes who develop increased pressure in the anterolateral compartment of the leg often experience pain attributable to compression of the superficial peroneal nerve at this location, similar to a transient compartment syndrome.74– 76 We believe that “growing pains” and some shin splint symptoms may be related to peroneal nerve compression as well.

13.15.2 Surgical Anatomy After emerging distal to the peroneus brevis muscle, the superficial peroneal nerve becomes more superficial until it pierces the deep fascia of the leg, usually ~ 12 cm proximal to the lateral malleolus. At this point, it most commonly divides into medial

Injury and Compression Neuropathy in the Lower Extremity

Fig. 13.49 Exposure and identification of the flexor retinaculum through the proximal incision. In the proximal incision, the exposure continues through the superficial fascia to identify the tibial vein. It is easier to first identify the “blue” vein than the “white” nerve. Deep to this vein, the tibial nerve is identified. In continuation and distal to the superficial fascia, the flexor retinaculum is identified. An aberrant muscle was present in this patient that was deep to the superficial fascia and flexor retinaculum. This muscle is divided.

and intermediate branches at the level of the inferior retinacular ligaments. There is some variability to the course of the superficial peroneal nerve, and both branches in patients with compression often travel in separate fibrous tunnels, typically up to 18 cm in length.74,77

13.15.3 Diagnosis Sensory deficit of the dorsum of the foot or lateral lower leg without corresponding weakness of the peroneus muscles is the hallmark of this entrapment. Pain is aggravated by forceful inversion of the foot, which causes traction of the nerve against its point of tethering as it pierces the deep fascia of the distal leg. Often the patient does not experience symptoms until strenuous or repetitive use of the leg ensues. In this case, sensory abnormalities may not be discernible at the time of evaluation. Examination may also reveal a bulging muscle at the expected site of the fascial defect that becomes more prominent with dorsiflexion. Even in the absence of this finding, a Tinel sign or scratch-collapse test within the expected region of this defect may be discernible.78 Of note, in patients with potential entrapment of the peroneal nerve at multiple sites, it can be difficult to ascertain whether potential compression sites are involved or whether

the nerve is simply aggravated by the more proximal compression. One useful tool to establish compression at multiple sites is the hierarchical scratch-collapse test. Ethyl chloride is used to topically numb an area that has proven positive with the scratch-collapse test. Following its application, patients will no longer collapse at that site. Examination of other potential compression sites will then collapse, while the primary site is numb. We have found that, using this technique, it is possible to ascertain the hierarchy of compression sites for a given nerve by numbing the sites that collapse and then continuing to test additional sites once the others are numb. Once the ethyl chloride has worn off, collapse at the original site will return. 78 Pain may radiate proximally up the front of the leg, occurring without the motor deficits that are evidence of entrapment at the fibular head. Nerve conduction studies may be useful in demonstrating a local conduction defect along the course of the superficial peroneal nerve in the absence of findings at the fibular head. Normal function of the extensor digitorum brevis (EDB) is expected with preserved first web space sensation.

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13.15.4 Surgical Technique If a muscle bulge is identified, this should be marked preoperatively and a longitudinal incision centered over this. In the

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Fig. 13.50 Release of the proximal flexor retinaculum and identification of the tibial nerve. The flexor retinaculum is proximally divided as far distally as the exposure will allow. The distal release of the flexor retinaculum will occur through the distal incision. The tibial nerve is identified deep to the tibial vein.

absence of this finding, the incision should be made two fingerbreadths lateral to the apex of the tibia centering over the region 10 to 12 cm proximal to the lateral malleolus (▶ Fig. 13.24). The incision can then be extended proximally or distally as necessary and is typically long (~ 18 cm). Once the subcutaneous tissue is cleared and the fascia defined, two linear septa are usually identified (▶ Fig. 13.25). The more medial usually contains a notable yellow “fat stripe.” The septum just lateral to this contains the nerve (▶ Fig. 13.26). The fascia in this location is divided longitudinally, revealing a V-shaped interfascial space within which this nerve runs (▶ Fig. 13.27). The nerve is followed distally, ensuring that no fascial entrapment remains (▶ Fig. 13.28). Care is taken to completely decompress the nerve proximally and distally and not to injure any small branches of the nerve, especially where it pierces the fascia and branches into the subcutaneous tissue (▶ Fig. 13.29; ▶ Fig. 13.30; ▶ Fig. 13.31). We also divide the fascial septum longitudinally and transversely with two to four cuts to completely loosen the fascial tunnel (▶ Fig. 13.32; ▶ Fig. 13.33). Thus, fasciotomy of the anterior and lateral compartment is typically included (▶ Fig. 13.34).

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13.15.5 Results Similar to fasciotomies for documented compartment syndrome, surgical decompression of the superficial branch of the peroneal nerve has met with reasonable success. Case studies report relief of pain, return of sensation, and return to athletic activity.79,80 In our experience with this patient population, frequently decompression at all three sites is performed in order to successfully relieve pain. In select cases, we have encountered traumatic injury to the lateral aspect of the ankle that results in neuropathic pain. These cases have been a challenge to manage due to their involvement of the multiple nerves rather than a single nerve. We could describe this type of case as similar to a radial sensory nerve injury in the upper extremity, where the lateral antebrachial cutaneous nerve can be involved and have an overlapping sensory territory with the radial sensory nerve. In these ankle injuries, a detailed examination is performed with the superficial peroneal nerve and sural nerve in mind to determine their involvement. Typically, the sural nerve has a neuroma and the superficial peroneal nerve may as well. These neuromas are excised and the nerves transposed. Compressed nerves are just released. Pain in the lateral calf may be compression of the lateral sural nerve (▶ Fig. 13.35).

Injury and Compression Neuropathy in the Lower Extremity

Fig. 13.51 Exposure and identification of the lateral plantar tunnel and the superficial fascia of the abductor hallucis. In the distal incision, a cutaneous branch of the medial plantar nerve is identified and protected upon exposure. The tendinous superficial fascia of the abductor hallucis is identified. Proximal and deep to this muscle, the lateral plantar tunnel is identified with the course of the tibial vessels. A septum is identified anterior to this tunnel and posterior to the medial plantar tunnel.

If these nerves were found to be involved, an appropriate surgical management would include proximal transposition of the superficial peroneal nerve and sural nerve, common peroneal nerve decompression, and exploration of the lateral sural nerve. The appropriate technique for a proximal transposition to resolve neuropathic pain is further described in the pain chapter and includes a proximal crush, cautery distal end cap, and proximal transposition. This set of surgeries has been successful in relieving significant pain from a case of a traumatic ankle injury that failed several attempts at surgical reconstruction. 81

13.16 Deep Peroneal Nerve 13.16.1 Historical Review In 1968 Marinacci82 described an entrapment beneath the extensor retinaculum over the anterior aspect of the ankle, which he referred to as “anterior tarsal tunnel syndrome.” This syndrome is characterized by a triad of weakness, pain, and sensory changes of the foot and ankle, specifically, in the first web space.83 We also describe, in addition, a second important site of entrapment of this nerve under the tendon of the extensor hallucis brevis (EHB) at the junction of the first and second cuneiform bones with the metatarsals. This entity has also been described with distal third tibia fractures.84

13.16.2 Surgical Anatomy Approximately 2.5 cm above the ankle, the distal deep peroneal nerve emerges from beneath the belly of the extensor hallucis longus muscle, lateral to its tendon (and usually the anterior tibial artery) and medial to the tendon of the EDL. The nerve passes under the superior, then inferior limb of the Y-shaped extensor retinaculum, where it divides into a medial and lateral branch. The division into these limbs occurs at the medial edge of the extensor digitorum tendons. These limbs then become the supero- and inferomedial limbs of the extensor retinaculum. Under the inferomedial limb, the talonavicular joint is a common location for compression of the deep peroneal nerve in plantar flexion. The medial branch of the deep peroneal nerve emerges from the extensor retinaculum and follows the dorsalis pedis artery until it terminates to provide sensation to the first web space, or potentially more of the dorsal surface of the medial two toes. The lateral branch passes laterally under the inferior limb of the extensor retinaculum, following which it innervates the EDB muscle from its deep surface. The nerve passes deep to the tendon of the extensor hallicus brevis. It crosses from a medial to lateral position with respect othe artery as it travels distally below the tendon.

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Fig. 13.52 Incision of the superficial fascia of the abductor hallucis. To expose the abductor hallucis, the tendinous superficial fascia is incised longitudinally along the course of the lateral plantar tunnel.

13.16.3 Diagnosis Patients with entrapment at these locations most commonly complain of aching or pain in the dorsum of the foot. Symptoms are usually aggravated with walking and relieved at rest. Sensation may be diminished in the distribution of this nerve compared to the surrounding territories. Tenderness to pressure, a positive scratch-collapse test, and a Tinel sign may be elicited over the nerve at the sites of entrapment, under the inferior limb of the extensor retinaculum or more distally, where it is compressed by the short extensor tendon to the great toe. Additionally, by resisting toe extension of both feet, asymmetry of the EDB may at times be noted. If this is present, the examiner should be aware that the primary site of compression must be the more proximal of the two. Electrodiagnostic testing is not helpful for diagnosis. Instead, a local anesthetic nerve block can be used to confirm the diagnosis. After injecting 3 mL of 1% lidocaine proximal to the site of the Tinel sign and waiting 15 minutes, the patient should be able to walk and stand on his or her toes without pain. If incomplete relief of pain is found, a more proximal associated site should be considered.

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13.16.4 Surgical Technique With the patient positioned supine, the limb is exsanguinated, and a tourniquet is applied on the thigh. A 3-cm incision is

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made between the extensor hallucis longus and EDL tendons over the course of the nerve. After coming through the subcutaneous tissue and carefully protecting the superficial peroneal nerve branches, we visualize the underlying tendons and fascia, then divide the supero- and inferomedial limbs of the extensor retinaculum. After exposing the superficial fascia, this is divided, and the tendon of the EHB is exposed (▶ Fig. 13.36; ▶ Fig. 13.37). The segment of this tendon overlying the nerve is then excised. The nerve is seen passing deep to this structure. Under this, a deep fascial layer is also found overlying the deep peroneal nerve and the dorsalis pedis artery, holding them flush to the underlying metatarsals. This is unroofed to relieve compression. Careful observation is made to exclude the contribution of a ganglion, bone spur, or adhesion of the nerve to adjacent structures. If one of these etiologies is visualized, appropriate dissection and excision of the culprit is undertaken.

13.17 Sural Nerve 13.17.1 Surgical Anatomy The sural nerve descends into the lower leg between the two heads of the gastrocnemius muscle. As it descends, it becomes more superficial and courses lateral to the tendocalcaneous region midway between the tendo-Achilles and the lateral malleolus. It courses with the short saphenous vein for the majority

Injury and Compression Neuropathy in the Lower Extremity

Fig. 13.53 Identification of the deep compressive fascia of the abductor hallucis. The abductor hallucis muscle is retracted distally and off the deep fascia of the abductor hallucis to expose the tendinous leading edge of the lateral plantar tunnel. This tendinous fascia deep to the abductor hallucis is divided to decompress the lateral plantar branch of the tibial nerve.

of its length. The sural nerve supplies sensation to the posterolateral lower leg and the lateral border of the foot. The common sural nerve is the coalescence of the lateral sural nerve, a branch of the common peroneal nerve, and the medial sural nerve, a branch of the tibial nerve. The common peroneal nerve proximal to the fibular neck gives off the lateral sural branches, which supply sensation to the lateral calf to the lateral aspect of the fifth toe. The medial sural nerve is given off the posterior tibial nerve and provides sensation to the lateral ankle, heel, and fifth toe. These nerves coalesce in most patients ~ 16 cm proximal to the lateral malleolus, either superficial or deep to the fascia. Our findings have confirmed that the lateral cutaneous nerve of the calf can become entrapped as it travels from the popliteal fossa through the fascia that joins the iliotibial tract to the deep fascia of the leg. Another potential site of compression is distally, where the nerve penetrates the fascia overlying the gastrocnemius muscle. This anatomy is highly variable. Nonsurgical management appears successful; however, compression of the sural nerve is an uncommon entity that is rarely reported in the literature. Sural neuromas, by contrast, are common, as is harvest of the sural nerve for graft or nerve biopsy. Although sural nerve biopsy is common, it can also be associated with morbidity. As our understanding of the

internal topography of peripheral nerves increases, so does our ability to more intelligently provide expendable motor and sensory nerve biopsies from both the upper and lower extremities. We advocate for these nerve biopsies to be performed by surgeons trained in the nuances of peripheral nerve surgery rather than general surgeons, as is the current practice. Management of sural neuromas is described in Chapter 20, but in general it involves identification of the sural nerve through a proximal, longitudinal incision, proximal clamping of the nerve, distal neurectomy and/or neuroma excision, and cauterization. The proximal nerve can then be transposed into muscle. The medial and lateral sural nerves are neurolyzed from each other so they can be transposed proximally at their own depths. Typically the lateral sural follows a more superficial path than the deeper medial sural.

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13.18 Tibial Nerve 13.18.1 Historical Review Compression of the tibial nerve at the leading edge of the soleus muscle is a relatively newly recognized entrapment. The soleal sling, or tendinous leading edge, of the soleus lies deep to the

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Fig. 13.54 Dividing the entire length of the deep fascia of the abductor hallucis. The deep fascia of the abductor hallucis is divided to expose the lateral plantar tunnel and decompress the lateral plantar branch of the tibial nerve. This nerve is found deep to the tibial vein. The surgeon is looking distally down the tunnel and retracting distally.

gastrocnemius muscles and has been shown to compress the tibial nerve following trauma.85 We have recently identified several patients presenting with calf pain, exacerbated by exercise. Similar to the relationship between the tendinous leading edge of the flexor digitorum superficialis and the median nerve in the volar forearm, the leading edge of soleus can compress the tibial nerve, causing transient ischemic symptoms. The scratchcollapse test can be helpful in identifying this entrapment, but rather than a light “scratch,” deep pressure over the entrapment site is needed because it is located deep in the calf. The patient will also have tenderness at this level, as compared to the contralateral leg. A Tinel sign is usually negative, likely due to the overlying muscle bulk.

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13.18.2 Surgical Anatomy The tibial nerve has contributions from L4 to S3 and is a branch of the sciatic nerve. It enters the lower leg after traveling through the popliteal fossa between the two heads of the gastrocnemius muscle. The nerve lies deep to the soleus muscle in the deep posterior compartment of the lower leg. It lies between the flexor digitorum longus and the flexor hallucis longus, before traveling behind the medial malleolus and into the tarsal tunnel.

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13.18.3 Surgical Technique The patient is positioned prone on the operating room table with an above-knee tourniquet. A gentle curvilinear incision is made just distal to the popliteal fossa over the junction of the proximal third/lower two-thirds of the lower leg and consistent with the origin of the soleus muscle. Care is taken to avoid injury to the lesser saphenous vein and the sural nerve, which travel just superficial to or within the gastrocnemius fascia and muscle. The midline raphe of the gastrocnemius is bluntly dissected proximally and further divided using microbipolar cautery distally to reveal the tendinous leading edge of the soleus muscle (▶ Fig. 13.38; ▶ Fig. 13.39). The nerve can be visualized as it passes beneath this tendinous edge, and multiple radially oriented releasing incisions are made in this leading edge to relieve compression from the nerve (▶ Fig. 13.40). Care should be taken to avoid damage to the posterior tibial artery, which runs with the tibial nerve. The surgeon passes a finger distally along the nerve to ensure that no further points of constriction are palpable. There is no need to reapproximate the gastrocnemius muscle following release. Fastidious control of hemostasis is required, and postoperative mobilization should be limited to prevent hematoma. We use a fibrin glue product and a drain in this region, as well as a pain pump.

Injury and Compression Neuropathy in the Lower Extremity

Fig. 13.55 Further division of the deep fascia of the abductor hallucis. Note the new orientation. The tendinous deep fascia of the abductor hallucis can extend distally, and it is important to identify and release all components of this fascia. The remaining deep fascia of the abductor hallucis is identified and released. The surgeon is now looking proximally up the tunnel from the foot of the table while retracting proximally.

13.19 Tarsal Tunnel Syndrome

13.19.2 Surgical Anatomy

13.19.1 Historical Review

In 1938 Horwitz87 presented the earliest description of the variations in the posterior tibial nerve. He described the terminal plantar nerves as taking their origin from the posterior tibial nerve 3.5 to 4 cm above the medial malleolus, with the more posterior branch giving off one or more calcaneal branches. In 1984 a similar study was undertaken that demonstrated the bifurcation occurring within 1 cm of the malleolar-calcaneal axis in the vast majority, although variations did exist (▶ Fig. 13.42). The calcaneal branching pattern was much more variable, originating either within or proximal to the tarsal tunnel and rarely emerging directly from the medial plantar nerve. The latter configuration can predispose to injury during release as this branch would run superficially over the lateral plantar branch, possibly being mistaken for additional fascia. The roof of the tarsal tunnel is formed from the thickening of the deep lower leg fascia, which becomes the flexor retinaculum, running from the medial malleolus to the calcaneus (▶ Fig. 13.43). The posterior tibial nerve enters the tarsal tunnel with the tendons of the tibialis posterior, flexor hallucis, and the FDL. After emerging from the retinaculum, the nerve divides into its medial and lateral plantar branches. These then each enter separate tunnels formed by fibrous origins (▶ Fig. 13.44). That of the lateral plantar nerve is formed by the origin of the plantar aponeurosis. That of the medial plantar

Kopell and Thompson, in 1960, described the possibility of entrapment of the posterior tibial nerve in the region of the ankle and foot.57 They even provided a figure demonstrating the medial and lateral plantar nerves entering into separate fibrous tunnels. In 1962 Keck coined the term tarsal tunnel syndrome, referring to a compression syndrome affecting the posterior tibial nerve as it passes beneath the flexor retinaculum on its way to the sole of the foot. Although reports have indicated a 90% response rate with division of this fascia alone, most authors now recommend extending the release to include the more distal tunnels of the medial and lateral plantar nerves and the calcaneal nerve as well. Symptoms generally involve the plantar surface of the foot, although most authors include the heel as well. The most common suggested source of this syndrome is trauma to the ankle with secondary swelling. Additionally, arthritis has been found to contribute. More recently, we have recognized the role of foot posture in the development and treatment of tarsal tunnel syndrome. We have used dedicated foot physiotherapists to assist in the management of tarsal tunnel syndrome in patients with the typical pronated ankle posture (▶ Fig. 13.41). Patients are encouraged to “curl” their toes, which re-creates the arch and corrects pronation.

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Fig. 13.56 Exposure and identification of the medial plantar tunnel and the fascia of the abductor hallucis. Note the original orientation. The dissection moves anteriorly to identify the medial plantar branch of the tibial nerve having a course deep to the tendinous fascia of the abductor hallucis through the medial plantar tunnel. A septum is identified posterior to this tunnel and anterior to the lateral plantar tunnel.

nerve is formed by the origin of the abductor hallucis brevis muscle. The division between these tunnels is a fibrous septum that originates from the fibro-osseous canal of the flexor hallucis longus tendon or directly from the calcaneus.

13.19.3 Diagnosis Paresthesias, pain, and numbness in the plantar aspect of the foot form the triad that is the hallmark of tarsal tunnel syndrome.88 Symptoms are usually most pronounced in the toes or beneath the metatarsal heads, but they can involve the heel as well. Occasionally, heel pain is the dominant symptom. This calcaneal branch irritation can be difficult to distinguish from a calcaneal bone spur, which is a common incidental finding in patients over 50 years of age. Tarsal tunnel symptoms can also radiate proximally into the calf region, and this may represent associated tibial nerve compression at the soleus arch. Some patients will complain of their toes “curling” or generalized cramping in their feet. Although perceived weakness is rare, occasionally actual weakness of the abductor hallucis may be discernible on examination, and weakness of the intrinsics can lead to clawing. Symptoms of tarsal tunnel syndrome are generally aggravated by walking or standing and in some patients are worse at night. Recently, the authors have noted that foot posture contributes significantly to tarsal tunnel syndrome, with patients frequently presenting with a unique foot position

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characterized by collapse of the arch and pronation of the ankle (▶ Fig. 13.41). Rest and elevation tend to ameliorate these symptoms, as does correction of the characteristic foot posture by instructing patients to curl their toes and strengthen the intrinsic foot muscles. This results in restoration of the arch and normal ankle posture. Leg trauma, diabetes, hypothyroidism, alcoholism, and chronic lower extremity edema all can predispose to this syndrome. Orthotics can provide a short-term solution; however, they are expensive, uncomfortable, and inconvenient. We try to encourage patients to correct poor foot posture and strengthen intrinsic muscles of their feet, in essence creating their own foot orthotic through foot physiotherapy exercises, just as we treat scapular muscle imbalance associated with thoracic outlet syndrome with physiotherapy and exercise, rather than with scapular taping. Physical examination may reveal swelling posterior to the malleolus with a Tinel sign in this region, particularly where the nerve enters the retinaculum. Additionally, disparate Tinel signs can often be elicited more distally in the medial or lateral plantar nerves, the former radiating into the first toe, and the latter referring to the fifth digit. As noted above, motor examination may reveal weakness or atrophy of the abductor hallucis. Patients with tarsal tunnel syndrome are often misdiagnosed with plantar fasciitis, dorsal sensory neuromas, or Mortos neuroma, although these can occur concurrently. Recurrent symptoms from an incomplete release are also common. The

Injury and Compression Neuropathy in the Lower Extremity

Fig. 13.57 Identification of the tendinous fascia of the abductor hallucis. The leading edge of the tendinous fascia of the abductor hallucis is identified superficial to the medial plantar nerve. This fascia is released to decompress the medial plantar branch of the tibial nerve. The scissors are in the medial plantar tunnel and pushing up against the septum to orient the surgeon and correct tunnel.

authors have found the scratch-collapse test to be extremely valuable in the investigation of tarsal tunnel syndrome, especially given the inconsistencies of electrodiagnostic studies (▶ Fig. 13.45).89–91 We also use the scratch-collapse test to show the utility of correction of poor foot posture by demonstrating that patients can “reverse” the positive scratch-collapse test by simply curling their toes, as described above. This motivates patients to engage in foot exercises. We use this same instruction to correct back and shoulder posture to “reverse” a positive scratch-collapse test over the parascapular muscles in patients with motor imbalance associated with thoracic outlet syndrome.

13.19.4 Surgical Technique With the patient in the supine position, the leg is exsanguinated and a thigh tourniquet is inflated. We routinely use two incisions to break up a longer scar for better wound healing and patient comfort (▶ Fig. 13.46; ▶ Fig. 13.47; ▶ Fig. 13.48). The first incision is based over the tibial neurovascular bundle beginning proximal to the medial malleolus. Keeping adequate distance from the malleolus ensures avoidance of damage to the distal saphenous nerve branches and facilitates identification of the proximal end of the flexor retinaculum (▶ Fig. 13.49). After coming through the subcutaneous tissue, the tibial nerve can be identified coursing with, but

slightly deep to, the vessels, which by nature of the blue-colored veins are easily identified. The flexor retinaculum is divided in its entirety (▶ Fig. 13.50). Once the tibial nerve has been adequately decompressed proximally, the dissection is taken distally through a separate incision based over the abductor muscle (▶ Fig. 13.51). As we dissect through this distal incision, we identify and protect the small cutaneous branch that comes from the medial plantar branch to innervate a small area on the medial plantar aspect of the instep of the foot. This nerve can be easily injured with plantar fascia release surgery. The fascia over the abductor hallucis muscle is divided, and this muscle is then retracted to expose the underlying fascia that forms the roof of this tunnel (▶ Fig. 13.52; ▶ Fig. 13.53). An instrument such as a Freer elevator can be inserted into the tunnel to confirm its trajectory. The roof of the tunnel is then divided, being careful to avoid injury to the nerve or vessels (▶ Fig. 13.54; ▶ Fig. 13.55). Typically, the first tunnel decompressed is the tunnel of the lateral plantar nerve. The medial plantar tunnel is more anteriorly located, and the abductor muscle is similarly retracted to identify the roof of this tunnel, which is then likewise divided (▶ Fig. 13.56; ▶ Fig. 13.57; ▶ Fig. 13.58). An instrument should be inserted into these tunnels once again to ensure that they are fully released and that no residual restriction remains. The septum between the two tunnels can

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Fig. 13.58 Dividing the fascia of the abductor hallucis. The fascia of the abductor hallucis is divided longitudinally along the course of the medial plantar tunnel and as far distally as possible to release the medial plantar tunnel. This will decompress the medial plantar branch of the tibial nerve. The septum that separates the medial and lateral plantar tunnels is seen.

be divided proximally, creating one large tunnel for the two nerves, but this maneuver is not necessary. We also release the proximal plantar fascia and reflect the abductor muscle distally to ensure that we can visualize a complete release of the medial and lateral plantar tunnels. We use a small retractor to reflect our 1-cm skin bridge between the two incisions to ensure complete decompression of the tibial nerve and its distal branches (▶ Fig. 13.59; ▶ Fig. 13.60; ▶ Fig. 13.61). The origin of the calcaneal nerve is identified usually proximally, and this branch is followed distally in its trajectory toward the heel, releasing any constricting fascia along this course. The existence of an accessory calcaneal branch should be considered both to avoid inadvertent transection and to ensure that all branches are adequately decompressed. Injury to this nerve can result in a scar that causes pain and can radiate to the heel.

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13.20 Morton Neuroma 13.20.1 Historical Review Common plantar digital nerve compression was one of the earliest nerve compression entities to be recognized. In 1876 Morton92 published the original description, in which he detailed the clinical presentation of 11 patients with symptoms in the fourth and fifth toes. Classically, this entity involves pain with walking between the third and fourth toes, with the latter being

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the most painful. Morton’s surgical solution involved resection of the fourth metatarsal head, as well as neurectomies of the adjacent nerves. The idea of performing neurectomies for this site of nerve entrapment has largely persisted to the present and been successful in alleviating the pain. However, we advocate treating this problem as a compression of the digital plantar nerves, with release of the intermetatarsal ligament as our first recommended operation.

13.20.2 Surgical Anatomy The lateral plantar nerve sends a branch to the web space between the third and fourth digits. Often this also receives a contribution from the medial plantar nerve. With toe flexion, the joining contributions from both nerves tether this branch and pull it proximally, which may predispose to this entrapment issue. The common plantar digital nerve crosses superficial to the intermetatarsal ligament between the third and fourth metatarsal heads, then divides into its terminal branches, which innervate the surfaces of the corresponding toes. With plantar flexion, weight is borne on the metatarsal heads, dorsiflexing the toes and pulling the common plantar digital nerve distally while it remains tethered proximally, as described above, by the flexor digitorum brevis. The common digital artery runs with this nerve and has been noted to undergo thickening and occlusion, making ischemia to the nerve a possible contributor. A second mechanism has been proposed that implicates the

Injury and Compression Neuropathy in the Lower Extremity

Fig. 13.59 Release of the calcaneal branch of the tibial nerve. Usually, the calcaneal branch of the tibial nerve will have a tunnel of its own. Release of the tunnel will decompress this cutaneous nerve. The calcaneal nerve branches from the tibial nerve proximally and posteriorly.

position of the nerve between the metatarsal heads. Tight shoes bring these bones close together, resulting in direct impingement upon this nerve with weight bearing, at which time these bones would normally spread. A metatarsal bursa in this region has also been implicated. Instead of a neuroma, pathologic specimens have demonstrated markedly thickened perineurium and intrafascicular epineurium. Loss of large myelinated fibers may be noted as well. Essentially, these specimens reflect the normal process of nerve compression instead of neuroma formation. Conservative management involves change in footwear, use of toe spreaders, and exercise to teach patients to spread and extend their toes.

13.20.3 Diagnosis The classic description of Morton neuroma is of pain between the third and fourth metatarsals, particularly with walking, that shoots into the toes and is relieved at rest and with the foot elevated. Symptoms do not worsen at night. On examination, pain can be elicited by pressure on the web space between the metatarsal heads.

13.20.4 Surgical Technique A number of potential surgical methods for decompression of the digital nerve have been described. The authors favor

avoiding an incision on the plantar (weight-bearing) surface of the foot, and instead making a 2-cm longitudinal incision over the affected web space (▶ Fig. 13.62). Retracting the metatarsal heads with a toe spreader instrument accompanied with digital plantar pressure allows access to the transverse intermetatarsal ligament, which is subsequently divided. This relieves compression on the digital nerve and makes neurectomy unnecessary. We would only proceed to neurectomy if this failed. In patients referred to us with increased pain after the typical dorsal neurectomy performed by other surgeons, we advocate a plantar approach through a non-weight-bearing incision (▶ Fig. 13.63). We bring an anatomy book into the operating room to facilitate identification of various structures. We identify the plantar digital nerves and use our tug test to pull on the digital nerves and ensure that we have the correct nerves and do not denervate the normal web space. With traction on the plantar nerves, the surgeon can see a “pull” in the skin of the individual web space. The involved nerve should be clamped with a hemostat proximally, divided and cauterized, then transposed deep and proximally so that the neuroma is well away from the plantar skin. Surgical decompression from a plantar approach is also possible; however, it creates a scar on the weight-bearing surface of the foot and is therefore not our preferred method of treatment (▶ Fig. 13.64).

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Fig. 13.60 Identification of the flexor retinaculum through the distal incision. The remaining distal component of the flexor retinaculum, which was not released from the proximal incision, is identified to make sure the retinaculum below the skin bridge is completely released.

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Fig. 13.61 Release of the distal flexor retinaculum. The remaining distal component of the flexor retinaculum is released to decompress the tibial nerve deep to the tibial vein.

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Fig. 13.62 Illustration of the pathomechanics of chronic nerve compression of the common plantar nerve to the third and fourth web spaces. The compression of this nerve results in Morton metatarsalgia. Note a proximal tethering of the nerve by its contributing branches (from the medial and lateral plantar nerves) as they pass around the flexor digitorum brevis, which pulls upon them during toe flexion. Note that with foot plantar flexion and weight bearing on the metatarsal heads, the common plantar digital nerve is stretched distally by the toes, while being compressed by the overlying intermetatarsal ligament, which is the site of the repetitive trauma to the nerve, as it is also intermittently compressed on each side by the metatarsal heads. (Used with permission from Mackinnon SE, Dellon AL, eds. Surgery of the Peripheral Nerve. New York, NY: Thieme; 1988:340.)

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Fig. 13.63 Digital nerve decompression for Morton neuroma. (a) A dorsal approach involving a longitudinal incision over the affected web space, retracting the metatarsal heads, and dividing the transverse intermetatarsal ligament, will release the digital nerve. (b) Increased magnification showing a released digital nerve.

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Fig. 13.64 Neurectomy and transposition for recurrent Morton neuroma. (a) A plantar approach involves a Brunner incision proximal to digital nerve neuroma. (b) The affected digital nerve is identified. (c) The affected digital nerve is distally transected and proximally crushed. (d) The proximal end of the affected nerve is cauterized. (e) After cautery and crush, the affected digital nerve is proximally transposed. (f) A hemostat is used to guide the proximal end of the nerve for an intermuscular proximal transposition along the course of the nerve.

13.21 Conclusion Surgeons are typically well versed in identifying and treating upper extremity compression neuropathies, especially carpal tunnel syndrome; however, they do not typically make the same extrapolation to the lower extremity. Dense sensory loss in the median nerve distribution associated with trauma in the forearm results in prompt decompression of the transverse carpal ligament. A complete foot drop in the situation of similar trauma to the knee or leg prompts a “wait and see” approach rather than consideration of a similar decompression of the peroneal nerve at the fibular head. We encourage surgeons to think about neurologic deficits in the lower extremity that localize to known areas of compression with the same rigor they currently use to manage the longest recognized entrapment neuropathy (carpal tunnel syndrome) at the wrist.

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13.22 References [1] Mackinnon SE, Dellon AL. Other lower extremity nerve entrapments. In: Mackinnon SE, Dellon AL, eds. Surgery of the Peripheral Nerve. New York: Thieme; 1988: 319–345 [2] Tarulli AW, Raynor EM. Lumbosacral radiculopathy. Neurol Clin 2007;25: 387–405 [3] Stevanato G, Vazzana L, Daramaras S, Trincia G, Saggioro GC, Squintani G. Lumbosacral plexus lesions. Acta Neurochir Suppl (Wien) 2007;100: 15–20 [4] Alexandre A, Corò L, Azuelos A. Microsurgical treatment of lumbosacral plexus injuries. Acta Neurochir Suppl (Wien) 2005;92:53–59 [5] Sivaraman A, Altaf F, Carlstedt T, Noordeen H. Intradural repair of lumbar nerve roots for traumatic paraparesis leading to functional recovery. J Spinal Disord Tech 2008;21:553–556

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[6] Acosta JA, Raynor EM. Electrophysiology of brachial and lumbosacral plexopathies. In: Blum AS, Rutkove SB. The Clinical Neurophysiology Primer. Totowa, NJ: Humana Press; 2007:299–311 [7] Karli N, Akgoz S, Chaudhry V. Lumbosacral plexopathies: etiology, frequency, and electrodiagnostic localization. J Clin Neuromuscul Dis 2007;8:195–201 [8] Planner AC, Donaghy M, Moore NR. Causes of lumbosacral plexopathy. Clin Radiol 2006;61:987–995 [9] Tung TH, Martin DZ, Novak CB, Lauryssen C, Mackinnon SE. Nerve reconstruction in lumbosacral plexopathy: case report and review of the literature. J Neurosurg 2005;102 Suppl:86–91 [10] Wilbourn AJ. Plexopathies. Neurol Clin 2007;25:139–171 [11] Kutsy RL, Robinson LR, Routt ML. Lumbosacral plexopathy in pelvic trauma. Muscle Nerve 2000;23:1757–1760 [12] Bhanushali MJ, Muley SA. Diabetic and non-diabetic lumbosacral radiculoplexus neuropathy. Neurol India 2008;56:420–425 [13] Dahele M, Davey P, Reingold S, Shun Wong C. Radiation-induced lumbo-sacral plexopathy (RILSP): an important enigma. Clin Oncol (R Coll Radiol) 2006;18:427–428 [14] You JS, Park YS, Park S, Chung SP. Lumbosacral plexopathy due to common iliac artery aneurysm misdiagnosed as intervertebral disc herniation. J Emerg Med 2011;40:388–390 [15] Abdelhamid MF, Sandler B, Awad RW. Ischaemic lumbosacral plexopathy following aorto-iliac bypass graft: case report and review of literature. Ann R Coll Surg Engl 2007;89:W12–3 [16] Abdellaoui A, West NJ, Tomlinson MA, Thomas MH, Browning N. Lower limb paralysis from ischaemic neuropathy of the lumbosacral plexus following aorto-iliac procedures. Interact Cardiovasc Thorac Surg 2007;6:501–502 [17] Souayah N, Sander HW. Lumbosacral magnetic root stimulation in lumbar plexopathy. Am J Phys Med Rehabil 2006;85(1):858-861 [18] Klimo P, Rao G, Schmidt RH, Schmidt MH. Nerve sheath tumors involving the sacrum: case report and classification scheme. Neurosurg Focus 2003;15:E12 [19] Payer M. Neurological manifestation of sacral tumors. Neurosurg Focus 2003;15:E1 [20] Siegmeth A, Müllner T, Kukla C, Vécsei V. [Associated injuries in severe pelvic trauma] Unfallchirurg 2000;103:572–581 [21] Birch R. Nerve injuries of the lower limbs. Foot Ankle Surg 2002;4:109–117 [22] Lang EM, Borges J, Carlstedt T. Surgical treatment of lumbosacral plexus injuries. J Neurosurg Spine 2004;1:64–71

Injury and Compression Neuropathy in the Lower Extremity [23] Harris WR, Rathbun JB, Wortzman G, Humphrey JG. Avulsion of lumbar roots complicating fracture of the pelvis. J Bone Joint Surg Am 1973;55:1436–1442 [24] Murata Y, Lee M, Mimura M, Murata A, Shimizu S. Partial avulsion of the cauda equina associated with a lumbosacral fracture-dislocation: a case report. J Bone Joint Surg Am 1999;81:1450–1453 [25] Chiou-Tan FY, Kemp K, Elfenbaum M, Chan KT, Song J. Lumbosacral plexopathy in gunshot wounds and motor vehicle accidents: comparison of electrophysiologic findings. Am J Phys Med Rehabil 2001;80:280–285, quiz 286–288 [26] Morelli V, Weaver V. Groin injuries and groin pain in athletes: part 1. Prim Care 2005;32:163–183 [27] Nakano KK. The entrapment neuropathies. Muscle Nerve 1978;1:264–279 [28] MacLeod DA, Gibbon WW. The sportsman’s groin. Br J Surg 1999;86:849–850 [29] Akita K, Niga S, Yamato Y, Muneta T, Sato T. Anatomic basis of chronic groin pain with special reference to sports hernia. Surg Radiol Anat 1999;21:1–5 [30] Ruge G. Verschiebungen in den Endgebieten der Nerven des Plexus lumbalis der Primaten [in German]. Morph Jahrb 1893;20:305–397 [31] Bardeen CR. A statistical study of the abdominal and border-nerves in man. Am J Anat 1902;1:203–228 [32] Murovic JA, Kim DH, Tiel RL, Kline DG. Surgical management of 10 genitofemoral neuralgias at the Louisiana State University Health Sciences Center. Neurosurgery 2005;56:298–303, discussion 298–303 [33] Reid V, Cros D. Proximal sensory neuropathies of the Leg. Neurol Clin 1999;17:655–667, viiiviii. [34] Choi PD, Nath R, Mackinnon SE. Iatrogenic injury to the ilioinguinal and iliohypogastric nerves in the groin: a case report, diagnosis, and management. Ann Plast Surg 1996;37:60–65 [35] Alfieri S, Di Miceli D, Doglietto GB. Prophylactic ilioinguinal neurectomy in open inguinal hernia repair. Ann Surg 2007;245:663 [36] Ducic I, Dellon AL. Testicular pain after inguinal hernia repair: an approach to resection of the genital branch of genitofemoral nerve. J Am Coll Surg 2004;198:181–184 [37] Perry CP. Peripheral neuropathies and pelvic pain: diagnosis and management. Clin Obstet Gynecol 2003;46:789–796 [38] Starling JR, Harms BA. Diagnosis and treatment of genitofemoral and ilioinguinal neuralgia. World J Surg 1989;13:586–591 [39] Lewin-Kowalik J, Marcol W, Kotulska K, Mandera M, Klimczak A. Prevention and management of painful neuroma. Neurol Med Chir (Tokyo) 2006;46:62– 67, discussion 67–68 [40] Stokvis A, van der Avoort DJ, van Neck JW, Hovius SE, Coert JH. Surgical management of neuroma pain: a prospective follow-up study. Pain 2010;151: 862–869 [41] Rab M, Ebmer And J, Dellon AL. Anatomic variability of the ilioinguinal and genitofemoral nerve: implications for the treatment of groin pain. Plast Reconstr Surg 2001;108:1618–1623 [42] McCrory P, Bell S. Nerve entrapment syndromes as a cause of pain in the hip, groin and buttock. Sports Med 1999;27:261–274 [43] Vernadakis AJ, Koch H, Mackinnon SE. Management of neuromas. Clin Plast Surg 2003;30:247–268, viivii. [44] Kim DH, Murovic JA, Tiel RL, Kline DG. Surgical management of 33 ilioinguinal and iliohypogastric neuralgias at Louisiana State University Health Sciences Center. Neurosurgery 2005;56:1013–1020, discussion 1013– 1020 [45] Vuilleumier H, Hübner M, Demartines N. Neuropathy after herniorrhaphy: indication for surgical treatment and outcome. World J Surg 2009;33: 841–845 [46] Stulz P, Pfeiffer KM. Peripheral nerve injuries resulting from common surgical procedures in the lower portion of the abdomen. Arch Surg 1982;117:324– 327 [47] Ducic I, Dellon AL, Taylor NS. Decompression of the lateral femoral cutaneous nerve in the treatment of meralgia paresthetica. J Reconstr Microsurg 2006;22:113–118 [48] Benezis I, Boutaud B, Leclerc J, Fabre T, Durandeau A. Lateral femoral cutaneous neuropathy and its surgical treatment: a report of 167 cases. Muscle Nerve 2007;36:659–663 [49] Siu TL, Chandran KN. Neurolysis for meralgia paresthetica: an operative series of 45 cases. Surg Neurol 2005;63:19–23, discussion 23 [50] Azuelos A, Corò L, Alexandre A. Femoral nerve entrapment. Acta Neurochir Suppl (Wien) 2005;92:61–62 [51] Busis NA. Femoral and obturator neuropathies. Neurol Clin 1999;17:633– 653, viivii. [52] Vázquez MT, Murillo J, Maranillo E, Parkin IG, Sanudo J. Femoral nerve entrapment: a new insight. Clin Anat 2007;20:175–179

[53] Morganti CM, McFarland EG, Cosgarea AJ. Saphenous neuritis: a poorly understood cause of medial knee pain. J Am Acad Orthop Surg 2002;10:130– 137 [54] Pendergrass TL, Moore JH. Saphenous neuropathy following medial knee trauma. J Orthop Sports Phys Ther 2004;34:328–334 [55] Worth RM, Kettelkamp DB, Defalque RJ, Duane KU. Saphenous nerve entrapment: a cause of medial knee pain. Am J Sports Med 1984;12:80–81 [56] Luerssen TG, Campbell RL, Defalque RJ, Worth RM. Spontaneous saphenous neuralgia. Neurosurgery 1983;13:238–241 [57] Kopell HP, Thompson WAL. Knee pain due to saphenousnerve entrapment. N Engl J Med 1960;263:351–353 [58] Bradshaw C, McCrory P, Bell S, Brukner P. Obturator nerve entrapment: a cause of groin pain in athletes. Am J Sports Med 1997;25:402–408 [59] Sorenson EJ, Chen JJ, Daube JR. Obturator neuropathy: causes and outcome. Muscle Nerve 2002;25:605–607 [60] Hollis MHL, DE, Jenson RP. Nerve entrapment syndromes of the lower extremity. EMedicine 2008 [61] Tipton JS. Obturator neuropathy. Curr Rev Musculoskelet Med 2008;1:234– 237 [62] Kitagawa R, Kim D, Reid N, Kline D. Surgical management of obturator nerve lesions. Neurosurgery 2009;65 Suppl:A24–A28 [63] Kim DH, Murovic JA, Tiel RL, Kline DG. Management and outcomes in 318 operative common peroneal nerve lesions at the Louisiana State University Health Sciences Center. Neurosurgery 2004;54:1421–1428, discussion 1428– 1429 [64] Stewart JD. Foot drop: where, why and what to do? Pract Neurol 2008;8:158–169 [65] Baima J, Krivickas L. Evaluation and treatment of peroneal neuropathy. Curr Rev Musculoskelet Med 2008;1:147–153 [66] Shizhen AX, T., Muzhi L. The microanatomy of peripheral nerves. In: Shizhen Z, Yongjain H, Wenchum Y. eds Microsurgical Anatomy. Lancaster, UK: MTP Press; 1985:299–350 [67] Sunderland S, Bradley KC. The cross-sectional area of peripheral nerve trunks devoted to nerve fibers. Brain 1949;72:428–449 [68] Kudoh H, Sakai T. Fascicular analysis at perineurial level of the branching pattern of the human common peroneal nerve. Anat Sci Int 2007;82:218–226 [69] Gillenwater J, Cheng J, Mackinnon SE. Evaluation of the scratch collapse test in peroneal nerve compression. Plast Reconstr Surg 2011;128:933–939 [70] Humphreys DB, Novak CB, Mackinnon SE. Patient outcome after common peroneal nerve decompression. J Neurosurg 2007;107:314–318 [71] Garozzo D, Ferraresi S, Buffatti P. Surgical treatment of common peroneal nerve injuries: indications and results: a series of 62 cases. J Neurosurg Sci 2004;48:105–112, discussion 112 [72] Bonnevialle P, Dubrana F, Galau B, et a. Common peroneal nerve palsy complicating knee dislocation and bicruciate ligaments tears. Orthop Traumatol Surg Res 2010;96:64–69 [73] Kim DH, Midha R, Murovic JA, Spinner RJ, Teil R. Kline and Hudson’s Nerve Injuries. 2nd ed. Elsevier; 2008 [74] Prakash , Bhardwaj AK, Singh DK, Rajini T, Jayanthi V, Singh G. Anatomic variations of superficial peroneal nerve: clinical implications of a cadaver study. Ital J Anat Embryol 2010;115:223–228 [75] Brief JM, Brief R, Ergas E, Brief LP, Brief AA. Peroneal nerve injury with foot drop complicating ankle sprain—a series of four cases with review of the literature. Bull NYU Hosp Jt Dis 2009;67:374–377 [76] Lorei MP, Hershman EB. Peripheral nerve injuries in athletes: treatment and prevention. Sports Med 1993;16:130–147 [77] Ducic I, Dellon AL, Graw KS. The clinical importance of variations in the surgical anatomy of the superficial peroneal nerve in the mid-third of the lateral leg. Ann Plast Surg 2006;56:635–638 [78] Davidge KM, Gontre G, Tang D, Boyd KU, Yee A, Damiano M, Mackinnon SE.. The hierarchial scratch collapse test for identifying multilevel ulnar nerve compression Hand 2014 [79] Rehman S, Joglekar SB. Acute isolated lateral compartment syndrome of the leg after a noncontact sports injury. Orthopedics 2009;32:523 [80] Slabaugh M, Oldham J, Krause J. Acute isolated lateral leg compartment syndrome following a peroneus longus muscle tear. Orthopedics 2008;31:272 [81] Watson CP, Mackinnon SE, Dostovsky JO, et al. Nerve resection, crush and relocaiton relieve complex regional pain syndrome type II: a case report. Pain. 2014;[epub ahead of print] [82] Marinacci AA. Medical and anterior tarsal tunnel syndrome Electromyography 1968;8:123–134 [83] DiDomenico LA, Masternick EB. Anterior tarsal tunnel syndrome. Clin Podiatr Med Surg 2006;23:611–620

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Injury and Compression Neuropathy in the Lower Extremity [84] Miki RA, Lawrence JP, Gillon TJ, Lawrence BD, Zell RA. Anterior tibial artery and deep peroneal nerve entrapment in spiral distal third tibia fracture. Orthopedics 2008;31 [85] Williams EH, Williams CG, Rosson GD, Dellon AL. Combined peroneal and proximal tibial nerve palsies. Microsurgery 2009;29:259–264 [86] Keck C. The tarsal-tunnel syndrome J Bone Joint Surg Am 1962;44:180–182 [87] Horwitz MT. Normal anatomy and variations of the peripheral nerve of the leg and foot: Application in operations for vascular diseases: Study of one hundred specimens Arch Surg 1938;36:626–636 [88] Franson J, Baravarian B. Tarsal tunnel syndrome: a compression neuropathy involving four distinct tunnels. Clin Podiatr Med Surg 2006;23:597–609

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[89] Bailie DS, Kelikian AS. Tarsal tunnel syndrome: diagnosis, surgical technique, and functional outcome. Foot Ankle Int 1998;19:65–72 [90] Ward PJ, Porter ML. Tarsal tunnel syndrome: a study of the clinical and neurophysiological results of decompression. J R Coll Surg Edinb 1998;43:35–36 [91] Galardi G, Amadio S, Maderna L, et al. Electrophysiologic studies in tarsal tunnel syndrome. Diagnostic reliability of motor distal latency, mixed nerve and sensory nerve conduction studies. Am J Phys Med Rehabil 1994;73:193–198 [92] Morton TG. Peculiar painful affection of fourth metatarsophalangeal articulation Am J Med Sci 1876;71–37

Brachial Plexus Injuries

14 Brachial Plexus Injuries Thomas H.H. Tung and Amy M. Moore

14.1 Introduction Traditionally, the surgical management of brachial plexus injuries has been associated with poor outcomes; consequently, operative intervention was seldom recommended. Furthermore, the complexity of the anatomy and the proximal nature of the injuries intimidated many surgeons and necessitated specialized training. Gradually, as our understanding of nerve injury and regeneration improved, and as surgical techniques, including nerve grafting for the management of nerve injuries, became more sophisticated, the functional outcomes of these procedures improved as well. The development of microneurosurgical technique with finer instrumentation and suture material has also enhanced technical precision and has facilitated regeneration after peripheral nerve injuries. However, over the past decade, the expansion and popularization of the use of nerve transfer technique have remarkably altered the results of functional recovery following brachial plexus surgery. An understanding of the internal topography of the brachial plexus, coupled with more distal nerve transfers to essentially convert these proximal injuries to more distal nerve injuries, has offered new options for recovery following these devastating injuries. This chapter will review the relevant anatomy, the history of the management of brachial plexus injuries, and the progression toward current surgical treatment. The epidemiology and mechanisms of traumatic brachial plexus injuries, as well as the diagnosis and evaluation of these patients, will be discussed. Finally, treatment options, detailed surgical technique, and postoperative management and outcomes will be described.

14.2 Historical Review Both Thucydides’ History of the Peloponnesian War (5th century BC) and Homer’s Iliad (8th century BC) described injuries of the brachial plexus secondary to shoulder trauma.1 In the 1st century BC in Rome, the first report of the diagnosis and treatment of brachial plexus trauma was by Galen and involved a patient who recovered hand sensation with conservative management. Since the time of Galen, the management of shoulder dislocations by shoulder traction was standard practice. However, it was not until the 18th century that Smellie first recognized this as a cause of brachial plexus injury, and surgical management at that time was not advocated.2 In 1861 Duchenne was the first to describe obstetrical brachial plexus injury, 3 and Erb recognized more isolated upper trunk involvement in 1875.4 The basis of medicine in the ancient literature was theory and dogma with little or no regard for anatomy or scientific method. Eventually, the dissection and study of human anatomy became prevalent in the 14th and 15th centuries in the Western world and challenged these ancient beliefs. Detailed illustrations of the brachial plexus by artists and anatomists, including Leonardo da Vinci, emerged from the period of the Renaissance in Europe.5 In the late 19th century, further definition of the detailed anatomy of the brachial plexus

accompanied a better understanding of the etiology of brachial plexus trauma. The first report of the primary repair of a brachial plexus injury appeared in 1900 by William Thorburn, who described an arm injury from a mill machine in a 16-year old patient. 6 Neuroma resection and primary repair were performed 7.5 months after the injury; after 4 years, the patient demonstrated good elbow and wrist flexion, minimal shoulder function, and no hand function with poor sensation. Harris and Low were the first to advocate the technique of neurotization, or nerve transfer, after root avulsions of the brachial plexus to reinnervate target muscles with functioning donor nerves and avoid more proximal dissection in the zone of injury.7 Many others are thought to have used this technique in the early 20th century, but no results were published, and the results of the surgical management of obstetrical brachial plexus lesions during this time were poor.8 Because such surgical procedures were also difficult, long, and required specialized training, the operative management of brachial plexus injuries was viewed negatively and was not advocated. Adult and pediatric brachial plexus surgery was therefore largely abandoned until such injuries emerged with increasing frequency during the world wars.5 During the Second World War, the prevalence of open penetrating injuries to the brachial plexus was high and led to a reevaluation of operative treatment. The emergence of new diagnostic modalities, such as cervical myelography in 1947, 9 electromyography (EMG) in 1948,10 the measurement of nerve action potentials in 1949,11 and the histamine test in 1954,12 contributed to a better understanding and classification of such injuries. Although the report of favorable results from surgical management appeared periodically from surgeons such as Davis and colleagues13 and Seddon,14 the predominant consensus of the time advocated conservative management of these injuries. In 1966, at the 10th SICOT (Société Internationale de Chirurgie Orthopédique et Traumatologique) meeting in Paris, a roundtable discussion was held under the chairmanship of Seddon and Merle ďAubigné and included all of the authorities in the field.15 The attendees concluded that (1) surgical exploration of the plexus, especially at the infraclavicular level, added no benefit to diagnosis or prognosis; and (2) surgical repair of the lesions was essentially impossible and did not ensure any effectively useful result.5 The primary focus was to establish the diagnosis of a supraganglionic lesion and loss of continuity by surgical exploration if necessary. If such a diagnosis could be confirmed, because of its poor prognosis, standard treatment included upper arm amputation, shoulder joint arthrodesis, and fitting with an upper arm prosthesis. If the diagnosis of a supraganglionic lesion could not be made, then the patient was managed conservatively for at least 2 years to provide the opportunity for spontaneous recovery, followed by arm amputation if none was forthcoming. In 1972 Seddon stated that the only role for surgery in a patient with a root injury was to confirm the diagnosis to shorten the waiting period before proceeding with amputation. Internal neurolysis was not recommended for fear of further injury and worsening the chance of some spontaneous recovery.15

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Brachial Plexus Injuries Meanwhile, during this time, microneurosurgical techniques were being developed with the advent of the operating microscope16–18 and smaller suture materials and instrumentation. The use of these techniques in the mid-1960s by Millesi17–19 and Narakas,20 and eventually others, progressively gained the favor of many surgeons worldwide and was responsible for changing the prevailing outlook of the management of these injuries. In 1975 Millesi presented at the SICOT meeting a study of 56 patients that he published 2 years later.21 With a followup of 5 years, 70% of patients showed recovery of function to some degree. Two patients were excluded who had avulsion of all five spinal roots. In 1977 Narakas reported a series of 107 patients with a follow-up of at least 2 years for 60 patients, managed by various combinations of neurolysis, nerve grafts, and nerve transfers.22 Like Millesi’s series, the results were much more encouraging with good or satisfactory outcomes for the majority of the patients. Additional case studies were soon published by Alnot et al. with similarly positive results.23 The outcomes following surgical management of obstetrical brachial plexus palsy were also greatly improved with refinement in surgical technique. In 1983 Tassin reported a series of 110 children reconstructed by Gilbert, who by 1984 had accumulated an experience of over 180 cases.24 These advancements permitted greater precision in nerve repair and grafting,5 and contributed to better outcomes and furthered interest in surgery of the brachial plexus. At this time, it also became evident that surgical reconstruction could offer improvement in pain syndromes associated with brachial plexus injury. In 1980 Wynn Parry described the incidence and natural history of chronic pain based on a series of 275 patients with follow-up from 3 to 30 years; he found that the incidence of chronic pain was significantly greater in those with root avulsion.25 In 1981 Narakas corroborated these findings and described the benefit of surgery to pain management.26 By 1989 an international experience of more than 4,000 cases had been accumulated.27 The current era of brachial plexus surgery has seen the popularization of distal nerve transfers both to enhance the results of more proximal reconstruction and as an alternative to anatomical reconstruction with nerve grafts. Although the use of nerve transfers was initially described in 1961 by Yeoman and Seddon for intercostal nerves,28 and in 1984 by Allieu for the spinal accessory nerve,29 only more recently has it become more accepted as a primary reconstructive option. The description of more distal intraplexus donor nerve branches including the thoracodorsal nerve in 1990 by Dai30 and medial pectoral nerves in 1993 by Mackinnon31 has allowed transfer closer to target muscles for faster reinnervation. In 1994 Oberlin et al. described the fascicular transfer by internal neurolysis of the ulnar nerve to reinnervate the biceps.32 In 2005 Mackinnon et al. recognized the importance of the brachialis for elbow flexion, expanded this procedure with a fascicular transfer from the median nerve to recover the brachialis muscle as well, and termed this musculocutaneous reconstruction the double fascicular transfer of either median or ulnar nerve fascicles to the biceps and brachialis branches.33 Innovative nerve transfers have also been described for the reconstruction of the complete brachial plexus palsy to provide more donor nerve options and the recovery of additional target muscle groups, such as those for hand function. These have included the contralateral lateral pectoral nerve by Gilbert in 1992,34 the phrenic nerve and

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contralateral C7 root with the use of a vascularized ulnar nerve graft by Gu in 1989 and 1991,35,36 and the partial contralateral C7 by Terzis in 1996.37 We recently used the nerve to the brachialis muscle to transfer to the nerve to the pronator and the anterior interosseous nerve (AIN) in the arm to restore hand function in patients with lower brachial plexus injury.38 The fascicles to the pronator muscle and the AIN can be identified in the arm in their standard locations or traced back proximally from their forearm location. A tenodesis from the median profundus to the ulnar profundus is done once reinnervation has occurred. As there has been a progressive increase in brachial plexus injuries as a result of motor vehicle and motorcycle accidents, advancements in trauma resuscitation and management have allowed more patients to survive the acute phase to become candidates for reconstruction. Modern techniques in brachial plexus surgery—neurolysis, nerve repair, nerve transfers, and nerve grafting—continue to evolve with progressively better results.

14.3 Surgical Anatomy The brachial plexus is formed by cervical spinal roots C5–T1 (▶ Fig. 14.1). Occasionally, the C4 root makes a significant contribution to a prefixed plexus with a much smaller contribution from T1. Alternatively, the T2 root contributes to the postfixed plexus accompanied by a small contribution from the C5 root. As the brachial plexus travels from the spinal cord to its target end-organs, the anatomical levels consist of roots, trunks, divisions, cords, and terminal cord branches and peripheral nerves. The spinal roots pass between the anterior and middle scalene muscles and then form three trunks, which travel in the inferior part of the posterior cervical triangle. The C5 and C6 roots join to form the upper trunk, C7 continues as the middle trunk, and C8 and T1 join to form the lower trunk. Moving from lateral to medial on the upper trunk, the sensorimotor topography is distinct and useful to know for reconstruction. In general, the most lateral one-quarter is suprascapular, the next one-quarter is deltoid followed by biceps, and the sensory group is more medially situated (▶ Fig. 14.2). In the middle trunk, two discrete separate fascicles lies on the superifical aspect that innervates the pectoral muscle. This can be easily teased from the middle trunk and used as a motor nerve transfer for suprascapular or accessory nerve function. The only division from the trunks is the suprascapular nerve, and it can be cleaved from the most lateral portion of the upper trunk very easily for a long distance proximal to its physical division from the upper trunk. This becomes very important for nerve transfer reconstruction. As they travel beneath the clavicle, the trunks separate into anterior and posterior divisions, which then unite in a consistent manner to form cords deep to the pectoralis minor muscle to make up the infraclavicular plexus. The cord names are based on their relationship to the axillary artery. The lateral cord is formed by the union of the anterior divisions of the upper and middle trunks (C5–C7), and the medial cord is the continuation of the anterior division of the lower trunk (C8, T1). The posterior cord consists of the posterior divisions of all three trunks (C5–T1). The terminal cord branches form the major peripheral nerves of the upper extremity. The innervation to the muscles of the shoulder girdle may also arise from the supraclavicular plexus at the trunk or root levels. The lateral and medial cords each provide a contribution to form

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Fig. 14.1 Anatomy of the brachial plexus showing the relationship of the roots, trunks, divisions, cords, and terminal branches with overlying musculoskeletal anatomy.

the median nerve, supplying the sensory and motor components of the nerve, respectively. In keeping with the cord contribution to the median nerve, the motor component of the median nerve is situated on the medial side of the nerve in the arm, and the sensory component is on the lateral side

(▶ Fig. 14.3). The lateral cord continues as the musculocutaneous nerve, and the medial cord becomes the ulnar nerve after the contribution to the median nerve. The terminal branches of the posterior cord include the axillary nerve to the deltoid and teres minor before continuing as the radial nerve. It should be

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Fig. 14.2 General fascicular anatomy of the upper and middle trunk of the brachial plexus.

noted that a branch from a cord may contain innervation from only some but not all of the roots that contribute to that cord (▶ Fig. 14.4). For example, the axillary nerve (C5, C6) arises from the posterior cord (C5–C8, T1). There are three branches that arise from the nerve roots. The long thoracic nerve is formed by branches of the fifth, sixth, and seventh nerve roots and innervates the serratus anterior muscle. The dorsal scapular nerve arises from the fifth and sixth cervical roots and supplies the levator scapulae and rhomboid muscles. These branches are clinically significant, as they provide clues to the level of injury in brachial plexus trauma and may guide surgical reconstruction, as described in the Diagnosis section below. The nerve to the subclavius muscle is the third branch; it is also formed by the fifth and sixth nerve roots but cannot be clinically assessed and therefore is not clinically important. The musculocutaneous nerve is one of the primary nerves for reconstruction or transfer in brachial plexus injuries, as it innervates the elbow flexors. As a terminal branch of the lateral cord, it quickly enters the coracobrachialis muscle, then travels distally between the biceps and brachialis muscles, innervating all three. In the distal upper arm, it continues as the lateral antebrachial cutaneous (LABC) nerve to provide sensation to the lateral volar aspect of the forearm. The proximal part of the musculocutaneous nerve is relatively tethered where it enters the coracobrachialis muscle and is therefore prone to an additional traction injury at this level in the setting of upper extremity traction. The intramuscular anatomy of the musculocu-

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taneous nerve is critically important for nerve transfer surgery and very predictable. The biceps branch enters the biceps muscle at the midhumeral (arm) level, the LABC branch is sandwiched between the biceps branch, which turns up into the muscle, and the brachialis branch, which turns down and in a medial direction into the brachialis muscle. The tug test is useful in confriming the LABC (▶ Fig. 14.5). Shoulder function is a high priority in brachial plexus palsies, and the suprascapular and axillary nerves are the target to reconstruct, with the suprascapular nerve being by far the most critical although we also reinnervate the long thoracic nerve. The suprascapular nerve (C5, C6) is a branch of the upper trunk of the supraclavicular plexus in the posterior triangle of the neck. It is in fact the only branch that occurs at the level of the trunks. It travels deep to the trapezius muscle, through the scapular notch, and innervates the supraspinatus and infraspinatus muscles. The scapular notch forms a distal compression point, and a release can and, if feasible, should be performed in conjunction with nerve transfer by excision of the ligament that forms the roof and otherwise bony passage. Associated compression of the suprascapular nerve at the notch is probably underrecognized in brachial plexus injuries. Release of this entrapment point improves suprascapular nerve function. The axillary nerve is a terminal branch of the posterior cord and travels through the quadrangular space to innervate the deltoid and teres minor muscles, as well as provide sensation to the overlying skin. The quadrangular space, which is made up of the humerus medially, the long head of the triceps laterally, the

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Fig. 14.3 Fascicular anatomy of the axillary, proximal median, and proximal ulnar nerve of the brachial plexus.

teres minor superiorly, and the teres major inferiorly, increases the susceptibility of the axillary nerve to traction injury and subsequent additional compression. The motor component of the axillary nerve makes up the superior three-quarters of the axillary nerve, but the sensory component lies in the inferior one-quarter and should be excluded from the motor reconstruction (▶ Fig. 14.3). The sensory component can be teased from the axillary nerve in the anterior approach, and traction on this inferior one-quarter portion will cause tenting of the posterior deltoid skin. Similarly, from a posterior approach, tugging on the sensory component of the nerve will produce the same skin indentation—an alternative motor sensory mapping technique. Posteriorly the axillary nerve separates into two large divisions with the anterior division being at more risk injury. Thus we evaluate anterior deltoid function for a separate injury pattern from the posterior division and may do a selective nerve transfer just to the anterior division if needed. Several other branches are clinically significant because of their potential use as donors for nerve transfer in reconstruction after a brachial plexus injury. The medial pectoral nerves (C8, T1) branch from the medial cord and innervate the sternocostal head of the pectoralis major muscle. The lateral pectoral

nerves (C5, C6) arise from the lateral cord to innervate the clavicular head of the pectoralis major, as well as the sternocostal head with the medial pectoral nerve. The functional status of the pectoralis major will help to localize the injury at the cord level. These branches can be most easily found deep to the pectoralis minor muscle and, if intact, can provide donor motor axons for transfer to restore elbow or shoulder function. The posterior cord gives off the upper, middle, and lower subscapular nerves before its terminal branches. The thoracodorsal nerve, also known as the long subscapular or middle subscapular branch, innervates the latissimus dorsi muscle and is a common donor nerve for transfer because of its size, length, and expendability. The upper or short subscapular nerve supplies the superior part of the subscapularis muscle, whereas the lower or inferior subscapular nerve innervates the lower subscapularis and the teres major muscles. The most current and promising options for functional reconstruction are based on an understanding of the internal topography of the brachial plexus and major peripheral nerves. Selective fascicular transfers require knowledge of specific topographical anatomy to optimize the reinnervation of target muscles and to minimize functional donor morbidity. Proximal

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Fig. 14.4 Intraneural topographical anatomy of the brachial plexus illustrating the extent of plexus formation and crossover after dissection by Kerr. (Used with permission from Kerr AT. The brachial plexus of nerves in the man: the variations in its formation and its branches. Am J Anat. 1918;23:285.)

reconstruction from the upper and middle trunks, as well as use of the whole or partial C7 as a source of donor fascicles, is a common technique. A consistent pattern of innervation is seen as one moves from the lateral or superior aspect of the upper trunk to the medial or inferior side. The lateralmost fascicles will contribute innervation to the suprascapular nerve, then the axillary nerve moving medially, musculocutaneous nerve, and sensory fascicles, which are present on the most medial aspect (▶ Fig. 14.2). The internal topography of the middle trunk is consistent with its branching pattern in divisions and cords. Internal neurolysis at the trunk level generally provides four to six fascicles, with the posterosuperior half innervating the shoulder muscles, and the anteroinferior half supplying elbow and wrist function.39 This is consistent at the level of the divisions, with the posterior division contributing to the axillary, radial, and thoracodorsal nerves, and the anterior division participating in musculocutaneous and median nerve function. 40

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The posterior division has been reported to contain twice the number of axons as the anterior division and is generally favored for hemi-C7 transfer.41 Knowledge of the topographical anatomy of the median and ulnar nerves in the upper arm is essential to the use of fascicular transfers for elbow flexion. The ulnar fascicular transfer as originally described by Oberlin uses a fascicle located on the lateral aspect of the nerve that innervates primarily flexor carpi ulnaris (FCU) function.32 Using a median nerve fascicle for more complete reinnervation of the elbow flexors as originally described by Mackinnon et al involves harvesting from the medial aspect, which usually contributes to flexor digitorum superficialis (FDS)/ flexor carpi radialis (FCR) function. 33 In general, the lateral cord contribution to the median nerve contains sensory axons, and the medial cord contribution provides motor axons. When reinnervating the biceps and brachialis muscles, it is important to know that after the biceps branch, the fascicles that

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Fig. 14.5 Tug test on sensory nerves. By gently “tugging” a sensory nerve proximally, dimpling of the skin territory that the nerve innervates occurs. This is a useful test to determine what territory the nerve innervates, in addition to determining the modality of the nerve.

ultimately become the LABC nerve are located laterally on the distal musculocutaneous nerve, and the medial side contains the fascicles to the brachialis. Sensory fascicular transfers can be performed at the level of the distal forearm or wrist to avoid dissection and scars on the palm. Because of the more distal location, fascicular anatomy more predictably corresponds with the location of the terminal branches. With internal neurolysis of the median nerve at the wrist, the most lateral or radial fascicle after the motor fascicle will innervate the first web space, and the most medial or ulnar fascicle corresponds to the third web space. The second webspace fascicles are found in the middle between the first and third web spaces. There is surprisingly little plexus formation in the median nerve proper even in the distal forearm between these webspace groups. Neurolysis of the ulnar nerve will demonstrate the motor axons on the medial or ulnar side and the sensory component on the lateral or radial side distal to the take-off of the dorsal cutaneous branch of the ulnar nerve. Such a working knowledge will allow transfer of the terminal AIN to the ulnar motor component at the wrist without the need to fully separate the motor and sensory components from the Guyon canal to the distal fore-

arm. Farther proximally in the forearm, proximal to the take-off of the dorsal cutaneous branch, the motor fascicle is sandwiched between the dorsal cutaneous fascicle located medially and the sensory fascicles to the fourth web space and fifth finger on the lateral side. It is a good practice to activate functional nerves with a standard handheld, battery-operated nerve stimulator (Vari-Stim III, Medtronic, Inc., Jacksonville, FL) during more routine nerve surgery, such as decompression, to learn intraneural topography, as direct stimulation will not be available during reconstructive procedures if the nerves are not functional.

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14.4 Epidemiology and Classification 14.4.1 Epidemiology Brachial plexus trauma is a devastating injury that involves young men in up to 90% of cases.1,42 The majority of these cases occur in motor vehicle accidents, with motorcycles involved in up to 84% of cases.43 In general, 0.67 to 1.3% of motor vehicle

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Brachial Plexus Injuries accidents and up to 4.2% of motorcycle accidents involve injury to the brachial plexus.42 The mechanisms of injury are variable but tend to be crush injuries after motor vehicle accidents; motorcycle accidents are more likely to cause root avulsion injuries because of the greater traction forces that occur on the unprotected body. Other common type of injuries are pedestrian/motor vehicle accidents, industrial accidents, and gunshot wounds. Lower velocity injuries, such as skiing, bicycling, and a fall from a height or down stairs, can result in brachial plexus palsies. A sudden force to the head or shoulder can stretch the brachial plexus, as is not uncommonly seen in sports injuries or in industrial or occupational accidents from a falling object. In traction injuries, downward displacement of the upper extremity causes a greater degree of injury at the level of the upper roots and trunks. Simultaneous neck flexion to the contralateral side distracts the head and neck from the shoulder and arm with a sudden increase in the neck–shoulder angle.44 This is a common mechanism in motorcycle accidents and sports injuries. Alternatively, upward displacement of the upper extremity forcefully increases the scapulohumeral angle and is more likely to injure the lower plexus. With severe forces, avulsion of the nerve or root may be seen, whereas lesser forces may produce only temporary palsies. Fixed attachments of the cervical roots to the vertebrae and prevertebral fascia limit the mobility of the brachial plexus. Consequently, iatrogenic traction palsies may occur at the extremes of upper extremity positioning for long surgeries.45 Plexus lesions have been reported in up to 38% of patients following cardiac surgery with median sternotomy.46 These are felt to represent a neurapraxia possibly due to compression of the medial cord between the clavicle and first rib during sternal retraction. Most of the neurologic symptoms resolve within the first few months, but a few may lead to long-term disability. It is important to note that such palsies, and other postoperative palsies, can occur with even so-called standard of care management in patients with subclinical compression neuropathies and other predisposing factors, such as hypothyroidism, diabetes mellitus, and obesity. Compression injury may play a greater role in more severe trauma involving a direct blow to the neck and shoulder region, such as that frequently seen in motor vehicle accidents, occupational injuries when a heavy falling object lands on the shoulder, and sports injuries with forceful contact, for example, football. In such cases, compression may occur in the costoclavicular space as the brachial plexus travels between the clavicle and first rib. Compression may also be due to adjacent structures that have sustained injury, including bone fragments or callous formation from a fractured clavicle, or hematoma or pseudoaneurysm from a vascular injury. Anatomical variants, such as cervical ribs, prominent transverse processes, and congenital fibrous bands that may contribute to neurogenic thoracic outlet syndrome, may also increase the susceptibility of the brachial plexus to trauma.47 The various mechanisms of injury are certainly not exclusive, and any combination or all may coexist to some degree in a patient to worsen the prognosis. Clearly, the position of the upper extremity and the magnitude of the force on the brachial plexus will affect the degree and extent of injury. Concomitant injuries are variable but frequent, especially following motor vehicle and motorcycle accidents, including fractures of the clavicle,

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ribs, humerus, and scapula, closed head injury, intra-abdominal injuries, and vascular injuries.48

Root Avulsion Different mechanisms of root avulsion have been described by Sunderland based on the amount of traction transmitted to the rootlets and the dural envelope (▶ Fig. 14.6).49 Displacement of the upper extremity causes a peripheral mechanism in which traction on the brachial plexus is transmitted to the rootlet and its dura mater sheath. The dura mater is less elastic and therefore will tear before the rootlet does. An imaging study such as cervical myelography will demonstrate a pseudomeningocele, but the nerve root may in reality still be intact. A more direct impact on the head and neck will cause a central mechanism in which the spinal cord is displaced to the contralateral side. In this case, traction is transmitted directly to the ipsilateral spinal root but not the dural sheath, causing disruption of the nerve root but not the dura. Other anatomical properties also influence injury patterns. The cervical roots are protected by the cervical fascia, which provides some protection against traction and makes them somewhat less likely to avulse than the C8 and T1 roots.44 The anterior spinal rootlets are also generally shorter than the posterior rootlets and are therefore more prone to avulsion. The level of the traumatic lesion in regard to the dorsal root ganglion (DRG), which contains the sensory cell bodies, affects the clinical presentation and the management (▶ Fig. 14.7).50 Injury proximal to the DRG, called a pre- or supraganglionic lesion, does not separate the peripheral sensory axon from its cell body; therefore, wallerian degeneration of the sensory nerve does not occur. In this case, electrical testing will demonstrate normal sensory action potentials because the viability of the sensory axons are maintained by their cell bodies, but clinically, there is sensory loss because these axons are no longer in continuity with the spinal cord. Injury distal to the DRG represents a post- or infraganglionic lesion and separates the peripheral sensory axons from their cell bodies. The peripheral sensory nerve will no longer be viable and will undergo wallerian degeneration, so no action potentials will be detected. Because the motor cell bodies are located within the spinal cord, all root avulsions cause degeneration of the motor axon, and no distinction relative to the cell body exists.51 The location of the lesion relative to the DRG provides information as to the potential feasibility of surgical reconstruction. An infraganglionic location indicates a more distal lesion and suggests that a healthy nerve stump is more likely to be present for grafting. A supraganglionic injury is much less likely to preserve a proximal nerve stump for grafting. A proximal avulsion may combine with a distal traction injury, in which case sensory nerve conduction studies would not be normal or would be reduced, depending on the degree of associated distal injury.

14.4.2 Diagnosis The patient with a brachial plexus injury is often seen initially with multisystem trauma in the emergency department and should be managed by the standard trauma resuscitation protocol. Because the patient is usually the first to detect the brachial

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Fig. 14.6 Injury mechanisms that may occur at the root level of the brachial plexus.

plexus palsy, the diagnosis may be delayed in the unconscious patient or if sedation or anesthesia is required.

History The mechanism of injury can be ascertained from a thorough history, which will facilitate the recognition of potential injury patterns by a focused physical examination. For motor vehicle

accidents, relevant information will include the speed at the time of the accident, the deployment of an airbag, whether seatbelts or a helmet was worn, and if the patient was ejected from the vehicle and how far. For occupational or industrial injuries, information about the involved machinery, the force and vector of pull that caused the injury, and any attempts to pull the patient’s arm from the machine by coworkers will help to evaluate the severity of the injury. Similarly relevant informa-

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Fig. 14.7 Pre- and postganglionic lesions. The illustration shows the distinction between a postganglionic lesion, in which sensory and motor axons are separated from their cell bodies, and both undergo wallerian degeneration, and a preganglionic lesion, in which the sensory axon maintains continuity with its cell body and therefore does not undergo wallerian degeneration, but is separated from the spinal cord and so does not provide sensory feedback.

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Brachial Plexus Injuries tion might include the weight and size of the falling object and where specifically the patient was struck, the height from which the object or patient fell, and how the patient landed from the fall. Any recovery of function since the injury should be noted and may alter the course of management. The management of pain will be problematic for a significant number of patients.52 The patient should be questioned about the nature and severity of the pain and the degree of relief that is provided by commonly prescribed medications. Our standard pain questionnaire is administered and provides quantitative and qualitative information about pain for reference as a baseline and to document changes (see Chapter 20). The pain may be episodic or constant in nature, may slowly improve as time passes, or may become a chronic issue. Referral to a pain specialist may become necessary if management with routine pain medications is not satisfactory. Fifty percent of nerve-injured patients are depressed and should be referred for evaluation. 53 The assessment of the patient as a candidate for surgery should include a general evaluation of the patient’s ability to cope with and compensate for a debilitating and life-altering injury and to manage potentially multiple operations and extended rehabilitation.1 The potential for the patient to return to gainful employment in any capacity is also considered, and vocational rehabilitation may be helpful.

Physical Examination A complete physical examination is critical for proper decision making and surgical management. Joint mobility in the hand, wrist, elbow, and shoulder should be evaluated. The importance of joint mobility should be stressed to the patient, and physical or occupational therapy should be prescribed if there is significant stiffness to optimize motor reconstruction.54 Scars on the upper extremity should be noted and may represent a peripheral nerve injury that will also require surgical management, or it may affect the availability of a potential donor nerve for transfer. Surgical scars from the management of orthopedic or vascular injury may also alter the surgical approach or overall reconstructive plan. The functional status of all muscle groups of the shoulder and upper extremity is fully evaluated in order to prioritize the reconstructive goals. Assessment of the number of potential nerve or muscle donors will help to generate a realistic reconstructive plan. The level and severity of injury can be estimated by the pattern of muscle denervation. Root avulsion injury can be diagnosed by the loss of function in those muscles whose nerve supply arises at the root level. Only a few of these muscles can be properly assessed by clinical examination. The long thoracic nerve (C5–C7) innervates the serratus anterior muscle, the dorsal scapular nerve (C4–C5) innervates the levator scapulae and the rhomboid muscles, and the phrenic nerve (C4–C5) innervates the corresponding hemidiaphragm. Denervation of the serratus anterior typically results in scapular winging, but this will be difficult to demonstrate in a patient with a paralyzed extremity. Only a very proximal lesion will result in the loss of function in these muscles and is consistent with a root avulsion injury. EMG studies will be helpful in assessing serratus anterior function. Avulsion of the C8–T1 roots will result in Horner syndrome (ptosis, miosis, and anhydrosis) due to injury to the cervical sympathetic fibers present at the same level that ultimately travel with

the trigeminal nerve to the orbit and contribute to oculopupillary function.50 At the trunk level, the suprascapular nerve (C5–C6) is the only nerve branch that can be assessed by physical examination. The suprascapular nerve is a branch of the upper trunk and innervates the supraspinatus and infraspinatus muscles, which abduct and externally rotate the shoulder. Denervation and atrophy of these muscles will result in prominence of the scapular spine. The supraspinatus specifically can be evaluated by the patient’s ability to externally rotate the shoulder against resistance (by blocking the forearm) with the elbow flexed if the musculocutaneous nerve is functioning. Numerous motor nerve branches arise at the cord level inferior to the clavicle. The lateral and medial pectoral nerve branches arise from the lateral and medial cords, respectively. Both the clavicular and sternocostal heads of the pectoralis major muscle are innervated by the lateral pectoral branches, whereas the medial pectoral branches supply only the sternocostal head. The pectoralis major muscle is easily palpated at the anterior axillary fold with adduction of the upper arm against resistance. The medial cord also gives rise to the medial antebrachial cutaneous (MABC) nerve, which provides sensation to the medial aspect of the volar forearm. The posterior cord has three motor branches to muscles of the posterior shoulder and axilla. The upper and lower subscapular nerves innervate the subscapularis muscle and the teres major muscle, respectively. The thoracodorsal nerve innervates the latissimus dorsi muscle, which can be directly assessed by palpating the posterior axillary fold while the patient coughs. The axillary nerve, which innervates the deltoid and teres minor muscles, is a terminal branch of the posterior cord. Denervation of the deltoid results in atrophy, which is readily apparent on physical examination and contributes to weakness or loss of shoulder abduction. The terminal cord branches make up the major peripheral nerves of the upper extremity. The lateral cord terminates as the musculocutaneous nerve, which innervates the coracobrachialis, biceps, and brachialis muscles and the sensory component to the median nerve. The medial cord terminates as the ulnar nerve and the motor component of the median nerve. The posterior cord terminates as the radial nerve. The functional status of the major peripheral nerves is evaluated by standard examination of hand and wrist function and their respective sensory territories.

14 Electrodiagnostic Studies EMG is performed on every patient prior to surgical management and is frequently repeated to monitor recovery of muscle function. Upon insertion of the EMG needle electrode, muscle denervated by a peripheral lesion, such as a brachial plexus injury, will exhibit spontaneous discharges (fibrillations) as compared to normal muscle, which will not show any electrical activity. Denervated muscle will continue to contract upon direct stimulation of its nerve for up to 72 hours, after which wallerian degeneration distal to the lesion will occur in any injury more severe than a neurapraxia, and neurotransmitters will no longer be present distal to the injury. However, because fibrillation potentials may not appear for up to 6 weeks following injury, EMG studies obtained before 6 weeks following

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Brachial Plexus Injuries nerve injury will be of limited utility. The results of EMGs will also reflect the severity of the injury and can therefore be used to follow the recovery of muscle function. Polyphasic lowamplitude potentials or nascent reinnervation potentials will appear prior to any clinical evidence of return of muscle function. As a muscle continues to recover, there will be a decline in the number of fibrillation potentials, and the return of and then a corresponding increase in the voluntary motor unit action potentials (MUAPs).55 MUAPs reflect distal motor sprouting from uninjured axons, whereas nascent units represent connections to motor end plates from regenerating injured axons. The presence of MUAPs or nascent units is a favorable sign for the eventual recovery of muscle function if present by 3 to 4 months past injury and should always be checked before proceeding with surgical reconstruction. If MUAPs are present, then recovery without surgical intervention is usually forthcoming. However, decompression of a “recovering” nerve at a known area of nerve compression will enhance ultimate function.

Radiographic Studies Plain radiographs can demonstrate fractures that may be helpful in evaluating the level and severity of injury, as well as the availability of certain potential donor nerves for transfer. A transverse process fracture of a cervical vertebra indicates a possible root avulsion injury because of the location of the deep cervical fascia between the transverse processes and the cervical roots.56 A clavicle fracture should alert the clinician to the possibility of compression injury to the underlying plexus or sharp injury by a bone fragment if there is comminution. If intercostal nerve transfers are being considered for the reconstruction of a complete brachial plexus injury, rib fractures demonstrated by plain films would prohibit their use as donor nerves. Similarly, a chest radiograph will evaluate diaphragmatic function and the status of the phrenic nerve for consideration as a potential donor motor nerve. A fracture of the scapula or first or second rib suggests a very severe injury with high force.

CT Myelography CT myelography combines the use of contrast material to visualize the integrity of the dural sheath around the nerve root and cervical computer tomography (CT) scanning. In root avulsion injury, tearing of the surrounding dural sheath heals by the formation of scar tissue and is visualized as a pseudomeningocele by CT/myelography. The absence of a root at a particular level is diagnostic of root avulsion. A pseudomeningocele is consistent with a root avulsion injury but is not diagnostic, as the dural sheath may remain intact despite root avulsion, or a dural tear may occur without root avulsion. This study is best obtained after at least 1 month from the time of injury after the dural sheath has had adequate time to heal. If performed too soon, the contrast dye may flow through the insufficiently healed dural tear into surrounding spaces and obscure the image, or any remaining blood clots may alter the distribution of the dye and lead to artifact. CT/myelography is commonly obtained and has a reported sensitivity and specificity of 95 and 98%, respectively.1,57

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Magnetic Resonance Imaging Magnetic resonance imaging (MRI) can also be used to evaluate the brachial plexus and offers some advantages over CT/myelography. First, patient sedation is not needed, as it is a noninvasive study. MRI can directly visualize the entire brachial plexus, as well as surrounding tissues, in sufficient detail to define anatomical relationships in three dimensions. Signs of tissue injury such as edema and inflammation will demonstrate increased signaling. Specifically, neuroma formation will be visualized as regional thickening on T1-weighted imaging and unusually increased signaling on T2-weighted imaging. The capability of MRI to image in multiple planes permits detailed visualization of the distal brachial plexus.58 The cervical roots are visualized best in the axial plane, and the trunks seen best in the oblique coronal plane; for the cords, the sagittal and oblique coronal planes are preferred. The introduction and popularization of nerve transfer technique make some of these tests moot. For example, with C5–C6 injuries, even if a very proximal stump of the C5 or C6 root is available, the more distal nerve transfer would be used to recover shoulder and elbow function without the use of nerve grafts in many situations. Studies that suggest complete avulsion will allow the surgeon to proceed with reconstructive surgery earlier, as no spontaneous recovery is anticipated. Newer techniques and protocols of MRI are emerging that offer more detailed three-dimensional imaging and may contribute to more precise surgical planning.59

14.4.3 Principles of Management In general, open injuries to the brachial plexus are managed with exploration and repair, if possible, depending on the mechanism of injury. As with any open nerve injury, if the mechanism involves rupture or avulsion, and the extent of the injury is unclear, definitive reconstruction with grafts is delayed, as discussed in more detail in the section Operative Management. All closed injuries undergo conservative management with the exception of confirmed root avulsions or disruption farther distally. The patient is observed and followed by clinical examination and EMG studies looking for evidence of functional muscle recovery for 3 months. If there are no signs of recovery of muscle function either clinically or electrically after 3 months, then surgical reconstruction is indicated.

Physical Therapy The maintenance of optimal joint mobility is important to maximize functional return whether from spontaneous recovery or surgical reconstruction. Physical or occupational therapy will be helpful for many patients, especially early during rehabilitation, and should be prescribed if necessary. Following reconstruction with nerve or muscle transfers, exercises for motor reeducation and strengthening will be essential once the target muscles have reinnervated for a successful outcome. There are a subset of plexus patients who even with excellent hand therapy have horrific hand stiffness.

Pain Management Severe brachial plexus injuries, especially avulsion injuries, are often associated with crippling neurogenic pain, which often

Brachial Plexus Injuries diminishes significantly after 1 year following injury. Motor and sensory reconstruction with peripheral nerve transfers will improve the pain. However, referral to pain management is frequently beneficial. Initially, medications such as Lyrica and tricyclic antidepressants may provide some relief or improvement and allow management by the surgeon. However, if the pain becomes chronic and debilitating, a referral to a pain management specialist should be made for optimal control. Management options may include a combination of medications from different classes, nerve blocks, or, if all else fails, further referral to a neurosurgeon for possible cauterization of the intraspinal dorsal root entry zone (DREZ).55 We do not recommend consideration of this procedure for at least 1 year following the injury.

