MRI of the Musculoskeletal System [2 ed.] 9783131165725, 9783131607928

Table of contents :
MRI of the Musculoskeletal System __ MRI of the Musculoskeletal System (2018)
MRI of the Musculoskeletal System __ 1 Relevant Magnetic Resonance Imaging Techniques (2018)
MRI of the Musculoskeletal System __ 2 The Spine (2018)
MRI of the Musculoskeletal System __ 3 The Shoulder (2018)
MRI of the Musculoskeletal System __ 4 elbowThe Elbow (2018)
MRI of the Musculoskeletal System __ 5 fingersThe Wrist and Fingers (2018)
MRI of the Musculoskeletal System __ 6 hipThe Hip and Pelvis (2018)
MRI of the Musculoskeletal System __ 7 kneeThe Knee (2018)
MRI of the Musculoskeletal System __ 8 lower legfootankleThe Lower Leg, Ankle, and Foot (2018)
MRI of the Musculoskeletal System __ 9 The Temporomandibular Joint (2018)
MRI of the Musculoskeletal System __ 10 muscle(s)The Muscles (2018)
MRI of the Musculoskeletal System __ 11 bone marrowBone Marrow (2018)
MRI of the Musculoskeletal System __ 12 bone tumorsBone and Soft Tissue Tumors (2018)
MRI of the Musculoskeletal System __ 13 osteoporosisOsteoporosis (2018)
MRI of the Musculoskeletal System __ 14 The Sacroiliac Joints (2018)
MRI of the Musculoskeletal System __ 15 jawsThe Jaws and Periodontal Apparatus (2018)
MRI of the Musculoskeletal System __ 16 Appendix (2018)
MRI of the Musculoskeletal System __ Index (2018)

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MRI of the Musculoskeletal System Second Edition

Maximilian Reiser, MD, FACR, FRCR Professor of Radiology Chairman of the Department of Clinical Radiology and Dean of Medicine Ludwig Maximilians University Munich, Germany

2062 illustrations

Thieme Stuttgart • New York • Delhi • Rio de Janeiro

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Martin Vahlensieck, MD Professor of Radiology Practice for Radiology and Nuclear Medicine Bonn, Germany

This book is an authorized translation of the 4th German edition published and copyrighted 2015 by Georg Thieme Verlag, Stuttgart. Title of the German edition: MRT des Bewegungsapparats Translator: Sarah Venkata, Medical Linguist / Science Writer, London, UK Illustrators: Christiane and Michael von Solodkoff, Neckargmünd, Germany 1st Italian edition 2003 2nd Spanish edition 2009 4th German edition 2015

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.

© 1999, 2018 Georg Thieme Verlag KG Thieme Publishers Stuttgart Rüdigerstrasse 14, 70469 Stuttgart, Germany +49 [0]711 8931 421, [email protected] Thieme Publishers New York 333 Seventh Avenue, New York, NY 10001 USA +1 800 782 3488, [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 de Janeiro, Thieme Publicações Ltda. Edifício Rodolpho de Paoli, 25º andar Av. Nilo Peçanha, 50 – Sala 2508 Rio de Janeiro 20020-906 Brasil +55 21 3172 2297 / +55 21 3172 1896 Cover design: Thieme Publishing Group Typesetting by DiTech Process Solutions Pvt. Ltd., India Printed in China by Everbest Printing Ltd., Hong Kong ISBN 978-3-13-1165725 Also available as an e-book: eISBN 978-3-13-1607928

54321

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Contents 1.

Relevant Magnetic Resonance Imaging Techniques . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2 M. Vahlensieck, F. Traeber, and J. Gieseke

Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2

1.1.1 1.1.2 1.1.3 1.1.4

Longitudinal and Transverse Magnetization . . . . . . . . . . . Measurement Time . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Spatial Assignment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Sequence . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

1.2

Spin-Echo Sequence . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2

1.2.1 1.2.2 1.2.3

T1 Contrast . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2 Proton Density–Weighted Image Contrast . . . . . . . . . . . . 2 T2 Contrast . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2

1.3

Turbo/Fast Spin-Echo Sequence . . . . . . . . . . . . . . . . . . . 2

1.4

Gradient-Echo Technique . . . . . . . . . . . . . . . . . . . . . . . . . 4

1.5

Ultrafast Magnetic Resonance Imaging Techniques . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6

2 2 2 2

1.10

Magnetization Transfer Contrast . . . . . . . . . . . . . . . . 11

1.11

Diffusion-Weighted Imaging and Diffusion-Weighted Body Suppression . . . . . . . . . . 13

1.12

Magnetic Resonance Angiography . . . . . . . . . . . . . . 13

1.12.1 Gated-Inflow Technique . . . . . . . . . . . . . . . . . . . . . . . . . . . 13 1.12.2 Phase Contrast Angiography . . . . . . . . . . . . . . . . . . . . . . . 14 1.12.3 Contrast Angiography . . . . . . . . . . . . . . . . . . . . . . . . . . . . 14

1.13

Relaxometry . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 14

1.14

Three-Dimensional Reconstruction . . . . . . . . . . . . . 14

1.15

Multiplanar Reformatting . . . . . . . . . . . . . . . . . . . . . . 15

1.16

Radial Acquisition . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 16 Spectroscopy and Spectroscopic Imaging . . . . . . . 16