Peripheral Entrapment Neuropathy Both the suprascapular and axillary nerves can develop distal entrapment sites at the suprascapular notch60–62 and quadrangular space,63,64 respectively, which could be decompressed to facilitate and maximize regeneration. This is readily performed at the same time as brachial plexus reconstruction. The suprascapular notch is present at the superior border of the scapula just medial to the base of the coracoid process. The roof of the notch is formed by the transverse scapular ligament, which is typically divided. The notch itself may be deep and narrow or wide and shallow and has been classified into six types. It is most commonly wide and U- or V-shaped, but in rare cases the ligament may be completely ossified.65 The suprascapular artery may run with the nerve through the notch but is usually over the ligament and joins the nerve in the supraspinous fossa, where the nerve is located medial to the vessels. In addition to the supraspinatus and infraspinatus muscles, the suprascapular nerve distal to the notch provides articular branches to both the glenohumeral and acromioclavicular joints,66 innervating up to two-thirds of the shoulder capsule.67 Entrapment at the suprascapular notch may be the result of trauma, a direct blow to the shoulder, or intrinsic or extrinsic compression, such as a tumor or cyst, or it may be idiopathic. Extremes of scapular position may cause traction on the nerve, which becomes taut and kinked over the edge of the ligament, creating a “sling effect” that leads to nerve irritation.61,65,66 Transmitted forces from direct trauma or traction injury to the shoulder or brachial plexus have been thought to be significant etiologic factors.68 The most common diagnostic findings are a deep and diffuse pain localized to the posterior and lateral aspects of the shoulder that may refer down the arm, to the neck, or to the upper anterior chest wall. In more severe cases, there may be muscle weakness and atrophy, along with electrical evidence of muscle denervation. In the setting of brachial plexus injury, these findings are nonspecific, and the most important sign will be tenderness to direct pressure over the suprascapular notch.60 The quadrangular space through which the axillary nerve passes is formed just beneath the shoulder joint by the long head of the triceps medially, the proximal humerus laterally, the teres minor superiorly, and the teres major inferiorly. Entrapment at this location, the quadrilateral space syndrome, can generally be characterized by pain poorly localized to the shoulder, paresthesia in a nondermatomal distribution, and discrete point tenderness in the quadrilateral space.69 An arteriogram may show compression of the posterior circumflex

humeral artery with shoulder abduction. Abnormal oblique fibrous bands may be found on exploration.69 The etiology is unclear, and most reported cases have been of insidious onset69,70 and rarely reported as posttraumatic.71–74 However, a traumatic etiology is supported by several factors, including involvement of the dominant extremity in most cases, rare bilateral involvement, and absence in cadaver dissections.69 It may also be related to repetitive trauma from the surrounding rotator cuff muscles. Fascial and fibrous bands are divided to decompress the space, but no muscle is divided.63 By themselves, entrapments at these sites are relatively infrequent disorders. Because brachial plexus injuries are usually severe and involve high-impact forces, the shoulder girdle is often involved in a large zone of injury. Even though the soft tissue injury may be focused on the region of the supraclavicular plexus, direct or traction forces may also lead to edema, inflammation, fibrosis, and scarring at these distal sites that can impede regeneration after nerve graft or transfer reconstruction. We therefore prefer the posterior approach for both the suprascapular and axillary nerves, as it readily allows decompression at the suprascapular notch and quadrangular space, respectively, when performing reconstruction, as described in more detail below. We believe that decompression of the suprascapular notch and quadrangular space should be done more frequently. In other situations of nerve injury, we recommend release of regenerating nerves at known areas of nerve compression. Patients should be examined for evidence of Tinel signs at known areas of nerve entrapment, and nerve release should be performed if these signs are present. This has been very helpful for recovery of median and ulnar nerve function with decompression at the cubital tunnel, Guyon canal, median forearm at the arcade of Frohse, and carpal tunnel. Thus, in brachial plexus injuries, consideration for decompression at these potential entrapment points should be given.

Neuralgic Amyotrophy (Parsonage-Turner Syndrome) Neuralgic amyotrophy is an uncommon disorder of unknown etiology that can occur in a sporadic or hereditary autosomal dominant pattern. Also known as brachial neuritis or Parsonage-Turner syndrome, it was first described by Parsonage and Turner in 1948 in 136 servicemen.75 Patients with neuralgic amyotrophy will be referred with nontraumatic brachial plexopathy and rarely require surgery. The disorder is characterized by an attack of severe neuropathic pain, followed by patchy paresis involving the upper extremities. It has been reported to have an incidence of 1.64 to 3.00 cases per 100,000 people based on data from the Mayo Clinic database and the United Kingdom.76,78 The precise etiology remains unclear but has been linked to a variety of factors, including infection, viral disease, surgery, immunization, trauma, and autoimmune mechanisms.79 In a recent case series of 199 patients with idiopathic brachial neuritis, 53.2% reported an antecedent event, with the most prevalent being infection (43.5%), exercise (17.4%), and surgery (13.9%), but the type of surgery was not specified. We have followed a small series of five patients with brachial neuritis following cervical spinal surgery with exposure of the cervical roots that form the brachial plexus. Two of these patients had other potentially contributing factors as well, including an

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Brachial Plexus Injuries upper respiratory and herpes simplex virus (HSV) infection. Influenza-like illnesses have been described in up to one-quarter of cases,80 and several viruses have been implicated, including Epstein-Barr, varicella zoster, coxsackie B, and parvovirus B19.81,82 Perioperative stress has been known to activate latent viral infection such as zoster presumably by suppression of the immune system.83 Cervical spine surgery may be a significant trigger of brachial neuritis secondary to either local manipulation of the roots of the brachial plexus or exposure to immunologic or inflammatory conditions.84 The most common presenting symptom is severe pain involving the shoulder that is frequently sudden, sometimes awakening the patient from sleep, and may radiate down the arm, sometimes extending below the elbow or up along the neck. Resolution of the pain after hours or even up to weeks will then be accompanied by delayed motor weakness. The patterns of weakness may include muscles innervated by one peripheral nerve, by multiple peripheral nerves, by one or more nerve trunks, or a combination of these.85 The most commonly involved nerves are the axillary (up to 70% of patients), the suprascapular, the long thoracic, and the musculocutaneous nerve.86– 88 Other less commonly affected nerves are the radial nerve, AIN, and median nerve.89–98 Muscle weakness is therefore most commonly noted in the deltoid, followed by the supraspinatus, infraspinatus, serratus anterior, biceps, triceps, and wrist and finger extensors, with atrophy occurring to varying degrees. Involvement of the diaphragm has been described, with patients reporting dyspnea and tachypnea.89 Sensory changes may also present generally in a distribution that reflects the affected nerves. The most common sensory presentation is hypesthesia over the lateral shoulder and upper arm, reflecting the sensory distribution of the axillary nerve, with the radial aspect of the forearm being the next most frequent site. The motor deficits are generally complete, whereas the sensory changes may be profound but not quite complete. Diagnosis is usually a clinical one based on history and physical findings, and EMG is usually the most helpful for localization and confirmation. The findings may be variable but generally demonstrate acute denervation, indicating an axonal neuropathy.92 There may be slowing of conduction velocities, especially distally, but they are frequently normal. 93 Findings evident within weeks of the onset of symptoms will generally show fibrillation potential, positive waves, delayed distal latencies, and decreased amplitude of action potentials. 87,88,93, 94 After several months there may be signs of early regeneration with polyphasic action potentials.86,88 MRI may be helpful but has also been controversial. 77,79 It has been reported to show high-intensity signals on T2-weighted images in the supraspinatus, infraspinatus, and deltoid muscles and diffuse atrophy of these same muscles in the long term but on a report of only three cases.95 Parsonage-Turner syndrome is usually benign and self-limiting with a favorable prognosis of full recovery by 3 years in 90% of patients.89 However, more recent reports have shown a less favorable outlook. Van Alfen and van Engelen in 2006 followed 246 patients with the disorder and found that almost one-third of patients suffered from chronic pain; the majority of patients still had persisting functional deficits after an average followup of more than 6 years.77 In general, the treatment is supportive for relief of pain and discomfort and may include

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analgesics, corticosteroid administration, rest, and even immobilization.96,97 Once the pain improves, many have advocated active rehabilitation with physical therapy to recover the previous level of mobility, range of motion, and strength. 86,97 There is usually no role for operative management in these cases because of the diffuse pathology and proximal location. The majority of patients can be managed satisfactorily with pain management and physical therapy, but in select circumstances, surgical intervention can be undertaken.98 We have performed nerve transfer reconstruction of motor function in several cases in which motor recovery was not forthcoming. Our practice is to reevaluate these patients at monthly intervals and proceed with nerve transfer if there remains no electrical evidence of reinnervation after 6 to 9 months, with the rationale being that denervation of more than 1 year will likely preclude any functional muscle recovery,99,100 and successful surgical intervention must be undertaken well prior to this.101 We have another group of patients with no spontaneous recovery after 6 to 9 months or even longer who respond to simple decompression. This implies a “double crush” type of scenario.

Radiation-Induced Brachial Plexopathy Radiation-induced brachial plexopathy (RIBP) is a neurologic impairment of a transient or permanent nature as a result of radiotherapy. The mechanism is incompletely understood but is believed to be secondary to localized ischemia and failure of cellular proliferation. Fibrosis of the neural and perineural soft tissue as a result of microvascular insufficiency leading to entrapment of nerve fibers is the end result.102–108 In addition, ischemic demyelination or metabolic disruption of axonal electrical properties as a result of nerve ischemia may result in persistent conduction block that is commonly observed in RIBP. 108–111 The incidence of RIBP is 1.2% of women irradiated for breast cancer and, in general, 4.5% among patients receiving chemotherapy compared to 0.6% without chemotherapy. 102, 112 The effect of chemotherapy is not completely understood, but it may enhance the effect of radiation on nerve tissue and consequently reduce the latency period of presentation. Johansson and colleagues analyzed the dose–response curve of RIBP by retrospective analysis of 150 patients with breast cancer.113 They advocated a greater awareness of the wide range of side effects from radiotherapy and the long latency period before clinical manifestation. They found that doses believed safe after 5 years may still cause serious late side effects well after the 5-year period regardless of treatment protocol. As such, any tendency toward the use of fewer, larger fractionation doses for economic benefit in patients with potentially curative disease is not recommended. Clinical manifestations of RIBP may begin anywhere from 6 months to 20 years after the completion of radiotherapy, with a median time of 1.5 years.114 The most common initial symptoms are motor weakness of the upper extremity, edema, and sensory changes, such as numbness, paresthesia, and dysesthesia. Pain is not common but when present will usually localize to the shoulder and proximal arm. The associated muscle paralysis is thought by most to be an axonal injury with muscle denervation. Because a conduction block or neurapraxia plays a significant role in the nerve injury, the axon itself may be viable and maintain the target muscle in a healthy state. The natural

Brachial Plexus Injuries history of RIBP has been variably reported. Pierce et al found that 80% of their RIBP patients experienced spontaneous improvement, whereas in 20% there was progressive deterioration.112 However, other investigators have observed that up to one-third of RIBP patients deteriorated quickly, while the other two-thirds remained stable for years.115,116 Imaging modalities, including CT, MRI, and positron emission tomography (PET) have been used to distinguish RIBP from a neoplastic process, the main differential diagnosis. MRI is the best study to image the brachial plexus, and a diffusely thickened plexus with signal intensity similar to skeletal muscle is consistent with RIBP-associated fibrosis.117–121 A neoplastic process, by contrast, would be visualized as a focal mass. A PET scan demonstrates malignant etiologies of brachial plexopathy with increased uptake of 18-fluoro-2-deoxy-D-glucose.122 A malignant etiology, either tumor recurrence or radiation-induced neoplasm, will present with a different pattern of neurologic involvement than RIBP. A tumor will present with more focal symptomatology,103,123 whereas RIBP is more diffuse because of the global extent of the radiation field and is less commonly very distal or proximal. Electrodiagnostic studies will demonstrate nerve conduction abnormalities in 90% of all patients with either neoplastic or radiation plexopathy. Myokymic discharge (abnormal spontaneous discharges accompanied by wavelike muscle quivering) is much more frequently seen in patients with radiation plexopathy (63%) than those with a neoplastic process (4%).124–126 However, nerve conduction studies will not be able to differentiate between RIBP and a neoplastic etiology of the brachial plexus.111 The presence of prolonged conduction block and its association with myokymic discharges has been strongly correlated with RIBP. 108–111 Even asymptomatic patients following radiotherapy have been shown to have some degree of segmental demyelination in brachial plexus fibers by electrophysiologic studies.126 Numerous supportive treatments have been recommended for RIBP. Physical therapy is essential to prevent lymphedema andatrophy and to maintain joint mobility.103 Medical therapy, including tricyclics, antiarrhythmics, anticonvulsants, nonsteroidal antiinflammatory drugs (NSAIDs), and steroids, may help to improve neuropathic pain.127 Anticoagulant agents have been reported to promote some recovery of motor function in RIBP theoretically by improving nerve ischemia as a possible pathogenic factor.128 As with any brachial plexus pathology, patients with chronic and intractable pain may be candidates for transcutaneous electrical nerve stimulation (TENS), dorsal column stimulator therapy, and DREZ lesions.103,127,129 The main focus of surgical management has been to release fibrotic tissue and any mechanical compression of the plexus and its nutrient vasculature and to improve its vascularity by transferring well-vascularized, nonradiated tissue or muscle around the plexus. Neurolysis alone may provide some relief of pain in a minority of patients. Others have advocated neurolysis with transfer of an omental or latissimus dorsi flap as a source of well-perfused tissue to improve ischemia.130–133 However, such interventions have not been consistently successful but have achieved some improvement in motor function and pain in some patients, with others reporting deterioration following such surgery.116,134 We have performed nerve transfer reconstruction to restore muscle function in this patient population

when conservative treatment and neurolysis were not successful. We have found in such cases target muscles in very healthy condition despite a prolonged period of loss of function and contraction upon stimulation of the distal nerve, indicating the presence of a proximal conduction block. Nerve transfers have excellent potential in these cases because there is no period of denervation prior to reconstruction. 135 This demonstrates that even with fibrillations on EMG, a significant component of the problem is chronic neurapraxia.

Accessory Nerve Injury There are several unique features to accessory nerve injury. Its small diameter and superficial location in the posterior triangle of the neck make it very susceptible for injury in the common situation, for example, of lymph node biopsies. Innervating the trapezius muscle, it has enormous importance in upper extremity function. The identification of an injury to the accessory nerve is often delayed because a portion of the trapezius muscle is usually functioning from the “accessory” accessory nerve; clinically, this can be a false-positive finding that contributes to a delay of diagnosis of a complete injury to the main accessory nerve. Similarly, electrodiagnostic studies are difficult because of the overlap of the paraspinal muscles and the fact that with some electrical activity in the upper trapezius muscle, the physicians caring for patients with these injuries can be given false assurance that this is a partial injury with an anticipated recovery. Patients with a complete injury of the main accessory nerve will not be able to abduct their arm past 90 degrees but will have a shoulder shrug from the partial innervation of the upper trapezius muscle. The scapular winging is most noticeable with eccentric contraction when the patient is asked to abduct the arm to 90 degrees, then slowly lower the arm back down to the side. Winging from the long thoracic serratus muscle palsy is most noticeable with forward flexion of the shoulder and seen most remarkably when the patient slowly lowers the arm from the forward flexed position. Because this nerve carries such important upper extremity function, injury to the accessory nerve is frequently involved in litigation. It is our contention that, given the fact that this is such a small nerve, injury to this nerve can be more a matter of informed consent than negligence. Although general anatomy textbooks tend to show the anatomy of the accessory nerve as fairly simplistic, in reality the small-diameter nerve anatomy in the posterior triangle is very complicated. There are multiple small cutaneous nerves in this area that can easily be mistaken for the accessory nerve. Some anatomical pointers can help with the identification of the accessory nerve, and it is important to accurately identify the proximal and distal portions of that nerve during repair. It is important to know with certainty that both the proximal and distal stumps of the accessory nerve have been accurately identified. We have seen situations where it is likely that inappropriate proximal and distal matching has occurred, and small cutaneous nerves have been misinterpreted as the injured, nonfunctioning motor accessory nerve. When doing an accessory nerve reconstruction, we often bring a detailed anatomy book into the operating room and note that the accessory nerve is more proximal in the neck than the greater auricular nerve. We may identify the greater auricu-

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Brachial Plexus Injuries lar and then look for the accessory nerve just above this. We identify the branch to the sternocleidomastoid and follow the accessory nerve distally into the posterior triangle region. The trauma from the original injury will be noted with a lot of scar tissue. We move distally to this area of trauma and attempt to identify the distal accessory nerve by gently spreading in the normal tissue distal to the area of injury but in line with the proximal accessory nerve. We call this slowly “wishing” the accessory nerve out. If we have any trouble identifying the distal accessory nerve, then we move even more distally and divide the trapezius muscle attachment from the clavicle and reflect some of the trapezius muscle off the clavicle. The distal accessory nerve is intimate with the trapezius muscle lying just on the posterior surface of the muscle. There will be several cutaneous nerves that are located just away from the muscle; these must not be confused with the distal accessory nerve, which is absolutely adjacent to the trapezius muscle. There have been situations where the injury on the accessory nerve is so proximal that we have not been able to successfully identify a proximal stump of the accessory nerve even when we have asked our otolaryngologic colleagues to assist with this identification. In these situations, we have used a portion of the middle trunk, separating the pectoral muscle branch fascicular group from the middle trunk and transferring this over as a nerve transfer to the distal accessory nerve with good results.136 In general, the results with reconstruction of the accessory nerve are excellent if performed in a timely fashion.

Operative Management Open Injuries Open injuries to the brachial plexus account for a minority of brachial plexus injuries and are treated as any other open peripheral nerve injury. Operative exploration and repair is usually indicated only for associated injuries to surrounding tissues, such as vascular structures. Only with a sharp transection injury should primary nerve repair be considered. Otherwise, any element of avulsion or crush injury will increase the zone of injury, which cannot be reliably determined at the initial exploration. If located, the proximal and distal nerve stumps can be tagged with suture to facilitate their identification at the time of definitive reconstruction or approximated if possible to minimize contraction of the nerve ends and the resulting size of the nerve gap. After 3 weeks, scar tissue formation has occurred sufficiently to accurately define the zone of injury, resect the injured nerve segments, and reconstruct the resulting gap as needed.50 Occasionally, the surgeon may wish to proceed with acute reconstruction. However, in these instances, it is important to resect proximally and distally so as not to be reconstructing within the zone of injury. In general, we would proceed with proximal reconstruction to control pain or for suprascapular or axillary nerve function but rely on distal motor nerve transfers if available for quicker recovery. Gunshot injuries generally cause mixed degrees of nerve injury, especially neurapraxia and axonotmesis, leading to a significant rate of spontaneous nerve regeneration and muscle reinnervation.137 Wound exploration at the time of injury is indicated only for associated injuries to vascular or other critical structures. Management is conservative for these patients for 4 to 5 months as compared to 3 to 4 months for closed injuries, as

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a higher percentage will recover some function spontaneously. If no signs of functional improvement either clinically or electrically are seen at that time, then operative management should proceed.

Closed Injuries Closed traction injuries are seen in the vast majority of patients referred for traumatic brachial plexus palsy. Management is nonoperative for at least 3 months following injury to permit evaluation for any spontaneous functional recovery. As discussed previously, we would allow 6 to 9 months of observation for cases of brachial neuritis. The importance of maintaining joint mobility of the shoulder, elbow, wrist, and digits should be stressed, and pain management should be optimized, including referral to a pain clinic if more routine pain medications are insufficient. After 3 months postinjury, the patient should be examined again clinically, and electrodiagnostic studies should be repeated. If there is some evidence of muscle reinnervation, whether clinically or electrically, then nonoperative management is continued, and the patient should be reassessed at periodic intervals. It is essential that the recovery of motor function occurs in an anatomical sequence consistent with nerve regeneration from proximal to distal. Recovery in a nonanatomical sequence suggests mixed degrees of injury, and operative management is indicated to reinnervate those target muscles that do not show evidence of recovery by 3 to 4 months. As an example, if a patient has good recovery of hand function but still remains without elbow flexion, then reinnervation of the musculocutaneous nerve should proceed.50

Exploration The patient is positioned on the operating table supine and with the ipsilateral upper extremity abducted on a hand table or arm board. The lower extremity, neck, or chest should be prepared in the field as necessary for the harvest of nerve grafts for reconstruction. If anatomical reconstruction of a proximal brachial plexus injury is planned, then a supraclavicular approach with the shoulder adducted is preferred. For distal reconstruction using nerve transfers, an infraclavicular exposure, or possibly even only a medial upper arm or back exposure may be sufficient. The use of paralytic medication should include only those that are short-acting if necessary during induction or withheld until the appropriate nerves have been exposed and a thorough functional assessment has been completed. The incision for a supraclavicular exposure can be transverse about 1 to 2 cm above the clavicle for suprascapular reconstruction (see Chapter 12). It is best extended along the posterior border of the lower sternocleidomastoid muscle if the roots are being explored (▶ Fig. 14.8). Retraction of the sternocleidomastoid anteriorly and dissection and mobilization of the supraclavicular fat pad superiorly will expose the proximal brachial plexus. Care should be taken to preserve any supraclavicular sensory nerves if they are functioning that are encountered during dissection of the fat pad. The roots will be located traveling between the anterior and middle scalene muscles, with the phrenic nerve running longitudinally across the anterior surface of the anterior scalene muscle. For an infraclavicular brachial plexus exposure, the in-

Brachial Plexus Injuries

Fig. 14.8 Transverse supraclavicular incision located ~1 to 2 cm above the clavicle for exposure of the proximal brachial plexus, trunks, and roots. If necessary, the incision can be extended superiorly along the posterior border of the sternocleidomastoid muscle or inferiorly along the deltopectoral groove and through the anterior axillary fold in a zigzag fasion to minimize scar contracture.

14 Fig. 14.9 This and the following seven figures are intraoperative photos of infraclavicular approach to the brachial plexus. This photo shows markings for the infraclavicular approach to the brachial plexus. The incision extends from the clavicle inferiorly along the deltopectoral groove, across the axillary fold in a zigzag manner to minimize contracture, and then extended inferiorly along the brachial sulcus.

cision extends from the clavicle to the anterior axillary fold along the deltopectoral groove, through the anterior axillary fold in a zigzag manner, then inferiorly in the brachial sulcus on the medial upper arm (▶ Figs. 14.9–14.16). To obtain full access to the brachial plexus, the pectoralis major muscle will have to be reflected medially after detaching its insertion from the humerus and the pectoralis minor divided superiorly near its origin. It is beneath the pectoralis minor muscle that the medial pectoral nerve branches from the medial cord will be located if use as a donor motor nerve for transfer

is being considered. We do not reconstruct the pectoralis minor. Intraoperative evaluation of the injured nerves is performed including gross examination, electrical stimulation, and sometimes intraoperative conduction studies, to determine the zone and degree of injury. Injured nerve segments can be determined by scarring and thickening of the epineurium with firmness and induration on palpation. Internal neurolysis of the injured segment will relieve compression from the surrounding scar tissue and the fascicles can be di-

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Fig. 14.10 Deep to the soft tissue of the skin, the pectoralis major muscle is identified with its insertion onto the proximal humerus. Distally, the median nerve is identified superficially, and the brachial vein is located just medial to the median nerve.

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Fig. 14.11 The pectoralis major is identified, and by using blunt dissection to surround the muscle, the tendinous insertion of the muscle is identified along the proximal humerus.

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Fig. 14.12 The pectoralis major muscle is taken down by sharply incising the tendinous insertion. A cuff of tendon is left on the humerus to allow for reattachment of the pectoralis major muscle at the end of the procedure.

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Fig. 14.13 The pectoralis major muscle has been released from the humerus at its tendinous insertion. Note that a cuff of tendon remains on the humerus for later reattachment.

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Fig. 14.14 The pectoralis major muscle is retracted using strong nonabsorbable sutures. Deep to the pectoralis major muscle, the biceps brachii muscle is identified. On the medial aspect of the biceps muscle, the median nerve is identified in the soft tissue.

rectly assessed. Further evaluation is made by direct nerve stimulation using a standard handheld, battery-operated nerve stimulator (Vari-Stim III) or by nerve to nerve intraoperative conduction studies to assess sensory nerves as well. If direct nerve stimulation causes muscle contraction or verified action potentials, then internal neurolysis only of the scarred segment of nerve is performed. If there is no nerve function or muscle contraction, then reconstruction is indicated with either neuroma resection and nerve grafts or distal nerve transfers.

Nerve Grafts

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Nerve grafts are indicated for the reconstruction of gaps due to direct nerve injury and transection, neuroma resection, or for nerve transfers using donor nerves that are too distant for direct transfer.138,139 In any instance, it is critical that all scarred nerve tissue be resected such that the proximal and distal nerve ends contain only healthy uninjured nerve fascicles. The most commonly used nerves for grafting in brachial plexus reconstruction are the MABC and the sural nerve. The MABC is convenient to use because it is harvested through the same medial upper arm exposure as the distal plexus and terminal branches, and there is frequently no donor morbidity as the nerve is often nonfunctional due to the injury. It is larger in caliber than the sural nerve and does not usually have branches in the upper arm until within a few centimeters of the elbow, so up to 25 cm can potentially be harvested. The sural nerves provide the largest source of nerve graft material, up to 30 to

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35 cm from each leg, depending on the length of the lower leg. Its sensory territory is the dorsolateral aspect of the foot and therefore is expendable. It derives from the tibial nerve in the popliteal fossa and the peroneal nerve at the fibular head, and its course is along the posterior midline of the lower leg, so it is more readily exposed with the patient in the prone position but can be harvested in the supine position with some effort with the hip and knee flexed as well. A single longitudinal incision will provide the best exposure of the sural nerve and its branches, or a series of four or more smaller incisions will minimize the donor scar. The use of endoscopic technique or a specialized nerve harvester can further minimize the number of incisions. In general, nerve grafts are most successful at ≤ 6 cm.

Motor Nerve Transfers In the case of root avulsion or a very high brachial plexus injury, the proximal nerve stump may not be present or accessible to permit graft reconstruction. Motor nerve transfer becomes the only reconstructive option available for these patients. We prefer reconstruction with distal motor nerve transfers as our first choice regardless of level of injury or proximal stump availability because of several advantages.140 This technique permits dissection in uninjured and unscarred tissue planes and minimizes the regeneration time and distance. Optimal muscle reinnervation is dependent on a sufficient quantity of regenerating motor axons reaching their target neuromuscular junctions within approximately 1 year following the injury. Consequently,

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Fig. 14.15 Deep to the pectoralis major muscle, the pectoralis minor muscle is identified as it inserts onto the clavicle. The pectoralis minor muscle is taken down from the clavicle with cautery and retracted. It is not reattached at the end of the procedure. In this exposure, the median nerve is identified medial to the biceps brachii muscle, and the ulnar nerve is seen just medial to the median nerve at this level.

the outcomes after proximal nerve repair or reconstruction with grafts are frequently poor because of the irreversible loss of the target motor end plates by degeneration and fibrosis. 141 The selection of motor nerves to donor muscles that are in close proximity to the target muscle(s) will minimize the regeneration distance and time and help ensure muscle rein-

nervation prior to permanent motor end plate loss. Unlike muscle transfers, because there are no tendon repairs and the muscle is left undisturbed in its anatomical position, adhesive scar formation that restricts muscle and tendon gliding is minimal, and original muscle biomechanics remains intact. Indeed, Guelinckx et al in an important study has

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Fig. 14.16 Division of the pectoralis minor and exposure of nerves. Once the pectoralis minor muscle is retracted, the medial pectoral nerves are identifiable in the fatty soft tissue medially. Laterally, the lateral cord of the brachial plexus is identified, and with gentle blunt dissection the terminal branches of the brachial plexus can be identified.

Fig. 14.17 Two-decade-old illustration demonstrating the relatively greater motor supply to the biceps than the brachialis muscles. B, biceps; BR, brachialis; CB, coracobrachialis; LABC, lateral antebrachial cutaneous nerve; MP, medial pectoral nerve. (Used with permission from Brandt KE, Mackinnon SE. A technique for maximizing biceps recovery in brachial plexus reconstruction. J Hand Surg Am 1993;18(4):726–733.)

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Fig. 14.18 (a) One-decade-old anatomy of the brachial plexus with musculocutaneous, median, and ulnar. (b) Illustration of double fascicle nerve transfer. FCR, flexor carpu radialis; FCU, flexor carpi ulnaris; LABC, lateral antebrachial cutaneous nerve. (Used with permission from Mackinnon SE, Novak CB, Myckatyn TM, Tung TH. Results of reinnervation of the biceps and brachialis muscles with a double fascicular transfer for elbow flexion. J Hand Surg Am 2005;30(5):978–985.)

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Fig. 14.19 An illustration showing improved understanding of the nerve supply to the biceps and brachialis muscles, as well as the topographical relationship of these branches with sensory lateral antebrachial cutaneous (LABC) nerve component. (a) Medial pectoral to musculocutaneous nerve transfer. (b) Double fascicular transfer demonstrating the topographical relationship of the donor motor fascicles of the ulnar and median nerves and transfer to nerve branches to the elbow flexors. The redundant flexor carpi ulnaris (FCU) fascicle of the ulnar nerve is transferred to the biceps branch of the musculocutaneous nerve, and the redundant or expendable motor fascicle of the median nerve is transferred to the brachialis branch.

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Fig. 14.20 Identifying locations of neurolysis on the median and ulnar nerve by first isolating the recipient biceps brachii and brachialis branches. The branches can be mobilized to determine the appropriate donor nerves and the locations of neurolysis for a tension-free repair. This image demonstrates the median nerve (flexor digitorum superficialis [FDS]/flexor carpi radialis [FCR] fascicle) as an appropriate donor nerve for the biceps brachii and the ulnar nerve (flexor carpi ulnaris [FCU] fascicle) for the brachialis. This step will prevent unnecessary intraneurolysis when isolating the donor fascicles. Superficial cutaneous nerves are protected to reach this exposure.

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Fig. 14.21 Isolating the donor median and ulnar nerve fascicles. The FDS/FCR fascicle is found on the ulnar aspect of the median nerve. The FCU fascicle is found on the radial aspect of the ulnar nerve. Intraoperative stimulation is used to confirm the appropriate donor nerve function, as well as the remaining intact median and ulnar nerve function.

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Fig. 14.22 Double fascicle nerve transfer. The double fascicular nerve transfer restores elbow flexion by reinnervating both the biceps brachii and brachialis muscles. The FDS/FCR fascicle of the median nerve is used to reinnervate the biceps brachii. The FCU fascicle of the ulnar nerve is used to reinnervate the brachialis. The donor nerves may reinnervate either recipient nerve for a tension-free repair. Please not we now typically do the ulnar to biceps and median to brachialis.

shown that the tendon repair impairs the recovery of muscle function more than neural or vascular repairs in a model of vascularized functional muscle transfer. 142 The choice of optimal donor nerve is based on factors such as the quantity of motor axons, location near the target muscle, and synergy of muscle function. Nerve branches that innervate muscle only or motor fascicles that can be readily neurolyzed from a mixed nerve, such as the FCU fascicle of the ulnar nerve, are preferred donor nerves.33,143 The use of donor nerves that innervate expendable muscles that provide a synergistic function to the target muscle will facilitate postoperative rehabilitation and motor reeducation and increase the likelihood of a successful result. If the donor muscle is nonsynergistic or even antagonistic, rehabilitation will be more difficult and extensive, and the outcome may be less favorable.144 Ideally, the donor nerve should be fully functional and uninjured; however, an injured but recovered donor nerve is frequently used, and even an injured nerve in which further recovery is anticipated may be considered based on limited donor availability. In this fashion, the recovering motor nerves “recover” into the critical muscle.

Elbow Function In general, functional reconstruction following a complete brachial plexus injury has traditionally focused first on restoring elbow flexion, followed by shoulder abduction. As such, the donor nerve with the largest caliber and greatest number of motor

axons should be used for elbow flexion. In our center at Washington University in St. Louis, Missouri, we use the following donor nerve branches in order of preference if availability permits, depending on the severity of the injury: redundant FCU fascicle of the ulnar nerve, redundant FCR or palmaris longus fascicle of the median nerve (usually together with the FCU fascicle for both biceps and brachialis reinnervation), FDS, medial pectoral nerves, thoracodorsal nerve, distal spinal accessory nerve, and intercostal nerves.

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Our first choice if available is the double fascicular transfer (DFT) consisting of a primarily FCU fascicle of the ulnar nerve to the biceps or brachialis branch of the musculocutaneous nerve and a primarily FCR, FDS, or palmaris longus fascicle of the median nerve to the brachialis or biceps branch.33 The median nerve is better transferred to the brachialis branch because motor reeducation is more synergistic (the median nerve links with pronation and the biceps with supination). This allows the transfer of regenerating motor axons very close to the neuromuscular junction of the elbow flexors with no donor morbidity. The FCU-to-biceps transfer was first described by Oberlin et al.32 Two decades ago the emphasis was on reinnervation of only the biceps, as demonstrated in ▶ Fig. 14.17, showing significantly greater innervation and axonal supply to the biceps as compared to the brachialis and the coracobrachialis, both of the latter two being given equal significance.145

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Fig. 14.23 (a) Illustration of a modified Oberlin transfer with flexor carpi ulnaris (FCU) fascicle transfer to the biceps branch of the musculocutaneous nerve augmented by transfer of the medial pectoral nerve to the brachialis branch with interposition nerve graft. (b) Intraoperative photo of a modified Oberlin transfer: (A) FCU fascicle transfer to biceps branch; (B) interposition nerve graft from the medial pectoral nerve (C) to the brachialis branch of the musculocutaneous nerve (D).

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Fig. 14.24 Thoracodorsal nerve-to-musculocutaneous nerve transfer. (a) Illustration of transfer of the thoracodorsal nerve to the biceps and brachialis branches of the musculocutaneous nerve. (b) Intraoperative photo of dissection of the anterior (1) and posterior branches (2) of the thoracodorsal nerve, and the biceps (3) and brachialis branches (4) of the musculocutaneous nerve transfer (shoulder to left; elbow to right). (c) Completed transfer of the thoradorsal nerve branches (1) to the musculocutaneous nerve branches (2). Nerve graft is rarely needed. The thoracodorsal nerve can also be tansferred directly to the musculocutaneous nerve proper.

However, we were the first to recognize the important contribution of the brachialis muscle to elbow flexion and recommend the DFT to reinnervate both the biceps and brachialis muscles (▶ Fig. 14.18) with Paul Manske (personal communication) confirming for us the overriding importance of the brachialis as the stronger elbow flexor.33 A more recent illustration of ours (▶ Fig. 14.19) reflects the progression of our understanding of the elbow flexors and demonstrates more accurately the anatomy of the musculocutaneous nerve in terms of the relative nerve supply to the biceps and brachialis muscles, as well as the internal topography of the motor branches in relation to the sensory LABC component. 146 For example, there are about 3,500 nerve fibers in the biceps and brachialis nerves respectively and over 7,000 in the LABC.

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While injury to C5,6 is a commonly seen pattern in upper brachial plexus injuries, involvement of the C7 can still occur. When this happens, the surgical management changes from a double fascicular transfer to a single fascicular transfer (FCU to biceps) with median to radial nerve transfers/ tendon transfers for C7 radial nerve loss. Injury to C7 results in flexor carpi radials (C6,C7) as potential donor, leaving flexor carpi ularnis to transfer to biceps brachii to restore elbow flexion. This is why that a précis examination and specific electrical studies must be performed as this will dictate the appropriate surgical management. In addition, pronation function may be weak and pronator teres is affected in these injuries.

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Fig. 14.25 Intercostal nerves-to-musculocutaneous nerve transfer. (a) Incisions for exposure of the intercostal nerves in the chest and the musculocutaneous nerve in the medial upper arm. (b) Intraoperative dissection of several intercostal nerves divided anteriorly and transposed posteriorly and superiorly toward the axilla. (c) Closer view. (d) Proximal end of reversed sural nerve graft after passing through the subcutaneous tunnel in the axilla to chest exposure and sutured to the distal ends of the intercostal nerves.

Complete Plexus Injuries Medial pectoral nerve branches and the thoracodorsal nerve are also good options if the median and ulnar nerves are not functioning, and a direct repair to the musculocutaneous nerve is usually possible. With a complete brachial plexus injury, the distal accessory nerve and intercostal nerves are usually available. The distal accessory will require a long nerve graft and, as discussed below, is generally reserved for transfer to the suprascapular nerve for shoulder function. The intercostal nerves are very small, and although direct transfer to the proximal musculocutaneous nerve in the axilla is feasible, the regeneration distance is still relatively long. Less favorable options are the contralateral partial C7 root and the phrenic nerve.29,147 Because the contralateral C7 root requires a very long nerve graft, usually the ulnar nerve is used as a vascularized nerve graft based on the supratrochlear vessels.148 However, this transfer is generally performed to recover finger flexion, as discussed below.

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The phrenic nerve, although a good quality motor nerve, is critical for respiratory function, and its use as a donor nerve for transfer causes potential long-term morbidity on diaphragmatic function, especially in patients who smoke. Patients with complete brachial plexus injuries have very limited donor nerve options for transfer, and the use of the phrenic nerve has the potential to contribute toward functional restoration. It has been used to recover elbow as well as shoulder and hand function with good results reported either by providing a greater number of donor motor axons for a target muscle or by allowing the reinnervation of more critical target muscles.35,36,149–154 However, use of the phrenic nerve has also been shown to measurably diminish respiratory function.35,149 Forced vital capacity (FVC), forced expiratory volume in 1 second (FEV 1), vital capacity (VC), and tidal volume (TV) were significantly reduced for over 1 year after use of a unilateral phrenic nerve, and recovery may take up to several years or more.150,155 Hypoxemia has also been reported with either unilateral or bilateral

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Fig. 14.26 Double nerve transfer involving the suprascapular nerve. (a) Landmarks for the location of the suprascapular and distal accessory nerves from a posterior approach. The distal accessory nerve is located 44% of the distance on a line drawn from the thoracic spine to the angle of the acromion on the shoulder. The suprascapular nerve is found traversing the suprascapular notch, which is located at the midpoint of a line drawn from the medial border of the scapula to the angle of the acromion. (b) Scapula from a posterior view. The suprascapular notch is at the midpoint between the medial border of the scapula and the acromion. Note the notch is located at the angle of the free edge of the scapula. Most anatomy texts incorrectly show this as a straight line, not angled.

phrenic nerve interruption.155–157 In contrast, use of intercostal nerves significantly reduced FVC, FEV1, and VC for less than 1 month, and TV was reduced for 6 months.150 The amount of reduction of each of these parameters was also significantly greater when the phrenic nerve was used as compared to intercostal nerves. Loss of diaphragmatic function can be devastating, and methods for restoration of diaphragm function include electrical pacing, usually reserved for patients with cervical quadriplegia or disorders of the central nervous system.158–162 Efforts have been made toward both repair of the phrenic nerve and nerve transfer. Although we have done a transfer from a rectus abdominis motor branch to the phrenic nerve in just one case, others have reported satisfactory results with similar nerve transfers, including use of the spinal accessory nerve136 or intercostal nerves as donor motor nerves.164 Future management options could include diaphragmatic transplantation for cases in which the diaphragm is not recoverable or available.165 Our colleagues in the Division of Cardiothoracic Surgery at our institution believe that using the phrenic nerve for transfer is ultimately a “very bad idea,” as pulmonary function may be significantly compromised as the patient ages, especially in smokers.

Specific Procedures to Restore Elbow Flexion Double Fascicular Transfer Intraoperative photos of a double fascicular transfer are shown in ▶ Fig. 14.20, ▶ Fig. 14.21, and ▶ Fig. 14.22.166 A longitudinal incision is made along the brachial sulcus in the middle third of the medial upper arm. After incising the brachial fascia, the musculocutaneous nerve is not usually immediately visualized but can be digitally palpated against the humerus in the proximal portion of the incision. Alternatively the LABC is found

distally just proximal to the elbow and followed proximally to the brachialis and biceps branches. The musculocutaneous nerve is identified traveling deep in the brachial sulcus between the biceps and brachialis muscles, and the branches to these muscles are isolated. The biceps branch arises from the musculocutaneous nerve in the midarm, which then divides farther distally into the LABC nerve and the brachialis branch, which projects deeper into the arm and is more medial. To confirm the LABC nerve, gentle traction on the nerve between the two motor branches produces a pulling on the skin in the proximal forearm. The median nerve is found closely approximated to the brachial vessels, and the ulnar nerve is located farther medially in the neurovascular sheath. Both are mobilized and verified by electrical stimulation. Topographically, the motor fascicles in the median nerve are found on the medial side of the median nerve and the sensory component on the lateral side of the median nerve. The expendable motor component of the ulnar nerve is located on the lateral or central portion of the ulnar nerve (▶ Fig. 14.20). But note the expendable portion of the median nerve is between the two critical and non-expendable pronator and anterior interosseous groups (see Chapter 6). To locate fascicles of appropriate caliber and sufficient length for direct transfer, internal neurolysis of these nerves is performed adjacent to the biceps and brachialis branches (▶ Fig. 14.21). The brachialis branch is neurolyzed proximally, divided, and moved toward the median or ulnar nerve to select the best match to the donor nerve. Care is taken to plan the location of the neurolysis of the donor nerve at an appropriate level opposite the recipient nerve to allow the transfer. Either the median or ulnar nerve is used as a donor for the biceps or brachialis transfer, depending on the ease to which they would transfer to the recipient nerve. A handheld nerve stimulator (Vari-Stim III) is used to confirm the function of these nerves

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Fig. 14.27 Course of the distal accessory nerve as it travels from proximal to distal on the deep surface of the trapezius muscle. The trapezius muscle is reflected to show that the nerve is on the anterior/deep surface of the muscle giving branches to the upper, middle, and lower trapezius muscles.

and to identify the expendable fascicles that innervate the FCR, FDS, or palmaris longus of the median nerve and the FCU of the ulnar nerve. The ground needle of the stimulator is placed close to the neurolyzed section of the donor nerve to allow for greater specificity of stimulation. In all cases, an expendable FCU fascicle of the ulnar nerve is used, as originally described.167,168 From the median nerve, a redundant FCR fascicle with or without innervation to the palmaris longus or an expendable FDS fascicle can be used. The selected donor fascicle is mobilized for up to 1 to 2 cm as permitted. Sufficient residual median and ulnar nerve function is verified and confirmed by electrical stimulation of the remainder of the donor nerve prior to transfer. The donor fascicle is divided as distally as necessary and the recipient nerve as proximally as necessary to facilitate a direct repair without tension throughout the range of movement of the extremity. The fascicle used for transfer usually makes up 15 to 20% of the entire nerve. The FCU fascicle of the ulnar nerve is coapted in an end-to-end fashion to the biceps or brachialis branch, and the motor fascicle of the median nerve is coapted directly to the recipient nerve branch using 9–0

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nylon suture and standard microneurosurgical technique (▶ Fig. 14.22). The following list details the operative steps to performing the DFT: 1. Identify and electrically stimulate the median nerve. 2. Distally, in the biceps/brachialis interval, identify the LABC. 3. Identify the BR nerve in the same biceps/BR interval. 4. Follow the musculocutaneous nerve proximally to the distal axilla and identify the biceps branch in the midarm. 5. Electrically stimulate the musculocutaneous nerve to ensure no function. 6. Use surface anatomy to visualize the course of the ulnar nerve behind the medial epicondyle and then identify and electrically stimulate the ulnar nerve in the incision. 7. Neurolyze the biceps, BR, and LABC nerves from the musculocutaneous nerve. 8. Move the BR and biceps branches toward the median and ulnar nerves. 9. Decide on the appropriate donor/recipient nerve configuration based on the best tension-free orientation but favor median to BR and ulnar to biceps.

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Fig. 14.28 (a) Anatomical relationship of the suprascapular nerve and its proximity to the distal accessory nerve as it travels inferiorly along the deep surface of the inferomedial portion of the trapezius muscle. (b) The suprascapular ligament is divided under direct visualization, and the suprascapular nerve is transected as proximally as possible to obtain length for a tension-free repair. The distal accessory nerve is divided as distally as possible for the same reason. Both ends are then transposed toward each other for a direct end-toend transfer. Work hard to follow donor as distal and recipient as proximal as possible otherwise you will need a graft, defeating the purpose of nerve transfer.

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Fig. 14.29 Landmarks for the location of the suprascapular and distal accessory nerves from a posterior approach. The thoracic spine, the medial border of the scapula, and the acromion are identified and marked. The distal accessory nerve is located 44% of the distance on a line drawn from the thoracic spine to the angle of the acromion on the shoulder. The suprascapular nerve is found traversing the suprascapular notch, which is located at exactly the midpoint of a line drawn from the medial border of the scapula to the angle of the acromion.

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Fig. 14.30 Intraoperative photo demonstrating the posterior approach to the suprascapular nerve. The trapezius muscle is split in line with the muscle fibers, and the suprascapular notch is initially palpated deep in the wound. Using deep retractors, the suprascapular ligament of the suprascapular notch is identified and exposed. A Kitner blunt dissecting instrument is used to fully visualize the ligament prior to division.

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Fig. 14.31 The suprascapular nerve is identified as it traverses the suprascapular notch. The suprascapular ligament has been divided in order to visualize and isolate the nerve.

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Fig. 14.32 The suprascapular nerve transected proximally.

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Fig. 14.33 Intraoperative photo demonstrating the identification of the distal accessory nerve. The trapezius muscle is split farther medially, and the nerve is identified on the deep surface of the muscle in the fat. It is then dissected distally as far as possible to obtain length for direct end-to-end coaptation.

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Fig. 14.34 Intraoperative photo demonstrating the proximity of the suprascapular nerve and distal accessory nerve. The distal accessory and its distal branches have not yet been transected in this image.

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Fig. 14.35 Intraoperative photo demonstrates the distal accessory and suprascapular nerves as they have been reflected toward each other for direct transfer. By transecting the donor nerve distally and the recipient nerve proximally, a direct tension-free coaptation is achieved.

10. Drape the donor nerve across the recipient nerve, ink the location of the proposed repair, and move the elbow back and forth to make sure that the greater excursion of the ulnar nerve near the elbow is taken into account when the location of the ulnar nerve neurolysis is planned. 11. Plan the fascicular neurolysis immediately distal to where the recipient easily crosses the donor nerve. 12. Neurolyze the donor fascicles from the median and ulnar nerve over a distance of ~ 1 cm. The median donor is located medial and anterior. The ulnar donor is located lateral and anterior. Identify and protect the pronator and AIN fascicles in the median nerve. 13. Place the ground of the nerve stimulator close to the neurolyzed section and stimulate the neurolyzed potential donor fascicle to ensure there is motor function. 14. Stimulate the portion of the median nerve not involved in the transfer to make sure there is good AIN function and pronation. 15. Stimulate the ulnar nerve not involved in the nerve transfer to ensure there is good intrinsic ulnar hand function and flexor digitorum profundus function to the fourth and fifth digits. 16. Divide the donor fascicles distally and set up the repair prior to placing the sutures to make sure there is no tension on the repair with movement of the extremity. 17. Check for a little bit of redundancy of the recipient nerve close to the repair to ensure no tension exists at the repair sites through full range of movement of the extremity. Use 9–0 suture.

18. Place some adhesion barrier (Seprafilm) or fibrin sealant (Tisseel) over the repair sites. 19. Immobilize the arm in a sling for 10 days.

Medial Pectoral Nerve-To-Musculocutaneous Nerve Transfer The musculocutaneous nerve is exposed through a longitudinal incision along the brachial sulcus of the medial upper arm and usually travels deep between the biceps and brachialis muscles. The incision is extended proximally in a zigzag fashion through the anterior axillary fold to minimize contracture, then along the deltopectoral groove to the clavicle. The pectoralis major muscle is exposed, and its insertion onto the humerus is dissected from surrounding tissue, isolated, and divided, taking care to leave a cuff of its tendon on the humerus adequate for suturing for reattachment. The pectoralis major muscle is then reflected medially, and the pectoralis minor muscle is exposed, isolated proximally, and divided. Large nonabsorbable sutures may be used to mark the proximal and distal sites of the tendon of the pectoralis major on the humerus and muscle to allow for the accurate reapproximation at the end of the surgery. This exposure allows mobilization of the musculocutaneous nerve proximally to its origin from the lateral cord of the brachial plexus to maximize length. Medial and inferior reflection of the pectoralis muscles will expose medial pectoral neurovascular structures traveling to their deep surface. Specifically, the pectoralis minor muscle must be divided, and with a nerve stimulator “tapping” on the deep surface of the pectoralis minor (not major), the functioning medial pectoral nerves can be identified.

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Fig. 14.36 (a) Intraoperative photo demonstrates the suprascapular notch and ligament. The suprascapular vessels are lateral and superficial to the suprascapular ligament. (b) The suprascapular nerve is identified after the suprascapular ligament has been divided. The suprascapular vessels are protected laterally. (c) The suprascapular nerve is transected proximally to obtain length and reflected superficially toward the distal accessory nerve. (d) The distal accessory nerve is directly coapted to the suprascapular nerve without tension. Patient prone, left shoulder, midline to right, shoulder to left, head above.

Usually, two or three medial pectoral nerve branches can be found, verified by electrical stimulation, and mobilized for several centimeters. These branches are then transected as distally as possible to maximize length and transposed laterally toward the musculocutaneous nerve, which is transected as proximally as possible to minimize the length of nerve graft required. A direct transfer to the distal stump of the transected musculocutaneous nerve is usually possible, and a short nerve graft is rarely needed (▶ Fig. 14.19a). This is because the musculocutaneous nerve can be neurolyzed proximally even into the lateral cord because the pectoralis major muscle is reflected. We have also used this transfer to the brachialis branch to augment the standard transfer of the FCU fascicle of the ulnar nerve to the biceps branch (▶ Fig. 14.23).146 The FCU fascicle transfer is performed as described previously in the section Double Fascicular Transfer.

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Thoracodorsal Nerve-To-Musculocutaneous Nerve Transfer The musculocutaneous nerve is exposed through a longitudinal incision along the brachial sulcus of the medial upper arm and usually travels deep between the biceps and brachialis muscles. Mobilization is performed as proximally as possible to maximize length, but visualization of its origin from the lateral cord of the brachial plexus is usually not possible without taking down the insertion of the pectoralis major muscle onto the humerus. A longitudinal incision is then made on the lateral chest wall in the midaxillary line several centimeters below the axilla. The anterior border of the latissimus dorsi muscle is exposed and elevated to expose the deep surface of the muscle and the thoracodorsal neurovascular pedicle. The thoracodorsal nerve can be verified by electrical stimulation and is then mobilized as proximally and distally as possible, including its anterior and

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Fig. 14.37 Reinnervation of an end-toside neurotization of the suprascapular nerve from the spinal accessory nerve to restore supra- and infraspinatus function and to preserve trapezius function. (a) In this case, a neurectomy at the coaptation site of the spinal accessory nerve was created to stimulate sprouting of the motor fibers. (b) In addition, an axonotmetic injury was created proximal to the end-to-side neurotization through a compression to induce reinnervation of the entire distal accessory nerve and trapezius muscle. (c) Wallerian degeneration proceeds distal to the axonotmetic injury following the compression. (d) Afterward, axonal regeneration proceeds through the native donor and into the recipient pathway through the end-toside repair. The lateral antebrachial cutaneous (LABC) graft was measured at 3 cm for this case. (Adapted with permission from Ray WZ, Kasukurthi R, Yee A, Mackinnon SE. Functional recovery following an end to side neurorrhaphy of the accessory nerve to the suprascapular nerve: case report. Hand (NY) 2010;5 (3):313–317.)

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Fig. 14.38 Supraclavicular incision for anterior approach spinal accessory to suprascapular end-to-side nerve transfer.

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Fig. 14.39 Anterior approach spinal accessory to suprascapular end-to-side nerve transfer. (a) Donor spinal accessory nerve was identified through the superior border of the trapezius. The upper trunk was also identified. (b) The recipient suprascapular nerve was neurolyzed away from the upper trunk. (c) A motor end-to-side nerve transfer occurred, which includes a partial neurectomy and a proximal crush of the donor nerve. This allows nerve fibers to proceed into the end of the recipient suprascapular nerve while preserving the spinal accessory nerve. An LABC nerve graft was required to bridge the gap for a tension-free repair.

posterior branches. A subcutaneous tunnel is created through the axilla superficially to avoid injury to major axillary structures connecting the chest and arm exposures. The thoracodorsal nerve branches are divided as distally as possible, and the nerve is transposed through the axillary tunnel and brought out through the superior end of the arm exposure. A direct transfer is then usually possible to the distal stump of the musculocutaneous nerve, which is transected as proximally as possible to maximize length and allow a direct repair to the thoracodorsal nerve. Occasionally, a short graft is needed (▶ Fig. 14.24).

Distal Accessory Nerve-To-Musculocutaneous Nerve Transfer

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This transfer is typically restricted to complete avulsion injuries. The musculocutaneous nerve is exposed through a longitudinal incision along the brachial sulcus of the medial upper arm and usually travels deep between the biceps and brachialis muscles. Mobilization is performed as proximally as possible to maximize length, but visualization of its origin from the lateral cord of the brachial plexus is usually not possible without taking down the insertion of the pectoralis major muscle onto the humerus. An angled or curvilinear incision is then made on the ipsilateral shoulder near the base of the neck along the anterior border of the trapezius muscle. The muscle is exposed and retracted posteriorly. The accessory nerve is usually found fairly superficially along the anterior border of the trapezius in the proximal portion of the exposure near the base

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of the neck or along the deep surface of the muscle in the distal portion of the exposure as the lateral clavicle is approached. The nerve stimulator is very helpful in identifying the accessory nerve. If there is difficulty finding it, then the trapezius muscle attachment to the clavicle can be divided and reflected. The nerve is very intimately related to the muscle. This is an important finding to identify the accessory nerve, as there are many nerves in this area. The accessory nerve also communicates with the second, third, and fourth cervical nerves, and the proximal portion may assume a rather plexiform arrangement, making identification of the proximal stump in the case of an injury difficult at times. The accessory nerve is then dissected as deep and posteriorly as possible to visualize branches to the upper trapezius. These are preserved, and the distal accessory nerve is transected as distally as possible to allow transposition more superficially out of the wound to facilitate suture repair. To spare as much of the upper and middle trapezius motor branches as possible, we have also dissected the distal accessory from the posterior approach just above the scapular spine and passed a nerve graft anteriorly for retrieval from an anterior approach to reach its target muscle. The musculocutaneous nerve is then transected as proximally as possible, and a reversed sural or MABC nerve graft is harvested, passed through a subcutaneous tunnel between the shoulder and arm exposures, and sutured to the proximal stump of the distal accessory nerve and the distal stump of the musculocutaneous nerve.

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Fig. 14.40 (a) Detailed illustration of the left shoulder (patient prone) and relevant anatomy surrounding the axillary nerve and the triceps branches of the radial nerve, which are identified by vessel loops. The axillary nerve traverses the quadrangular space whose borders are the teres minor superiorly, the teres major inferiorly, the long head of the triceps medially, and the humerus laterally. The radial nerve and its triceps branches traverse the triangular space whose borders are the teres major superiorly, the long head of the triceps medially, and the humerus laterally. The medial head of the triceps branch lies superficial to the medial head of the triceps muscle. (b) Detailed illustration of the nerve transfer of the medial triceps branch of the radial nerve to the axillary nerve. The sensory branch of the axillary nerve (i.e., the superior lateral cutaneous nerve) is identified and transferred end to side to the lateral aspect of the radial nerve to provide sensation to the lateral shoulder and upper arm.

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Intercostal Nerve(s)-To-Musculocutaneous Nerve Transfer This transfer is also restricted to computer avulsion injuries. The musculocutaneous nerve is exposed through a longitudinal incision along the brachial sulcus of the medial upper arm and usually travels deep between the biceps and brachialis muscles. Mobilization is performed as proximally as possible to maxi-

Fig. 14.41 Intraoperative photo of the posterior right shoulder and the markings for the incision used for a triceps-to-axillary nerve transfer. The incision is made on the posterior shoulder along the posterior border of the deltoid muscle, extended past the posterior axillary fold, then inferiorly for ~ 5 to 7 cm along the posterior arm.

mize length, but visualization of its origin from the lateral cord of the brachial plexus is usually not possible without taking down the insertion of the pectoralis major muscle onto the humerus. A long, curvilinear incision is then made on the ipsilateral chest running obliquely from the midaxillary line along the axis of the ribs anteriorly to approximately the level of the midclavicular line. Placement just below or near the inframammary fold will provide a less conspicuous donor scar (▶ Fig. 14.25a). Wide undermining of the skin flaps is performed to expose several levels of the rib cage. Three rib levels are chosen, usually T4–T6. The soft tissues along the inferior border of the rib are elevated by subperiosteal dissection, the periosteal layer is incised, and the intercostal neurovascular bundle is exposed and mobilized both anteriorly and posteriorly to maximize length (▶ Fig. 14.25b,c). The intercostal motor branches are small and are identified by electrical stimulation. Larger branches are often sensory nerves. Motor branches supplying the rectus abdominis muscle may also be encountered, usually beneath the lower rib levels, and are generally larger than intercostal motor nerves. These should be used as donors if encountered to maximize the quantity of motor axons for transfer. The intercostal nerves are divided as anteriorly (distally) as possible and the musculocutaneous nerve transected as proximally as possible for a direct transfer or to minimize the length required of the nerve graft. A direct transfer requires more extensive mobilization of the intercostal nerves and limited shoulder abduction to prevent disruption of the repair site. A subcutaneous tunnel is

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Fig. 14.42 (a) Detailed illustration of the right posterior shoulder and relative anatomy of the radial nerve and its triceps branches. (b) Fascicular anatomy of the radial nerve and the triceps branches as they traverse the triangular space. Note that the sensory component of the radial nerve is on the lateral aspect of the radial nerve. The medial triceps branch is colored green.

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Fig. 14.43 Intraoperative photos of the posterior right shoulder exposure showing the (a) relative anatomy of the axillary nerve and radial nerve with the triceps branches. The inset demonstrates the branching of the medial triceps branch when dissected distally into the muscle. (b) Direct transfer of the distal stump of the branch to the medial head of the triceps to the proximal stump of the axillary nerve. Given the significant amount of length on the medial triceps branch, the coaptation to the axillary is performed without tension, allowing full range of motion of the shoulder. Care is taken to follow the axillary nerve as proximally as possible into the quadrangular space, so it is divided at its “smallest diameter” location in order to include the teres minor branch and to provide a better size match for the nerve to the medial head of the triceps.

created through the axilla superficially between the chest and arm exposures to pass the proximal musculocutaneous nerve. A reversed sural or MABC nerve graft if used is harvested, passed through this tunnel, and sutured directly to the intercostal and musculocutaneous nerves (▶ Fig. 14.25d). Caution should be used when harvesting intercostal nerves. Complications can include pleural tear, pleural effusion, respiratory problems, and risk increases with the number of intercostal nerves being used. Ipsilateral rib fracture may limit the availability of the intercostal nerves but is not a contraindication.169

Shoulder Function The next priority is the functional reconstruction of shoulder abduction, which includes reinnervation of the supra- and infraspinatus muscles and the deltoid. The distal accessory nerve is a standard transfer to the suprascapular nerve, which innervates the supra- and infraspinatus muscles. It is readily available even following a complete brachial plexus injury, and the trapezius provides a synergistic function. This transfer can be

performed from either the anterior or posterior approach with a direct repair usually being feasible with either approach. We frequently use the posterior approach because it also permits release at the suprascapular notch, preserves more innervation of the upper trapezius, provides a wider exposure to facilitate the nerve repair, and allows a more distal transfer to minimize the regeneration time and distance.170 The disadvantage of the posterior approach is that the patient must be positioned in the prone position, which does not allow simultaneous dissection on other regions (arm, chest) and further lengthens the surgical time because of repositioning, reprepping, and draping. However, if the need for long nerve grafts is certain, one or both sural nerves can be harvested simultaneously when prone. The prone position does however facilitate simultaneous triceps to axillary nerve transfer. We have also been very happy with an anterior approach to the accessory and suprascapular nerves. We make a partial epineurotomy in the accessory nerve and coapt the suprascapular nerve to it in an end-to-side repair. Just proximal to the repair we will crush the nerve with a jeweler’s forceps for 30 seconds

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Fig. 14.44 (a) Intraoperative photos of the end-to-side transfer of the sensory branch of the axillary nerve (i.e., superior lateral cutaneous branch of the axillary nerve) to the sensory fascicle of the radial nerve. (b) The sensory component of the radial nerve is located on the lateral aspect of the radial nerve (green). The sensory branch of the axillary nerve is coapted to the sensory fascicle in an end-to-side manner to restore sensation to the lateral shoulder and upper arm. (c) Fascicular anatomy of the radial nerve and the triceps branches as the nerve exits the triangular space. Note the location of the sensory component of the radial nerve (green) on the lateral aspect of the nerve.

to make an axonotmetic injury of all accessory fibers. We have found this results in very little accessory nerve donor deficit. A transfer to the axillary nerve to reinnervate the deltoid should also be considered if donor nerve availability permits. A triceps branch (usually to the medial head) is a good option for direct transfer if available and can be performed from a posterior approach concomitant with the posterior distal accessory-tosuprascapular nerve transfer. Transfer of medial pectoral nerve branches is also a good option if they are not being used to restore elbow flexion and can provide a direct repair. The thoracodorsal nerve is a good quality donor nerve if available and can reach directly to the axillary nerve, but it will be more difficult to rehabilitate because the latissimus muscle is antagonistic to the deltoid. If only the restoration of elbow flexion is possible, then a shoulder fusion remains an option to recover a limited degree of shoulder abduction. We have also reinnervated the serratus anterior muscle with a direct transfer from intercostal nerves to the long thoracic nerve to improve winging and scapular rotation. This is a straightforward transfer, especially if exposure of intercostal nerves following a complete injury is already necessary to restore elbow flexion. We will generally use three intercostal levels for elbow flexion and one or two nerves for the long thoracic nerve to the serratus anterior, depending on the size of the donor nerves. With isolated cases of long thoracic nerve palsies, we suggest using pectoral fascicles taken from the

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middle trunk and transferring these to the long thoracic nerve in the supraclavicular area using a standard supraclavicular brachial plexus decompression approach, as described above. To recover the lower slips of the serratus muscle, we combine this with a thoracodorsal nerve-to-long thoracic nerve transfer in the axillary. Thus, the ipsilateral C7 pectoral transfer will reinnervate the upper serratus, and the thoracodorsal-to-long thoracic transfer will reinnervate the more distal serratus muscle slips.

Specific Procedures to Recover Shoulder Function Double Nerve Transfer (accessory to suprascapular nerve, triceps branch to axillary nerve) These transfers are performed with the patient in the prone position. A transverse incision is made ~ 7 to 8 cm in length and 2 cm above the scapular spine. The suprascapular nerve is located at approximately the midpoint of a line drawn from the medial border of the scapula to the angle of the acromion, which is palpated as the bony prominence on the lateral shoulder just above the humeral head (▶ Fig. 14.26). The supraspinatus muscle is exposed and retracted inferiorly to expose the superior border of the scapula. At the medial base of the coracoid process, the suprascapular ligament is exposed and divided to decompress the suprascapular notch. The supra-

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14 Fig. 14.45 Illustration of the nerve transfer of the medial triceps branch of the radial nerve to the axillary nerve using a posterior approach. The sensory branch is excluded from the motor nerve transfer. To prevent kinking and tension of the medial branch of the triceps as it is coapted to the axillary nerve, the teres major muscle fascia is partially divided at the inferior aspect of the muscle.

scapular nerve is then mobilized superiorly above the scapula and transected as proximally as possible to provide enough length of nerve to transpose more superficially toward the distal accessory nerve. At the medial portion of the exposure, the trapezius muscle is elevated, and the distal accessory neurovascular bundle is readily identified deep to the muscle. The distal accessory nerve is located 44% medial to the midpoint of a line drawn from the thoracic spine to the angle of the acro-

mion on the shoulder. The distal accessory nerve is dissected and mobilized both proximally and distally as much as possible, then divided distally. “Look” for the accessory nerve with a nerve stimulator at this 44% point in the fat below, not in the trapezius muscle. The proximal nerve is transposed laterally to reach the suprascapular nerve, and a direct repair is performed (▶ Figs. 14.27– 14.36).

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Fig. 14.46 Triceps-to-axillary nerve transfer. (a) Intraoperative photo of the posterior right shoulder and the markings for the incision used for a triceps-to-axillary nerve transfer. The incision is made on the posterior shoulder along the posterior border of the deltoid muscle, extended past the posterior axillary fold, then inferiorly for ~ 5 to 7 cm along the posterior arm. (b) Intraoperative photos of the dissection of the axillary nerve. The red vessel loop surrounds the entire axillary nerve as it exits the quadrangular space. (c) The axillary nerve has been transected proximally in the quadrangular space to ensure including the branch to the teres minor. The sensory branch of the axillary nerve is excluded at this point to maximize regeneration into the muscles innervated by the axillary nerve. Note as you progress proximally the cross sectional area of the axillary nerve greatly decreases for better size match with the medial triceps nerve.

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To further minimize any potential donor morbidity, transfer can be performed in an end-to-side fashion with a partial neurectomy and crush injury to the accessory nerve to enhance motor regeneration with a good functional outcome (▶ Fig. 14.37; ▶ Fig. 14.38; ▶ Fig. 14.39).171 To reconstruct the axillary nerve, an oblique incision is made on the posterior shoulder along the posterior border of the deltoid muscle, extended past the posterior axillary fold, then inferiorly for ~ 5 to 7 cm along the posterior arm (▶ Figs. 14.40– 14.46).

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The interval between the deltoid and triceps muscles is dissected, and the teres major muscle is exposed deep in this interval as it inserts onto the posterior aspect of the humerus. Dissection superior to the teres major will expose the axillary nerve as it travels through the quadrangular space made by the teres minor superiorly, the teres major inferiorly, the long head of the triceps medially, and the humerus laterally. The first time you do this, bring a good anatomy book into the operating room with you. You will be impressed by the large size of the axillary nerve. Remember that the inferior branch of the nerve is

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Fig. 14.47 (a) Intraoperative photo demonstrating a transected spinal accessory nerve and its distal branches lying on the anterior surface of the trapezius muscle. (b) The spinal accessory nerve is reconstructed using an MABC nerve graft.

sensory, and tugging on this branch will result in traction on the skin overlying the deltoid. The large superior portion of the nerve will be motor to the deltoid, and the teres minor branch will come off proximally and run in a superomedial direction. It is critical to reinnervate the teres minor branch (▶ Fig. 14.43; ▶ Fig. 14.46b). If there is scarring in this region, for example, after shoulder surgery, remember that the axillary nerve is superior to the vessels, and be prepared to find the sensory portion of the axillary nerve first; keep looking and moving proximally into the quadrangular space. In this posterior approach there are two clear motor branches of the axillary nerve, the posterior easily identified and the anterior is much deeper. Look for that deeper anterior branch then follow the entire axillary nerve carefully, as for proximal as possible. Divide the tricep tendon, not the muscle, for exposure. Divide the axillary nerve as proximally as possible, as you will need the length, and your repair will be done at the smaller trunk of the axillary nerve and not out in the larger diameter branches. Multiple branches are identified, including the branch to the teres minor and the sensory branch. Inferior to the teres major, the radial nerve and its triceps branches are exposed as they pass through the triangular space whose borders are made by the teres major superiorly, the long head of the triceps medially, and the humerus laterally. The branch to the medial head of the triceps is verified by electrical stimulation, divided as distally as possible, and transposed superiorly toward the axillary nerve. The axillary nerve is divided as proximally as possible and transposed inferiorly toward the medial triceps branch for a direct repair. Division of some of the inferior tendinous portion of the teres major muscle reduces tension on the repair by effectively shortening the distance (▶ Fig. 14.40). Colbert and Mackinnon have modified Leechavengvong’s procedure to use the branch to the medial head of the triceps. This medial triceps fascicle is essentially “predis-

sected” and lies right on top of the radial nerve. It has a very long length and is very easily dissected, unlike the other triceps branches, which are shorter and quickly become intramuscular in location.172

Partial Middle Trunk Nerve Transfer A fascicle of the middle trunk to the pectoral muscle is an expendable donor for long thoracic accessory and suprascapular nerves. A supraclavicular brachial plexus exposure is performed through a transverse incision made a fingerbreadth above the clavicle. The omohyoid is divided and the supraclavicular fat pad mobilized and retracted to expose the brachial plexus. The suprascapular nerve is identified as it arises from the upper trunk in the lateral aspect of the upper trunk. The anterior scalene muscle may be divided, protecting the phrenic nerve from injury, to allow exposure of all of the root levels. The middle trunk is isolated and verified by electrical stimulation. Internal neurolysis with fascicular dissection is performed to isolate pectoral motor fascicles that will be used for transfer. When doing this procedure, you will be able to identify a fascicular group that when stimulated results in primarily pectoralis muscle function. This fascicular group is divided as distally as possible and the suprascapular nerve transected as proximally as possible to minimize the length of nerve graft required. The ipsilateral partial middle trunk transfer is used for reconstruction of the injured accessory nerve when the proximal stump is not available (▶ Figs. 14.47–14.55). It can also be transferred to the long thoracic nerve in isolated long thoracic nerve palsies. Dissection of the middle trunk proceeds as described in the previous paragraph. The accessory nerve is identified as it emerges from behind the superoposterior border of the sternocleidomastoid muscle and travels inferiorly just deep to the anterior border of the trapezius muscle. If the injury to the accessory nerve is high in the neck, it may be possible to mobilize sufficient length of the distal nerve to allow

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Fig. 14.48 Orientation for pectoral fascicle of the middle trunk-to-spinal accessory nerve transfer. The supraclavicular incision is marked from the lateral border of the sternocleidomastoid to the trapezius muscle. The lateral border of the sternocleidomastoid is marked.

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Fig. 14.49 Dividing the anterior free border of the trapezius for identification of the spinal accessory nerve. The free edge of the trapezius muscle is identified deep to the platysma muscle. Through the platysma muscle, the supraclavicular nerves are identified and protected. This free edge is divided to reflect a short portion of the trapezius to expose the spinal accessory nerve, which is immediately adjacent to the trapezius muscle.

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Fig. 14.50 Identifying the spinal accessory nerve. The spinal accessory nerve is intimate to the undersurface of the trapezius muscle. The released edge of the trapezius muscle is reflected posteriorly to facilitate easier identification of the accessory nerve.

transposition toward the brachial plexus and a direct transfer with the pectoral fascicle. If sufficient length is not available, then a MABC nerve graft will allow a tension-free transfer. If decompression of the brachial plexus per se is not indicated, a less extensive exposure of the brachial plexus roots just lateral to the scalene muscles is sufficient for neurolysis of the middle trunk, and division of the anterior scalene muscle is not necessary. We have reported a case of this transfer in a patient with neuritis resulting in accessory nerve palsy. 136 The brachial plexus was decompressed through a standard supraclavicular approach, the middle trunk was mobilized and internal neurolysis identified a fascicular component that innervated pectoralis muscle function. Proximal mobilization of the accessory nerve allowed a direct transfer to the middle trunk fascicle. After 7 months, functional muscle testing showed Medical Research Council (MRC) Grade 4 recovery of

lower and middle trapezius function. At 1 year postoperatively, the patient had recovered full range of motion of his shoulder with good trapezius function and only mild scapular winging. He recovered forward flexion of his shoulder to 142 degrees (▶ Fig. 14.56).

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Medial Pectoral Nerve-to-Axillary Nerve Transfer Exposure of the axillary nerve from an anterior approach requires a full infraclavicular brachial plexus exposure with an incision extending from the clavicle along the deltopectoral groove, in a zigzag manner through the anterior axillary fold to minimize contracture, then extending inferiorly along the medial brachial sulcus to the midarm (▶ Figs. 14.57–14.61).173 The pectoralis major muscle is exposed, and its insertion onto the humerus is isolated and then taken down, being sure to leave a cuff of tendon on the humerus sufficient for anchoring

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Fig. 14.51 Identifying the middle trunk of the brachial plexus. In this exposure, the brachial plexus is located deep to the divided omohyoid muscle. The brachial plexus is located lateral to the anterior scalene muscle. The suprascapular nerve is identified as it branches from the upper trunk. Deep to the upper trunk, the middle trunk is identified. During this exposure, the long thoracic nerve is identified lateral to the middle scalene and protected.

sutures when reattaching onto the humerus. The pectoralis major muscle is then reflected medially and the pectoralis minor muscle is exposed, isolated proximally, and divided and not repaired. Medial and inferior reflection of the pectoralis muscles will expose medial pectoral neurovascular structures traveling to their deep surface. Usually, two or three medial pectoral nerve branches can be found on the deep surface of the pectoralis minor muscle, verified by electrical stimulation, and mobilized for several centimeters. Do not look for them under the pectoralis major muscle. These branches are then transected as distally as possible to maximize length and transposed laterally. The neurovascular sheath of the plexus is incised at the level of the shoulder joint to expose the distal cord level. The axillary artery is mobilized to identify the posterior circumflex humeral branch, which serves as the main landmark to find the axillary nerve. The axillary nerve can be found just above this major

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branch point of the axillary artery. The axillary nerve is mobilized as much as possible, then divided proximally to minimize the graft length required to reach from the medial pectoral nerves to the axillary nerve. Again, the LABC or the MABC from the medial arm exposure can be used for grafting.

Thoracodorsal Nerve-to-Axillary Nerve Transfer Exposure of the axillary nerve from an anterior approach requires a full infraclavicular brachial plexus exposure with an incision extending from the clavicle along the deltopectoral groove, in a zigzag manner through the anterior axillary fold to minimize contracture, then extending inferiorly along the medial brachial sulcus to the midarm. The pectoralis major muscle is exposed, and its insertion onto the humerus is isolated and then taken down, being sure to leave a cuff of tendon on the

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Fig. 14.52 Identifying the donor pectoral fascicles of the middle trunk. (a) The pectoral fascicular group is identified on the anterior surface of the middle trunk and innervates the pectoralis major. Two pectoral fascicles are commonly found. Note that the upper trunk is retracted medially. (b) The microforceps delineate the pectoral fascicle on the anterior surface of the middle trunk.

humerus sufficient for anchoring sutures when reattaching onto the humerus. The pectoralis major muscle is then reflected medially. The neurovascular sheath of the plexus is incised at the level of the shoulder joint to expose the distal cord level. The axillary artery is mobilized to identify the posterior circumflex humeral branch, which serves as the main landmark to find the axillary nerve. The axillary and radial nerves can be found just above this major branch point of the axillary artery. The axillary nerve is mobilized as much as possible, then divided proximally to maximize length for transposition. A longitudinal incision is then made on the lateral chest wall in the midaxillary line several centimeters below the axilla. The anterior border of the latissimus dorsi muscle is exposed and elevated to reveal the deep surface of the muscle and the thoracodorsal neurovascular pedicle. The thoracodorsal nerve can be verified by electrical stimulation and is then mobilized as proximally and distally as possible, including its anterior and posterior branches. A subcutaneous tunnel is created through the axilla superficially to avoid injury to major axillary structures connecting the chest and arm exposures. The thoracodorsal nerve branches are divided as distally as possible, and the nerve is transposed through the axillary tunnel and brought out through the superior end of the arm exposure. A direct transfer is then usually possible to the distal stump of the axillary nerve.

We prefer medial pectoral to axillary nerve transfer because of ease of motor reeducation.

Two-Level Nerve Transfer for Long Thoracic Nerve Palsy Restoration of serratus anterior muscle function is important for excellent shoulder function. We have previously described using a branch of the thoracodorsal nerve from the latissimus muscle to innervate the long thoracic nerve (▶ Fig. 14.62).174 We now combine this transfer with a second transfer more proximal at the level of the supraclavicular plexus (▶ Fig. 14.63; ▶ Fig. 14.64; ▶ Fig. 14.65).174 A nerve fascicle to the pectoral muscles is identified in the middle trunk and transferred to the long thoracic nerve immediately as it exits from the middle scalene muscle (▶ Fig. 14.66). In this way, we reinnervate all the muscle slips of the serratus.

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Intercostal Nerve(s)-to-Long Thoracic Nerve Transfer A long curvilinear incision is made on the ipsilateral chest running obliquely from the midaxillary line along the axis of the ribs anteriorly approximately to the level of the midclavicular line. Placement just below or near the inframammary fold will provide a less conspicuous donor scar. Wide undermining of

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Fig. 14.53 Selecting the donor fascicle from the pectoral fascicular group. Two fascicles to the pectoralis major are identified on the anterior surface of the middle trunk. These fascicles are confirmed with stimulation, and the fascicle that elicits a stronger response is selected for the donor nerve for transfer. A length of 2 cm will be dissected for the nerve transfer.

the skin flaps is performed to expose several levels of the rib cage. One or two rib levels are chosen. The soft tissues along the inferior border of the ribs are elevated by subperiosteal dissection, the periosteal layer is incised, and the intercostal neurovascular bundle is exposed and mobilized both anteriorly and posteriorly to maximize length. The intercostal motor branches are small and are identified by electrical stimulation. Larger branches are often sensory nerves. Motor branches supplying the rectus abdominis muscle may also be encountered, usually at the lower rib levels, and are generally larger than intercostal motor nerves. These should be used as donors if encountered to maximize the quantity of motor axons for transfer. The long thoracic nerve is identified running longitudinally along the lateral chest wall just beneath the axilla. Before visualization, it can often be palpated by running the fingers along the lateral chest wall. Once identified, it is mobilized superiorly and inferiorly and separated from the vessels that make up the long

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thoracic neurovascular bundle. The intercostal nerves are then divided as anteriorly (distally) as possible and transposed laterally toward the long thoracic nerve, which is divided as superiorly (proximally) as possible and transposed inferiorly and anteriorly for a direct transfer (▶ Fig. 14.67). If intercostal nerves are also being used to transfer to the musculocutaneous nerve, this will usually use intercostal nerve T3–T5; intercostal nerve T6 ± T7 will be used for the long thoracic nerve. Otherwise, intercostal levels T3–T4 can be used for the long thoracic nerve for an easier and closer transfer.

Triceps Function Using the same posterior approach as for a medial triceps nerve-to-axillary nerve transfer, we have successfully restored triceps function when it has been absent (▶ Fig. 14.68; ▶ Fig. 14.69; ▶ Fig. 14.70).175 If the radial nerve but not the

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Fig. 14.54 Neurolyzing the donor pectoral fascicle to transfer to the recipient spinal accessory nerve. A length of at least 2 cm of the donor fascicle is dissected distally. Posterior/medial to the pectoral fascicles is the fascicle to the triceps brachii, which can be confirmed by electrical stimulation.

triceps is functioning, then a fascicle to the extensor carpi radialis longus can be teased from the radial nerve and transferred to a triceps nerve. In general, the topography of the radial nerve is sensory lateral and finger and thumb extension medial with wrist extension in the middle. We have also taken an FCU fascicle from the ulnar nerve to the triceps nerve using this posterior approach or an anterior approach. Intercostal nerves can be used but require a more time-consuming dissection.176

Hand Function Complete Plexus Injuries The reconstruction of hand function remains the most difficult because of the longer distance to the finger flexors. Few options usually remain after the more commonly used donor nerves have been used for elbow and shoulder function. The contralateral C7 root as a whole or partial transfer has been previously mentioned using an ipsilateral vascularized ulnar nerve as a long graft with the distal graft sutured to the median nerve.

However, the results are generally suboptimal both in terms of the quality of target muscle reinnervation and the difficulty of rehabilitating the injured extremity independently from the contralateral donor extremity.29,148 For these reasons, we do not advocate using this procedure. The abundance of intercostal nerves allows use of two or three levels for transfer to a long nerve graft even if intercostal nerve transfers are already used to reinnervate the elbow flexors and the serratus anterior. This allows the first stage of a staged free functional muscle transfer for hand function to be performed at the time of brachial plexus reconstruction. The use of free functional muscle transfers to restore some hand function is discussed below in the section Muscle Transfers.

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Lower Plexus Injuries Patients with a lower brachial plexus injury are also appropriate candidates for more distal nerve transfers as primary management after partial injury or partial recovery of hand function.

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Fig. 14.55 Pectoral fascicle of middle trunk to the spinal accessory nerve transfer. The nerves in this transfer are neurolyzed to sufficient length to avoid any tension by dividing the donor pectoral fascicle distally and the recipient spinal accessory nerve proximally.

For a persistent median nerve deficit, transfer of expendable branches of the radial nerve177 or the brachialis branch38,178 of the musculocutaneous nerve can be performed to restore AIN and pronator function (▶ Fig. 14.71). We have now mapped the internal topography of the median nerve in the arm to know that the fascicles to the AIN lie medial and deep. The fascicles to the palmaris longus and flexor carpi radialis and flexor digitorum sublimis lie medial and superficial. The sensory component of the median nerve is laterally located. The fascicle to the pronator lies between the motor and sensory groups as a distinct, easily neurolyzable fascicle on the anterior aspect of the nerve. If C7 is involved, then the supinator (C5) can be transferred to restore posterior interosseous nerve (PIN) function and wrist extension.179 Take the brachaialis donor nerve as distal as possible and use all of it to cover the recipient median motor deficit especially AIN, and if C7 is also involved, the pronator and FCR. Once recovery has occurred distal tendon transfers and a tenodesis of the profunda will be performed. The terminal branch of the AIN can also be used to reconstruct ulnar intrinsic hand function if

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satisfactory median nerve function has been recovered without distal ulnar nerve recovery. In complete C8T1 injuries, distal AIN is not available. We have transferred the extensor digiti quinti/extensor carpi ulnaris branches of the PIN with a nerve graft to the deep ulnar motor branch with recovery of intrinsic function.180 Such distal nerve transfers are generally used for the management of nerve injuries that occur distal to the brachial plexus and are described in detail in Chapter 5.

Other Specific Procedures to Restore Hand Function Contralateral Partial C7-to-Median Nerve Transfer with Vascularized Ulnar Nerve Graft A supraclavicular brachial plexus exposure is performed on the contralateral side through a transverse incision made a fingerbreadth above the clavicle. The omohyoid is divided and the supraclavicular fat pad mobilized and retracted to expose the brachial plexus. The anterior scalene muscle is divided, protecting the phrenic nerve from injury, to allow exposure of

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Fig. 14.56 Patient with left accessory nerve palsy. (a) The patient is unable to abduct his left arm preoperatively. (b) An intraoperative image is shown of the left base of the neck. Head is to upper right and left shoulder to lower left. The distal accessory nerve was identified (white asterisk), and a proximal C7 motor component (white arrow) was transferred to it. (c,d) One year postoperatively, the patient regained full range of motion of his left upper extremity.

all of the root levels. The C7 root is isolated and verified by electrical stimulation. Internal neurolysis with fascicular dissection is performed to isolate the posterosuperior half that will be used for transfer. This fascicular group is divided as distally as possible to allow more superficial transposition to facilitate suturing to the nerve graft. If preferred, the divisions of the middle trunk can be exposed with more distal dissection, and generally the posterior division is favored for partial transfer. On the ipsilateral arm, an incision is made from the axilla along the medial brachial sulcus to the elbow, between the medial epicondyle and the olecranon to mobilize the ulnar nerve from the cubital tunnel, then inferiorly along the ulnar aspect of the volar forearm to the ulnar side of the wrist. The ulnar nerve is mobilized entirely from the axilla to the wrist, dividing motor and sensory branches in the forearm, but the superior ulnar collateral pedicle vascularizing the proximal ulnar nerve in the upper third of the arm is kept intact (▶ Fig. 14.72a). A subcutaneous tunnel is created from the axilla across the chest to the contralateral supraclavicular region. A small counterincision midway across the chest will facilitate passage of

the nerve graft. The ulnar nerve is transected at the wrist and the distal end passed through the subcutaneous tunnel across the chest and delivered to the contralateral supraclavicular exposure for direct suturing to the hemi-C7 root that was previously divided (▶ Fig. 14.72b). In the ipsilateral upper arm, the proximal ulnar nerve is divided above the superior ulnar collateral vessels, which are preserved. The median nerve is divided at this level, and the distal stump of the ulnar nerve is transposed inferiorly and sutured directly to the distal stump of the median nerve for a transfer from the contralateral hemi-C7 root to the ipsilateral median nerve via a long vascularized ulnar nerve graft (▶ Fig. 14.72c). Because of the long length of the graft, the vascularity of the ulnar nerve graft is important to maximize the rate of regeneration. Therefore, some groups advocate performing the transfer in two stages if bleeding from the distal ulnar nerve at the wrist after transection is insufficient. The ulnar nerve is still transposed at this stage, but division of the proximal ulnar nerve and suture to the median nerve are performed at the second stage after several months to preserve sufficient

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Fig. 14.57 Medial pectoral nerve-to-axillary nerve transfer. Intraoperative photo of the exposed brachial plexus at the level of the cords and terminal branches. An infraclavicular exposure is performed with elevation of the pectoralis major muscle and division of the pectoralis minor muscle. The medial pectoral nerves are identified deep to the pectoralis minor muscle and protected using a vessel loop. The medial and lateral cords of the brachial plexus are then identified. The lateral cord and axillary vessels are retracted medially to expose the posterior cord, which has been identified and surrounded using a vessel loop. The biceps brachii muscle is retracted laterally, facilitating the exposure. The anterior circumflex humeral vessels cross over the radial nerve/posterior cord and are a landmark for identifying the axillary nerve.

vascularity to the ulnar nerve graft to maintain a higher rate of regeneration.

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Intercostal Nerve(s)-to-Sural Nerve Graft (First Stage for Free Functional Muscle Transfer) A long curvilinear incision is made on the ipsilateral chest running obliquely from the midaxillary line along the axis of the ribs anteriorly approximately to the level of the midclavicular line. Placement just below or near the inframammary fold will provide a less conspicuous donor scar. Wide undermining of the skin flaps is performed to expose several levels of the rib cage. Usually two or three rib levels are chosen. If this procedure is performed at the same time as intercostal nerve transfers to the musculocutaneous nerve, then lower rib levels will be used. The soft tissues along the inferior border of the ribs are elevated by subperiosteal dissection, the periosteal layer is in-

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cised, and the intercostal neurovascular bundle is exposed and mobilized both anteriorly and posteriorly to maximize length. The intercostal motor branches are small and are identified by electrical stimulation. Larger branches are often sensory nerves. Motor branches supplying the rectus abdominis muscle may also be encountered, usually at the lower rib levels, and are generally larger than intercostal motor nerves. These should be used as donors if encountered to maximize the quantity of motor axons for transfer. The intercostal nerves are then divided as anteriorly (distally) as possible and transposed laterally. A small counterincision is made on the medial aspect of the upper arm, and a subcutaneous tunnel is created between the chest and arm incisions superficially across the axilla. The sural nerve is used as a reversed graft, passed through the subcutaneous tunnel, and at the chest sutured directly to the intercostal nerve branches. The distal end of the graft is delivered into the arm

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Fig. 14.58 The medial pectoral nerves are identified under the divided pectoralis minor muscle. The posterior cord is identified by retracting the lateral cord and the axillary vessels medially. In this image, the anterior circumflex humeral vessels have been ligated to expose the axillary nerve as it traverses deep to the vessels. The axillary nerve is dissected proximally to obtain as much length as possible for reflection into the wound for the nerve transfer.

exposure and can be tagged with permanent suture to facilitate identification at the second stage.

Sensory Nerve Transfers Restoring sensation to the hand should be routinely considered, as many of the available donor sensory nerves are readily dissected in the same exposures being used for the motor nerve transfers. Sensation in the thumb, index, and long fingers can be restored by nerve transfer to the lateral cord contribution to the median nerve. Alternatively, transfer can be performed to the ulnar nerve in the upper arm to restore sensation to the ulnar hand and digits. At a second stage, the nerve branch to the fourth web space can be directly transferred to the nerve that innervates the first web space to supply sensation to the thumb and index finger. Donor sensory nerve options include the intercostal sensory nerve branches, supraclavicular nerves, the LABC, and intercostobrachial nerve. The choice of donor can be dictated by the

exposure(s) required for the motor nerve transfers. The intercostal sensory nerves are routinely encountered while harvesting the intercostal motor branches, and supraclavicular nerves are usually seen more superficially during a supraclavicular exposure for the brachial plexus or the anterior exposure of the distal accessory and supraspinatus nerves. The intercostobrachial nerve can be identified either during dissection of other axillary structures or when creating a subcutaneous tunnel through the axilla for other nerve transfers or grafts. Sensory nerve transfers may also be performed at the level of the distal forearm or palm in conjunction with motor nerve transfers or secondarily. The transfers are discussed in detail in Chapter 5. Transfer at a distal level will allow a more rapid recovery of sensation to facilitate postoperative therapy and motor reeducation following functional reconstruction. The functioning ulnar nerve can be used as a donor for transfer for more critical median nerve sensation in high median nerve injuries and can be performed at the level of the hand or distal forearm

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Fig. 14.59 (a) The axillary nerve has been transected proximally and tagged with a small blue monofilament suture. The medial pectoral nerves have been dissected and transected distally. (b) Despite transecting the donor nerves distally and the recipient nerve proximally, there is still a nerve gap present in this patient.

as a direct nerve transfer, such as transfer of the dorsal cutaneous branch (▶ Fig. 14.73) or noncritical branches in the hand. The common and proper digital nerves are exposed and dissected to the level of the web space, and the nerve branch to the fourth web space is transferred directly to the branch to the first web space. We use an end-to-side technique to restore protective sensation to noncritical territories, such as the donor third web space or second web space (▶ Fig. 14.74). The third web space can be used as a donor branch to restore more critical border digit sensation in a similar manner in the palm, or a sensory fascicular transfer technique at the level of the distal forearm can be done. We prefer this technique when using the nerve branch to the third web space as the donor nerve, as in a high ulnar nerve injury or upper brachial plexus palsy. The internal topography of both the median and ulnar nerves at the wrist is well defined and predictable. The motor and sensory components of each nerve are readily identified and separated; in particular, the fascicle to the third web space is readily neurolyzed for more than half the length of the forearm proximal to the wrist. However, we have not found the sensory components of the ulnar nerve to the fourth web space and to the ulnar border of the small finger to be easily separated at this level. Therefore, we prefer transfer of the digital nerve branches in the palm when using the fourth web space branch as the donor nerve and fascicular transfer at the distal forearm when reconstructing ulnar nerve sensation using the

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whole sensory component as the recipient nerve. For an upper brachial plexus injury (C5C6), the sensory fascicle to the third web space can be transferred to the first web space for critical thumb and index finger sensation (▶ Fig. 14.75). As with all nerve transfers, the donor fascicle is divided as distally as possible and the recipient fascicle divided as proximally as possible to maximize length and minimize tension at the repair site. The fascicular transfer technique avoids scars on the contact surfaces of the palm, avoids potential injury to the palmar vascular arches, and can be combined with other procedures, such as the terminal AIN transfer to the deep ulnar motor branch or sideto-side flexor tenodesis through the same exposure. These transfers are discussed in more detail in Chapter 5.

Muscle Transfers Functional muscle transfers are indicated for salvage of a failed nerve reconstruction after a brachial plexus injury, for the patient in whom reinnervation of target muscles is no longer feasible, or as primary reconstruction rather than nerve transfers and/or grafts.54,181 The decision to transfer muscles or nerves depends on the surgeon’s training, experience, and comfort level. Regional pedicled muscle transfers are most commonly performed for elbow flexion, and suitable donor muscles include the latissimus dorsi, the sternocostal head of the pectoralis major, the Steindler flexorplasty, and the long head of the triceps

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Fig. 14.60 Intraoperative photo demonstrates the exposure and harvest of the medial brachial cutaneous and the medial antebrachial cutaneous (MABC) nerves to be used as a nerve graft. The nerves originate from the medial cord and course distal, and the MABC nerve lies on the surface of the basilic vein.

muscle, even though it is antagonistic.69 Conventional tendon transfers in the forearm always remain an option for the reconstruction of hand function if the availability of donor muscles and tendons permits.182 Free functional muscle transfers are used primarily to reconstruct hand function or elbow flexion if no functioning regional muscles are available. The most commonly used donor muscles are the gracilis, the latissimus dorsi, and the pectoralis major. The long length of the gracilis muscle when used as a free motorized transfer allows the simultaneous reconstruction of both elbow and limited hand function in the patient with late presentation or who is referred long after the injury. With the muscle origin near the shoulder, the distal gracilis tendon can be sutured to the forearm tendons to restore both elbow flexion and finger flexion or extension. Frequently, tenolysis in the forearm secondarily may enhance hand function with improved although still limited range of motion of the fingers. A second gracilis transfer can be performed, also using additional intercostal nerve motors, to restore opposing finger function, as in the “double Doi” procedure.183

Secondary Procedures Secondary surgery remains an option in the latter reconstructive stages to provide additional improvement in extremity function. A shoulder fusion is always available as a backup option following a failed nerve reconstruction or in patients where such nerve transfers are not available. Because the trapezius muscle is still functional in these patients, the provided scapular rotation will translate into a limited amount of shoulder abduction if the glenohumeral joint is fused. A wrist fusion may also be used to help stabilize the wrist for improved hand function or to allow transfer of recovered wrist flexors or extensors for the reconstruction of hand function.

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Postoperative Management The period of immobilization after reconstruction depends on the method of reconstruction and the presence of nerve grafts or nerve or tendon repairs. Direct nerve repairs are typically immobilized for 1 week, depending on the laxity of the repairs and their ability to accommodate the patient’s range of joint

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Fig. 14.61 The medial pectoral nerves are transferred to the axillary nerve with the use of an MABC nerve graft. The nerves are coapted without tension.

motion. If nerve grafts have been used, there is no tension at the repair sites; therefore, only a few days of immobilization is usually necessary. For tendon or muscle transfers, 3 to 4 weeks of immobilization is followed by gentle range of motion exercises to limit adhesive scarring at the repair sites that may interfere with normal muscle or tendon excursion. If the insertion of the pectoralis major onto the humerus was taken down, shoulder immobilization for 4 weeks will be needed for satisfactory healing. Physical therapy will help the patient gradually recover as much passive range of motion at the involved joints as possible. Clinical evidence of target muscle reinnervation generally will not be apparent for several months to 1 year postoperatively, depending on the regeneration distance required to reach the target motor end plates. At one month post operatively, long before reinnervation has occurred, therapy is focused on motor reeducation to stimulate cortical remapping and more spontaneous target muscle activation.144

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Outcomes The interpretation of results of brachial plexus reconstruction has been difficult for several reasons. Because most brachial plexus injuries represent combined lesions with varying degrees of nerve injury to multiple elements of the brachial plexus, the precise staging and quantification of such injuries are difficult to standardize. The lack of consensus as to the best surgical approach to these patients with reconstruction varying widely from neurolysis and proximal anatomical reconstruction

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with nerve grafts to the use of a variety of distal nerve transfers or a combination of approaches further complicates the analysis of outcomes. Many referring physicians remain unaware of the sensitive timing of surgical management. Consequently, many referrals are made after the “window of opportunity” has shut. The outcome of functional reconstruction of the injured brachial plexus depends on the level and severity of the injury and the timing of surgical management. Because of the longer distance from which nerve regeneration must occur to reinnervate target muscles, the results generally are inferior for proximal injuries as compared to more distal lesions. Also, the greater the delay in surgical reconstruction, the less likely that functional restoration will be satisfactory because of the degeneration and fibrosis of the neuromuscular junction. Early results of proximal anatomical nerve graft reconstruction were less optimistic by current standards. Narakas in 1980 reported on 100 cases of nerve grafting after a follow-up of at least 3 years with a general approach of cable graft reconstruction of the upper three roots.184 For supraclavicular or retroclavicular lesions, he classified his results as 21% good, 43% fair, and 36% poor or none. Infraclavicular and distal lesions had better outcomes with 33% good, 40% fair, and 27% poor or none. However, he did not define his classification of the results. Millesi in 1984 reported a series of 158 cases treated with a variety of surgical approaches.185 He defined useful function as meeting the following criteria: no subluxation of the shoulder joint, some active control of the shoulder, some amount of external rotation but not necessarily abduction, and strong elbow flexion. He was

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Fig. 14.62 Thoracodorsal-to-long thoracic nerve transfer. The thoracodorsal nerve is an available donor to transfer into the recipient long thoracic nerve to reinnervate the distal serratus anterior muscle slips. Do this transfer as proximal on the long thoracic nerve as possible. The more proximal muscle slips are the most important for function.

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Fig. 14.63 Two-level nerve transfer procedure to restore long thoracic nerve function. Dashed lines indicate anatomical reference to the clavicle. (a) Nerve transfers to restore long thoracic nerve function occurred at two levels to reinnervate both proximal and distal parts of the serratus anterior muscle. (b) Proximally, pectoral nerve fascicles were neurolyzed from the middle trunk and transferred to reinnervate the upper portion of the long thoracic nerve. (c) Distally, a branch of the thoracodorsal nerve was transferred to reinnervate the lower portion of the long thoracic nerve. (Used with permission from Ray WZ, Pet MA, Nicoson MC, et al. Two-level motor nerve transfer for the treatment of long thoracic nerve palsy. J Neurosurg 2011:115(4):858–864.)

able to obtain 72.2% useful function in 23 patients treated with neurolysis only, 70.3% useful function in 89 cases of nerve graft reconstruction, and 40.9% useful function in 44 nerve transfers using the intercostal nerves. Such early reports using different evaluation methods illustrate the difficulty in comparing the results of various approaches from different institutions and to more recently reported series. However, a recent review of 31 studies including 299 patients with upper brachial plexus injuries demonstrated significantly better outcomes for elbow flexion and shoulder function with dual nerve transfers versus traditional nerve grafting.186 Kline and colleagues used the Lousiana State University Health Sciences Center (LSUHSC) scoring system,187 which is much like the more commonly used modified Medical Research Council (MRC) system (▶ Table 14.1).188 The difference is that, like Millesi’s classification, it scores overall extremity global function rather than specific movements, such as elbow flexion or shoulder abduction. It also assigns grade 2 (considered fair) to movement against gravity, which corresponds to an MRC grade 3, but specifies further as proximal muscles contract against gravity, but distal muscles

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do not contract, whereas LSUHSC grade 3 is proximal muscles contract against gravity, and some distal muscles do too. However, it is also based on a maximum 5-point score, so care is needed in comparing these results with others. Also, it is very difficult to interpret and compare specific motor functions, and therefore different techniques, for specific actions. Notwithstanding that, in a series of 208 patients with complete C5–T1 injuries treated with proximal nerve grafts, only 35% recovered an overall functional outcome of LSUHSC grade 3 (considered moderate) or better.189 As a result, Kline et al more recently combined proximal nerve graft repair with various nerve transfers using the accessory, thoracodorsal, medial pectoral, and intercostal nerves as donors with an improvement in the scores for shoulder and biceps function.190,191 Bentolilia and Sedel reported on a series of 63 patients in which both proximal grafting and nerve transfer techniques were employed.192 For elbow flexion, 44 patients had proximal graft reconstruction, and 19 received nerve transfer from the spinal accessory alone or spinal accessory with intercostal nerves or a proximal graft. In the nerve graft group, 28 of 44 patients (63%) achieved good recovery of biceps function (grade

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Fig. 14.64 Distal nerve transfer to restore long thoracic nerve function using a branch of the thoracodorsal nerve as a donor. (a) The long thoracic and thoracodorsal nerves were identified through an incision made below the right axilla. The long thoracic nerve was identified superficial to the serratus anterior, and the thoracodorsal nerve was identified on the latissimus dorsi. (b) The thoracodorsal nerve was transferred to reinnervate the distal long thoracic nerve. (Used with permission from Ray WZ, Pet MA, Nicoson MC, et al. Two-level motor nerve transfer for the treatment of long thoracic nerve palsy. J Neurosurg 2011:115(4):858–864.)

3 + or better), and the remaining had poor recovery. In the nerve transfer group, 11 of 19 (58%) recovered good function, and the remaining had fair or poor recovery. Recovery of muscles for hand and wrist function from proximal grafts was only 16% for good function. Four significant prognostic factors were the delay between the accident and surgery, a previous operation on a vascular lesion, the presence of vasomotor problems, and a Horner sign. With the increasing use of nerve transfers for this patient population by multiple centers, there has been an accumulating base of literature reporting the results of such techniques. Because many of these techniques are quite new, many series have limited numbers of patients but are still useful in summarizing outcomes. The outcomes after distal motor nerve transfers have been consistent, and especially in cases of very proximal injuries or root avulsions, have been predictably superior to reconstruction with long nerve grafts. The MRC grading system has been most commonly used to assess specific motor functions, sometimes augmented by the maximum weight that can be lifted to quantify strength. Distal nerve transfers allow the transfer of regenerating motor axons often very close to the motor end plate for faster reinnervation and the recovery of elbow flexion. Two series have reported the results of fascicular transfers from the median and ulnar nerves to the biceps and brachialis branches of the musculocutaneous nerve. Mackinnon et al reported on six patients with a mean follow-up of 20.5 months.33 Recovered elbow flexion strength was MRC grade 4 + /5 in four patients and 4/5 in two (▶ Fig. 14.76). Evidence of reinnervation of target muscles was noted at a mean of 5.5 months following surgery. Liverneaux et al reported the results of 10 patients using the same technique and

obtained elbow flexion strength of 4/5 in all patients. 193 In neither series was any permanent sensory or motor donor morbidity noted in ipsilateral hand function. The contribution of the brachialis muscle is clearly demonstrated by the superior strength obtained by reinnervation of both the biceps and brachialis muscles as compared to the reinnervation of the biceps only. Teboul et al had previously reported the transfer of an ulnar nerve fascicle to the biceps branch of the musculocutaneous nerve in 32 patients.194 Of those, 20 patients obtained a good result of MRC grade 4, 4 patients got a fair result of grade 3, and 8 patients had a poor result of grade 2 or worse. Eleven patients underwent a secondary Steindler flexorplasty to further improve elbow flexion strength. More recently, Ray and colleagues reported on a series of 29 patients with a mean follow-up of 19 months.166 All but one patient regained elbow flexion (97%). Eight patients recovered MRC grade 5/5, 15 patients had 4/4, and 4 patients recovered 3/5 strength. Again, there was no functional morbidity noted. If median or ulnar nerve function is not present, the thoracodorsal nerve has been a good and reliable source of donor motor axons in our experience, but the literature has been scant, possibly because of perceived donor morbidity. Although there is weakening in shoulder adduction strength, the effect on an upper extremity that already lacks elbow and hand function and has no or weak shoulder abduction is in reality functionally insignificant in most cases. A patient who has come to rely on holding objects between the upper extremity and lateral chest should be made aware of weakening shoulder adduction as a trade-off to recover elbow flexion. Novak et al reported on a series of six patients in which the thoracodorsal nerve was used to reinnervate both the biceps and brachialis muscles and re-

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Fig. 14.65 Proximal nerve transfer to restore long thoracic nerve function using pectoral nerve fascicles as donors. (a) Two pectoral nerve fascicles were neurolyzed from the identified middle trunk through a right-sided supraclavicular approach. Two branches of the long thoracic nerve were identified lateral to the middle trunk. (b) Two pectoral nerve fascicles were transferred to reinnervate two branches of the proximal long thoracic nerve. (c) Nerve repair was accomplished with good size match by neurotizing each pectoral fascicle with an individual branch of the long thoracic nerve. (Used with permission from Ray WZ, Pet MA, Nicoson MC, et al. Two-level motor nerve transfer for the treatment of long thoracic nerve palsy. J Neurosurg 2011:115(4):858–864.)

covered MRC grade 5 strength in one patient, 4 in four patients, and 2 in one patient.195 Samardzic et al. reviewed a series of 27 thoracodorsal nerve transfers to the musculocutaneous nerve in 12 cases and to the axillary nerve in 14 cases. 196 Eight patients underwent thoracodorsal nerve–only transfer for elbow flexion, and two recovered excellent function corresponding to MRC grade 4 + , five obtained good function of grade 4, and one recovered fair function of grade 3. Four other patients had transfer of thoracodorsal nerve plus the intercostal, subscapular, or long thoracic; of those, one had an excellent result, and three had a good result. Although not our first choice, when preferred donors are not available (median, ulnar), the thoracodorsal nerve is a consistent and reliable donor motor nerve that recovers good or better elbow flexion in most cases. Branches of the medial pectoral nerve also provide good donor motor fascicles for transfer. The dissection is more extensive, as it requires detaching the insertion of the pectoralis major muscle from the humerus and reflecting it and the pectoralis minor muscle medially to expose their deep surface and their neurovascular supply. The branches are smaller, so several need to be harvested to provide a reasonable size match for the musculocutaneous nerve. With appropriate healing of the

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muscle insertion to the humerus, donor morbidity is low, as the pectoralis major muscle maintains innervation by the lateral pectoral nerve. In 1993 Brandt and Mackinnon reported on a series of four patients who underwent transfer of branches of the medial pectoral nerve to the musculocutaneous nerve.145 The terminal LABC branch was transposed proximally in an attempt to neurotize the biceps. Three patients recovered grade 4 elbow flexion strength, and one obtained grade 3. The first evidence of reinnervation was noted at 6 to 8 months after reconstruction. A larger series was reported by Samardzic et al and included 25 patients who had medial pectoral nerve transfers, 14 to the musculocutaneous nerve and the other 11 to reinnervate the axillary nerve.197 In the elbow flexion group, two patients obtained an excellent result (4 +), four had a good result (4), three had a fair result (3), and one was classified as a bad result (no movement). In four patients, medial pectoral nerve transfer was augmented by spinal accessory or intercostal nerve transfers. Two of these patients had an excellent result, one obtained a good result, and one got a bad result. The overall functional recovery of elbow flexion has been ~ 80 to 85% of cases but limited by greater dissection and smaller and shorter donor motor branches, which may require a graft in many cases.

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Fig. 14.66 Illustration of pectoral fascicle to proximal long thoracic nerve transfer. The pectoral fascicle is an available donor to transfer to the recipient long thoracic nerve to reinnervate the proximal serratus anterior muscle slips. Two pectoral fascicles can be used.

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Fig. 14.67 (a) Intraoperative photo of the long thoracic nerve (1) transected superiorly and transposed inferiorly (to the right) next to the intercostal nerve and (2) divided anteriorly and transposed superiorly. (b) Nerve branches sutured (1) and other transposed intercostal nerves on background (2). Orientation: head to left, feet to right.

14 Total brachial plexus injuries are more difficult to manage with less promising results because of the lack of intraplexus donor availability. In such cases, the most commonly used donors are the distal accessory and intercostal nerves. When dissecting the distal accessory nerve, it is important to spare more proximal motor branches to the upper and midtrapezius muscle and harvest the portion distal to these branches to preserve shrugging and some scapular rotation, which is important functionally after a shoulder fusion. A relatively long nerve graft will then be required for transfer to the musculocutaneous nerve through a subcutaneous tunnel. The reported outcomes have been inferior to those obtained from the use of the intraplexus motor donors described above and comparable in general to or a little better than that obtained from the experience with intercostal nerves. Songcharoen et al reported on their ex-

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perience with 577 spinal accessory nerve transfers for shoulder function and elbow flexion.198 An interpositional nerve graft was necessary for transfer to the musculocutaneous nerve, and recovery time was about 1.5 years. Useful motor function defined as MRC grade 3 or better was obtained in 74% of cases. Specific patient details and timing of reconstruction after injury were not provided. Intercostal nerves are used when the preferred motor donor nerves described previously are not available. They are limited by their very small size and distance from target muscles, and they require a long and tedious harvest with unclear long-term effects on pulmonary function when harvesting multiple rib levels. We would not advise using intercostal nerves when there has been ipsilateral rib fractures or ipsilateral phrenic nerve injury, or if the phrenic nerve is also being used for trans-

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Fig. 14.68 Illustration of ulnar nerve flexor carpi ulnaris (FCU) fascicular transfer to the medial head of the triceps motor branch. Note: right posterior arm with head to right and feet to left and patient prone. (a) When approached from the posterior aspect, the ulnar nerve is found medially, deep to the long head of the triceps. (b) Transfer was performed to reinnervate the medial head of the triceps brachii. Denervated muscle is depicted in red, innervated muscle in green, innervated nerve in yellow, and denervated nerve in purple; right arm, patient prone, posterior approach. (Used with permission from Pet MA, Ray WZ, Yee A, Mackinnon SE. Nerve transfer to the triceps after brachial plexus injury: report of four cases. J Hand Surg Am 2011;36(3):398–405.)

fer. Terzis and Kostopolous described a series of 718 intercostal nerve transfers for elbow flexion, extension, and shoulder function in 2007.199 They found the lower intercostal nerves (T7– T10) to yield better results than the upper intercostals (T3–T6), and the use of three or more intercostal nerves to be better than two nerves. For elbow flexion, they obtained good or excellent results in 72% of cases. Songcharoen et al described their experience with 22 intercostal transfers to the musculocutaneous nerve.198 A good result of MRC grade 3 or better was obtained in 65% of cases, with an average time of recovery to grade 3 of 12 months. The maximum strength recovered in their series was flexion to 90 degrees while lifting a weight of 5 kg. Chuang and colleagues reviewed an original series of 66 patients using three intercostal nerves for transfer to the musculocutaneous nerve without grafts for a success rate of 67% for motor function of grade 4 or better.200 More recently, Chuang updated his experience with an average incidence of 80% for recovery of elbow flexion strength of grade 3 or better.201 A meta-analysis of 1,088 nerve transfers conducted by Merrell et al. revealed an overall success rate of 66%, with 72% of transfers exhibiting recovery of at least grade 3/5 and 37% achieving at least grade 4/5 elbow flexion.202 We do not advocate the use of the phrenic nerve as a donor, but many do and mainly for the reconstruction of elbow flex-

ion. Gu and Ma described the use of the phrenic nerve in a series of 180 patients who underwent surgery dating back to 1970.149 Of 65 patients who had follow-up of more than 2 years, 84.6% recovered elbow flexion of grade 3 or better. The time required for recovery of grade 3 strength was on average 9.5 months. One patient had a transient respiratory problem in the postoperative period, and pulmonary function tests demonstrated decreased pulmonary capacities during the first year after surgery that improved in the second year. Songcharoen et al accumulated an experience of 306 phrenic nerve transfers by 2005, with 151 patients having follow-up of more than 2 years.198 This series included transfers to the suprascapular and axillary nerves for shoulder function, as well as the musculocutaneous nerve for elbow flexion, for which the reported success rate was 60% for MRC grade 3 or better. However, they found that 73% of patients had diminished pulmonary function postoperatively, with the vital capacity reduced by an average of 9.4%, but gradually improving to the preoperative level after anywhere from 6 to 24 months. The recovery of shoulder function is usually much better than that achieved with a shoulder fusion but not as good as elbow flexion. Initial experience began with the reinnervation of preferably the suprascapular nerve or the axillary nerve with outcomes roughly comparable to or a little better than that

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Fig. 14.69 Current knowledge of the internal topography of the radial nerve at the level of the triceps branches as determined by intraoperative electrical stimulation. The three territories identified are, from medial to lateral, finger extensors, wrist extensors, and sensory component (right arm, patient prone, posterior approach). (Used with permission from Pet MA, Ray WZ, Yee A, Mackinnon SE. Nerve transfer to the triceps after brachial plexus injury: report of four cases. J Hand Surg Am 2011;36(3):398–405.)

achieved with shoulder fusion. Recent reports have demonstrated a level of function achieved with shoulder fusion of abduction of 47.5 degrees (range 30–60 degrees) and flexion of 56.6 degrees (range 30–75 degrees) in a series of six cases. 203 A larger series reported by Chammas et al in 1996 included 18 patients who underwent glenohumeral arthrodesis following a brachial plexus injury, with an average follow-up of 6 years. 204 The average motion recovered was 60 degrees of abduction and flexion, 14 degrees of extension, 48 degrees of internal rotation, and 0 degree of external rotation. The most common complications were nonunion requiring revision with bone grafting, and humeral fracture, which can be managed nonoperatively. The experience of Songcharoen et al with 577 spinal accessory nerve transfers included transfer to both the suprascapular and the axillary nerves.198 The best results came from the direct transfer of the distal spinal accessory nerve to the suprascapular nerve, with a success rate of 80% for useful motor recovery of MRC grade 3 or better. An example of a good result was shoulder abduction of 70 degrees, flexion of 60 degrees, and external rotation of 30 degrees. On average, 17.5 months postoperatively was required to recover a level of grade 3 function. Terzis and Kostas reported on 118 patients with reinnervation of the suprascapular nerve.205 In 80 patients, the distal spinal accessory nerve was used as a direct transfer (65 patients) and with an interposition nerve graft (15 patients). With a di-

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rect transfer, recovery of an average muscle grading of 3.9 was obtained with shoulder abduction of 58 degrees, as compared to grade 3.1 and shoulder abduction of 44 degrees when a nerve graft was required. The results of transfer from the spinal accessory nerve were also better than the use of other extraplexus donors, which included the dorsal scapular nerve and C3 and C4 plexus donors. In this series, use of the distal accessory nerve as a direct transfer provided a comparable result to the use of intraplexus donors from C5–C8, with an average muscle grading of 3.8 and shoulder abduction of 58 degrees with less dissection and operative time. Reinnervation of the axillary nerve as an alternative to the suprascapular nerve yields useful but inferior results to transfer to the suprascapular nerve. Songcharoen et al. described the transfer of the accessory to the axillary nerve as a secondary alternative and required an interposition nerve graft.198 In this series, 60% of patients recovered useful motor function of grade 3 or better, with a good result being abduction of 60 degrees and flexion of 45 degrees. In a series of 266 patients who underwent nerve transfers to reconstruct shoulder function, Chuang found that restoration of shoulder abduction will usually have better results in patients with upper root avulsion (C5–C7) than those with total or global root avulsion because of the complexity of the shoulder joint and the contribution and coordinated movement of many muscles.201

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Fig. 14.70 Intraoperative photos of the ulnar nerve-to-FCU fascicular transfer to the motor branch of the medial head of the triceps. (a) Posterior approach to the radial and ulnar nerves. (b) The donor FCU fascicle of the ulnar nerve (outlined) and the recipient radial nerve branch to the medial head of the triceps are identified. (c) The nerves are coapted in an end-to-end fashion (right arm, patient prone, posterior approach). (Used with permission from Pet MA, Ray WZ, Yee A, Mackinnon SE. Nerve transfer to the triceps after brachial plexus injury: report of four cases. J Hand Surg Am 2011;36(3):398–405.)

Fig. 14.71 Illustration of brachialis-to-anterior nerve transfer. To restore anterior interosseous nerve (AIN) function, the brachialis branch is an available donor for transfer. The transfer occurs in the middle of the arm where the recipient anterior interosseous fascicle is located on the posterior/medial aspect of the median nerve. This fascicle has a distal course that rotates more laterally before it branches into the AIN nerve from its posterior/lateral aspect of the median nerve. If C7 is also involved, use the brachialis to innervate AIN, pronator and FCR. Follow the donor brachialis branches more distally than this drawing illustrates to achieve a greater cross sectional donor nerve diameter and move regeneration closer to recipient end plates.

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Fig. 14.72 (a) The superior ulnar collateral pedicle vascularizing the proximal ulnar nerve in the upper third of the arm. The patient is oriented with the shoulder to the right, elbow to the left. (b) A subcutaneous tunnel is created from the axilla across the chest to the contralateral supraclavicular region. The ulnar nerve is transected at the wrist and the distal end passed through the subcutaneous tunnel across the chest and delivered to the contralateral supraclavicular exposure for direct suturing to the hemi-C7 root that was previously divided. (c) Direct transfer of the distal end of the vascularized ulnar nerve graft to the distal stump of the transected median nerve (1) in the upper arm in conjunction with intercostal nerve transfers (2). The patient is oriented with the axilla to the right, elbow to the left.

Clearly, the best results for shoulder function come from reinnervation of both the suprascapular and axillary nerves simultaneously. This has been confirmed by meta-analysis of 1,088 nerve transfers by Merrell et al when compared to transfer to a single nerve.202 Transfer of a triceps branch of the radial nerve to the axillary nerve from the posterior approach was first described by Witoonchart et al and Leechavengvongs et al in an anatomical and then clinical study.206,207 The clinical series consisted of seven patients who underwent transfer of the nerve branch to the long head of the triceps to the anterior branch(es) of the axillary nerve from a posterior shoulder approach, along with distal accessory-to-suprascapular nerve transfer. All patients recovered MRC grade 4 deltoid function, of which five were classified as an excellent result, and the other two had a good result. Six patients recovered grade 4/5 external shoulder rotation, and one had grade 3/5. The average shoulder abduction was 124 degrees with a range of 70 to 160 degrees. Subluxation of the glenohumeral joint was resolved in all patients, and none complained of any donor motor deficit.

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Bertelli and Ghizoni reported on a series of suprascapular and axillary nerve reinnervation cases with the accessory nerve and the nerve to the long or lateral head of the triceps. 208 Ten patients underwent shoulder reconstruction as well as nerve transfer for elbow flexion. Shoulder abduction was graded at 4 in three patients and 3 in the remaining patients. External rotation strength was grade 4 in two patients, 3 in five patients, and 2 in three patients. The average shoulder abduction recovered was 92 degrees, with a range of 65 to 120 degrees. No evidence of donor site deficits was observed in any patients. We have used the double nerve transfer technique at our institution and have been very pleased with our results (▶ Fig. 14.77). We modified Wittonchart and Leechavenvong’s procedure to use the medial triceps branch and we also recognize that the anterior division of the axillary nerve may have an unrecoverable injury requiring transfer while the posterior branch may have a lesser injury. We also try to reinnervate the long thoracic nerve whenever possible, and the technique of a partial injury to the accessory nerve with proximal crush

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Fig. 14.73 (a) The functioning ulnar nerve can be used as a donor for transfer for more critical median nerve sensation in high median nerve injuries, which can be performed as a direct nerve transfer, such as transfer of the dorsal cutaneous branch to the first and second web space branches of the median nerve. Note the end to side nerve transfer of the distal non critical third webspace median nerve to the ulnar nerve. (b) This transfer can also be performed at the wrist/distal forearm, which is our preferred approach.

described previously appears to result in little if any accessory nerve deficit. The recovery of hand function is the most challenging goal because of the distal location of the target muscles.209 Such reconstruction frequently relies on a free functional muscle transfer. The contralateral C7 root has been used in its entirety or in part to reconstruct elbow flexion or hand function.30,210 Gu et al reviewed a series of 32 patients who underwent contralateral C7 root transfer with a follow-up of over 2 years.211 Of those 32, 14 patients had transfer to the median nerve for hand function. For motor recovery, 7 patients obtained finger flexion of grade 3 or better (50%), and 12 recovered sensation of grade 3 or better (85.7%). A larger series was reported by Waikakul et al with 96 patients undergoing transfer of the anterior division of the contralateral C7 root for hand function with a follow-up of more than 3 years.212 All patients underwent other simultaneous nerve transfers for shoulder and elbow function. Sensory recovery was very satisfactory, with 83% obtaining grade 3 or better. However, motor function was much less promising, with only 33% recovering pronation of grade 3, 29% obtaining wrist flexion to grade 3, and only 21% recovering finger flexion to grade 3. The superior results obtained by Gu may have been related to the use of either the

whole C7 root or the posterior division, which has been reported to contain twice the number of motor fibers as the anterior division, and staging the transfer to improve the vascularity of the ulnar nerve graft. 30 Songcharoen et al had the largest series of 111 patients with contralateral C7 transfer to the median nerve.198 With a followup of more than 3 years, 30% recovered good motor function (grade 3), and 20% obtained grade 2 function. The reconstruction of sensation is much better with the recovery of protective sensation (sensory grade 2/5 or more) of up to 83%. Approximately 50% of patients regained S3 sensation, and 33% obtained S2 sensation. The average time to MRC grade 3 motor function and sensory grade 3 recovery was 35 months. Postoperative donor morbidity occurred in 97% of patients and included sensory alteration in the index fingertip, median nerve distribution, or shoulder area, but all had resolved by 7 months with an average of 3.75 months. Three patients were found to have postoperative contralateral motor donor morbidity with weakness of triceps function to grade 4/5 and finger extension to grade 2/5. The triceps weakness had resolved in 2 months. We agree with others that the results of partial C7 transfer are poor and do not justify the risk of donor-site morbidity.213

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Fig. 14.74 (a) Illustration of sensory nerve transfers in the hand to restore median nerve sensation. (b) For sensory reconstruction, the common and proper digital nerves are exposed and dissected to the level of the web space, and the nerve branch to the fourth web space is transferred directly to the branch to the first web space. The distal stump of the branch to the second web space is transferred in an end-to-side manner to a functioning ulnar nerve branch to restore protective sensation without donor morbidity.

Table 14.1 Modified Medical Research Council Grading System of the Functional Status after Peripheral Nerve Injury and Reconstruction*

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Grade

Definition

5

Normal strength

5-

Barely detectable weakness

4+

Same as grade 4, but muscle holds the joint against moderate to maximal resistance

4

Muscle holds the joint against a combination of gravity and moderate resistance

4-

Same as grade 4, but muscle holds the joint only against minimal resistance

3+

Muscle moves the joint fully against gravity and is capable of transient resistance but collapses abruptly

3

Muscle cannot hold the joint against resistance but moves the joint fully against gravity

3-

Muscle moves the joint against gravity but not through full mechanical range of motion

2

Muscle moves the joint when gravity is eliminated

1

A flicker of movement is seen or felt in the muscle

0

No movement

* This is applied for specified joint function.

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Fig. 14.75 Transfer of the third web space fascicle of the median nerve to the first web space for critical thumb and index finger sensation for an upper brachial plexus injury (C5–C6). The distal stump of the third web space fascicle is transferred end to side back to the first web space fascicle to restore protective sensation to the donor third web space territory (inset).

Free functional muscle transfers provide a final option once the “window of opportunity” for the reinnervation of target muscles has closed. An experienced and specialized team can provide reliable and consistent results. Barrie et al recovered functional results for elbow flexion using a single gracilis muscle transfer in 79% of cases.214 The use of intercostal or spinal accessory donor motor nerves provided comparable results. In 2 of 17 patients in this series, however, no clinically detectable muscle function was obtained despite evidence of muscle survival. Doi et al described the use of a double free-muscle technique to restore elbow flexion and both wrist and digit flexion and extension.215 They reported a success rate of 96% for excellent elbow flexion, with 65% of patients achieving more than 30 degrees of total active motion of the fingers with the second muscle transfer. The authors felt that a muscle transfer for both elbow flexion and wrist extension (63% with grade 4/5 or better) diminished the overall result for elbow flexion

strength as compared to transfer for elbow flexion alone (79%), and that grasp function was less reliable.216 Terzis and others have reached a similar conclusion, that prehension is less consistently restored when a single muscle is used for two functions and that possibly only elbow flexion should be reconstructed.217–220 However, Chuang has been able to achieve satisfactory results using the gracilis muscle transfer for the recovery of double function.221 The effect of surgical reconstruction for brachial plexus injury on careers and life in general has been evaluated in a long-term patient-reported outcome study.43 For the group of patients who had gainful employment at the time of their injury, 54% were able to return to work and most of them within 1 year following injury. Job satisfaction was reported to be moderate to high in 70% of this group of patients as compared to 85% of the general population. Of those who were unable to return to work, most felt that the impairment resulting from their injury

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Fig. 14.76 (a,b) Postoperative follow-up after double fascicular transfer to reinnervate biceps and brachialis muscles showing excellent recovery of elbow flexion with Medical Research Council grade 4 + /5 strength.

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Fig. 14.77 (a,b,c) Double nerve transfer reconstruction of left shoulder function in this patient with excellent restoration of deltoid contour and function with full range of active shoulder motion.

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Brachial Plexus Injuries was the responsible factor. However, 78% of those after brachial plexus injury as compared to 90% of the general population were satisfied with their quality of life in general. A more recent study has found that up to 87% of patients were satisfied with the results of reconstruction, and 83% would undergo the surgery again, despite considerable persistent disability. 222 Lower quality of life outcomes have been associated with higher injury severity scores, delayed surgical repair, and smoking.223 Taken together, most patients remained happy and satisfied with their work despite abnormal motor function and sensation with long-term physical impairment. Overall happiness at work and with life in general therefore was not felt to be too heavily dependent on upper extremity function. Thus, unlike the past, when brachial plexus surgery was associated with much pessimism, the results of surgical reconstruction continue to improve and warrant an optimistic outlook for these unfortunate patients.

14.5 Conclusion Brachial plexus trauma is a debilitating injury that results in permanent impairment of upper extremity function. Timely management is required for the best possible recovery of motor function. Many surgical techniques exist for the management of such injuries and include primary repair of an acute injury, neurolysis, neuroma resection and nerve graft reconstruction, motor and sensory nerve transfers, and muscle and tendon transfers. Additional procedures may provide further enhancement of function, such as shoulder and wrist fusion. The optimal management plan and surgical technique will vary with the mechanism, severity, and level of the injury, as well as the surgeon’s training and experience. Postoperative rehabilitation will be facilitated by a multidisciplinary approach, including expertise in physical therapy and motor reeducation and pain management if necessary. The entire reconstructive process frequently requires multiple procedures in a staged fashion over many years and extended and intensive rehabilitation. With the continued evolution and understanding of the management of such injuries, the compliant and motivated patient with a committed and experienced surgical team can expect good functional restoration and maintain a fulfilling and gratifying life.

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Brachial Plexus Injuries [158] Onders RP, Elmo MJ, Ignagni AR. Diaphragm pacing stimulation system for tetraplegia in individuals injured during childhood or adolescence. J Spinal Cord Med 2007;30 Suppl 1:S25–S29 [159] Taira T, Hori T. Diaphragm pacing with a spinal cord stimulator: current state and future directions. Acta Neurochir Suppl (Wien) 2007;97:289–292 [160] Mitsuyama T, Taira T, Takeda N, Hori T. Diaphragm pacing with the spinal cord stimulator. Acta Neurochir Suppl (Wien) 2003;87:89–92 [161] Chervin RD, Guilleminault C. Diaphragm pacing for respiratory insufficiency. J Clin Neurophysiol 1997;14:369–377 [162] Chervin RD, Guilleminault C. Diaphragm pacing: review and reassessment. Sleep 1994;17:176–187 [163] Tubbs RS, Pearson B, Loukas M, Shokouhi G, Shoja MM, Oakes WJ. Phrenic nerve neurotization utilizing the spinal accessory nerve: technical note with potential application in patients with high cervical quadriplegia. Childs Nerv Syst 2008;24:1341–1344 [164] Krieger LM, Krieger AJ. The intercostal to phrenic nerve transfer: an effective means of reanimating the diaphragm in patients with high cervical spine injury. Plast Reconstr Surg 2000;105:1255–1261 [165] Krupnick AS, Gelman AE, Okazaki M, et al.. The feasibility of diaphragmatic transplantation as potential therapy for treatment of respiratory failure associated with Duchenne muscular dystrophy: acute canine model. J Thorac Cardiovasc Surg 2008;135:1398–1399 [166] Ray WZ, Pet MA, Yee A, Mackinnon SE. Double fascicular nerve transfer to the biceps and brachialis muscles after brachial plexus injury: clinical outcomes in a series of 29 cases. J Neurosurg 2011;114:1520–1528 [167] Weber RV, Mackinnon SE. Nerve transfers in the upper extremity. J Am Soc Surg Hand 2004;4:200–213 [168] Tung TH, Weber RV, Mackinnon SE. Nerve transfers for the upper and lower extremities. Oper Tech Orthop 2004;14:213–222 [169] Kovachevich R, Kircher MF, Wood CM, Spinner RJ, Bishop AT, Shin AY. Complications of intercostal nerve transfer for brachial plexus reconstruction. J Hand Surg Am 2010;35:1995–2000 [170] Bahm J, Noaman H, Becker M. The dorsal approach to the suprascapular nerve in neuromuscular reanimation for obstetric brachial plexus lesions. Plast Reconstr Surg 2005;115:240–244 [171] Ray WZ, Kasukurthi R, Yee A, Mackinnon SE. Functional recovery following an end to side neurorrhaphy of the accessory nerve to the suprascapular nerve: case report. Hand (NY) 2010;5:313–317 [172] Colbert SH, Mackinnon SE. Posterior approach for double nerve transfer for restoration of shoulder function in upper brachial plexus palsy. Hand (NY) 2006;1:71–77 [173] Ray WZ, Murphy RK, Santosa KB, Johnson PJ, Mackinnon SE. Medial pectoral nerve to axillary nerve neurotization following traumatic brachial plexus injuries: indications and clinical outcomes. Hand (NY) 2012;7:59–65 [174] Ray WZ, Pet MA, Nicoson MC, Yee A, Kahn LC, Mackinnon SE. Two-level motor nerve transfer for the treatment of long thoracic nerve palsy. J Neurosurg 2011;115:858–864 [175] Pet MA, Ray WZ, Yee A, Mackinnon SE. Nerve transfer to the triceps after brachial plexus injury: report of four cases. J Hand Surg Am 2011;36:398–405 [176] Gao K, Lao J, Zhao X, Gu Y. Outcome after transfer of intercostal nerves to the nerve of triceps long head in 25 adult patients with total brachial plexus root avulsion injury. J Neurosurg 2013;118:606–610 [177] Hsiao EC, Fox IK, Tung TH, Mackinnon SE. Motor nerve transfers to restore extrinsic median nerve function: case report. Hand (NY) 2009;4:92–97 [178] Mackinnon SE, Yee A, Ray WZ. Nerve transfers for the restoration of hand function after spinal cord injury. J Neurosurg 2012;117:176–185 [179] Ray WZ, Mackinnon SE. Clinical outcomes following median to radial nerve transfers. J Hand Surg Am 2011;36:201–208 [180] Barbour JR, Gontre G, Daliwal G, Mackinnon SE. Transfer of the extensor digiti quinti and extensor carpi ulnaris branches of the posterior interosseous nerve to the motor branch of the ulnar nerve to restore intrinsic hand function: case report and anatomic study. J Hand Surg Am 2012 [181] Doi K, Hattori Y, Kuwata N, et al.. Free muscle transfer can restore hand function after injuries of the lower brachial plexus. J Bone Joint Surg Br 1998;80:117–120 [182] Burkhalter WE. Early tendon transfer in upper extremity peripheral nerve injury. Clin Orthop Relat Res 1974;104:68–79 [183] Doi K, Kuwata N, Muramatsu K, Hottori Y, Kawai S. Double muscle transfer for upper extremity reconstruction following complete avulsion of the brachial plexus. Hand Clin 1999;15:757–767 [184] Narakas AO. The surgical treatment of traumatic brachial plexus lesions. Int Surg 1980;65:521–527

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[185] Millesi H. Brachial plexus injuries: management and results. Clin Plast Surg 1984;11:115–120 [186] Garg R, Merrell GA, Hillstrom HJ, Wolfe SW. Comparison of nerve transfers and nerve grafting for traumatic upper plexus palsy: a systematic review and analysis. J Bone Joint Surg Am 2011;93:819–829 [187] Kline DG, Hudson AR. Nerve Injuries: Operative Results for Major Injuries, Entrapments, and Tumors. Philadelphia, PA: WB Saunders; 1995 [188] John J,, Medical Research Council. Grading of muscle power: comparison of MRC and analogue scales by physiotherapists. Int J Rehabil Res 1984;7:173–181 [189] Kim DH, Cho YJ, Tiel RL, Kline DG. Outcomes of surgery in 1019 brachial plexus lesions treated at Louisiana State University Health Sciences Center. J Neurosurg 2003;98:1005–1016 [190] Kline DG, Tiel RL. Direct plexus repair by grafts supplemented by nerve transfers. Hand Clin 2005;21:55–69 [191] Sulaiman OA, Kim DD, Burkett C, Kline DG. Nerve transfer surgery for adult brachial plexus injury: a 10-year experience at Louisiana State University. Neurosurgery 2009;65 Suppl:A55–A62 [192] Bentolila V, Nizard R, Bizot P, Sedel L. Complete traumatic brachial plexus palsy: treatment and outcome after repair. J Bone Joint Surg Am 1999;81:20– 28 [193] Liverneaux PA, Diaz LC, Beaulieu JY, Durand S, Oberlin C. Preliminary results of double nerve transfer to restore elbow flexion in upper type brachial plexus palsies. Plast Reconstr Surg 2006;117:915–919 [194] Teboul F, Kakkar R, Ameur N, Beaulieu JY, Oberlin C. Transfer of fascicles from the ulnar nerve to the nerve to the biceps in the treatment of upper brachial plexus palsy. J Bone Joint Surg Am 2004;86-A:1485–1490 [195] Novak CB, Mackinnon SE, Tung TH. Patient outcome following a thoracodorsal to musculocutaneous nerve transfer for reconstruction of elbow flexion. Br J Plast Surg 2002;55:416–419 [196] Samardzic MM, Grujicic DM, Rasulic LG, Milicic BR. The use of thoracodorsal nerve transfer in restoration of irreparable C5 and C6 spinal nerve lesions. Br J Plast Surg 2005;58:541–546 [197] Samardzic M, Grujicic D, Rasulic L, Bacetic D. Transfer of the medial pectoral nerve: myth or reality? Neurosurgery 2002;50:1277–1282 [198] Songcharoen P, Wongtrakul S, Spinner RJ. Brachial plexus injuries in the adult —nerve transfers: the Siriraj Hospital experience. Hand Clin 2005;21:83–89 [199] Terzis JK, Kostopoulos VK. The surgical treatment of brachial plexus injuries in adults. Plast Reconstr Surg 2007;119:73e–92e [200] Chuang DC, Yeh MC, Wei FC. Intercostal nerve transfer of the musculocutaneous nerve in avulsed brachial plexus injuries: evaluation of 66 patients. J Hand Surg Am 1992;17:822–828 [201] Chuang DC. Nerve transfers in adult brachial plexus injuries: my methods. Hand Clin 2005;21:71–82 [202] Merrell GA, Barrie KA, Katz DL, Wolfe SW. Results of nerve transfer techniques for restoration of shoulder and elbow function in the context of a metaanalysis of the English literature. J Hand Surg Am 2001;26:303–314 [203] Wong EL, Kwan MK, Loh WY, Ahmad TS. Shoulder arthrodesis in brachial plexus injuries—a review of six cases. Med J Malaysia 2005;60 Suppl C:72–77 [204] Chammas M, Meyer zu Reckendorf G, Allieu Y. Arthrodesis of the shoulder for post-traumatic palsy of the brachial plexus: analysis of a series of 18 cases Rev Chir Orthop Repar Appar Mot 1996;82:386–395 [205] Terzis JK, Kostas I. Suprascapular nerve reconstruction in 118 cases of adult posttraumatic brachial plexus. Plast Reconstr Surg 2006;117:613–629 [206] Witoonchart K, Leechavengvongs S, Uerpairojkit C, Thuvasethakul P, Wongnopsuwan V. Nerve transfer to deltoid muscle using the nerve to the long head of the triceps: 1. An anatomic feasibility study. J Hand Surg Am 2003;28:628–632 [207] Leechavengvongs S, Witoonchart K, Uerpairojkit C, Thuvasethakul P. Nerve transfer to deltoid muscle using the nerve to the long head of the triceps: 2. A report of 7 cases. J Hand Surg Am 2003;28:633–638 [208] Bertelli JA, Ghizoni MF. Reconstruction of C5 and C6 brachial plexus avulsion injury by multiple nerve transfers: spinal accessory to suprascapular, ulnar fascicles to biceps branch, and triceps long or lateral head branch to axillary nerve. J Hand Surg Am 2004;29:131–139 [209] Flores LP. Brachial plexus surgery: the role of the surgical technique for improvement of the functional outcome. Arq Neuropsiquiatr 2011;69:660–665 [210] Chuang DC. Contralateral C7 transfer (CC-7T) for avulsion injury of the brachial plexus. Tech Hand Up Extrem Surg 1999;3:185–192 [211] Gu Y, Xu J, Chen L, Wang H, Hu S. Long term outcome of contralateral C7 transfer: a report of 32 cases. Chin Med J (Engl) 2002;115:866–868

Brachial Plexus Injuries [212] Waikakul S, Orapin S, Vanadurongwan V. Clinical results of contralateral C7 root neurotization to the median nerve in brachial plexus injuries with total root avulsions. J Hand Surg [Br] 1999;24:556–560 [213] Sammer DM, Kircher MF, Bishop AT, Spinner RJ, Shin AY. Hemi-contralateral C7 transfer in traumatic brachial plexus injuries: outcomes and complications. J Bone Joint Surg Am 2012;94:131–137 [214] Barrie KA, Steinmann SP, Shin AY, Spinner RJ, Bishop AT. Gracilis free muscle transfer for restoration of function after complete brachial plexus avulsion. Neurosurg Focus 2004;16:E8 [215] Doi K, Muramatsu K, Hattori Y, et al.. Restoration of prehension with the double free muscle technique following complete avulsion of the brachial plexus. Indications and long-term results. J Bone Joint Surg Am 2000;82:652–666 [216] Bishop AT. Functioning free-muscle transfer for brachial plexus injury. Hand Clin 2005;21:91–102 [217] Terzis JK, Kostopoulos VK. Free muscle transfer in posttraumatic plexopathies: part 2. The Elbow Hand (NY) 2009

[218] Doi K, Hattori Y, Ikeda K, Dhawan V. Significance of shoulder function in the reconstruction of prehension with double free-muscle transfer after complete paralysis of the brachial plexus. Plast Reconstr Surg 2003;112:1596–1603 [219] Barrie KA, Steinmann SP, Shin AY, Spinner RJ, Bishop AT. Gracilis free muscle transfer for restoration of function after complete brachial plexus avulsion. Neurosurg Focus 2004;16:E8 [220] Berger AC, Hierner R, Kleinschmidt L. Palliative surgery: the elbow and forearm. in: Gilbert A, ed. Brachial Plexus Injuries. London: Dunitz Martin; 2001:23–130 [221] Chuang DC. Neurotization and free muscle transfer for brachial plexus avulsion injury. Hand Clin 2007;23:91–104 [222] Kretschmer T, Ihle S, Antoniadis G, et al.. Patient satisfaction and disability after brachial plexus surgery. Neurosurgery 2009;65 Suppl:A189–A196 [223] Dolan RT, Butler JS, Murphy SM, Hynes D, Cronin KJ. Health-related quality of life and functional outcomes following nerve transfers for traumatic upper brachial plexus injuries. J Hand Surg Eur Vol 2012;37:642–651

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15 Obstetrical Brachial Plexus Palsy Alison K. Snyder-Warwick and Gregory H. Borschel

15.1 Introduction The first recorded case of obstetrical brachial plexus paralysis is attributed to the British physician William Smellie in 1768. He noted bilateral arm paralysis in a newborn that he had delivered by applying traction to the head with forceps: [L]astly, I moved the handles towards the [p]ubis, and delivered the woman of a child, whose face was swelled, and whose head was compressed like that described in the former case: the long compression had rendered the arms paralytic for several days, though this misfortune was soon remedied by friction and embrocations.1 The term obstetrical paralysis was introduced by Guillaume Duchenne in 1872. He described a case of an infant delivered by forceps with the shoulder held in internal rotation with the elbow extended but with hand motion intact.2 In 1874 Wilhelm Erb described C5–C6 paralysis.3 The first report describing operative treatment for obstetrical brachial plexus palsy was in 1903. In this series, Kennedy described excision of the neuroma, followed by suture coaptation of the cut ends of the plexus.4 He was able to demonstrate partial return of shoulder abduction and elbow flexion in three patients who underwent operation at age 2 months. In the same year, Thorburn described the most common presentation of obstetrical brachial plexus palsy, along with its anatomical implications: [W]e have paralysis with loss of Faradic reaction, and subsequently atrophy of the biceps, brachialis anticus, deltoid, long and short supinators, teres minor and supra- and infraspinati, a group of symptoms capable of production by injury at the junction of the fifth and sixth cervical roots to form the upper cord of the plexus. In such cases the shoulder is flaccid and rotated inwards, the forearm is extended and the hand lies prone.5 James Sever, in 1916 and in a follow-up report in 1925, recommended against operating on the brachial plexus itself. He felt that most cases were nonoperative, but in some cases he advocated releasing the pectoralis major and subscapularis muscles, while leaving the nerves themselves undisturbed. 6–8 Because of Sever’s reports, obstetrical brachial plexus paralysis was subsequently managed without operating on the peripheral nerves themselves until the advent of the microsurgical era. Improved instrumentation, lighting, and understanding of anatomy and pathophysiology led to renewed interest in operative management in the 1970s.9–11 During the microsurgical era, Narakas proposed an injury severity classification system based on his experience with over 1,000 cases of obstetrical brachial plexus palsy.12–16 A type I injury heals spontaneously within weeks and typically affects C5– C6. A type II injury does not recover full shoulder function, but elbow function is adequate; usually this represents a C5–C7 lesion. Tendon transfers are sometimes needed for wrist and dig-

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ital extension. A type III injury is more extensive with avulsion of the C7 spinal root, plus an injury to the lower trunk, sometimes including T1. The clinical presentation at birth may include Horner syndrome, which resolves by definition. A type IV injury presents like a type III injury, but the Horner syndrome persists, indicating likely avulsion of C8–T1. A type V injury involves C5–T1. The Horner syndrome does not resolve. Narakas considered paralysis of both the rhomboid and serratus anterior muscles a particularly poor prognostic sign for spontaneous recovery. In the 1980s, Alain Gilbert popularized the most common indication for operative management in obstetrical brachial plexus paralysis. He advocated neuroma excision and interpositional nerve grafting in cases where no elbow flexion was present at age 3 months (see Indications for Primary Brachial Plexus Exploration, below).17–19 He proposed lack of elbow flexion by age 3 months as the major indication for neuroma excision and sural nerve grafting (“primary surgery”). The indications for and timing of surgical intervention in cases in which there is a subtotal injury are controversial. Multidisciplinary brachial plexus centers with sufficiently large numbers of patients are few in number, and each one applies different indications and techniques. This lack of international consensus has resulted in difficulty in interpreting results across centers consistently and has hampered progress in improving diagnostic and therapeutic techniques.

15.2 Etiology Obstetrical brachial plexus injuries occur at an incidence of 0.5 to 3.0 injuries per 1,000 live births.20–24 Injury may result from multifactorial causes. Traditionally, brachial plexus injury is thought to result from positioning during birth, although neural compression secondary to instrumentation or manipulation, uterine contraction, clavicular fracture, and hematoma are other possible causes. Positioning may cause an increase in the neck–shoulder angle, particularly in cases of shoulder dystocia or difficult delivery, resulting in a stretch to the brachial plexus that may exceed the neural tensile stress tolerance and produce injury. Frequently, these multifactorial etiologies produce a mixed-type neural injury, ranging from neurapraxia to complete root avulsion.

15.3 Nomenclature Although the term obstetrical brachial plexus palsy is probably the most common label for this condition, many different terms have been used. Obstetricians, especially those in the United States and other litigious societies, object to the use of the word obstetrical because it implies a departure from standard of care during delivery. Many brachial plexus surgeons favor terms other than obstetrical. However, there is currently no consensus among brachial plexus surgeons as to what the most appropriate alternative label would be. Some suggested alternatives are perinatal brachial plexus palsy, birth brachial plexus palsy, infant brachial plexus palsy, newborn brachial plexus injury, neonatal

Obstetrical Brachial Plexus Palsy brachial plexus injury, neonatal brachial plexopathy, birth-related brachial plexus palsy, and congenital brachial plexus palsy. For simplification, we will use the term obstetrical brachial plexus palsy throughout this chapter to refer to injuries to the brachial plexus noted in the perinatal period. Most lesions affect the upper plexus and could be classified as Erb type. About 25% of lesions affect all branches of the plexus, and these are referred to as “total palsies.” Klumpke paralysis (an isolated lower plexus lesion) is not seen in obstetrical palsy.25–27

15.4 Evaluation 15.4.1 Perinatal History Infants are seen as early as possible postpartum. At our center, we prefer to examine the infants in the newborn nursery if at all possible; if that is not possible, we prefer to see them before age 1 month. Predisposing factors, related to the patient as well as to the patient’s mother, are determined. The prenatal history is elicited to determine maternal factors, such as diabetes, preeclampsia, prolonged duration of labor, and previous obstetrical complications. Factors related to delivery are determined, such as presentation (vertex, breech, or other), use of instrumentation, occurrence of shoulder dystocia, complicated delivery, and need for caesarean section. The history includes the immediate postpartum history, including the 1- and 5-minute Apgar scores. Child-related factors included in the history are the gestational age, birth weight, and presence of perinatal complications, such as respiratory distress, diaphragmatic paralysis, fractures of the clavicle or humerus, shoulder dislocation, presence of Horner syndrome, and torticollis. Developmental delay can sometimes confound the diagnosis of a brachial plexus lesion; therefore, information regarding developmental milestones is noted. Increased global tone may indicate a cortical insult. Shoulder dislocations and clavicular, rib, and humeral fractures can also present with a nonfunctional upper extremity that resembles a brachial plexus injury. Careful interviews are important to delineate brachial plexus injuries from other confounding conditions. Several factors have been associated with obstetrical brachial plexus injury. Infants with brachial plexus injuries frequently have birth weights that are, on average, 0.5 to 1 kg (1 to 2 lbs.) greater,20 and infants weighing > 4 kg (9 lbs.) are at increased risk.24,28 Macrosomia related to maternal diabetes is associated with brachial plexus injury as well,29 and tight glycemic control in diabetic mothers has been shown to reduce the incidence of shoulder dystocia. In a review of 655 cases of obstetrical brachial plexus palsy, Al-Qattan et al27 found 39% of those patients had a history of maternal diabetes. Infants with a history of maternal diabetes in the setting of brachial plexus injury were more likely to have a complete plexus palsy compared to infants with a brachial plexus injury and nondiabetic mothers. They also noted that infants with brachial plexus injury and diabetic mothers had larger birth weights compared to infants with brachial plexus injury and nondiabetic mothers. In cases of suspected fetal macrosomia in the setting of maternal diabetes, some authors recommend elective cesarean section, although this recommendation is controversial (see below). A brachial plexus injury in a previous delivery has also been associated

with subsequent deliveries complicated by brachial plexus injury,30 and maternal body mass index (BMI) > 30 kg/m2 is associated with shoulder dystocia.31 Shoulder dystocia occurs when the shoulder impinges on the maternal pelvis, precluding progression of delivery. Infant positioning with this complication can result in lateral traction on the infant’s head, increasing the neck–shoulder angle and causing a traction injury to the brachial plexus.28 Shoulder dystocia is associated with a 100-fold increased risk of brachial plexus injury.24 It is present in 7% of cases with maternal diabetes.31,32 In infants < 4 kg (9 lbs.), the incidence of shoulder dystocia is 0.6 to 1.4%. Conversely, in infants > 4 kg, the incidence of shoulder dystocia is 5 to 9%.33 Unfortunately, current prenatal ultrasound techniques are unable to determine prenatal weight accurately enough to recommend cesarean section in borderline cases. Preventive cesarean section for suspected fetal macrosomia > 4 kg based on ultrasonic evaluation is not recommended by the American College of Obstetrics and Gynecology because best estimates show that it would require 100 cesarean sections to prevent a single brachial plexus injury.34 Other authors, however, have recommended elective cesarean section for cases of suspected fetal macrosomia.35,36 Once shoulder dystocia is diagnosed, however, it is very difficult to treat. Various maneuvers have been proposed to address it. Suprapubic pressure is applied in an effort to free the shoulder from the pubic symphysis, and positioning the mother to support her weight on her knees and palms is sometimes advocated to straighten the path for delivery. Other intrapartum techniques, such as the Wood maneuver, in which the attendant uses a hand to internally rotate the infant, have been proposed, but a Cochrane review has demonstrated little utility of such maneuvers.37,38 Besides shoulder dystocia, use of instrumentation during delivery and a prolonged labor are associated with brachial plexus injury.39 Clavicular and humeral fractures are associated with brachial plexus injuries.40 In the absence of a true brachial plexus lesion, these fractures may result in involuntary splinting secondary to pain, producing a “pseudoparalysis” resembling a true brachial plexus lesion. Others have postulated that a clavicular fracture in the setting of shoulder dystocia may be protective by permitting downward rotation of the shoulder and preventing increased longitudinal stress to the brachial plexus.41 No statistical correlation, however, has determined improved long-term prognosis with humeral or clavicular fracture.40 Whereas the most common birth presentation associated with brachial plexus injury is vertex vaginal delivery, breech27, 42 and cesarean delivery have been reported with brachial plexus injury as well. Brachial plexus injury occurring after breech is frequently associated with C5–C6 avulsions42 and Erb palsy.27 A recent retrospective review of 698 infants with obstetrical brachial plexus palsy reported 35 patients with breech presentations. Patients with breech delivery demonstrated a higher incidence of bilateral brachial plexus injury, smaller birth weights, and lower incidence of spontaneous recovery of shoulder abduction and flexion in the setting of upper Erb palsy compared to infants with cephalic presentation and upper Erb palsy.27 Although somewhat counterintuitive, brachial plexus injury after caesarean delivery may relate to trauma sustained during unsuccessful attempts at vaginal delivery or possibly upon delivery through the uterine incision.43

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15.4.2 Physical Examination Examination by a multidisciplinary care team, including experienced physical and occupational therapists, is critical in assessing motor function and capacity in activities of daily living. The physical examination findings dictate the treatment. To facilitate the motor examination, infants are placed in an unobstructive, safe environment, such as on a large exercise mat. The chest and upper extremities of infants are uncovered to allow full evaluation of the motor exam. Older children who are capable of following verbal or visual instructions may stand for the examination. Absence of factors suggestive of a nonbrachial plexus origin of motor weakness is verified. Tension and posturing of the head and neck are assessed to delineate the presence of torticollis. Children with brachial plexus lesions tend to look away from the affected side. The etiology is not well understood, but it may be related to intrauterine head positioning or trauma to the ipsilateral neck muscles.44 The presence of torticollis necessitates physiotherapy to prevent deformational plagiocephaly or sternocleidomastoid (SCM) muscle contracture.45 Rarely, surgical release of the SCM muscle is required in cases of refractory torticollis. Upper extremity posturing may indicate the level of plexus injury. Upper plexus injury, known as Erb palsy, affects the C5, C6, and occasionally C7 roots. An upper extremity is held in the classic “waiter’s tip” position (▶ Fig. 15.1), with the shoulder adducted and internally rotated, the elbow extended, the forearm pronated, and the wrist and fingers flexed. A lower plexus injury, referred to as “Klumpke paralysis,” involves the roots of C8 and T1 in isolation and typically does not occur with obstetrical brachial plexus injuries.25 Intermediate brachial plexus injury, however, has been described in obstetrical brachial plexus injury and involves C7 ± C8 and T1.46 Upper extremity posturing in intermediate plexus injury is variable, depending on the involved levels. Elbow flexion is demonstrated in patients with isolated C7 root avulsions. Total brachial plexus injuries, affecting C5, C6, C7, C8 ± T1, present as a “flail limb” with no elicitable motor activity. After noting upper extremity resting posture, the patient is assessed for evidence of trauma in the vicinity of the brachial plexus, such as clavicular, humeral, or rib fractures, ecchymoses, or scarring indicative of previous fat necrosis. The shoulder is assessed for dislocation or subluxation. A winged scapula indicates long thoracic nerve injury (C5, C6, and C7). Symmetry of the torso during respiration is assessed to evaluate for evidence of phrenic nerve dysfunction. The phrenic nerve arises from C3, C4, and C5; its dysfunction, therefore, may indicate an upper plexus injury.47 Horner syndrome, on the other hand, indicates a lower plexus injury, with T1 root injury proximal to the separation of the sympathetic fibers from the somatic motor fibers. Injury to these preganglionic sympathetic fibers presents as the classic signs of ipsilateral ptosis, anhidrosis, miosis, and apparent enophthalmos. The essential element of the physical examination is the motor exam, which guides treatment and is indicative of prognosis. The Active Movement Scale (AMS) developed at Toronto’s Hospital for Sick Children (▶ Table 15.1) is a validated instrument that is applicable to patients of any age, regardless of ability for voluntary cooperation.45,48–50 The AMS allows the examiner to determine grades for movements of the upper

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Fig. 15.1 Posturing of the upper extremity in a patient with Erb palsy. This patient demonstrates the classic “waiter’s tip” posturing, with the shoulder adducted and internally rotated, the elbow extended, the forearm pronated, and the wrist and fingers flexed.

extremity. A test score is generated by converting the raw scores to converted scores. The sum of the converted scores is the test score. If the test score is > 3.5, then nonoperative management is recommended. In the AMS, 15 movements are assessed (shoulder abduction, flexion, internal and external rotation, elbow flexion and extension, forearm pronation, and wrist, finger, and thumb flexion and extension) and scored from 0 to 7. The Medical Research Council (MRC) scale 51 and the Mallet scale52 are other commonly used scoring systems to assess upper extremity motor function; however, neither is universally applicable to patients of all age ranges.53

15.5 Preoperative Planning A brachial plexus injury was previously thought not to be amenable to surgical management after initial attempts

Obstetrical Brachial Plexus Palsy Table 15.1 The Hospital for Sick Children Active Movement Scale Observation

Score

Converted Score

No contraction

0

0

Contraction, no motion

1

0.3

Motion ≤ half range

2

0.3

Motion > half range

3

0.6

Full motion

4

0.6

Motion ≤ half range

5

0.6

Motion > half range

6

1.3

Full motion

7

2.0

Gravity eliminated

Against gravity

Source: Used with permission from Clarke HM, Curtis CG. An approach to obstetrical brachial plexus injuries. Hand Clin 1995;11:563–580.

produced mixed results. Advances in microsurgery resulted in renewed interest in surgical management of this problem. Early operative intervention, consisting of nerve grafts and nerve transfers performed at ~ 3 to 9 months of age, has become the mainstay of treatment for appropriate brachial plexus injuries.54 Current approaches to management are outlined here.

15.5.1 Indications for Primary Brachial Plexus Exploration Most infants with obstetrical brachial plexus injuries do not require operative management, as upper extremity function improves spontaneously. Patients who demonstrate early and rapid improvement of mild paralysis often demonstrate complete or nearly complete recovery.55 Spontaneous complete recovery rates have been reported as high as 93% by 4 months of age.56 In contrast, patients with severe paralysis, or flail limb, Horner syndrome (▶ Fig. 15.2), and no evidence of improvement demonstrate poor functional outcomes without operative intervention. 57 The difficulty in the management of infants with obstetrical brachial plexus lesions is determining the appropriate management for patients who demonstrate clinical pictures between these two extremes. There currently is no consensus regarding indications for operative intervention or the precise timing of any proposed surgical management. Traditionally, the absence of elbow flexion at 3 months of age has been considered the standard indication for operative management of an obstetrical brachial plexus injury. Gilbert and colleagues19,5,8,59,60 first suggested this indication when they noted poor shoulder outcomes at 5 years and increased secondary procedures in patients who lacked biceps function at 3 months. This criterion has been challenged and elaborated upon in the literature in the ensuing years, with timelines for operative management selection ranging from 3 to 9 months of age.55,61–63 Michelow et al2,4 reported that poor recovery was incorrectly predicted 12% of the time with absence of biceps function alone at age 3 months, leading to unnecessary surgical

Fig. 15.2 The presentation of a 3-month-old infant with a total brachial plexus injury. Note the left Horner syndrome (manifested by left upper eyelid ptosis) accompanied by a complete lack of tone in the left upper extremity (“flail arm”).

intervention. They reported that this rate of incorrect prediction of poor recovery was reduced to 5.2% when evaluation of elbow flexion was combined with elbow, wrist, finger, and thumb extension at 3 months of age. This compilation of motor evaluations is the Toronto Test Score.54 Chuang et al reviewed their experience with operative management of obstetrical brachial plexus palsy in 78 infants.64 Patients who underwent surgery at an average age of 19 months displayed similar shoulder and elbow functional outcomes as infants who underwent reconstruction at an average age of 4.9 months. Hand function, however, displayed minimal or no improvement in patients who underwent reconstruction after infancy. Chuang and colleagues therefore advocated early (age ~ 3 mo) surgical intervention in patients with absent elbow and hand function, but continued observation in patients with absent elbow flexion but intact hand function. If elbow flexion is not present by 6 months of age, the authors advocated surgical intervention. Fisher et al reviewed the management of 209 patients with brachial plexus injuries over a 4-year period. 65 Patients were categorized into four groups based on the presence of elbow flexion at age 3 months and operative or nonoperative intervention. At a follow-up period of 3 years, there were no functional differences among the groups. Early elbow flexion alone was found to be an insufficient criterion to dictate operative or nonoperative management. The authors of this chapter combine motor assessments at 3, 6, and 9 months of age to determine the need for operative intervention. At any of these time points, surgical management may be recommended if indicated. At 3 months, the patient is

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Obstetrical Brachial Plexus Palsy assessed using the Toronto Test Score.45,48,54 The test score assesses not only biceps function, but also elbow, wrist, finger, and thumb extension according to the AMS. Scores are then converted and summated (▶ Table 15.1). A test score < 3.5 is strongly predictive of poor recovery, and operative management is then recommended. The Toronto Test Score has been validated for use in determining indications for surgical intervention.45,48 At 6 months of age, the patient’s motor exam is again assessed with the AMS to assess for the presence or absence of improvement from previous exams. Absence of improvement of a low score on the AMS may be an indication for operative management. At 9 months of age, the infant is assessed with the “cookie test.” A lightweight cookie is placed in the hand on the affected upper extremity, and the humerus is held adducted against the child’s thorax. If the child is capable of sufficient elbow flexion to successfully reach the cookie to the mouth without flexing the neck > 45 degrees, then the child passes the cookie test, and nonoperative intervention is usually recommended.45 Brachial plexus lesions are complex injuries. No single algorithm for treatment may universally correctly predict management decisions. Determinations for operative intervention must be made based on the individual patient’s unique circumstances and motor performance over sequential time points. If a child initially demonstrates recovery but then fails to progress or has a persistent partial deficit, operative management may be recommended despite adequate performance on the above-mentioned scoring systems.

15.5.2 Preoperative Radiologic Evaluation Once surgical management has been recommended, patients undergo standardized preoperative imaging consisting of diaphragmatic ultrasonography and computed tomography (CT) myelography or magnetic resonance imaging (MRI). Diaphragmatic ultrasonography documents preoperative phrenic nerve function. CT myelography determines the presence of pseudomeningoceles, which, in the absence of visible ventral rootlets, predicts root avulsion with a specificity of 0.98. 66 MRI may also demonstrate pseudomeningoceles, but with the advantages of noninvasive technique and no exposure to ionizing radiation. For these reasons, some centers have favored MRI over CT myelography.61,67

15.6 Operative Management: Brachial Plexus Exploration, Nerve Grafting, and Nerve Transfers

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Once the decision for operative intervention has been reached, many reconstructive options are available. Brachial plexus reconstruction requires intraoperative decisions based on the neural lesions present, the resulting neural gap, and the amount of available neural donor tissues. We describe here the operative technique used at the Hospital for Sick Children, as previously described,53 then review options for brachial plexus reconstruction.

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15.6.1 Operative Preparations Care in the preparation for a lengthy and complex surgical procedure can have numerous benefits, from increased efficiency to improved patient outcomes. Communication among the members of the teams involved in the operative management of the patient with brachial plexus injury is paramount, particularly between the anesthesia and surgical teams. Simple maneuvers, such as suturing the nasal endotracheal tube to the membranous nasal septum and using a clear plastic drape over the head to allow visualization of the endotracheal tube by the anesthesia team during the procedure, can prevent disastrous complications.68 In addition, discussions regarding avoidance of excess intravenous fluid resuscitation can prevent pulmonary edema postoperatively. Proper positioning facilitates dissection and exposure of the plexus. If nerve grafts are certain to be required, the patient positioning may begin prone to facilitate bilateral sural nerve harvest and then transition to supine positioning for exposure to the plexus. Throughout this lengthy operation, all pressure points should be adequately padded to prevent pressure necrosis. Increased intraoperative communication and an outlined plan for the procedure help prevent complications.

15.6.2 Sural Nerve Harvest The sural nerves provide an excellent source of nerve graft material in brachial plexus reconstruction. Harvest of bilateral sural nerves provides a large length of graft material, up to 13 to 15 cm per leg in a 10-kg infant when the nerve is transected proximally at its branch point from the tibial nerve. Nerve harvest leaves minimal donor site morbidity with an insensate patch at the lateral foot. This region of sensory loss is measurable and permanent, but evaluation of older children who have undergone sural harvest during infancy are often unaware of this region of sensation loss.69,70 Multiple approaches for sural nerve harvest have been described. At the Hospital for Sick Children, sural harvest is completed via an endoscopically assisted approach using three transverse incisions in the posterior leg at the lateral malleolus, the distal belly of the gastrocnemius, and the popliteal fossa, as previously described.69,71 The use of the endoscope facilitates identification of the peroneal communicating branch. Once sural harvest is completed, the proximal ends of the nerves are marked, and the nerve grafts are placed in a secure, sterile container.46

15.6.3 Exposure of the Brachial Plexus After harvest of the sural nerves is completed, a supine position is achieved to allow access to the brachial plexus. Many incisions may be used to facilitate plexus exposure, but we prefer a supraclavicular approach46 with a V-shaped incision coursing vertically along the posterior border of the SCM muscle and then gently curving transversely at the clavicle (▶ Fig. 15.3). This approach allows adequate exposure with a resultant inconspicuous scar. The first goal of the operative management of an obstetrical brachial plexus injury is to determine the anatomy of the lesion. The skin and thin platysma muscle of the pediatric patient are

Obstetrical Brachial Plexus Palsy modate infraclavicular exposure; inferior clavicular retraction is usually sufficient.

15.6.4 Neuroma Resection

Fig. 15.3 Preoperative markings for supraclavicular exposure of the brachial plexus. A small rolled towel is placed under the upper back to facilitate exposure. The neck is placed in gentle extension, and the head is turned away from the operative side.

incised. Dissection proceeds along the posterior border of the SCM. The clavicular head of the SCM is divided at its insertion to facilitate exposure. The external jugular vein may need to be divided. The supraclavicular sensory nerves are encountered coursing around the lateral SCM and the clavicle. These nerves may be required for additional nerve graft material and thus are divided distally to preserve neural length while allowing adequate exposure. The transverse cervical artery is divided. The omohyoid is identified and divided at its tendinous midpoint condensation after sutures are placed in either side of the tendon to facilitate repair and preservation of this important surgical anatomical landmark in the neck. After division, the fat pad of Brown is visible and can be swept laterally to facilitate exposure of the brachial plexus. Laterally, the suprascapular vessels are identified and transected to permit increased exposure of the neuroma affecting the brachial plexus. Visualization of a nerve passing from lateral to medial indicates the phrenic nerve, as it is the only nerve in the neck with this course. The phrenic nerve travels distally from C4 and must be carefully dissected from C4 and C5. It is stimulated to evaluate diaphragmatic response. The remainder of the neuroma is dissected, systematically identifying the nerve root at each level. The C4 root, located by following the supraclavicular sensory nerves proximally, serves as a landmark for identifying the C5 root. Care is taken to identify and preserve the long thoracic nerve as it branches from the C5, C6, and C7 roots. An empty foramen is indicative of likely root avulsion. Inability to locate a nerve root may be due to root avulsion and retraction within the neuroma. The trunks of the plexus are identified. The upper and middle trunks may be adherent, depending on the location of the neuroma. The suprascapular nerve is visualized exiting the posterior division of the upper trunk laterally. The dorsal scapular artery, located between either the upper and middle trunks or the middle and lower trunks, requires division for exposure. The subclavian artery overlies the lower trunk. Careful dissection allows exposure of the C8 and T1 roots. The T1 root lies adjacent to the parietal pleura of the chest. A bubble test should be performed after dissection to confirm the integrity of the pleura. Typically, clavicular resection is not required to accom-

The roots are stimulated to determine functional results in the upper extremity. Dissection of the plexus is completed to incorporate the neuroma in its entirety. The neuroma is then transected at its midportion. Dissection proceeds distally until soft, healthy nerve is identified. Dissection distally is ensured to be free from scar by performing frozen sections. The distal nerves are transected at the healthy appearing portion, and the fascicular pattern is assessed. The nerve may require further “breadloafing” if intrafascicular scarring is grossly apparent. The distal ends of the nerve are tagged to facilitate subsequent identification during reconstruction. The level of proximal transection is then determined. Proximally, transection is performed, again, at supple, healthy-appearing nerves. Root avulsions are also noted. The proximal nerve stumps are evaluated by frozen sections to ensure neural adequacy for reconstruction. Specimens for frozen section are examined with a neuropathologist to ensure no evidence of fibrosis, indicating resection outside the zone of injury, before reconstruction is performed. For the proximal nerve stumps, histologic information must be combined with the intraoperative appearance, stimulation, and radiologic imaging evaluations to guide management. Nerves with intraforaminal ruptures may appear normal histologically. In the case of the distal stump, the absence of scarring indicates appropriateness for nerve reconstruction.

15.6.5 Reconstruction of the Brachial Plexus Only after appropriate preparation of the proximal and distal nerve targets can successful brachial plexus reconstruction be performed. Priority is given to restoration of function of the hand, followed by the elbow and the shoulder. Planning for the reconstruction may incorporate nerve grafting, nerve transfers, or a combination of the two techniques, depending on the anatomy of the lesion, the resulting neural defect, and the amount of available grafting material.

15.6.5.1 Nerve Grafting Reconstruction is performed as anatomical grafting, or reconstructing the intended target from the original root, when possible. Cable grafting is planned by measuring the resultant nerve defect compared to the available lengths of sural nerve graft. Typically, the resulting nerve defects measure 2.5 to 4.5 cm in length and therefore may be grafted with six to nine sural nerve cables. If additional grafts are required, the cervical plexus may be used as a donor site. The sural grafts are reversed to minimize axonal drop-off, and grafts are arranged according to internal topography when appropriate. When the proximal stump is not available to innervate the intended distal nerve, other sources of axons must be used, either from within the plexus (intraplexus neurotization) or from outside the plexus (extraplexus neurotization). After the grafts are appropriately arranged for reconstruction, nerve coaptations are performed with fibrin glue (Tisseel,

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Obstetrical Brachial Plexus Palsy

Fig. 15.4 Sural nerve grafts are arranged in the desired location, and fibrin glue is used for nerve coaptations. No sutures are necessary for the nerve graft coaptations.

Baxter International, Deerfield, IL) (▶ Fig. 15.4). A recent metaanalysis reports decreased granulomatous reaction and improved axonal regeneration in peripheral nerve coaptations completed with fibrin glue instead of sutures, although few human studies were available for inclusion in the analysis. 72 In addition, the use of fibrin glue allows proximal transection and reconstruction of proximal stumps, which would be difficult, if not impossible, to perform with the use of sutured coaptations.

important to recall that the suprascapular nerve lies medial and deep to the suprascapular vessels. The suprascapular ligament, a known compression site of the suprascapular nerve, can be simultaneously released with the posterior approach, which not only may facilitate regeneration, but also improves exposure of the suprascapular nerve, allowing a more distal coaptation that decreases the time to target muscle reinnervation. The main disadvantage is that it requires a separate exposure, thus adding operative time.

15.6.5.2 Nerve Transfers Nerve transfers are indicated when there is a lack of donor motor axons from the roots of the brachial plexus, such as in the case of root avulsion. Nerve transfers may permit reconstruction of motor deficits with purely motor nerves and allow reconstruction with a single neural coaptation. They may be useful in cases that present late or in cases of otherwise good spontaneous recovery when a specific isolated movement fails to recover. The more commonly used nerve transfers are described, and results are reviewed in the next section.

15.6.5.2.1 Spinal Accessory Nerve Transfer Transfer of the distal part of the spinal accessory nerve to the suprascapular nerve is a commonly performed nerve transfer for obstetrical brachial plexus palsy. From an anterior approach, the spinal accessory nerve is relatively easy to dissect and transfer to the suprascapular nerve for restoration of supra- and infraspinatus muscle function.46,73 Alternatively, this transfer may be performed via a posterior approach with the patient prone.74,75 Regardless of approach, the spinal accessory nerve is located deep in the trapezius muscle and is traced distally to preserve the proximal branches serving the upper and middle trapezius (▶ Fig. 15.5). A posterior approach allows a more distal transection of the spinal accessory nerve, decreasing the distance required for regeneration to the target muscle. It is

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15.6.5.2.2 Intercostal Nerve Transfer Intercostal nerve transfers can also be used in cases of insufficient donor axons.76 Three or more intercostal nerves may be used. These nerves are usually long enough to be transferred reliably to the musculocutaneous nerve for restoration of elbow flexion. The incision for harvesting of the intercostal nerves is begun at the midaxillary line and extended to a point inferior and medial to the nipple at the level of the fourth intercostal space. The inferior pectoralis major muscle is dissected from the intercostal muscles. The periosteum is incised over the ribs, and the periosteum is then elevated over the inferior margin of each rib. An incision is made through the reflected periosteum, revealing the neurovascular bundle. The periosteal incision is then carried medially 1 cm beyond the nipple and mobilized proximally to the posterior axillary line to deliver the maximum length of nerve. Kawabata et al recommend bundling the intercostal nerves together with fibrin glue, then performing a coaptation to the musculocutaneous nerve with sutures. 77

15.6.5.2.3 Oberlin Transfer Oberlin transfer of a redundant branch to the flexor carpi ulnaris to the biceps nerve has been used in obstetrical brachial plexus palsy reconstructions.78,79 Noaman et al proposed four indications for use of the Oberlin transfer in obstetrical brachial

Obstetrical Brachial Plexus Palsy

Fig. 15.5 Distal spinal accessory nerve transfer to the suprascapular nerve. Preservation of the proximal fibers to the trapezius prevents shoulder droop. (Used with permission from Mackinnon SE, Colbert SH. Nerve transfers in the hand and upper extremity surgery. Tech Hand Up Extrem Surg 2008;12:20−33.)

15 plexus palsy.79 The first situation is when primary surgical exploration of the plexus demonstrates isolated avulsion of the C5 and C6 roots. This is generally a rare finding in obstetric paralysis, but it may occur in breech delivery. In these cases, shoulder stability can be obtained by accessory to suprascapular nerve transfer, and elbow flexion can be achieved by using Oberlin nerve transfer. The second indication is late presentation. In these cases, the results of reconstruction of the brachial plexus using nerve grafts or neurotization of the plexus in the neck are severely compromised by the prolonged period of denervation

to the biceps muscle. Motor reinnervation of the biceps occurs within 3 months after Oberlin transfer; thus, elbow flexion is restored before permanent atrophy of the muscle. The third indication is spontaneous recovery of the upper obstetrical brachial plexus palsy without biceps function. The fourth indication is a conducting neuroma in continuity of the upper trunk with nearly normal shoulder function and no biceps function. 79 An incision in the bicipital groove allows exposure of the nerve to the biceps from the musculocutaneous nerve. The ulnar nerve is then identified, and the motor fascicles on the

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Obstetrical Brachial Plexus Palsy anterior and lateral side of the nerve are located. Redundant fibers to the flexor carpi ulnaris are identified, dissected under the operating microscope, and prepared for transfer to the nerve to the biceps. A tension-free repair is then performed.

15.6.5.2.4 Double Fascicular Nerve Transfer Humphreys and Mackinnon proposed reconstruction of the biceps and brachialis branches of the musculocutaneous nerve with redundant motor donor fascicles of both the median and ulnar nerves.80 This transfer has been performed in adult patients and older children in cases of traumatic (i.e., nonobstetrical) injury. The median or ulnar nerve may serve as the donor for either branch, and the optimal donor match should be selected on an individual basis intraoperatively. The donor for the nerve to the brachialis should be selected first, as it may have limited length. The motor fascicles of the median nerve are located medially, whereas motor fascicles of the ulnar nerve are typically located centrally and laterally. Redundant fascicles are taken from the median nerve, while preserving anterior interosseous nerve and thumb intrinsic function. Similarly, redundant fascicles are taken from the ulnar nerve, while preserving hand intrinsic function. Such a strategy may be useful for delayed presentations, or cases managed nonoperatively that fail to regain useful elbow flexion (i.e., pass the cookie test).

15.6.5.2.5 Medial Pectoral Nerve Transfer to the Musculocutaneous Nerve Transfer of the medial pectoral nerve to the musculocutaneous nerve has been reported in obstetrical brachial plexus palsy. 81 When necessary, the incision can be made in combination with a supraclavicular approach by extending the incision into the deltopectoral groove. Alternatively, it can be made without the supraclavicular incision by marking a zig-zag incision from the deltopectoral groove into the axilla and then distally to the bicipital groove to gain access to the musculocutaneous nerve. The pectoralis major muscle insertion is transected, and the pectoralis minor muscle is divided at its origin from the coracoid process. A nerve stimulator is used to locate the medial pectoral nerves as they enter the pectoralis minor muscle. It is important to realize that the lateral pectoral nerves are usually connected to the medial pectoral nerves, as documented in a detailed anatomical study by Aszmann et al.82 However, only those fibers that are seen entering the muscle directly and stimulate well should be used for the transfer. If a branch is seen entering the muscle and stimulates vigorously, then it is transected where it enters the muscle. In most upper plexus lesions, the medial pectoral nerves stimulate well. Coaptation to the musculocutaneous nerve usually can be achieved with favorable size match.

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15.6.5.2.6 Contralateral C7 Transfer Chuang et al reported contralateral C7 transfer in obstetrical brachial plexus reconstruction, but the authors state that “the practice of using contralateral C7 transfer has been considered infrequently and is ineffective in infant obstetrical brachial plexus palsy because of poor cooperation for rehabilitation.”64 Nevertheless, some centers are using this transfer in cases of

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five root avulsions. Such cases are very rare, however. Surgeons in Asia have been performing this transfer, but North American surgeons have been reluctant to adopt its use out of concern for the unaffected extremity. Chen et al reported use of this transfer in seven children with panplexus obstetrical lesions. 83 They performed the transfer using vascularized ulnar nerve from the affected extremity or sural nerve grafts. Transfer of C7 to the median nerve, lateral cord, or musculocutaneous nerve was performed, in combination with other nerve transfers with variable results.

15.6.5.2.7 Hypoglossal Nerve Transfer Reports of hypoglossal nerve transfer for reconstruction of obstetrical brachial plexus lesions have been described.84,85 Longterm motor deficits of the tongue, however, make this nerve transfer undesirable. Its use, therefore, is no longer advocated.

15.6.5.2.8 Phrenic Nerve Transfer Transfer of the phrenic nerve to the brachial plexus has been used extensively in adults but not in children. The main concern is that infants and small children are obligate diaphragmatic breathers; therefore, division of the phrenic nerve would produce an unacceptably high rate of respiratory complications. Nevertheless, this transfer has been reported in obstetrical brachial plexus palsy.86

15.6.6 Adjunctive Management Muscle imbalance at the shoulder can lead to additional functional impairments in the upper extremity in children with obstetrical brachial plexus injuries. Glenohumeral motion is unaffected only in patients who have complete functional recovery by the age of 2 months.55 In the setting of brachial plexus injury, the dually innervated internal rotators of the shoulder remain largely unaffected, whereas external shoulder rotation and abduction movements are weak or absent. The resulting muscle imbalance may result in internal shoulder rotation contracture, glenohumeral joint deformity, and posterior dislocation, all of which further inhibit upper extremity function. Maintenance of range of motion is important to prevent detrimental sequelae. Botulinum toxin A has been used to decrease muscle force in unaffected muscles, such as the internal shoulder rotators, to prevent contractures, improve passive range of motion, improve muscle balance during the period of neuroregeneration after brachial plexus reconstruction, and potentially allow for cortical motor reorganization.87,88

15.7 Postoperative Management The wounds are closed with absorbable monofilament suture in layers, with all suture material buried, and cyanoacrylate skin adhesive is applied. This allows the child to bathe without fear of damaging the closure. A Velpeau stockinette sling is applied. This simple sling keeps the shoulder in adduction for an immobilization period of 3 weeks. The family can easily learn to replace or tighten it when necessary. After 3 weeks of immobilization, the infant is allowed to move freely. Additional casts and splinting are not required.

Obstetrical Brachial Plexus Palsy Recovery of movement may be noted as early as 3 months postoperatively. Preoperative motion is typically regained by 3 to 6 months postoperatively, and functional improvements continue for 3 to 4 years before plateauing. Secondary procedures, including additional nerve transfers, tendon transfers, or osteotomies, are sometimes indicated to correct residual problems.

15.8 Outcomes Assessment of specific clinical outcomes in obstetrical brachial plexus palsy is hampered by the fact that there is no universally accepted outcome measure. Many centers report range of motion in terms of degrees of joint angle. Others use various scores, including the Mallet score for shoulder function and the Raimondi score for hand function, as well as the British MRC score for muscle strength. Probably the most universally applicable outcome measure is the AMS, because this scale can be applied in infants and also in cooperative older patients. Many techniques for brachial plexus reconstruction are advocated by different surgeons worldwide. In obstetrical brachial plexus palsy, surgical intervention may entail neurolysis, neuroma resection and interpositional grafting, or nerve transfer. Neurolysis was shown to be beneficial for the treatment of conducting neuromas-in-continuity at 12-month follow-up in patients with Erb palsy but not in those with total plexus palsies.89 Capek et al compared 26 patients in which neuroma resection and interpositional nerve grafting was performed to 17 patients who underwent neurolysis alone.90 They found that resection of the neuroma did not adversely affect the total limb motion scores. In addition, all patients who underwent neuroma excision and grafting regained their preoperative baseline function by 3 to 6 months postoperatively. The significance of this work is that the surgeon may resect the neuroma without fear of downgrading function in children who are deemed operative candidates using the Toronto Test Score. Lin et al retrospectively reviewed prospectively collected data comparing neurolysis alone to neuroma resection and grafting in 108 patients undergoing reconstruction of obstetrical brachial plexus lesions.91 At a 4-year follow-up interval, patients with Erb palsy who underwent neurolysis alone demonstrated no functional improvement, whereas those patients treated with neuroma resection and nerve grafting achieved significant functional improvements in seven tested movements. Similarly, in patients with total brachial plexus palsies, there were no significant functional improvements at 4 years in 15 tested movements in patients treated with neurolysis alone, whereas 11 of 15 movements significantly improved at 4 years in patients treated with neuroma resection and interpositional nerve grafting. In 2005 O’Brien et al published a series of 52 children treated with brachial plexus exploration and sural nerve grafting.61 The mean age of operation was 9.79 months, although the authors state a preference to operate at age 6 months. They found that children with C5–C6 injury achieved an MRC score ≥ 3/5 in the biceps in 92%, triceps 92%, and deltoid 83%. Children with a C5– C7 injury achieved an MRC score ≥ 3/5 in the biceps in 76%, triceps 76%, and deltoid 72%. Children with a C5–C8 and T1 injury achieved an MRC score ≥ 3/5 in the biceps in 73%, triceps 53%, and deltoid 67%. Complications included two wound infections and one case of postoperative hemidiaphragmatic paralysis.

In 2006 Gilbert et al reported their 20-year experience. The authors found that 80% of children with C5–C6 lesions achieve good or excellent shoulder function following neuroma excision and grafting at 4 years.92 The indication for exploration was lack of biceps function at age 3 months. In C5–C7 lesions, 61% had good or excellent shoulder function at 4 years. Those with complete lesions achieved average, good, or excellent results in 77% at 8 years. Elbow function was reported as almost always excellent, with 81% of children with complete lesions demonstrating good or excellent results at 8 years. Hand function was rated as “useful” in 76%. El-Gammal et al reported their results after reconstruction via neurolysis, grafting, and/or nerve transfer for total brachial plexus palsy in 35 children.93 The best functional outcomes were achieved for elbow flexion and extension (77% good or excellent) and worst for thumb and wrist extension (28% and 31% good or excellent, respectively). Nerve transfer procedures have met with good results. Transfer of the distal spinal accessory nerve to the suprascapular nerve appears to produce results that are statistically not distinguishable from sural nerve grafting from C5 to the suprascapular nerve. Tse et al reviewed 177 patients who had undergone suprascapular nerve reconstruction by either sural nerve grafting from the C5 root or spinal accessory nerve transfer.94 At 3 years postoperatively, there were no differences in external shoulder rotation scores on the AMS between the two techniques. Similarly, Terzis and Kostas noted no significant differences in motor grading in 53 patients who underwent suprascapular nerve reconstruction via direct neurotization from the spinal accessory nerve or intraplexus donors compared to reconstruction using a nerve graft, although they described a trend toward increased range of shoulder abduction in direct reconstructions.95 They reported good or excellent results in 96% of patients for supraspinatus function and 75% of patients for infraspinatus function. External shoulder rotation achieved Mallet grade III or IV in 41 of 50 patients who underwent surgical reconstruction. In a study by Pondaag et al, there were no differences in function as assessed by angle of true glenohumeral rotation, passive external rotation, and Mallet hand-to-head motion.96 In a study by van Ouwerkerk et al, transfer of the spinal accessory nerve to the suprascapular nerve was performed from a posterior approach.97 When used in otherwise spontaneously recovered patients, the transfer improved external rotation dramatically: all 54 patients initially had no active external rotation (Mallet II score), and at 2 years, 40 of those patients achieved Mallet IV external rotation, 10 achieved Mallet III external rotation, and 4 remained at Mallet II external rotation. The authors recommended waiting 10 months to perform this transfer in cases where spontaneous recovery appears to be otherwise proceeding well, conjecturing that additional central motor learning pathways become disrupted if the transfer is performed too early, resulting in decreased cortical integration. Intercostal nerve transfers to the musculocutaneous nerve were performed in 31 cases in a report by Kawabata et al.77 Two intercostal nerves were used in 26 cases, and three were used in 5 cases. MRC grade M4 biceps function was achieved in 26 of 31 patients (84%). In the 12 patients who underwent an operation before age 5 months, all achieved MRC grade M4 biceps function. Similarly, El-Gammal et al reported improved function with intercostal nerve transfer to various recipient nerves for

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Obstetrical Brachial Plexus Palsy brachial plexus reconstruction in 46 patients with 62 neurotization procedures.98 They found improved results with earlier operative intervention (age < 9 mo), although this result was not statistically significant. Good or excellent motor results were achieved in 76% of cases. Motor reconstruction was most reliable for elbow flexion, with 93.5% of patients achieving good or excellent results. Intercostal neurotization showed improved restoration of elbow flexion compared to grafting of the upper trunk in a separate series.93 In a study by Noaman et al, Oberlin transfer was performed in seven patients.79 Of these patients, five obtained Gilbert-Raimondi elbow scores of 4 or 5. MRC biceps grade M4 or M5 function was achieved in four patients. No children had deficits involving the ulnar nerve. The authors’ recommended indications for this transfer are listed above, under Operative Management. Al Qattan reported MRC scores of M5 (Toronto Test Score of 7) in both patients in his 2002 study.78 His recommended indications include isolated avulsion of C5 and C6 and late presentations. Transfer of the medial pectoral nerves to the musculocutaneous nerve, as reported in a series of 25 cases by Blaauw and Slooff in 2003, resulted in signs of reinnervation of the biceps and brachialis at 2 months after transfer.81 Reinnervation was largely complete 6 months after transfer. The mean age at operation was 5.3 months. Seventeen of 25 patients achieved antigravity elbow flexion, and 5 achieved elbow flexion with gravity eliminated; 3 children recovered no biceps/brachialis function. Those who did not achieve antigravity elbow flexion were then treated with Steindler flexorplasty. A review of 20 patients with obstetrical brachial plexus injuries treated with medial pectoral nerve transfer to the musculocutaneous nerve resulted in sufficient elbow flexion to reach the hand to the mouth in 80% of patients.99 Contralateral C7 transfer to the median nerve produced variable results in a retrospective review by Chen et al. 83 They noted MRC grade S3 or better sensory function in all patients postoperatively. When they used the C7 transfer to reinnervate biceps, they were able to obtain MRC grade M3 function in three of four cases. When they used C7 for median nerve function, they achieved M3 or greater median nerve function in two of seven cases. Half of their obstetrical cases had “substantial” synchronous movement or sensation. Lin et al reviewed their experience with staged contralateral C7 transfer to both the musculocutaneous and median nerves.100 They demonstrated improved biceps motor function of M3 or M4 in seven of nine patients and M2 in two patients. Median nerve function in the hand (wrist and finger flexion) fared less well with no motor improvement in two of nine patients, M2 function in two patients, and M3 or M4 function in five patients at an average follow-up of 50 months. All nine of these infants displayed synchronous motion from the donor limb. Lin et al recently reported improved functional results after contralateral C7 transfer in the treatment of infants with obstetrical brachial plexus injuries.101 Better than or equal to half range of motion against gravity (M2 +) was achieved in 11 of 15 patients after reconstruction of the upper trunk or lateral cord with the contralateral C7 after an average 47-month follow-up. Shoulder function on the donor side was reported to be fully recovered by 4 weeks postoperatively.

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Children with obstetrical brachial plexus palsy but without significant hand impairment are able to perform self-care activities without significant limitation, as assessed by the Pediatric Evaluation of Disability Inventory (PEDI). Those children with hand impairment have a deficit in self-care activities. Children with obstetrical brachial plexus palsy but without hand impairment fared no differently on the PEDI than their unaffected peers.102 Although children affected with obstetrical brachial plexus palsies demonstrate lower scores for global and upper extremity function compared to pediatric norms, they participate in organized sports activities at a rate similar to their unaffected peers. Whereas up to 42% of these children perceive a disability related to their sport, the majority of children participated in multiple sports and did not experience increased rates of injury compared to their unaffected peers.103

15.9 Conclusion Management of obstetrical brachial plexus palsy remains challenging. Although the majority of children do not require operative management, those that do can often be treated successfully with a variety of techniques. Appropriate timing of surgical intervention is critical for optimization of results. The gold standard of neuroma excision and sural nerve grafting may be supplemented by newer techniques, such as selective distal nerve transfers. Outcomes analysis continues to be a valuable tool for assessing the optimal management for patients with obstetrical brachial plexus injuries.

15.10 References [1] Smellie W. A collection of cases and observations in midwifery. Vol 2. 4th ed. London: Wilson & Nicol; 1768 [2] Duchenne GBA. De l’Électrisation localisée et de son application à la pathologie et à la thérapeutique par courants induits et par courants galvaniques interrompus et continus. 3rd ed. Paris: Librairie JB Baillière; 1872 [3] Erb, W. Über eine eigenthümliche Localisation von Lähmungen im Plexus brachialis. Verhandlungen. Naturhistorisch-medizinischer Verein. Heidelberg 1874;2:130–136 [4] Kennedy R. Suture of the brachial plexus in birth paralysis of the upper extremity. BMJ 1903;1:298–301 [5] Thorburn W. Obstetrical paralysis. J Obstet Gynaecol Br Emp 1903;3:454–458 [6] Abe Y, Doi K, Kawai S. An experimental model of peripheral nerve adhesion in rabbits. Br J Plast Surg 2005;58:533–540 [7] Sever JW. Obstetric paralysis: report of eleven hundred cases. JAMA 1925;85:1862–1865 [8] Sever JW. Obstetric paralysis: its etiology, pathology, clinical aspects and treatment, with a report of four hundred and seventy cases. Am J Dis Child 1916;12:541–578 [9] Millesi H, Ganglberger J, Berger A. Erfahrungenmit der MikrochirurgieperiphererNerven. Chir Plast Reconstr 1967;3:47–55 [10] Sunderland S. A classification of peripheral nerve injuries producing loss of function. Brain 1951;74:491–516 [11] Narakas A, Verdan C. Les greffesnerveuses. ZeitschriftfürUnfallmedizin und Berufskrankheiten. Revue de Médicine des Accidents et des Maladies Professionelles 1969;62:137–152 [12] Narakas AO. Injuries to the brachial plexus. In: F W Bora Jr., ed. The Pediatric Upper Extremity: Diagnosis and Management. Philadelphia, PA: WB Saunders; 1986:247–258 [13] Narakas A. Brachial plexus surgery. Orthop Clin North Am 1981;12:303–323 [14] Narakas AO. The treatment of brachial plexus injuries. Int Orthop 1985;9:29–36 [15] Narakas AO. Obstetrical brachial plexus injuries. In: D W. Lamb, ed. The Paralysed Hand. Vol 2. Edinburgh, Scotland: Churchill Livingstone; 1987:116–135

Obstetrical Brachial Plexus Palsy [16] Narakas AO, Hentz VR. Neurotization in brachial plexus injuries. Indication and results. Clin Orthop Relat Res 1988;237:43–56 [17] Gilbert A. Obstetrical brachial plexus palsy. In: R Tubiana, ed. The Hand. Vol 4. Philadelphia, PA: WB Saunders; 1993:575–601 [18] Gilbert A, Khouri N, Carlioz H. Exploration chirurgicale du plexus brachial dans la paralysieobstétricale. Constatations anatomiques chez 21 malades opérés. Rev Chir Orthop Repar Appar Mot 1980;66:33–42 [19] Gilbert A, Tassin J-L. Obstetrical palsy: a clinical, pathologic, and surgical review. In: JK Terzis, ed. Microreconstruction of Nerve Injuries. Philadelphia, PA: WB Saunders; 1987:529–553 [20] Eng GD, Binder H, Getson P, O’Donnell R. Obstetrical brachial plexus palsy (OBPP) outcome with conservative management. Muscle Nerve 1996;19:884–891 [21] Strömbeck C, Krumlinde-Sundholm L, Forssberg H. Functional outcome at 5 years in children with obstetrical brachial plexus palsy with and without microsurgical reconstruction. Dev Med Child Neurol 2000;42:148–157 [22] Levine MG, Holroyde J, Woods JR, Siddiqi TA, Scott M, Miodovnik M. Birth trauma: incidence and predisposing factors. Obstet Gynecol 1984;63:792– 795 [23] Hardy AE. Birth injuries of the brachial plexus: incidence and prognosis. J Bone Joint Surg Br 1981;63-B:98–101 [24] Michelow BJ, Clarke HM, Curtis CG, Zuker RM, Seifu Y, Andrews DF. The natural history of obstetrical brachial plexus palsy. Plast Reconstr Surg 1994;93:675–680, discussion 681 [25] Foad SL, Mehlman CT, Ying J. The epidemiology of neonatal brachial plexus palsy in the United States. J Bone Joint Surg Am 2008;90:1258–1264 [26] al-Qattan MM, Clarke HM, Curtis CG. Klumpke’s birth palsy: does it really exist? J Hand Surg ( Br ) 1995;20:19–23 [27] Al-Qattan MM, El-Sayed AAF, Al-Zahrani AY, et al. Obstetric brachial plexus palsy in newborn babies of diabetic and non-diabetic mothers. J Hand Surg Eur Vol 2010a;35:362–365 [28] Al-Qattan MM, El-Sayed AAF, Al-Zahrani AY, et al. Obstetrical brachial plexus palsy: a comparison of affected infants delivered vaginally by breech or cephalic presentation. J Hand Surg Eur Vol 2010;35:366–369 [29] Gilbert A, Brockman R, Carlioz H. Surgical treatment of brachial plexus birth palsy. Clin Orthop Relat Res 1991;264:39–47 [30] Wikström I, Axelsson O, Bergström R, Meirik O. Traumatic injury in large-fordate infants. Acta Obstet Gynecol Scand 1988;67:259–264 [31] Al-Qattan MM, El-Sayed AAF, Al-Kharfy TM, et al. Obstetric barachial plexus injury in subsequent deliveries. Canadian Journal of Plastic Surgery 1996;4:203–204 [32] Mehta SH, Blackwell SC, Bujold E, Sokol RJ. What factors are associated with neonatal injury following shoulder dystocia? J Perinatol 2006;26:85–88 [33] Keller JD, López-Zeno JA, Dooley SL, Socol ML. Shoulder dystocia and birth trauma in gestational diabetes: a five-year experience. Am J Obstet Gynecol 1991;165:928–930 [34] Baxley EG, Gobbo RW. Shoulder dystocia. Am Fam Physician 2004;69:1707– 1714 [35] Rouse DJ, Owen J, Goldenberg RL, Cliver SP. The effectiveness and costs of elective cesarean delivery for fetal macrosomia diagnosed by ultrasound. JAMA 1996;276:1480–1486 [36] Conway DL, Langer O. Elective delivery of infants with macrosomia in diabetic women: reduced shoulder dystocia versus increased cesarean deliveries. Am J Obstet Gynecol 1998;178:922–925 [37] Langer O, Berkus MD, Huff RW, Samueloff A. Shoulder dystocia: should the fetus weighing greater than or equal to 4000 grams be delivered by cesarean section? Am J Obstet Gynecol 1991;165:831–837 [38] Athukorala C, Crowther CA, Willson K, Austrailian Carbohydrate Intolerance Study in Pregnant Women (ACHOIS) Trial Group. Women with gestational diabetes mellitus in the ACHOIS trial: risk factors for shoulder dystocia. Aust N Z J Obstet Gynaecol 2007;47:37–41 [39] Athukorala C, Middleton P, Crowther CA. Intrapartum interventions for preventing shoulder dystocia. Cochrane Database Syst Rev 2006:CD005543 [40] de Chalain TM, Clarke HM, Curtis CG. Case report: unilateral combined facial nerve and brachial plexus palsies in a neonate following a midlevel forceps delivery. Ann Plast Surg 1997;38:187–190 [41] al-Qattan MM, Clarke HM, Curtis CG. The prognostic value of concurrent clavicular fractures in newborns with obstetric brachial plexus palsy. J Hand Surg Br 1994;19:729–730 [42] Métaizeau JP, Gayet C, Plenat F. Les lésions obstétricales du plexus brachial. Chir Pediatr 1979;20:159–163 [43] Gilbert A, Razaboni R, Amar-Khodja S. Indications and results of brachial plexus surgery in obstetrical palsy. Orthop Clin North Am 1988;19:91–105

[44] Clarke HM, Curtis CG. Examination and prognosis. In: A. Gilbert, ed. Brachial Plexus Injuries. London: Martin Dunitz; 2001:159–172 [45] Losee JE, Mason AC. Deformational plagiocephaly: diagnosis, prevention, and treatment. Clin Plast Surg 2005;32:53–64, viii [46] Clarke HM, Curtis CG. An approach to obstetrical brachial plexus injuries. Hand Clin 1995;11:563–580, discussion 580–581 [47] Marcus JR, Clarke HM. Management of obstetrical brachial plexus palsy evaluation, prognosis, and primary surgical treatment. Clin Plast Surg 2003;30:289–306 [48] Al-Qattan MM, Clarke HM, Curtis CG. The prognostic value of concurrent phrenic nerve palsy in newborn children with Erb’s palsy. J Hand Surg Br 1998;23:225 [49] Curtis C, Stephens D, Clarke HM, Andrews D. The active movement scale: an evaluative tool for infants with obstetrical brachial plexus palsy. J Hand Surg Am 2002;27:470–478 [50] Bae DS, Waters PM, Zurakowski D. Reliability of three classification systems measuring active motion in brachial plexus birth palsy. J Bone Joint Surg Am 2003;85-A:1733–1738 [51] Aydın A, Mersa B, Erer M, Ozkan T, Ozkan S. Early results of nerve surgery in obstetrical brachial plexus palsy [in Turkish] Acta Orthop Traumatol Turc 2004;38:170–177 [52] British Medical Research Council. Aids to the Investigation of Peripheral Nerve Injuries. London: His Majesty’s Stationary Office; 1943 [53] Mallet J. Paralysie obstétricale du plexus brachial. Traitement des séquelles. Primauté du traitement de l’épaule—méthode d’expression des résultats. Rev Chir Orthop Repar Appar Mot 1972;58 uppl 1:166–168 [54] Borschel GH, Clarke HM. Obstetrical brachial plexus palsy. Plast Reconstr Surg 2009;124 Suppl:144e–155e [55] Waters PM. Comparison of the natural history, the outcome of microsurgical repair, and the outcome of operative reconstruction in brachial plexus birth palsy. J Bone Joint Surg Am 1999;81:649–659 [56] Gordon M, Rich H, Deutschberger J, Green M. The immediate and long-term outcome of obstetric birth trauma: 1. Brachial plexus paralysis. Am J Obstet Gynecol 1973;117:51–56 [57] Al-Qattan MM, Clarke HM, Curtis CG. The prognostic value of concurrent Horner’s syndrome in total obstetric brachial plexus injury. J Hand Surg ( Br ) 2000;25:166–167 [58] Bahm J, Gilbert A. Behandlungs strategie beigeburts traumatischen Plexus paresen. Monatsschr Kinderheilkd 1997;145:1040–1045 [59] Gilbert A. Long-term evaluation of brachial plexus surgery in obstetrical palsy. Hand Clin 1995;11:583–594, discussion 594–595 [60] Gilbert A, Whitaker I. Obstetrical brachial plexus lesions. J Hand Surg Br 1991;16:489–491 [61] O’Brien DF, Park TS, Noetzel MJ, Weatherly T. Management of birth brachial plexus palsy. Childs Nerv Syst 2006;22:103–112 [62] Laurent JP, Lee R, Shenaq S, Parke JT, Solis IS, Kowalik L. Neurosurgical correction of upper brachial plexus birth injuries. J Neurosurg 1993;79:197–203 [63] Hale HB, Bae DS, Waters PM. Current concepts in the management of brachial plexus birth palsy. J Hand Surg Am 2010;35:322–331 [64] Chuang DCC, Mardini S, Ma HS. Surgical strategy for infant obstetrical brachial plexus palsy: experiences at Chang Gung Memorial Hospital. Plast Reconstr Surg 2005;116:132–142, discussion 143–144 [65] Fisher DM, Borschel GH, Curtis CG, Clarke HM. Evaluation of elbow flexion as a predictor of outcome in obstetrical brachial plexus palsy. Plast Reconstr Surg 2007;120:1585–1590 [66] Chow BC, Blaser S, Clarke HM. Predictive value of computed tomographic myelography in obstetrical brachial plexus palsy. Plast Reconstr Surg 2000;106:971–977, discussion 978–979 [67] Yılmaz K, Calişkan M, Öge E, Aydinli N, Tunaci M, Ozmen M. Clinical assessment, MRI, and EMG in congenital brachial plexus palsy. Pediatr Neurol 1999;21:705–710 [68] La Scala GC, Rice SB, Clarke HM. Complications of microsurgical reconstruction of obstetrical brachial plexus palsy. Plast Reconstr Surg 2003;111:1383– 1388, discussion 1389–1390 [69] Capek L, Clarke HM. Endoscopically assisted sural nerve harvest in infants. Semin Plast Surg 2008;22:25–28 [70] Lapid O, Ho ES, Goia C, Clarke HM. Evaluation of the sensory deficit after sural nerve harvesting in pediatric patients. Plast Reconstr Surg 2007;119:670– 674 [71] Capek L, Clarke HM, Zuker RM. Endoscopic sural nerve harvest in the pediatric patient. Plast Reconstr Surg 1996;98:884–888 [72] Sameem M, Wood TJ, Bain JR. A systematic review on the use of fibrin glue for peripheral nerve repair. Plast Reconstr Surg 2011;127:2381–2390

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Obstetrical Brachial Plexus Palsy [73] Kawabata H, Kawai H, Masatomi T, Yasui N. Accessory nerve neurotization in infants with brachial plexus birth palsy. Microsurgery 1994;15:768–772 [74] Bahm J, Noaman H, Becker M. The dorsal approach to the suprascapular nerve in neuromuscular reanimation for obstetric brachial plexus lesions. Plast Reconstr Surg 2005;115:240–244 [75] Colbert SH, Mackinnon SE. Nerve transfers for brachial plexus reconstruction. Hand Clin 2008;24:341–361, v [76] Hattori Y, Doi K, Fuchigami Y, Abe Y, Kawai S. Experimental study on donor nerves for brachial plexus injury: comparison between the spinal accessory nerve and the intercostal nerve. Plast Reconstr Surg 1997;100:900–906 [77] Kawabata H, Shibata T, Matsui Y, Yasui N. Use of intercostal nerves for neurotization of the musculocutaneous nerve in infants with birth-related brachial plexus palsy. J Neurosurg 2001;94:386–391 [78] Al-Qattan MM. Oberlin’s ulnar nerve transfer to the biceps nerve in Erb’s birth palsy. Plast Reconstr Surg 2002;109:405–407 [79] Noaman HH, Shiha AE, Bahm J. Oberlin’s ulnar nerve transfer to the biceps motor nerve in obstetric brachial plexus palsy: indications, and good and bad results. Microsurgery 2004;24:182–187 [80] Humphreys DB, Mackinnon SE. Nerve transfers. Operative Techniques in Plastic and Reconstructive Surgery 2002;9:89–99 [81] Blaauw G, Slooff AC. Transfer of pectoral nerves to the musculocutaneous nerve in obstetric upper brachial plexus palsy. Neurosurgery 2003;53:338– 341, discussion 341–342 [82] Aszmann OC, Rab M, Kamolz L, Frey M. The anatomy of the pectoral nerves and their significance in brachial plexus reconstruction. J Hand Surg Am 2000;25:942–947 [83] Chen L, Gu YD, Hu SN, Xu JG, Xu L, Fu Y. Contralateral C7 transfer for the treatment of brachial plexus root avulsions in children - a report of 12 cases. J Hand Surg Am 2007;32:96–103 [84] Blaauw G, Sauter Y, Lacroix CL, Slooff AC. Hypoglossal nerve transfer in obstetric brachial plexus palsy. J Plast Reconstr Aesthet Surg 2006;59:474–478 [85] Malessy MJ, Hoffmann CF, Thomeer RT. Initial report on the limited value of hypoglossal nerve transfer to treat brachial plexus root avulsions. J Neurosurg 1999;91:601–604 [86] Xu J, Cheng X, Dong Z, Gu Y. Remote therapeutic effect of early nerve transposition in treatment of obstetrical brachial plexus palsy. Chin J Traumatol 2001;4:40–43 [87] Ezaki M, Malungpaishrope K, Harrison RJ, et al. botulinum toxin A injection as an adjunct in the treatment of posterior shoulder subluxation in neonatal brachial plexus palsy. J Bone Joint Surg Am 2010;92:2171–2177 [88] Price AE, Ditaranto P, Yaylali I, Tidwell MA, Grossman JA. Botulinum toxin type A as an adjunct to the surgical treatment of the medial rotation deformity of the shoulder in birth injuries of the brachial plexus. J Bone Joint Surg Br 2007;89:327–329

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[89] Clarke HM, Al-Qattan MM, Curtis CG, Zuker RM. Obstetrical brachial plexus palsy: results following neurolysis of conducting neuromas-in-continuity. Plast Reconstr Surg 1996;97:974–982, discussion 983–984 [90] Capek L, Clarke HM, Curtis CG. Neuroma-in-continuity resection: early outcome in obstetrical brachial plexus palsy. Plast Reconstr Surg 1998;102:1555–1562, discussion 1563–1564 [91] Lin JC, Schwentker-Colizza A, Curtis CG, Clarke HM. Final results of grafting versus neurolysis in obstetrical brachial plexus palsy. Plast Reconstr Surg 2009;123:939–948 [92] Gilbert A, Pivato G, Kheiralla T. Long-term results of primary repair of brachial plexus lesions in children. Microsurgery 2006;26:334–342 [93] El-Gammal TA, El-Sayed A, Kotb MM, et al. Total obstetric brachial plexus palsy: results and strategy of microsurgical reconstruction. Microsurgery 2010b;30:169–178 [94] Tse R, Marcus JR, Curtis CG, Dupuis A, Clarke HM. Suprascapular nerve reconstruction in obstetrical brachial plexus palsy: spinal accessory nerve transfer versus C5 root grafting. Plast Reconstr Surg 2011;127:2391–2396 [95] Terzis JK, Kostas I. Outcomes with suprascapular nerve reconstruction in obstetrical brachial plexus patients. Plast Reconstr Surg 2008;121:1267– 1278 [96] Pondaag W, de Boer R, van Wijlen-Hempel MS, Hofstede-Buitenhuis SM, Malessy MJ. External rotation as a result of suprascapular nerve neurotization in obstetric brachial plexus lesions. Neurosurgery 2005;57:530–537, discussion 530–537 [97] van Ouwerkerk WJ, Uitdehaag BM, Strijers RL, et al. Accessory nerve to suprascapular nerve transfer to restore shoulder exorotation in otherwise spontaneously recovered obstetric brachial plexus lesions. Neurosurgery 2006;59:858–867, discussion 867–869 [98] El-Gammal TA, Abdel-Latif MM, Kotb MM, et al. Intercostal nerve transfer in infants with obstetric brachial plexus palsy. Microsurgery 2008;28:499–504 [99] Wellons JC, Tubbs RS, Pugh JA, Bradley NJ, Law CR, Grabb PA. Medial pectoral nerve to musculocutaneous nerve neurotization for the treatment of persistent birth-related brachial plexus palsy: an 11-year institutional experience. J Neurosurg Pediatr 2009;3:348–353 [100] Lin H, Hou C, Chen D. Modified C7 neurotization for the treatment of obstetrical brachial plexus palsy. Muscle Nerve 2010;42:764–768 [101] Lin H, Hou C, Chen D. Contralateral C7 transfer for the treatment of upper obstetrical brachial plexus palsy. Pediatr Surg Int 2011;27:997–1001 [102] Ho ES, Curtis CG, Clarke HM. Pediatric Evaluation of Disability Inventory: its application to children with obstetric brachial plexus palsy. J Hand Surg Am 2006;31:197–202 [103] Bae DS, Zurakowski D, Avallone N, Yu R, Waters PM. Sports participation in selected children with brachial plexus birth palsy. J Pediatr Orthop 2009;29:496–503

Facial Nerve Injury

16 Facial Nerve Injury Gregory H. Borschel, Tessa A. Hadlock, Christine B. Novak, and Alison K. Snyder-Warwick

16.1 Introduction Facial paralysis, whether acquired or congenital, causes great concern and produces substantial morbidity. Children with isolated facial paralysis are often perceived as learning impaired, despite possessing normal intelligence. Families of individuals suffering from facial paralysis benefit from prompt diagnosis and formulation of a treatment plan. Facial paralysis was considered a nonoperative condition until the 19th century. The first operative case of nerve reconstruction for facial paralysis was likely performed by Sir Charles Ballance in 1895.1 The first case was formerly attributed to Drobnick, who was reported as having performed, in 1879, a transfer of the spinal accessory nerve to the facial nerve, resulting in improved facial symmetry.2 However, further investigation has shown that Drobnick would have been only 21 years old at the time and still a student.3 Ballance in 1895 performed an end-to-side transfer of the spinal accessory nerve to the facial nerve in an 11-year-old boy, who developed acquired facial paralysis after an operation for otitis media. The case was described in a paper in the British Medical Journal in 1903.1

16.2 Etiology Among adult patients, most cases of facial paralysis are acquired. The most common causes of facial paralysis among adults in a study by Cha et al were Bell palsy (54.9%), infection (26.8%), trauma (5.9%), iatrogenic (2.0%), and tumors (1.8%), whereas the most frequent causes of acquired facial palsy in children were Bell palsy (66.2%), infection (14.6%), trauma (13.4%), birth trauma (3.2%), and leukemia (1.3%). Infections resulting in facial paralysis are usually caused by herpes simplex, varicella zoster virus, Lyme disease, or bacterial processes in the middle ear and mastoid.4 In a study of pediatric facial paralysis by Evans et al, 35 cases of facial paralysis were reviewed. The etiologies were infectious (13); traumatic (7); iatrogenic (5); congenital (4); Bell/idiopathic (3); relapsing (2); and neoplastic (1).5 Peak age distributions for both infectious and traumatic etiologies were bimodal: 1 to 3 and 8 to 12 years. In a similar study by Shih et al, 56 cases of pediatric facial paralysis were reviewed, and a similar distribution was found.6 In a series of approximately 2,000 patients treated at the facial nerve center of one of the authors (TAH), among both adult and pediatric patients, the distribution of etiologies was dominated by Bell palsy and vestibular schwannoma extirpation, followed by head and neck malignancy and iatrogenic injuries (▶ Fig. 16.1).7 Other documented etiologies and associations for facial paralysis are toxoplasmosis, human immunodeficiency virus (HIV), infections following cochlear implants, fibrous dysplasia of the temporal bone, middle ear or parotid tumors, Wegener granulomatosis, mandibular distraction osteogenesis, stroke, dental extraction, Epstein-Barr virus infection, Melkersson-Rosenthal syndrome, Möbius syndrome, hemifacial microsomia, intrapartum injury, hereditary mandibular branch paralysis (also termed congenital unilateral lower lip paralysis [CULLP]),

myasthenia gravis, and other neuromuscular disorders. A classification system for the multiple etiologies has been proposed in which the various etiologies have been collated into groups for ease of communication between specialists.8

16.3 Anatomical Considerations 16.3.1 Facial Nerve The facial nerve comprises an intracranial portion and both intra- and extratemporal segments, with special considerations for damage in each segment. Motor fibers to the muscles of facial expression (plus the stylohyoid, posterior belly of the digastric muscle, and stapedius) make up the majority of axons contained within the facial nerve. The remaining fibers of the facial nerve include visceral motor fibers (salivary and lacrimal function), general sensory fibers (to the external auditory canal), and special sensory fibers (taste fibers via the chorda tympani). Impulses from the motor cortex are projected through the internal capsule into the seventh cranial nerve nucleus. Input to the frontal branch portion of the facial nucleus is bilateral, whereas impulses to other muscles of facial expression decussate to the contralateral facial nucleus. This arrangement is the basis for the clinical finding of ipsilateral sparing of brow elevation in cases of central unilateral facial paralysis. Fibers then exit the pons and enter the temporal bone, where the nerve is vulnerable to both shear stresses and compressive neuropathies. The internal topography of the facial nerve at this level is variable. The intracranial segment of the nerve consists of the facial motor nucleus in the brainstem, as well as a short segment in the cerebellopontine angle (CPA). The facial motor nucleus is most vulnerable during the resection of pilocytic astrocytomas, cavernous brainstem hemangiomas, and other benign and malignant brainstem processes, as well as in cerebrovascular accidents involving the brainstem. In the CPA, the nerve is subject to iatrogenic manipulation during the extirpation of vestibular schwannomas, meningiomas, and other CPA tumors. The intratemporal segment of the nerve (▶ Fig. 16.2) is vulnerable to crush or transection injury from temporal bone fractures; 50% of transverse temporal bone fractures result in facial paralysis, and 20% of longitudinal temporal bone fractures yield facial paralysis. Of these, all require steroid treatment, and unfavorable evoked elecromyography (EMG) studies (< 10% action potential amplitude of facial muscles compared to the normal side) 72 hours following injury may prompt surgical decompression when medically feasible. The geniculate ganglion region is the putative location of latent herpes simplex virus, which is responsible for Bell palsy. The geniculate region is susceptible to the development of both geniculate ganglion hemangiomas and facial nerve schwannomas, each ordinarily heralded by an atypical paralysis pattern (multiple episodes of Bell palsy–type symptoms on a single side or long-term flaccidity in the absence of a parotid malignancy). Although management of intratemporal tumors varies on a case-by-case basis, the general

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Fig. 16.1 Distribution of etiology of facial paralysis at the facial nerve center of one of the authors (TAH).

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Fig. 16.2 The course of the facial nerve through the temporal bone. Used with permission from Cheney M, Hadlock T. Facial Surgery, Plastic and Reconstructive. London: CRC Press; 2014.

parotid gland. Upon exiting the parotid gland, the facial nerve has 8 to 15 branches. Distally, there is massive arborization and interconnection of the branches, resulting in significant functional overlap; a single zygomaticobuccal branch may innervate the orbicularis oculi and the orbicularis oris. The three or four branches of the temporal division run obliquely along the undersurface of the temporoparietal fascia after crossing the zygomatic arch 3 to 5 cm from the lateral orbital margin. They are most susceptible to injury along the lateral border of the frontalis muscle, where there is little adipose tissue, and the nerves are virtually subcutaneous. These nerves innervate the frontalis and the upper orbicularis oculi muscles. The zygomaticobuccal division consists of five to eight branches with significant innervation overlap such that one or more branches may be divided without causing weakness. These nerves innervate the lip elevators and the lower orbicularis oculi muscles, as well as the orbicularis oris and buccinator. The branches to the zygomaticus major and minor musculature are crucial in microsurgical facial paralysis reconstruction. The mandibular division has one to three branches, whose course begins up to 2 cm posterior to the ramus of the mandible, crossing the mandible halfway between the angle and the symphysis. These branches lie on the deep surface of the platysma and cross superficial to the facial vessels ~ 3.5 cm from the edge of the parotid, innervating the depressor anguli oris, the depressor labii inferioris, the mentalis muscle, and sometimes the upper platysma and orbicularis oris. The cervical division has one branch that leaves the parotid below the angle of the mandible and runs on the deep surface of the platysma, entering it at the junction of the superior and middle thirds.

16.3.2 Facial Muscles consensus is that removal and cable grafting are warranted when a patient functions at a level equal or inferior to that which would be achievable through a nerve graft. Middle ear surgery places the intratemporal segment at risk, with the horizontal segment most vulnerable during stapes surgery and the vertical segment at risk during mastoid surgery. The extratemporal facial nerve (▶ Fig. 16.3) is subject to damage during penetrating facial injury or during parotid or temporomandibular joint surgery . Rarely, rhytidectomy can lead to neurapraxia (grade I injury) or higher grade nerve injuries, including segmental branch transection. Upon exiting the temporal bone at the stylomastoid foramen, the nerve passes between the superficial and deep lobes of the parotid gland. The nerve then divides into two main trunks, which further divide within the parotid gland to form divisions. Traditionally, it has been taught that this results in five divisions of the facial nerve: frontotemporal, zygomatic, buccal, marginal mandibular, and cervical. There are different branching patterns and frequent interconnections among branches.8 These interconnections result in redundant motor function. Some branches may be difficult to isolate, and the term zygomaticobuccal, for example, may be more appropriate. At their exit from the parotid gland, the facial nerve branches lie ~ 10 mm from the skin surface. They become progressively more superficial medially. The temporal branch may be only a few millimeters deep to the surface and 5 cm distal to the

The facial muscles can largely be thought of as either sphincter dilators or constrictors. They consist of 17 paired muscles and one unpaired muscle, the orbicularis oris. The functions of the frontalis, orbicularis oculi, zygomaticus major, levator labii superioris, orbicularis oris, and depressor labii inferioris are the most clinically significant. The frontalis muscle is a bilateral broad muscle 5 to 6 cm in width and 1 mm thick. It originates from the galea aponeurotica, inserting onto the superciliary ridge of the frontal bone and into fibers of the orbicularis oculi, procerus, and corrugator supercilii, as well as the overlying skin. It acts to dynamically elevate the brow and prevents brow ptosis with its resting tone. The orbicularis oculi muscle constricts the sphincter of the eyelids. It is a continuous sheet of muscle with pretarsal (covering the tarsus), preseptal (covering the septum), and orbital (covering the orbital margin) components. In the lower eyelid, the orbital portion overlies the origins of the zygomaticus major, levator labii superioris, levator labii superioris alaeque nasi, and part of the masseter. Multiple motor nerve branches enter the muscle just medial to its lateral edge. The zygomaticus major originates from the lower lateral portion of the body of the zygoma, with the orbicularis oculi and the zygomaticus minor covering the upper part. The zygomaticus major lies along a line from the helical root to the oral commissure, where it inserts into the modiolus (the point of insertion of the zygomaticus major and minor, orbicularis oris,

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Fig. 16.3 The facial nerve nucleus is located in the brainstem, travels through the cerebellopontine angle, then courses intratemporally before exiting at the stylomastoid foramen. Each of the extratemporal facial nerve branches provides specific movement. (Reprinted with permission from DNA Illustrations Inc., www.dnaillustrations.com.)

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buccinator, risorius, levator anguli oris, and depressor anguli oris). The nerve fibers enter the deep surface of the muscle (as is the case with all the muscles of facial expression except for the levator anguli oris, buccinator, and mentalis, which are innervated from their superficial surfaces). The lower lip depressors are the depressor labii inferioris and depressor anguli oris. The platysma, through its insertions into the other lower lip depressors and the modiolus, is also a lower lip depressor.

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16.4 Evaluation Evaluation of the patient with facial paralysis centers on establishing a diagnosis, assessing the protection of the cornea, and determining the remaining level of function of each branch of the facial nerve. A thorough history and physical examination are critical. Details of onset are important for diagnosis. Sudden onset paralysis suggests an infectious process, trauma, or cerebrovascular accident. If the paralysis is of gradual onset, then

Facial Nerve Injury Table 16.1 The House-Brackmann Facial Nerve Grading Scale

Table 16.2 The Yanagihara Scale

Grade Definition

Scale of five rating*

I

Normal symmetrical function in all areas

At rest

0

1

2

3

4

II

Slight weakness noticeable only on close inspection Complete eye closure with minimal effort Slight asymmetry of smile with maximal effort Synkinesis barely noticeable; contracture or spasm absent

Wrinkle forehead

0

1

2

3

4

Blink

0

1

2

3

4

Slight closure of eye

0

1

2

3

4

Tight closure of eye

0

1

2

3

4

Closure of eye on the involved side only

0

1

2

3

4

Wrinkle nose

0

1

2

3

4

Whistle

0

1

2

3

4

Grin

0

1

2

3

4

Depress lower lip

0

1

2

3

4

III

IV

Obvious weakness but not disfiguring May not be able to lift eyebrow Complete eye closure and strong but asymmetrical mouth movement with maximal effort Obvious but not disfiguring synkinesis, mass movement, or spasm Obvious disfiguring weakness Inability to lift brow Incomplete eye closure and asymmetry of mouth with maximal effort Severe synkinesis, mass movement, and spasm

V

Motion barely perceptible Incomplete eye closure, slight movement of corner of mouth Synkinesis, contracture, and spasm usually absent

VI

No movement, loss of tone; no synkinesis, contracture, or spasm

tumor must be suspected. For acute onset cases, a Lyme titer is drawn in endemic areas (eastern United States), and a thorough head and neck examination is performed. The status of the middle ear is evaluated for the presence of fluid, cholesteatoma, or canal processes such as vesicles, necrotizing otitis externa, or tumor. The tongue is examined for fissuring, and a detailed cranial nerve examination is performed. In relapsing cases or cases that do not follow a recognizable pattern of onset or recovery, radiographic imaging and additional hematologic studies for autoimmune phenomena and rare disorders are appropriate. For facial paralysis noted at birth, establishing an etiology, when possible, is extremely beneficial to treatment planning, because not all cases are developmental. Some are caused by injury to the facial nerve, either in utero or during delivery. Therefore, such cases should be judiciously observed over time for improvement. Early electrodiagnostic testing can sometimes help distinguish these conditions. If there is any improvement in function over time, the cause is likely not a developmental abnormality of the facial nerve or nucleus, but more likely of a traumatic nature. If the level of function does not improve, then the cause is likely a failure of formation of the facial nerve or nucleus. For acquired cases of facial weakness, aside from attempting to determine etiology, establishing the health of the cornea is imperative early in facial paralysis management. The presence or absence of Bell reflex should be noted. Bell reflex is present when the globe rotates cephalad on attempted eyelid closure, moistening and protecting the cornea. It is absent when the globe fails to rotate upward, thereby exposing the cornea to the air. In cases where the cornea is not protected, most patients can be acutely managed with eye drops (artificial tears), lubricating ointment, and/or nightly eye taping. Patients with congenital facial paralysis tolerate more corneal exposure than adults or patients with acquired facial paralysis, and they are less likely to require operative intervention for the eyelid in childhood.

* The scale consists of normal, slight paralysis, moderate paralysis, severe paralysis, and total paralysis, for which points 4, 3, 2, 1, and 0, respectively, are awarded. Source: From Berg T, Jonsson L, Engström M. Agreement between the Sunnybrook, House-Brackmann, and Yanagihara facial nerve grading systems in Bell’s palsy. Otol Neurotol 2004;25(6):1020–1026, with permission.

A special situation arises when the cornea is insensate, secondary to trigeminal nerve dysfunction. In these cases, the patient is unable to feel the cornea, predisposing it to additional injury. Corneal sensation can be assessed by using wisps of cotton obtained from a cotton-tipped applicator. The patient is instructed to look away from the examiner, and the cotton is touched to the sclera on the temporal side of the cornea. A fluorescein slit lamp examination by an ophthalmologist can detect corneal ulceration; patients with insensate corneas require formal ophthalmologic evaluation. More aggressive management with eyelid weighting and/or tarsorrhaphy may be indicated. Reconstruction of corneal sensation has been previously described, 9 but with limited clinical experience. The function of the branches of the facial nerve is determined by asking the patient to perform a series of movements. The patient is asked to maximally elevate the brows, forcefully close the eyelids, close the eyelids as with sleeping, produce a maximal smile, produce his or her “best” smile, grimace (as in showing the teeth), and puff out the cheeks or pucker, and still photographs of each of these expressions is documented, along with the face in repose. A video record documents the degree of movement and helps determine the effectiveness of various dynamic interventions. Various subjective grading systems have been proposed to document function. The most widely used is the House-Brackmann scale,10 which became the standard scale under the Facial Nerve Disorders Committee of the American Academy of Otolaryngology–Head and Neck Surgery (▶ Table 16.1), and has been recently revised to account for synkinetic movement.11 The House–Brackmann scale, expressed as a score of I to VI, is easy and rapid to apply, but it does not differentiate among the branches of the facial nerve. It is primarily useful in following recovery among patients following acoustic neuroma surgery or other conditions in which all of the branches of the facial nerve are affected. It is not useful in cases of isolated branch paralysis or cases of congenital paralysis.

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Fig. 16.4 The Sunnybrook Facial Grading System. (Courtesy of Sunnybrook Health Science Centre, Toronto, Ontario, Canada.)

Other scales have been proposed that evaluate facial nerve function in a similar overall manner.12,13 The Sunnybrook system14 was developed to provide the clinician with a means of documenting individual regional functions of the facial nerve during recovery (▶ Fig. 16.4). The resulting composite score, out of a possible 100, takes into account resting symmetry, voluntary excursion, and synkinesis. The Yanagihara system (Table 16.2) is used widely in Japan.15,16 It uses 10 different movements, where each movement is assigned a score of 0 to 4; the maximum score is 40. Synkinesis is not accounted for in this scale. Comparisons of these and other popular grading scales have determined that, although the systems are not interchangeable, they are somewhat congruent in their assessment of individual patients. 12,16,17 Facial motion has been assessed directly using a number of tools, including simple measurement of muscle excursion with a handheld ruler 18,19 and video-based motion capture systems.20–26 The Massachusettes Eye and Ear Infirmary has developed user-friendly software that uses iris diameter as a scale of reference to determine measurements of facial features on still

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digital photographs.27–29 Some have incorporated video in a postoperative rehabilitation program.30,31 The most critical aspect in assessment of the patient with facial paralysis is orderly recording of facial function by zone. One author (TAH) finds that a worksheet assists in rigorous zonal assessment (▶ Fig. 16.5). The brow is assessed for symmetry and excursion. The eyelids are assessed for closure and laxity. The nasal base is assessed for nasal valve collapse, the nasolabial fold examined as to its effacement or hyperprominence, and the oral commissure is assessed for symmetry and excursion with smiling, with attention to both retraction and elevation of the oral commissure and lower lip depressor function. These movements are also each assessed for their involuntary presence during attempts at other facial zone movements. In addition, speech is assessed for difficulty pronouncing bilabial consonants, such as b and p.

16.5 Management The approach to management of patients with facial paralysis depends on several factors, including the duration of paralysis,

Facial Nerve Injury

Fig. 16.5 Worksheet for use in zonal assessment of resting and dynamic function in facial paralysis.

age of the patient, branches involved, and level of motivation for surgery. Several authors have proposed algorithmic approaches to the surgical management of this condition.32–39 Whenever possible, the native muscles should be reinnervated, as they are the most capable of producing the wide array of movements normally present with intact facial expression. If the proximal facial nerve stump is available, most surgeons would favor primary repair or cable grafting to reestablish continuity between the facial motor nucleus and the facial musculature. With acute facial nerve transections, the repair should be done as soon as possible. If the repair is done within the first 72 hours of injury, then stimulation of the distal stumps is possible.40 Stimulation greatly facilitates identification of important branches. If a minimal tension repair is not possible, then an autologous nerve graft should be performed. Either sural or great auricular nerve grafts are typically used. When the proximal facial nerve stump is not available, such as following extensive skull base surgery with facial nerve sacrifice at the brainstem, then an alternative neural source can be used to connect to the distal facial nerve stump to reach the facial musculature. This procedure, termed reinnervation, employs the contralateral facial nerve (cross-facial nerve grafting), the ipsilateral masseteric branch of the trigeminal nerve, the ipsilateral hypoglossal nerve, or the partial spinal accessory nerve. Cross-facial nerve grafting, described by Scaramella and Tobias41 in 1973 and by Smith42 independently in 1972, possesses the major advantage that the return of function is spontaneous and can produce true emotion-based expression, whereas the other neural sources all require physical therapy and neuromuscular retraining.

16.5.1 Technique Cross-facial nerve grafting is performed under general anesthesia (▶ Fig. 16.6). A preauricular incision is marked, and the subcutaneous tissues may be infiltrated with epinephrine. Dissection is carried out at the level of the superficial muscular aponeurotic system (SMAS), superficial to the parotidomasseteric fascia. Parallel to the level of the lateral canthus, the facial nerve branches emerge from the parotid gland. At this level, fine scissors dissection is employed. Multiple branches of the facial nerve are seen emanating from the parotid, and these are mapped with a bipolar nerve stimulator to determine their function. Usually there is significant crossover between branches, such that transecting one or two branches will not result in weakening the nonparalyzed side. The surgeon must ensure that a branch remains to power each movement on the nonparalyzed side. While detectable temporary donor site motor deficits have been reported,43 in one author’s experience (TAH) of 55 cases, only a single case revealed minor changes in smile vector on the healthy side. It is best to be selective, such that a branch intended to power lip elevation comes from a pure lip elevator on the nonparalyzed side. Similarly, if the surgeon wishes to power eyelid closure, it is best to select a pure eye closure branch. Once the branches are selected, the nerve graft (usually the reversed sural nerve) is tunneled to reach the contralateral preauricular region. Harvest of the sural nerve usually produces low morbidity, but the patient should expect decreased sensation over the dorsolateral foot. In a study by Meek et al, 20 to 30% of patients experienced a mild level of pain even years after

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Facial Nerve Injury harvest (neuromatous pain).44,45 Coaptations are performed under the operating microscope with 9–0 or 10–0 nylon sutures, under no tension. Clinically apparent movement results after sufficient regeneration occurs along the nerve graft (~ 1 mm/d) to reach the target, usually ~ 6 months. An advancing Tinel sign indicates that regeneration is progressing. Outcomes for cross-facial nerve grafting vary. Smith reported a series of three patients in whom a sural nerve graft was coapted between donor buccal and zygomatic branches to affected branches on the paralyzed side using a two-stage technique.42 Improved symmetry was obtained. Scaramella published a long-term series of 11 patients who underwent single-stage cross-facial nerve grafting and reported that 5 had good tone, and 3 had fair tone; he considered 2 of the cases failures.46 Anderl reported a series of 15 patients who underwent crossfacial nerve grafting using four grafts per patient to reanimate individual regions and concluded that the “result was satisfying (> 50%) where the preoperative conditions were favorable.”47 He stressed the importance of timing, with earlier reinnervation yielding better outcomes. Baker and Conley used the lower division of the facial nerve for the donor, which was coapted to a sural nerve graft and then the entire cross-sectional area of the recipient facial nerve.48 They reported on a series of 10 patients, 6 of whom experienced “fair” improvement, and the remainder gaining no improvement. Galli et al reported on a series of five patients who underwent mapping and cross-facial nerve grafting with “successful” results.49 When the reconstruction is done early, results tend to be better.50 Terzis and Konofaos recommended doing the procedure before 6 months’ denervation time had elapsed.37 A study of 72 patients who underwent primary cross-facial nerve grafting showed that results were good or excellent in 73% (JK Terzis, unpublished data). In either reinnervation or grafting, controversy exists as to how long the facial musculature remains receptive to reinnervation before it becomes end stage (irretrievable atrophy and fibrosis).3,6,51–53 Terzis and Konofaos proposed a timeframe of 6 months’ denervation, after which a nerve-based reconstruction would be unlikely to succeed. They noted, however, that in certain situations they violated their own guideline and obtained good results with cross-facial nerve grafts performed after 6 months of denervation.37

16.5.2 Regional Considerations The Brow The paralyzed brow and upper face require treatment to achieve the best overall symmetry and function. It is difficult to achieve dynamic reconstruction of the brow, except in cleanly transected frontal branch paralysis, in which early exploration and repair yield dynamic function. Frequently, surgeons employ static procedures to reposition the brow and restore peripheral vision. The direct brow lift is a simple method of improving symmetry between the paralyzed and nonparalyzed brows and results in reliably good patient satisfaction.54–56 It is straightforward and can be performed under local anesthesia.55 The skin cephalad to the brow is marked for excision by manually simulating the lift with the patient seated upright. The marking is made in the form of an ellipse. The height of the ellipse is determined by the amount required to lift the brow to

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its desired position. The inferior incision lies just cephalad to the brow. The neurovascular bundles are marked, and an incision is made down to the subcutaneous fat, preserving the neurovascular bundles. Laterally, the dissection may be made just superficial to the frontalis muscle. Following excision, the wounds are closed. Outcome studies using this technique show that the procedure is reliable, safe, and produces favorable satisfaction levels. Among 54 patients with an average follow-up of 11 months, 52 rated their satisfaction as good or high; 3 brows had persistent hypesthesia or paresthesia, and 22 had at least transient sensory changes.55 In a study by Ueda et al, the technique was able to alleviate obstruction of visual fields in 85%. 9 Although direct brow lifting is straightforward, it has been largely replaced by techniques that avoid visible scarring. Endoscopic brow lifting has been used increasingly over the past decade, gaining popularity because it avoids the long scars previously required by direct techniques. It has been used in facial paralysis for correction of brow asymmetry. The technique is similar to that used for cosmetic endoscopic brow lifting.57–62 Briefly, with the patient seated upright, the difference between sides is measured, and markings are made. A line is drawn from the midpupillary line vertically. The paramedian access incision is centered on this line behind the hairline. The region of greatest elevation is generally at the junction of the middle and lateral one-third of the brow in women and flatter in men. Another incision is planned posterior to the hairline to assist with access for instruments. The temporal incision is marked posterior to the hairline, centered over a line extending from the lateral nasal ala through the lateral canthus. The brow and adjacent tissues are subperiosteally infiltrated with local anesthetic containing epinephrine (in an adult, e.g. 60 mL bupivicaine 0.125% with epinephrine 1:400,000). The paramedian incisions are carried subperiosteally, and elevators are used to elevate posterior and anterior to nearly the supraorbital rim. The 30-degree endoscope is then introduced, and the supraorbital and supratrochlear bundles are identified and protected. The dissection proceeds into the temporal pocket, which is developed superficial to the deep temporal fascia (i.e., superficial to the investing fascia of the temporalis muscle; if there is doubt as to the level, an incision can be made in the deep temporal fascia to verify the level by visualizing the temporalis muscle directly underneath). The pockets are connected, and then the suspension is performed either with sutures in a bone tunnel, screw and staple fixation, or using the Endotine (Coapt Systems Inc., Palo Alto, CA), such that the brow is slightly overcorrected in position compared to the contralateral brow. We have used a 3.5-mm Endotine, combined with a 2–0 PDS (polydioxanone) suture from the superficial temporal fascia anteriorly to the deep temporal fascia posteriorly through the temporal incision. Outcome studies of endoscopic brow lifting show that the procedure can be durable and provide safe, reliable results with high patient satisfaction. In one study, 31 adult patients with acquired unilateral facial paralysis underwent endoscopic brow lifting. The average difference in preoperative brow height was 6 mm, and the postoperative difference at 1 year was 1.3 mm. No complications were noted, although one patient required a revision using a direct brow lift. Kinzel et al found a high level of patient satisfaction among patients undergoing endoscopic brow lift for cosmetic indications. 60

Facial Nerve Injury

Fig. 16.6 Early reconstructions of unilateral facial paralysis may utilize a specific branch or branches of the facial nerve from the unaffected side of the face to reconstruct specific movements. Care is taken to ensure donor redundancy and functional specificity. Nerve grafts, usually from the sural nerve, are coapted between the functional donor nerve branch and the affected facial nerve target branch. (Reprinted with permission from DNA Illustrations Inc., www.dnaillustrations.com.)

16 In a series by Rautio and Pignatti, 12 patients underwent endoscopic brow lift for facial paralysis. They noted adequate correction in 10 of 12 patients. 61

Upper Eyelid Paralysis in the upper eyelid is caused by the inability of the orbicularis oculi muscle to constrict the sphincter of the palpebral

fissure. In most patients with facial paralysis, the oculomotor and trigeminal nerves are intact. For these patients, corneal exposure is sometimes controllable with eye drops during the day (e.g., 0.5% or 1.0% methylcellulose) and lubricating ointment at night. If the trigeminal nerve is not intact, then sensation to the cornea is impaired, and the risk of developing a corneal ulcer becomes significant. Terzis et al proposed innervating the corneas of such patients with a transfer of the contralateral

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Facial Nerve Injury supraorbital and supratrochlear nerves to the ipsilateral insensate cornea.63 The procedure was able to restore protective sensation to the cornea, improving visual acuity and decreasing recurrence of corneal ulceration. When patients lack orbicularis oculi function or have an unsatisfactory Bell reflex, and/or the cornea is insensate, they benefit from surgical management of the upper lid. Either static or dynamic procedures can be performed for upper lid paralysis. Use of gold weights for upper lid loading has been popular for years, as it is relatively easy to perform and generally produces reliable, safe results.64 Newer platinum chain implants (Spiggle & Theis GmbH, Dieburg, Germany) have become available that offer certain advantages over gold weights.64 Although gold weights are only available in rigid single-component implants, multilink platinum chain implants are able to effectively change their radius to better fit the contour of the globe with upper eyelid excursion. Platinum also has a greater density than gold (21.5 g/cm3 vs. 19.4 g/cm3), allowing the implants to be of smaller volume and therefore less prominent. A recent report of 105 cases of thin-profile platinum eyelid weights revealed lower complication rates and superior aesthetic results compared with gold.65 Regardless of the type of implant, weights may be implanted through an incision in the supratarsal crease or through an incision 2 mm cephalad to the ciliary margin. The amount of weight is selected preoperatively by testing the weight on the patient’s eyelid using a temporary adhesive. The weight should be centered on the point of maximal lagophthalmos. Dissection is carried through the orbicularis oculi muscle to the level of the tarsal plate. The weight is then secured to the tarsus, and the skin and muscle are closed over the weight.66 Reported complications of lid loading include implant migration (8–10%), extrusion (3–7%), wound infection (7–10%), excessive ptosis (15–25%), residual lagophthalmos (8–15%), and astigmatism (7–24%).64,67,68 In a meta-analysis of 38 publications on 1,000 cases, Schrom et al found that complete lid closure can be obtained in 84.5% with rigid gold implants. Postoperative complication rates were 13.4% for prominence or bulging of the implant, 6.4% for migration, 6.8% for extrusion, 11.5% for corneal astigmatism, and 7.0% for postoperative infections. 69 Following static periocular treatment for paralytic lagophthalmos, patients report improved periocular comfort and quality of life.70

severe cases, or a staged approach can be used, such that the upper lid is managed first and the lower lid second when indicated. A tarsal strip procedure is often sufficient to correct paralytic ectropion. A lateral canthotomy is performed, and the lower lid is measured for skin resection by pulling it superolaterally, thus overlapping the lateral canthal tendon. The extra skin, muscle, and conjunctiva are removed, leaving a strip of tarsal plate. A double-armed permanent or absorbable suture (e.g., 4–0 or 5–0 PDS) is placed in the Whitnall tubercle, inside the orbit through the periosteum. The tarsal strip is then secured with a horizontal mattress suture. The muscle is repaired, and the skin is closed with fast-absorbing gut sutures. The lateral canthus should be closed so that the angle is sharp, not rounded (▶ Fig. 16.7).

Nasal Valve Many patients with flaccid facial paralysis suffer with ipsilateral nasal valve collapse, which can be corrected using a simple fascia lata sling technique (▶ Fig. 16.8). The maneuver, which can be performed alone or in combination with static or dynamic smile reanimation procedures, contributes significantly to relieving nasal obstruction in this population.71

The Nasolabial Fold The nasolabial fold is frequently malpositioned as a result of facial paralysis and can be effaced or hyperprominent, depending

Lower Eyelid The primary stabilizers of the lower lid are the tarsal plate and the medial and lateral canthal tendons. The capsulopalpebral fascia is analogous to the levator muscle of the upper eyelid. The orbicularis oculi muscle, when paralyzed, results in decreased support of the lower lid, leading to paralytic ectropion. In older patients, involutional ectropion may also be present, exacerbating the degree of ectropion. The snap test may be used to assess the degree of lid laxity: if the lower lid, when pulled away from the globe, is able to “snap” back into position without blinking, then the snap test is considered normal. Paralytic ectropion should be addressed surgically when upper lid procedures alone are insufficient to correct corneal exposure and when the lacrimal punctum sits too far from the surface of the globe to collect tears effectively. Lower lid operations can be done at the same time as upper lid operations in

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Fig. 16.7 Pre- (a) and postoperative (b) views of a patient experiencing severe lower lid malposition from a left facial schwannoma, corrected with a tarsal strip technique. Used with permission from Lindsay R, Smitson C, Edwards C, Cheney M, Hadlock T. Correction of the Nasal Base in the Flaccidly Paralyzed Face: An Orphaned Problem in Facial Paralysis. Plast Reconstr Surg. 2010 Oct;126(4):185e-186e.

Facial Nerve Injury

Fig. 16.8 Nasal valve correction. Left: Surgical steps in passing fascia lata from the temporal area to the nasal ala. Right: Pre- and postoperative basal views of the nose. Used with permission from Lindsay R, Smitson C, Edwards C, Cheney M, Hadlock T. Correction of the Nasal Base in the Flaccidly Paralyzed Face: An Orphaned Problem in Facial Paralysis. Plast Reconstr Surg. 2010 Oct;126(4):185e-186e.

on the nature of the paralysis. Adjustments to this zone are designed to improve facial symmetry and involve either a two-stitch nasolabial fold modification (▶ Fig. 16.9)33 or simple cosmetic filler therapy for improved balance.

Oral Commissure and Smile Reconstruction of the midface can be accomplished using static techniques, regional muscle, or free muscle. The surgeon and patient choose a method based on motivation, expectations, prognosis, and physiologic age. Free muscle transfer is the most complex of these approaches, but it also offers the most natural smile when successful. Preoperative evaluation for free gracilis transfer includes a complete assessment of the vessels and nerves to determine which are available for use. The recipient vessels are assessed by palpation. Usually the facial vessels are the preferred recipient site, and these are readily palpable or able to be detected with a handheld Doppler ultrasound probe. If the facial vessels are not available, the superficial temporal artery and vein may be used. In rare clinical circumstances, the ipsilateral facial nerve can be used to power a free muscle, though more commonly, a cross-facial nerve graft is used, employing techniques described earlier in this chapter. Briefly, in a cross-facial nerve graft procedure, the sural nerve is harvested from the leg using multiple small incisions or endoscopically.72,73 A contralateral branch of the facial nerve supplying the lip elevators is selected with the assistance of a bipolar nerve stimulator. After

determining redundancy, that branch is transected and prepared for coaptation to the sural nerve graft. The graft is tunneled from the paralyzed side to the nonparalyzed side using a hemostat or other passer, through an upper buccal sulcus incision. Coaptation between the graft and the functioning facial nerve branch is completed, then the distal end of the nerve graft is marked and/or secured to the maxillary periosteum at the level of the canine root using a nonabsorbable suture to facilitate locating the nerve graft during the second stage. After a cross-facial nerve graft, 6 to 9 months are needed for the axons to regenerate through the graft. A Tinel sign can be followed to guide the timing of the second stage. For the muscle transfer, the operation begins as follows: Markings are made preoperatively that mirror the nasolabial crease on the nonparalyzed side. Once anesthesia is induced, the thigh and face are prepped and draped. A small shoulder roll facilitates access. Slight reverse Trendelenburg positioning and rolling the table away from the surgeon are helpful. Plain epinephrine (10 mL, 1:400,000) is infiltrated subcutaneously prior to the incision. A preauricular incision is made, extending from within the temporal hair, above the helical root, onto or in front of the tragus. The incision extends behind the ear and then under the angle of the jaw anteriorly (▶ Fig. 16.10). The scalpel is used for the first part of the dissection, switching to low-current electrocautery once a subcutaneous plane has been established. Fine tenotomy scissors are used to dissect the facial vein, located near the anterior border of the masseter, and the facial artery is located medial to the vein. The facial vein

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Facial Nerve Injury

Fig. 16.10 Preauricular incision used for either cross-facial nerve grafting or gracilis muscle transfer.

Fig. 16.9 Nasolabial fold modifications. (a) Introducing a nasolabial fold. Note suture placement medial to the desired location of the neonasolabial fold. (b) Effacing the hyperprominent nasolabial fold. Note suture placement lateral to the hyperprominent fold, similar to aesthetic facelifting techniques. Used with permission from Hadlock TA, Greenfield LJ, Wernick-Robinson M, Cheney ML. Multimodality approach to management of the paralyzed face. Laryngoscope. August 2006;116:1387.

usually bifurcates in the midface, and this is usually a convenient level at which to ligate the facial artery and vein. The vessels are then turned down toward the incision in preparation to receive the muscle transfer. Correct positioning of muscle inset sutures is critical at the oral commissure. These sutures (usually 1–0 to #1 Vicryl) are placed in the native musculature or residual fascia at the level of the previous location of the facial artery. The pull of the sutures is tested intraoperatively to ensure adequate excursion and symmetry (▶ Fig. 16.11). Usually three to five such anchoring sutures are used. In the case of a previous cross-facial nerve graft, the distal stump of the donor nerve is accessed through the upper buccal sulcus incision. If the masseteric branch of the trigeminal nerve is to be used, an incision is made using the electrocautery 1 cm inferior to the zygomatic arch and 3 cm anterior to the tragus. 74 Fine tenotomy scissors are used to dissect through the masseter

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muscle, and a handheld nerve stimulator is helpful in locating the obliquely coursing nerve. The nerve runs along the deep surface of the masseter, from the posterosuperior to the anteroinferior muscle borders.75,76 The nerve is dissected proximally and distally. The nerve is transected at the point where it begins to branch distally (▶ Fig. 16.12). The gracilis muscle is harvested through an upper thigh incision (▶ Fig. 16.13). The vascular pedicle is isolated, protected, and dissected proximally to the level of the profunda femoris. The gracilis branch of the obturator nerve is identified entering the muscle ~ 1 cm proximal to the vascular pedicle. The nerve is dissected into the pelvis, with the help of lighted retractors. The muscle is split longitudinally to reduce its bulk (▶ Fig. 16.14). Approximately 50% of the cross-sectional area of the muscle can be removed from the region away from the neurovascular pedicle, and the range of transferred muscle is ordinarily 10 to 40 g (▶ Fig. 16.15). The nerve may be stimulated with a nerve stimulator to ensure that the muscle contracts following debulking. A measurement from the helical root to the oral commissure is taken. An additional centimeter is added to either side of the muscle to account for length lost with suturing. Prior to division of the vascular pedicle of the gracilis muscle, horizontal mattress 3–0 Vicryl sutures are passed though the proximal and distal ends of the muscle to reinforce the security of the anchoring sutures. The muscle is brought to the face after ligating the vessels, and the insetting sutures are secured by passing through the muscle behind the row of mattress sutures, such that the anchoring sutures are secured with two of the mattress sutures. After medial muscle inset, the artery and vein are repaired with interrupted 9–0 or 10–0 nylon sutures, or a venous coupling device. The nerve coaptation is then executed in tensionless fashion. The temporal muscle insertion is carried out, securing the temporal end of the muscle to the deep temporal fascia. A small Penrose drain is left below the earlobe. The wound is gently irrigated, then closed in layers. A custom thermoplastic splint is employed by one author (GHB), where it is sutured to the scalp and placed in the mouth to protect the muscle anchor suture line. The patient is maintained with the head elevated, and a soft diet is maintained for 2 weeks. Contractile function in the

Facial Nerve Injury

Fig. 16.11 Anchoring sutures have been placed into the region of the oral commissure. The pull is tested intraoperatively to ensure adequate excursion and symmetry.

free muscle may be observed as early as 6 weeks in cases of transfer of the motor nerve to the masseter and within 6 to 12 months when using a cross-facial nerve graft. A course of neuromuscular rehabilitation is very helpful to maximize the excursion of the muscle transfer (▶ Fig. 16.16), although most of the rehabilitation can be performed in a home program. Outcome studies of free muscle transfer generally suffer from both low numbers and nonstandardized outcome measures. In 2009 Terzis and Olivares reported a series of adult patients in which free muscle transfer was used.77 The authors analyzed a series of 24 patients who underwent staged reconstruction with a cross-facial nerve graft followed by gracilis muscle transfer. Follow-up was a minimum of 5 years. They found that the muscle continued to gain excursion even after 2 years. There was no evidence of a decrease in function, either clinically or by EMG, after 2 years. Examining pediatric outcomes from the same procedure, the same authors concluded that long-term outcomes in children improved beyond 2 years, without detrimental effects on the growing craniofacial skeleton.78 The

failure rate for free functional muscle transfer to the face is variable but is reported from 9 to 21% for adults and children.79-81 Overall results are considered excellent or good in ~ 50% of patients.80 Bhama and colleagues recently presented outcomes in a series of 154 gracilis free tissue transfers (GFTT) over a 10-year period at a single institution. They reported an overall failure rate of 9%, with a decreased failure rate in flaps innervated by the masseteric branch of the trigeminal nerve. In all comers, smile excursion and symmetry with smile improved following GFTT. Patients with flaps innervated by the masseteric branch of the trigeminal nerve experienced significantly greater postoperative excursion when compared with flaps innervated by a cross-face nerve graft.82 In a separate publication, the authors highlight the complexity of clinical outcomes research in patients with facial nerve injuries. They also cite the need for continued vigilance in recording preoperative, intraoperative, and postoperative data when treating patients with facial nerve disorders.83

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Fig. 16.12 The masseteric branch of the trigeminal nerve is dissected. This nerve can usually be located 3 cm medial to the tragus and 1 cm inferior to the zygomatic arch. A dissection through the majority of the thickness of the masseter muscle is necessary to locate the nerve.

Additional procedures are occasionally needed following free muscle transfer or nerve transfer to further refine the result. Terzis and Olivares in 2009 analyzed outcomes from 31 patients who underwent secondary procedures following free muscle transfer, and found that a partial temporalis muscle transfer was frequently needed as an adjunctive procedure following cross-facial nerve graft or other nerve transfer, such as partial hypoglossal-to-facial nerve transfer.81 Free muscles innervated by the masseteric branch have greater excursion than those innervated by a cross-facial nerve graft.19,84,85 The rehabilitation of masseteric branch–innervated muscle transplants is slightly more involved than when a crossfacial nerve graft is used. Nevertheless, 66 to 82% of patients achieve the ability to smile without active biting. 85–87 Therapy is coordinated by the occupational, physical, or speech therapist and is directed toward achieving maximal voluntary excursion, as well as overall balance and symmetry. Complications include infection and nonfunction or weak function of the free muscle transfer. In cases of weak or insufficient excursion of the muscle, further procedures may be indicated. If the muscle has strong contractile function but has pulled away from the insertion, it can potentially be reinserted by reopening the preauric-

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ular incision, dissecting the distal insertion and then reinserting it into the commissure, although this is somewhat risky and may jeopardize the function of the free muscle. If the muscle is weak, but the insertion is correctly positioned, the muscle can be plicated to gain additional power, or a temporalis (or partial temporalis) muscle flap can be placed to augment the contractile function of the muscle.

Lower Lip Paralysis of the marginal mandibular branch of the facial nerve can be effectively treated by weakening the contralateral side.88 The treatment is as effective for isolated lower lip weakness as for establishing lower lip balance after successful smile reanimation. An algorithm for lower lip management has been proposed (▶ Fig. 16.17),89 in which successively longer periods of contralateral lower lip weakening are employed, beginning with a simple local anesthetic injection and progressing to permanent resection of the depressor labii inferioris if the patient likes the effect and oral competence is not jeopardized. When using botulinum toxin, though the effect is usually quite satisfactory (▶ Fig. 16.18), the weakening will resolve with

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Fig. 16.13 The gracilis muscle is harvested through an incision in the upper thigh.

Fig. 16.14 The gracilis muscle has been split longitudinally to reduce its crosssectional area and minimize bulk. Contractility of the muscle with nerve stimulation is verified after muscle dissection.

time (usually ~ 3 to 6 months), and the injection must be repeated. Some surgeons favor dynamic techniques for the lower lip,90 although these are not widely employed, based on the simplicity of the former approach.

16.6 Rehabilitation Facial asymmetry resulting from injury to the facial nerve may have profound social and psychological consequences.91,92 An injury that causes a disruption to facial nerve function will

result in muscle degeneration and loss of facial movement. However, cortical changes will also occur with the loss of motor function. With muscle reinnervation, motor function will return; however, the preinjury motor cortex may not remap in the same pattern following injury.93–95 Neuromuscular reeducation will assist in optimizing muscle strength, facial symmetry, and cortical mapping. Rehabilitation programs that include only passive modalities such as electrical muscle stimulation will not promote motor reeducation. Exercise programs that include only mass facial movements will not recruit and strengthen weaker muscles and will not minimize synkinetic movements.

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16 Fig. 16.15 Transfer of only a segment of the gracilis muscle to the face reduces bulk. The gracilis is harvested with its neurovascular pedicle, and continued contractile function is confirmed with a nerve stimulator after dissection before transfer to the face. (Reprinted with permission from DNA Illustrations Inc., www.dnaillustrations.com.)

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Fig. 16.16 A 6-year-old girl presented with congenital facial paralysis. She underwent single-stage transfer of the gracilis muscle innervated by the masseteric branch of the trigeminal nerve. Strong reinnervation was present at 6 weeks following surgery. She was able to fine-tune her symmetry using a home-based program of neuromuscular rehabilitation. (a) Preoperative photograph. (b) Six-week postoperative photograph. (c) Three-month postoperative photograph. This patient was able to transition from requiring a conscious biting effort to spontaneous emotional control of the muscle: at 6 weeks, she needed to consciously bite down to activate the muscle. At 3 months, she was able to activate the muscle without voluntary effort.

Successful rehabilitation to facilitate facial symmetry must include selective muscle control with appropriate cortical input to permit recruitment of target muscles.91,96–106 Rehabilitation techniques are effective and continue to benefit patients even up to 3 years after facial nerve injury.107–109

Nonoperative treatment is often recommended following facial nerve injury, and many rehabilitation treatments, including exercise, electrical muscle stimulation, biofeedback, and motor reeducation, have been described for these patients.96–98,101–104, 106,110,111 Typically, following injury to the facial nerve, patients present with no movement of the facial muscles even with maximal effort, resulting in eating, drinking, and speaking difficulties. Although complete recovery following Bell palsy has been reported in 70 to 96% of patients, those with incomplete recovery present with a broad range of facial paresis and/or synkinesis.112,113 The resultant facial asymmetry is a result of ongoing weakness as well as synkinesis. Synkinetic motion, defined as an unintended movement that accompanies a volitional facial movement, may preclude the recruitment of a specific muscle or movement. If this aberrant movement is antagonistic to the intended motion, then decreased excursion may result. Synkinesis often includes eye narrowing or eye closure with movement of the mouth; for example, aberrant movement in the orbicularis oculi will occur with recruitment of the orbicularis oris or risorius muscles. These aberrant synkinetic movements will contribute to facial asymmetry. Patients that present with a flaccid facial paralysis require education for eye care to prevent injury to the cornea. Nonoperative therapy is of limited value in patients with no evidence of recovery. Patients are often referred for electrical muscle stimulation, although the therapeutic value of this treatment has yet to be established.114 With denervated muscle, direct current or galvanic stimulation is required to produce a muscle contraction.114,115 Those who advocate the use of direct current electrical stimulation do so with the intent that it will minimize muscle atrophy prior to muscle reinnervation. However, there is no empirical evidence or randomized controlled trials to support the efficacy of electrical muscle stimulation with external electrodes to prevent muscle degeneration. Once the muscle has been reinnervated, it is theoretically possible to use an alternating current to produce a muscle contraction. However, in patients with synkinesis, electrical stimulation can produce mass facial movements and induce more synkinesis but will not assist in decreasing the aberrant movement. In one author’s experience (CBN), patients with synkinesis do not benefit from electrical muscle stimulation and may in fact develop more synkinesis than those not receiving such stimulation. Treatment strategies that use neuromuscular retraining and promote selective motor control and facial symmetry appear more efficacious. Exercises that emphasize mass facial movement and/or maximal muscle contraction have only limited value in patients with facial nerve palsy. Patients with low facial tone or flaccid facial muscles may be instructed in general exercises with an emphasis on maximal contraction and movement. This will encourage movement as the facial muscles begin to reinnervate. Once there is evidence of muscle reinnervation, however, patients should not continue with exercises of mass movement but rather should be instructed in exercises that emphasize motor control and facial symmetry. Exercises that encourage mass movements and maximal effort will increase synkinetic motions and thus increase the appearance of facial asymmetry. With evidence of facial muscle reinnervation as determined by clinical evaluation (visual or biofeedback) or EMG, neuromuscular retraining should be instituted to increase motor control and selective muscle contraction.

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Fig. 16.17 Algorithm for management of lower lip asymmetry. Used with permission from Lindsay R, Smitson C, Cheney M, Hadlock T. A Systematic Algorithm for the Management of Lower Lip Asymmetry, Am J Otolaryngol. 2011 Jan-Feb;32(1):1-7.

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Facial muscles may demonstrate true muscle weakness, or they may simply appear weak due to restricted excursion from synkinesis of an antagonistic muscle. Exercises that encourage mass facial movements and general electrical muscle stimulation will result in mass action of the facial muscles, and in many patients this will increase synkinesis. These exercises and modalities will not promote selective muscle recruitment or

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decrease synkinesis and will result in a less than optimal outcome.

16.6.1 Neuromuscular Reeducation Neuromuscular reeducation involves selective muscle recruitment to increase muscle excursion and strength and to de-

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Fig. 16.18 Examples of contralateral lower lip weakening (a–d). Both patients demonstrate left lower lip weakness, and both were treated with 5 IU botulinum toxin to the right depressor labii inferioris. Used with permission from Lindsay R, Smitson C, Cheney M, Hadlock T. A Systematic Algorithm for the Management of Lower Lip Asymmetry, Am J Otolaryngol. 2011 Jan-Feb;32(1):1-7.

crease synkinesis. Muscle reeducation using a program of specific home exercises and surface EMG biofeedback has been shown to be efficacious in the treatment of patients following facial nerve injury.91,96,100–106,116 Ross et al conducted a prospective randomized controlled trial to evaluate the efficacy of feedback training in patients with facial nerve paresis.103 Patients (n = 25) who had a long-standing facial nerve paresis were randomized to exercises using a mirror or EMG biofeedback and exercises with a mirror. The duration of treatment was 1 year. There were seven patients who lived a far distance from the treatment facility; these patients served as control subjects. Following 1 year of treatment, there were statistically significant improvements in the facial movement symmetry in the patients who had mirror exercises and mirror exercises with EMG biofeedback as compared to controls. Similarly, Nakamura et al conducted a randomized controlled trial that included 27 patients with complete facial palsy.102 The patients in the treatment group received retraining exercises to reduce synkinetic eye closure with mouth movements. The authors reported a significant decrease in synkinetic eye closure after 10 months of retraining. Cronin and Steenerson conducted a retrospective chart review of 24 patients with facial palsy who were treated with neuromuscular retraining and found improvement in facial movement with neuromuscular facial retraining.101 These studies provide evidence to support neuromuscular retraining with a home exercise program as an efficacious treatment for patients following facial nerve injury, including patients with long-standing paresis.

16.6.2 Patient Treatment Upon initial presentation, patients should be instructed in eye care and protection. In patients with low facial tone, the initial exercises may be directed toward mass facial movements; these

exercises may include maximal effort facial movements and cocontractions of the entire face. However, it is important to follow these patients closely, and when there is evidence of early muscle reinnervation with synkinesis, mass facial movements should be discontinued. Exercise programs that continue with this strategy may reinforce an abnormal movement pattern and tend to increase the degree of synkinesis, muscle tone, and facial asymmetry. Neuromuscular retraining is necessary to increase selective voluntary muscle movement and thus decrease the aberrant movement associated with synkinesis. Patients with facial nerve paresis are often concerned about their uneven smile or the eye closure that occurs with mouth movements and/or chewing; therefore, their goals for therapy are to improve an uneven smile or to decrease the degree of eye closure. These are difficult goals and can only be achieved with control of the synkinesis. The initial treatment must be directed toward the decrease of the synkinesis and resting muscle tone. An understanding of the basic anatomy, physiology, and nerve injury and recovery will help the patient to understand the strategies and exercises for neuromuscular retraining. Patient education is a key component of successful treatment. Initially, it is necessary to increase patient awareness of the increased facial tone and the small stimuli that will increase muscle activity.96 Training to incorporate relaxation of these muscles is needed to minimize facial tone. Many patients with facial paresis often sit in a head-forward slouching position, with the head tilted toward the side with the facial paresis. Postural correction should include increased awareness of the head position and its effect on facial tone. Many patients in which the platysma muscle is involved with their synkinesis will notice increased facial tone and increased synkinetic movements with head-forward postures. Patients should also be instructed to avoid excessive chewing on the affected side, such as chewing gum, because mass facial movements will increase facial

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Facial Nerve Injury tone and thus increase synkinesis. Some practitioners also caution patients regarding stimulants, such as caffeinated drinks and nicotine. Massage and bilateral light face-tapping exercises may be used to promote sensory stimulation and blood flow to the affected side of the face.96 In some cases, injection of botulinum toxin may be useful to decrease aberrant synkinetic movements.33,39,108,109,117 Strategies to decrease resting tone are critical in overall rehabilitation. Although increased resting tone is often a problem on the affected side of the face and may affect facial symmetry, hyperactivity on the unaffected side of the face will also contribute to the apparent asymmetry. Strategies such as face tapping and light massage may help to encourage muscle relaxation. Surface EMG biofeedback can be a useful education tool to assist patients in learning how to relax the muscles and to decrease resting muscle tone.103 A four-channel EMG unit may be used to monitor the muscles on the affected and unaffected sides of the face to allow the patient to observe muscle activity in normal muscles and those with increased tone. The initial goal in facial neuromuscular retraining is to minimize synkinesis, with progression to isolated voluntary facial movements. In some cases, it is very difficult to eliminate the synkinesis. Van Swearingen and Brach advocate permitting patients to increase the voluntary movement despite the development of synkinesis.106 As the muscle excursion increases, the patient can incorporate strategies to decrease the synkinetic movements. Although for many patients the goal is to improve their smile, the action necessary for this motion requires many muscles to act and relax synergistically. One must increase control of individual muscles, and the timing of when to begin isolated voluntary movements is based on evaluation of the patient’s response to retraining. To regain motor control of composite movements required for facial motion, it is necessary to regain controlled isolated voluntary movements and increase effort once muscle control is regained. As with many other neuromuscular retraining programs,118 simultaneous contractions of the contralateral side can facilitate retraining. These movements can be facilitated with visual feedback, and exercises using a source of biofeedback such as a mirror or surface EMG are essential to understand and learn this movement. With success of small facial movements on the unaffected side, the movement is initiated on the affected side. The isolated movement is performed to the extent that there is no simultaneous synkinetic movement, and the movement appears symmetrical with the contralateral side. Slow onset of muscle activity is encouraged because fast facial movements will promote improper muscle recruitment and perpetuate synkinesis. EMG biofeedback and observation using a mirror can be used to help the patient initiate the voluntary movement and to control synkinesis. Visualization of the movement on the unaffected side in a mirror or with EMG biofeedback can provide visual cues to assist in performing the correct movement on the affected side. This type of biofeedback training can be useful in reducing synkinetic aberrant motions with voluntary movement. EMG biofeedback training may be used with either a two- or four-channel EMG unit. To encourage relaxation of the overactive muscles and to decrease resting tone, one channel may be placed on the affected side and one channel on the unaffected side. This will provide the patient with visual and/or

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auditory feedback of the normal activity and of the reinnervated muscles, which are often overactive even at rest. With retraining of motion and to minimize aberrant movement, both channels may be placed on the affected side, with one channel on the synkinetic muscles and the other channel to increase voluntary control. For example, one channel may be placed on the risorius muscle or orbicularis oculi to control aberrant synkinetic muscle activity, and the second channel may be placed on the orbicularis oris to increase active motion. This method will permit the patient to observe the active movement and the concurrent synkinetic muscle activity. If a four-channel EMG biofeedback unit is available, the other two channels can be placed on the contralateral unaffected muscles to observe the desired normal action. This type of visual and/or auditory feedback is immediate and allows the patient to correctly learn to increase the voluntary movement while minimizing the synkinetic muscle activity. Muscle physiology and the response of reinnervated muscle will guide the timing and duration of exercise sessions. Brach and Van Swearingen reported facial muscle fatigue even in healthy normal subjects.119 Because the facial muscles fatigue quickly, the exercise program must be planned accordingly. Patients are able to perform only a few trials of a particular muscle action prior to fatigue, so rest is required before resuming the exercise. Patients should be instructed in controlled onset of movement and holds with few repetitions. More frequent exercise sessions throughout the day are preferable to one long exercise session. With more control gained over the aberrant synkinetic motions, increased effort of voluntary movement and muscle excursion can be achieved. In many cases, EMG biofeedback may be a useful tool for neuromuscular retraining; however, many patients will not have access to this modality at home or at some therapy centers. Exercise programs that use visual feedback with a mirror have also been shown to be efficacious. These programs may be of greater use for many patients because they may be performed easily and more frequently. Initial retraining exercises to increase muscle strength and excursion should begin with muscles that are easier to isolate. With increased control to correctly recruit the appropriate muscle, more muscles and actions can be incorporated in the home program. If available, EMG biofeedback training provides the patient with accurate and immediate feedback to ensure that the appropriate muscles are being recruited. These learned strategies, however, should then be transferred to the exercises with mirror feedback to allow more frequent exercise sessions. Because of the importance of adequate eye closure, specific exercises such as target training to improve eye closure should be instituted in the early rehabilitation program. A handheld mirror is positioned below the face. The patient is instructed to gaze down into the mirror and attempt to close the eye. By using the mirror, the eye is used as a target to maintain it in a downward position. This promotes increased activity of the orbicularis oculi for eye closure. With improvement of eye closure in the downward position, the mirror (and thus the target) is moved to a more horizontal position to increase the excursion of the orbicularis oculi muscle. With neuromuscular retraining, initial improvements that occur in the first few months are usually a result of increased patient understanding of the activities that stimulate and per-

Facial Nerve Injury petuate synkinesis. As the patient learns to decrease resting muscle tone, to minimize exacerbation of the synkinesis, and to decrease hyperactivity of the affected side, facial symmetry improves. Increased muscle excursion and selective muscle recruitment require more complex neuromuscular reeducation and progress at a much slower rate. As indicated in the efficacy trials, many months of neuromuscular retraining and an appropriate home exercise program are necessary to improve facial movement and to attain facial symmetry.

16.6.3 Postoperative Neuromuscular Retraining Following surgical reconstruction such as nerve repair, grafting, transfers, or cross-facial nerve graft with free muscle transfer, rehabilitation strategies to achieve facial symmetry are essential to maximize outcome. Many of the same neuromuscular retraining strategies as described previously are implemented. The specific reeducation program will be determined by the surgical procedure and patient assessment. In the early postoperative period, patient education regarding wound healing and eye care is instituted. Direct facial nerve repair or grafting will result in reinnervation of the facial muscles and some degree of synkinesis. Therefore, neuromuscular retraining may follow the strategies as previously described. Selective muscle recruitment, minimizing synkinetic movements, and facial symmetry may be facilitated with mirror or biofeedback training. Nerve transfers using the masseteric branch of the trigeminal nerve-to-facial nerve or cross-facial nerve transfers require specific reeducation to recruit the facial muscles. With evidence of muscle reinnervation, patients should begin specific exercises to increase muscle control and strength. Nerve transfers such as the masseter nerve branch to the facial nerve initially require the patient to “contract” the donor muscle for contraction of the recipient reinnervated muscles. In these cases, the patient is instructed to “bite down” or “clench the teeth” to elicit a contraction in the reinnervated facial muscles. This is best performed with visual feedback, which can be provided with a mirror. The initial goal is to produce a contraction symmetrical to the contralateral side. Because of the weakness of the reinnervated facial muscles, this will require less effort from the unaffected side. With increased strength and control, the patient attempts to perform this action without biting down and to achieve a symmetrical appearance between the affected and unaffected side. With a cross-facial nerve graft and free muscle transfer, the retraining is easier, because most facial movements are bilateral. Therefore, contraction of the unaffected side of the face will produce a contraction on the contralateral side. Like the other retraining strategies, the goal should be directed toward motor control and facial symmetry.

16.7 Conclusion Facial paralysis is a complex condition requiring meticulous, zonal, ongoing management. Surgical approaches vary with age, motivation, prognosis, and local soft tissue factors.

Continuous reassessment and a layered management strategy involving medical, surgical, and rehabilitative strategies lead to optimal outcomes.

16.8 References [1] Van de Graaf RC, IJpma FF, Nicolai JP. Sir Charles Alfred Ballance (18561936) and the introduction of facial nerve crossover anastomosis in 1895. J Plast Reconstr Aesthet Surg 2009;62:43–49 [2] B. S. L’état actuel de la chirurgie nerveuse. Paris: J Rueff; 1902 [3] van de Graaf RC, Nicolai JP, IJpma FF. Re: cross-facial nervegraft: past and present. J Plast Reconstr Aesthet Surg 2008;61:462–463 [4] Cha CI, Hong CK, Park MS, Yeo SG. Comparison of facial nerve paralysis in adults and children. Yonsei Med J 2008;49:725–734 [5] Evans AK, Licameli G, Brietzke S, Whittemore K, Kenna M. Pediatric facial nerve paralysis: patients, management and outcomes. Int J Pediatr Otorhinolaryngol 2005;69:1521–1528 [6] Shih WH, Tseng FY, Yeh TH, Hsu CJ, Chen YS. Outcomes of facial palsy in children. Acta Otolaryngol 2009;129:915–920 [7] Hohman MH, Hadlock TA. Etiology, diagnosis, and management of facial palsy: 2000 patients at a facial nerve center. Laryngoscope. 2014; [epub ahead of print] [8] Tzafetta K, Terzis JK. Essays on the facial nerve: 1. Microanatomy. Plast Reconstr Surg 2010;125:879–889 [9] Ueda K, Harii K, Yamada A. Long-term follow-up study of browlift for treatment of facial paralysis. Ann Plast Surg 1994;32:166–170 [10] House JW, Brackmann DE. Facial nerve grading system. Otolaryngol Head Neck Surg 1985;93:146–147 [11] Vrabec JT, Backous DD, Djalilian HR, et alFacial Nerve Disorders Committee. Facial nerve grading system 2.0. Otolaryngol Head Neck Surg 2009;140:445– 450 [12] Berg T, Jonsson L, Engström M. Agreement between the Sunnybrook, HouseBrackmann, and Yanagihara facial nerve grading systems in Bell’s palsy. Otol Neurotol 2004;25:1020–1026 [13] Engström M, Jonsson L, Grindlund M, Stålberg E. House-Brackmann and Yanagihara grading scores in relation to electroneurographic results in the time course of Bell’s palsy. Acta Otolaryngol 1998;118:783–789 [14] Ross BG, Fradet G, Nedzelski JM. Development of a sensitive clinical facial grading system. Otolaryngol Head Neck Surg 1996;114:380–386 [15] Yanagihara N. On standardised documentation of facial palsy (author’s transl) [in Japanese] Nippon Jibiinkoka Gakkai Kaiho 1977;80:799–805 [16] Satoh Y, Kanzaki J, Yoshihara S. A comparison and conversion table of the House-Brackmann facial nerve grading system and the Yanagihara grading system. Auris Nasus Larynx 2000;27:207–212 [17] Coulson SE, Croxson GR, Adams RD, O’Dwyer NJ. Reliability of the “Sydney,” “Sunnybrook,” and “House Brackmann” facial grading systems to assess voluntary movement and synkinesis after facial nerve paralysis. Otolaryngol Head Neck Surg 2005;132:543–549 [18] Manktelow RT, Zuker RM, Tomat LR. Facial paralysis measurement with a handheld ruler. Plast Reconstr Surg 2008;121:435–442 [19] Bae YC, Zuker RM, Manktelow RT, Wade S. A comparison of commissure excursion following gracilis muscle transplantation for facial paralysis using a cross-face nerve graft versus the motor nerve to the masseter nerve. Plast Reconstr Surg 2006;117:2407–2413 [20] Kecskes G, Herman P, Kania R, et al. Lengthening temporalis myoplasty versus hypoglossal-facial nerve coaptation in the surgical rehabilitation of facial palsy: evaluation by medical and nonmedical juries and patient-assessed quality of life. Otol Neurotol 2009;30:217–222 [21] He S, Soraghan JJ, O’Reilly BF. Objective grading of facial paralysis using local binary patterns in video processing. Conf Proc IEEE Eng Med Biol Soc 2008;2008:4805–4808 [22] Terzis JK, Olivares FS. Use of mini-temporalis transposition to improve free muscle outcomes for smile. Plast Reconstr Surg 2008;122:1723–1732 [23] Frey M, Michaelidou M, Tzou CH, et al. Three-dimensional video analysis of the paralyzed face reanimated by cross-face nerve grafting and free gracilis muscle transplantation: quantification of the functional outcome. Plast Reconstr Surg 2008;122:1709–1722 [24] Frey M, Giovanoli P, Michaelidou M. Functional upgrading of partially recovered facial palsy by cross-face nerve grafting with distal end-to-side neurorrhaphy. Plast Reconstr Surg 2006;117:597–608

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[55] Booth AJ, Murray A, Tyers AG. The direct brow lift: efficacy, complications, and patient satisfaction. Br J Ophthalmol 2004;88:688–691 [56] Putterman AM. Intraoperatively controlled small-incision forehead and brow lift. Plast Reconstr Surg 1997;100:262–266 [57] Ducic Y, Adelson R. Use of the endoscopic forehead-lift to improve brow position in persistent facial paralysis. Arch Facial Plast Surg 2005;7:51–54 [58] Mavrikakis I, DeSousa JL, Malhotra R. Periosteal fixation during subperiosteal brow lift surgery. Dermatol Surg 2008;34:1500–1506 [59] Noel CL, Frodel JL. Eyebrow position recognition and correction in reconstructive and cosmetic surgery. Arch Facial Plast Surg 2008;10:44–49 [60] Kinzel R, Kaduk WM, Cuzalina A, Podmelle F, Metelmann HR. Indication, technique and clinical out come of the endoscopic assisted forehead and brow lift [in German] Mund Kiefer Gesichtschir 2005;9:6–11 [61] Rautio J, Pignatti M. Endoscopic forehead lift for ptosis of the brow caused by facial paralysis. Scand J Plast Reconstr Surg Hand Surg 2001;35:51–56 [62] Ramirez OM. Endoscopic subperiosteal browlift and facelift. Clin Plast Surg 1995;22:639–660 [63] Terzis JK, Dryer MM, Bodner BI. Corneal neurotization: a novel solution to neurotrophic keratopathy. Plast Reconstr Surg 2009;123:112–120 [64] Berghaus A, Neumann K, Schrom T. The platinum chain: a new upper-lid implant for facial palsy. Arch Facial Plast Surg 2003;5:166–170 [65] Silver AL, Lindsay RW, Cheney ML, Hadlock TA. Thin-profile platinum eyelid weighting: a superior option in the paralyzed eye. Plast Reconstr Surg 2009;123:1697–1703 [66] Bergeron CM, Moe KS. The evaluation and treatment of lower eyelid paralysis. Facial Plast Surg 2008;24:231–241 [67] Seiff SR, Sullivan JH, Freeman LN, Ahn J. Pretarsal fixation of gold weights in facial nerve palsy. Ophthal Plast Reconstr Surg 1989;5:104–109 [68] Schrom T. Lidloading in facial palsy Laryngorhinootologie 2007;86:634– 638 [69] Schrom T, Wernecke K, Thelen A, Knipping S. Results after lidloading with rigid gold weights—a meta-analysis Laryngorhinootologie 2007;86:117–123 [70] Henstrom DK, Lindsay RW, Cheney ML, Hadlock TA. Surgical treatment of the periocular complex and improvement of quality of life in patients with facial paralysis. Arch Facial Plast Surg 2011;13:125–128 [71] Lindsay RW, Smitson C, Edwards C, Cheney ML, Hadlock TA. Correction of the nasal base in the flaccidly paralyzed face: an orphaned problem in facial paralysis. Plast Reconstr Surg 2010;126:185e–186e [72] Hadlock TA, Cheney ML. Single-incision endoscopic sural nerve harvest for cross face nerve grafting. J Reconstr Microsurg 2008;24:519–523 [73] Capek L, Clarke HM. Endoscopically assisted sural nerve harvest in infants. Semin Plast Surg 2008;22:25–28 [74] Borschel G, Kawamura D, Ksukurthi R, et al. The motor nerve to the masseter muscle: an anatomic and histomorphometric study to facilitate its use in facial reanimation. J Plast Reconstr Aesthet Surg 2012;65:363–366 [75] Klebuc M, Shenaq SM. Donor nerve selection in facial reanimation surgery. Semin Plast Surg 2004;18:53–60 [76] Zuker RM, Goldberg CS, Manktelow RT. Facial animation in children with Möbius syndrome after segmental gracilis muscle transplant. Plast Reconstr Surg 2000;106:1–8, discussion 9 [77] Terzis JK, Olivares FS. Long-term outcomes of free-muscle transfer for smile restoration in adults. Plast Reconstr Surg 2009;123:877–888 [78] Terzis JK, Olivares FS. Long-term outcomes of free muscle transfer for smile restoration in children. Plast Reconstr Surg 2009;123:543–555 [79] Hadlock TA, Malo JS, Cheney ML, Henstrom DK. Free gracilis transfer for smile in children: the Massachusetts Eye and Ear Infirmary experience in excursion and quality-of-life changes. Arch Facial Plast Surg 2011;13:190– 194 [80] O’Brien BM, Pederson WC, Khazanchi RK, Morrison WA, MacLeod AM, Kumar V. Results of management of facial palsy with microvascular free-muscle transfer. Plast Reconstr Surg 1990;86:12–22, discussion 23–24 [81] Terzis JK, Olivares FS. Mini-temporalis transfer as an adjunct procedure for smile restoration. Plast Reconstr Surg 2009;123:533–542PubMed [82] Bhama PK, Weinberg JS, Lindsay RW, et al. Objective outcomes analysis following microvascular gracilis transfer for facial reanimation: a review of 10 years’ experience. JAMA Facial Plast Surg. 2014;16:85–92 [83] Bhama PK, Gilkilch RE, Weinberg JS, et al. Optimizing total facial nerve patient management for effective clinical outcomes research. JAMA Facial Plast Surg. 2014;16:9–14 [84] Coombs CJ, Ek EW, Wu T, Cleland H, Leung MK. Masseteric-facial nerve coaptation—an alternative technique for facial nerve reinnervation. J Plast Reconstr Aesthet Surg 2009;62:1580–1588

Facial Nerve Injury [85] Manktelow RT, Tomat LR, Zuker RM, Chang M. Smile reconstruction in adults with free muscle transfer innervated by the masseter motor nerve: effectiveness and cerebral adaptation. Plast Reconstr Surg 2006;118:885–899 [86] Woollard AC, Harrison DH, Grobbelaar AO. An approach to bilateral facial paralysis. J Plast Reconstr Aesthet Surg 2010;63:1557–1560 [87] Rubin LR, Rubin JP, Simpson RL, Rubin TR. The search for the neurocranial pathways to the fifth nerve nucleus in the reanimation of the paralyzed face. Plast Reconstr Surg 1999;103:1725–1728 [88] Hussain G, Manktelow RT, Tomat LR. Depressor labii inferioris resection: an effective treatment for marginal mandibular nerve paralysis. Br J Plast Surg 2004;57:502–510 [89] Lindsay RW, Edwards C, Smitson C, Cheney ML, Hadlock TA. A systematic algorithm for the management of lower lip asymmetry. Am J Otolaryngol 2011;32:1–7 [90] Terzis JK, Kalantarian B. Microsurgical strategies in 74 patients for restoration of dynamic depressor muscle mechanism: a neglected target in facial reanimation. Plast Reconstr Surg 2000;105:1917–1931, discussion 1932– 1934 [91] Brach JS, VanSwearingen J, Delitto A, Johnson PC. Impairment and disability in patients with facial neuromuscular dysfunction. Otolaryngol Head Neck Surg 1997;117:315–321 [92] Coulson SE, O’Dwyer NJ, Adams RD, Croxson GR. Expression of emotion and quality of life after facial nerve paralysis. Otol Neurotol 2004;25:1014–1019 [93] Bach y Rita P. Central nervous system lesions: sprouting and unmasking in rehabilitation. Arch Phys Med Rehabil 1981;62:413–417 [94] Bach-y-Rita P. Brain plasticity as a basis for recovery of function in humans. Neuropsychologia 1990;28:547–554 [95] Merzenich MM, Jenkins WM. Reorganization of cortical representations of the hand following alterations of skin inputs induced by nerve injury, skin island transfers, and experience. J Hand Ther 1993;6:89–104 [96] Balliet R, Shinn JB, Bach-y-Rita P. Facial paralysis rehabilitation: retraining selective muscle control. Int Rehabil Med 1982;4:67–74 [97] Brach JS, Van Swearingen JM. Physical therapy for facial paralysis: a tailored treatment approach. Phys Ther 1999;79:397–404 [98] Brach JS, Van Swearingen JM, Lenert J, Johnson PC. Facial neuromuscular retraining for oral synkinesis. Plast Reconstr Surg 1997;99:1922–1931, discussion 1932–1933 [99] Brown DM, Nahai F, Wolf S, Basmajian JV. Electromyographic biofeedback in the reeducation of facial palsy. Am J Phys Med 1978;57:183–190 [100] Brudny J, Hammerschlag PE, Cohen NL, Ransohoff J. Electromyographic rehabilitation of facial function and introduction of a facial paralysis grading scale for hypoglossal-facial nerve anastomosis. Laryngoscope 1988;98:405–410 [101] Cronin GW, Steenerson RL. The effectiveness of neuromuscular facial retraining combined with electromyography in facial paralysis rehabilitation. Otolaryngol Head Neck Surg 2003;128:534–538

[102] Nakamura K, Toda N, Sakamaki K, Kashima K, Takeda N. Biofeedback rehabilitation for prevention of synkinesis after facial palsy. Otolaryngol Head Neck Surg 2003;128:539–543 [103] Ross B, Nedzelski JM, McLean JA. Efficacy of feedback training in long-standing facial nerve paresis. Laryngoscope 1991;101:744–750 [104] Segal B, Hunter T, Danys I, Freedman C, Black M. Minimizing synkinesis during rehabilitation of the paralyzed face: preliminary assessment of a new small-movement therapy. J Otolaryngol 1995;24:149–153 [105] Segal B, Zompa I, Danys I, et al. Symmetry and synkinesis during rehabilitation of unilateral facial paralysis. J Otolaryngol 1995;24:143–148 [106] Van Swearingen JM, Brach JS. Changes in facial movement and synkinesis with facial neuromuscular reeducation. Plast Reconstr Surg 2003;111:2370– 2375 [107] Lindsay RW, Robinson M, Hadlock TA. Comprehensive facial rehabilitation improves function in people with facial paralysis: a 5-year experience at the Massachusetts Eye and Ear Infirmary. Phys Ther 2010;90:391–397 [108] Kollewe K, Mohammadi B, Dengler R, Dressler D. Hemifacial spasm and reinnervation synkinesias: long-term treatment with either Botox or Dysport. J Neural Transm 2010;117:759–763 [109] Boroojerdi B, Ferbert A, Schwarz M, Herath H, Noth J. Botulinum toxin treatment of synkinesia and hyperlacrimation after facial palsy. J Neurol Neurosurg Psychiatry 1998;65:111–114 [110] Diels HJ, Combs D. Neuromuscular retraining for facial paralysis. Otolaryngol Clin North Am 1997;30:727–743 [111] Farragher D. Trophic stimulation. Nurs Stand 1990;5 Suppl P:10–11 [112] Axelsson S, Lindberg S, Stjernquist-Desatnik A. Outcome of treatment with valacyclovir and prednisone in patients with Bell’s palsy. Ann Otol Rhinol Laryngol 2003;112:197–201 [113] Hato N, Matsumoto S, Kisaki H, et al. Efficacy of early treatment of Bell’s palsy with oral acyclovir and prednisolone. Otol Neurotol 2003;24:948–951 [114] Eberstein A, Eberstein S. Electrical stimulation of denervated muscle: is it worthwhile? Med Sci Sports Exerc 1996;28:1463–1469 [115] Michlovitz SL. Is there a role for ultrasound and electrical stimulation following injury to tendon and nerve? J Hand Ther 2005;18:292–296 [116] Barbara M, Monini S, Buffoni A, et al. Early rehabilitation of facial nerve deficit after acoustic neuroma surgery. Acta Otolaryngol 2003;123:932–935 [117] Filipo R, Spahiu I, Covelli E, Nicastri M, Bertoli GA. Botulinum toxin in the treatment of facial synkinesis and hyperkinesis. Laryngoscope 2012;122:266–270 [118] Duff SV. Impact of peripheral nerve injury on sensorimotor control. J Hand Ther 2005;18:277–291 [119] Brach JS, Van Swearingen J. Measuring fatigue related to facial muscle function. Arch Phys Med Rehabil 1995;76:905–908

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Tendon Transfers for Functional Reconstruction

17 Tendon Transfers for Functional Reconstruction J. Megan Patterson, Martin I. Boyer, Charles A. Goldfarb, and Douglas M. Sammer

17.1 Introduction Peripheral nerve injuries are usually treated by primary direct nerve repair whenever possible. In patients with injuries that preclude primary repair, nerve grafting or nerve transfer may provide satisfactory muscle reinnervation and outcome. However, there remains a subset of patients who do not recover satisfactory function. Additionally, some patients may present in such a delayed fashion that reinnervation is unlikely to occur due to prolonged muscle denervation. Another group of patients may be more efficiently served with initial tendon transfers rather than nerve reconstruction. Still others may be best served by a combination of nerve reconstruction and tendon transfers. This chapter reviews the common tendon transfers used in patients with palsies of the radial, ulnar, and median nerves.

17.2 History The polio epidemics that swept through Europe in the 1800s led directly to the development of tendon transfers. Most of the early tendon transfers were devised to improve lower extremity function in patients with poliomyelitis. World Wars I and II resulted in vast numbers of patients with upper extremity injuries, and surgeons were able to gain a career’s worth of experience in tendon transfer surgery within a few years. This rapidly led to the expansion and refinement of tendon transfer techniques in the upper extremity.1

17.3 Principles of Tendon Transfer Over the years, several tendon transfer principles have been described and refined (▶ Table 17.1). Although adherence to these principles does not guarantee a successful outcome, to ignore them invites failure. A tendon transfer should be performed only after soft tissue equilibrium has been achieved. In other

words, the tendon transfer will function optimally only if it lies in a soft tissue bed that is free from healing wounds, edema, and scar tissue. In some cases, large areas of scar or skin graft may need to be resected and resurfaced with a flap prior to performing the tendon transfer. In other cases, the tendon transfer can be rerouted to avoid areas of scar tissue. Joints must be supple and free from contracture prior to tendon transfer. A tendon transfer will not move a stiff joint. Although this seems intuitive, it is not uncommon for the surgeon to encounter patients who present for tendon transfer who have had no hand therapy and who have severe contractures. Splinting and intensive hand therapy should be initiated at the time of injury to maintain full passive motion in anticipation of future tendon transfers. In some cases, contracture releases are required. These should be performed prior to tendon transfer surgery. Contracture release should not be performed at the same time as the tendon transfer, as contracture releases require early mobilization, and tendon transfers require a period of immobilization postoperatively. The donor muscle–tendon unit (MTU) should be expendable such that its transfer does not result in a clinically significant functional impairment. It is of no use to restore one function but lose another equally important function. When possible, it is preferable to perform a tendon transfer that is synergistic. Synergistic muscles are those that work together to perform certain activities (i.e., wrist extension and finger flexion, or wrist flexion and finger extension). An example of a synergistic transfer is the flexor carpi radialis (FCR)-to-extensor digitorum communis (EDC) transfer, in which a wrist flexor is used to restore finger extension. Retraining following a synergistic tendon transfer is easier than after a nonsynergistic transfer. Additionally, whenever possible, the donor MTU should have similar strength and amplitude to the MTU that it is replacing. In the normal adult hand, the wrist flexors and extensor have ~ 33 mm of excursion. Extrinsic finger extensors have 50 mm of

Table 17.1 Principles of Tendon Transfers

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Soft tissue equilibrium

Transfers should pass through a healthy bed of soft tissue, free from scar, inflammation, or wound.

Supple joints

Joints must be supple prior to performing tendon transfer. Contracture releases must be done as a first stage prior to tendon transfers.

Expendable donor

Transfer of the donor should not result in a clinically significant functional deficit.

Adequate strength

The donor must have adequate strength, similar to that of the muscle whose function it is replacing.

Adequate excursion

The donor must have enough excursion to move the joint through a useful range of motion. If not, the tenodesis effect may be required to augment joint motion.

Single tendon, single function

A transfer should be used to restore one function. Performing multiple functions dilutes transfer strength and makes retraining difficult.

Synergy

Synergistic transfers result in easier retraining (eg, transferring a wrist flexor for finger extension).

Straight line of pull

A transferred muscle tendon unit will be strongest if it has a straight line of pull. Direction changes, although sometimes necessary, make the transfer weaker. However, a transfer should not pass through more than one pulley, or strength and excursion will be greatly diminished.

Tendon Transfers for Functional Reconstruction excursion, and the extrinsic finger flexors have 70 mm of excursion.2 If an MTU with inadequate excursion is used, the patient will not achieve full motion. In these cases, the tenodesis effect can sometimes be used to increase the effective excursion of the tendon transfer. For example, when the FCR (33-mm excursion) is transferred to the EDC (50-mm excursion) for restoration of finger extension, the donor MTU will have inadequate excursion to provide full finger extension. However, if the patient flexes the wrist during attempted finger extension, the effective excursion of the transfer is increased, and the patient can achieve full extension. The strength of the MTU is equally important. A donor MTU that is too strong will result in unbalanced movement, poor joint posture, or even a contracture. A donor MTU that is too weak will have inadequate power to achieve the desired function. When considering donor strength, it is easiest to compare relative strength of the various upper extremity muscles. 3 For example, the strongest forearm MTUs are the brachioradialis and flexor carpi ulnaris (FCU), with a relative strength of 2. The remaining wrist flexors and extensors, the finger flexors, and the pronator teres all have a relative strength of 1. The finger extensors have a relative strength of 0.5, that is, approximately half that of the finger flexors and wrist motors. The weakest donor MTUs are the thumb extensors and abductor and the palmaris longus, with a relative strength of 0.1 each. It is preferable to use a donor MTU that has normal strength rather than a muscle affected by nerve injury or trauma, because a transferred MTU will usually lose one motor grade after transfer. 3 In general, a single MTU should be transferred to replace a single function. Requiring a tendon transfer to perform more than one function (e.g., finger and wrist extension) will result in inadequate motion and strength and will make retraining more difficult. The exception to this rule is when a single tendon is used to restore the exact same function in multiple digits, such as using a single tendon to restore metacarpophalangeal (MCP) extension in all five fingers. Finally, when possible, a tendon transfer should be performed in such a way as to create a straight line of pull from the muscle origin to the tendon insertion. Significant direction changes along the course of the transfer result in a weakening of transfer strength. This principle becomes important when deciding whether to perform an endto-side or end-to-end transfer. For example, the pronator teres is commonly transferred to the extensor carpi radialis brevis (ECRB) to restore wrist extension in patients with radial nerve palsy. If recovery of the ECRB is anticipated, this transfer should be performed in an end-to-side fashion. Although this results in a direction change and may weaken the transfer somewhat, the transfer is performed in this fashion so that the ECRB can contribute to wrist extension when it recovers. However, if no recovery is anticipated, the transfer should be performed in an end-to-end fashion, creating a straight and more effective line of pull. In some cases, a direction change is necessary to achieve the optimum line of pull for a desired motion. For example, the superficialis opponensplasty involves a transfer of the flexor digitorum superficialis (FDS) to the thumb abductor pollicis brevis (APB) insertion. If performed with a straight line of pull, this transfer will result in too much palmar abduction. To achieve true opposition, the tendon must pass from the area of the pisiform, across the palm, to the APB insertion. This requires the creation of a soft tissue pulley at the level of the pisiform. This

direction change will result in a weakening of the transfer but is required in this case to achieve the desired motion. In addition to the principles described above, careful surgical technique will help improve the success of the transfer. First, the donor muscle belly should be mobilized proximally to allow for an improved line of pull and to permit full excursion. This is particularly important in certain muscles with heavy fascial attachments and limited excursion, such as the brachioradialis. Careful attention must be given to the tensioning of the transfer. Proper tensioning of the tendon transfer is one of the most difficult parts of a tendon transfer operation. In general, it is probably better to make the transfer a little too tight rather than too loose. Although an overly tight transfer will loosen to some degree over time, a transfer that is too loose will never tighten up. However, there is some evidence in the literature that most tendon transfers are set with too much tension. Fridén and Lieber measured intraoperative sarcomere length after tendon transfers were performed using standard tensioning techniques and found that almost all of the tendon transfers were too tight, resulting in suboptimal sarcomere length and an active force generation of only 28% of normal. 4 In another study, these same authors explored the use of laser diffraction for making intraoperative sarcomere length measurements to determine the optimum tension at which to set a tendon transfer. 5 Although these techniques are still experimental, they may become useful in the future for assisting with tension setting in the operating room. Evaluating the tenodesis effect can often provide an additional means of ensuring that adequate tension has been achieved. For example, in an FCR-to-EDC transfer, the MCP joints should fully extend with the wrist passively flexed. With the wrist passively extended, the surgeon should be able to passively flex the fingers to the palm. A tapered needle should be used, as it will cause less damage to the tendon than a cutting needle. A 3–0 or 4–0 braided polyester suture is usually adequate, but the size of the suture and the repair technique must reflect the size of the tendon and the planned postoperative therapy protocol. A Pulvertaft weave technique using a tendon weaver or anchoring the transfer to bone usually provides adequate fixation to allow for early range of motion.3 Most transfers are immobilized for 3 to 4 weeks postoperatively in the position that minimizes tension on the transfer. Supervised active range of motion is begun at 3 to 4 weeks, and passive motion begins at 6 weeks. Strengthening is usually started at 8 weeks postoperatively. Splinting is weaned, and patients are allowed to gradually return to full activity at 3 months postoperatively. Early active motion may be appropriate in some patients.

17.3.1 Tendon Transfers for Ulnar Nerve Palsy Anatomy and Physical Exam 17

The ulnar nerve originates from the medial cord of the brachial plexus, receiving fibers from the C8 and T1 nerve roots. The ulnar nerve provides innervation to the FCU and the ulnar half of the flexor digitorum profundus (FDP) in the proximal forearm. In the hand, the ulnar nerve innervates the hypothenar muscles, the ring and small finger lumbricals, the adductor

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Tendon Transfers for Functional Reconstruction pollicis, the interossei, and the deep head of the flexor pollicis brevis (FPB). The intrinsic paralysis that results from ulnar nerve palsy causes a difficulty with grasp due to asynchronous motion of the MCP and interphalangeal (IP) joints.6 In the normal hand, finger flexion is initiated at the MCP joint powered by the intrinsic muscles, followed by IP joint flexion powered by the extrinsic finger flexors. This produces a normal cupping motion during finger flexion, making it possible to grasp objects with the fingers. In patients who have lost intrinsic function, finger flexion begins at the IP joints, with late secondary MCP flexion, resulting in a rolling motion of the fingers during flexion. This rolling motion pushes objects out of the palm in a proximal direction and makes grasping objects quite difficult. Patients also have weakness of pinch due to loss of adductor pollicis and first dorsal interosseous (FDI) function. Patients with an ulnar nerve deficit will present with characteristic physical exam findings.3,7 Wartenberg sign is an inability to adduct the small finger and is one of the earliest signs of ulnar nerve dysfunction. This loss of adduction is caused by weakness of the third palmar interosseous muscle and the unopposed pull of the radial nerve innervated extensor digiti minimi and EDC to the small finger. Loss of interosseous function results in impaired lateral movements of the digits and an inability to cross the fingers. Duchenne sign is clawing of the ring and small fingers (MCP hyperextension and IP flexion). Clawing is due to the loss of MCP joint flexion and IP joint extension due to weakness of the ulnar nerve innervated interossei and lumbricals. The extrinsic finger flexors and extensors are unopposed by the intrinsics, resulting in MCP hyperextension and IP flexion. The small finger is more affected than the ring finger. Index and long fingers are less involved due to intact median nerve innervation of the first and second lumbrical muscles. Dual median and ulnar innervation of the ring finger is present in 50% of people and may protect from clawing of the ring finger. 8 It should be noted that clawing is more severe in cases of low ulnar nerve palsy, in which the FDP to the ring and small fingers is intact. In high ulnar nerve palsy, clawing can occur, but it is much less severe. This is because the only functioning extrinsic flexors of the ring and small finger are the FDS muscles. It should be noted that in the case of a repaired high ulnar nerve injury, clawing will become worse as the nerve regenerates and reinnervates the FDP to the ring and small fingers. Worsening of clawing in a high ulnar nerve palsy should be considered a sign of improving, not worsening, ulnar nerve function. Froment sign is hyperflexion of the thumb IP joint during key pinch. It is caused by weakness of the adductor pollicis muscle and subsequent use of the flexor pollicis longus (FPL) to stabilize the joint during key pinch. Froment sign may be seen in conjunction with Jeanne sign, which is a hyperextension deformity of the thumb MCP joint during attempted pinch due to volar plate laxity. Susan E. Mackinnon emphasized (personal communication) that there exists a “pseudo Froment sign” in patients with weakness but not complete paralysis of the intrinsic muscles, as well as hyperlaxity of the joints in the thumb. This pseudo Froment sign implies that the IP joints of the two thumbs show comparatively different posturing, even if the palsied thumb does not show hyperflexion per se. Thus, it is

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important to simultaneously compare the IP joint positioning of the normal and abnormal thumbs. Although these are common physical exam findings seen with ulnar nerve paralysis, it is important to note that variation may exist due to interconnections from the median to the ulnar nerve. A Martin–Gruber connection may occur from the median nerve to the ulnar nerve in the forearm and is present in 17% of individuals.9 For example, the presence of a Martin–Gruber connection can result in partial preservation of intrinsic hand function in the setting of a complete high ulnar nerve laceration.

Low Ulnar Nerve Palsy Splints can be used to address ulnar nerve dysfunction and help prevent claw deformity. The lumbrical bar splint is a handbased, static splint that maintains the MCP joints in slight flexion and therefore allows the extrinsic extensors, acting through the lateral bands, to extend the IP joints. Dynamic splints, such as the Wynn–Parry splint, can also be used to prevent MCP hyperextension and help to initiate flexion of the MCP joint. Unfortunately, these splints are often bulky, poorly tolerated, and not an ideal long-term solution if nerve recovery is not expected.8 The primary goals of tendon transfers for low ulnar nerve palsy are to correct clawing and improve lateral (key) pinch. It should be noted that the loss of key pinch is often well compensated and may not present a functional problem. Prior to surgical intervention, a discussion with the patient must be had to determine the patient’s priorities and his or her perception of the most significant deficit. ▶ Table 17.2 lists some common transfers for ulnar nerve palsy.

Transfers to Correct Claw Deformity Surgical options for correcting claw deformity are tenodesis, capsulodesis, and tendon transfer. Tenodesis and capsulodesis are passive procedures that are most appropriate for patients who are able to extend their IP joints when their MCP hyperextension is passively corrected (Bouvier test).10 Tenodesis and capsulodesis both function as an internal anticlawing splint, preventing MCP hyperextension. These static procedures are not effective in patients who are unable to extend their IP joints when their MCP hyperextension is corrected. These procedures do not improve grip strength or synchrony of finger flexion. In addition, they often stretch out with time, resulting in recurrence of the claw finger deformity.3 However, because they are straightforward and do not require complex rehabilitation, they may be appropriate in some patients. The Zancolli MCP capsulodesis tightens the volar plate to prevent MCP hyperextension, thereby allowing the extrinsic extensors to extend the IP joints.11 The capsulodesis is performed through a transverse incision in the distal palmar crease. The A1 pulley is divided, and the flexor tendons are retracted to expose the volar plate. The proximal origin of the volar plate is released, advanced proximally, and anchored to the metacarpal neck. The capsulodesis should be performed to provide 20 to 30 degrees of MCP flexion contracture. Advancing and inserting the volar plate into bone provides more lasting results than volar plate plication alone.

Tendon Transfers for Functional Reconstruction Table 17.2 Common Tendon Transfers* Ulnar nerve palsy Claw deformity

1. Tenodesis or MCP capsulodesis 2. ECRL through the lumbrical canals to the lateral bands using a free tendon graft 3. FDS rerouted and sutured to the A1 pulley (Zancolli)

Thumb pinch

1. ECRB between long and ring finger metacarpals to the adductor pollicis tendon using a free tendon graft (with or without fusion of MCP or IP joints if necessary) 2. EIP to adductor pollicis (may not require graft)

Wartenberg sign

1. Transfer EDQ to radial side of the small finger extensor hood

Median nerve palsy Thumb opposition

1. 2. 3. 4. 5.

EIP-to-APB insertion EDQ-to-APB insertion (useful transfer when other options are not available) PL (Camitz) FDS of ring finger APB (low median nerve palsy) Two-stage FCU/FDS opponensplasty

High median nerve palsy

1. BR to FPL (or fusion of the IP joint of the thumb) 2. Side-to-side tenodesis of the FDP if the index and long fingers to the ring and small fingers 3. ECRL to FDP of the index and long fingers

Radial nerve palsy Wrist extension

1. PT to ECRB

Finger extension

1. FCR/FCU to EDC 2. FDS to EDC (Boyes transfer)

Thumb extension

1. PL to EPL 2. FDS to EPL

* Authors’ preferences italicized. Abbreviations: APB, abductor pollicus brevis, BR, brachioradialis; ECRB, extensor carpi radialis brevis; ECRL, extensor carpi radialis longus; EDC, extensor digitorum communis; EDQ, extensor digiti quinti; EIP, extensor indicis proprius; EPL, extensor pollicus longus; FCR, flexor carpi radialis; FCU, flexor carpi ulnaris; FDP, flexor digitorum profundus; FDS, flexor digitorum superficialis; FPL, flexor pollicis longus; IP, interphalangeal; MCP, metacarpophalangeal; PL, palmaris longus; PT, pronator teres.

Two primary tendon transfer options exist to address claw finger deformity. The authors’ preferred method is to transfer the extensor carpi radialis longus (ECRL) or FCR to the lateral bands using a free tendon graft (palmaris longus, plantaris, or toe extensors).3,12 The ECRL is usually the donor tendon of choice; however, FCR is used in cases where ECRL is needed to power another transfer. The ECRL tendon is passed around the radial aspect of the forearm, lengthened with free tendon grafts, passed volar to the intermetacarpal ligaments, and inserted into the lateral band of the proximal phalanges of the affected fingers. Alternatively, a dorsal route may be used. The slips of free graft used to extend the ECRL are passed through the respective intermetacarpal spaces, through the lumbrical canals (volar to the deep intermetacarpal ligaments), and out to the lateral bands. The transfer should be tensioned with the wrist in maximum dorsiflexion, the IP joints extended, and the MCP joints maximally flexed. A second option is to reroute the ring flexor digitorum superficialis (FDS) and suture it to the A1 pulley (Zancolli lasso procedure), the lateral bands (Stiles–Bunnell intrinsic transfer), or the proximal phalanx (Burkhalter).3,12,13 Insertion onto the pulley system or onto the proximal phalanx provides only active MCP flexion, whereas insertion onto the lateral band also provides active IP extension. The advantages of the FDS transfers are that they are technically easier than using the ECRL or FCR and do not require tendon grafting. One disadvantage is that, unlike the ECRL or FCR transfer, they do not add to grip strength and may even reduce grip strength in an already weak

hand. Furthermore, in cases of high ulnar nerve palsy in which ring and small FDP function is absent, the surgeon must take care not to use the ring or small FDS as a donor MTU. The Zancolli lasso procedure is performed by making an incision in the distal palmar crease over the ring and small fingers. The A1 pulley and proximal portion of the A2 pulley are exposed. The FDS tendon is divided 2 cm distal to its bifurcation, and both slips are passed volarly through the tendon sheath and sutured back to themselves proximal to the A1 pulley, forming a loop.11 The transfer is tensioned with maximal pull on the FDS with the wrist in neutral position and the MCP joints flexed to 35 degrees. Although this procedure effectively corrects claw deformity and allows coordinated finger flexion, it does not significantly improve grip strength and can lead to a “swan neck” deformity due to the loss of FDS support to the proximal interphalangeal (PIP) joint. In fact, as noted above, in patients with an already weakened grip strength, transfer of the FDS may lead to substantial worsening of grip. The modified Stiles–Bunnell transfer also uses the FDS tendon as a motor to correct claw finger deformity. 14,15 The FDS of the ring or long fingers may be used. In patients with high ulnar nerve palsy, the long finger FDS is preferred. The FDS from the long finger is released ~ 2 cm distal to its bifurcation, and the tendon is divided longitudinally for ~ 5 cm. These tendon slips are redirected through the radial lumbrical canals of the ring and small fingers volar to the deep intermetacarpal ligament. They are then inserted into the radial lateral bands of the ring and small fingers. The transfer

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Tendon Transfers for Functional Reconstruction should be tensioned with the wrist in neutral and the ring and small fingers in the intrinsic plus position. This transfer will improve clawing and MCP flexion by replacing interossei and lumbrical function of the small and ring fingers; however, it will not improve strength and power grip as well as the ECRB or FCR transfers, and is therefore less desirable in younger patients and those with high functional demands. Complications of this procedure include swan neck deformity and PIP flexion contracture. Alternatively, the transferred FDS tendons may be inserted into the proximal phalanx using a drill hole.13 This insertion provides MCP flexion but not IP extension. However, it does decrease the incidence of postoperative swan neck deformity by avoiding the additional extension force at the PIP joint that occurs with transfers to the lateral band. The FDS transfer may also be sutured directly into the A2 pulley, which will result in improved MCP flexion. In cases where there has been attenuation of the central slip due to long-standing deformity, the FDS may be sutured directly into the remnant of the central slip. This will improve extension at the PIP joint but will increase the risk of PIP hyperextension.

Transfers to Improve Thumb Pinch Thumb pinch is often well compensated in patients with ulnar nerve palsy and may not require reconstruction. However, some patients have a profound loss of pinch strength and benefit from a tendon transfer. Many tendon transfers have been described for restoring thumb pinch. Although most are effective in improving thumb balance, cosmesis, and function, they do not provide significant improvements in pinch or adduction strength.8 The ECRB transfer, however, has been shown to double pinch strength and thus is our preferred transfer. 16 Either the brachioradialis or ECRB lengthened with a tendon graft may be used. The tendon is passed between the long and ring finger metacarpals from dorsal to volar, allowing the long metacarpal to serve as a pulley for the rerouted tendon. In the palm it is directed toward the thumb, passing deep (dorsal) to the flexor tendons and neurovascular structures, and is inserted on the adductor pollicis tendon. The transfer is tensioned with the wrist in neutral and the thumb held tightly against the radial volar border of the index finger. Tenodesis should be checked to ensure appropriate tensioning of the transfer. With the wrist flexed, the thumb should adduct against the index metacarpal,

and with the wrist extended, the thumb should be easily abducted away from the palm. Arthrodesis of the thumb MCP joint may be required to improve stability of the thumb when MCP hyperextension is present (Jeanne sign). If the MCP joint is stable, but the patient has a significant Froment sign, arthrodesis of the IP joint may be performed. The extensor indicis proprius (EIP)-to-adductor pollicis transfer is useful for improving key pinch (▶ Fig. 17.1). This transfer does not add as much strength, but it has the advantage of not requiring a tendon graft. The EIP is harvested as distally as possible from the level of the proximal phalanx of the index finger and retrieved into a longitudinal dorsal hand incision. It is then passed through the long/ring intermetacarpal space and to the adductor pollicis insertion in the same fashion as the ECRB transfer. It is important to repair the sagittal band over the index finger and to suture the distal stump of the EIP to the adjacent index EDC. Despite these precautions, there may be a small amount of extension lag at the index MCP joint.

Additional Transfers for Low Ulnar Nerve Palsy Loss of FDI function also contributes weak key pinch. However, it should be noted that in most cases the FDI does not require reconstruction, because the index finger can be stabilized against the adjacent fingers during pinch. Despite this, there are several tendon transfers designed to address loss of FDI function, including EIP, ECRL, APB or abductor pollicis longus (APL), extensor digiti quinti (EDQ), FDS, and palmaris longus transfers.12 The APL is a common choice because its vector is most closely in line with that of the FDI. Only one slip of the APL is needed, but a tendon graft is necessary to provide adequate length. Some patients may benefit from correction of a Wartenberg deformity. This can be corrected by transferring the EDQ to the small finger radial collateral ligament or the radial side of the A2 pulley.17 However, it should be noted that in some patients the abducted position of the small finger is functional. Correction of a Wartenberg sign by adducting the small finger to the hand may result in difficulty with certain activities, such as typing.

17 Fig. 17.1 Extensor indicis proprius (EIP)-to-adductor pollicis tendon transfer. (a) Incisions for EIP distal tendon harvest and insertion into the adductor pollicis muscle. (b) Harvest of EIP tendon occurs distally. (c) The EIP tendon is tunneled through subcutaneous tissue to the adductor pollicis.

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Fig. 17.2 Exposure and identification of flexor digitorum profundus (FDP) tendons with visible lines. Dotted lines portray the individual FDP tendons.

Transfers for High Ulnar Nerve Palsy In addition to the above transfers, patients with high ulnar nerve palsy may benefit from transfers to restore DIP flexion of the small and ring fingers. This is most easily accomplished by side-to-side tenodesis of ring and small FDP to the FDP of the long and index fingers (▶ Figs. 17.2–17.6).18 In patients for whom independent functioning of the index FDP is important, the ring and small finger FDP should be tenodesed to the long finger FDP alone. Alternatively, the ECRL (elongated with a tendon graft) can be used to power the FDP of the small and ring fingers. The FCR should not be used as a donor MTU in patients with high ulnar nerve palsy, as this would take away the only remaining wrist flexor. When performing a tendon transfer to restore small and ring FDP function, it is important to tell patients with mild or no clawing that they may develop new clawing or have a worsening in clawing after restoration of FDP function. In some cases, performing an FDP reconstruction may result in clawing that is severe enough to require an anticlawing tendon transfer.

17.3.2 Tendon Transfers for Median Nerve Palsy Anatomy and Physical Exam The median nerve originates from the lateral and medial cords of the brachial plexus and receives fibers from the C5, C6, C7, C8, and T1 nerve roots. The sensory component of the median nerve travels through the lateral cord and the motor component through the medial cord. All muscles of the volar forearm

except for the FCU and the ulnar half of the FDP are innervated by the median nerve. Additionally, the median nerve innervates the thenar muscles, as well as the most radial two lumbricals. The anatomy of the median nerve is described in more detail in Chapter 9. The two predominant problems for with patients with low median nerve palsy are the sensory deficit and the lack of thumb opposition.3,19 The loss of the most radial two lumbricals does not usually cause a significant functional deficit because the ulnar nerve–innervated interossei remain functional. In addition, patients with high median nerve palsy experience a loss of thumb IP flexion, along with a loss of index and long finger IP flexion.3 They may also experience weakness of forearm pronation and wrist flexion, although these movements are usually well compensated.

Transfers for Low Median Nerve Palsy ▶ Table 17.2 listed some of the common transfers for median nerve palsy. In cases of low median nerve palsy, tendon transfers are performed to restore thumb opposition. Occasionally, these transfers are paired with a bony procedure, such as thumb MCP or IP joint arthrodesis to provide stability. Four different MTUs are commonly used in opponensplasties: the abductor digiti quinti (ADQ), EIP, palmaris longus, and FDS.18–21 In 1921 Huber described the use of the ADQ to restore thumb opposition.18 The Huber transfer is primarily used in patients with congenital absence of the thenar musculature, but it may be useful in patients in whom other transfers are not available. The ADQ is identified through an incision on the ulnar border of the hand. The muscle is dissected free of its fascial compart-

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Fig. 17.3 Identifying the division between the median- and ulnar-innervated FDP tendons. Forceps are used in this image to visualize the division between the median- and ulnar-innervated FDP tendons. The ulnar-innervated FDP tendons are sutured to the median-innervated FDP tendons to complete the FDP tenodesis in an ulnar nerve injury.

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Fig. 17.4 Establishing the appropriate tension on the ulnar-innervated FDP tendons and insertion of the first suture. The ulnar-innervated FDP tendons are retracted proximally for tension (arrow) and to improve the effectiveness of the FDP tenodesis. The insertion of the first suture is important, as it sets the tension. First, the suture is inserted in the ulnar-innervated FDP tendons; next, the tension is set on the ulnar-innervated FDP tendons; lastly, the suture is inserted into the median-innervated FDP (specifically, the FDP tendon to the long finger) and tied off.

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Fig. 17.5 The first suture for the FDP tenodesis. The following sutures are inserted easily, as the tension is already set by the first suture.

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Fig. 17.6 FDP tenodesis. The independent FDP tendon to the long finger is not included in this tenodesis, and the FDP tendon to the long finger is what drives the function of the ulnar-innervated FDP tendons for ulnar nerve injuries.

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Fig. 17.7 Atrophy of thenar muscles. (a,b) This patient had a median nerve injury that is evident with the atrophy of the thenar muscles. Extensor indicis proprius (EIP) opponensplasty: (c) Incision for harvest of the distal EIP tendon. (d) The tendon is routed in the posterior/ulnar direction and tunneled through the subcutaneous fascia to the abductor pollicis brevis.

ment distally to its two insertions onto the base of the proximal phalanx and the extensor apparatus. Proximally, it is dissected to its origin on the pisiform. Care must be taken not to dissect on the radial side of the ADQ at its origin, because this is the location of the neurovascular pedicle. The ADQ is then passed through a wide subcutaneous tunnel at the base of the palm and inserted on the APB tendon. Transfer of the ADQ has the advantage of restoring bulk to the thenar eminence, which is particularly important in patients with congenital thenar hypoplasia. The ADQ also has a similar length, strength, and direction of pull to the muscles that it is replacing. The EIP opponensplasty, described in 1956 by ChouhyAguirre and Zancolli and popularized by Burkhalter, is our opponensplasty of choice (▶ Fig. 17.7).20 The EIP tendon is divided as distally as possible over the proximal phalanx of the index finger and withdrawn proximal to the extensor retinaculum through a distal dorsal forearm incision. It is passed subcutaneously to a small incision at the ulnar side of the wrist. The EIP tendon is then tunneled across the palm subcutaneously and inserted at the APB insertion. The EIP is an excellent donor choice because it has adequate length and strength, no pulleys are required (the ulna serves as

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the pulley), and its transfer results in minimal functional loss to the index finger. It is important to repair the index finger sagittal band and to suture the distal stump of the EIP to the adjacent index EDC in order to minimize extension lag at the MCP joint. An alternative transfer is the EDQ opponensplasty. Although a weak transfer, it is strong enough to position the thumb in opposition. Like the EIP transfer, it does not require the creation of a pulley and usually does not require elongation with a tendon graft. The EDQ opponensplasty is particularly useful in situations in which other donor MTUs are not available. The palmaris longus, or Camitz, transfer is primarily used in cases of long-standing carpal tunnel syndrome associated with severe thenar wasting, resulting in loss of thumb opposition. 21 The Camitz transfer is performed at the time of carpal tunnel release. It is therefore important to plan the incision to allow harvest of the palmaris longus, which must be taken with a long extension of superficial palmar fascia. The extended palmaris longus is then transferred to the APB insertion. This transfer does not result in restoration of true opposition, but rather functions more as an abductorplasty.

Tendon Transfers for Functional Reconstruction

Fig. 17.8 Flexor digitorum superficialis (FDS) (ring)-to-abductor pollicis brevis (APB) tendon transfer. (a) The FDS tendon of the ring finger is harvested distally. (b) The FDS ring tendon is tunneled through the subcutaneous fascia toward the APB. (c) The tendon of the APB is identified. (d) The FDS ring tendon is sutured into the tendon of the APB.

The FDS tendon from the ring finger can be used to restore thumb opposition (superficialis opponensplasty) (▶ Fig. 17.8).3, 7,19 The FDS to the ring finger is harvested at to the palmar digital crease and withdrawn proximally into the palm. For the correct line of pull, a pulley must be created at the level of the pisiform. There are multiple methods for creating an opponensplasty pulley, but this can be achieved simply by creating a loop out of the radial half of the FCU tendon at the level of the pisiform. After passing the FDS through the FCU pulley, it is passed through a subcutaneous tunnel across the palm and inserted on the APB insertion. A number of problems can occur with this transfer. Adhesions may limit tendon gliding through the pulley. The pulley can lengthen or migrate, decreasing the effectiveness of the transfer. As with any FDS transfer, PIP joint hyperextension or weakening of grip strength may occur. Additionally, it should be remembered that the superficialis opponensplasty can only be performed in patients with low median nerve palsy, because the FDS is denervated in high median nerve palsy. Further complicating the issue is the fact that many low median nerve palsies are a result of a laceration at the level of the wrist, often with concomitant injury to the flexor tendons. A previously injured or repaired FDS tendon should not be used for this transfer.1 Alternative pulley options have been described for the FDS tendon transfer. Bunnell described using a loop of FCU at the

level of the pisiform. 22 Guyon canal can also be used as a pulley, although ulnar nerve compression may result. 19 The distal end of the transverse carpal ligament and the ulnar border of the palmar aponeurosis have also been described. 23 The location of the pulley will determine the line of pull of the transfer. A line of pull originating at the level of the pisiform is ideal. In general, a pulley proximal to that level will result in more palmar abduction than is necessary, and a pulley distal to that level will result in more flexion than is necessary. The choice of pulley location should be based on both surgeon preference and patient need. Postoperatively, the thumb should be held in a position of maximal opposition for 3 to 4 weeks, at which point graduated range of motion exercises are begun.

Transfers for High Median Nerve Palsy Patients with high median nerve palsy will require an opponensplasty, although the superficialis opponensplasty is not an option. A two-stage opponensplasty can be used to restore thumb opposition with FCU/FDS (▶ Fig. 17.9). In addition, patients will benefit from transfers to restore thumb and index (and sometimes long) finger flexion.3,19 Thumb IP flexion can be restored by transferring the brachioradialis or ECRB to the FPL (▶ Fig. 17.10). 3 Alternatively,

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Fig. 17.9 Flexor carpi ulnaris (FCU)/ flexor digitorum superficialis (FDS) two-stage opponensplasty. This allows for the extension of a tendon while preserving the integrity of the tendon graft. (a) In the first stage, the FDS tendon to the ring finger is distally harvested. (b) The distal end of the FDS tendon is sutured into the distal end of the FCU. (c) After the tendon junction has healed, the second-stage opponensplasty occurs. The FCU/FDS tendon junction is mobilized, and the proximal end of the FDS ring tendon is divided. (d) The FDS ring tendon is then mobilized toward the abductor pollicis brevis. (e) The FCU/FDS tendon junction is observed to be intact and healed. (f) The distal FDS ring tendon is sutured into the tendon of the abductor pollicis brevis.

IP fusion may be performed. Distal interphalangeal (DIP) flexion of the index and long fingers may be restored by side-to-side tenodesis of all four FDP tendons or by using the ECRL as a donor tendon. 3,19 Our procedure of choice is to transfer the brachioradialis to the FPL and perform a side-to-side tenodesis of the FDP of the index and long fingers to the ring and small fingers. In patients who require independent functioning of the index finger, the ECRL transfer is performed. There is no need to restore function to the index and long FDS if adequate function is restored to the FDP.

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17.3.3 Tendon Transfers for Radial Nerve Palsy Anatomy and Physical Exam The radial nerve is a continuation of the posterior cord of the brachial plexus and receives fibers from the C5, C6, C7, C8, and T1 nerve roots. It gives off branches to the triceps before entering the anterior compartment of the arm. The radial nerve then crosses anterior to the elbow between the brachioradialis and the brachialis, after which it divides into the

Tendon Transfers for Functional Reconstruction

Fig. 17.10 Brachioradialis–to- flexor pollicis longus (FPL) tendon transfer. The brachioradialis is mobilized and transferred to the FPL.

posterior interosseous nerve (PIN) and the superficial sensory branch of the radial nerve. The radial nerve proper provides motor branches to the bracioradialis and ECRL. The ECRB receives motor innervation from the radial nerve proper, the superficial branch of the radial nerve, or the PIN.24 The PIN provides innervation to the supinator, EDC, extensor carpi ulnaris (ECU), EDQ, APL, extensor pollicis longus (EPL), extensor pollicis brevis (EPB), and EIP. High radial nerve palsy results in an inability to extend the wrist, the MCP joints, and the thumb. Patients with PIN palsy (low radial nerve palsy) will have preserved radial wrist extension due to intact function of the ECRL, which is innervated prior to the branching of the PIN. In addition to a loss of extension, patients with radial nerve palsy notice substantially decreased grip strength due to an inability to stabilize the wrist during power grip.1 When examining the patient with radial nerve palsy, it is important to differentiate between IP and MCP extension. Patients with isolated radial nerve palsy will have preserved IP joint extension, and this should not be mistaken for intact finger extension. In addition, the patient may unconsciously use the tenodesis effect to provide a small amount of MCP extension. The surgeon should stabilize the wrist in the

neutral position when examining for MCP extension to prevent the tenodesis effect. The goals of tendon transfer for radial nerve palsy include restoration of wrist extension, MCP extension, and thumb extension. Tendon transfers for radial nerve palsy date to the late 1800s; since that time, there have been over 50 modifications described. As they are performed today, tendon transfers for radial nerve palsy are among the most reliable and effective tendon transfers. ▶ Table 17.2 lists some of the common tendon transfers for radial nerve palsy. A common combination of tendon transfers for radial nerve palsy includes 1) pronator teres to ECRB; 2) FCR to EDC; and 3) PL to EPL (▶ Figs. 17.11–17.32).

Transfers to Restore Wrist Extension The pronator teres is most commonly used to restore wrist extension and is our preferred donor MTU (▶ Fig. 17.12; ▶ Fig. 17.13).3 It is typically transferred to the ECRB, because insertion on the ECRL can result in excessive radial deviation of the wrist (▶ Fig. 17.22). The pronator teres is a good donor MTU because it is of adequate strength and preserves the wrist flexors for other uses. The pronator teres–to-ECRB transfer can be

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Tendon Transfers for Functional Reconstruction performed early after high radial nerve injury, acting as an internal splint while the nerve regenerates. In these situations, it is best to perform the tendon transfer in an end-to-side fashion using a Pulvertaft weave, so that the ECRB can contribute to

wrist extension when it becomes reinnervated (▶ Fig. 17.24; ▶ Fig. 17.25; ▶ Fig. 17.26). When reinnervation is not anticipated, the transfer should be done in an end-to-end fashion, to create a straighter and more effective line of pull. When harvesting the pronator teres at its insertion, it is important to include a strip of periosteum along with the tendon. Because the pronator teres tendon is short, the additional length provided by the periosteal extension makes insertion using a Pulvertaft weave possible (▶ Fig. 17.14; ▶ Fig. 17.15).

Transfers to Restore Finger Extension

Fig. 17.11 Orientation for tendon transfers for radial nerve palsy. A long incision is made over the volar forearm to expose the donor tendons (pronator teres, flexor carpi radialis, and palmaris longus) and a recipient tendon (extensor carpi radialis brevis [ECRB]). A second, shorter incision is made over the dorsal distal forearm to expose the recipient tendons (extensor digitorum communis [EDC] and extensor pollicis longus [EPL]). A third short incision is made at the base of the thumb to mobilize and reroute the extensor pollicis longus. In a smaller arm, this tendon transfer can be achieved with one long, volar incision that can be reflected dorsally to access the recipient tendons.

Because finger extension and wrist flexion are synergistic, either the FCU or FCR can be used to restore digital extension. Our tendon transfer of choice to restore finger extension is the FCR-to-EDC transfer (▶ Fig. 17.27; ▶ Fig. 17.28; ▶ Fig. 17.29). There are a number of reasons for this: 1. The FCU is stronger than the FCR, and its sacrifice results in substantial weakening of wrist flexion and loss of the dartthrowing motion. 2. Harvest of the FCU removes the only remaining ulnar deviator of the wrist, resulting in radial deviation, particularly in patients with PIN palsy. 3. The FCU has a shorter tendinous portion and a more distal muscle belly that requires significant proximal dissection. The FCR can be transferred subcutaneously around the radial or ulnar borders of the distal forearm (▶ Fig. 17.16; ▶ Fig. 17.23; ▶ Fig. 17.27), or through the interosseous membrane. It is usually passed around the ulnar border of the wrist/distal

17 Fig. 17.12 Exposure and identification of the donor pronator teres. The pronator teres tendon is identified between the radial vessels and the superficial branch of the radial nerve. The radial sensory nerve is located deep to the brachioradialis and is exposed by retracting the brachioradialis laterally.

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Fig. 17.13 Exposure of the pronator teres and its periosteal extension for mobilization. A long exposure is needed to mobilize the pronator teres and its periosteum attachment. The periosteum is exposed distally to acquire sufficient length for the pronator teres–to-ECRB tendon transfer.

17 Fig. 17.14 Mobilizing the pronator teres periosteum from the radius. A curved elevator is used to release the periosteum from the radius, allowing for additional length of the pronator teres tendon.

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Fig. 17.15 Release of the pronator teres tendon from the radius. The pronator teres tendon and its periosteal attachment are released from the radius for the pronator teres–to-ECRB tendon transfer.

17 Fig. 17.16 Identifying the donor flexor carpi radialis (FCR). The FCR is identified superficially in the volar forearm. The incision is extended distally to expose its tendon for mobilization for transfer.

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Fig. 17.17 Identifying the donor palmaris longus. The palmaris longus is identified just medial to the flexor carpi radialis and is exposed distally for mobilization for transfer. When exposing the palmaris longus, it is especially important to protect the median nerve. The muscle attachments to the surrounding fascia are freed to ensure good excursion.

17 Fig. 17.18 Identifying the recipient EDC. The EDC is identified through a second dorsal incision proximal to the extensor retinaculum. Individual EDC tendons are identified and confirmed by tugging on the respective tendons and observing for finger extension. The extensor indicis proprius (EIP) is not used for this tendon transfer. Avoid dividing the extensor retinaculum distally, as this will cause bowstringing.

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Fig. 17.19 Identifying the recipient EPL. The EPL is identified deep and lateral to the EDC. It can be identified by tugging on the tendon and observing thumb interphalangeal joint extension.

17 Fig. 17.20 Identifying the EPL tendon through a second incision. An incision is made at the base of the thumb to mobilize the EPL tendon. At this location, the superficial branch of the radial nerve is identified and protected adjacent to the EPL. In this case of complete radial nerve palsy, however, this sensory nerve is nonfunctioning.

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Fig. 17.21 Rerouting the EPL tendon. The EPL is divided proximally at the dorsal forearm to mobilize its tendon. The EPL tendon is then rerouted to the volar exposure for the palmaris longus-to-EPL tendon transfer.

17 Fig. 17.22 Identifying the recipient ECRB. The ECRB is located radial to the extensor carpi radialis longus (ECRL). The ECRL is found dorsal to the brachioradialis. The superficial sensory branch can be noted to have a course between the brachioradialis and the ECRL.

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Fig. 17.23 Dividing the donor tendons of the pronator teres, flexor carpi radialis (FCR), and palmaris longus. The donor tendons are divided distally to mobilize for tendon transfers.

17 Fig. 17.24 Identifying the donor pronator teres–to-recipient ECRB tendon transfer. The pronator teres is passed over the brachioradialis and ECRL to attach to the ECRB using a Pulvertaft weave. The first setting of the weave should be tendon to tendon. The periosteal extension of the pronator teres will be used to bolster the strength of the tendon transfer distally.

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Fig. 17.25 Setting the tension for the pronator teres-to-ECRB tendon transfer. The tension is set with the first juncture of the repair being tendon to tendon. The tension is set with the wrist extended and the ability to passively flex the wrist.

17 Fig. 17.26 Pronator teres-to-ECRB tendon transfer. The repair is made with a Pulvertaft weave with three to five passes. The Pulvertaft weave is used without dividing the recipient tendon in case the radial nerve eventually reinnervates to some degree.

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Fig. 17.27 Mobilizing the flexor carpi radialis (FCR) tendon through the dorsal exposure. The FCR is mobilized and passed to the dorsal forearm to weave into the EDC. The FCR-to-EDC tendon transfer is completed with the wrist/fingers in extension.

17 Fig. 17.28 Weaving the FCR tendon through the EDC tendons. The FCR tendon is weaved through all four EDC tendons and should not include the EIP.

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Fig. 17.29 FCR–to-EDC tendon transfer. The first juncture of the weave sets the tension with the wrist/fingers in extension. After setting the tension, additional weaves through the EDC will secure this tendon transfer.

17 Fig. 17.30 The EPL is rerouted to the anterior exposure. The EPL is rerouted anteriorly for the palmaris longus-to-EPL tendon transfer. The tension is set for this repair with the thumb/wrist in extension.

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Fig. 17.31 Setting the tension for the palmaris longus-to-EPL tendon transfer. The EPL was rerouted anteriorly. The palmaris longus will attach to the EPL in a Pulvertaft weave. Tension for this repair is set with the thumb/wrist in extension. Once the tension is set, the thumb should still be able to be passively flexed.

17 Fig. 17.32 Palmaris longus-to-EPL tendon transfer. The tendon transfer is completed with a Pulvertaft weave using the palmaris longus and EPL. Tension is checked following the first suture and after completing the weave.

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Tendon Transfers for Functional Reconstruction forearm to prevent excess radial deviation. In addition, keeping it to the ulnar side of the wrist leaves the radial side of the wrist and forearm free for transfers to restore thumb extension.3 The extensor tendons can be left under the extensor retinaculum and the transfer performed proximal to the extensor retinaculum (▶ Fig. 17.18; ▶ Fig. 17.28). This results in a direction change that may cause some weakening of the transfer. However, it results in a better orientation of the extensor tendons and prevents bowstringing. Alternatively, the extensor tendons can be withdrawn distally from the extensor retinaculum and the transfer performed superficial to the extensor retinaculum. This results in a straighter line of pull and a potentially stronger transfer, but it also creates a less natural line of pull. Because the excursion of the FCR (33 mm) is inadequate to fully extend the MCP joints, finger extension must be augmented with the tenodesis effect. It should be remembered that patients who undergo wrist arthrodesis will not be able to use the tenodesis effect to augment finger extension. In this situation, the FDS transfer (70-mm excursion) should be considered. The Boyes transfer uses the FDS as a donor for restoring finger extension.25 The FDS tendon is identified through a small incision over the A1 pulley in the palm. The FDS is harvested at this level rather than distally over the proximal phalanx because harvesting the FDS tendon distally can cause a loss of volar support to the PIP joint and may result in a hyperextension deformity. The FDS is withdrawn into a longitudinal incision in the volar forearm, then passed around the distal forearm or through the interosseous membrane to insert into the digital extensors. If transferred through the interosseous membrane, the opening should be made just proximal to the pronator quadratus and should be large to minimize adhesion formation. Boyes described using the FDS of the long finger to restore EDC function, and the FDS of the ring finger to restore EIP and EPL function.25

Transfers to Restore Thumb Extension Although normal thumb function requires a functioning EPL, EPB, and APL, satisfactory function can be gained by simply restoring the EPL.3 The palmaris longus is the most commonly used MTU for restoring thumb extension and is our transfer of choice (▶ Fig. 17.30; ▶ Fig. 17.31; ▶ Fig. 17.32). It is transferred around the radial border of the wrist to the EPL, which should be released from its fibro-osseous tunnel and transposed radially (▶ Fig. 17.20; ▶ Fig. 17.21; ▶ Fig. 17.30). Transposing the EPL out of the third extensor compartment allows a straighter line of pull, which is important for a weak motor like the palmaris longus. In addition, it allows the tendon transfer to provide some degree of radial abduction in addition to IP extension. Care must be taken to avoid overtightening of the transfer, as this will result in hyperextension of the MCP joint of the thumb. If the palmaris longus is not available, the ring FDS is commonly used to restore thumb extension.

17.3.4 Tendon Transfers for Elbow Function Indications Loss of elbow flexion significantly limits the usefulness of the upper extremity. If the hand cannot be positioned in space by

controlled movement at the elbow, the presence of normal hand movement is of diminished use. The most common indication for tendon transfers to restore elbow flexion is a brachial plexus injury in which nerve repair, reconstruction, or transfer has failed. In addition, if neurologic reconstruction does not result in M4 or greater function, then a tendon transfer to augment the strength of elbow flexion can be considered. Less commonly, tendon transfers for elbow flexion may be considered in patients with tetraplegia, in patients with congenital upper extremity differences such as arthrogryposis, and in extremities with loss of muscle or tendon substance. Elbow extension is less important for hand positioning because it can be compensated for by gravity. Although elbow extension is less crucial than flexion, in select situations tendon transfers may be indicated to restore elbow extension.

Transfers for Elbow Flexion Multiple tendon transfers have been described for the restoration of elbow flexion. The pectoralis major and minor, latissimus dorsi, and triceps muscles may be transferred to the biceps to provide elbow flexion. The Steindler flexorplasty differs from the above transfers and involves the proximal transposition of the origin of the flexor pronator mass, thereby converting it to an elbow flexor. Other transfers, such as the sternocleidomastoid transfer described by Bunnell, are of primarily historical interest.26

Steindler Flexorplasty First described by Steindler in 1918, the modified procedure described by Mayer and Green is the basis of the operation performed today.27,28 Because the Steindler flexorplasty involves the proximal transposition of the flexor-pronator mass from the medial epicondyle, the forearm flexors and pronator teres must be innervated and have good strength. By moving the origin of these muscles proximally, their moment arm across the elbow is increased, allowing them to act as elbow flexors. A curvilinear incision is made over the medial arm and forearm, centered over the medial epicondyle. The incision should extend at least 10 cm above and below the elbow. In the forearm, the incision overlies the pronator teres, and in the arm it should curve anteriorly toward the midline. The skin is incised, and the skin flaps are elevated, taking care to preserve the medial antebrachial cutaneous nerve. The ulnar nerve is identified and dissected as in an ulnar nerve transposition, taking care to preserve the motor branches to the FCU. Next, the median nerve and brachial artery are identified in the proximal aspect of the incision. The median nerve is dissected in a proximal-to-distal direction into the proximal forearm. Motor branches, including those to the pronator teres, FCR, FDS, and palmaris longus, must be carefully preserved. Once the nerve dissections have been performed, an epicondylectomy is performed. This can be done with an osteotome or a sagittal saw. The epicondyle fragment should be ~ 2.5 cm in diameter and ~ 5.0 mm thick. Care should be taken to avoid injury to the medial collateral ligament of the elbow. The medial epicondyle is then grasped with a clamp, and gentle distal traction is provided. The flexor muscles and pronator teres are dissected free from the anterior surface of the elbow

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Tendon Transfers for Functional Reconstruction joint and from the anterior surface of the ulna. During this process, it is important to preserve the motor branches from both the median and ulnar nerves. The dissection is performed as far distally as necessary to allow proximal transposition of the medial epicondyle by 5 to 7 cm. The elbow must be flexed to 120 to 130 degrees to allow full proximal transposition. While protecting the median nerve and brachial artery, the denervated brachialis muscle is divided longitudinally down to the anterior surface of the humerus. Subperiosteal dissection is performed, and a bur is used to roughen the cortical bone, preparing a site for the epicondyle. The epicondyle should be transposed 5 to 7 cm proximal to its original location and should be transferred to the anterior, not medial, surface of the humerus. This anterior position improves supination and helps prevent pronation contracture. Fixation is performed with a 3.5-mm bicortical screw. The medial epicondyle drill hole can be enlarged or overdrilled and a washer used to lag the medial epicondyle fragment to the humerus. The tourniquet is let down, hemostasis is achieved, and the skin is closed. The elbow is splinted in 120 degrees of flexion until bony union is achieved, followed by progression of active motion. No attempt should be made to overcome the resultant flexion contracture of the elbow. It should be noted that the technique works best in patients who have some degree of preoperative Steindler effect (augmentation of elbow flexion strength, or maintenance of elbow flexion position by forceful wrist and/or finger flexion, with pronation).29 One limitation of the Steindler flexorplasty is that the transferred muscles cannot be used for tendon transfers in the hand. Patients should be counseled preoperatively that an elbow flexion contracture of 30 to 50 degrees is expected. This flexion contracture increases the mechanical advantage of the transfer, and no attempt should be made to correct it. When used in patients with a preoperative Steindler effect, a functional range of motion can be expected. Lifting power will not likely exceed 5 lbs. (2.3 kg).29

Triceps-to-Biceps Transfer The anterior transposition of the triceps to the biceps for restoration of elbow flexion was first described by Bunnell in 1948 and subsequently modified and popularized by Carroll. 30,31 The primary drawback of the triceps-to-biceps transfer is the resultant loss of elbow extension. Elbow extension is somewhat compensated for by gravity, but loss of active elbow extension results in difficulty with activities such as using crutches, turning the wheels of a wheelchair, and pushing up from a lying or sitting position. It also limits the ability to lift the hands above the head. Alternatively, the long head of the triceps can be selectively transferred, preserving active elbow extension, as described by Haninec and Szeder and Naidu et al.32,33 The long head of the triceps is functionally and electromyographically independent from the other two heads and can be used selectively for transfer. Although an attractive option, selective transfer of the long head of the triceps has not been extensively studied. The operative technique for the triceps transfer was described by Carroll and Hill.34 A midline longitudinal incision is made on the posterior arm, extending distally across the olecranon and along the subcutaneous border of the proximal one-third of the ulna. Skin flaps are elevated. The ulnar

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nerve is exposed medially at the elbow and is protected. Working in a distal-to-proximal direction, a long strip of periosteum is raised from the ulnar shaft in continuity with the triceps tendon insertion. The triceps is then mobilized from the distal one-third of the humeral shaft, protecting the radial nerve. The tendinous portion of the flap is rolled and sutured into a tube in preparation for transfer. The biceps tendon is exposed through an incision in the antecubital fossa, and a subcutaneous tunnel is created laterally between the antecubital incision and the posterior incision. The tubed triceps tendon is passed through the tunnel and inserted on the biceps tendon using a Pulvertaft weave. This should be done with maximum tension on the transfer with the elbow in 90 degrees of flexion and the forearm supinated. The elbow is immobilized at 90 degrees for 4 weeks before active flexion is started. Carroll and Hill presented a series of 15 patients with arthrogryposis or paralytic disorders treated with tricepsto-biceps transfer. 34 In the six patients with paralytic disorders, the active range of motion against gravity ranged from 90 to 135 degrees, with the exception of one patient who fell and disrupted the tendon transfer. In 1998 Rostoucher et al published a series of 60 patients who underwent tendon transfers to restore elbow flexion, 26 of which were triceps-to-biceps transfers. 35 Of the 26 triceps transfers, 12 patients had very good results (120 degrees of active flexion with motor grade of 4 or 5), and 10 had good results (< 120 degrees, but with motor grade of 4 or 5). One of the 26 transfers failed.

Pectoralis-to-Biceps Transfer Pectoralis transfers for elbow flexion have been described using the pectoralis major, pectoralis minor, or both.26,36 The use of the pectoralis muscle for flexorplasty was first described by Schulze-Berge in 1917, in which a portion of the biceps tendon was turned proximally and sutured to the pectoralis major, a technique no longer employed today.37 In 1946 Clark described the transfer of the pectoralis major muscle for restoring elbow flexion.38 Although variations exist, the pectoralis tendon is usually elongated with a fascia lata graft, allowing insertion on the biceps tendon.39 A curvilinear incision is made across the antecubital fossa, and the biceps tendon is dissected out. A subcutaneous tunnel extending from the antecubital fossa to the anterior axillary fold is created bluntly. Next, an incision is made from the anterior shoulder down the upper arm along the insertion of the pectoralis tendon. The pectoralis major tendon is circumferentially dissected and freed from the humerus, followed by partial mobilization of the muscle on its anterior and posterior surfaces. A fascia lata graft is obtained from the thigh, measuring approximately 20 × 10 cm. The fascia lata graft is rolled and sutured into a tube, then is passed through the subcutaneous tunnel. It is inserted on the biceps tendon using a Pulvertaft weave. The distal incision is closed, and the elbow is flexed to 90 degrees. The fascia lata graft is then inserted into the pectoralis tendon under maximum tension. The elbow is immobilized for 3 to 4 weeks prior to starting active motion. One drawback of the pectoralis transfer is that it can result in internal rotation of the shoulder. In addition, using the pectoralis for a tendon transfer may further weaken an already weak

Tendon Transfers for Functional Reconstruction shoulder. In some patients it may destabilize the shoulder enough that a shoulder arthrodesis is required. In a series published by Beaton et al, patients had a mean postoperative arc of motion of ~ 90 degrees, similar to that obtained following Steindler flexorplasty in their series.39

Latissimus Dorsi-to-Biceps Transfer The latissimus dorsi can also be used to restore elbow flexion. Unlike the triceps and pectoralis transfers, the latissimus transfer is often performed as a “bipolar” muscle transfer, involving division of both the origin and insertion of the latissimus dorsi.40 The latissimus dorsi muscle is transferred to the bed of the biceps, rotated on its neurovascular pedicle. The insertion of the latissimus is weaved into the proximal tendinous origin of the biceps at the coracoid process, and the fibrous origin of the latissimus is weaved into the biceps tendon distally at the elbow. Like the pectoralis transfer, latissimus transfers may result in destabilization of the shoulder.

17.4 Conclusion When nerve repair or reconstruction fails or is not possible, tendon transfers may be used to improve upper extremity function. Adherence to the principles of tendon transfer and close attention to surgical technique are important in order to prevent complications and optimize outcomes.

17.5 References [1] Sammer DM, Chung KC. Tendon transfers: 1. Principles of transfer and transfers for radial nerve palsy. Plast Reconstr Surg 2009;123:169e–177e [2] Boyes JH. Selection of a donor muscle for tendon transfer. Bull Hosp Jt Dis 1962;23:1–4 [3] Richards RR. Tendon transfers for failed nerve reconstruction. Clin Plast Surg 2003;30:223–245, vivi. [4] Fridén J, Lieber RL. Evidence for muscle attachment at relatively long lengths in tendon transfer surgery. J Hand Surg Am 1998;23:105–110 [5] Lieber RL, Fridén J. Intraoperative measurement and biomechanical modeling of the flexor carpi ulnaris-to-extensor carpi radialis longus tendon transfer. J Biomech Eng 1997;119:386–391 [6] Riordan DC. Tendon transplantations in median-nerve and ulnar-nerve paralysis. J Bone Joint Surg Am 1953;35-A:312–320, passimpassim. [7] Sammer DM, Chung KC. Tendon transfers: 2. Transfers for ulnar nerve palsy and median nerve palsy. Plast Reconstr Surg 2009;124:212e–221e [8] Kalainov DM, Cohen MS. Tendon transfers for intrinsic function in ulnar nerve palsy. Atlas Hand Clin 2002;7:19–39 [9] Leibovic SJ, Hastings H. Martin-Gruber revisited. J Hand Surg Am 1992;17:47–53 [10] Bouvier SHV. Note sur une paralysie partielle des muscles de la main. Bull Acad Nat Med (Paris) 1851;18:125 [11] Zancolli EA. Claw-hand caused by paralysis of the intrinsic muscles: a simple surgical procedure for its correction. J Bone Joint Surg Am 1957;39-A:1076– 1080

[12] Tse R, Hentz VR, Yao J. Late reconstruction for ulnar nerve palsy. Hand Clin 2007;23:373–392, viivii. [13] Burkhalter WE, Strait JL. Metacarpophalangeal flexor replacement for intrinsic-muscle paralysis. J Bone Joint Surg Am 1973;55:1667–1676 [14] Stiles HJ, Forrester-Brown MF. Treatment of Injuries of the Peripheral Spinal Nerves. London: Henry Frowde and Hodder & Stoughton; 1922 [15] Bunnell S. Surgery of the intrinsic muscles of the hand other than those producing opposition of the thumb. J Bone Joint Surg Am 1942;24:1–31 [16] Smith RJ. Extensor carpi radialis brevis tendon transfer for thumb adduction —a study of power pinch. J Hand Surg Am 1983;8:4–15 [17] Blacker GJ, Lister GD, Kleinert HE. The abducted little finger in low ulnar nerve palsy. J Hand Surg Am 1976;1:190–196 [18] Littler JW, Cooley SG. Opposition of the thumb and its restoration by abductor digiti quinti transfer. J Bone Joint Surg Am 1963;45:1389–1396 [19] Brand PW. Tendon transfers for median and ulnar nerve paralysis. Orthop Clin North Am 1970;1:447–454 [20] Burkhalter W, Christensen RC, Brown P. Extensor indicis proprius opponensplasty. J Bone Joint Surg Am 1973;55:725–732 [21] Terrono AL, Rose JH, Mulroy J, Millender LH. Camitz palmaris longus abductorplasty for severe thenar atrophy secondary to carpal tunnel syndrome. J Hand Surg Am 1993;18:204–206 [22] Bunnell S. Opposition of the thumb. J Bone Joint Surg Am 1938;20:269–284 [23] Thompson TC. A modified operation for opponens paralysis. J Bone Joint Surg Am 1942;26:632–640 [24] Abrams RA, Ziets RJ, Lieber RL, Botte MJ. Anatomy of the radial nerve motor branches in the forearm. J Hand Surg Am 1997;22:232–237 [25] Chuinard RG, Boyes JH, Stark HH, Ashworth CR. Tendon transfers for radial nerve palsy: use of superficialis tendons for digital extension. J Hand Surg Am 1978;3:560–570 [26] Bunnell S. Restoring flexion to the paralytic elbow. J Bone Joint Surg Am 1951;33-A:566–571, passim [27] Steindler A. Orthopedic reconstruction work on hand and forearm. New York Medical Journal 1918;108:1117–1119 [28] Mayer L, Green W. Experiences with the Steindler flexorplasty at the elbow. J Bone Joint Surg Am 1954;36-A:775–789, passim [29] Hentz VR, Doi K. Traumatic brachial plexus injury. In: Green DP, Hotchkiss RN, Pederson WC, Wolfe SW, eds. Green’s Operative Hand Surgery. 5th ed. Philadelphia, PA: Elsevier; 2005:1319–1371 [30] Bunnell S. Surgery of the Hand. 2nd ed. Philadelphia, PA: JB Lippincott; 1948 [31] Carroll RE. Restoration of flexor power to the flail elbow by transplantation of the triceps tendon. Surg Gynecol Obstet 1952;95:685–688 [32] Haninec P, Szeder V. Reconstruction of elbow flexion by transposition of pedicled long head of triceps brachii muscle. Acta Chir Plast 1999;41:82–86 [33] Naidu S, Lim A, Poh LK, Kumar VP. Long head of the triceps transfer for elbow flexion. Plast Reconstr Surg 2007;119:45e–47e [34] Carroll RE, Hill NA. Triceps transfer to restore elbow flexion: a study of fifteen patients with paralytic lesions and arthrogryposis. J Bone Joint Surg Am 1970;52:239–244 [35] Rostoucher P, Alnot JY, Touam C, Oberlin C. Tendon transfers to restore elbow flexion after traumatic paralysis of the brachial plexus in adults. Int Orthop 1998;22:255–262 [36] Segal A, Seddon HJ, Brooks DM. Treatment of paralysis of the flexors of the elbow. J Bone Joint Surg Br 1959;41-B:44–50 [37] Schulze-Berge VSR. Ersatz der beuger des vorderarmes (bizeps and brachialis) durch den pectoralis major. Deutsche Med Wochenschr 1917;43:433 [38] Clark JMP. Reconstruction of biceps brachii by pectoral muscle transplantation. Br J Surg 1946;34:180 [39] Beaton DE, Dumont A, Mackay MB, Richards RR. Steindler and pectoralis major flexorplasty: a comparative analysis. J Hand Surg Am 1995;20:747–756 [40] Zancolli E, Mitre H. Latissimus dorsi transfer to restore elbow flexion: an appraisal of eight cases. J Bone Joint Surg Am 1973;55:1265–1275

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Tumors of the Peripheral Nervous System

18 Tumors of the Peripheral Nervous System John R. Barbour and Kirsty U. Boyd

18.1 Introduction Peripheral nerve sheath tumors (PNSTs) constitute less than 5% of tumors of the extremities and are an infrequent finding for even those surgeons specializing in peripheral nerve disorders. A limited number of large series have been published over the past 2 decades, attempting to summate the experience of managing these rare tumors at medical centers specializing in tertiary care management (▶ Table 18.1). Symptoms of a nerve tumor can include pain, palpable masses or thickening in the extremity, paresthesias, and weakness. Diagnosis can be facilitated with magnetic resonance imaging (MRI), ultrasonography, computed tomography (CT), ultrasound, or electromyography (EMG), although the findings are often inconclusive until surgical exploration and biopsy. 1 The majority of PNSTs are benign schwannomas or neurofibromas (▶ Fig. 18.1); however, many other benign tumors can involve peripheral nerves, including lipofibromatous hamartomas, granular cell tumors, perineuromas, intraneural ganglion cysts, lipomas, desmoid tumors, and intraneural hemangiomas. Clinically, it is important to distinguish between schwannomas and neurofibromas due to the higher risk of nerve dysfunction after attempted neurofibroma excision. Malignant transformation of PNSTs is rare. Identification of malignant PNSTs is important because they are associated with a high rate of recurrence, morbidity, and mortality. The plexiform subtype of neurofibromas should also be distinguished from other subtypes of schwannomas and neurofibromas because such neurofibromas pose a substantial risk of malignant degeneration or recurrence. When associated with neurofibromatosis, malignant transformation occurs with an incidence upward of 10%, with nerve sheath cell sarcoma occurring much more frequently than malignant schwannomas.

18.2 Neoplasms of Nerve Sheath Origin 18.2.1 Historical Background Friedrich von Recklinghausen10 first emphasized the relationship between the tumors of the skin and the nerves in neurofibromatosis in 1882. Although later determined to be a sufferer of Proteus syndrome, Joseph Merrick (the “Elephant Man”) was presented in 1884 as a dramatic case of neurofibromatosis by British surgeon Frederick Treves, which brought much media attention to the condition. The condition as it was described by von Recklinghausen, now called neurofibromatosis type 1 (NF1), accounts for ~ 90% of all cases of neurofibromatosis. In 1910 Verocay11 postulated that some peripheral nerve tumors arose from Schwann cells, and molecular studies have shown the origin is from neural crest cells due to disruption in nerve growth factor. Stout12 introduced the term neurolemmoma in 1935. This term was replaced by the more appropriate schwannoma by Ehrlich and Martin in 1943.13 Neurolemmoma, which referred to the neuroectodermal origin, is considered less specific than the term schwannoma, which refers to the cell type involved.

18.2.2 Schwannoma Schwannomas arise from the nerve sheath and can occur anywhere within the peripheral nervous system. In general, they grow slowly and present with a palpable mass with few or absent neurologic deficits. The eighth cranial nerve is involved more than any other cranial nerve, and a tumor at this location is referred to as an acoustic neuroma. The clinical presentation of acoustic neuroma is quite variable; however, most patients with an acoustic neuroma present with unilateral hearing loss, tinnitus, and vestibular symptoms. Patients with larger

Table 18.1 Epidemiology of Peripheral Nerve Sheath Tumors Reference

No. of Patients

Years Enrolled

Corresponding Institution

120

1912–1983

Mayo Clinic, Rochester, MN

104

1959–1990

Western Infirmary, Glasgow, Scotland

Donner et al4

288

1968–1991

Louisiana State University, New Orleans

Artico et al5

119

1980–1995

La Sapienza University, Rome, Italy

Wong et al6

134

1975–1993

Mayo Clinic, Phoenix, AZ

Cashen et al7

80

1972–1997

Massachusetts General Hospital, Boston

Kim et al8

546

1969–1999

Stanford University, Palo Alto, CA Louisiana State University, New Orleans

Anghileriet al9

205

1976–2002

Istituto Nazionale dei Tumori, Milan, Italy

Ducatman et Kehoe et

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al2

al3

Tumors of the Peripheral Nervous System

Fig. 18.1 Illustrations of typical schwannoma and neurofibroma appearance and morphology. (a) Typical schwannoma appearance, with crosssectional view. Notice that normal, unaffected fascicles run around the tumorous mass and are displaced outwardly. (b) Typical neurofibroma appearance, with cross-sectional view at the midportion of the mass. Notice that all fascicles are affected and intertwined within the mass. No normal fascicles exist for exclusion. (Used with permission from Mackinnon SE, Dellon AL, eds. Surgery of the Peripheral Nerve. New York, NY: Thieme;1988:541.)

tumors may develop trigeminal nerve dysfunction, facial nerve dysfunction, and symptoms of increased intracranial pressure. Brainstem and cerebellar compressive symptoms present in the very late stage of the disease with massive tumor and manifest as ipsilateral upper or lower extremity dysfunction, ataxia, and gait disturbance. Schwannomas tend to be solitary but can be numerous, and multiple schwannomas along a single nerve path have been reported. Solitary schwannomas that are enucleated very rarely recur, and malignant transformation in a solitary schwannoma has been reported in only 12 cases in the literature. Patients with peripheral nerve tumors are frequently asymptomatic, occasionally reporting only a small palpable tumor mass. There may be some sensory disruption, and palpation of the nerve may lead to a provocative Tinel-like response. When palpable, the tumor may be mobile in a transverse, or side-to-side, but not along the long axis of the nerve. Clinically, schwannomas may mimic a lipoma or ganglion at the level of the skin. Schwannomas within the spinal canal may assume a dumbbell shape that extends into or out of the canal along a nerve root. Compression of the spinal cord can lead to weakness, numbness, stiffness, trouble controlling bladder or bowel function, and paralysis. Compression of the nerve root can lead to pain shooting down the arms or legs, weakness, or numbness.

Incidence Schwannomas are the most common peripheral nerve tumors in adults, with a peak onset between 30 and 50 years of age,

although all ages can be affected. They present with an overall equal gender distribution, although there is a 2:1 female predominance with cranial nerve and intracranial lesions. Schwannomas comprise ~ 8% of all intracranial tumors and ~ 29% of primary spinal tumors, but they remain uncommon in the peripheral nerve distribution, representing < 5% of tumors within the hand.14,15 Studies have also shown a disproportionately higher incidence of schwannomas within the upper extremities, occurring twice as often as in the lower extremity. 3 This is in contrast to neurofibromas, which are equally distributed throughout the nervous system.

Histology The electron microscopic characteristics of Schwann cells demonstrate a double basement membrane, which differentiates a Schwann cell from a fibroblast. Although the epineurium of the peripheral nerve is composed of fibroblasts, the perineurium is composed of perineural fibroblasts, which closely resemble the basement membrane of Schwann cells. These perineural cells are variants of traditional Schwann cells, although they do not produce myelin. These cells give rise to more invasive neurofibromas and the Schwann cells to less invasive schwannomas. Nerve fibers are not found within the schwannoma itself. The schwannoma itself tends to displace the fascicles of the nerve outwardly, causing them to appear stretched out over the tumor. On gross examination, schwannomas are encapsulated and on transverse sectioning are either solid or cystic. Histologically, there are two pattern types of schwannomas, Antoni A

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Tumors of the Peripheral Nervous System and Antoni B. Both types may be found within the same tumor. An Antoni A pattern is characteristically cellular, made up of spindle-shaped cells that often can align themselves into a palisade formation (Verocay bodies). Collagen fibers, produced by the Schwann cell, may be found within these highly cellular tumors. The Antoni B pattern is less cellular, with a loose arrangement of spindle cells in a clear, mucinous matrix. The neoplastic cells are spindle cells that stain for S-100 and Leu-7. Secondary changes, including hyalinization, cysts, microhemorrhages, and even mineralization, are observed. A schwannoma initiates from a single fascicle within the main nerve and displaces the rest of the nerve.

Variants Variants of schwannomas include ancient, cellular, and melanotic. Many cases previously assumed to be malignant schwannomas are in fact benign cellular schwannomas. Cellular schwannomas are a rare variant of the benign schwannoma that demonstrate hypercellularity and nuclear atypia. A differentiation between benign cellular and malignant schwannomas is that in the former, no more than six mitotic figures per 40 highpowered fields (HPFs) are noted, and no areas of frank necrosis are seen. Necrosis is typically not present in the cellular schwannomas variant, as it is in malignant schwannomas. Likewise, central cystic formation within the tumor on CT or MRI is more characteristic of a benign schwannoma. Ultrasound examination has been recommended for the differentiation. These tumors highlight the necessity of making a histologic diagnosis of the nature of the peripheral nerve tumor with careful pathologic analysis. Prognosis of a benign cellular schwannoma is equal to that of other benign schwannomas.

Radiologic Evaluation In the case of tumors intrinsic or extrinsic to nerves, MRI may be useful in planning surgical resection and can also help identify anatomical situations in which en bloc resection is not advised. High-resolution MRI (magnetic resonance neurography [MRN]) allows the identification and characterization of lesions primarily and secondarily affecting nerves, the relation to surrounding important anatomical structures, and the extent of intrinsic or extrinsic nerve involvement. MRN can often differentiate between neurofibromas and schwannomas based on characteristic findings and an understanding of the intraneural anatomy. Neurofibromas are usually centrally located within the nerve sheath and have fascicles running through the tumor, often expanding the tumor in fusiform fashion. Schwannomas, by contrast, are usually eccentrically located and are more encapsulated than neurofibromas. MRI is helpful in differentiating between these two tumors, with an accuracy of 60 to 79%. 16 Neurofibromas more commonly demonstrate a target sign, which is a peripheral, hyperintense rim and a central hypointense region on a T2-weighted MRI. Schwannomas more commonly have diffuse contrast enhancement on a T1-weighted MRI (▶ Fig. 18.2). Most PNSTs are hypoechoic on ultrasound and have posterior acoustic enhancement, making their appearance simulate that of a ganglion cyst. If so, blood flow on color and Doppler sonography can distinguish a PNST from a cystic lesion. If a solid mass

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is identified, peripheral nerve continuity should be evaluated, because continuity would suggest a PNST rather than a separate mass. Although MRI and ultrasound can be used to assist in differentiating between benign and malignant tumors, these techniques are not consistently reliable.14 The presence of a target sign is mildly suggestive of a benign PNST, whereas gallium uptake by the tumor is suggestive of a malignant PNST.17,18 Additionally, infiltrated margins seen on ultrasound are suggestive of malignancy.19 Although a preoperative biopsy has been shown to increase the accuracy of diagnoses, the risks associated with a biopsy far outweigh the benefits. These procedures pose a risk of injuring the adjacent nerve, an increased risk of nerve injury at definitive removal, and subsequent need for nerve grafting or nerve transfer. Consequently, MRI and tertiary referral without biopsy are recommended when a PNST is suspected.

Surgical Therapy Schwannomas and neurofibromas can be completely resected with acceptable morbidity, although microscopic magnification is indicated to avoid damage to the nerve fibers. Surgery is successful in preserving function in 90% of schwannomas, 80% of neurofibromas, and 66% of neurofibromas in those with NF1. Patients whose schwannomas are treated by excision through intracapsular enucleation may have temporary sensory and/or motor dysfunction, but few have long-term neurologic deficits. Approximately 80% of patients who have benign nerve sheath tumors experience improvement or elimination of their pain. Patients who had previously undergone biopsy or surgery have poorer outcomes. Recurrences are quite rare when complete resection has been achieved. The tumor can be enucleated from the nerve without injury to any of the nerve fascicles. Excision of the nerve in order to remove the benign tumor is unacceptable in the event of schwannomas. When resection is performed by experienced nerve surgeons, these tumors can be reached in both superficial and deep locations, including the brachial plexus, lumbosacral plexus, and paraspinal region (▶ 18.3–18.14).20–23 Neighboring neural elements should be mobilized and preserved. The neural elements should be identified and protected proximally and distally to the tumor itself prior to attempting direct resection. A longitudinal epineurotomy should be made in a “bare area,” of the tumor (devoid of fascicular structure).24 Intraoperative electrophysiology or nerve stimulation can help to identify safe zones in which dissection can be performed, assist to determine functioning and nonfunctioning fascicles, and therefore facilitate resection.25,26 In schwannomas, there frequently is a single entering and exiting fascicle into the tumor (▶ Fig. 18.15). Reconstruction of this fascicle is not necessary, and neurologic effect does not occur. These fascicles have been demonstrated electrophysiologically to be nonfunctional. This is in contrast to neurofibromas, where there typically are several involved fascicles that remain functioning. In these cases, interfascicular dissection can typically preserve most functioning fascicles. The tumor may be removed as a solitary mass once the correct plane has been defined and the entering and exiting fascicles are identified. In a situation in which functioning fascicles are lost, but proximal and distal portions of the nerve can be identified, recon-

Tumors of the Peripheral Nervous System

Fig. 18.2 Schwannoma magnetic resonance imaging (MRI). (a) A large schwannoma was located within the tibial nerve. A posterior approach was taken, and the nerve was identified between the two heads of the gastrocnemius muscle. (b) The nerve was clearly identifiable on MRI of the lower extremity and can be seen as a hyperdense lesion within the lining of the tibial nerve. (c) The schwannoma was removed by opening the epineurium at a “bare area” and separating the uninvolved fascicles until the single feeding fascicle was identified.

struction can be performed using interpositional grafts or nerve conduits. If patients endorse symptoms of median nerve compression, an associated carpal tunnel release may improve symptoms, as the fibrofatty tissue is extraneural and can be excised. Permanent neurologic dysfunction is more common following resection of tumors in the proximal arm and in tumors that are immobile, painful, and > 4 cm in size.

18.2.3 Neurofibroma The neurofibromatoses are two distinct and well-described autosomal dominant genetic syndromes caused by mutations in genes coding for neurofibromin (NF1) and merlin (NF2). These deficits predispose patients to the development of both benign and malignant PNSTs. Both the schwannoma and the neurofibroma arise from a cell with a double basement membrane characteristic of a Schwann cell; however, the neurofibroma can also arise from the perineural fibrocyte that is embryologically more primitive than the Schwann cell. Unlike the schwannoma, the neurofibroma is intimately associated with nerve fibers running through the tumor (▶ Fig. 18.1b). The invasiveness within the nerve may relate to the more primitive cell of origin. Unlike the schwannoma, which is intraneural but essentially separate from the nerve tissue, nerve fibers are found within the neurofibroma itself. For this reason, it is much more com-

Fig. 18.3 Schwannoma case 1: orientation and history. A 70-year-old man presented with a painless enlarging mass on the volar aspect of the left wrist. Shown here is appropriate marking for proximal and distal access to the mass, including plans for an open carpal tunnel release.

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Fig. 18.4 Schwannoma case 1: exposure of schwannoma. A wide incision to expose the affected nerve proximally and distally was performed, including release of the carpal tunnel at the wrist. Note the fusiform swelling of the median nerve.

mon for the patient with a neurofibroma to complain of neurologic abnormalities. Four main types of neurofibromatoses have been described: central, peripheral, visceral, and forme fruste. Central neurofibromatosis is characterized by tumors of the central nervous system, including gliomas, meningiomas, schwannomas, and neurofibromas. Peripheral neurofibromatosis is characterized by multiple cutaneous tumors and plexiform neuromas. Visceral neurofibromatosis is characterized by neurofibromas and ganglioneuromas of the autonomic nervous system. The formes frustes involve a limited number of café-au-lait spots and cutaneous neurofibromas of a given region of the body (▶ 18.16–18.19).

Incidence The incidence of NF1 is 1 in 3,000 live births. The incidence of NF2, which is more severe, is 1 in 30,000 live births.24 Diagnostic criteria are presented in ▶ Table 18.2. Many patients with the disease will have trivial manifestations; however, the tendency toward malignancy, the complexity of presentations, and the high incidence of this problem make neurofibromatosis a disease entity of importance.

Histology Neurofibromatosis is a disorder of neural crest–derived cells that has a diverse clinical presentation extending from a few subcutaneous nodules to a devastating disease involving many

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organs in the body with a tendency toward malignancy. The genetic disorder involves an autosomal dominant mutant gene that has full penetrance but variable expression. Cardinal features are café-au-lait spots of the skin and neurofibromas in the peripheral, autonomic, and central nervous systems (▶Figs. 18.16–18.20). Although the schwannoma is composed almost entirely of Schwann cells, the neurofibroma is of a more mixed composition. Histologically, the tumor cells are fusiform and present in a mucoid matrix with numerous collagen fibers present. Unlike schwannomas, the nerve is involved in the tumor, and nerve fibers are present within the proper tumor itself. The majority of neurofibromas found in the skin will be solitary and not associated with neurofibromatosis. Plexiform neurofibromas are seen only in patients with neurofibromatosis and not as isolated entities (▶ Fig. 18.19). All patients with a solitary neurofibroma should be examined for clinical evidence of neurofibromatosis. Bundles of Schwann cells and axons are noted in the connective tissue matrix. Nerve fibers are seen within the tumor itself, which is a feature not found in schwannomas. Plexiform neurofibromas are clinically recognized as a mass of redundant soft tissue, with thickened nerves that occasionally can be palpated superficially through the skin. Grossly, these plexiform neurofibromas appear as tortuous swellings of nerve tissue with nodules running along the course of the nerve. It is often difficult at the time of surgery to determine whether the lesion is benign or malignant because plexiform neurofibromas have the same fusiform oval tumors along the course of the nerve trunk as do malignant schwannomas. The cut section of the malignant

Tumors of the Peripheral Nervous System

Fig. 18.5 Schwannoma case 1: identifying the longitudinal plane for resection. (a) Following a wide proximal and distal exposure of the nerve, the tumor was exposed and circumferentially controlled. Fusiform expansion of the entire median nerve was encountered with displaced fascicles at the periphery of the tumor mass. (b) The tumor was retracted and twisted to inspect the entire external surface and to locate the area with the greatest and least number of nerve fibers. (c) After circumferential inspection, an area with no superficial fascicles was identified for entering the tumor. (d) The line for incision is drawn with a surgical marker to mark the planned incision along the edge of the fascicle nearest the “bare area” of the tumor.

tumors often shows areas of hemorrhage or necrosis, and the microscopic appearance of these malignant tumors shows aggressive mitotic activity.

Variants Plexiform neurofibromas in involved nerves may result in flabby redundant tissue. In addition, there may be hypertrophy of peripheral nerve trunks or even gigantism of any involved limb. Histologically, these lesions may show elements of a normal nerve associated with a disorderly arrangement of Schwann cells, axon, and collagen. These tumors will have an anaplastic

appearance similar to fibrosarcoma, and malignant degeneration may occur. Management of an isolated plexiform neurofibroma involving a major peripheral nerve is initially managed based on findings from tissue biopsy. Plexiform lesions affecting multiple fascicles generally are not completely resectable without major neurologic compromise unless they are located within expendable branches. As long as there is little concern for malignancy, the patient can be managed nonoperatively. Resection is indicated for concern of malignant transformation; however, limited resection and internal neurolysis may be helpful for those with refractory neuropathic pain. The incidence of malignant

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Fig. 18.6 Schwannoma case 1: isolating the schwannoma. (a) A # 15 scalpel blade is used to incise the epineurium along the side of the fascicle closest to the “bare area” of the tumor. (b) A periosteal elevator is used to dissect the tumor from the nerve. (c) Posterior pressure from a finger, which is placed behind the nerve, allowed for the tumorous portion to be “pushed” out of the nerve with the help of the freer elevator. If the surgeon is in the correct plane the removal is easy. If it is not easy then go a bit deeper to a tissue plane a bit closer to the tumor. (d) The tumor is removed. It usually can be found to have a single entering and exiting fascicle with no other connections to the native nerve fibers.

transformation (reported to be nearly 10%) is usually heralded by rapid loss of neurologic function or the presence of pain. In these instances, a high rate of local recurrence occurs after inadequate local resection, and radical local excision is advocated. Various combinations of conventional and plexiform lesions of schwannomas or neurofibromas may coexist in the same location in some patients who have or do not have neurofibromatosis. These tumors are locally destructive and do not spread via the lymphatic channels. Intraneural extension over a long distance has been noted. Unfortunately, these tumors are notoriously radioresistant.

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Surgical Therapy Although the degree of preoperative nerve dysfunction is usually minor, excision of the neurofibroma when it is intimately involved with a peripheral nerve conveys potential loss of nerve function. In spite of the teaching (▶ Fig. 18.1), that suggests a neurofibroma cannot be removed without lost function, frequently the mass can be excised or at least debulked without significant functional deficit. We always try to debulk the tumor using similar technique to a schwannoma. Surgical exploration and excision are required under the following circumstances: diagnosis, pain, cosmetic considerations, progressive

Tumors of the Peripheral Nervous System

Fig. 18.7 Schwannoma case 1: resecting the schwannoma. (a) The entering fascicle was transected, and the tumor was removed en masse without neurologic deficit. (b) With the tumor removed, the normal unaffected fibers were seen running in the normal direction. No need for closing the epineurium. (c) Macroscopic evaluation of the schwannoma demonstrates a smooth walled mass with distinct borders.

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Fig. 18.8 Schwannoma case 2: orientation and history. A 28-year-old woman with a known history of neurofibromatosis and multiple café-au-lait spots was referred following failed resection of a median nerve schwannoma. The patient presented with a healed volar forearm incision over the palpable tumor.

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Fig. 18.9 Schwannoma case 2: exposure of the schwannoma. Following wide proximal and distal exposure of the nerve, the tumor was exposed and circumferentially controlled. Fusiform expansion of the entire median nerve was encountered with displaced fascicles at the periphery of the tumor mass.

Fig. 18.10 Schwannoma case 2: identifying the longitudinal plane for resection. After circumferential inspection, the “bare” an area with no superficial fascicles is identified for entering the nerve to remove the tumor. The ink mark is in line with the fascicle—tumor junction.

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Fig. 18.11 Schwannoma case 2: elevating the epineurium. After incising the epineurium, a periosteal elevator is used to dissect the schwannoma from the uninvolved fascicles. If the elevator is in the correct deep plane the tumor will shell out easily. If it does not come out easily the surgeon is in too superficial a plane.

Fig. 18.12 Schwannoma case 2: posterior digital pressure to isolate the schwannoma. A finger can be placed behind the tumor to apply gentle pressure and facilitate the separation of the tumor from the normal fascicles of the median nerve.

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Fig. 18.13 Schwannoma case 2: schwannoma removal. The entering fascicle can be transected, and the tumor can be removed en masse without neurologic deficit. The entering and exiting fascicle is nonfunctional and does not need to be reconstructed.

Fig. 18.14 Pre- and postoperative pain evaluations. All patients undergoing a nerve-related procedure in our practice complete pre- and postoperative pain evaluations. This patient’s pain evaluations demonstrated the characteristic descriptors used by many patients with nerve pain (cramping, throbbing, aching, tingling, dull). A substantial improvement in the level of pain was observed, which is often seen in patients after removal of the nerve sheath tumor.

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Fig. 18.15 Entering and exiting fascicle within a schwannoma. A large schwannoma was observed within the median nerve at the wrist. This image depicts the single fascicle, which characteristically can be found entering and exiting the schwannoma after it has been completely neurolyzed from the unaffected fascicles. This single fascicle can be sacrificed without neurologic deficit in most patients, and the expected long-term outcome is excellent.

Fig. 18.16 Benign neurofibroma case: history and imagining. A 56-year-old man presented with a benign neurofibroma of the medial and lateral cords of the brachial plexus. (a) Photo of the left chest, demonstrating a subtle mass in the infra-clavicular region. (b) Sagittal section from a computed tomography scan of the neck shows the soft tissue tumor in the proximal brachial plexus.

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Fig. 18.17 Benign neurofibroma case: exposure of the brachial plexus and neurofibroma. Intraoperative photo shows the exposed tumor within the infraclavicular brachial plexus. The pectoralis muscle was divided to provide full exposure of the goose egg-sized tumor proximally and distally.

Fig. 18.18 Benign neurofibroma case: resection of a neurofibroma. Photo of the brachial plexus following careful dissection and removal of the tumor mass. Because the tumor was known to be benign from intraoperative pathology specimens, near-complete excision was performed without sacrificing upper extremity motor function. Intraoperative nerve stimulation was used to ensure that no critical nerves were divided.

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Fig. 18.19 Plexiform neurofibroma case: imaging of plexiform neurofibroma. A 21-year-old female patient with neurofibromatosis presented with several months of tingling and numbness in the left upper extremity. (a) Coronal section of magnetic resonance imaging of the chest demonstrates the large brachial plexus neurofibroma that displaced the lung inferiorly. (b) Transverse plane of the upper chest. Large tumor is hyperintense on T2weighted image. (c) Positron emission tomography (PET) scan demonstrates intense [18F]-2-fluoro-2-deoxy-d-glucose (FDG) uptake. A lesion with these characteristics on FDG-PET imaging was indicative of malignant degeneration into a neurofibrosarcoma. The increased area of uptake in the left C6 nerve root region corresponded to a nerve sheath tumor. The mild uptake on PET favored a benign process. (d) Three-dimensional reconstruction of a chest computed tomography scan, including bone and soft tissue windows. (e) Posteroanterior chest radiograph shows the soft tissue mass overlying the left upper chest.

Table 18.2 Neurofibromatosis: Features Distinguishing NF1 from NF2 Neurofibromatosis Type 1 (NF1) (Requires two or more of the following) ●

● ● ● ● ● ●

Six or more brownish lesions on the skin, > 5 mm in greatest diameter in preadolescents and > 15 mm in adolescents and adults Two or more neurofibromas Freckling in the armpits or groin Optic glioma Two or more Lisch nodules, or small masses on the iris of the eyes Bone lesions (sphenoid dysplasia) A first-degree relative with NF1

neurologic deficits, compression of adjacent tissues, and suspicion of a malignant tumor. Excision of the neurofibroma will be indicated only in rare instances; some neurofibromas can be successfully debulked without loss of neurologic function (▶ Fig. 18.16; ▶ Fig. 18.17; ▶ Fig. 18.18). In these scenarios, neural continuity may need to be restored with either a primary nerve repair or nerve grafting. The rare, very proximal tumor that is thought to be benign may be better followed rather than excised if removal is deemed potentially morbid, especially when it is an incidental and asymptomatic finding. Excision of a schwannoma when there has not been a prior incisional biopsy should be able to be performed without a neurologic deficit (▶ Figs. 18.8–18.13). In contrast to schwannomas, attempts at microsurgical separation of a neurofibroma from intact fascicles often results in nerve damage. Intraoperative electrophysiologic monitoring has been suggested as an aid to excising only nonfunctional fascicles. Pain has been reported to

Neurofibromatosis Type 2 (NF2) (Requires either of the following) ● ●

Eighth cranial nerve masses on both sides (bilateral) An immediate relative with NF2 and either an eighth nerve mass on one side or two of the following: neurofibroma, meningioma, glioma, schwannoma

improve or remain unchanged in 56 to 82% of patients, with a minority of patients reporting worsening pain. Motor strength has been shown to decrease in 15 to 50% of patients following excision of solitary neurofibromas. As with schwannomas, more proximal tumors typically fare worse. If nerve resection is attempted, direct repair or nerve grafting should be performed. Rarely, this repair will restore function, but it does help to prevent neuroma formation. As with schwannomas, recurrence after neurofibroma excision is uncommon.

18.2.4 Schwannomatosis Schwannomatosis is characterized by the development of multiple schwannomas, but without the involvement of vestibular schwannomas. Although the clinical features, diagnostic criteria, and genetics of NF1 and NF2 are widely known, those of schwannomatosis are less frequently encountered.27,28 Criteria

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Fig. 18.20 Malignant neurofibroma case: history and imaging. A 27-year-old male patient with neurofibromatosis type 1 presented with pain and an enlarging mass in the left chest/shoulder region. (a) Anterior photo shows the palpable mass and abduction of the left arm. (b) Lateral photo demonstrates the projection of the tumor. (c) Transverse section from computed tomography (CT) scan of the chest shows the soft tissue mass within the left axilla. (d) Three-dimensional reconstruction of the chest CT. (e) Coronal section of the chest CT shows the tumor arising from the nerve sheath.

Table 18.3 Diagnosis of Schwannomatosis Definite Schwannomatosis

Presumptive/Probable Schwannomatosis

Two or more pathologically proved schwannomas AND Lack of radiographic evidence of vestibular nerve tumor after 18 years of age

Two or more pathologically confirmed schwannomas without cranial nerve VIII dysfunction after 30 years of age OR Two or more pathologically confirmed schwannomas in a limited distribution (single limb) without cranial nerve VIII dysfunction at any age

are listed in ▶ Table 18.3. Patients with schwannomatosis may develop conventional and plexiform lesions centrally or peripherally but not within their vestibular nerves, differentiating them from patients with NF2.29 Patients who have neurofibromatosis and schwannomatosis are prone to developing peripheral nerve tumors. Familial cases of schwannomatosis with autosomal dominance have been described. Families with schwannomatosis have been found to have a germline mutation of INI1/SMARCB1, which is located near the gene marker D22S1174 identified on chromosome 22 in patients who have NF2.30 Distinction of patients who have schwannomatosis from those who have NF2 is necessary in that patients with NF2 oc-

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casionally develop intracranial and spinal tumors such as meningiomas and have different priorities for surveillance (hearing screens).31 Similar to NF2, sporadic schwannomatosis seems to have a prevalence of 1 in 30,000, whereas the prevalence of familial schwannomatosis is unknown. Localized (segmental) forms of neurofibromatosis and schwannomatosis have also been documented.

18.2.5 Granular Cell Tumors Granular cell tumors are infrequent neoplasms encountered in the forearm and hand. These lesions appear to arise from neural elements and are noted to occur in extremely close association

Tumors of the Peripheral Nervous System with peripheral nerves. Multicentricity has been noticed in nearly 15% of cases, although wide excision of the tumor is thought to be completely curative. An extremely rare malignant variant of the tumor has been described and is difficult to differentiate from the benign lesion. These malignant variants are highly aggressive and necessitate wide excision and consideration of chemotherapy and/or radiation.

18.2.6 Malignant Nerve Sheath Tumors Malignant peripheral nerve sheath tumors (MPNSTs) constitute a heterogeneous group of malignant tumors that arise from major or minor peripheral nerve branches or sheaths of peripheral nerve fibers and are derived from Schwann cells or pluripotent cells of neural crest origin.32 Patients who have MPNSTs demonstrate aberrations in chromosome 17q 11.2–22 and show loss of NF1 gene expression, with a resultant increase in Ras oncogene expression. MPNSTs represent 5 to 10% of soft tissue sarcomas and are malignant neoplasms that generally arise in the presence of a neurofibroma or schwannoma.33 The term currently includes tumors from different classification schemes used in the past (neurosarcoma, neurofibrosarcoma, malignant neuroma). The molecular events of malignant transformation are a topic of interest. NF1 is a tumor suppressor gene syndrome in which germline mutations result in inactivation of neurofibromin, the NF1 gene product. The functional role of neurofibromin is to inactivate p21-Ras guanine triphosphate (GTP), which is the active form of the Ras protein. This loss of functional neurofibromin in NF1-associated tumors results in increased activated p21-Ras GTP levels and subsequent increases in cell growth and proliferation.34,35 Subsequent somatic NF1 mutations inactivate the normal NF1 allele, which results in tumor genesis. Nonetheless, loss of neurofibromin and resultant p21-Ras hyperactivation occurs in Schwann cells from both benign PNSTs and MPNSTs, and additional genetic alterations are likely required to permit the transformation of cells from a benign tumor to the malignant cells of an MPNST.36 Recent studies have shown that DNA amplification and upregulation of both topoisomerase type IIa (TOP2A) and epidermal growth factor receptor (EGFR), as well as genomic deletions and inactivation of the cyclin-dependent kinase inhibitor 2A (CDKN2A) and tumor protein p53 (TP53) genes, are linked to malignant transformation and MPNST development.37 MPNSTs represent a challenge by virtue of their aggressive nature. Unfortunately, they are associated with a poor prognosis and limited treatment options. Studies have demonstrated a significantly higher incidence of local recurrence and postoperative nerve dysfunction with MPNSTs than benign PNSTs.38 Malignancy can occur de novo or from previously benign nerve cells and is suspected when the tumor exhibits an irregular shape, unclear or invasive margins, presence of intratumoral lobulation, high signal intensity areas on T1-weighted imaging, or nonhomogeneous contrast enhancement (▶ Fig. 18.21).

Presentation The diagnosis of these tumors remains problematic because it is based primarily on clinical suspicion. Any patient with

a history of NF1, NF2, or schwannomatosis who presents with a tumor showing a rapid increase in size, new or progressive neurologic symptoms, or increasing pain should be suspected of having malignant degeneration. Detailed history and physical examination are the foundation of the assessment. Note should be made of when the mass or deficit was noticed. A rapid increase in the size of a mass or rapid onset of symptoms should immediately raise concern for the possibility of a malignant transformation. All four extremities should have motor examination grading and a sensory examination. The location and extent of any motor weakness or sensory deficit should be defined, and the sensory examination should focus on specific dermatomal distributions. Reflexes should be examined, and the patient should be checked for provocative signs (Tinel, Phalen) overlying the suspected tumor. Inquiry should also be made about numbness, “pins and needles,” or “electric shock” type paresthesias. We have developed algorithms for low and high suspicion for malignancy (▶ Fig. 18.22; ▶ Fig. 18.23).

Incidence Approximately 5 to 10% of all soft tissue sarcomas diagnosed in the United States each year are MPNSTs, with an incidence of 0.001% in the general population (▶ 18.24–18.29).39 These tumors occur with equal frequency in men and women, and there is no racial association.40 Malignant degeneration potentially can occur in any of the affected lesions in a patient with neurofibromatosis; however, NF1 has a significantly stronger association with MPNSTs than NF2.41 MPNSTs have been found to occur in 2 to 10% of patients with NF1; conversely, up to 50% of all patients with an MPNST have NF1.42 Most studies show that the peak incidence of MPNSTs is in the seventh decade in isolated cases but in the third or fourth decade in persons with NF1, although malignant tumors may occur at a younger age in either group.2,35,43 Most MPNSTs occur in patients who have NF1, with a cumulative lifetime risk of up to 10%. Individuals who have NF1 and plexiform neurofibromas are 18 times more likely to develop MPNSTs than patients who do not have internal plexiform neurofibromas.44 An incidence of malignant transformation between 3 and 10% has been described if the neurofibroma involves the major nerve trunks. Ten percent of MPNSTs occur in patients who have undergone radiation treatments for other diseases, and those malignancies occur an average of 12 to 15 years after the exposure.45 The effect of radiation on peripheral nerves has been described, and the incidence of radiation-induced MPNSTs reported in large series ranges from 5.5 to 11.0% in patients both with and without NF1.2,6 Metastases to the lung, liver, brain, soft tissue, bone, regional lymph nodes, skin, or retroperitoneum are commonly seen (▶ Figs. 18.30– 18.40).

Imaging The most conclusive test for a patient with a potential neurofibrosarcoma is a tumor biopsy; however, MRI, radiographs, CT scans, and bone scans can aid in localizing a tumor and/or possible metastasis. Needle biopsy is generally encouraged due to the low risk of pain or neurologic deficit, but it is often incon-

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Fig. 18.21 Epithelioid sarcoma case: history and imaging. A 30-year-old man presented with persistent pain and tingling in his left hand after carpal tunnel surgery. (a) Skin incision markings made prior to surgery allow access to the tumor within the forearm. (b) Sagittal section of magnetic resonance imaging (MRI) of the left upper extremity show the mass within the median nerve. (c) Transverse section of the MRI shows the tumor within the nerve sheath. Preoperative radiation oncology consult was obtained.

clusive. In general, it is advocated to perform a complete excisional biopsy to minimize sampling error and decrease the risk of nerve damage from multiple procedures. The gold standard for imaging of peripheral nerve tumors has become MRI. Contrast scans should always be ordered to evaluate the enhancing quality of the mass. Information on the enhancing qualities of the mass, combined with its appearance on T1 and T2 images, can give valuable clues as to the histopathologic findings that may be encountered. The sensitivity of MRI for diagnosing MPNSTs is reported to be > 80%, but conventional MRI techniques can suffer from spatial and resolution limitations, as well as motion artifacts. Our experience with MRI is that, although it will localize the tumor, it is not accurate with regard to tissue typing nor malignant potential. MRN offers enhanced visualization and definition of peripheral nerve lesions and produces higher resolution images of the nerves with greater separation from the surrounding soft tissue. Whether a tumor is benign or malignant cannot be discerned definitively from any radiologic test alone. Areas of hemorrhage or necrosis, heterogeneous enhancement, and cystic areas suggest a malignancy but are also seen in benign tumors. PET with FDG is a technique that allows the visualization and quantifica-

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tion of glucose metabolism in cells and reflects the greater metabolism of malignant tumors (▶ Fig. 18.20).46 FDG-PET and PET CT are sensitive and specific diagnostic tools for MPNSTs in individuals who have NF1 and have become integral in the diagnosis and management of this complex condition. 46

Classification and Grading Classification of MPNSTs is based on the classifications used for soft tissue sarcomas. Grades 1 to 3 indicate the number of mitotic figures and the degree of nuclear and cellular atypia, as well as the tumors’ macroscopic size.35 Mitotic rates are evaluated per high-powered field (HPF). Greater than 5 mitotic rates per 10 HPFs is classified as a high-grade MPNST, because a single mitotic figure may be significant in a tumor with hypercellularity and nuclear atypia.41 Greater than 5% cellular staining of MIB-1 proliferation marker is also considered to be high grade.47 Tumor size at surgery is stratified to be > or < 5 cm. Patients with neurogenic sarcomas > 5 cm present twice as often with neurologic motor or sensory deficits compared to patients who have neurogenic sarcomas ≤ 5 cm. Additionally, tumor size correlates with pathologic grade, which predicts survival rate

Tumors of the Peripheral Nervous System

Fig. 18.22 Algorithm for low preoperative suspicion for malignancy.

and risk of metastatic spread. The most aggressive grade III tumors are found in patients who have neurogenic sarcomas > 5 cm.2,35,48 MPNSTs are often graded using the Enneking classification system. The Enneking system classifies sarcomas and nerve tumors of the extremities by histologic appearance and likelihood of metastasizing as stage I (low-grade sarcomas; < 25% chance of metastasis), stage II (high-grade sarcomas; > 25% chance of metastasis), or stage III (any grade; already metastasized). It further classifies tumors as type A (intracompartmental) or type B (extracompartmental). Type A tumors are contained within fascial planes and are more likely to be controlled with surgical resection than type B tumors.49

Histology Histologic examination should cover sections stained with conventional tinctorial stains, including hematoxylin and eosin (H&E) and reticulin. The histologic diagnosis is often difficult, given their heterogeneity and differentiation. MPNSTs are nonencapsulated infiltrating tumors composed of spindle cells arranged in a whorling pattern with irregular nuclei, cyst

formation, and nuclear palisading. There are several distinct histologic features, such as proliferation of tumor in the subendothelial zones of vessels with neoplastic cell herniation into the vessel lumen and proliferation of small vessels in the walls of the large vessels that are characteristic of MPNSTs. Mitotic figures are readily visible, with > 1 per HPF, and 50 to 90% of cases are immunoreactive with S-100 protein staining.50 Necrosis, pseudocystic change, or hemorrhage may also be found. The pathologic criteria for malignancy are invasion of surrounding tissues by tumor cells, vascular invasion, nuclear pleomorphism, necrosis, and the presence of mitoses. Although intraoperative frozen sections are not definitive, they may be of use in suggesting malignancy if there are frequent mitoses. Using the H&E-stained sections, MPNSTs are graded based on cellularity, nuclear pleomorphism, anaplasia, mitotic rate (mitotic figures in 10 HPFs), microvascular proliferation, and degree of necrosis/invasion. The diagnosis of an MPNST cannot be made from examination of H&E sections alone, because sarcomas arising from fibroblasts or smooth muscle cells may have a similar appearance. The histologic analysis includes immunostaining for desmin, myogenin, vimentin, S-100, proliferative activity marker MIB-1, and expression of p53, p27, and p16

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Fig. 18.23 Algorithm for high preoperative suspicion for malignancy.

oncogenes. Three immunohistochemical markers (S-100, Leu-7, myelin basic protein), although not definitively diagnostic, are highly supportive of an MPNST.2,51 On electron microscopy, features suggestive of a neurogenic origin include wavy, buckled, or comma-shaped nuclei arranged in sweeping fascicles with extensive perineural and intraneural spread of the tumor. Proliferation of the tumor in the subendothelial zones of vessels and neoplastic cells herniating into the lumen are also supportive.

Treatment The surgical management of MPNSTs remains controversial but historically involves wide local excision (▶ Figs. 41–46).35 Gross inspection of MPNSTs commonly demonstrates a fusiform, fleshy, tan-white mass with areas of degeneration and secondary hemorrhage. The nerve proximal and distal to the tumor may be thickened because of spread of the tumor along the epineurium, and it is not always feasible to demonstrate the origin from a nerve, especially when it arises from a small peripheral

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branch. Intraoperative motor stimulation can be helpful in identifying functional motor nerves in the vicinity of peripheral nerve tumors and is most helpful in complex, plexiform neurofibromas.38 Only complete excision before metastasis is likely to give a good prognosis.52 The reported local recurrence rate of MPNSTs after gross total resection is upward of 65%.53 Local aggressive resection and control are thought to decrease the risk for metastasis and result in a better overall prognosis. In some theories, microscopically positive margins may be an indication of a highly aggressive tumor rather than being a reflection of inadequate resection. The ultimate aim of surgery is complete removal of the lesion with tumor-free margins (▶ Fig. 18.21; ▶ Figs. 18.24–18.29; ▶ Fig. 18.38; ▶ Fig. 18.39; ▶ Fig. 18.40).2,54 Complete excision with limb preservation cannot always be accomplished, however. In situations where limb salvage is not possible, amputation proximal to the tumor should be performed after histologic confirmation of malignancy. Select patients benefit from preoperative chemotherapy to reduce the size of the tumor and to assess response, and all patients with residual

Tumors of the Peripheral Nervous System

Fig. 18.24 Epithelioid sarcoma case: exposure of nerve sarcoma. Following wide curvilinear skin incision, the nerve was exposed and frozen section obtained which tested positive for high-grade sarcoma. With the assistance of radiation oncology, the sarcoma was resected with surrounding tissues and await permanent section report where margins tested negative.

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Fig. 18.25 Epithelioid sarcoma case: epithelioid sarcoma. The entirety of the tumor was excised, including the median nerve ends proximally and distally.

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Fig. 18.26 Epithelioid sarcoma case: resection of nerve sarcoma. Following excision, the distal ends of the median nerve were isolated, and the nerve gap was found to be 8 cm.

18

Fig. 18.27 Epithelioid sarcoma case: secondary tissue resection for negative margins. Two weeks later with the oncology surgeon a wide resection was performed after permanent sections confirmed high grade malignancy.

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Fig. 18.28 Epithelioid sarcoma case: tissue resection. The wound bed was inspected following resection of the margins to ensure complete hemostasis and coverage of critical structures.

18 Fig. 18.29 Epithelioid sarcoma case: brachytherapy. Brachytherapy catheters were placed with assistance of the radiation oncologists.

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Fig. 18.30 Lipofibroma case: orientation and history. A 49-year-old man presented with neuropathic pain and a large mass on the volar aspect of the right wrist. The patient had several previous failed carpal tunnel releases and a resection and nerve graft and transfer reconstruction was planned. A large incision was planned from the midpalm to the mid-forearm and included an open carpal tunnel release. This incision allows for proximal and distal identification of the nerve before dissecting directly down onto the tumor.

Fig. 18.31 Lipofibroma case: exposure of the lipofibroma. Following complete dissection, the median nerve was identified, and the large lipofibroma identified. Note that the distal dissection has been performed to include the terminal sensory components to the median nerve.

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Fig. 18.32 Lipofibroma case: magnification of exposure. Distal sensory branches exiting the lipofibroma were identified. A sensory branch of the ulnar nerve was identified to serve as a donor for an end-to-side sensory nerve transfer. Proximal median nerve entering the lipofibroma was identified.

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Fig. 18.33 Lipofibroma case: resection of lipofibroma. Following removal of the tumor, the deficit was determined, and appropriate options for grafting was considered.

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Fig. 18.34 Lipofibroma case: lipofibroma. Back table dissection of the nerve tumor showing a lengthwise distance of 10 cm of the median nerve. Cross section of the tumor in the midsection demonstrating multiple fascicles of the median nerve, which were densely interwoven within the tumor.

Fig. 18.35 Lipofibroma case: sural nerve graft harvests. Bilateral sural nerves were harvested as autologous cable grafts for reconstruction.

tumor margins or close margins on pathology should be considered for chemotherapy and radiation oncology consultation.55 Compared to schwannomas, neurofibromas are more likely to have multiple nerve fascicles entering and exiting at the poles of the tumor. The surface of the tumor is mapped using a

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nerve stimulator to find an area in which the tumor can be approached safely and an interfascicular dissection performed for its removal. The nonfunctioning fascicles can be sacrificed, and functioning fascicles are traced through the tumor with an attempt to preserve them when possible. If there are functional

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Fig. 18.36 Lipofibroma case: nerve grafting and transfers for reconstruction. Intraoperative photos demonstrate the sural nerve grafts from the proximal median nerve in the forearm to the distal transected sensory nerves in the level of the palm. The recurrent thenar branch of the median nerve was not involved in the tumor and therefore was protected and not reconstructed.

fascicles that must be sacrificed, then nerve grafting can be used to bridge the defects, or nerve transfer techniques can be employed to recover function more rapidly. Nerve continuity after removal of malignant brachial and lumbosacral plexus lesions is not often advocated, as the adjuvant radiation and chemotherapy compromise the ability of the axons to find their path to the target organ, and results following reconstruction are suboptimal. Furthermore, survival after an MPNST is often not long enough for reinnervation to occur.54 Amputation may be indicated for extensive MPNSTs and for tumors that recur after adequate excision.41 Our practice is to resect the tumor obtaining negative microscopic margins, arrange for postoperative brachytherapy and/or external beam radiation, and reconstruct distal to the operative site with nerve transfers.

Radiotherapy Although external beam or catheter-directed brachytherapy radiation improves local control in the areas with minimal residual disease, operative resection represents the basis of treatment with consideration for neoadjuvant chemotherapy preoperatively in order to enhance resectability (▶ Fig. 18.29).56 Additionally, although radiotherapy provides local control

and delays onset of recurrence, it has little effect on long-term survival. Adjuvant radiotherapy should be given whenever possible for intermediate- to high-grade lesions and for low-grade tumors after a marginal excision. Adjuvant radiotherapy involves irradiation of the entire operative field, with a 5-cm field margin. Neoadjuvant radiotherapy involves irradiation of the tumor alone with a 5-cm margin. The usual dose administered is 6,000 to 7,000 cGy. Irradiation before surgery has been recommended if the location, size, and distribution of the tumor make it more technically difficult to provide optimal radiotherapy after excision; if dissection may be anticipated along major critical structures (with the possibility of leaving microscopic disease in critical structures); or if remote tissue flaps or skin grafts are required for wound coverage after resection. Postoperative radiotherapy is recommended as part of a uniform treatment policy for MPNSTs, much like other high-grade soft tissue sarcomas, even if clear surgical margins are obtained.

Chemotherapy Because of the rare nature of MPNSTs, appropriately conducted, multicenter trials on the effectiveness of chemotherapy on MPNSTs do not exist, and most current data are based on case

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Fig. 18.37 Lipofibroma case: magnification of nerve grafting and transfers for reconstruction. Critical sensory territories (first web space) were reconstructed with nerve grafts, and the noncritical sensory territories (second/third web spaces) were reconstructed with end-to-side nerve transfers from a digital sensory branch of the ulnar nerve.

series or regimens successful for other soft tissue sarcomas. However, systemic chemotherapy has been used in the treatment of metastatic disease,35 and administration of neoadjuvant chemotherapy has been postulated to reduce the need for amputation and permit wide excision with negative margins at the time of surgery. Few drugs have been proven to be effective. Treatments include single-agent doxorubicin or a combination of doxorubicin and ifosfamide, with a partial response rate of 20 to 25%. 57 First-line agents are ifosfamide and doxorubicin, although carboplatin and etoposide have been used with promising results in metastatic MPNST refractory to first-line therapy.58 Dacarbazine has also been noted to have activity against MPNSTs and is combined with doxorubicin in the cyclophosphamide, vincristine, Adriamycin, and dacarbazine (CYVADIC) regimen. 57 Studies have shown the role of TOP2A and CD117 overexpression in certain cases as important markers for TOP2A inhibitors such as etoposide and doxorubicin and inhibitors of KIT-like imatinib mesylate (Gleevec).41,59 Additionally, chemotherapy may be useful in the neoadjuvant setting to achieve tumor regression in patients with unresectable primary tumors. Although chemotherapy is not curative, there is a benefit at 10 years for progression-free survival for local and distant relapse; however, the magnitude of any overall survival benefit is small (4%).60

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Prognosis MPNSTs have a poor prognosis, and the prognosis seems to be worse in patients who have NF1.61 These tumors have such a poor prognosis because metastases to the lung, liver, brain, soft tissue, bone, regional lymph nodes, skin, or retroperitoneum are common.2 Hematogenous metastatic spread occurs most commonly to the lungs. Centrally located paraspinal MPNSTs have more aggressive behavior than peripherally located tumors, mainly because of the difficulty in excising them completely.46 In general, malignant tumors are treated with postoperative external beam or brachytherapy catheter-directed radiation treatment (▶ Fig. 18.29). The 5-year survival rates in large series have been reported to range between 16 and 52%. Malignant degeneration in a patient with neurofibromatosis is associated with a higher mortality rate than a similar change in an isolated neurofibroma. The reported 5-year survival rate for patients who have MPNSTs without NF1 is as high as 50%; it drops to as low as 10% for MPNSTs in patients who have NF1.61 Adverse prognostic factors include large size (> 5 cm), high tumor grade, advanced histology, positive surgical margins, and associated NF1. 35 Even with aggressive therapy, local recurrence occurs in 50% of patients.53 Studies using preoperative radiotherapy or interstitial radiotherapy have demonstrated that patients with

Tumors of the Peripheral Nervous System

Fig. 18.38 Malignant small B-cell lymphoma case: exposure of the brachial plexus and radial nerve lymphoma. A 56-year-old woman presented with radial nerve palsy related to a tumor within the posterior cord of the brachial plexus and extending into the radial nerve proper. Intraoperatively, the tumor did not appear to be benign and a biopsy was taken, which was interpreted as sarcoma, round cell type, non-spindle, possibly Ewing and most likely malignant. Intraoperative consultation with the radiation oncologist suggested wide excision and given the preliminary cell type external beam radiation not brachytherapy. Her final pathology was small cell, non-Hodgkin lymphoma.

tumor-positive margins ultimately develop locally recurrent or distant metastatic disease.

18.3 Neoplasms of Nonneural Origin 18.3.1 Fibrolipomatous Hamartoma Fibrolipomatous hamartoma (FLH) of the neural structures of the hand is a rare lesion. The typical management is several surgeries over years, progressing from decompression, to neurolysis, and finally resection and reconstruction only for severe pain and dysfunction. Patients who have FLH may present with neuropathy by itself or in combination with gigantism of the digits in the hand or foot from involvement of the median, plantar, or digital nerves. These lesions occur most commonly in the median nerve. They also have been observed in the radial, ulnar, digital, superficial peroneal, plantar, and cranial nerve distributions (median nerve compression within the carpal tunnel). Larger masses may cause numbness or weakness, similar to that seen in carpal tunnel syndrome, and surgical intervention is indicated only for compression type symptoms. These lesions are characterized by fibrofatty proliferation causing epineural and perineural fibrosis. MRI characteristically shows an enlarged fu-

siform nerve with fascicles that are isointense on T1-weighted images and hyperintense on T2 weighting. MRI may demonstrate that these lesions appear to be similar to a coaxial cable in the axial plane and linear in the coronal plane and have “skip lesions,” longitudinal involvement within the same nerve, or even involvement of other nerves within the same limb. These patients typically present before age 30. Of all persons with this tumor, nearly two-thirds exhibit macrodactyly due to the bony overgrowth and progression of subcutaneous fat. Resection is indicated only if the FLH occurs in expendable nerves, as neurologic deficit will result after excision of this benign lesion (▶ Figs. 18.47–18.51). Similarly, debulking of the tumor is not widely performed. In contrast, intraneural lipomas (lipomas occurring within the epineurium of nerves) can be identified readily based on findings of fat within the nerve on MRI, and these lesions can be resected safely.62 In the differential diagnosis of patients with lipofibromatosis of the nerve is interstitial neuritis, or Dejerine-Sottas disease. This is a familial condition with local swelling of a peripheral nerve caused by hypertrophic interstitial neuropathy. The histologic findings in Dejerine-Sottas disease is one of Schwann cell proliferation and myelin sheath degeneration without fatty infiltration of the nerve. Unfortunately, because this tumor involves the nerve directly, excision will result in loss of nerve function, and graft reconstruction will be required.

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Fig. 18.39 Malignant small B-cell lymphoma case: resection of the radial nerve lymphoma. (a) The tumor was excised from the unaffected proximal portion, leaving the axillary nerve intact. (b) The tumor mass following complete surgical excision.

18.3.2 Peripheral Nerve Lipomas Peripheral nerve lipomas can exist in virtually any nerve distribution, but they are most commonly described involving the median nerve. When involved at this level, associated macrodactyly has been described. These tumors often present as a soft mass in the palm in childhood or early adulthood, and symptoms are usually slowly progressive. Patients may complain of pain and sensory abnormalities, as well as motor weakness in the median nerve distribution. Symptoms of median nerve compression and carpal tunnel syndrome can arise secondary to this tumor mass; however, carpal tunnel release usually provides only temporary relief. The tumor may progress distally and may even involve the digital nerves themselves. Extensive microsurgical neurolysis is possible because the fibrofatty tumor is present circumferentially around the nerve. Surgical debulking and precise removal of large amounts of tissue preserving full nerve function is possible (▶ Figs. 18.52–18.56). Occasionally, the tumor will need to be excised to control pain, and in this scenario nerve grafting should be performed to preserve sensibility to the hand. Intraneural lipomas, hemangiomas, and ganglia have all been

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described and usually present with a palpable mass and neurologic symptoms from direct nerve compression. The conditions can all be treated surgically with microscopic neurolysis and excision of the mass without resultant nerve function loss.

18.3.3 Intraneural Ganglia Intraneural ganglia are an interesting phenomenon that can occur within any peripheral nerve, but most commonly they affect the peroneal nerve near the knee and result in a foot drop (▶ Figs. 18.57–18.61). These are histologically characterized as lesions with mucin within the epineurium and usually occur following a remote history of direct or indirect trauma. The pathogenesis is controversial, but evidence supports a jointrelated articular pathology rather than a de novo origin.63 Intraneural ganglia are thought to be derived from degenerative synovial joints. Joint fluid penetrates through a capsular rent and dissects by the path of least resistance within the epineurium of nerves by way of articular branches, typically causing intrinsic compression of the nerve. In contrast, common simple

Tumors of the Peripheral Nervous System

Fig. 18.40 Malignant small B-cell lymphoma case: reconstruction of the radial nerve with median-to-radial nerve transfers. The radial nerve deficit was reconstructed with distal nerve transfers in the forearm. The nerve to the flexor carpi radialis (median) was transferred to the posterior interosseus nerve (radial), and the nerve to the flexor digitorum superficialis (median) was transferred to the extensor carpi radialis brevis (radial). Patient was treated with external beam radiation with excellent long term survival.

18 Fig. 18.41 Malignant peripheral nerve sheath tumor case 1: imaging of a malignant tumor. (a) Sagittal section from preoperative magnetic resonance imaging (MRI) shows high-density uptake in the region of the sciatic nerve. (b) Transverse sections from MRI show the tumor emanating from the sciatic nerve proper. (c) Photo of the encapsulated tumor following complete surgical excision. (d) Cross-section of the tumor mass.

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Fig. 18.42 Malignant peripheral nerve sheath tumor case 1: exposure of a malignant nerve tumor. A 52-year-old female patient presented with lower extremity pain and tingling. A posterior curvilinear incision was made in the posterior thigh crease to allow for wide exposure (inset for reference). Tumor measured 5.3 × 2.1 cm.

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Fig. 18.43 Malignant peripheral nerve sheath tumor case 1: resection of a malignant nerve tumor. The sciatic nerve was carefully identified and protected. The mass was identified as protruding from the lateral portion of the sciatic nerve and was fully excised with circumferential margins without removing the unaffected portions of the sciatic nerve.

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Fig. 18.44 Malignant peripheral nerve sheath tumor case 2: orientation and imaging. A 29-year-old male patient presented with a rapidly enlarging mass in the left axilla that caused pain and numbness in the left arm. (a) Photo of the mass within the left axilla, including preoperative skin markings. The tumor was involving the skin within the axilla. (b) Magnetic resonance imaging (MRI) of the chest was consistent with a peripheral nerve sheath tumor originating from the medial antebrachial cutaneous nerve. (c) Sagittal section of the chest MRI shows the dimensions of the tumor and its relation to the surrounding muscles.

18 Fig. 18.45 Malignant peripheral nerve sheath tumor case 2: exposure of a medial antebrachial cutaneous nerve tumor. The tumor was approached circumferentially by wide exposure and identification of all other branches of the brachial plexus.

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Fig. 18.46 Malignant peripheral nerve sheath tumor case 2: malignant medial antebrachial cutaneous nerve tumor. Prior to complete surgical excision, the tumor was confirmed to arise from the medial antebrachial cutaneous nerve.

Fig. 18.47 Lipofibromatous hamartoma case: orientation and history. A 22-year-old female patient presented with a palpable mass in the midpalm, consistent with a lipofibromatous tumor involving the median nerve. (a) Anteroposterior photograph of the right palm shows the palpable and elevated mass within the midpalm and extending toward the third web space. (b) Lateral photograph of the right palm with the prominent mass visible.

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Fig. 18.48 Lipofibromatous hamartoma case: exposure of the tumor. Intraoperative photo shows the exposed nerve to the third web space as it branches from the median nerve in the proximal palm. The entire portion of the nerve fascicle was affected, beginning at the carpal tunnel.

Fig. 18.49 Lipofibromatous hamartoma case: proximal and distal exposure of median nerve. Following isolation of the nerve in the palm, wide proximal exposure was obtained by extending the incision proximal to the carpal tunnel and identifying the proximal edge of the normal nerve.

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Fig. 18.50 Lipofibromatous hamartoma case: resection of the tumor. Following surgical excision of the affect portion, the proximal and distal ends were exposed, and the nerve deficit was measured to plan for interposition or nerve transfer to return sensibility to the third web space.

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Fig. 18.51 Lipofibromatous hamartoma case: reconstruction and proximal transposition. The distal portion of the nerve to the third web space was coapted to the radial digital nerve to the long finger in an end-to-side fashion, to maintain important sensibility to the web space. The proximal nerve ending was protected and transposed proximally to prevent painful neuroma.

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Tumors of the Peripheral Nervous System ganglia, which also may form from synovial joints, dissect outside a nerve, but they may extrinsically compress nerves. The size, shape, and direction of spread of these cysts are influenced by external pressure.64 Decompression provides immediate relaxation of the nerve; however, recurrence rates are high. We recommend concurrent tibial-fibular fusion at the time of the ganglion excision to reduce recurrence.

18.3.4 Perineuromas Perineuromas are rare benign peripheral nerve tumors that can also develop as extraneural tumors. They occur most commonly

Fig. 18.52 Lipoma case: orientation and history. A 57-year-old woman presented with pain within the superficial peroneal nerve territory and a palpable bilobed mass within the course of the nerve.

in children and young adults and typically cause gradually progressive weakness and sensory loss involving an extremity. Perineuromas demonstrate morphologic, ultrastructural, and immunohistochemical features that distinguish them from schwannomas and neurofibromas. Perineuromas show a female predominance, and there is no association with neurofibromatosis. MRI usually reveals a lesion that is isointense on T1 weighting, hyperintense on T2 weighting, and has homogeneous smooth enhancement over the affected segment. These lesions occur over a variety of anatomical sites and equally throughout the upper and lower extremities. The tumors are almost always grossly well circumscribed but are not encapsulated. Intraneural perineuromas (also termed localized hypertrophic neuropathy) show concentric intraneural lamellar proliferation of perineural cells resulting in a fusiform swelling of a segment of nerve. MRI usually reveals a fusiform lesion that may vary over a short to long segment. Perineuromas have pseudo-onion bulbs on H&E staining and are negative for S-100 at the outer leaflets (areas of pseudo-onion bulbs) but are positive in the core, where the nerve fibers may be, and positive for epithelial membrane antigen (EMA).65 There are EMA-positive cells surrounding a central core of axons, positive for S-100 and neurofilament. This cellular pathology may be a reactive process in response to nerve damage, as it commonly occurs in the interosseous nerve of young adults. However, intraneural perineuroma, soft tissue perineuroma, and localized hypertrophic neuropathy may all show deletions of chromosome 22.

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Fig. 18.53 Lipoma case: proximal exposure. The superficial peroneal nerve was exposed and identified proximal to the tumor.

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Fig. 18.54 Lipoma case: exposure of the lipoma. A dissection, from proximal to distal along the superficial peroneal nerve, exposed the lipoma deep to the nerve.

18 Fig. 18.55 Lipoma case: isolating the lipoma. The lipoma was isolated from the superficial peroneal nerve and was observed to have a superficial attachment to the nerve.

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Fig. 18.56 Lipoma case: resecting the lipoma. The lipoma was resected from the superficial peroneal nerve, while keeping the nerve intact. A large lipoma mass (7 cm in length) was removed.

Fig. 18.57 Ganglion cyst case: history and imaging. (a) A 51-year-old man presented with progressively weakened dorsiflexion at his left ankle. Physical examination revealed a palpable mass at the fibular neck and a positive Tinel sign on provocation. (b) Magnetic resonance imaging revealed high-contrast lobules along the peroneal nerve.

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Fig. 18.58 Ganglion cyst case: peroneal nerve decompression at the fibular head. After skin incision and sharp dissection, a large ganglion within the nerve sheath of the common peroneal nerve is encountered, and the nerve is proximally and distally decompressed in its anatomical bed by widely dividing the superficial fascia.

Fig. 18.59 Ganglion cyst case: exposure of the peroneal nerve. The posterior crural intermuscular septum was divided to relieve distal compression. Note the gray-like appearance of the peroneal nerve.

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Fig. 18.60 Ganglion cyst case: removal of cyst fluid. The ganglion cyst on the peroneal nerve is incised and drained to relieve pressure. The cysts are incised and decompressed at multiple levels along the nerve. Specifically the ganglion is not excised.

Fig. 18.61 Ganglion cyst case: the articular fascicular connection to the joint is ligated.

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18.4 Conclusion Benign and malignant peripheral nerve tumors arise from major or minor peripheral nerve branches, are derived from Schwann cells or pluripotent cells of neural crest origin. and are infrequently seen in clinical practice. A complete physical examination and detailed history should be taken to determine neurologic deficits and potential likelihood of malignant transformation, which carries a poor prognosis. The majority of nerve tumors are benign, with schwannomas and neurofibromas being more common. MRI remains the gold standard of diagnostic imaging, and advances in uses specifically for nerve visualization have led to specified MRN protocols. Resection of benign schwannomas and many neurofibromas can be performed with little to no expected neurologic deficit due to the understanding we have of the peripheral nervous system. It is clinically important to distinguish between schwannomas and neurofibromas due to the higher risk of nerve dysfunction after ill-advised neurofibroma excision. Recent advancements in molecular sequencing and technical accomplishments in treating nerve pathology have allowed improved outcomes in the treatment of peripheral nerve tumors. Further improvements involve the understanding of preoperative imaging characteristics, sophistication of pharmacological and operative interventions, and comprehension of the pathologic findings. Continuing technical advances by surgeons involved in diagnosing and treating diseases of the peripheral nervous system should allow even greater accuracy with MRN or with a combination of MRI and other imaging modalities, such as ultrasound and PET. Understanding molecular genetics should help to develop targeted therapies that can further help to develop operative and nonoperative strategies for management.

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[12] Stout AP. The peripheral manifestations of specific nerve sheath tumor (Neurilemoma) Am J Cancer 1935;24:751–96 [13] Ehrlich HE, Martin H. Schwannomas (Neurilemomas) in the head and neck Surg Gyn Ob 1943;76:577–83 [14] Strickland JW, Steichen JB. Nerve tumors of the hand and forearm. J Hand Surg Am 1977;2:285–291 [15] Stack HG. Tumors of the hand. BMJ 1960;1:919–922 [16] Baser ME, Friedman JM, Evans DG. Increasing the specificity of diagnostic criteria for schwannomatosis. Neurology 2006;66:730–732 [17] Levine E, Huntrakoon M, Wetzel LH. Malignant nerve-sheath neoplasms in neurofibromatosis: distinction from benign tumors by using imaging techniques. AJR Am J Roentgenol 1987;149:1059–1064 [18] Bhargava R, Parham DM, Lasater OE, Chari RS, Chen G, Fletcher BD. MR imaging differentiation of benign and malignant peripheral nerve sheath tumors: use of the target sign. Pediatr Radiol 1997;27:124–129 [19] Reynolds DL, Jacobson JA, Inampudi P, Jamadar DA, Ebrahim FS, Hayes CW. Sonographic characteristics of peripheral nerve sheath tumors. AJR Am J Roentgenol 2004;182:741–744 [20] Ganju A, Roosen N, Kline DG, Tiel RL. Outcomes in a consecutive series of 111 surgically treated plexal tumors: a review of the experience at the Louisiana State University Health Sciences Center. J Neurosurg 2001;95:51–60 [21] Das S, Ganju A, Tiel RL, Kline DG. Tumors of the brachial plexus. Neurosurg Focus 2007;22:E26 [22] Dafford K, Kim D, Reid N, Kline D. Pelvic plexus tumors. Neurosurg Focus 2007;22:E10 [23] Cherqui A, Kim DH, Kim SH, Park HK, Kline DG. Surgical approaches to paraspinal nerve sheath tumors. Neurosurg Focus 2007;22:E9 [24] Spinner RJ, Amrami KK. What’s new in the management of benign peripheral nerve lesions? Neurosurg Clin N Am 2008;19:517–531, vv. [25] Kwok K, Davis B, Kliot M. Resection of a benign brachial plexus nerve sheath tumor using intraoperative electrophysiological monitoring. Neurosurgery 2007;60 Suppl 2:316–320, discussion 320–321 [26] Russell SM. Preserve the nerve: microsurgical resection of peripheral nerve sheath tumors. Neurosurgery 2007;61 Suppl:113–117, discussion 117–118 [27] MacCollin M, Chiocca EA, Evans DG, et al. Diagnostic criteria for schwannomatosis. Neurology 2005;64:1838–1845 [28] Huang JH, Simon SL, Nagpal S, Nelson PT, Zager EL. Management of patients with schwannomatosis: report of six cases and review of the literature. Surg Neurol 2004;62:353–361, discussion 361 [29] Woodruff JM. Pathology of tumors of the peripheral nerve sheath in type 1 neurofibromatosis. Am J Med Genet 1999;89:23–30 [30] Hulsebos TJ, Plomp AS, Wolterman RA, Robanus-Maandag EC, Baas F, Wesseling P. Germline mutation of INI1/SMARCB1 in familial schwannomatosis. Am J Hum Genet 2007;80:805–810 [31] Westhout FD, Mathews M, Paré LS, Armstrong WB, Tully P, Linskey ME. Recognizing schwannomatosis and distinguishing it from neurofibromatosis type 1 or 2. J Spinal Disord Tech 2007;20:329–332 [32] Baehring JM, Betensky RA, Batchelor TT. Malignant peripheral nerve sheath tumor: the clinical spectrum and outcome of treatment. Neurology 2003;61:696–698 [33] Woodruff JM, Selig AM, Crowley K, Allen PW. Schwannoma (neurilemoma) with malignant transformation: a rare, distinctive peripheral nerve tumor. Am J Surg Pathol 1994;18:882–895 [34] Guha A, Lau N, Huvar I, et al. Ras-GTP levels are elevated in human NF1 peripheral nerve tumors. Oncogene 1996;12:507–513 [35] Angelov L, Davis A, O’Sullivan B, Bell R, Guha A. Neurogenic sarcomas: experience at the University of Toronto. Neurosurgery 1998;43:56–64, discussion 64–65 [36] Carroll SL, Ratner N. How does the Schwann cell lineage form tumors in NF1? Glia 2008;56:1590–1605 [37] Spurlock G, Knight SJ, Thomas N, Kiehl TR, Guha A, Upadhyaya M. Molecular evolution of a neurofibroma to malignant peripheral nerve sheath tumor (MPNST) in an NF1 patient: correlation between histopathological, clinical and molecular findings. J Cancer Res Clin Oncol 2010;136:1869– 1880 [38] Levi AD, Ross AL, Cuartas E, Qadir R, Temple HT. The surgical management of symptomatic peripheral nerve sheath tumors. Neurosurgery 2010;66:833– 840 [39] Hajdu SI. Peripheral nerve sheath tumors: histogenesis, classification, and prognosis. Cancer 1993;72:3549–3552 [40] D’Agostino AN, Soule EH, Miller RH. Sarcomas of the peripheral nerves and somatic soft tissues associated with multiple neurofibromatosis (Von Recklinghausen’s disease). Cancer 1963;16:1015–1027

Tumors of the Peripheral Nervous System [41] Ferner RE, Gutmann DH. International consensus statement on malignant peripheral nerve sheath tumors in neurofibromatosis. Cancer Res 2002;62: 1573–1577 [42] Yohay K. Neurofibromatosis types 1 and 2. Neurologist 2006;12:86–93 [43] Scherberich A, Tucker RP, Degen M, Brown-Luedi M, Andres AC, Chiquet-Ehrismann R. Tenascin-W is found in malignant mammary tumors, promotes alpha8 integrin-dependent motility and requires p38MAPK activity for BMP2 and TNF-alpha induced expression in vitro. Oncogene 2005;24:1525–1532 [44] Tucker T, Wolkenstein P, Revuz J, Zeller J, Friedman JM. Association between benign and malignant peripheral nerve sheath tumors in NF1. Neurology 2005;65:205–211 [45] Schwarz J, Belzberg AJ. Malignant peripheral nerve sheath tumors in the setting of segmental neurofibromatosis: case report. J Neurosurg 2000;92:342– 346 [46] Kourea HP, Bilsky MH, Leung DH, Lewis JJ, Woodruff JM. Subdiaphragmatic and intrathoracic paraspinal malignant peripheral nerve sheath tumors: a clinicopathologic study of 25 patients and 26 tumors. Cancer 1998;82:2191– 2203 [47] Yamaguchi U, Hasegawa T, Hirose T, et al. Low grade malignant peripheral nerve sheath tumour: varied cytological and histological patterns. J Clin Pathol 2003;56:826–830 [48] LeVay J, O’Sullivan B, Catton C, et al. Outcome and prognostic factors in soft tissue sarcoma in the adult. Int J Radiat Oncol Biol Phys 1993;27:1091–1099 [49] Enneking WF. A system of staging musculoskeletal neoplasms. Instr Course Lect 1988;37:3–10 [50] Johnson MD, Glick AD, Davis BW. Immunohistochemical evaluation of Leu-7, myelin basic-protein, S100-protein, glial-fibrillary acidic-protein, and LN3 immunoreactivity in nerve sheath tumors and sarcomas. Arch Pathol Lab Med 1988;112:155–160 [51] Hirose T, Hasegawa T, Kudo E, Seki K, Sano T, Hizawa K. Malignant peripheral nerve sheath tumors: an immunohistochemical study in relation to ultrastructural features. Hum Pathol 1992;23:865–870 [52] Ghosh BC, Ghosh L, Huvos AG, Fortner JG. Malignant schwannoma: a clinicopathologic study. Cancer 1973;31:184–190 [53] Murphey MD, Smith WS, Smith SE, Kransdorf MJ, Temple HT. From the archives of the AFIP. Imaging of musculoskeletal neurogenic tumors: radiologic-pathologic correlation. Radiographics 1999;19:1253–1280

[54] Bhattacharyya AK, Perrin R, Guha A. Peripheral nerve tumors: management strategies and molecular insights. J Neurooncol 2004;69:335–349 [55] Landy H, Feun L, Markoe A, et al. Extended remission of a recurrent median nerve malignant peripheral nerve sheath tumor after multimodal treatment: case report. J Neurosurg 2005;103:760–763 [56] Grobmyer SR, Maki RG, Demetri GD, et al. Neo-adjuvant chemotherapy for primary high-grade extremity soft tissue sarcoma. Ann Oncol 2004;15:1667– 1672 [57] Bramwell V, Rouesse J, Steward W, et al. Adjuvant CYVADIC chemotherapy for adult soft tissue sarcoma—reduced local recurrence but no improvement in survival: a study of the European Organization for Research and Treatment of Cancer Soft Tissue and Bone Sarcoma Group. J Clin Oncol 1994;12:1137–1149 [58] Steins MB, Serve H, Zühlsdorf M, Senninger N, Semik M, Berdel WE. Carboplatin/etoposide induces remission of metastasised malignant peripheral nerve tumours (malignant schwannoma) refractory to first-line therapy. Oncol Rep 2002;9:627–630 [59] Skotheim RI, Kallioniemi A, Bjerkhagen B, et al. Topoisomerase-II alpha is upregulated in malignant peripheral nerve sheath tumors and associated with clinical outcome. J Clin Oncol 2003;21:4586–4591 [60] Sarcoma Meta-analysis Collaboration. Adjuvant chemotherapy for localised resectable soft-tissue sarcoma of adults: meta-analysis of individual data. Lancet 1997;350:1647–1654 [61] Doorn PF, Molenaar WM, Buter J, Hoekstra HJ. Malignant peripheral nerve sheath tumors in patients with and without neurofibromatosis. Eur J Surg Oncol 1995;21:78–82 [62] Marom EM, Helms CA. Fibrolipomatous hamartoma: pathognomonic on MR imaging. Skeletal Radiol 1999;28:260–264 [63] Spinner RJ, Atkinson JL, Scheithauer BW, et al. Peroneal intraneural ganglia: the importance of the articular branch. Clinical series. J Neurosurg 2003;99:319–329 [64] Spinner RJ, Amrami KK, Wolanskyj AP, et al. Dynamic phases of peroneal and tibial intraneural ganglia formation: a new dimension added to the unifying articular theory. J Neurosurg 2007;107:296–307 [65] Hahn AF, Mauermann ML, Dyck PJ, Keegan BM. A 16-year-old girl with progressive weakness of the left leg. Neurology 2007;69:84–90

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Surgical Management of Chronic Headaches, Migraines, and Neuralgias

19 Surgical Management of Chronic Headaches, Migraines, and Neuralgias

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Ivica Ducic

19.1 Introduction Multiple types of headaches are recognized by the International Headache Society and other national and international experts and organizations, and new and evolving definitions are further delineating the characteristics, pathophysiology, and treatment of headaches.1–4 Although definitions of some common headaches (▶ Table 19.1) point to their differences, the nomenclature remains confusing, as not only do different types of headaches have overlapping symptoms, but also different types of headaches or migraines can be present in the same patient at different times. Thus, it comes as no surprise that many of these patients remain misdiagnosed, thereby significantly diminishing the chance for a successful treatment outcome.5 Our understanding of headache pathophysiology now acknowledges the combinations of rather than the individual role of vascular, hormonal, central, and peripheral nervous system variables.6–13 Because of the multifactorial etiology, various clinical presentations, including headaches, migraines, and neuralgias, and number of different specialists involved in treating patients, treatment options are countless. Unfortunately, none are ideal, mostly due to specialists’ focus on a single variable, incomplete understanding of pathophysiology, and lack of a multidisciplinary approach.14–16 As discussed throughout this chapter, a team approach and multidisciplinary treatment options, properly timed and synced, provide the best chance for yielding improved outcomes.16 To simplify terminology for the purposes of this chapter, commonly encountered conditions such as chronic daily headaches, migraine headaches, postoperative headaches, occipital neuralgia, frontotemporal trigeminal neuralgia, posttraumatic headaches, postherpetic neuralgia, and other less commonly encountered conditions will be referred to as chronic headaches. Migraine headache, a well-documented form of chronic headache, is characterized by at least a 3-month history of headaches occurring 15 or more days per month, meeting criteria for migraine on 8 or more days per month, in the absence of medication overuse (▶ Table 19.1).1–4 One out of three patients with migraines experience aura prior to migraine, developing over 15 to 20 minutes while lasting less than 60 minutes. Overall, migraine is reported to affect about 12% of the U.S. population, while chronic migraine prevalence globally is ~ 1% (0.5– 2.2%).17–19 Considering that migraine sufferers are typically adults in their prime earning years, with prevalence being highest for those ages 25 to 45 years, this debilitating condition is responsible for a significant loss of productivity.20,21 The estimated cost of migraine treatments in the United States alone is about $14 billon, with an additional $13 billion associated with loss of work.22 It also has a severe negative effect on a patient’s quality of life, as well as family and social functioning.5 It is not surprising, then, that a search for a better understanding of the pathophysiology of migraines and other forms of chronic headaches, and thus an avenue for better treatment, is intense. Regardless if one or a combination of the aforementioned types of

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CH is present, three separate anatomical regions can be affected: the frontal, temporal, and occipital area of the head. As is further discussed, each area, individually or in combination, may pose as a pathophysiological trigger for a patient’s chronic headache (migraine, headache, and/or neuralgia). Frontotemporal trigeminal neuralgia (FTTN) is a relatively sparsely documented cause of chronic headaches (▶ Table 19.1).23–25 It presents as unilateral or bilateral frontal and/or temporal headache, with pain or pressure over the supraorbital, supratrochlear, infratrochlear, zygomaticotemporal, and/or auriculotemporal nerves. The differential diagnosis may be somewhat challenging, as it shares features with migraine and cluster headaches; trigeminal neuralgia; sinusitis; visual, nasal, septal/turbinate, or temporomandibular joint (TMJ) abnormalities; and SUNCT (short-lasting, unilateral, neuralgiform headache with conjunctival injection and tearing) syndrome.26–29 Following the exclusion of these variables, several different treatment modalities have been used with varying degrees of success, including glycerol injection, local anesthetic blockade, trigeminal ganglion ablation or decompression, radiofrequency ablation, peripheral nerve stimulation, acupuncture, and neurolysis.30–33 In rare instances, patients with chronic posttraumatic or postsurgical FTTN-related chronic headaches will have an underlying discrete neuroma entrapped in scar tissues that can be identified and resected to achieve a successful therapeutic end.34,35 It has been estimated that 60% of patients with this infirmity will require some form of support from society. The intangible burden of suffering on the patient can be devastating as well, causing relationship disturbances, emotional liability, and even suicidal ideation. This problem translates to a high socioeconomic cost in terms of missed work, disability benefits, and early retirement.36 In other cases, the supraorbital, supratrochlear, intratrochlear, zygomaticotemporal, and/or auriculotemporal nerves bear no distinct lesion but may suffer from compression by the corrugator supercilii muscle, supraorbital fibrous arch, supraorbital notch or foramen, temporalis muscle, or adjacent structures that can lead to a chronic and severe headache syndrome.28,37,38 These patients have often undergone extensive diagnostic testing or have taken numerous neuroleptic or analgesic medications without benefit. Surgical management of FTTN-related chronic headaches has been previously reported in the literature; however, the details of the operation have been vague, and the patient series has been limited. Outlined later in this chapter are the anatomy, indications for intervention, and the types of surgical treatment available. Occipital neuralgia (ON) is another well-documented form of chronic headache. A refractory and often disabling disorder, it is characterized by chronic headaches of moderate to severe intensity localized to the occipital region. It presents as unilateral or bilateral, mostly constant aching, burning, throbbing, or shooting occipital pain, often radiating to the top of the scalp or anteriorly to the eye, face, or neck (▶ Table 19.1). No specific age range or differences in prevalence between men and women are reported. Patients often complain of difficulty lying on

Surgical Management of Chronic Headaches, Migraines, and Neuralgias Table 19.1 Diagnosis and Classification of Common Headache Disorders Headache Type Migraine headache

Clinical Features ●

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Tension headache

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Cluster headache

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Cervicogenic headache

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Occipital neuralgia

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Frontotemporal trigeminal neuralgia

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Significance

Episodic headache lasting 4 to 72 hours with any two of unilateral; throbbing; moderate to severe; worsened by movement; and any one of nausea or vomiting; photophobia and phonophobia. Chronic migraine: at least a 3-month history of headaches occurring ≥ 15 d/mo, meeting criteria for migraine on ≥ 8 d/mo, in the absence of medication overuse

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Usually bilateral, dull, pressing, bandlike tightening Mild to moderate, lasts 30 minutes to 7 days Sensitivity to light or sound but no nausea May affect frontal, frontotemporal, and occipital area No worsening with exertion

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Severe, excruciating, unilateral, orbital pain If untreated, lasts 15–180 minutes Affects orbital, periorbital, or temporal regions Autonomic symptoms (any 2 of): rhinorrhea, lacrimation, facial sweating, ptosis, eyelid edema, conjunctival injection

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Usually unilateral: neck, occipital, or frontotemporal Associated with neck movement or head position Ipsilateral shoulder, neck, or nonradicular arm pain Typically constant or intermittent but rarely throbbing

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Aching, burning, and throbbing pain that typically starts at the base of the head and radiates to the scalp Unilateral or bilateral Tender occipital nerves on pressure Often difficulties lying on back of head (“pillow“ sign) Pain behind the eye; hypersensitive occipital scalp

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Unilateral or bilateral frontotemporal pain or pressure Tender zygomaticotemporal, auriculotemporal, supraorbital, and/or supratrochlear nerves

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● ●

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● ●

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Most common headache Affects women more than men Episodic tension headaches occur < 15 d/mo, chronic ≥ 15 d/mo No associated symptoms

Peak incidence: age 20–40 years 5 times more common in men than women May occur once to 8 times a day, in cycles from 1 week to every year Episodic cluster headaches occur for < 1 year, chronic occur for ≥ 1 year No specific age range Affects both men and women equally Associated with cervical spine abnormalities; rarely dizziness or nausea

No specific age range Affects both men and women equally Involves greater, dorsal, lesser occipital nerves, and/or C2 or C3 nerve roots Retro-orbital pain with severe attacks

No specific age range Can be present with sinus problems, TMJ abnormality, deviated septum, malocclusion, eye problem

Chronic daily headache

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Headache of any kind lasting ≥ 15 d/mo for at least 3 months

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Evolving definitions are a work in progress by many national and international societies

Postoperative headache and Posttraumatic headache

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Following previous head and neck surgical intervention or trauma, respectively May involve frontal, temporal, and/or occipital region May present as neuralgia, headache, and/or migraine

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No specific age or gender predisposition Pain location mostly within operative field Onset with surgery or trauma Multidisciplinary approach required

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●

● ● ●

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Affects 10% of adult U.S. population, 5% of young children, 10% of adolescents 3 times more common in women than men (21 vs. 7 million) Peak incidence: age 25–45 years Family history of migraine common Severely disabling and difficult to manage Chronic migraine is associated with substantially more frequent headaches, comorbid pain and affective disorders, and fewer pain-free intervals when compared to episodic migraines

Abbreviation: TMJ, temporomandibular joint. Source: Data from Headache Classification Committee of the International Headache Society. Classification and diagnostic criteria for headache disorders, cranial neuralgias and facial pain. Cephalalgia 1988;8(Suppl 7):1–96; and Headache Classification Committee of the International Headache Society. The International Classification of Headache Disorders 2nd ed. Cephalalgia 2004;24:1–160.

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Surgical Management of Chronic Headaches, Migraines, and Neuralgias the back of their head due to occipital scalp hypersensitivity (“pillow” sign) and can have severe occasional retro-orbital pain, especially when pressure is applied over tender occipital nerves. Tenderness is usually distributed over the greater, dorsal, and/or lesser occipital nerves, while abnormal C2 or C3 nerve roots can equally present as ON. Many patients suffer for years, translating into diminished productivity, dependence on pain medications, and frustration on the part of the patient and physician. Since it was first described in 1821, numerous etiologies have been theorized and a variety of interventions employed in the treatment of ON. The most probable etiology is thought to be compression of the occipital nerve(s) by adjacent structures. 39–44 ON probably represents a specific disorder that exists along a continuum of posttraumatic pain, whiplash, cervical spine abnormality, tension headache, chronic daily headache, and migraine.1,4,16, 41 Related labels that have been applied include Arnold neuralgia, posterior cervical sympathetic syndrome, cervical migraine, occipital neuritis, cervicogenic headache, and spinally transformed migraine.45–47 Although controversy exists regarding diagnostic criteria and nomenclature, the pertinent findings tend to be occipital headache/pain despite optimized medical care, tenderness over the occipital nerves, and temporary headache elimination by anesthetic block of the occipital nerve on the affected side(s). 16,48,49 Various treatment modalities have been employed, including neuromodulation, C2 gangliotomy, C2 gangliectomy, C2–C3 rhizotomy, C2–C3 root decompression, radiofrequency lesioning, subdermal denervation, neurectomy, and neurolysis with or without section of the inferior oblique muscle. 16,38,43,44,50–56 These interventions have enjoyed varying degrees of success, although many studies suffer from a limited sample size. Before defining the pathophysiologic mechanisms responsible for the various types of chronic headache, let us review the relevant peripheral nerve anatomy.

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19.2 Anatomy 19.2.1 Supraorbital, Supratrochlear, and Infratrochlear Nerves The trigeminal nerve arises from the lateral aspect of the pons. The sensory root gives rise to the gasserian ganglion, which lies within the petrous part of the temporal bone in the posterior cranial fossa. The first division of the trigeminal nerve, the ophthalmic nerve (V1), arises from the anteromedial gasserian ganglion, then passes through the wall of the cavernous sinus below the trochlear nerve.33,57 It then divides into the frontal, lacrimal, and nasociliary branches, which enter the orbit by means of the superior orbital fissure. The frontal branch lies just above the levator complex and divides into the supraorbital (SON), supratrochlear (STN), and infratrochlear (ITN) nerves, typically before their exit from the skull. These nerves provide sensation to the skin of the forehead, the medial angle of the eye, and the upper eyelid (but not the cornea).30 The SON typically exits the frontal bone by means of a palpable notch or foramen along the middle third of the supraorbital rim. This exit may vary and can be located anywhere along, above, or even lateral and superior to the supraorbital rim. 58 The STN typically leaves no notch or impression on the frontal bone. Beyond the orbital rim, the SON has two consistent divisions: a superficial or medial division that passes above the frontalis muscle to innervate skin on the forehead and the anterior margin of the scalp, and a deep or lateral division that travels distally along the lateral forehead between the galea and the pericranium. 59,60 Clinically, the SON can be located by means of palpation with the fingernail or along a line in the midsagittal plane perpendicular to the edge of the medial limbus. The STN is located between 8 and 10 mm medial to the supraorbital nerve. Like the STN, the ITN and SON branches pass under or through the corrugator muscle that can function as a nerve compression site

Fig. 19.1 Frontotemporal nerves involved with headaches.

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Surgical Management of Chronic Headaches, Migraines, and Neuralgias (▶ Fig. 19.1). It is this superficial location, in addition to passage through the supraorbital notch or foramen, with minimal soft tissue coverage and abutting the noncompressible frontal bone, that render the SON, STN, and ITN susceptible to damage. Injury can be acute, surgery- or trauma-related SON, STN, or ITN neuroma, or it can be the result of chronic nerve compression. In either case, FTTN-related CH may be the unfavorable outcome, mandating more than medical treatment alone.

19.2.2 Zygomaticotemporal and Auriculotemporal Nerves The zygomaticotemporal nerve (ZTN) is a branch of the maxillary division (V2) of the trigeminal nerve and is completely sensory in nature. The maxillary nerve emerges from the trigeminal ganglion, passes through the foramen rotundum, then courses on the upper part of the posterior surface of the maxilla, where in the pterygopalatine fossa it gives off the zygomatic branch.57 The nerve then courses toward the orbit and its lateral wall along the inferior orbital fissure, bifurcating into the zygomaticotemporal and zygomaticofacial branches. The ZTN passes along the inferolateral angle of the orbit, provides a branch to the lacrimal gland, then traverses a bony canal in the zygomatic bone to enter into the temporal fossa, where it courses between the bone and the temporalis muscle. It pierces the deep temporal fascia ~ 2 cm above the zygomatic arch (6–7 mm lateral to the lateral orbital rim and 7–8 mm superior to the nasion horizontal line) to innervate the skin of the temporal area (▶ Fig. 19.1). As it pierces the temporal fascia, it sends a small parasympathetic branch toward the lateral angle of the orbit, into the lacrimal gland. A horizontal branch of the ZTN communicates with the auriculotemporal nerve.61,62 A second branch of the ZTN can sometimes be found, where the nerve goes through or under the temporalis muscle, piercing it lateral to the lateral orbital rim. It is the portion of the nerve’s course through the temporal fossa and temporalis muscle that poses a potential compression site for the ZTN, serving as a possible generator for tenderness and a source of FTTN-related chronic headaches. The auriculotemporal nerve (ATN) comes off the posterior trunk of the mandibular nerve (V3). It emerges from behind the TMJ, posterior to the superficial temporal vessels, and courses over the posterior root of the zygoma, then divides into superficial temporal branches. 57 The nerve branches include the superior auricular (providing sensation to the skin of the tragus/helix), external acoustic meatus (skin of the meatus, tympanic membrane), articular (posterior part of the TMJ), parotid (secretomotor fibers to the gland), and superficial temporal (skin in the temporal region). The superficial temporal branches accompany the superficial temporal artery in the temporal region and communicate with the facial and zygomaticotemporal nerves.61,63 Unlike the ZTN, the ATN does not appear to have a proven compression site, although intraoperative observations indicate direct mechanical ATN irritation by superficial temporal artery and fibrous bands along its course. Nerve tenderness on exam and positive temporary effect of nerve blocks are highly suggestive of ATN involvement.

19.2.3 Greater, Lesser, and Dorsal Occipital Nerves

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The greater occipital nerve (GON) arises from the dorsal ramus of C2 deep to the inferior oblique muscle, at which point C2 branches.57 The medial branch of C2 is the GON, which runs transversely along the inferior oblique and is covered by the splenius capitis, the longissimus, and the semispinalis capitis muscles. Occasionally, the nerve travels within the substance of the inferior oblique muscle. The nerve then turns upward to pierce the semispinalis capitis. Here the nerve runs rostrolaterally before emerging into the scalp by piercing the aponeurotic fibrous attachments of the trapezius and sternocleidomastoid to the superior nuchal line.64 In this aperture (trapezial tunnel), the occipital artery and occasionally the lymph nodes are in intimate association with the GON.65 Immediately below the superior nuchal line, the nerve divides into several terminal branches; medial branches innervate the occipital skin, extending to the parietal scalp, and lateral branches pass into the region behind the pinna, connecting with the lesser occipital nerve (LON) (▶ Fig. 19.2). It has been demonstrated that the GON has an average diameter of 3.8 ± 1.6 mm and emerges from the semispinalis capitis muscle 14.9 ± 4.5 mm lateral to the midline and 30.2 ± 5.1 mm inferior to the occipital protuberance. The nerve almost always (98.5%) pierces the body of the semispinalis capitis muscle, and in 6.1% of individuals, it is split by fibers of this muscle or in the trapezial tunnel. It is important to note that in 43.9% of patients, the GONs on the right and left sides can be asymmetric, in either horizontal or vertical axes.64–68 These observations serve as a correction to several anatomical misconceptions depicted in some anatomical atlases relating to GON anatomy (▶ Fig. 19.3). The LON arises from the dorsal rami of C2 and occasionally C3. It ascends toward the occiput parallel to the posterior border of the sternocleidomastoid muscle, occasionally piercing it.57 Its average diameter is 1.2 ± 1.6 mm. Near the cranium, it perforates the sternocleidomastoid fascia, where it is susceptible to compression, and continues superiorly over the occiput, where it innervates the mastoid and lateral occipital skin, communicating medially with the GON.65,69,70 Some variability in anatomy exists, but the nerve tends to emerge from the posterior border of the sternocleidomastoid muscle above the point of emergence of the great auricular nerve (▶ Fig. 19.2; ▶ Fig. 19.3). This point is ~ 60 to 70 mm from the midline and 40 to 60 mm inferior to a line drawn between the lowest points of the external auditory canals. The dorsal occipital nerve (DON) arises from the dorsal rami of C3. The third cervical dorsal ramus courses medial to the posterior intertransverse muscle, dividing into medial and lateral branches. Its medial branch runs between the spinalis capitis and semispinalis cervices muscles, piercing the splenius and trapezius to innervate the skin.57,65,69,70 Deep to the trapezius, it gives rise to the lateral branch, the third/dorsal occipital nerve, which pierces the trapezius on its course to the skin of the lower occipital region, where it lies medial to the GON and connects with it. Communications between the GON and DON are not uncommon (▶ Fig. 19.2; ▶ Fig. 19.3).

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Surgical Management of Chronic Headaches, Migraines, and Neuralgias

Fig. 19.2 Anatomy of the occipital nerves.

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Fig. 19.3 Anatomical variations of occipital nerves.

19.3 Pathophysiology 19.3.1 Peripheral and Central Sensitization Role in Triggering and Maintaining Chronic Headaches and Migraine Headaches The humoral and cellular mechanisms of headache have been well studied, yet no consensus exists as to the exact pathway of pain generation. Over the past few decades, proposed mechanisms have included peripheral and central sensitization, referred pain, parasympathetic activation, and pain transmission, blending both neuronal and vascular variables. Interleukin type 1 (IL-1), tumor necrosis factor (TNF), and nitric oxide have also been implicated as promoting mediators, particularly for

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hyperalgesia.6–13 Despite the existence of complex molecular– biological mechanisms, it seems clear when reviewing the body of literature on this topic that there is often a peripheral trigger, such as nerve irritation, that touches off the central pain cascade (▶ Fig. 19.4). Nerve irritation and hyperexcitability of peripheral nociceptors may lead to central sensitization and pain evoked by nonnoxious stimuli.71 The response of these types of headache to peripheral nerve block further strengthens this theory. Similarly, connections between the trigeminal nucleus and the upper four cervical roots may form the anatomical substrate for the spread of cervical pain from the neck to the head.72 The proximity of the occipital artery to the GON has also been postulated to cause nerve compression and paroxysmal, throbbing pain.73,74 As summarized by the author and suggested by the literature, five sources of potential entrapment are observed for the GON,

Surgical Management of Chronic Headaches, Migraines, and Neuralgias

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Fig. 19.4 Pathophysiology: peripheral nerve involvement in headaches.

three for the LON, and two for the DON that can lead to occipital neuralgia-related chronic migraines or headaches. Similarly, four potential compression sites have been observed for the SON/STN/ITN, one for the ZTN, and two for the ATN (▶ Table 19.2) Although controversy continues, ranging from definitions to CH treatments, it is important to acknowledge that the underlying pathophysiology has its peripheral and central mechanisms, most likely supporting each other, regardless of the nature of the first generator that initiated the headache (▶ Fig. 19.5). By understanding the often overlapping symptomatology of various types of chronic headaches and migraines, it is important to focus treatment on targeting one or more possible causative mechanisms. Thus, it is the author’s opinion that, although the initial medical treatment may focus primarily on various central sensitization components, surgical treatment of peripheral sensitization should be considered soon after medical treatment is seen as plateauing or is found to be ineffective. This means that focus should not be not only on symptoms and definitions, but also on search for the potential peripheral sensitization site, including nerve compression triggering the central sensitization and thus any form of chronic headache.16 Supporting this concept is the finding that,

although many patients may present with the same type of chronic migraine or headache, prescribed migraine medications help some patients but not others, and certain patients only partially. Different mechanisms—peripheral nerve involvement, whether central, metabolic, or a combination—give rise to the same symptomatic complex, characterized by the same headache category. Therefore, understanding the negative feedback of these different mechanisms on each other necessitates multidisciplinary treatments, including surgical intervention that supplements the medical care of patients with migraines and chronic headaches.

19.4 Diagnostic Evaluation and Workup Patients with any form of chronic headache require specialized providers, such as neurologists and anesthesia pain specialists with expertise and interest in the treatment of headaches. These providers should establish a proper diagnosis based on a thorough evaluation and workup. For patient safety reasons, it is important that, unless supervised by a physician specialized in headache management, other medical providers or physi-

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Surgical Management of Chronic Headaches, Migraines, and Neuralgias Table 19.2 Chronic Headache, Migraine, and Neuralgias: Nerve Compression Sites

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Nerve

Associated Migraine/Chronic Headache Peripheral Compression Sites

Greater occipital

Occipital

● ● ● ●

●

Lesser occipital

Occipital

● ● ●

Dorsal occipital

Occipital

● ●

Supraorbital-supratrochlear

Frontal

Spine/C2, C3 nerve root Sternocleidomastoid muscle (SCM) SCM fascia attaching to the mastoid Spine/C2, C3 nerve root Trapezius muscle and fascia

●

Supraorbital foramen/notch Corrugator muscle Supraorbital/trochlear vasculature Frontalis muscle (rarely)

● ● ●

Zygomaticotemporal

Temporal

●

Temporalis muscle

Auriculotemporal

Temporal

●

Superficial temporal artery Deep fascial bands

●

Fig. 19.5 Pathophysiology: headache versus migraine mechanisms.

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Spine/C2 nerve root Inferior oblique muscle Semispinalis capitis muscle Trapezial tunnel (trapezius muscle and its aponeurotic attachments to occipital bone) Angiolymphatics (occipital artery/vein and/or lymph node within or at the distal trapezial tunnel)

Surgical Management of Chronic Headaches, Migraines, and Neuralgias cians with no expertise or interest in the treatment of patients with any form of chronic headache should not serve as the first-line providers to these patients, primarily to minimize medical mistakes, misdiagnoses, and well-intentioned but improper treatments. After establishing a proper diagnosis and initiating medical treatment (▶ Table 19.1), the specialist should monitor a patient’s progress.16 Once an acute/episodic migraine, neuralgia, or headache becomes chronic despite appropriate medical treatment (headache of any kind lasting 15 or more days per month, for at least 3 months), consideration should be given to peripheral nerve involvement, triggering that patient’s type(s) of headaches. In such case, tenderness over the nerve at a known compression site (▶ Table 19.2) should be suggestive, while observation of positive, although temporary, response to a peripheral nerve block is confirmatory for a tested peripheral trigger point site.16,48,49,72,75 A positive, transient response to a nerve block is defined as headache/migraine relief lasting a few hours, a few days, or even a few weeks. Unless the patient is allergic, a longer-acting anesthetic with steroid may yield the best results. The physician may opt to use a minimal dose of steroids or not at all in the frontotemporal region to prevent steroid-induced skin discoloration or subcutaneous soft tissue wasting, with the corresponding negative aesthetic outcome. A nerve block can be administered at those locations to observe the best response. The following sites for nerve blocks, based on patient complaints and presentation, can be suggested: ● GON: 3 cm below the occipital protuberance and 2 to 3 cm lateral from the midline ● DON: 3 cm below the occipital protuberance and 1 to 2 cm lateral from the midline ● LON: 3 cm below the occipital protuberance’s horizontal line and ~ 5 to 6 cm lateral to the occipital protuberance (follow the posterior border of the sternocleidomastoid attachments to the mastoid) ● SON-STN (frontal headaches): corrugator muscle area, just into/above the eyebrow ● ZTN (temporal headaches): 1 cm lateral to the lateral orbital rim and ~ 1 cm superior to the lateral canthal area, into the temporalis muscle ● ATN (temporal headaches): 1 cm anterior to the ear with the line horizontal to the top of the helix (along the superficial temporal artery path, above the sideburn) If the nerve block has no response, it can be repeated in a few weeks; at that time, it can be given at a slightly different site, compensating for possible anatomical variations, particularly in the occipital area.16,65,76 An alternative and significantly more expensive diagnostic modality is local injection of botulinum toxin A), which acts directly on muscle tone and vascular physiology.38,77,78 About 15 units of freshly prepared drug can be administered into each anatomical region (right around the nerves, not all over the head/neck). The drug effect may take 1 to 2 weeks. In my practice, I find nerve block applicable in > 90% of patients, as the only diagnostic agent used, while botulunum toxin A is reserved for patients with sporadic ON/migraine/ chronic headache or those not responding to blocks. This way, a nerve block provides the same information (involvement of blocked nerves in pathophysiology of headache/migraine/neuralgia pain) but at about one-tenth the cost of a botulinum toxin

A diagnostic procedure. Certainly, routine office administration precautions (allergy check, aspiration prior to anesthetic injection, single-use sterile supplies, practitioner’s familiarity with the procedure, etc.) are required when handling either nerve block or botulinum toxin A. In addition, the practitioner may choose to block one anatomical region at a time, in order to define its role in the patient’s headache/migraine pathogenesis, further facilitating decision making for what type of surgery and what anatomical region require priority. Patients with ON-related migraine or chronic headache, in the presence of neck pain, would need to have potential spinerelated pathology ruled out. If identified and if it warrants surgical intervention as determined by a spine surgeon, this should take place prior to peripheral nerve surgery on the occipital nerves. Likewise, patients with FTTN-related chronic migraines or headaches may need to have an evaluation by several different specialists, given they also have symptoms suggesting a deviated septum and sinus related problems (ear, nose, and throat specialist), malocclusion and TMJ problems (dentist/oral surgeon), and vision-related concerns (ophthalmologist). Peripheral nerve surgery can then be considered if these evaluations have been addressed; see box below.

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Indications for Surgical Treatment of Chronic Headaches ● ●

●

●

●

●

Patient under the care of a headache specialist Established diagnosis of chronic headache or one of its forms (see ▶ Table 19.1) Other medical, drug-induced, or anatomically specific pathologies ruled out and addressed if symptomatic, including ○ Cervical, spine, and brain abnormalities ○ Deviated nasal septum and sinus problems ○ Visual issues ○ Dental problem (e.g., malocclusion, temporomandibular joint abnormality) Failure of conservative treatment (headache/migraine/neuralgia symptoms present for at least 3 months despite headache specialist supervised medical treatment) Positive (although temporary) response to a nerve block or botulinum toxin A Patient is suitable surgical candidate

19.5 Surgical Technique 19.5.1 Patients with Frontal or Temporal Neuralgia-related Chronic Headache or Migraine With the patient in the supine position, upon administration of local anesthetic and under general anesthesia, the dissection of the SON, STN, and/or ITN on the affected side(s) is performed by means of an upper eyelid skin crease incision.32 The dissection is performed in anatomical layers through the preseptal plane toward the orbital rim. The corrugator supercilii muscle is identified and the SON, STN, and ITN followed. The nerves, dissected under loupe magnification, are decompressed by means

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Fig. 19.6 (a) Access incisions for an open approach to the supraorbital/ supratrochlear nerves (SON/STN). (b) Intraoperative open view: SON/STN.

of releasing the corrugator supercilii muscle and the supraorbital notch/foramen where indicated (▶ Fig. 19.6). The same procedure can be performed endoscopically, using three ports in the frontal scalp when bilateral access is needed. 38,79 Subperiosteal dissection is carried just superior to the SON/STN exit from the supraorbital rim, while muscle resection is performed under direct vision, with care being taken to identify and preserve nerve branches (▶ Fig. 19.7). In those cases where traumatic neuroma is being treated, open excision rather than decompression of the nerve is required, and end-to-end proximal stump nerve implantation can be considered to minimize neuroma recurrence.34 The endoscopic approach to ZTN decompression is performed using an anterotemporal incision that can serve by itself for the nerve access or that can be combined with lateral ports used for SON/STN access.38 Endoscopic dissection is carried under direct vision, staying on top of the deep temporal fascia and taking care not to violate the plane carrying the frontal branch of the facial nerve. Once the ZTN is encountered adjacent to the lateral orbital rim, the transection can be performed (▶ Fig. 19.8). If the ATN needs to be excised as well, a separate, more posterior vertical incision is made, and the ATN and superficial temporal artery are accessed and the nerve transected (▶ Fig. 19.8a).

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Fig. 19.7 (a) Access incisions for an endoscopic approach to the supraorbital/supratrochlear/zygomaticotemporal nerves (SON/STN/ ZTN). (b) Intraoperative endoscopic view: SON/STN.

19.5.2 Patients with Occipital Neuralgia-related Chronic Headache or Migraine With the patient in the prone position and under general anesthesia, proper positioning is ensured so that no focal pressure is applied to the eyes or extremities. Head and neck position should be neutral to slightly flexed, so that neck extension, which can obscure intraoperative visualization, is minimized. The incision for GON access is marked ~ 2 to 3 cm below the occipital protuberance and extends ~ 3 cm on each side of the midline (▶ Fig. 19.9). The incision is deepened through anatomic planes to expose the trapezius. A vertical incision is then developed over the trapezius fascia, enabling access to the DON and GON. If a small branch of the DON is identified within the field, it can be resected under tension and allowed to retract into the musculature so that it will not become entrapped by

Surgical Management of Chronic Headaches, Migraines, and Neuralgias

Fig. 19.8 (a) Access incisions for an open or endoscopic approach to the zygomaticotemporal/auriculotemporal nerves (ZTN/ATN). (b) Intraoperative endoscopic view: ZTN.

scar within the dissection field and cause a painful neuroma. Careful dissection is then continued to identify the GON, typically as it emerges from the semispinalis capitis muscle (SSCM) (▶ Fig. 19.10). Dissection is first carried proximally, removing the small medial piece of the SSCM abutting the GON, then inferiorly to release the inferior obliquus capitis muscle (IOCM) fibers overlying the GON.16,32,65 In ~ 6% of patients, the nerve is found to be split within the substance of the SSCM (▶ Fig. 19.11), in which case the muscle fibers are released. Approximately 40% of patients have GON asymmetries between the two sides, either in the vertical or the horizontal plane (▶ Fig. 19.12; ▶ Fig. 19.13).16,65 Dissection is then carried distally, releasing the nerve within the trapezial tunnel (the site where the GON penetrates through the trapezial fascial attachments to the occiput). This 1- to 2-cm tunnel has an oblique superolateral direction and often contains angiolymphatics, another possible compression variable to be acknowledged.16,65 Usually at its superolateral distal end the occipital artery and vein cross the GON. If the vessels are found to impinge on the nerve, they are dissected free and ligated. If present, any enlarged and abutting lymph nodes in direct contact with the nerve are also removed from the tunnel, further decompressing the nerve. The same incision can often be used to treat the opposite side when needed. The wound is closed in anatomical layers without drains. The same approach is used if GON transection and implantation are indicated, except in that case implantation of the proximal stump of the GON is performed deeply and under the SCCM. Microsurgical instruments and techniques, as well as 4.0 magnifying loupes, are used for all peripheral nerve surgery procedures. If a unilateral LON excision is performed concurrently, a small 3-cm incision is made at a separate site lateral to the first incision, over the path of the LON, which is identified over the middle third of the posterior border of the sternocleidomastoid muscle. The LON can be decompressed or excised and its proximal stump implanted into muscle. If bilateral GON decompression and LON decompression or transection is performed, a

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Fig. 19.9 Access incisions for an approach to the greater occipital/dorsal occipital nerves (GON/ DON).

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Fig. 19.10 Intraoperative view showing the normal appearance of a bilateral greater occipital nerve piercing the semispinalis capitis muscle.

modified approach is employed.16 Two separate incisions are made, one on each side, each to access the ipsilateral GON and LON (▶ Fig. 19.14). In this way, two rather than three or four incisions are made to access all nerves. The entire outpatient procedure for either occipital or frontotemporal nerves takes ~ 1 hour. One variable (anatomical area) is surgically treated (occipital vs. frontotemporal) at the time, with 3 to 4 months of observation needed before proceeding with the next anatomical region. This approach has two advantages. First, the true response at the first anatomical region can be determined; in some patients, this prevents pain from spreading to other areas (e.g., from the occipital to the frontal areas), thus minimizing the need for unnecessary additional procedures. However, if FTTN continues despite adequate surgical treatment of the occipital region, then the frontotemporal area is addressed. Second, operative time with either surgery is often under 1 hour, which is well tolerated by patients and permits rapid recovery.

19.6 Discussion Although most important aspects related to the surgical treatment of patients with chronic headaches has been discussed, a

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number of questions remain to be answered. Upon review of the current literature, it is clear that conflicting information is available, further complicating the proper treatment of patients with any form of chronic headache. The reported prevalence of FTTN in patients with frontal or temporal chronic or migraine headaches has been estimated to be 0.5 to 1.0%.17,29,36 Often patients with FTTN have undergone pharmacologic or more invasive treatments to alleviate their symptoms. Some of the procedures for the treatment of trigeminal neuralgia (glycerol injection, ganglionic section, thermocoagulation, and the Janetta procedure) may be of therapeutic benefit, but they are often too radical or invasive to be appropriately considered in FTTN due to SON/STN nerve compression.30 Similarly, pharmacologic management that may be appropriate for migraines, cluster headaches, and SUNCT syndrome can of little benefit in patients with FTTN. 14,28 Acupuncture has been reported to be of some therapeutic benefit. 31 Local anesthetic injection of the nerves in the frontotemporal region has been reported to be helpful; however, these injections often provide short-term relief and must be repeated frequently.28,80,81 Supraorbital nerve avulsion has also been considered; however, symptoms tend to recur in 6 to 12 months. 30 Occasionally, a neuroma is found at the time of exploration or is

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Fig. 19.11 Intraoperative view of a left greater occipital nerve split with muscle fibers.

clinically palpated preoperatively. Reported events leading to traumatic neuroma of the SON, STN, or ZTN include brow lift, motor vehicle collision, shrapnel injury, orbital enucleation, halo fixation, frontal bone fracture, and even insect bite. 82–86 In these cases, resection of the neuroma with implantation, rather than decompression, is the most appropriate treatment. 34 Purely compressive causes, including “swim goggle” headache, postoperative scarring, anesthesia mask, cryptic hemangioma, and blunt trauma, have also been described.29,34,38,87,89 Thus, FTTN-related migraine or chronic headache due to compression appears to be most amenable to SON/STN decompression, with or without ZTN/ATN transection, if the temporal component of headache is also present.38 Surgical intervention should be considered upon failure of conservative treatment in patients with tenderness over relevant frontotemporal nerves and positive response to nerve blocks or botulinum toxin A. Occipital pain can arise from other conditions, such as Arnold-Chiari malformation, tumors, vertebrobasilar insufficiency, meningitis, arthritis, gout, polyneuropathy, syphilis, malaria, torticollis, myositis, mastoiditis, postherpetic neuralgia, upper respiratory tract infection, and temporal arteritis.43,90–92 For this reason, neurologic consultation is often recommended prior to surgery. Various treatment modalities have been employed in the treatment of ON.14 Nonsteroidal antiinflammatory drugs

and narcotics tend to provide only transient relief and require frequent, repetitive use.93,94 Ergot derivatives are controversial, with some authors claiming a short-term effect, possibly mediated by constriction of the occipital artery, whereas others find that they are completely ineffective.14,94 Local anesthetic injection alone or in conjunction with corticosteroids may provide lasting pain relief.48 Ethyl alcohol injection may improve symptoms but is associated with high recurrence rates, while epidural corticosteroids have not been shown to be effective.95,96 Different medical treatment regimens may be successfully applied to a specific headache type, but their value in some patients can be limited and may require frequent adjustments. Botox (onabotulinumtoxinA), according to the drug’s prescribing information, is approved in the treatment of headaches in adults (older than 18 years) with chronic migraine who have 15 or more days each month with headache lasting 4 or more hours each day. It has been shown to be effective with a limited duration, although neck weakness has been a complication in 27% of patients.38,77,78 When compared to a placebo group, onabotulinumtoxinA significantly reduced the mean frequency of headache and migraine days and headache and migraine episodes, and it improved patients’ functioning and quality of life.15,97 In these studies, Botox was administered by injection as a minimum dose of 155 units over 31 sites across 7 head and

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Fig. 19.12 Intraoperative view of the left and right greater occipital nerve (GONs), horizontally asymmetric, with the right GON piercing the semispinalis capitis muscle next to the midline raphe, and the left GON ~ 4 cm away from the midline. Blue marker indicates the right half of the midline raphe.

neck muscles. Another 40 units were administered over 8 sites across 3 head and neck muscles, based on the follow-the-pain approach. Despite the reported promising effects of Botox treatments, several important concerns remain. Considering that it only recently received approval from the U.S. Food and Drug Administration for its use in migraine patients, it has yet to be determined what its long-term effects are. For example, what true long-term side effects can be expected as head and neck muscles carrying on an important dynamic and neck-stabilizing function are repeatedly paralyzed and thus inactivated? Based on a suggested Phase REsearch Evaluating Migraine Prophylaxis Therapy (PREEMPT) protocol, using 155 to 200 units of onabotulinumtoxinA per patient during one treatment session costs about $1,300 to $2,500.9,7 Considering this and the fact that onabotulinumtoxinA administration needs to be repeated every few months, this is an extraordinarily expensive treatment modality. Studies are needed to examine its long-term effects and cost-effectiveness. Radiofrequency ablation (RFA) has been identified as a less invasive treatment modality, mostly applied by anesthesia pain specialists. RFA involves the percutaneous insertion of a catheter (typically under fluoroscopic guidance) that is directed

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toward the nerve of interest.98 High-frequency alternating current delivered in a continuous mode induces thermal injury to the targeted tissue and thus ablation of the nerve. Pulsed radiofrequency (RF) signal delivered at a sublethal intensity/frequency in short high-voltage bursts may produce more poorly defined changes in nerve physiology, presently with unknown long-term outcomes. Available reports in the literature are mostly small sample case reports. One of them followed a patient after RFA of the GON, demonstrating 60 to 70% pain relief over 5 months. The treatment had to be repeated for continued efficacy; long-term results remain unknown.54 Another study of 15 patients demonstrated pain relief lasting 8.8 months after RF neurotomy of the C3–C6 dorsal rami; however, during follow-up, it was found that the pain tended to recur.99 A review of the literature identified three studies, each with more than 10 patients and including the same variables and outcomes, which allowed comparison to other invasive treatment modalities.100–102 Overall, 72 out of 131 patients (55%) showed improvement, with a 4.9% complication rate. In my experience, a number of patients who had had RFA performed elsewhere went on to fail decompression and subsequently required nerve excision to diminish their pain. It appears that RFA further con-

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Fig. 19.13 Intraoperative view of the left and right greater occipital nerves, asymmetric in the vertical plane, piercing the semispinalis capitis muscle at different vertical planes.

Fig. 19.14 Recommended incisions to access the greater and lesser occipital nerves bilaterally.

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Surgical Management of Chronic Headaches, Migraines, and Neuralgias tributes to nerve damage, as those patients who continue to have headaches following RFA often have increased pain that is reminiscent of neuroma in continuity. This should be an important component of the preoperative discussion with patients, who may ultimately require nerve excision instead of decompression. Future prospective studies, if focused on 2- and 5year outcomes, and an associated relapse rate following RFA, may provide answers to outstanding questions, and thus define the real value of RFA treatment of chronic headaches. Neuromodulation (nerve stimulators) have been evaluated as an invasive treatment modality. It involves implantation of a battery-operated generator, connected by wires to electrodes placed in the vicinity of the targeted nerve tissue. A review of the literature identified nine studies, each with more than 10 patients, using the same outcome variables.47,50,103–109 Overall, 126 of 184 patients (68%) showed improvement. The complication rates in this study were 37% minor (lead site pain, contact dermatitis, loss of effect, current leak) and 31.5% major (unintended lead “migration,” device infections, faulty hardware requiring reoperation). Another study found 16 of 30 patients (53%) experienced > 50% pain improvement, at a mean followup of 35 months, and a similar study identified 7 out of 14 patients (50%) reporting > 50% pain relief, at a mean follow-up of 22 months.47,50 It is unclear, however, what the true 5-year long-term benefit of neuromodulation is. Taking into consideration the significant cost of the device itself, the implantation procedure, the potential for explantation in the event of infection, and the need for additional surgical sites and scars, patient informed consent needs to be rather comprehensive. Lastly, the idea that the treatment with a nerve stimulator focuses solely on symptom management leaves many patients unsettled knowing that the actual cause of their chronic headaches is not addressable with neuromodulation. Surgical interventions represent an invasive treatment modality, with numerous approaches reported. Peripheral nerve surgery strategies aim to address the underlying pathophysiology and anatomical cause of the headaches: nerve compression. Early C2 and C3 nerve root decompression surgery identified the C3 facet spur, whose removal led to complete pain relief at 11 months’ follow-up.43 Microsurgical C2 ganglionectomy has been advocated following a series of four patients with complete pain relief after 24 months, with one patient suffering pain recurrence.52,56 These patients experienced transient nausea and dizziness postoperatively, and one patient had a cerebrospinal fluid leak. C1–C4 rhizotomy has been reported in 17 patients with ON, with 68.8% of patients considering the procedure worthwhile.53 Numbness in the affected dermatomes was present after the procedure. Subdermal denervation of the affected skin segments has been reported.55 In these patients, two large scalp flaps were elevated, containing the occipitofrontalis muscle, to expose the GON and LON. These were then excised and the flaps replaced. Three patients were reported to have received “satisfactory results” from this procedure. Avulsion neurectomy of the GON has been performed in 22 patients, with 70% demonstrating pain relief at 18 months.55,56 About 30% of these patients experienced scalp hypersensitivity, dysesthesia, neuroma, or recurrence. Neurolysis of the GON at the deep neck fascia and trapezial tunnel was found to provide short-term pain relief in 66% of patients at 18 months’ follow-up, however, pain was found to have

19

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recurred in all but four patients.44 Interestingly, 80% of patients did not regret the surgery, and 40% wanted to try the identical operation again. These authors postulated that they might have not released the nerve deep enough, as the semispinalis muscle was not addressed. The semispinalis muscle was sectioned in a study of 34 patients, with 100% demonstrating an improvement in headache pain.38 Similarly, in a series of 13 patients with whiplash trauma and occipital headache, release of the nerve at the trapezial tunnel as well as the semispinalis resulted in 72.2% reporting good or excellent pain relief.41 Surgical neurolysis with sectioning of the inferior oblique muscle was reported in 10 patients, with 70% patient satisfaction at a mean follow-up of 37 months.110 One of the largest studies to date of 206 patients demonstrated that 80% of patients experienced meaningful (> 50% relief) pain relief at a minimum of 12 months’ follow-up.16 Forty-three percent of the patients who benefited from surgery had complete elimination of ON. Although the remaining 57% of patients did not have complete elimination, they reported that their headaches were less frequent and severe and that their medications became more efficacious. In comparison to other procedures, the GON is not damaged, but rather decompressed. If and when the LON is excised, the resultant sensory defect in the mastoid area behind the ear is minor. These results suggest that ON is stimulated by peripheral nerve entrapment. About 20% of patients who experienced < 50% relief were considered treatment failures, most likely due to GON’s inability to regenerate despite decompression. Besides continued medical management, patients were offered subsequent nerve excision if they still had tenderness over the GON and were responsive to nerve blocks. Most of the patients who had subsequent excisions were helped, but some of them were not or had scalp hypersensitivity and continued pain, mandating continued medical pain management. To minimize failures, attention must be focused on abnormal branching of the GON, the course of the DON and LON, and the relationship of the GON and occipital vessels/lymph nodes.16,65, 67,69 In addition, careful attention to other compression sites for the same nerve is mandatory, along with adherence to the proposed treatment algorithm (▶ Table 19.2; ▶ Fig. 19.15). A review of the literature identified 14 studies, each with more than 10 patients, using the same outcome variables, which allowed data comparison to peripheral nerve surgery and other invasive treatments.16,38,78,110–119 A total of 1,072 of 1,253 patients (86%) benefited from surgical treatment of their chronic headaches. Associated total minor complications were noted in 139 patients (11.1%). When compared to other invasive treatment options, positive outcomes for peripheral nerve surgery (86%) were above those for neuromodulation (68%) and RFA (55%). The evidence-based data indicate that peripheral nerve surgery, which targets the anatomical cause of chronic headaches, has the best chance of reversings a patient’s condition when compared to other available treatment modalities. When surgical treatment of migraine headaches was compared to placebo, 15 of 26 sham patients (57.7%) and 41 of 49 study patients (83.7%) experienced at least 50% reduction in migraines. Furthermore, 28 of 49 study patients (57.1%) reported complete elimination of migraines, compared to only 1 of 26 sham patients (3.8%), thus indicating that peripheral trigger sites were involved in the pathogenesis of patients’ migraines and that their deactiva-

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Fig. 19.15 Recommended algorithm for the management of chronic headaches and migraines.

tion led to improvement.111 Similarly, excessive weight in patients with very large breasts appears to create chronic pressure and tension via trapezial muscle and fascia on peripheral nerves in the occipital region, triggering ON, migraines, and chronic headaches in these patients.120 Breast reduction appears to eliminate this type of tension and pressure, thereby improving or eliminating ON, migraine, and other forms of chronic headache in patients with large breasts. Finally, any surgery and trauma, including post-concussion sports injuries, can directly affect peripheral nerves in the occipital, frontal, and/or temporal region, causing different types of chronic headache, migraine or neuralgia.16,34,121 Successful surgical treatment in these patients only serves as another confirmation of an existing peripheral trigger responsible for patients’ chronic headaches.

19.7 Conclusion The diagnosis and management of chronic headaches, migraines, and neuralgia is a controversial and evolving topic. Although many investigators argue that surgery is an invasive treatment for chronic headaches, the partial benefit or failure of medical management in many patients mandates exploration

of this and other options. Thus, indications for peripheral nerve surgery (as listed above) are recommended for all patients whose symptoms are present with any condition included in ▶ Table 19.1, despite appropriate medical treatment for at least 3 months prescribed by a headache specialist. Surgical treatment, mostly decompression and, to a lesser degree, nerve transection/excision, provides safe pain relief to a subset of patients with FTTN- and ON-related chronic headaches or migraines, by addressing the causative nerve compression. Clearly, more work needs to be done before a consensus is developed; however, it is hoped the concepts discussed here can help better standardize indications and applicable surgical techniques, supplementing current medical care.

19.8 References [1] International Headache Society. The International Classification of Headache Disorders. www.i-h-s.org [2] Headache Classification Committee of the International Headache Society. Classification and diagnostic criteria for headache disorders, cranial neuralgias and facial pain. Cephalalgia 1988;8 Suppl 7:1–96 [3] Martin V, Elkind A. Diagnosis and classification of primary headache disorders. In: Standards of care for headache diagnosis and treatment. Chicago, IL: National Headache Foundation; 2004:4–18

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[33] Tucker SM, Tarlov EC. Intraorbital surgery for trigeminal neuralgia. Ophthal Plast Reconstr Surg 2005;21:11–15 [34] Ducic I, Larson EE. Posttraumatic headache: surgical management of supraorbital neuralgia. Plast Reconstr Surg 2008;121:1943–1948 [35] Freidman RM, Rohrich RJ, Finn SS. Management of traumatic supraorbital neuroma. Ann Plast Surg 1992;28:573–574 [36] Lipton RB, Stewart WF, Reed M, Diamond S. Migraine’s impact today: burden of illness, patterns of care. Postgrad Med 2001;109:38–40, 43–45 [37] Pareja JA, Caminero AB. Supraorbital neuralgia. Curr Pain Headache Rep 2006;10:302–305 [38] Guyuron B, Kriegler JS, Davis J, Amini SB. Comprehensive surgical treatment of migraine headaches. Plast Reconstr Surg 2005;115:1–9 [39] Beruto LJ, Ramos MM. Decades de med y cirug pract. 1821;3:145–169 [40] Bogduk N. The anatomy of occipital neuralgia. Clin Exp Neurol 1981;17:167– 184 [41] Magnússon T, Ragnarsson T, Björnsson A. Occipital nerve release in patients with whiplash trauma and occipital neuralgia. Headache 1996;36:32–36 [42] Becser N, Bovim G, Sjaastad O. Extracranial nerves in the posterior part of the head: anatomic variations and their possible clinical significance. Spine 1998;23:1435–1441 [43] Poletti CE. Proposed operation for occipital neuralgia: C-2 and C-3 root decompression: case report. Neurosurgery 1983;12:221–224 [44] Bovim G, Fredriksen TA, Stolt-Nielsen A, Sjaastad O. Neurolysis of the greater occipital nerve in cervicogenic headache: a follow-up study. Headache 1992;32:175–179 [45] Bovim G, Bonamico L, Fredriksen TA, Lindboe CF, Stolt-Nielsen A, Sjaastad O. Topographic variations in the peripheral course of the greater occipital nerve: autopsy study with clinical correlations. Spine 1991;16:475–478 [46] Ballesteros-Del Rio B, Ares-Luque A, Tejada-Garcia J, Muela-Molinero A. Occipital (Arnold) neuralgia secondary to greater occipital nerve schwannoma. Headache 2003;43:804–807 [47] Slavin KV, Colpan ME, Munawar N, Wess C, Nersesyan H. Trigeminal and occipital peripheral nerve stimulation for craniofacial pain: a single-institution experience and review of the literature. Neurosurg Focus 2006;21:E5 [48] Naja ZM, El-Rajab M, Al-Tannir MA, Ziade FM, Tawfik OM. Occipital nerve blockade for cervicogenic headache: a double-blind randomized controlled clinical trial. Pain Pract 2006;6:89–95 [49] Ashkenazi A, Matro R, Shaw JW, Abbas MA, Silberstein SD. Greater occipital nerve block using local anaesthetics alone or with triamcinolone for transformed migraine: a randomised comparative study. J Neurol Neurosurg Psychiatry 2008;79:415–417 [50] Slavin KV, Nersesyan H, Wess C. Peripheral neurostimulation for treatment of intractable occipital neuralgia. Neurosurgery 2006;58:112–119, discussion 112–119 [51] Stechison MT, Mullin BB. Surgical treatment of greater occipital neuralgia: an appraisal of strategies. Acta Neurochir (Wien) 1994;131:236–240 [52] Wang MY, Levi AD. Ganglionectomy of C-2 for the treatment of medically refractory occipital neuralgia. Neurosurg Focus 2002;12:E14 [53] Kapoor V, Rothfus WE, Grahovac SZ, Amin Kassam SZ, Horowitz MB. Refractory occipital neuralgia: preoperative assessment with CT-guided nerve block prior to dorsal cervical rhizotomy. AJNR Am J Neuroradiol 2003;24:2105–2110 [54] Navani A, Mahajan G, Kreis P, Fishman SM. A case of pulsed radiofrequency lesioning for occipital neuralgia. Pain Med 2006;7:453–456 [55] Martin BC, Fagan PJ. The surgical therapy of certain occipital headaches. Plast Reconstr Surg 1964;33:266–268 [56] Sharma RR, Devadas RV, Pawar SJ, Lad SD, Mahapatra AK. Current status of peripheral neurectomy for occipital neuralgia. Neurosurg Q 2005;15:232–238 [57] Standring S, ed. Gray’s Anatomy. 39th ed. London: Elsevier; 2005 [58] Beer GM, Putz R, Mager K, Schumacher M, Keil W. Variations of the frontal exit of the supraorbital nerve: an anatomic study. Plast Reconstr Surg 1998;102:334–341 [59] Janis JE, Ghavami A, Lemmon JA, Leedy JE, Guyuron B. The anatomy of the corrugator supercilii muscle: 2. Supraorbital nerve branching patterns. Plast Reconstr Surg 2008;121:233–240 [60] Fallucco M, Janis JE, Hagan RR. The anatomical morphology of the supraorbital notch: clinical relevance to the surgical treatment of migraine headaches. Plast Reconstr Surg 2012;130:1227–1233 [61] Totonchi A, Pashmini N, Guyuron B. The zygomaticotemporal branch of the trigeminal nerve: an anatomical study. Plast Reconstr Surg 2005;115:273–277 [62] Janis JE, Hatef DA, Thakar H, et al. The zygomaticotemporal branch of the trigeminal nerve: Part II. Anatomical variations. Plast Reconstr Surg 2010;126:435–442

Surgical Management of Chronic Headaches, Migraines, and Neuralgias [63] Janis JE, Hatef DA, Ducic I, et al. Anatomy of the auriculotemporal nerve: variations in its relationship to the superficial temporal artery and implications for the treatment of migraine headaches. Plast Reconstr Surg 2010;125:1422–1428 [64] Mosser SW, Guyuron B, Janis JE, Rohrich RJ. The anatomy of the greater occipital nerve: implications for the etiology of migraine headaches. Plast Reconstr Surg 2004;113:693–697, discussion 698–700 [65] Ducic I, Moriarty M, Al-Attar A. Anatomical variations of the occipital nerves: implications for the treatment of chronic headaches. Plast Reconstr Surg 2009;123:859–863, discussion 864 [66] Bogduk N. The clinical anatomy of the cervical dorsal rami. Spine 1982;7:319–330 [67] Natsis K, Baraliakos X, Appell HJ, Tsikaras P, Gigis I, Koebke J. The course of the greater occipital nerve in the suboccipital region: a proposal for setting landmarks for local anesthesia in patients with occipital neuralgia. Clin Anat 2006;19:332–336 [68] Becser N, Bovim G, Sjaastad O. Extracranial nerves in the posterior part of the head: anatomic variations and their possible clinical significance. Spine 1998;23:1435–1441 [69] Dash KS, Janis JE, Guyuron B. The lesser and third occipital nerves and migraine headaches. Plast Reconstr Surg 2005;115:1752–1758, discussion 1759–1760 [70] Tubbs RS, Salter EG, Wellons JC, Blount JP, Oakes WJ. Landmarks for the identification of the cutaneous nerves of the occiput and nuchal regions. Clin Anat 2007;20:235–238 [71] Ashkenazi A, Levin M. Three common neuralgias: how to manage trigeminal, occipital, and postherpetic pain. Postgrad Med 2004;116:16–18, 21–24, 31– 32 passim [72] Kerr FW. Central relationships of trigeminal and cervical primary afferents in the spinal cord and medulla. Brain Res 1972;43:561–572 [73] Shimizu S, Oka H, Osawa S, et al. Can proximity of the occipital artery to the greater occipital nerve act as a cause of idiopathic greater occipital neuralgia? An anatomical and histological evaluation of the artery-nerve relationship. Plast Reconstr Surg 2007;119:2029–2034, discussion 2035–2036 [74] Ducic I, Felder JM, Janis JE. Occipital artery vasculitis not identified as a mechanism of occipital neuralgia-related chronic migraine headaches. Plast Reconstr Surg 2011;128:908–912 [75] Bogduk N. Local anesthetic blocks of the second cervical ganglion: a technique with application in occipital headache. Cephalalgia 1981;1:41–50 [76] Caputi CA, Firetto V. Therapeutic blockade of greater occipital and supraorbital nerves in migraine patients. Headache 1997;37:174–179 [77] Ashkenazi A, Silberstein SD. Botulinum toxin and other new approaches to migraine therapy. Annu Rev Med 2004;55:505–518 [78] Janis JE, Dhanik A, Howard JH. Validation of the peripheral trigger point theory of migraine headaches: single-surgeon experience using botulinum toxin and surgical decompression. Plast Reconstr Surg 2011;128:123–131 [79] Ramirez OM, Pozner JN. Endoscopically assisted supraorbital nerve neurolysis and correction of eyebrow asymmetry. Plast Reconstr Surg 1997;100:755– 758, discussion 759–760 [80] Klein DS, Schmidt RE. Chronic headache resulting from postoperative supraorbital neuralgia. Anesth Analg 1991;73:490–491 [81] Parris WCV. Chronic headache resulting from postoperative supraorbital neuralgia. Anesth Analg 1992;74:934–935 [82] Benvenuti D. Endoscopic brow lifts with injury to the supraorbital nerve and neuroma formation. Plast Reconstr Surg 1999;104:297–298 [83] Sutula FC, Weiter JJ. Orbital socket pain after injury. Am J Ophthalmol 1980;90:692–696 [84] Messmer EP, Camara J, Boniuk M, Font RL. Amputation neuroma of the orbit: report of two cases and review of the literature. Ophthalmology 1984;91:1420–1423 [85] Okubo K, Asai T, Sera Y, Okada S. A case of amputation neuroma presenting proptosis. Ophthalmologica 1987;194:5–8 [86] Wirta DL, Dailey RA, Wobig JL. Eyelid neuroma associated with swim goggle use. Arch Ophthalmol 1998;116:1537–1538 [87] Jacobson RI. More “goggle headache”: supraorbital neuralgia. N Engl J Med 1983;308:1363–1364 [88] O’Brien JC. Swimmer’s headache, or supraorbital neuralgia. Proc (Bayl Univ Med Cent) 2004;17:418–419 [89] Sharma RR, Pawar SJ, Lad SD, Netalkar AS, Musa MM. Frontal intraosseous cryptic hemangioma presenting with supraorbital neuralgia. Clin Neurol Neurosurg 1999;101:215–219 [90] Weinberger LM. Cervico-occipital pain and its surgical treatment: the myth of the bony millstones. Am J Surg 1978;135:243–247

[91] Tancredi A, Caputi F. Greater occipital neuralgia and arthrosis of C1–2 lateral joint. Eur J Neurol 2004;11:573–574 [92] Jundt JW, Mock D. Temporal arteritis with normal erythrocyte sedimentation rates presenting as occipital neuralgia. Arthritis Rheum 1991;34:217–219 [93] Martelletti P, van Suijlekom H. Cervicogenic headache: practical approaches to therapy. CNS Drugs 2004;18:793–805 [94] Martelletti P. Inflammatory mechanisms in cervicogenic headache: an integrative view. Curr Pain Headache Rep 2002;6:315–319 [95] Koch D, Wakhloo AK. CT-guided chemical rhizotomy of the C1 root for occipital neuralgia. Neuroradiology 1992;34:451–452 [96] Martelletti P, Di Sabato F, Granata M, et al. Failure of long-term results of epidural steroid injection in cervicogenic headache. Eur Rev Med Pharmacol Sci 1998;2:10–14 [97] Aurora SK, Dodick DW, Turkel CC, et alPREEMPT 1 Chronic Migraine Study Group. OnabotulinumtoxinA for treatment of chronic migraine: results from the double-blind, randomized, placebo-controlled phase of the PREEMPT 1 trial. Cephalalgia 2010;30:793–803 [98] Lord SM, Bogduk N. Radiofrequency procedures in chronic pain. Best Pract Res Clin Anaesthesiol 2002;16:597–617 [99] van Suijlekom HA, van Kleef M, Barendse GA, Sluijter ME, Sjaastad O, Weber WE. Radiofrequency cervical zygapophyseal joint neurotomy for cervicogenic headache: a prospective study of 15 patients. Funct Neurol 1998;13:297–303 [100] Vanelderen P, Rouwette T, De Vooght P, et al. Pulsed radiofrequency for the treatment of occipital neuralgia: a prospective study with 6 months of follow-up. Reg Anesth Pain Med 2010;35:148–151 [101] Huang JH, Galvagno SM, Hameed M, et al. Occipital nerve pulsed radiofrequency treatment: a multi-center study evaluating predictors of outcome. Pain Med 2012;13:489–497 [102] Choi HJ, Oh IH, Choi SK, Lim YJ. Clinical outcomes of pulsed radiofrequency neuromodulation for the treatment of occipital neuralgia. J Korean Neurosurg Soc 2012;51:281–285 [103] Weiner RL, Reed KL. Peripheral neurostimulation for control of intractable occipital neuralgia. Neuromodulation 1999;2:217–221 [104] Popeney CA, Aló KM. Peripheral neurostimulation for the treatment of chronic, disabling transformed migraine. Headache 2003;43:369–375 [105] Oh MY, Ortega J, Bellotte JB, Whiting DM, Aló K. Peripheral nerve stimulation for the treatment of occipital neuralgia and transformed migraine using a C1–2-3 subcutaneous paddle style electrode: a technical report. Neuromodulation 2004;7:103–112 [106] Melvin EA, Jordan FR, Weiner RL, Primm D. Using peripheral stimulation to reduce the pain of C2-mediated occipital headaches: a preliminary report. Pain Physician 2007;10:453–460 [107] Schwedt TJ, Dodick DW, Hentz J, Trentman TL, Zimmerman RS. Occipital nerve stimulation for chronic headache—long-term safety and efficacy. Cephalalgia 2007;27:153–157 [108] Paemeleire K, Van Buyten JP, Van Buynder M, et al. Phenotype of patients responsive to occipital nerve stimulation for refractory head pain. Cephalalgia 2010;30:662–673 [109] Saper JR, Dodick DW, Silberstein SD, McCarville S, Sun M, Goadsby PJ, ONSTIM Investigators. Occipital nerve stimulation for the treatment of intractable chronic migraine headache: ONSTIM feasibility study. Cephalalgia 2011;31:271–285 [110] Gille O, Lavignolle B, Vital JM. Surgical treatment of greater occipital neuralgia by neurolysis of the greater occipital nerve and sectioning of the inferior oblique muscle. Spine 2004;29:828–832 [111] Guyuron B, Reed D, Kriegler JS, Davis J, Pashmini N, Amini S. A placebo-controlled surgical trial of the treatment of migraine headaches. Plast Reconstr Surg 2009;124:461–468 [112] Guyuron B, Kriegler JS, Davis J, Amini SB. Five-year outcome of surgical treatment of migraine headaches. Plast Reconstr Surg 2011;127:603–608 [113] Dirnberger F, Becker K. Surgical treatment of migraine headaches by corrugator muscle resection. Plast Reconstr Surg 2004;114:652–657, discussion 658– 659 [114] Bearden WH, Anderson RL. Corrugator superciliaris muscle excision for tension and migraine headaches. Ophthal Plast Reconstr Surg 2005;21:418–422 [115] Poggi JT, Grizzell BE, Helmer SD. Confirmation of surgical decompression to relieve migraine headaches. Plast Reconstr Surg 2008;122:115–122, discussion 123–124 [116] de Ru JA, Schellekens PPA, Lohuis PJFM. Corrugator supercilii transection for headache emanating from the frontal region: a clinical evaluation of ten patients. J Neural Transm 2011;118:1571–1574

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Painful Sequelae of Peripheral Nerve Injuries

20 Painful Sequelae of Peripheral Nerve Injuries Stephen H. Colbert “Physical pain is not a simple affair of an impulse, traveling at a fixed rate along a nerve. It is the resultant of a conflict between a stimulus and the whole individual.” —René Leriche, The Surgery of Pain

20.1 Introduction Pain is a very general term that has a wide variety of meanings, from the most nonphysical, such as the philosophical idea of pain and the general concept of suffering, to the more concrete, such as the neurophysiologic response to a noxious stimulus. Nevertheless, all definitions of pain are joined by the common concept of an association with something unpleasant. The word itself stems from the Greek and Latin roots meaning “punishment.” The clinical importance of pain has been so recognized that it has become the “fifth vital sign” despite the universal understanding that pain is a subjective symptom rather than an objective sign. Strictly defined, pain is a subjective cognitive experience, a perception, often diametrically opposed to pleasure, but is distinct from nociception, the physiologic response to a noxious stimulus. This distinction becomes clear with the recognition that pain exists in two major varieties, physical and mental. Although physical pain may exist in association with nociception, it is more properly the resultant effect of the nociceptive response, the former being on a conscious level and the latter on a subconscious level. Additionally, nociception does not necessitate pain, and pain can exist in the absence of nociception, such as with mental or emotional pain. This discussion will focus on physical pain, which is more relevant to the theme of this text and its clinical practice, yet it is well recognized that physical and emotional pain are generally closely associated and coexistent. The International Association for the Study of Pain (IASP) established a definition of pain in 1979 as an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage.1 This definition was derived from a previous definition by Harold Merskey in 1964.2 The IASP statement notes that pain is always subjective and, though biologically associated with potential tissue damage, is defined entirely by the psychological experience, regardless of the cause or presence of a stimulus. Biologically, pain is an evolutionary survival tool or defense mechanism that encourages the subject to end and to avoid the noxious stimulus that may be threatening the existence or integrity of the physical being. It is a stimulus for behavioral learning for selfpreservation and healing, as a painful injured body part is protected and thus encouraged to heal. Pain is a common and expected consequence of nerve injury and an occasional untoward consequence of nerve surgery. Pain, however, can become chronic, can exist in the absence of an appropriate stimulus, and can be an abnormal response to a normally nonpainful stimulus. In other words, pain can become pathologic, seemingly no longer serving as a survival mechanism or in any

defense capacity. These pathologic pain conditions are not only some of the most mysterious physiologically but also some of the most difficult to treat clinically. This chapter will begin by discussing the normal physiology of pain, then follow with a broader discussion on pathologic pain responses, in particular, that most commonly addressed by the extremity surgeon or peripheral nerve surgeon, the complex regional pain syndromes (CRPSs). It also addresses our thoughts and techniques for the surgical management of painful neuromas and painful neuroma-in-continuity. In the pain management and neurosurgical literature, there exists great pessimism on the success of surgery to treat CRPS II (causalgia), but this is definitely not our experience.3,4

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20.2 Normal Pain Response 20.2.1 Physiology Pain reception, that is, nociception, is perhaps the most important sensory system due to its protective characteristics. Pain may be characterized by its time course, location, and quality. Acute pain is brief, lasting only seconds, minutes, or hours. Prolonged pain lasts days to weeks. Chronic pain lasts many months to years. Pain may be somatic or visceral. Somatic pain may be superficial or deep, with deep pain in joints, ligaments, bone, muscle, and blood vessels being poorly localized, dull and achy and mediated by fewer numbers of nociceptors. Visceral pain is mediated by even fewer nociceptors and is even more dull, vague, and often referred to nonvisceral locations. To begin to understand the physiology of pain, it is convenient to review three components: the receptors, the intrinsic neural pathways, and the extrinsic regulators of those pathways. Nociceptors are the receptors that respond to noxious stimuli. There are two basic types of nociceptors, Aδ and C, which are traditionally labeled “free nerve endings” and are named for the types of afferent fibers with which they are associated. Aδ and C fibers are both relatively small. Aδ fibers have thin myelin and conduct more slowly than the larger, more heavily myelinated fibers. C fibers are unmyelinated and conduct more slowly than any other fibers. Aδ receptors are mechanoreceptors that respond to mechanical deformation of the skin that may be damaging, such as pinch. C receptors respond to noxious hot thermal or chemical stimuli. Thus, Aδ fibers tend to mediate fast, sharp pain, whereas C fibers tend to mediate slow, burning pain. Cold thermal nociceptors exist as well but are less common than Aδ and C nociceptors. These nociceptors respond to primary noxious stimuli and are further sensitized by chemical mediators that result from tissue damage, such as histamine, serotonin, acetylcholine, prostaglandins and bradykinins. In the absence of injury or other inflammatory response, these nociceptors are largely dormant and relatively unresponsive. The sensory cell bodies of these axons are smaller than those associated with the larger myelinated axons, and they have a different neurochemical profile, including the most recognized substance involved in nociception, substance P. Substance P is a peptide in the family of tachykinins, called neurokinins in

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Painful Sequelae of Peripheral Nerve Injuries mammals. It is a neuroactive peptide produced and released by the primary afferent neurons acting to regulate the excitability of the secondary sensory neurons in the dorsal horn. Substance P acts in concert with the excitatory neurotransmitter glutamate in the central nervous system (CNS). It is found in different locations within the CNS, as well as at the terminal endings of primary sensory afferent fibers, where it is thought to contribute to inflammation associated with pain.5 The gate control theory of pain, first proposed by Melzack and Wall in 1965,6 is the foundation for most modern theories of pain perception and multiple avenues for treatment. The theory states that interneurons in the spinal cord act as a gate that is opened by the stimulating effect of the nociceptive afferent fiber input and is closed by the inhibitory effect of nonnociceptive afferent fiber input. That is, activity of the nonnociceptive, larger, faster, more heavily myelinated Aβ fibers inhibits transmission of pain signals to the brain. It has since been recognized that pain physiology is much more complex, with differential pathways modulated by descending signals from the brain and brainstem as well. Nociceptive signals are transmitted to the brain via several different pathways. The most prominent of these is the spinothalamic tract. The secondary neurons are located in laminae I, V, VI, and VII of the dorsal horn. Their axons cross the midline, ascend in the anterolateral white matter of the contralateral spinal cord, and terminate in the central lateral and ventral posterolateral nuclei of the thalamus. The tertiary neurons in the thalamic nuclei send axons to the ipsilateral somatosensory cortex of the postcentral gyrus and to the associated cortical areas. There are at least four other well-defined nociceptive pathways that involve the reticular formation of the brainstem, midbrain periaqueductal gray matter, additional thalamic nuclei, hypothalamus, basal ganglia, and other cortical areas. The degree to which nociceptive signals result in the perception of pain involves all of these mechanisms and is thus quite complex. It involves both stimulatory and inhibitory pathways. Ascending pathways can be separated into two main systems, a teleological advanced “first pain” system involving the higher somatosensory cortex that mediates the discriminative aspect of pain and a more primitive “second pain” system involving the reticular tracts and the “lower” cortex that mediates the motivational and affective aspects of pain, that is, its unpleasantness. The spinothalamic tract connection to the primary somatosensory cortex through the lateral thalamus constitutes the discriminative system. The spinoreticulothalamic tracts involve the medial thalamus and project to the frontal cortex, the anterior cingulated gyrus, and constitute the motivational-affective system. Descending modulatory pathways have generally inhibitory effects on spinal cord dorsal horn neurons. The periaqueductal gray is the most prominent regulator of these descending inhibitory signals. It has excitatory connections to other brainstem nuclei, which in turn have inhibitory connections to the dorsal horn nociceptor cells. For good reviews of the neurophysiology of pain, the reader is referred to Cross7 and Willis and Westlund.8

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20.2.2 Treatment The mainstay of treatment for physiologic pain responses is pharmacologic. Reducing the inflammatory response that leads

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to nociceptor excitability with aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) can attenuate pain sensation. Pain may also be alleviated through inhibitory modulators, such as primary afferent neuron membrane serotonin and opiate receptors. NSAIDs and opioid medications are logically combined with behavioral modifications and other therapeutic maneuvers that prevent further stimulation of pain, such as immobilization, protection, and cooling and elevation to limit edema. For peripheral nerve surgeons and other hand and extremity surgeons whose work may involve manipulation of peripheral nerves, prevention is probably the best defense against pain. The pain response is attenuated and the sensitization of the receptors can be inhibited by blockade with local anesthetic prior to nerve transection or manipulation, providing a reduced pain perception postoperatively.9–12 These measures are generally adequate in the absence of an abnormal pain response; conversely, they are most frequently insufficient when an abnormal pain response occurs.

20.3 Abnormal Pain Response In addition to the expected normal physiologic pain response to injury, there are two categories of abnormal pain responses that beleaguer both the patient and the peripheral nerve surgeon: painful neuromas and pain syndromes.

20.3.1 Neuromatous Pain Overview Any swelling of a nerve can technically be defined as a neuroma. Generally today, most medical terms with the same Greek suffix have become limited to neoplasia. However, the more common definition of neuroma, and the one assumed in this chapter, applies predominantly to traumatic neuroma, or the growth or swelling at the site of nerve injury (▶ Fig. 20.1). The natural response following nerve injury is development of the growth cone and subsequent nerve regeneration. Wallerian degeneration occurs distally as Schwann cells proliferate, and the axons degenerate and are resorbed, while proximally axons will make an effort to reestablish contact with their distal targets. Teleologically, this represents the body’s effort to repair itself and restore its original form. Inevitably, the initial process of regeneration at the site of nerve injury involves the creation of a neuroma. Supernumerary sprouts emanate from the injured axons and “search” for their lost targets. Stimulation of these fibers creates an unpleasant paresthetic or painful sensation. This response to percussion creates the clinical Tinel-Hoffman sign, or Tinel sign, named for French neurologist Jules Tinel and German physiologist Paul Hoffman, serving as physicians opposite each other during World War I. When the appropriate distal connections are made and terminal targets are reinnervated, regeneration is ideal, and the irritation abates. In this situation, the neuroma resolves. However, if proper regeneration is disrupted, and proper terminal connections are not made, a neuroma may persist. Nerve fibers become tangled and disoriented, contained within dense, disorganized connective tissue (▶ Fig. 20.2). Such neuromas tend to be very mechanically sensitive and clinically relevant. These are labeled painful neuromas.

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Fig. 20.1 Peripheral neuromas. (a) The patient had a sural neuroma treated with two previous procedures to relocate and implant the nerve into muscle. The nerve end had been left too distal in the leg and under tension. In our surgery, we excised this neuroma, proximally crushed the sural nerve, and moved the nerve very proximally, deep in a muscle interval and with no tension. (b) A pseudoneuroma was observed in a second case where the ulnar nerve was compressed at the cubital tunnel.

Fig. 20.2 (a) Histologic assessment of a neuroma reveals extra-fascicular collateral sprouting of fibers. This particular specimen is a digital sensory nerve. (b) Histologic assessment of a radial pseudoneuroma reveals intact fascicles with Renaut bodies, which are commonly present in compressed nerves.

Historically, studies have shown that resection, often with additional mechanical measures such as crush, cauterization, or ligation, and relocation of the nerve ending into bone or muscle can limit the degree of neuroma formation and consequent symptoms (▶ Fig. 20.3).13,14 These findings

have been supported by Mackinnon’s work.15–18 In particular, implantation of the free nerve ending into muscle or bone limits the disorganized nerve fiber development and the proliferative response of connective tissue stroma and fibroblasts.

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Fig. 20.3 Surgical management of peripheral neuroma. (a) A neuroma forms at the distal end of the nerve following injury. (b) The neuroma is excised, and the proximal end is capped through cautery. The nerve proximally is crushed as far proximally as possible to induce a second-degree nerve injury. (c) After a proximal crush and cautery, the nerve is transposed proximally intermuscularly. We hypothesize that the proximal crush injury (Sunderland II) "resets" the central changes that occur in the spinal cord and brain after a neurectomy.

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In most cases, the nerve does not invade the muscle, but is instead confined by it. If motion occurs at the implantation site, the nerve may become mechanically stimulated or dislodged from within the substance of the muscle (▶ Fig. 20.4). If the free nerve end is placed or subsequently comes to rest in a superficial position, patients may have pain with direct stimulation or palpation of the resultant neuroma. These two situations represent the main reasons for persistent or recurrent painful neuroma following implantation into muscle. Thus, when treating painful neuromas surgically, it is important to bury the free nerve end as deep as possible into a position with as little motion as possible and in a proximal direction with no tension at all. We never “sew” it in place but instead use 10 cc’s of fibrin glue. Dorsi et al (Belzberg’s group) have developed a model of neuropathic pain to investigate the mechanisms of neuroma pain.19 They emphasize that following peripheral nerve transection pain can develop from direct stimulation of the neuroma distinct and independent from hyperalgesia and allodynia that can develop at a location distant from the site of the actual injury yet within the territory of the injured nerve (▶ Fig. 20.5). This model emphasizes that the nerve surgeon must be cognizant of these two sources for pain following nerve injury, that is, both the injured end of the proximal nerve segment and the distal denervated nerve. We have always emphasized that the first line of management for a painful nerve injury is to reconstruct the injured nerve and restore continuity of the peripheral nervous system (▶ Fig. 20.6; ▶ Fig. 20.7). This allows the proximal divided nerve to properly regenerate and prevent neuroma formation. We emphasize the neuroma as being the site of the main pain following nerve transection, and we recommend in almost all situations reconstructing the peripheral nervous system with a

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nerve repair, graft, or conduit. We now recognize that this maneuver is not just controlling proximal neuroma pain but also preventing the pain that comes from the distal portion of the nerve and its sensory receptors. Thus, reconstructing the nerve does indeed help with pain following nerve injury, not just because it controls proximal neuroma formation, but also because it allows satisfactory reinnervation into the distal territory. Surgeons need to be cognizant of managing the neuroma and of trying to satisfactorily reinnervate the distal nerve. Along this line, we make every attempt to reinnervate the distal divided sensory nerves when we harvest nerve grafts, especially in patients who have a pain component to their injury. We take the divided, denervated distal stump of the donor nerve and turn it end to side into an adjacent normal sensory nerve. We know from all of our experimental work that the end-to-side technique will allow for some degree of spontaneous sensory collateral sprouting (although it will not allow for motor sprouting unless there is direct in jury to the motor axons). For example, one of our donor nerves of choice for digital reconstruction is the anterior branch of the medial antebrachial cutaneous (MABC) nerve. The distal end of the divided anterior branch of the MABC nerve can be easily turned end to side into the normal intact posterior branch of the MABC nerve or MBC nerve (▶ Fig. 20.8). This will allow for some spontaneous end-to-side sprouting from the posterior branch into the distal portion of the anterior branch to not only result in decreased donor deficit but also help to reinnervate the distal territory of the divided anterior branch of the MABC nerve. The recent animal model by Dorsi et al really emphasizes for us the importance of not only managing the neuroma itself as a focus of pain but also understanding that the distal denervated portion of the nerve, unless it is satisfactorily reinnervated, will itself be a source of hyperalgesia and allodynia.19

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Fig. 20.4 Histologic assessment of a nerve embedded in a muscle. (a) Transverse section of the sensory branch of the radial nerve, which has been placed into the adbuctor pollicis longus and extensor pollicis longus muscles. Nerve fibers are seen to be invading the muscle. They are not confined by the muscle bed, but are apparent between muscle fibers. (b) However, the nerve is mostly capped by muscle (Toluidine blue; 169x). (Used with permission from Dellon AL, Mackinnon SE. Treatment of the painful neuroma by neuroma resection and muscle implantation. Plast Reconstr Surg 1986;77:427−436.)

Evaluation and Non-Surgical Management of Neuromas The goals of management of patients who present with painful neuromas are to relieve pain and restore function. These require keen diagnosis and selection of patients for intervention, as well as following basic principles when intervening surgically. Yet, as the previous discussion hints, the best management is prevention. As pain may have many causes, sometimes multiple and coexistent, it is important to distinguish the patient with isolated neuroma pain from the patient with an accompanying pain syndrome. A careful history and physical examination will allow this distinction. In addition to identifying the time course, location, duration, quality, and inciting and alleviating factors, we advocate use of a visual analogue scale, a body diagram, and a dedicated pain questionnaire, such as the example in the Appendix of Chapter 2 of this book. Other assessment tools are the Hospital Anxiety and Depression Scale (HADS),20 the Pain Disability Index (PDI) function,21,22 the Brief Pain Inventory Interference Scale (BPI-1) function,23 and the Short Form Health

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Survey (SF12v2) for health-related quality of life.24 Combining the description of pain with its location and intensity can help distinguish neuromatous pain, which is focal, brief, intermittent, sharp, and often intense, from nonneuromatous pain, which may be diffuse and of varying quality and duration (▶ Fig. 20.9). Initial management of neuromatous pain should involve pharmacologic trials and desensitization physiotherapy. Pharmacologic management may include narcotics, anxiolytics, and antiepileptics such as gabapentin and pregabalin. We find pregabalin vastly superior to gabapentin and in fact no longer recommend gabapentin. Caution is suggested with long-term use of medications with addiction potential. Occasionally, a patient will have an unclear diagnosis, although neuroma may be high on the list of differentials. Examination techniques such as rapid alternating movements, rapid grip exchange, simultaneous tasks, and assessment of intratest variability can be used to assess patient reliability if the history is not definitive and if malingering is suspected. A more affective technique that may be both diagnostic and therapeutic is an anesthetic nerve block. Patients who respond well to one or more nerve blocks are

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Fig. 20.5 Neuroma pain and hyperalgesia pain. (a) Pain from neuroma formation is well known; however, hyperalgesia pain resulting from adjacent sensory territories collaterally sprouting into deinnervated territory is underrecognized. (b) Surgical management via nerve graft addresses both neuroma pain and hyperalgesia pain. (c) Surgical management via proximal transposition addresses neuroma pain, but it does not necessarily address hyperalgesia pain. (d) Strategies for addressing hyperalgesia pain during a proximal transposition include end-to-side sensory nerve transfers, in which the distal deinnervated end is transferred to the side of an adjacent functional sensory nerve.

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Fig. 20.6 Restoring continuity following nerve injury with a nerve graft. (a) The patient presented with continued neuroma pain following a failed nerve repair (reconstruction of the radial digital branch of the median nerve to the long finger). (b) The failed reconstruction was excised outside the zone of injury. (c) The digital branch was reconstructed with a lateral antebrachial cutaneous nerve graft to restore continuity of the nerve.

Fig. 20.7 Histologic assessment of a failed nerve reconstruction with continued neuroma pain. (a,d) Distal to the neuroma, regenerated nerve fibers were observed; however, the patient presented with pain specific to the neuroma and within the digital territory. (b,e) Nerve fibers within the neuroma had a longitudinal and cross-sectional orientation. (c,f) Proximal to the neuroma, normal nerve fibers were observed (Toluidine blue; 40x, 400x).

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Fig. 20.8 Medial antebrachial cutaneous (MABC) nerve graft and end-to-side nerve transfer to restore donor deficit. (a) The MABC is an available donor nerve for graft reconstructions. (b) After harvesting, an end-to-side sensory nerve transfer can be performed to restore rudimentary sensation to the donor territory. In this case, the distal end of the MABC was transferred to the side of a functional medial brachial cutaneous (MBC) nerve via a perineural window. Nerve fibers will collaterally sprout from the MBC into the MABC.

Fig. 20.9 Pain descriptions for neuromatous and nonneuromatous pain. The pain evaluation is an important tool for distinguishing types of pain and helping with the diagnosis. Patients with similar presenting diagnoses may have very different pain distributions.

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Fig. 20.10 Neuroma pain managed with a nerve grafting. (a) In this case, the patient had a complete ulnar nerve injury with complaints of neuropathic pain within the ulnar nerve territory. (b) Nerve grafting was elected due to the location of injury and to restore continuity of the ulnar nerve. The sensory and motor modalities were matched with two medial antebrachial cutaneous nerve grafts for the sensory component, and a motor nerve graft (from gracilis) for motor reconstruction.

much better candidates for surgical management than those who do not. Those who do not respond often will give a history of getting worse following the nerve block. Surgical treatment of neuroma is not recommended in these patients. Our examination of the patient with nerve pain always starts by assuming the patient indeed has real pain. Next we review the first page of our pain evaluation with the patient so we can confirm the location and quality of the pain and whether there are different types of pain in different locations (▶ Fig. 20.9). We then ask the patient if he or she can touch the area of pain. The patient’s response to this is the key to knowing whether we can help surgically. For example, if a patient with a radial sensory nerve injury can easily massage and touch the dorsal radial aspect of the wrist, and hand, the most we would do is decompress the nerve at the brachioradialis/extensor carpi radialis longus (ECRL) entrapment point. We would not operate on the nerve itself. By contrast, if the patient will not even touch the area of pain, we will not touch it either. We will do a “blow” scratch-collapse test (SCT) and look for a proximal Tinel sign away from the area of pain. Although there will be a very strong and painful Tinel sign at the actual site of the nerve injury or neuroma, ~ 4 to 6 cm proximal to this there will be a less painful Tinel sign. Emphasize to the patient that you will not touch the area of pain, then start proximal to the nerve injury site and tap along the nerve(s) you suspect are involved. This lets you identify the nerves innervating the neuroma without hurting the patient. The patient will be able to concentrate and tell you where her or she feels the distribution of pain, which basically tells you what nerves are involved. Over the last few years, we have had much success with the SCT combined with ethyl chloride spray in the evaluation and assessment of patients with painful nerve injuries. In these patients, electrodiagnostic tests will not be able to measure C and Aδ fibers; imaging studies are also not helpful. In Chapter 2, the SCT is well described, and videos of

specific patient examinations using this test are available at nervesurgery.wustl.edu. By using all of these techniques, the peripheral nerve surgeon can accurately identify patients with painful neuromas and select those who will most likely benefit from surgical treatment.

Surgical Management of Neuromas Surgical management of painful neuromas follows basic principles designed to treat the pain and restore function whenever possible: (1) repair nerve continuity whenever possible (▶ Fig. 20.10; ▶ Fig. 20.11); (2) resect the neuroma and bury it within a deep tissue with minimal chance of mechanical stimulation, when the nerve cannot be reconstructed and/or sensation is not critical (▶ Fig. 20.12); (3) “crush” the nerve you are transposing as far proximally as possible to create a second-degree, axonotmetic injury to allow a longer period of relative painless “brain silence” as the nerve regenerates distally (our experience is that nerve regeneration associated with a seconddegree injury is less painful than the neuroma associated with a fifth-degree injury); and (4) restore sensation in the denervated territory in the acute setting of nerve transection using an endto-side sensory nerve transfer of the transected distal nerve to an adjacent normal nerve. Neuromas commonly occur posttraumatically at the digits and amputation stumps and along the courses of known superficial sensory nerves. With the availability of biodegradable nerve conduits and processed acellular nerve allografts (ANAs), nerve gaps in the noncritical digits with a receptive distal segment can be reconstructed with no new donor deficit. We use autografts for all critical sensory nerves and ANAs only for noncritical, small-diameter, small gap sensory nerves (▶ Fig. 20.13; ▶ Fig. 20.14). These tools allow the preservation of autologous donor nerve sites and thus reduce the potential for a separate site of potential neuroma.

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Fig. 20.11 Neuroma pain managed with sensory nerve transfers. (a,b) In this case, the patient presented with a failed conduit repair of the ulnar nerve at the cubital tunnel. The patient presented more than 1 year after the nerve injury, too late for motor nerve transfers. (c,d) To restore critical sensation and address hyperalgesia pain, sensory nerve transfers were elected. Specifically, the third web space of the median nerve was transferred end to end to the sensory component of the ulnar nerve, and the dorsal cutaneous branch was transferred end to side to the third web space of the median nerve. (e) Neuromatous pain was addressed by proximally crushing the ulnar nerve, cauterizing the proximal end, and transposing the ulnar nerve proximally and intermuscularly.

If these reconstructive efforts fail, then common or proper digital nerves should be moved to the deep dorsal surface of the hand, away from the palmar touch surface to prevent mechanical stimulation. In amputation stumps or in situations where there is no appropriate distal nerve segment and sensation is not critical, neuromas should be resected and buried proximally into bone or deep muscle with little excursion or other risk of mechanical stimulation. It is strongly recommended not to leave denervated skin at the stump closure site, in order to avoid the presence of a neurochemical stimulus for neuroma formation; thus further shortening of the digit may be necessary (▶ Figs. 20.15–20.18). Likewise, for primary ray amputations, most commonly the index, the digital nerves should be dissected well beyond the level of skin closure so that they may be transposed proximally tension-free and buried into bone, such as the third metacarpal, without denervating the remaining skin flaps. Where sensation is critical, such as the ulnar touch surface of the thumb and the radial touch surface of the index, and previous attempts to restore nerve continuity have failed or the tissue injury is too severe, then locoregional flaps (e.g., Littler

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flaps) or even distant innervated tissue flaps may be helpful to restore sensation (▶ Figs. 20.19–20.26). Recently we completed cadaver studies demonstrating that there is surprisingly little plexus formation between specific digital nerve fascicular bundles in the median nerve even into the forearm. This knowledge allows us to move “problem” digital nerves well out of the hand to avoid leaving the “new” neuroma in the hand. The superficial sensory nerves of the dorsoradial wrist deserve special mention. The radial sensory nerve has been appropriately called the “unforgiving nerve” (J.H. Coert, unpublished data). Mackinnon believes that this nerve is known to be so resistant to surgical treatment because the pain is actually coming from adjacent noninjured nerves (e.g., lateral antebrachial cutaneous [LABC], dorsal cutaneous ulnar [DCU], posterior cutaneous nerve of the forearm, and palmar cutaneous nerve) that collaterally sprout into the radial sensory territory. As well, it seems that these nerves can variably be the source of pain. One day blocking the LABC helps, another day blocking the DCU helps. These nerves tend to be particularly sensitive and susceptible to mechanical irritation. They may become irritated by

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Fig. 20.12 Neuroma pain managed with proximal transposition. (a) In this case, the patient had a distal humeral facture, which was treated with an open reduction/internal fixation. Following this, the patient had complaints of neuropathic pain at the posterior aspect of the proximal forearm. This pain was consistent with the territory of the posterior cutaneous branch of the radial nerve. The old incision is delineated with dotted lines. (b) The posterior cutaneous branch of the radial nerve was exposed proximal to the injury and previous surgical site. (c) The nerve was transected, capped with cautery, and proximally crushed with hemostat. (d) Following this, the nerve was transposed proximally and intermuscularly and kept in place with 10 cc’s of fibrin glue.

the presence of de Quervain disease, and primary nerve entrapment may be overlooked or misdiagnosed as de Quervain disease. Irritation or injury also may occur during treatment of distal radius fractures or carpal bone fractures, particularly with percutaneous intervention, or with surgical treatment of basilar thumb arthritis. The superficial branch of the radial (SBR) nerve and the terminal branches of the LABC nerve have relatively little soft tissue coverage and are subject to a significant range of movements across the mobile wrist. The sensory distribution of these nerves is not considered critical. Care must be taken preoperatively to identify the involved nerves, as the territories of these nerves overlap in 75% of cases (▶ Fig. 20.27).25 Repeat exams and diagnostic nerve blocks are valuable and often necessary in this process (▶ Fig. 20.28). Even when distal sensation is successfully restored following reconstruction of these nerves, or when only a portion of the nerve is injured and is treated with resection and burying, pain is often not adequately relieved. Thus, we recommend treatment with careful and thorough identification of involved nerves, neuroma resection, burying of the proximal segment ends into the deep surface of the brachioradialis muscle, and side-to-end repair of the distal segment to an available intact

sensory nerve in proximity such as the median nerve (▶ Fig. 20.29). We also will do a complete tenotomy of the brachioradialis tendon if a nerve repair or grafting of the radial sensory nerve is performed. We will also cut and repair the radial sensory nerve at a proximal second level in the forearm and repair with a 3-cm acelluarlized nerve allograft to move the regenerative front more proximal.

20.3.2 Pain Syndromes Classification of Pain Syndromes Although earlier descriptions of similar cases exist,26 Silas Weir Mitchell provided the first clear description of limb pain and dystrophy following nerve injury based on his extensive care for American Civil War soldiers.27,28 He wrote, “Long after the trace of the effects of a wound has gone. . . neuralgic symptoms are apt to linger, and too many carry with them throughout long years this final reminder of the battlefield.” The term causalgia, after the Greek for “heat pain” or “burning pain,” is reported to be originally attributed to Robley Dunglison. 29 However, the publication of Mitchell’s text in 1864, Gunshot

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Fig. 20.13 Examination of a sharp, lacerating injury to a digital nerve. This patient immediately presented to our institution with a sharp laceration wound to the right hand, which an outside institution had irrigated and sutured. The patient reported loss of sensation at the radial aspect of the long finger. (a,b) The purple X’s indicate the distribution of sensory loss. (c) Although the laceration was only a few centimeters across, the patient described a deep stab injury. A Tinel sign (purple star) was present near the site of the injury.

Fig. 20.14 Surgical management of a sharp, lacerating injury to a noncritical digital nerve using an acellular nerve allograft (ANA). (a) Upon exploration, the digital artery was found to be transected. The digital nerve to the radial aspect of the long finger was found to be intact but injured. (b) The digital nerve had been longitudinally injured by the sharp object. (c) The zone of injury was identified and resected until healthy nerve was seen at both proximal and distal ends. (d) A 2-cm ANA (Avance Nerve Graft, AxoGen Inc., Alochua, FL) was used to bridge the nerve gap for a tension-free repair. The nerve repair was tested for tension by putting the long finger through full flexion and extension.

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Fig. 20.15 An examination of neuropathic pain following an amputation. This 27-year-old male patient presented with a below-knee amputation and pain following the amputation along the lateral side of the stump. The patient is prone and the right leg is prepped.

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Fig. 20.16 Exposure of peroneal and sural nerves in a case of neuropathic pain following amputation. The peroneal and sural nerves were initially identified and exposed at the fibular head. To attain sufficient length for proximal transposition, a second proximal incision was made and the peroneal nerve exposed.

Wounds and Other Injuries of Nerves, along with coauthors Morehouse and Keen, and Mitchell’s subsequent international recognition, would establish him as the authority on this subject.27 In 1900 Paul Sudeck, and in 1901 Robert Kienbock described the clinical and radiographic pictures of what came to be known as Sudeck atrophy, acute osteopenia in the setting of a pain syndrome.30 Although René Leriche proposed pathologic activity of the sympathetic nervous system as an etiologic factor and developed treatment with periarterial sympathectomy,31 the term reflex sympathetic dystrophy (RSD) is attributed to James Evans. 32,33 Evans distinguished

RSD from causalgia by noting that in some cases, the predominant symptoms are related to sympathetic changes rather than pain and that the changes that occur are often remote from any site of injury.34 Oscar Steinbrocker is credited with introducing the term shoulder–hand syndrome, describing a reflex sympathetic dystrophy of the upper extremity occurring usually after CNS insult, commonly stroke. 35 Algodystrophy, meaning “painful dystrophy,” describes two prominent manifestations without reference to location or cause and is a term introduced and more commonly used in Europe.36

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Fig. 20.17 Surgical management of peroneal and sural nerves in a case of neuropathic pain following amputation. The peroneal and sural nerves were transected above the injury, capped with cautery, and crushed proximally.

Fig. 20.18 Transposition of peroneal and sural nerves in a case of neuropathic pain following amputation. Following transection, cautery, and crush, the peroneal and sural nerves were transposed proximally and deep. The nerves are shown draped proximally just prior to being directed under the muscle in this proximal direction.

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Fig. 20.19 Case presentation of a gunshot wound to the hand. A 5-year-old girl presented to our institution with a gunshot wound to the ulnar aspect of the hand. Initial exploration and small finger amputation were completed. The sensory component of the ulnar nerve was injured with segmental loss and need for soft tissue coverage. She had significant pain relating to the small finger amputation.

Fig. 20.20 Illustration of a gunshot wound and nerve injury within the hand. The gunshot wound occurred at the ulnar palmar aspect of the hand, which transected the ulnar sensory nerve branches distal to its branch point from the deep motor branch of the ulnar nerve.

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Fig. 20.21 Surgical management and reconstruction of ulnar nerve sensation. The small finger required amputation. Due to the blast injury, there was poor soft tissue coverage at the palm, preventing long nerve grafts. 1. The median sensory nerve branch to the ulnar aspect of the index finger was selected as the donor nerve to transfer into the ulnar sensory nerve branch to the ulnar aspect of the ring finger for restoration of critical sensation. 2. The ulnar nerve sensory component in the forearm was harvested proximally as an autologous expendable nerve graft. 3. An acellular nerve allograft was used as an extender to allow proximal transposition of the ulnar nerve sensory component intramuscularly to prevent painful neuroma formation. 4. To restore rudimentary sensation back to the donor nerve sensory territory, an end-to-side nerve transfer to the median sensory branch to the radial aspect of the long finger was performed.

Fig. 20.22 Identification of the donor digital nerve branch for nerve transfer. An incision was made on the palmar aspect of the hand between the index and long fingers. The digital nerve to the ulnar aspect of the index finger was identified as the donor nerve. This digital nerve was chosen as the donor for two reasons: the sensation to the ulnar aspect of the index finger is relatively expendable, and the index finger was the farthest from the site of the blast injury and was grossly intact. The adjacent digital nerve to the radial aspect of the long finger is also noted.

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Fig. 20.23 Identification of the sensory component of the ulnar nerve as the nerve graft and prevention of neuroma formation. Using intrafascicular neurolysis, the sensory component of the ulnar nerve is identified on the radial aspect of the ulnar nerve. A microvessel is seen separating the sensory from the motor component of the ulnar nerve.

Fig. 20.24 Harvesting the sensory component of the ulnar nerve as the nerve graft. (a,b) The sensory component of the ulnar nerve is harvested as a 3.5-cm nerve graft. The motor component of the ulnar nerve was protected and kept intact.

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Fig. 20.25 Donor nerve and interposition nerve graft for nerve transfer and end-to-side nerve transfer to restore rudimentary sensation to the donor nerve territory. An interposition nerve graft from the sensory component of the ulnar nerve was coapted to the proximal end of the donor digital branch of the median nerve to the ulnar aspect of the index finger. To restore rudimentary sensation to the donor nerve territory, the distal end of the ulnar index finger branch of the median nerve was end-to-side transferred and coapted to the side of the radial long branch of the median. Note that this is a unique case where the ulnar nerve sensory component is being used as expendable graft material. This is because the small finger was amputated as part of the initial injury. The objective was to reinnervate the ulnar aspect of the ring finger by distal nerve transfers.

Given the myriad names attributed to seemingly similar pathologic processes, clarity of terminology was sought in the early 1990s. In 1994 the distinction between RSD and causalgia was maintained as each became a subtype of a more general classification called complex regional pain syndrome (CRPS),37,38 which represents excessive regional pain, sensory changes, and vasomotor changes following a noxious event. CRPS type I corresponds to RSD, that is, occurring without a definable nerve lesion. CRPS type II corresponds to causalgia, that is, occurring with a definable nerve lesion. Critical to the definition of these entities is the lack of an identifiable pathologic condition that can logically account for the degree of symptomatology. The IASP has supported this consensus definition of CRPS, as well as a multiaxis taxonomy for all types of chronic pain, patterned much like the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV), involving characterization of regional, systemic, temporal, intensity/duration, and etiologic axes. This latter system is cumbersome and beyond the scope of this text; thus, we will focus on the former systems specific to CRPS subtypes that are far more relevant to the hand and peripheral nerve physician.

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Pathophysiology of Complex Regional Pain Syndrome Hyperalgesia is defined as an increased response to a normally painful stimulus or a reduced threshold for pain. It may be primary, at the site of injury, or secondary, at a site remote from the injury. Allodynia is pain resulting from a normally nonpainful or innocuous stimulus. It is these aspects, along with the chronicity, that generally characterize pain syndromes. The exact pathophysiologic mechanisms of these responses, as well as the vasomotor responses in CRPS, are not thoroughly understood; however, inflammatory, immunologic, and neurogenic factors have all been implicated. Birklein’s and Weber’s groups implicated neuropeptides and neurogenic inflammation in the etiology of CRPS, 39,40 particularly finding elevated calcitonin gene-related peptide (CGRP)– and substance P-mediated plasma protein in the early stages of CRPS. More recently, Fechir, Gerber, and Birklein41have pointed out that these mechanisms may account for development of pathology in “warm” CRPS, one clinical subtype of CRPS as suggested by Bruehl et al.42 “Warm” CRPS involves increased skin temperature and occurs following trauma, whereas “cold” CRPS involves acutely decreased skin temperature that develops

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Fig. 20.26 Acellular nerve allograft (ANA) as an extender from the sensory component of the ulnar nerve for intermuscular transposition. (a) A 5.5-cm ANA (Avance Nerve Graft, AxoGen) is used. (b) The ANA is coapted to the proximal end of the sensory component of the ulnar nerve, transposed proximally, and buried deep within the forearm musculature to prevent painful neuroma formation.

spontaneously or following minimal trauma. Birklein points out that even though similarities exist between acute trauma and CRPS with regard to inflammatory responses, evidence prior to the early 2000s suggests a paucity of proinflammatory cells and lack of response to NSAIDs, and the type of acute hyperalgesia differs between those with acute trauma and those with CRPS.43 In trauma, hyperalgesia exists to both heat and mechanical stimuli; in acute CRPS type I (RSD), it exists only to mechanical stimuli. The mechanical sensitivity seems to be partially mediated through central sensitization. These findings are supportive of a role for neurogenic inflammation where peripheral and central neuropeptides lead to peripheral and central sensitization. As stated previously with regard to the normal physiologic pain response, the peripheral nociceptors are thought to be sensitized by inflammatory mediators.44–46 Üçeyler et al investigated proinflammatory and antiinflammatory cytokine messenger RNA (mRNA) and protein levels in CRPS patients and controls.47 They found elevated mRNA levels of proinflammatory cytokines tumor necrosis factor (TNF) and interleukin-2 (IL-2), as well as elevated serum levels of IL-2 in patients with CRPS; mRNA levels of antiinflammatory cytokines interleukin-4 (IL-4) and interleukin-10 (IL-10) were reduced along with protein levels of transforming growth factor beta 1 (TGFβ1) in those with CRPS.47 This reveals an overall proinflammatory cytokine profile in CRPS. Animal studies have shown that proinflammatory cytokines TNF-α, interleukin-1β (IL-1β), and inter-

leukin-6 (IL-6) promote the release of CGRP from sensory nerves.48 This may suggest a possible relationship between inflammatory cytokines and neurogenic inflammation. The role of the sympathetic nervous system in chronic pain syndromes is unclear, as some chronic pain syndromes seem to be “sympathetically mediated” (sympathetic maintained pain, SMP),49 and some do not (sympathetic independent pain, SIP).50 Sympathetic blockade decreases pain symptoms in a subset of patients with CRPS but not in others. The senior author of this chapter and editor of this text has reported on the role of the sympathetic nervous system in maintaining pain and distinguishing it from other factors that maintain the pain.18,51,52 Recalling the “warm” and “cold” types of CRPS, clearly the behavior of the sympathetic nervous system is variable early and may change over time in CRPS. Nevertheless, in addition to the often-evident clinical findings, the bulk of recent evidence suggests a role of the sympathetic nervous system in CRPS. Recalling the comparison of acute trauma to CRPS, Berklein’s group has also found differences in sympathetic nerve function in these respective settings with failure of autonomic system vasoconstriction in affected limbs of those with CRPS but not those with acute trauma.43 This correlates with an earlier finding from the same group that vasomotor function is decreased acutely and sudomotor function is increased acutely in CRPS.53,54 It is important to note that the vasomotor findings by Birklein’s group involve responses to mental arithmetic tasks, but

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Painful Sequelae of Peripheral Nerve Injuries

Fig. 20.27 Cadaveric dissection showing the overlap between the radial sensory nerve and lateral antebrachial cutaneous (LABC) nerve. (a) The radial sensory nerve is visible on the background, and the LABC nerve is held on a hemostat. The LABC nerve completely overlaps the territory of the radial sensory nerve and is just superficial to the radial sensory nerve. (b) The radial sensory nerve and LABC nerve demonstrate no overlap. This pattern was found in 25% of dissections. (Used with permission from Mackinnon SE, Dellon AL. The overlap pattern of the lateral antebrachial cutaneous nerve and the superficial branch of the radial nerve. J Hand Surg [Am] 1985;10:522−526.)

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no abnormal response was found to other forms of vasomotor stimulation. This implies that the dysfunction may begin predominantly in the central sympathetic-associated nervous system. Comparatively, following trauma, increased skin temperature is associated with neuropeptide release from sensory nerve endings and vasodilatory chemical release from mast cells and leukocytes predominantly in the periphery.55 Sympathetic vasoconstriction is thought to reduce neurogenic inflammation.56 Thus, the dysfunction of sympathetic vasoconstriction not only may lead directly to increased inflammation in CRPS, but may also enhance it by indirectly promoting neurogenic inflammation. Drummond has extensively studied the role of the sympathetic nervous system in CRPS, and recently, Gibbs et al presented an excellent review of evidence and proposed a theory of how the sensory and sympathetic systems interact in SMP.57 They identified an association between noradrenaline and sensitized cutaneous pain and proposed mediation by inflammation-sensitized α-adrenoceptors, either on or near very closely associated pain afferent fibers. They also re-

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ported a lack of evidence for ephaptic, or nonsynaptic electric, communication in favor of chemical coupling of the sympathetic and sensory systems and adrenoceptor-mediated supersensitivity. Mechanisms may include an alteration to cutaneous sensory innervation with a reduction in C and A-delta fiber density, central and peripheral sensitization, and increase in the release of pro-inflammatory cytokines and neuropeptides, alterations in sympathetic nervous system function, and altered processing of nociceptive stimuli from cortical reorganization. 59 Finally, neurogenic factors involved in CRPS include the CNS. As stated in the previous paragraph, some of the involvement of the sympathetic nervous system appears to be central. Central sensitization of the spinal cord in opioid-induced hyperalgesia may be mediated by the neurotransmitters glutamate, via action on N-methyl-D-aspartate (NMDA) receptors,58 and cholecystokinin from the rostral ventromedial medulla (RVM). 60 In addition, studies have found reorganization of both the sensory61 and motor62 cerebral cortex in CRPS patients.

Painful Sequelae of Peripheral Nerve Injuries

Fig. 20.28 Diagnostic nerve blocks used to determine the origin of the neuropathic pain. (a) The lateral antebrachial cutaneous (LABC) nerve is blocked in the proximal forearm adjacent to the cephalic vein. The radial sensory nerve is blocked just dorsal to the muscle tendon junction of the brachioradalis muscle. The nerves are blocked well proximal to the dorsoradial wrist area. (b) The LABC nerve is blocked in the proximal forearm. The forearm is “divided” longitudinally into thirds. The nerve lies adjacent to the cephalic vein at the junction of the lateral and middle thirds. It lies just medial to the brachioradialis muscle. (c) The radial sensory nerve lies just dorsal to the musculotendinous junction of the brachioradialis muscle. (Used with permission from Mackinnon SE, Dellon AL, eds. Surgery of the Peripheral Nerve. New York, NY: Thieme; 1988:481,484.)

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Fig. 20.29 Surgical management of neuropathic pain in the radial sensory and lateral antebrachial cutaneous (LABC) nerve territories. (a) In this case, the patient had an injury to the dorsal radial aspect of the wrist. She had a carpometacarpal arthroplasty and carpal tunnel release with no relief of pain along the dorsal radial aspect of the wrist. (b) Previous incision marked along the wrist. (c) Upon exposure, the neuroma was identified along the dorsal radial aspect of the wrist to be the radial sensory nerve. The LABC nerve was not found to be involved. (d) In a proximal incision, the radial sensory nerve was exposed to attain sufficient transposable length. The neuroma was then excised, capped with cautery, crushed proximally, and transposed proximally.

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Painful Sequelae of Peripheral Nerve Injuries As the difference between SMP and SIP, or “warm” or “cold” CRPS, suggests, different factors may maintain pain in patients with pain syndromes. In addition to functional factors, psychological factors, such as secondary gain, may maintain pain in some patients, and anxiety, stress, and somatization may predispose to CRPS or similar symptoms.63,64

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20.3.3 Diagnosis of Complex Regional Pain Syndrome Overview Pain is the most significant reason patients seek medical attention. Although it may occur at virtually any age, patients affected by CRPS are usually in their third or fourth decade of life, and females outnumber males 3:1 to 4:1.65–67,68,69 It tends to affect the upper and lower extremities, and the most common causes are surgery, crush injuries, strains, and fractures.65–67 Importantly, a small but rather consistent percentage of patients do not recall any inciting or associated event, 65,66 which raises questions about the pathophysiology and diagnosis of CRPS. Along with the definition and classification of CRPS, the IASP introduced diagnostic criteria for the two types of CRPS in 1994:37,38

International Association for the Study of Pain Diagnostic Criteria for Complex Regional Pain Syndrome Types I and II 1. Presence of inciting noxious event without (type I) or with (type II) an identifiable nerve injury 2. Spontaneous or continuous pain, allodynia, or hyperalgesia not limited to a single nerve territory and disproportionate to any inciting event 3. Edema, changes in skin blood flow, temperature, abnormal sudomotor activity, or trophic changes in the region of the pain at some time point 4. Absence of an alternative diagnosis that would otherwise account for the degree of pain and dysfunction [1 not necessary for diagnosis; 2 to 4 necessary for diagnosis]

The implementation of these standardized criteria represents an effort to facilitate clinical recognition and scientific study of these pain syndromes. However, Bruehl et al noted that the sensitivity of these criteria is high, but the specificity is as low as 0.36 with a high tendency for false-positive diagnosis in patients with non-CRPS neuropathic pain, such as diabetic neuropathy.65,70 They proposed a modification of diagnostic criteria, initially for research purposes, but logically adapted for clinical purposes, called the Budapest criteria, based on the work done by an international panel of experts in Budapest, Hungary, in 2003.70–72 The Budapest citeria retain the exceptional sensitivity of the IASP criteria (0.99), but greatly improve upon the specificity (0.68):

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Modified Budapest Research Diagnostic Criteria for Complex Regional Pain Syndrome 1. Continuing pain disproportionate to any inciting event 2. At least one symptom in three of the four following categories: 1. Sensory: hyperesthesia and/or allodynia 2. Vasomotor: temperature asymmetry, skin color change, skin color asymmetry 3. Sudomotor: edema, abnormal sweating, asymmetric sweating 4. Motor: reduced range of motion, motor dysfunction (weakness, tremor, dystonia), trophic changes (e.g., hair, nail, skin) 3. At least one sign at time of evaluation in two or more of the following categories: 1. Sensory: evidence of hyperalgesia, allodynia 2. Vasomotor: evidence of temperature asymmetry, skin color change or asymmetry 3. Sudomotor: evidence of edema, abnormal sweating, or asymmetric sweating 4. Motor: evidence of reduced range of motion, motor dysfunction (weakness, tremor, dystonia), trophic changes (e.g., hair, nail, skin) 4. There is no other diagnosis that better explains the signs and symptoms.

Findings fall into three categories: pain and sensory, autonomic, and trophic. Autonomic findings include vasomotor and sudomotor signs, such as edema (80% of patients), 41 skin color changes, skin temperature changes (80% of patients), 73 and abnormal sweating patterns (55% of patients). 74 Motor and dystrophic findings include muscle weakness, stiffness, or decreased range of motion; dystonia (30% of patients); 75 and tremor (50% of patients).76 Sensory changes can be heightened or lowered and occur in up to 90% of patients. 41 Common to all diagnostic criteria, however, and the most identifiable feature, is disproportionate pain following an inciting event that has no other identifiable cause. Patients describe excruciating, burning, sharp, shooting pain, as well as achy pain. Pain occurs within the affected body part, usually the upper or lower extremity. Traditionally, CRPS has been described as occurring in three sequential stages.77,78 Stage I, the acute stage, is associated with the classic symptoms of pain and sensory abnormalities, as well as vasomotor and sudomotor signs; stage II, occurring at 3 to 6 months after onset, exhibits continued or increased symptoms and signs of stage I, with the development of motor and dystrophic signs and symptoms; and stage III, the late stage, is characterized by decreased pain with increased dystrophic changes. The presence of these distinct sequential stages has not been supported by more recent investigation and is largely refuted by the statistical analysis performed by Bruehl et al. 42 They noted that the patients with the longest duration of pain had fewer motor and dystrophic changes, as did the group with the shortest pain duration; thus, the presence of severe dystrophic

Painful Sequelae of Peripheral Nerve Injuries changes does not imply the expectation of a greater duration of pain symptoms. Their analysis found a distinction between patients with a relatively limited syndrome duration of either predominantly vasomotor findings or predominantly pain and sensory findings, and a separate group displaying the more classic florid syndrome findings of a longer duration who are much more likely to have dystrophic and motor changes.

Clinical Diagnosis Clinically, pain should be characterized as thoroughly as possible, including onset, duration, location, quality, and greatest and average intensity. This is best performed with a standardized, patient-completed questionnaire and visual analogue scale (pain questionnaire; see ▶ Fig. 20.29). Simple observation of the patient’s posture and degree of protective nature of the involved extremity provides insight as to the severity of pain as well as the patient’s ability to cope. Observation alone allows identification of many of the aforementioned findings, the presence or absence of which should be noted. In the more traditional, florid cases, patients will treat the extremity as a foreign object, nonself, and will protect it from any stimulation. It is always advisable to ask the patient if he or she will allow the extremity to be touched before beginning any physical examination. As allowed, assessments of sensation to light touch, skin temperature, range of motion, and sweating should all be made (▶ Fig. 20.30; ▶ Fig. 20.31). Skin temperature and sweating can be assessed subjectively or objectively. After acclimatizing to a standard, controlled room temperature, skin temperature may be measured by an

infrared thermal camera at the fingertips of the involved extremity and compared to the contralateral, uninvolved extremity. Sweating may be measured quantitatively with the Quantitative Sudomotor Axon Reflex Test (QSART), which uses iontophoresis to measure acetylcholine-stimulated sweat production, or qualitatively with the thermoregulatory sweat test, which assesses regional sweat production in response to elevated body temperature via a whole-body starchlike test in a warm ambient environment.

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Ancillary Diagnostic Studies In addition to the aforementioned qualitative and quantitative sensory and autonomic tests, electrodiagnostic abnormalities may help distinguish CRPS type II from type I. However, there is little other diagnostic value in these tests and no clearly identifiable value in determining treatment. Given the practical difficulties in obtaining electrodiagnostic studies in patients with pain and their limited value, they are not recommended. The single most valuable diagnostic study for CRPS is the three-phase bone scan. The three-phase image technique is performed on the hands and wrists. A radioisotope is injected, and images are captured with a gamma camera at different times following injection. The first phase occurs immediately and results in angiographic images. This is followed immediately by the second phase, called the blood pool or tissue phase, which shows uptake in involved soft tissue in the few minutes following injection. The third, or delayed, phase occurs 3 to 6 hours after injection and reveals activity in bone. Some diagnostic centers recommend a fourth phase 24 hours after injection to

Fig. 20.30 Examination of a patient with reflex sympathetic dystrophy and complex regional pain syndrome. The patient exhibited trophic skin changes, swelling, and marked joint stiffness in the right hand. This manifests in the inability to make a fist.

Fig. 20.31 Three-phase bone scan of reflex sympathetic dystrophy and complex regional pain syndrome. (a) Marked joint stiffness and trophic skin changes were exhibited in the right hand. (b) The three-phase hand scan demonstrated increased perfusion of the soft tissue in the right forearm and hand in the immediate static postinjection images. (c,d) The delayed images demonstrated increased uptake along the right periarticular surfaces of the fingers when compared to the left side.

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Painful Sequelae of Peripheral Nerve Injuries attempt to increase specificity in the diagnosis of other pathologies. Studies may be interpreted as normal, focally abnormal, or diffusely abnormal. Findings in CRPS include increased uptake in all three phases at the involved extremity location. The first two phases generally show diffuse asymmetric uptake, and the delayed phase shows increased asymmetric periarticular uptake, which has become the defining diagnostic feature of bone scintigraphy for CRPS. Although reports in the literature vary as to the overall sensitivity and specificity in CRPS,79,80 the sensitivity and specificity have been shown to be excellent for early SMP.81,82 These scans tend to identify those patients with the most florid expressions and greatest degree of trophic changes70 and tend to be more valuable earlier in the course of disease.83,84 Plain radiographs are usually normal early in the disease process but may show late demineralization and resorption. Magnetic resonance imaging (MRI) has revealed abnormal findings of thickening of the skin and edema of the skin, soft tissues, joints, bone, and, most recently, skeletal muscle in patients with CRPS.85 Standard T1-weighted images show low signal, whereas fat saturation or gadolinium-enhanced T1 images, T2 images, and T2 STIR (T2 Short Tau Inversion Recovery) images show high signal. MRI is promoted as a superior diagnostic imaging technique because it can distinguish among CRPS, bone necrosis, infection, and tumor86; it is also preferred when the sensitivity or specificity of a bone scan is questioned. However, MRI findings of bone edema tend to be absent and may be completely normal late in the disease process or when dystrophy predominates.87 Consequently, bone scans can be more useful than MRI in monitoring treatment.

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20.3.4 Treatment of Complex Regional Pain Syndrome The effective treatment of CRPS requires an experienced multidisciplinary approach with physiotherapy as the main modality, but also pharmacologic and interventional therapies. Although the focus of treatment begins with pain and edema control, followed by functional restoration once the diagnosis is made, a more preemptive strategy of prevention is highly recommended.

Preventive Measures The majority of inciting events are spontaneous and unpredictable, but there are some situations when the peripheral nerve surgeon can intervene prior to a potentially inciting event. Various reports identify displaced and reduced fractures and tight application of a plaster cast as associated with the higher incidence of CRPS seen with distal radius fractures.88,89,90 Pressures under casts of patients who develop CRPS have been found to be higher than those who do not develop a pain syndrome.91 However, whether the pressure is a cause or effect is unclear. There are various anecdotal reports touting the relative benefit of one form of treatment of distal radius fractures over the other, but there are, perhaps surprisingly, no high-quality comparative studies or clear evidence reported in the literature regarding the effect of fracture treatment on the development of CRPS.92 Zollinger et al reported on the preventive effects of vitamin C against CRPS, and their findings have been

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corroborated by at least one other group.93,94,95 Administration of vitamin C, 0.5 to 1.0 g orally for 45 to 50 days postinjury, is associated with a reduced incidence of CRPS in patients with distal radius fractures and may eventually prove to be beneficial in other situations. Much of the other research on potential preventive measures for CRPS has focused on risk factors for recurrent CRPS. Despite the common belief in multiple measures to prevent recurrent disease, such as perioperative analgesia, minimally invasive procedures, minimal tourniquet usage, early postoperative mobilization, and perioperative administration of calcitonin, their true benefits remain unproven.92 These measures have been touted as a means of treatment of CRPS, and benefits in this setting remain to be seen.96 Zyluk92 reports a 2% overall CRPS recurrence rate, similar to that found by Veldman and Goris, 97 at 3%. Recurrence tended to be spontaneous, and apparently unrelated to reoperation, as no specific preventive measures were undertaken in those who did undergo reoperation on the involved extremity. Dellon et al98 recently reported 80% “excellent” or “good” results from targeted peripheral nerve surgical intervention, involving neurolysis, joint denervation, or neuroma resection, in select patients with a diagnosis of ongoing CRPS type I of at least 6 months of nonsurgical treatment, evidence of nerve compression, and response to nerve blockade.98 This suggests that some patients with a diagnosis of CRPS type I may have a significant component of ongoing nerve injury similar to CRPS type II, and that surgical intervention, even that involving the affected nerves, is not only safe but potentially therapeutic. However, these studies are limited by their retrospective, uncontrolled design. Definitive conclusions generally require more rigorous, prospective, controlled studies, which are naturally rendered prohibitive by the nature of this particular disease process. Conventional dogma generally suggests avoidance of operative intervention in patients with a history of CRPS until all signs and symptoms of the disease have resolved. Although no definitive conclusions may be drawn regarding reoperative risk, it is somewhat comforting to find such low percentages of recurrence reported. Dexmedetomidine, a clonidine-like α2 receptor agonist that has sedative, analgesic, sympatholytic, and anxiolytic effects, has been shown to reduce postoperative pain and analgesic requirements when used either intravenously preoperatively or as a component of intraoperative intravenous regional anesthesia.99,100,101,104 Although no studies exist evaluating its effect on CRPS, we believe its effect profile is ideally designed to help prevent development of postoperative pain syndromes and recommend its use (0.5 μg/kg ideal body weight) in at-risk surgical cases. Given the aforementioned pathophysiologic theories, we also recommend direct local anesthetic infiltration prior to any planned nerve transection to prevent sensitization. Future clinical studies will help determine the validity of these recommendations.

Treatment Measures Prevention of CRPS is ideal, but most cases, by their nature, are associated with an inciting event that is generally spontaneous and thus not preventable. In these situations, early recognition and intervention are key. Treatment is multidisciplinary and involves pharmacologic, physiologic, psychologic, and interven-

Painful Sequelae of Peripheral Nerve Injuries tional modalities, with physiotherapy as the centerpiece. The focus of treatment is on early pain relief, edema control, and restoration of function.

Pharmacologic Treatment Very few controlled studies exist regarding most reported treatments, but some treatment options do have the support of a few small controlled studies.102,103 Both prednisolone105 and methylprednisolone106 have had success at reducing pain over the course of 1 to 3 months, and bisphosphonates have shown success at reducing pain and swelling and increasing range of motion in CRPS type I.107,108 Oxygen-free radical scavengers, particularly topical dimethyl sulfoxide (DMSO) and oral N-acetyl-cysteine (NAC), have shown benefit in single randomized controlled studies. DMSO appears to be beneficial in “warm” CRPS type I,109,110 and NAC appears to be beneficial in “cold” CRPS type I.110 Baclofen has been used to treat dystonia. Many pharmacologic therapies have reported benefits that have not been proven or have shown no significant benefit upon more rigorous evaluation, including calcitonin, phentolamine, and pharmacologic sympathetic blockade. 96,111 Despite the absence of direct study in CRPS, we support the use of pregabalin, an anticonvulsant with analgesic and anxiolytic activity that has predominantly been used for the treatment of fibromyalgia and diabetic neuropathic pain. An alternative to pregabalin is gabapentin, an older anticonvulsant with in our experience interior therapeutic effects on neuropathic pain. Other medications that may play a role in the treatment of CRPS are antidepressants, either trycyclics (TCAs), selective serotonin reuptake inhibitors, or selective serotonin and norepinephrine reuptake inhibitors (SNRIs), particularly when depressive psychiatric manifestations exist. Anesthetic transdermal patches are sometimes useful for treating pain and sensory symptoms, particularly for those patients with very limited or focal manifestations. There is no doubt that opioids have a role in pain relief, and although they should not be denied, reliance on them or development of dependence should be avoided. Given the complexity of these pharmacologic treatment options and the usual prolonged duration of symptoms, pain management specialists have an important role in this aspect of patient treatment and are valuable members of the multidisciplinary management team.

Psychological Treatment Psychiatric abnormalities or overt illnesses should be treated by a psychiatrist. Associated or underlying depression, anxiety, and personality disturbances should be treated with the appropriate pharmacologic and psychotherapeutic measures. Otherwise, these factors will present considerable obstacles to overcoming the fear of the pain and prevent progression of management. Additionally, cognitive behavioral therapy is valuable in virtually all patients to overcome pain phobia and extremity neglect and to promote progression of physiotherapeutic modalities, as discussed below.

Sympathetic Blockade Sympathetic nerve blocks have long been used in both the diagnosis and treatment of CRPS and RSD or SMP before adoption of

the current nomenclature. Even though there are more controlled studies on sympathetic blockade in the treatment of CRPS than on any other single treatment, the role of sympathectomy is not clear.96 Given the lack of clear evidence for surgical sympathectomy for SMP in CRPS and its potential complications, it is only rarely recommended. Pain relief from sympathetic blockade is generally transient and not curative, though sometimes quite dramatic. Although it is not expected to be curative, pharmacologic regional sympathetic block may have diagnostic value and adjunct therapeutic value in some patients. Blocks are usually performed with intravenous regional phentolamine or guanethidine, or more appropriately for diagnostic purposes with local anesthetic at the stellate ganglion (cervicothoracic) for the upper extremity and at the lumbar paravertebral sympathetics for the lower extremity. Block of sympathetic function with maintenance of somatic function should be confirmed for a valid diagnostic test.111 Such blocks are performed as part of a multimodality approach.

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Somatic Blockade Despite the lack of an expected prolonged effect, both sympathetic and somatic nerve blockades with anesthetics may have significant value in temporarily reducing pain and allowing patients to undergo more effective physiotherapy. Somatic nerve blocks may take the form of epidural, brachial plexus, lumbar plexus, or intrathecal anesthetic administration. Both sequential interventions and indwelling catheters have been used.111

Neurostimulation The principle of neurostimulation and its effect on pain perception has its foundation in the gate control theory; however, the precise mechanism of action is unconfirmed. The process involves modulation of the central or peripheral pain pathways with a specific electric current sufficient to block pain pathways without blocking other sensory or motor pathways. Pulsed radiofrequency has been found to be an effective treatment at the dorsal root ganglia for cervical radicular pain and is similar in efficacy at the suprascapular nerve to steroid injections for chronic shoulder pain.112 The stimulation of the pulsed radiofrequency appears to modulate synaptic transmission, neuron morphology, and pain signaling.112 Transcutaneous electrical nerve stimulation (TENS) is an effective treatment for hyperalgesia and pain of various causes. It involves transmission of a high- or low-frequency current through surface electrodes resulting in analgesic effects through activation of central opioid receptors and peripheral opioid and α2-noradrenergic receptors.113 The peripheral mechanism seems to involve the deeper tissue large-diameter afferents rather than the cutaneous small fiber afferents,114 and the central mechanism involves inhibition of release of glutamate and aspartate.115 A Cochrane database review found insufficient evidence to support individual use of TENS in acute pain,116 but there is some suggestion based on laboratory models that it may have value in CRPS type II,117 as well as evidence of effectiveness in CRPS type I in children. 118 Peripheral nerves can be stimulated directly with invasive placement of peripheral nerve stimulators. The application of these is currently best reserved for select patients when other

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Painful Sequelae of Peripheral Nerve Injuries modalities have failed. They have the most reliable response in those patients with CRPS type II.119,120 However, to date, there have been no published randomized controlled trials evaluating peripheral nerve stimulators; also, there are complications associated with their use, such as infections, lead migration, and nerve injury, and the revision rate is relatively high. Nevertheless, published reports show significant benefit in a large proportion of patients, and there is a low risk of any serious adverse event.119,120,121,122 Finally, central nerves may be targeted with spinal cord stimulation (SCS), by placement of indwelling electrodes and a battery pack following successful trial stimulation. There is evidence of effective pain relief, even in late cases following failed management by other techniques, as well as improvement in quality of life.123,124 Olsson et al report on a series of 7 adolescent females, all with favorable outcomes after SCS. 98,125 A task force of the European Federation of Neurological Societies evaluated the evidence for different methods of neurostimulation to develop therapy guidelines, and concluded that SCS is efficacious in CRPS type I and failed back surgery syndrome.126 Their evaluation also found inadequate evidence regarding peripheral nerve stimulation. Others have reported benefits of SCS in refractory angina pectoris and pain of peripheral vascular disease.127 Kemler and Furnée evaluated the cost efficacy of SCS and found its inclusion to be more effective and less expensive than standardized treatments for CRPS type I without SCS.128 Kemler et al reported on some of the longest follow-up (5 years) of patients with CRPS type I treated with SCS and finds that the beneficial effect of SCS on pain diminishes with time, yet patients report a continued higher treatment satisfaction.129

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Physiotherapy The modalities discussed above are not only valuable in reducing pain symptoms but also critical in allowing the performance of physiotherapy. The degree of pain routinely discourages any use of the affected limb, but active use is necessary to preserve limb function. It is often very difficult to convince the patient of this necessity. Maximizing pain control increases the patient’s ability to perform physiotherapy, and thus promotes active involvement of the patient in his or her treatment, allows him or her to see the extremity in use, and provides beneficial psychological encouragement. It is important for therapy to occur below the patient’s pain threshold level so as not to exacerbate pain symptoms, decrease compliance, and be generally counterproductive. Once pain is sufficiently managed, the initial focus of physiotherapy is gradual desensitization. Initial stimuli should be non-nociceptive, such as mild temperature changes, pressure, motion, and massage. Edema control is another early goal of physiotherapy to promote the subsequent and final goals of increased range of motion and strength. Exercises should be active, rather than passive, for range of motion, and strength exercises should be isometric to avoid pain exacerbation. Graded motor imagery (GMI) is a three-stage program consisting of implicit motor imagery (left/right handedness), explicit motor imagery (imagined movements), and mirror image therapy. Mirror image therapy and biofeedback are heavily recommended to assist with overcoming the psychological obstructions and help advance motion therapy. Finally, work-

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specific occupational therapy should be employed to help reengage the patient in a productive daily life.130

20.4 Controversy A significant component of a nerve surgeon’s practice is treating patients with the painful sequelae of nerve injury. By contrast, the dogma in the nonsurgical pain literature is that “re-cutting injured nerves in neuropathic pain patients necessarily has disastrous consequences.”131 This commentary was a response to a case report recently published wherein neuromas of the sural and peroneal nerves were excised and proximally transposed to give long-standing significant pain relief for young women who had suffered neuropathic pain for 13 years.132 This “no surgical approach” is based on the assumption that the generators of pain migrate from the periphery to the central nervous system. This centralization transitions to chronicity, making surgical manipulation of any impulse generator within the peripheral nerve system unsuccessful in relieving pain.133,134,135,136,137 Based on this case report, Devor and Tal challenge us as nerve surgeons to critically review and report the techniques that we espouse and know dramatically improve the lives of many of our patients with neuropathic pain.

20.5 Conclusion Pain is a complex concept with a variety of meanings and realworld implications extending from the most abstract to the molecular. Yet all of its forms maintain a basic, underlying essence that, though difficult to define singularly, is universally understood. Clinically, pain is an unfortunate symptom with which the peripheral nerve surgeon must be familiar. It may present as a normal response to injury or a very abnormal and recalcitrant occurrence without any identifiable cause. In any presentation, it is not to be ignored. Attention to neuromatous pain begins with prevention, proceeds with physiotherapy, and ends with careful surgical selection and treatment. Successful treatment of CRPS requires early recognition and intervention with a focus not only on pain management, but also on psychological management and on functional rehabilitation.138

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Index Note: Page numbers set bold or italic indicate headings or figures, respectively.

A Accessory nerve – course of 420 – in partial middle trunk nerve transfer 435–437 – in thoracic outlet syndrome surgery 330 – injury 405 – palsy 319, 443 – to musculocutaneous nerve transfer 428 – to suprascapular nerve transfer 419–432, 432, 433–434 Acellularized nerve allograft (ANA) 92, 97–98, 175, 176–177, 179–180, 188 Acetylcholine receptor 24 Action potentials – compound muscle fiber –– amplitude of 61, 62 –– area of 61, 62 –– defined 60 –– duration of 62, 62 –– in axon loss 65 –– in demyelination 67 –– in motor nerve conduction studies 63 –– latency of 62, 62 – motor unit –– defined 64 –– in axon loss 65 –– in axonotmesis 59 –– in brachial plexus injury 402 –– in neurapraxia 59 –– in neurotmesis 59 –– in perioperative assessment for nerve transfer 103 –– in ulnar nerve compression 262 –– morphology of 64 – sensory nerve –– amplitude of 61, 62 –– area of 61, 62 –– defined 60 –– duration of 62, 62 –– in axon loss 65 –– in demyelination 67 –– in sensory nerve conduction studies 62 –– latency of 62, 62 Activating transcription factor (ATF) 13 Activator protein 1 (AP-1) 11 Adson test 315, 318 Allograft 89, 95–98 – See also Conduits nerve, See also Grafts nerve – acellularized 92, 97–98, 169, 175, 176–177, 179–180, 188 – cold preservation of 194 – experiences 196, 196 – for animal bite 197 – for intercostal neuralgia 197, 199– 202 – for median nerve reconstruction 196–197 – for peroneal nerve reconstruction 197

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– for posterior tibial nerve reconstruction 197 – for radial nerve reconstruction 197 – for sciatic nerve reconstruction 196 – for tibial nerve reconstruction 196 – for ulnar nerve reconstruction 196– 197, 198 – history of 169, 193 – immunosuppression and 193, 194, 195, 202 – in gunshot wound 197 – pretreatment of 194 – regeneration and 193 – rejection 92, 194, 196 – Schwann cell migration in 193, 194, 203 – tacrolimus and 195 – vascularized composite 199, 203 ALPHA-helical region 12 Amplitude of evoked response 61, 62 ANA See Acellularized nerve allograft (ANA) Anatomical variations – brachial plexus 313, 392 – cubital tunnel syndrome and 255 – median nerve 211 – posterior tibial nerve 371, 381 – scalenes 313 – ulnar nerve 254 Anconeus epitrochlearis cubital tunnel syndrome and 255 Anesthesia – in carpal tunnel release 223 – in nerve transfer 103 – in tetraplegic patients 162–163 Anesthetics nerve injury from 7, 8 Angiography in vascular thoracic outlet syndrome 327 Animal bite allograft for 197 Anterior crural intermuscular septum in peroneal neuropathy 347, 350, 354, 367 Anterior interosseous nerve (AIN) – anatomy 161 – as donor nerve 87, 90 – brachialis transfer to 131–132 –– in median nerve restoration 131, 138–140 –– in tetraplegia 158, 160 – extensor carpi radialis brevis branch transfer to 126, 127, 128, 132–137 – flexor digitorum superficialis transfer to –– for anterior interosseous nerve palsy 246 –– technique 128, 132–137 – function restoration 128, 133–137 – in median-to-radial nerve transfer 112 – in reverse end-to-side supercharge transfer 141, 148 – palsy 129, 246, 246 – to flexor carpi ulnaris transfer 128, 133 – to median recurrent motor branch nerve transfer 118, 119 – to ulnar nerve transfer 137, 139, 141–146 Anterior tarsal tunnel syndrome 377

– See also Deep peroneal nerve neuropathy , See also Tarsal tunnel syndrome Anterior transmuscular transposition for cubital tunnel syndrome 262, 263–270 – alternative techniques for 271 – distal intermuscular septum in 263, 266–267 – fascial flaps in 270 – flexor carpi ulnaris branch in 269– 270 – flexor carpi ulnaris in 263, 268 – intramuscular 271 – medial antebrachial cutaneous nerve in 264, 272 – medial intermuscular septum in 264–265 – median antebrachial cutaneous nerve in 272 – Osborne band in 263 – subcutaneous 271 – submuscular 271 – T fascia in 263, 268–269 – ulnar nerve in 263, 265, 268–269 AP-1 See Activator protein 1 (AP-1) Arcade of Frohse 291, 297, 299, 303 Arcade of Struthers 254, 282 Area of evoked response 61 Arginase-1 12 Artemin (ARTN) 15, 15 Arterial graft 169 Arterial thoracic outlet syndrome 311, 314 – See also Thoracic outlet syndrome (TOS) – angiography in 327 – history in 326 – physical examination in 327 ARTN See Artemin (ARTN) ATF See Activating transcription factor (ATF) Autograft 85, 86–95 – See also Grafts nerve Avance 169, 175 – See also Acellularized nerve allograft (ANA) Avulsion injury brachial plexus 76 Axillary artery in ulnar nerve blood supply 254 Axillary nerve – fascicular anatomy of 395 – in brachial plexus anatomy 393, 394 – in brachial plexus injury 403 – in Parsonage-Turner syndrome 404 – medial pectoral nerve transfer to 437, 444–448 – thoracodorsal nerve transfer to 438 – topographical anatomy of 3 – triceps branch transfer to 419–432, 432, 433–434 – tug testing of 395 AxoGuard Nerve Connector 169 Axon loss See Wallerian degeneration Axonal transport 17 Axonotmesis 6, 7, 59, 75 – See also Injury nerve Axons – in nerve fiber anatomy 1

– in preferential motor reinnervation 18 – retraction of in injury 4, 5

B BDNF See Brain-derived neurotrophic factor (BDNF) Bernhardt-Roth syndrome See Meralgia paresthetica Berrettini branch 254 BETA-chain 12 Biceps flexor carpi ulnaris transfer to 412, 415 Bicipital aponeurosis 208 Blood supply – intrinsic during mobilization 255 – nerve 18 – to ulnar nerve 254 Bone marrow stromal cells nerve conduits and 186 ''Border nerves'' See Genitofemoral nerve , See Iliohypogastric nerve , See Ilioinguinal nerve Brachial neuritis See Parsonage-Turner syndrome Brachial plexus – anatomy 313, 392, 393-394 – fascicular anatomy of 394 – in thoracic outlet syndrome 312– 313 – in thoracic outlet syndrome surgery 326, 328–331, 334, 334–335 – intraneural topographical anatomy of 395, 396 – lateral cord of 392, 393, 394 – medial cord of 392, 393 – posterior cord of 392, 393 – provocative test for 47 Brachial plexus injury – accessory nerve injury in 405 – avulsion 76 – by compression 398 – closed 406 – CT myelography in 402 – dorsal root ganglion in 398, 400 – electrodiagnostic studies in 401 – electromyogram in 72, 401 – epidemiology of 397 – fractures in 402 – gender and 397 – historical review of 391, 399 – iatrogenic 398 – imaging in 402 – in cardiac surgery 398 – in gunshot wounds 406 – magnetic resonance imaging in 402 – management principles 402 – motor nerve transfers in 410 – motor unit action potentials in 402 – open 406 – operative management of 407–412, 414–419, 422–428, 430–447 –– exploration in 406, 407 –– infraclavicular exposure in 407, 407–412 –– medial antebrachial cutaneous nerve grafts in 410

Index –– median nerve in 408, 411 –– pectoralis major in 407, 408–410 –– pectoralis minor in 411–412 –– supraclavicular exposure in 406 – pain in 401, 402 – Parsonage-Turner syndrome in 403 – peripheral entrapment neuropathy in 403 – physical examination in 401 – physical therapy for 402 – plain radiography in 402 – postganglionic lesions in 398, 400 – preganglionic lesions in 398, 400 – quadrilateral space syndrome in 403 – radiation-induced 404 – root avulsion in 398, 399–400 – shoulder function in 419–431, 431, 432, 432, 433–448 Brachial plexus neuritis See ParsonageTurner syndrome Brachialis in radial nerve decompression at spiral groove 294, 398 Brachialis nerve – anatomy 161, 209, 413 – to anterior interosseous nerve transfer 131–132 –– in median nerve restoration 131, 138–140 –– in tetraplegia 158, 160 Brachioradialis – in posterior interosseous decompression 295, 298–299 – in radial nerve decompression at spiral groove 294 – in radial sensory branch decompression 306–307 Brain-derived neurotrophic factor (BDNF) 15 ''Bread loafing'' 76, 80

C c-Jun 11, 13 cAMP See Cyclic adenosine monophosphate (cAMP) cAMP response element binding protein (CREB) 11, 12, 13 Capitate in carpal tunnel anatomy 212 Carpal tunnel anatomy 212 Carpal tunnel compression test 214 Carpal tunnel release (CTR) – anesthesia in 223 – complex regional pain syndrome after 229 – complications in 226, 229 – endoscopic –– advantages of 222 –– open versus 222 – in obese patients 225, 225 – incidence of 212 – incision in 220 – medial antebrachial cutaneous nerve graft in 219 – median nerve injury in 226, 229 – nerve wrap in 188 – neurolysis in 224 –– revision 232, 239 – neuroma resection in 218 – open –– advantages of 223 –– versus endoscopic 222 – outcomes with 225 – palmar aponeurosis in 223

– revision 227, 228–229, 229, 230–239 – transverse carpal ligament in 221– 222, 224 – transverse palmar cutaneous branch of ulnar nerve in 224 Carpal tunnel syndrome (CTS) – anatomic causes of 219 – clinical presentation of 212 – corticosteroid injections for 221 – diagnosis of 212 – electrodiagnostic studies in 216, 217 – etiology of 217 – gender and 212 – history of 212 – incidence of 212 – nocturnal relief of 219 – nonsurgical treatment of 220 – pain evaluation in 214, 214 – Phalen test in 214 – physical examination in 214 – provocative tests in 214 – recovery expectation in 215, 217, 225 – repetitive hand work and 218 – risk factors for 217 – splinting for 220 – Ten sign in 214 – thenar wasting in 213, 214 – Tinel test in 214 – vibration exposure and 218 Carpometacarpal arthroplasty 297 Cervical rib 313 Cervical spine disease thoracic outlet syndrome versus 316 cJun-N-terminal-kinases (JNKs) 13 Clavicle fracture in brachial plexus injury 402 Clawing – in ulnar nerve compression 260, 261 – in ulnar nerve injury 137, 141 CMAPs See Compound muscle fiber action potentials (CMAPs) Collagen – endoneurial 1, 1 – in nerve conduits 169, 171, 172, 173–174, 176, 181, 186 Common peroneal nerve See Peroneal nerve Complex regional pain syndrome after carpal tunnel release 229 Compound muscle fiber action potentials (CMAPs) 60-67 Compression neuropathy See also Carpal tunnel syndrome (CTS) , See also Cubital tunnel syndrome , See also Pronator syndrome , See also Ulnar nerve compression – evaluation of 41, 41, 42–46, 47, 48 – pathophysiology of 25, 26–28 – pressures in 25 – provocation testing in 45, 46, 47 Computed tomography (CT) – in thoracic outlet syndrome 322 – myelography in brachial plexus injury 402 Conduction block in nerve injury 6 Conduction velocity (CV) 62 Conduits nerve 84, 94 – See also Allograft – acellularized nerve allografts versus 175, 176 – collagen 169, 171, 172, 173–174, 176, 181, 186

– – – –

evidence on 170, 171, 173 failed 181, 181–183, 186 in large diameter nerves 182 poly(DL-lactide-ε-caprolactone) 169, 172 – polyglycolic acid 169, 170, 171, 173–174, 182 – preferential motor innervation and 189, 189 – Schwann cells and 182, 184, 186 – use recommendations 188 – volume 181, 189 Corticosteroid injections for carpal tunnel syndrome 221 Costoclavicular test 315, 318 CREB See cAMP response element binding protein (CREB) Crossed fingers in ulnar nerve compression 259 Cubital tunnel syndrome – anatomic variations and 255 – anterior transmuscular transposition for 262, 263–270 – complications in surgery for 272, 272 – etiology of 254, 256–257 – in situ decompression for 271 – medial epicondylectomy for 271 – nerve conduction velocities in 262 – nonoperative management of 262 – outcomes 272 – pathophysiology of 254, 256–257 – recurrent –– revision surgery for 278–282, 282, 283–285 –– scarring in 281 – supercharge end-to-side nerve transfer 283 – ulnar nerve excursion and 256, 256 – ulnar nerve subluxation and 256, 257 Cumulative trauma disorder 314, 314 Cyclic adenosine monophosphate (cAMP) 11, 12

D DASH See Disabilities of the Arm Shoulder and Hand (DASH) De Quervain tenosynovitis release 297 Deep peroneal nerve neuropathy – diagnosis of 378 – historical review of 377 – surgical anatomy in 377 – surgical technique for 367–368, 378 Degeneration See Neurodegeneration Demyelinating conduction block 67, 69 Demyelinating conduction slowing 67, 68 Demyelination focal on electrodiagnostic testing 67, 68–69 DFT See Double fascicular transfer (DFT) Diabetes – carpal tunnel syndrome and 217 – cubital tunnel syndrome and 254 – femoral nerve neuropathy and 357 – lumbosacral radiculoplexus neuropathy in 340 – recovery and 77 Diabetic amyotrophy 340 Disabilities of the Arm Shoulder and Hand (DASH) 51–52

Distal intermuscular septum in anterior transmuscular transposition for cubital tunnel syndrome 263, 266–267 Dorsal cutaneous branch of ulnar nerve (DCU) 123 – as donor site 89 – in anterior interosseous nerve-to-ulnar nerve transfer 143 – in median nerve sensory restoration 119, 121–123, 124–125 – in ulnar nerve compression 260 – lateral antebrachial cutaneous nerve transfer to 139, 143 Dorsal root ganglion (DRG) in brachial plexus injury 398, 400 Dorsal scapular nerve in brachial plexus anatomy 394 Double crush theory 314 Double fascicular transfer (DFT) 413– 414, 415, 415, 417, 419-432 DRG See Dorsal root ganglion (DRG) Duchenne sign in ulnar nerve compression 260, 261

E EAST See Elevated arm stress test (EAST) Effort-induced thrombosis 311 – See also Thoracic outlet syndrome (TOS) Electrical stimulation nerve regeneration and 19 Electrodiagnostic examination (EDX) – assessment 61-69 – in brachial plexus injuries 401 – in carpal tunnel syndrome 216, 217 – in cubital tunnel syndrome 73, 262 – in femoral nerve neuropathy 359 – in perioperative assessment for nerve transfer 103 – in pronator syndrome 245 – in tetraplegia 162 – in thoracic outlet syndrome 323, 325 – in ulnar nerve compression 262 Electromyography (EMG) – in Parsonage-Turner syndrome 404 – in perioperative assessment for nerve transfer 103 Elevated arm stress test (EAST) 315, 317, 318 End-to-side (ETS) nerve transfer 22, 23, 83, 83 – regeneration in 84 – supercharge 83 –– history of 283 –– in cubital tunnel syndrome 283 –– technique 141, 147–148 Endoneurium – in compression neuropathy 27 – in nerve fiber anatomy 1, 1–2 – in nerve injury 6 Endoscopic carpal tunnel release (ECTR) – advantages of 222 – open versus 222 Epineurium – in compression neuropathy 27 – in nerve fiber anatomy –– external 1, 1–2 –– internal 1–2

621

Index Evoked potentials in thoracic outlet syndrome 325 Evoked response parameters 61 Extensor carpi radialis brevis (ECRB) – branch –– in median-to-radial nerve transfer 114 –– in nerve transfer for wrist drop 104, 105 –– to anterior interosseous nerve transfer 126, 127, 128, 132–137 –– to pronator nerve branch transfer 126, 126, 127, 127–130, 130 – in median-to-radial nerve transfer 114–115 – in posterior interosseous decompression 295, 299–300, 302 – in wrist extension 104 – tendon in radial tunnel decompression 296, 305 – tendon transfer with pronator teres tendon 106–108 Extensor carpi radialis longus (ECRL) – in posterior interosseous decompression 295, 298–299 – in radial sensory branch decompression 306 – in wrist extension 104 – nerve anatomy 161 External epineurium in nerve fiber anatomy 1, 1–2 Extracelluar matrix molecules in nerve regeneration 14

F Fascicles – anatomy of 1, 3–4 – in brachial plexus 394 – in median nerve 2, 4, 208 – in nerve fiber anatomy 1, 2 – in nerve injury 7 – in nerve repair 81, 83 – in ulnar nerve 2, 3 – internal topography with 2, 3 Femoral nerve – in lumbosacral plexus anatomy 338, 339 – neuropathy –– diabetes and 357 –– diagnosis of 358 –– electrodiagnostic studies in 359 –– historical review of 357 –– results in 359 –– surgical treatment of 359 First web space-to-third web space nerve transfer 119, 120–121 FK-506 19, 20–21 – in allografting 92, 195 Flexor carpi radialis (FCR) – in double fascicular transfer 415, 420 – in median-to-radial nerve transfer 111, 113, 113, 115 , 116 – in nerve transfer for wrist drop 104, 105 Flexor digitorum brevis in Morton neuroma 387 Flexor digitorum superficialis (FDS) – branch –– in median-to-radial nerve transfer 113, 113, 116

622

––

in nerve transfer for wrist drop 104, 105 ––– for anterior interosseous nerve palsy 246 ––– technique 128, 132–137 –– to pronator teres nerve transfer 128–129 – fascicle 4, 420 –– in double fascicular transfer 415 – in median-to-radial nerve transfer 109, 112–113, 115 – tendon in carpal tunnel anatomy 212 Flexor pollicis longus (FPL) – in anterior interosseous nerve palsy 246 – tendon in carpal tunnel anatomy 212 Flexor retinaculum – in carpal tunnel anatomy 212 – in tarsal tunnel anatomy 380 Fluorescent labeling in vivo 30 Foot drop in peroneal neuropathy 364, 369 Foot posture in tarsal tunnel syndrome 370 Fourth web space common digital nerve in median nerve sensory restoration 119 Fracture – distal radius 256 – hook of hamate 256 – humeral radial nerve injury in 289, 289 – in brachial plexus injury 402 – Monteggia radial nerve injury and 290 Froment sign 49 – in ulnar nerve compression 259, 260, 261 – in ulnar nerve injury 141 Furcal nerve in lumbosacral plexus anatomy 338

G GDNF See Glial-derived neurotrophic factor (GDNF) GEM Neurotube 170 Gender – brachial plexus injury and 397 – carpal tunnel syndrome and 212 – cervical rib and 313 – pronator syndrome and 235 – thoracic outlet syndrome and 314 Genitofemoral nerve – in lumbosacral plexus anatomy 338, 339 – neuropathy –– diagnosis of 350 –– historical review for 345 –– nerve blocks in 351 –– pain in 347 –– results in 353 –– surgical anatomy in 350 –– surgical technique for 341, 352 Glial-derived neurotrophic factor (GDNF) 15, 15, 16 Globular domain 12 Globular region 12 Gracilis nerve as donor nerve 87, 91– 93

Grafts nerve See also Allograft, See also Harvesting – allograft 89, 95–98 – autograft 85, 86–95 – disadvantages of 86 – end-to-side nerve transfer 22, 23 – for brachial plexus injury 410 – for radial nerve injury 293, 301, 307 – neuroma in 86, 98 – regeneration in 86, 86 – size of 85 – vascularized 19, 86 Grip strength 49 ''Growing pains'' 374 Growth-associated protein 43 (GAP43) 11 Gunshot wounds – allograft reconstruction for 197 – as injury mechanism 76, 79–80, 82 – brachial plexus injury in 406 – nerve wrap in 181 – radial nerve injury in 290 Guyon canal – in carpal tunnel anatomy 212 – in ulnar nerve anatomy 251, 253, 254 Guyon canal compression – nonoperative management of 274 – operative management of 273–274, 274, 275–277 – recurrent 282 Guyon canal syndrome and ulnar nerve compression at wrist 256

H Ha lstead test 315, 318 Hamate in carpal tunnel anatomy 212 Hand dynamometers 49 Harvesting – anterior interosseous nerve in 87, 90 – distal segment of injured nerve in 89 – end-to-side nerve transfer in 22 – gracilis nerve in 87, 91–93 – lateral antebrachial cutaneous nerve in 87, 89 – medial antebrachial cutaneous nerve in 86, 87–88, 410 – posterior interosseous nerve in 87, 90 – proximal segment of injured nerve in 87, 94–95 – sural nerve in 86, 86–87 HDAC5 See Histone deacetylase 5 (HDAC5) Histone deacetylase 5 (HDAC5) 11 – nerve compression 256, 258–259 Hook of hamate fracture 256 Human acellularized nerve 169 Humeral fracture radial nerve injury in 289, 289 Hypothenar hammer syndrome 256

I Iliohypogastric nerve – in lumbosacral plexus anatomy 338, 339 – neuropathy

–– diagnosis of 350 –– historical review for 345 –– nerve blocks in 351 –– pain in 347 –– results in 353 –– surgical anatomy in 350 –– surgical technique for 341, 352 Ilioinguinal nerve – in lumbosacral plexus anatomy 338, 339 – neuropathy –– diagnosis of 350 –– historical review for 345 –– nerve blocks in 351 –– pain in 347 –– results in 353 –– surgical anatomy in 348 –– surgical technique for 341, 352 Imaging See Magnetic resonance imaging (MRI) , See Plain radiography , See Transcutaneous peripheral nerve imaging Immunosuppression See also Tacrolimus – allografts and 193–194, 194, 195, 202 – Schwann cells and 194 Inducible nitric oxide synthase (iNOS) 29 Inferior gluteal nerve in lumbosacral plexus anatomy 338, 340 Injection injury 7, 8, 290 Injury nerve See also Regeneration – classification of 6, 6, 7, 75-77 – evaluation of 41, 41, 42–46, 47, 48, 78 – extracellular matrix molecules in 14 – in children 5 – in gunshot wounds 76, 79–80, 82 – injection 7, 8 – mechanisms of 5, 76, 77–80 – neurotrophin factors in 15, 15 – open 76, 77–79, 101 – preferential motor reinnervation in 16, 17–18 – regenerating unit in 4, 5 – Schwann cell in 4, 5, 10, 13, 193 – smoking and 77 – Tinel sign in 6 – traction 76, 101, 398 – transcriptional control of nerve regeneration in 10, 12 – Wallerian degeneration in 4, 5, 6, 8, 9–11 – zone of 79–80 iNOS See Inducible nitric oxide synthase (iNOS) Integrin 12, 14 Intercostal nerve(s) – to long thoracic nerve transfer 432 – to musculocutaneous nerve transfer 418, 430 Intercostal neuralgia 197, 199–202 ''Internal splint'' for wrist drop 106 Intrapartum maternal lumbosacral plexopathy 341

L Lacerations – as injury mechanism 76, 77–78 – nerve conduit for 181, 183–184 – nerve wrap for 181, 184

Index – ulnar nerve 138 Lacertus fibrosus 208 Laminin 12, 14 Lasègue maneuver 340, 341 Latency in nerve conduction studies 61, 62 Lateral antebrachial cutaneous nerve (LABC) – as donor nerve 87, 89 – in brachial plexus anatomy 394 – in brachialis-to-anterior interosseous nerve transfer 139 – in double fascicular transfer 419 – in median-to-radial nerve transfer 110 – in sensory restoration of radial nerve distribution 116, 117 – radial sensory nerve versus 296 – to dorsal cutaneous ulnar nerve transfer 139, 143 – tug testing of 397 Lateral epicondylitis 292, 296, 305 Lateral femoral cutaneous nerve (LFC) – in lumbosacral plexus anatomy 338, 339 – in meralgia paresthetica 342, 354 Lateral intermuscular septum – in radial nerve decompression at spiral groove 295–296 – in radial nerve palsy 290 Lateral pectoral nerves in brachial plexus anatomy 395 Lipomas radial nerve injury with 290 LMN See Lower motor neurons (LMNs) in spinal cord injury Long thoracic nerve – in brachial plexus anatomy 394 – in partial middle trunk nerve transfer 435, 438 – in thoracic outlet surgery 312, 329, 331, 334, 335–336 – intercostal nerve transfer to 432 – palsy 318 –– two-level nerve transfer for 439 Lower extremity injury neuropathy See also Lumbosacral – historical review of 338 – lumbosacral plexus in 338, 339 Lower motor neurons (LMNs) in spinal cord injury 159–160 Lumbosacral plexopathy anatomy 338, 339 – diabetes and 340 – etiology of 340, 340 – in pregnancy 341 – neoplastic processes in 343 – nonsurgical etiologies in 340 – radiation-induced 340 – trauma and 344 – vascular etiologies in 340, 341 Lumbosacral radiculoplexus neuropathy (LRPN) 340

M MAG See Myelin-associated glycoprotein (MAG) Magnetic resonance imaging (MRI) – in brachial plexus injury 402 – in nerve transfer assessment 103 – in Parsonage-Turner syndrome 404 – in thoracic outlet syndrome 322 – in ulnar nerve compression 262

MAPKs See Mitogen-activated protein kinases (MAPKs) Martin-Gruber anastomosis 210, 210, 254 MCP-1 See Monocyte chemotactic protein-1 (MCP-1) Medial antebrachial cutaneous nerve (MABC) – as donor nerve 86, 87–88, 301, 410 – in anterior transmuscular transposition for cubital tunnel syndrome 264, 272, 272, 281 – in partial middle trunk nerve transfer 435, 435 – in radial nerve injury repair 301 Medial epicondylectomy for cubital tunnel syndrome 271 Medial intermuscular septum – in anterior transmuscular transposition for cubital tunnel syndrome 264–265 – in revision surgery for cubital tunnel syndrome 280 Medial pectoral nerves – in brachial plexus anatomy 395 – musculocutaneous transfer to 413, 416, 425 – to axillary nerve transfer 437, 444– 448 Median nerve See also Palmar cutaneous nerve branch (PCM) – allograft reconstruction of 196–197, 198, 207 – anatomy 208, 209 – decompression for pronator syndrome 239–244, 245, 245, 246 – fascicles 208 – in brachial plexus anatomy 393 – in brachial plexus surgery 411 – in brachialis-to-anterior interosseous nerve transfer 138–139 – in carpal tunnel anatomy 212 – in carpal tunnel release 217 – in double fascicular transfer 414– 415, 419 – in lower plexus injury restoration of 131, 132, 138–140 – in radial nerve repair 306 – in Riche-Cannieu motor anastomosis 211, 254 – innervation 213 – Martin-Gruber anastomosis and 210, 210, 254 – musculocutaneous nerve transfer to in tetraplegia 159 – provocative test for 47 – sensory deficit –– intramedian sensory nerve transfer 123 –– ulnar nerve transfer for 121, 122– 125 – sensory restoration 118, 120–122, 125 –– upper plexus 123 – to radial nerve transfer 106, 109– 116 – topographical anatomy of 2–3, 4, 208 – variations 211 Median nerve injury – in carpal tunnel release 226, 229 – nerve transfer for 116, 117 – reconstruction techniques for 97, 98

– thumb opposition and 117 Median nerve neuropathy 207 – See also Carpal tunnel syndrome (CTS) Median recurrent motor branch anterior interosseous nerve transfer to 118, 119 Meralgia paresthetica – diagnosis of 355 – historical review of 354 – nonsurgical treatment of 355 – surgical anatomy in 354 – surgical technique for 342, 355 Merkel cell neurite complex 41 Mesoneurium 1, 1, 27 Metastatic disease in lumbosacral plexopathy 343 – See also Neoplasms MHCs See Myosin heavy chains (MHCs) MHQ See Michigan Hand Outcomes Questionnaire (MHQ) 52 Microtubules in axonal transport 17 Microvessels – in compression neuropathy 27 – in nerve fiber anatomy 1 Mitogen-activated protein kinases (MAPKs) 10, 15 Monocyte chemotactic protein-1 (MCP1) 10 Monteggia fracture radial nerve injury 290 Morton neuroma – diagnosis of 385 – historical review of 384 – pain in 385 – recurrent 388 – surgical anatomy in 384 – surgical technique for 385, 387 Motor evaluation 49 Motor nerve conduction studies 63, 63 – See also Nerve conduction studies (NCSs) Motor unit action potential (MUAP) – defined 64 – in brachial plexus injury 402 – in nerve injury 59 – in perioperative assessment for nerve transfer 103 – in ulnar nerve compression 262 – morphology of 64 Motor unit defined 25 MRI See Magnetic resonance imaging (MRI) MUAP See Motor unit action potential (MUAP) Muscle imbalance evaluation of 50 Musculocutaneous nerve – anatomy 161, 393, 394 – distal accessory nerve transfer to 428 – in brachialis-to-anterior interosseous nerve transfer 132, 138 – in double fascicular nerve transfer 419 – intercostal nerve transfer to 418, 430 – medial pectoral transfer to 413, 416, 425 – thoracodorsal nerve transfer to 417, 426 – to median nerve transfer in tetraplegia 159

Myelin-associated glycoprotein (MAG) 11, 29 Myeloid differentiation primary response gene 88 (MYD88) 10 Myocytes 24–25 Myosin heavy chains (MHCs) 24

N Neonates motor nerve injury in 6 Neoplasms – lumbosacral plexopathy and 343 – radial nerve injury with 290 Nerve block – in genitofemoral nerve 351 – in iliohypogastric nerve 351 – in ilioinguinal nerve 351 – in obese patients 351 – in obturator neuropathy 363 Nerve conduction studies (NCSs) – general 60- 69 – in carpal tunnel syndrome 216 – in cubital tunnel syndrome 262 – in thoracic outlet syndrome 325 – in ulnar nerve compression 262 – latency in 61, 62 – mixed 63 – motor 63, 63 – sensory 61, 62 Nerve growth factor (NGF) 15 NeuraGen 169, 172, 174 – See also Conduits nerve Neural mobility evaluation 50 Neuralgic amyotrophy See ParsonageTurner syndrome Neurapraxia 6, 7, 59, 75 – See also Injury nerve NeuraWrap 169, 172, 181 Neurite outgrowth inhibitor (Nogo) 11, 12 Neurodegeneration mechanisms of 8, 9–11 – See also Wallerian degeneration Neurofibromatosis type 1 343 NeuroFlex 169, 172 – See also Conduits nerve Neurogenic thoracic outlet syndrome 311, 314, 314 – cervical spine disease versus 316 – computed tomography in 322 – electrodiagnostic testing in 323, 325 – history in 316 – imaging in 322 – magnetic resonance imaging in 322 – muscle imbalance in 317, 319 – obesity and 314 – physical examination in 316 – plain radiography in 322 – posture and 314,, 315, 317, 321 – scapular winging in 319, 321 – scratch-collapse test in 320, 321, 321–323 – sensory evaluation in 323 – serratus anterior in 318, 321 – somatosensory evoked potentials in 325 – Spurling test in 316, 317 – Tinel sign in 321 – two-point discrimination in 325 Neurolac 169 Neuroma – in grafting 86, 98 – in gunshot wound 79

623

Index – in laceration 89 – in zone of injury 79 – Morton –– diagnosis of 385 –– historical review of 384 –– recurrent 388 –– surgical technique for 385, 387 – suture line 10 NeuroMatrix 169, 172 NeuroMend 169, 172 Neuromuscular anatomy and physiology 24, 26–28, 30–31 Neurotmesis 6, 7, 59, 75 Neurotrophic factors 15, 15 Neurotrophins 15, 15 Neurotropism – in nerve conduits 181 – in nerve injury 4 Neurotube 169 Neurturin (NRTN) 15, 15 Node of Ranvier – in nerve fiber anatomy 1 – in nerve injury 4 Nogo See Neurite outgrowth inhibitor (Nogo) Novak/Mackinnon/Patterson test 315 NRTN See Neurturin (NRTN)

O Obese patients – carpal tunnel release in 225, 225 – meralgia paresthetica in 354 – nerve blocks in 351 Obesity thoracic outlet syndrome and 314 Obturator nerve – in lumbosacral plexus anatomy 338, 339 – neuropathy –– diagnosis of 363 –– historical review of 362 –– nonsurgical treatment of 363 –– surgical treatment of 346, 363 Osborne band – cubital tunnel syndrome and 255 – in anterior transmuscular transposition for cubital tunnel syndrome 263 – in ulnar nerve anatomy 251

P Paget-Schroetter syndrome 311 – See also Thoracic outlet syndrome (TOS) Pain evaluation 51 Pain evaluation questionnaire 51, 55, 258, 260 Pain postoperative neuropathic 99 Palmar aponeurosis in carpal tunnel release 223 Palmar carpal ligament in carpal tunnel anatomy 212 Palmar cutaneous nerve branch (PCM) – in carpal tunnel release 223 – in carpal tunnel syndrome presentation 212 – in median nerve anatomy 4, 210, 211 – in ulnar nerve decompression in Guyon canal 274, 275

624

– transverse in carpal tunnel release 224 Palmaris longus (PL) – branch –– in median-to-radial nerve transfer 111 –– in nerve transfer for wrist drop 104, 105 – fascicle 4 Pancoast tumor 322 Parsonage-Turner syndrome – diagnosis of 404 – in anterior interosseous nerve palsy 246 – in brachial plexus injury 403 – magnetic resonance imaging in 404 – outcomes in 404 – permanent neuropathy in 101 – presentation of 404 – viral infection and 404 Partial middle trunk nerve transfer 435, 435, 436–443 Patient evaluation See also Electrodiagnostic examination (EDX) , See also Physical examination – grading systems in 49 – in tetraplegia 161 – in ulnar nerve compression 256, 258–261 – motor evaluation in 49 – nerve conduction studies in 60, 61 – pain evaluation in 51 – patient-reported assessment in 51 – posture in 50 – self-report questionnaires in 51 – sensory evaluation in 41, 41, 42–46, 47, 48 – test selection in 50 Patient factors in outcomes 77 Patient-reported assessment 51 Patient-Specific Functional Scale (PSFS) 52 PCM See Palmar cutaneous nerve branch (PCM) Pectoral fascicles in partial middle trunk nerve transfer 439–442 Pectoralis major in brachial plexus surgery 407, 408–410 Pectoralis minor in brachial plexus surgery 411–412 Penetrating injury 76, 78, 101 Pentazocine injection radial nerve injury and 290 Perineurium – in compression neuropathy 27 – in nerve fiber anatomy 1, 1–2 Peroneal nerve – allograft reconstruction of 197 – compression scratch collapse test in 48 – deep 369 –– neuropathy of ––– diagnosis of 378 ––– historical review of 377 ––– surgical anatomy in 377 ––– surgical technique for 367–368, 378 – in lumbosacral plexus anatomy 338 – neuropathy –– diagnosis of 369 –– foot drop in 364, 369 –– historical review of 364 –– results in 373

–– ––

surgical anatomy in 346, 366 surgical technique for 348–356, 371 – superficial entrapment of –– diagnosis of 375 –– historical review of 374 –– pain in 375 –– results in 366, 376 –– surgical anatomy in 374 –– surgical technique for 356–366, 375 – superficial sensory branch of 369 – topography 369 Peroneal nerve injury iatrogenic 290 Persephin (PSPN) 15, 15 Pes anserine bursitis 360 PGA See Polyglycolic acid (PGA) Phalen test in carpal tunnel syndrome 214 Phrenic nerve – as donor nerve 418 – in thoracic outlet anatomy 312 – in thoracic outlet surgery 326–327, 334, 335–336 – respiratory function and 418–419 Physical examination See also Patient evaluation , See also Provocation testing – in brachial plexus injury 401 – in carpal tunnel syndrome 214 – in radial nerve injury 292 – in tarsal tunnel syndrome 382 – in tetraplegia 162 – in thoracic outlet syndrome 315 –– neurogenic 316 –– vascular 327 – in ulnar nerve compression 258, 259, 261 Physical therapy – for brachial plexus injury 402 – for thoracic outlet syndrome 328 PIN See Posterior interosseous nerve (PIN) Pinch strength 49 Pisiform in carpal tunnel anatomy 212 PKA See Protein kinase A (PKA) PKC See Protein kinase C (PKC) Plain radiography – in brachial plexus injury 402 – in thoracic outlet syndrome 322 PMR See Preferential motor reinnervation (PMR) Poly(DL-lactide-ε-caprolactone) 169, 172 Polyglycolic acid (PGA) conduit 169, 170, 171, 173–174, 182 – See also Conduits nerve Polyvinyl alcohol 169 Porcine small intestinal submucosa 169 Posterior crural intermuscular septum in peroneal neuropathy 350–352, 367 Posterior cutaneous nerve of forearm 295 Posterior femoral cutaneous nerve in lumbosacral plexus anatomy 338, 339 Posterior interosseous nerve (PIN) – as donor nerve 87, 90 – decompression 295, 297–305

– in extensor carpi radialis brevis-toanterior interosseous nerve transfer 129 – in median-to-radial nerve transfer 113, 114–115 – in nerve transfer for wrist drop 104, 105, 106 – in radial nerve injury repair 306 – supinator transfer to in tetraplegia 159 Posterior tibial nerve – allograft reconstruction of 197 – variations in 371, 381 Posterior ulnar recurrent artery (PURA) in ulnar nerve blood supply 254 Postoperative care for nerve transfers 148 Postoperative rehabilitation in nerve repair 99 Postoperative splinting in nerve transfer 104 Posture – evaluation 50 – in tarsal tunnel syndrome 370 – neurogenic thoracic outlet syndrome and 314, 315 Precursor cells skin-derived nerve conduits and 186 Preferential motor reinnervation (PMR) 16, 17–18, 189, 189 Pregnancy – carpal tunnel syndrome and 219, 221 – femoral nerve entrapment and 357 – lumbosacral plexopathy in 341 – meralgia paresthetica and 354 Pressure thresholds cutaneous 44, 44 Pronator quadratus (PQ) fascicle 4 Pronator syndrome – clinical presentation of 235 – electrodiagnostic testing in 245 – gender and 235 – median nerve decompression for 239–244, 245, 245, 246 – nonsurgical treatment of 245 – provocative testing in 245 – risk factors for 235 – sleeping habits and 235 Pronator teres (PT) – branch –– extensor carpi radialis brevis transfer to 126, 126, 127, 127– 130, 130 –– flexor carpi ulnaris nerve transfer to 130 –– flexor digitorum superficials nerve transfer to 128–129 – fascicle 4 – function restoration 127–130, 130 – in median-to-radial nerve transfer 106, 111, 111–112 – tendon –– in median-to-radial nerve transfer 110 –– in wrist drop 106–108 Protein kinase A (PKA) 11, 12 Protein kinase C (PKC) 11 Provocation testing – for chronic nerve compression 45, 46, 47 – in carpal tunnel syndrome 214 – in pronator syndrome 245 – in tarsal tunnel syndrome 370

Index – in ulnar nerve compression 260 Pseudo-Froment sign in ulnar nerve compression 261 Pseudoangina 316 PSFS See Patient-Specific Functional Scale (PSFS) Pudendal nerve in lumbosacral plexus anatomy 339, 340

Q Quadrangular space 394, 403 Quadrangular space syndrome 403 Questionnaire – pain evaluation 51, 55 – self-report 51

R Radial nerve – allograft reconstruction of 197 – anatomy 291, 291 – in brachial plexus anatomy 393 – median nerve transfer to 106, 109– 116 – provocative test for 47 – sensory restoration in distribution of 116, 117 Radial nerve decompression – at spiral groove 294, 294, 295–297 – in radial tunnel 295, 297–305 – in sensory branch 296, 305–308 – postoperative care for 306 – results with 306 Radial nerve injury – closed 293 – compression in 290 – diagnosis of 292 – etiology of 289, 289 – from neoplasms 290 – grafting for 293, 301, 307 – historical perspective on 289 – iatrogenic 290 – in gunshot wounds 290 – in humeral fracture 289, 289 – in lateral epicondylitis 292 – injection 290 – Monteggia fracture and 290 – nerve transfer for 104, 105–109, 293, 306, 308 – open 293 – orthopedic 289, 289 – physical examination in 292 – primary repair of 293, 301, 307 – reconstructive technique for 98, 99 – surgical anatomy in 291, 291 – tendon rupture versus 292, 301 – tendon transfers for 293, 307 – wrist drop in 104 Radial recurrent artery 291 Radial vessels – in median-to-radial nerve transfer 109, 110–111 – in posterior interosseous decompression 300 Radiation-induced brachial plexopathy (RIBP) 404 Radiation-induced lumbosacral plexopathies 340 Radius fracture distal 256 Rapid Exchange Grip (REG) 49 Rapid simultaneous grip (RSG) test 49

Recurrent thenar nerve 4 REG See Rapid Exchange Grip (REG) Regenerating unit 4, 5 Regeneration See also Injury nerve – accelerated 19, 20–21 – acellularized nerve allografts and 177–178, 180 – allografts and 193 – blood supply and 18 – electrical stimulation and 19 – extracelluar matrix molecules in 14 – in end-to-side nerve repair 84 – in grafting 86, 86 – nerve conduits and 170, 174 – neurotrophic factors in 15, 15 – neurotrophins in 15, 15 – tacrolimus and 195 – transcriptional control of 10, 12 Rehabilitation in nerve repair 99 – in nerve transfer for wrist drop 104 Rejection of allografts 92, 194, 196 Repair nerve See also Grafts nerve, See also Transfer nerve – epineurial 81, 83 – fascicular 81, 83 – postoperative rehabilitation in 99 – tension and 84 – tension-free 82 – timing of 78 – type of 83 Repetitive hand work carpal tunnel syndrome and 218 Repetitive stress disorder 314, 314 Respiratory function phrenic nerve and 418–419 Reverse end-to-side supercharge transfer 141, 147–148 Revision surgery – for carpal tunnel release 227, 228– 229, 229, 230–239 – for ulnar nerve decompression 276, 278–285 RevolNerv 172, 174 – See also Conduits nerve Rho-associated kinases (ROCKs) 11, 12, 15 Rib(s) – cervical 313 – fracture in brachial plexus injury 402 – in thoracic outlet syndrome surgery 332–333, 334, 334 RIBP See Radiation-induced brachial plexopathy (RIBP) Riche-Cannieu motor anastomosis 211, 254 ROCKs See Rho-associated kinases (ROCKs) Roos test 315, 317, 318 Root avulsion in brachial plexus injury 398, 399–400 RSG See Rapid simultaneous grip (RSG) test Ruffini end-organ 41

S Sacral nerve in lumbosacral plexus anatomy 339 Sacral plexus in lumbosacral plexus anatomy 338, 339 Sacral sheath tumors 343 Saphenous nerve

– in lumbosacral plexus anatomy 339 – neuropathy –– diagnosis of 361 –– historical review of 360 –– results with 362 –– surgical anatomy in 360 –– surgical treatment of 343–345, 361 Saw injury 197 ''Saturday night palsy'' 290 Scalene – hypertrophy 313 – variations 313 Scalene test 315, 318 Scalenus minimus 313 Scalenus syndrome 311 – See also Thoracic outlet syndrome (TOS) Scaphoid in carpal tunnel anatomy 212 Scapula fracture in brachial plexus injury 402 Scapular notch 394 Scapular winging – in accessory nerve injury 405 – in thoracic outlet syndrome 319, 321 Schwann cell – allograft rejection and 194 – allografts and 193, 194 – basement membrane 1 – immunosuppression and 194 – in allografts 96, 203 – in nerve fiber anatomy 1, 1, 10 – in nerve injury 4, 5, 10, 13, 193 – in vascularized composite allograft 199–200, 203 – in Wallerian degeneration 8, 9 – nerve conduits and 182, 184, 186 – toll-like receptors and 10 Schwannomas 343 Sciatic nerve – in lumbosacral plexus anatomy 338, 339 – reconstruction allograft in 196 Scratch-collapse test (SCT) 47, 48 – in tarsal tunnel syndrome 370, 372, 382 – in thoracic outlet syndrome 320, 321, 321–323 – in tibial nerve compression 380 – in ulnar nerve compression 261 SCT See Scratch collapse test (SCT) Seddon’s classification system 6 Self-report questionnaires 51 Semmes-Weinstein monofilament 44, 44 Sensory evaluation 41, 41, 42–46, 47, 48 – cutaneous pressure thresholds in 44, 44 – in thoracic outlet syndrome 323 – light moving touch in 42, 42, 43 – provocation testing in 45, 46, 47 – scratch collapse test in 47, 48 – two-point discrimination in 44, 45, 50 – vibration thresholds in 42, 43 Sensory nerve action potentials (SNAPs) – amplitude of 61, 62 – area of 61, 62 – defined 60 – duration of 62, 62

– in axon loss 65 – in demyelination 67 – in sensory nerve conduction studies 62 – latency of 62, 62 Sensory nerve conduction studies 62 – See also Nerve conduction studies (NCSs) Sensory restoration – median nerve 118, 120–122 – radial nerve distribution 116, 117 – ulnar nerve 137, 141, 141, 142–143, 149–153 Serratus anterior in thoracic outlet syndrome 318, 321 SETS See Supercharge end-to-side (SETS) nerve transfer Shin splints 374 Shoulder nerve transfers – anterior approach to 431 – double nerve transfer in 419–432, 432, 433–434 – in brachial plexus injury 419–431, 431, 432, 432, 433–448 – medial pectoral nerve-to-axillary nerve transfer in 437, 444–448 – partial middle trunk nerve transfer in 435, 435, 436–443 – posterior approach to 431 – thoracodorsal-to-axillary nerve transfer 438 Sibson fascia 313 Silicone nerve conduit See also Conduits nerve Sleeping habits pronator syndrome and 235 Smoking – carpal tunnel syndrome and 217 – injury recovery in 77 SNAPs See Sensory nerve action potentials (SNAPs) Soleal sling 379 Somatosensory evoked potentials (SSEPs) in thoracic outlet syndrome 325 Spinal accessory nerve – in partial middle trunk nerve transfer 435–437 – in thoracic outlet syndrome surgery 330 – palsy 319, 443 Spinal cord injury (SCI) at cervical level – anesthetic considerations with 162– 163 – brachialis-to-anterior interosseous nerve transfer in 158, 160 – classification of hand surgery in 159 – electrodiagnostic testing in 162 – functional needs in 162 – historical perspective 157 – history in 161 – incidence of 157 – lower motor neurons in 159–160 – musculocutaneous nerve-to-median nerve transfer in 159 – nerve transfer procedures for 157, 158, 159, 163, 164–166 – novel nerve transfer treatment options in 163 – pathophysiology in 160 – patient evaluation in 161 – perioperative considerations with 162

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Index – physical examination in 162 – supinator-to-posterior interosseous nerve transfer in 159 – surgical anatomy in 160 – tendon transfers in 157 – upper motor neurons in 160 Spiral groove radial nerve decompression at 294, 294, 295–297 Splinting – for carpal tunnel syndrome 220 – in nerve transfer 104, 148 Spurling test in neurogenic thoracic outlet syndrome 316, 317 SSEPs See Somatosensory evoked potentials (SSEPs) Stem cells adipose-derived nerve conduits and 186 Stretch injuries 76, 101 Subcostal nerve in lumbosacral plexus anatomy 339 Subscapular nerves in brachial plexus anatomy 395 SUCA See Superior ulnar collateral artery (SUCA) Sunderland classification system 6 Supercharge end-to-side (SETS) nerve transfer 83 – history of 283 – in cubital tunnel syndrome 283 – regeneration in 84 – reverse technique 141, 147–148 Superficial peroneal nerve entrapment – diagnosis of 375 – historical review of 374 – pain in 375 – results in 376 – surgical anatomy in 374 – surgical technique for 356–366, 375 Superior gluteal nerve in lumbosacral plexus anatomy 340 Superior ulnar collateral artery (SUCA) in ulnar nerve blood supply 254 Supinator – branch –– in median-to-radial nerve transfer 115 –– to posterior interosseous nerve transfer in tetraplegia 159 – in median-to-radial nerve transfer 114–115 – in posterior interosseous decompression 296, 303–304 – in radial nerve anatomy 291 Supraclavicular plexus 394 Supracondylar process 208 Suprapleural membrane 313 Suprascapular nerve – accessory nerve transfer to 419–432, 432, 433–434 – distal accessory nerve transfer to 431 – in brachial plexus anatomy 392, 394 – in brachial plexus injury 403 – in Parsonage-Turner syndrome 404 – in partial middle trunk nerve transfer 435, 438 – in scratch collapse test 49 Suprascapular notch 403 Supraspinatus in double nerve transfer 432 Sural nerve – as donor nerve 86, 86–87 – biopsy 379

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– common 379 – compression 379 – lateral 379 – medial 379 – surgical anatomy of 378 Sympathetic trunk in lumbosacral plexus anatomy 339

T T fascia in anterior transmuscular transposition for cubital tunnel syndrome 263, 268–269 Tacrolimus 19, 20–21 – in allografting 92, 195 – regeneration and 195 Tarsal tunnel syndrome – diagnosis of 382 – foot posture and 370 – historical review of 381 – pain in 382 – physical examination in 382 – provocation testing in 370 – scratch-collapse test in 370, 372, 382 – surgical anatomy in 371–372, 381 – surgical technique for 373–383, 383, 384–386, 388 – Tinel sign in 382 TCL See Transverse carpal ligament (TCL) Ten Test 9, 42 – in carpal tunnel syndrome 214 – in ulnar nerve compression 260 Tendon transfers 101–102 – for finger flexion 126 – for radial nerve injury 293, 301, 307 – in tetraplegia 157 – in wrist drop 106, 106–108 – nerve transfers versus 102, 157, 159 Tennis elbow 292, 296, 305 Tension, nerve repair and 84 Tetraplegia – anesthetic considerations with 162– 163 – brachialis-to-anterior interosseous nerve transfer in 158, 160 – classification of hand surgery in 159 – electrodiagnostic testing in 162 – functional needs in 162 – historical perspective 157 – history in 161 – incidence of 157 – lower motor neurons in 159–160 – musculocutaneous nerve-to-median nerve transfer in 159 – nerve transfer procedures for 157, 158, 159, 163, 164–166 – novel nerve transfer treatment options in 163 – pathophysiology in 160 – patient evaluation in 161 – perioperative considerations with 162 – physical examination in 162 – supinator-to-posterior interosseous nerve transfer in 159 – surgical anatomy in 160 – tendon transfers in 157 – upper motor neurons in 160 Thenar fascicle 4 Thenar nerve recurrent 4 Thenar wasting 213, 214

Third web space common digital nerve in median nerve sensory restoration 119 Third web space fascicle in ulnar nerve sensory restoration 142, 149–150 Third web space-to-first web space nerve transfer 119, 120–121 Thoracic outlet syndrome (TOS) – anatomy in 312, 312, 313–314 – arterial 311, 314 –– angiography in 327 –– history in 326 –– physical examination in 327 – diagnosis of 314, 315 – gender and 314 – history of 311 – management of 323–327, 327, 328– 336 – neurogenic 311, 314, 314 –– cervical spine disease versus 316 –– computed tomography in 322 –– electrodiagnostic testing in 323 –– electromyography in 325 –– history in 316 –– imaging in 322 –– magnetic resonance imaging in 322 –– muscle imbalance in 317, 319 –– nerve conduction studies in 325 –– obesity and 314 –– physical examination in 316 –– plain radiography in 322 –– posture and 314, 315 –– scapular winging in 319, 321 –– scratch-collapse test in 320, 321, 321–323 –– sensory evaluation in 323 –– serratus anterior in 318, 321 –– shoulder posture in 317, 321 –– somatosensory evoked potentials in 325 –– Spurling test in 316, 317 –– Tinel sign in 321 –– two-point discrimination in 325 – pathophysiology of 312, 312, 313– 314 – physical examination in 315 – physical therapy for 328 – recurrent 335 – scratch collapse test in 48 – serratus anterior in 321 – surgical treatment of 323–332, 332, 333–336 – venous 311, 314 –– angiography in 327 –– history in 326 –– physical examination in 327 – vibration thresholds in 43 Thoracodorsal nerve – in brachial plexus anatomy 395 – to axillary nerve transfer 438 – to musculocutaneous nerve transfer 417, 426 Thumb – metacarpophalangeal joint arthrodesis 297 – opposition 117 – radial aspect of fascicle 4 Tibial nerve – compression –– historical review of 379 –– scratch-collapse test in 380 –– surgical anatomy in 380

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surgical technique for 368–370, 380 – in lumbosacral plexus anatomy 338 – in tarsal tunnel release 375–376, 380, 383, 383, 385 – reconstruction allograft in 196 Timing – of electrodiagnostic examination 70 – of nerve repair 78 Tinel sign – in carpal tunnel syndrome 214 – in nerve injury 6 – in tarsal tunnel syndrome 382 – in thoracic outlet syndrome 321 – in ulnar nerve compression 260 TLR See Toll-like receptor (TLR) Toll-like receptor (TLR) in injury 10 TOS See Thoracic outlet syndrome (TOS) Tourniquet in nerve transfers 104 Tourniquet palsy 6 Traction injuries 76, 101, 398 Transcriptional control of nerve regeneration 10, 12 Transcutaneous peripheral nerve imaging 29, 30–31 Transfer nerve See also Repair nerve – anesthesia for 103 – for forearm and hand 101, 104–117, 119–153, 154 – for tetraplegia 157, 158, 159, 163, 164–166 – history of 101 – indications for 102 – motor unit action potentials in perioperative assessment for 103 – perioperative assessment for 103 – postoperative care for 148 – postoperative splinting in 104 – principles of 102 – splinting in 104, 148 – tendon transfers versus 102, 157, 159 – tourniquet in 104 Transport axonal 17 Transverse carpal ligament (TCL) – in carpal tunnel anatomy 210, 212 – in carpal tunnel release 221–222, 223–224 Transverse palmar cutaneous branch of ulnar nerve in carpal tunnel release 224 Transverse process fracture in brachial plexus injury 402 Transverse septocostal ligament 313 Trapezius in thoracic outlet syndrome 317, 321 Trauma See Fracture , See Gunshot wounds , See Lacerations , See Penetrating injury , See Spinal cord injury (SCI) Triceps branch-to-axillary nerve transfer 419–432, 432, 433–434 Triquetrum in carpal tunnel anatomy 212 Tug test 397 Tumors See Neoplasms Tuning fork 42, 43 Two-point discrimination 44, 45, 50 – in thoracic outlet syndrome 325 Type I collagen in nerve conduits 169, 171, 172 – See also Conduits nerve

Index

U Ulnar artery in carpal tunnel anatomy 212 Ulnar collateral arteries in ulnar nerve blood supply 254 Ulnar nerve – allograft reconstruction of 196–197, 198 – anatomy 251, 252–253 – anterior interosseous nerve transfer to 139, 144–146 – blood supply to 254 – compression points of 253 – distribution 258 – dorsal cutaneous branch of 123 –– as donor site 89 –– in anterior interosseous nerve-toulnar nerve transfer 143 –– in median nerve sensory restoration 119, 121–123, 124–125 –– in ulnar nerve anatomy 251 –– in ulnar nerve compression 260 –– lateral antebrachial cutaneous nerve transfer to 139, 143 – excursion 256, 256 – fascicular anatomy of 395 – in anterior transmuscular transposition for cubital tunnel syndrome 263, 265, 268–269 – in brachial plexus anatomy 393, 395 – in carpal tunnel anatomy 212 – in double fascicular transfer 414 – in elbow 251, 253 – in forearm 251, 253 – in hand 253 – in median sensory deficit transfer 121, 122–125 – in reverse end-to-side supercharge transfer 141, 147 – in Riche-Cannieu motor anastomosis 211, 254 – in upper arm 251, 252 – in wrist 253

– Martin-Gruber anastomosis and 210, 210, 254 – provocative test for 47 – radial fascicular group of 251, 253 – sensory restoration 137, 141, 141, 142–143, 149–153 – subluxation 256, 257 – topographical anatomy of 2, 3, 253 – ulnar fascicular group of 251, 253 – variations 254 Ulnar nerve compression See also Cubital tunnel syndrome , See also Guyon canal compression – at forearm 256 – at multiple sites 276, 278 – at wrist 256 – crossed fingers in 259 – Duchenne sign in 260, 261 – electrodiagnostic studies in 262 – electromyography in 262 – etiology of 254, 256–257 – finger abduction/adduction in 259 – Froment sign in 259, 260, 261 – history in evaluation of 256, 258– 259 – imaging in 262 – magnetic resonance imaging in 262 – motor unit action potentials in 262 – nerve conduction studies in 262 – pain questionnaire in 258, 260 – pathophysiology of 254, 256–257 – patient evaluation in 256, 258–261 – physical examination in 258, 259, 261 – provocation testing in 260 – proximal to elbow 254 – pseudo-Froment sign in 261 – scratch-collapse test in 261 – Ten Test in 260 – Tinel sign in 260 – ultrasound in 262 – Wartenberg sign in 259, 260, 261 Ulnar nerve decompression

– failed 276, 278–285 – in cubital tunnel syndrome 262, 263–270 – in Guyon canal compression 273– 274, 274, 275–277 Ulnar nerve injury – clawing in 137, 141 – Froment sign in 141 – muscle function and sensory loss in 137, 141–143 – reconstructive techniques for 97, 98 Ultrasound in ulnar nerve compression 262 UMNs See Upper motor neurons (UMNs) Unmyelinated axon in nerve fiber anatomy 1, 1–2 Upper arm – ulnar nerve compression in 254 – ulnar nerve in 251, 252 Upper motor neurons (UMNs) in tetraplegia 160

V Variations anatomical – brachial plexus 313, 392 – cubital tunnel syndrome and 255 – median nerve 211 – posterior tibial nerve 371, 381 – scalenes 313 – ulnar nerve 254 Vascular endothelial growth factor (VEGF) 28–29 Vascular leash of Henry 291 Vascularized composite allotransplantation (VCA) 199, 203 VCA See Vascularized composite allotransplantation (VCA) VEGF See Vascular endothelial growth factor (VEGF) Venous thoracic outlet syndrome 311, 314

– See also Thoracic outlet syndrome (TOS) – angiography in 327 – history in 326 – physical examination in 327 Vertebraseptocostal ligament 313 Vibration exposure in carpal tunnel syndrome 218 Vibration thresholds 42, 43 – in thoracic outlet syndrome 325 Vibrometers 42 Viral infection Parsonage-Turner syndrome and 404

W Wallerian degeneration – in brachial plexus injury 398, 400 – in compression neuropathy 27, 28 – in nerve injury 4, 5, 6 – mechanisms of 8, 9–11 – on electrodiagnostic examination 65, 66 Wartenberg sign in ulnar nerve compression 259, 260, 261 Web space fascicles 4 – See also Fourth web space common digital nerve , See also Third web space common digital nerve Weinstein Enhanced Sensory Test 9 Wld mouse 9, 11 Work-related upper extremity musculoskeletal disorder 314, 314 Wraps nerve 169, 181, 184–185, 187– 188 Wright hyperabduction 315, 318 Wrist See also Carpal tunnel Wrist drop 104, 104, 105–109 Wrist flexion 126, 126, 127–133 Wrist ulnar nerve compression at 256

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