1.6

Fat Suppression . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6

1.17

1.6.1 1.6.2 1.6.3 1.6.4 1.6.5

Chemical-Selective Saturation . . . . . . . . . . . . . . . . . . . . . . . Chopper-Dixon Method . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Modified Dixon Technique . . . . . . . . . . . . . . . . . . . . . . . . . . . Short-Tau Inversion Recovery . . . . . . . . . . . . . . . . . . . . . . . . Water Excitation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

6 7 7 7 7

1.17.1 Hydrogen Spectroscopy . . . . . . . . . . . . . . . . . . . . . . . . . . . 16 1.17.2 Phosphorus Spectroscopy . . . . . . . . . . . . . . . . . . . . . . . . . 19 1.17.3 Carbon Spectroscopy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 21

1.7

Contrast Media and Contrast Dynamic Enhancement . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9

1.18.1 Cine Mode . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 21 1.18.2 Very Fast Sequences . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 21

1.8

Magnetic Resonance Arthrography . . . . . . . . . . . . . . . 9

1.8.1 1.8.2

Direct Magnetic Resonance Arthrography . . . . . . . . . . . . 9 Indirect Magnetic Resonance Arthrography . . . . . . . . . . . 9

1.9

Cartilage Imaging and Parameter Maps (Quantitative Magnetic Resonance Imaging) . . . 11

2.

1.18

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1.1

Cinematic Examinations . . . . . . . . . . . . . . . . . . . . . . . . 21

1.19

Magnetic Resonance Myelography . . . . . . . . . . . . . 21

1.20

Magnetic Resonance Neurography . . . . . . . . . . . . . 21

1.21

Magnetic Resonance Imaging of Prostheses . . . 21

The Spine . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 28 K.M. Friedrich and M. Breitenseher

2.1

Imaging . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 28

2.4

Spondylitis and Spondylodiscitis . . . . . . . . . . . . . . . . 49

2.1.1 2.1.2 2.1.3

Indications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 28 Hardware . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 28 Examination Protocols . . . . . . . . . . . . . . . . . . . . . . . . . . . . 28

2.4.1 2.4.2 2.4.3

Pyogenic and Specific Spondylitis . . . . . . . . . . . . . . . . . . 52 Rheumatoid Arthritis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 53 Seronegative Spondyloarthropathy . . . . . . . . . . . . . . . . 55

2.2

Anatomy and Physiology . . . . . . . . . . . . . . . . . . . . . . . 30

2.5

Posttraumatic Spinal Changes . . . . . . . . . . . . . . . . . . 56

2.2.1 2.2.2 2.2.3 2.2.4 2.2.5 2.2.6

Bone Marrow and Osseous Elements . . . . . . . . . . . . . . . Neuroforamina . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Intervertebral Disks . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Ligaments . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Dural Sac, Spinal Cord, and Spinal Nerves . . . . . . . . . . . Imaging Artefacts . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

2.5.1 2.5.2 2.5.3

Posttraumatic Changes to the Intervertebral Disks and Ligaments . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 56 Posttraumatic Bone Changes . . . . . . . . . . . . . . . . . . . . . . . 59 Posttraumatic Changes to the Spinal Canal . . . . . . . . . . 62

2.6

Postoperative Spinal Changes . . . . . . . . . . . . . . . . . . 65

2.3

Degenerative Conditions of the Spine . . . . . . . . . . 41

2.6.1 2.6.2

The Postoperative Intervertebral Disk . . . . . . . . . . . . . . 65 The Postoperative Bony Spine . . . . . . . . . . . . . . . . . . . . . . 69

2.3.1

Bone and Bone Marrow Changes along the Vertebral Body End Plates . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 41 Intervertebral Disk Changes . . . . . . . . . . . . . . . . . . . . . . . 44 Changes to the Zygapophysial Joints . . . . . . . . . . . . . . . . 47

2.7

Tumors of the Spine . . . . . . . . . . . . . . . . . . . . . . . . . . . . 71

2.7.1 2.7.2

Development of Spinal Tumors . . . . . . . . . . . . . . . . . . . . . 71 Localization of Tumors . . . . . . . . . . . . . . . . . . . . . . . . . . . . 72

2.3.2 2.3.3

30 37 39 39 39 41

v

Contents 2.7.3 2.7.4 2.7.5

3.

Common Benign Tumors and Tumorlike Lesions . . . . . 72 Common Malignant Primary Tumors . . . . . . . . . . . . . . . 74 Common Malignant Secondary Tumors . . . . . . . . . . . . . 76

2.8

Clinical Significance of Magnetic Resonance Imaging . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 78

2.8.1

Acknowledgment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 80

The Shoulder . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 84 M. Vahlensieck and C. Pfirrmann

Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 84

3.9

Disorders of the Synovial Lining and Joint Capsule . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 122

3.2

Examination Technique . . . . . . . . . . . . . . . . . . . . . . . . . 84

3.2.1 3.2.2 3.2.3 3.2.4

Patient Positioning . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Coil Selection . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Sequences and Parameters . . . . . . . . . . . . . . . . . . . . . . . . Special Imaging Techniques . . . . . . . . . . . . . . . . . . . . . . .

3.9.1 3.9.2 3.9.3 3.9.4 3.9.5 3.9.6

Arthritis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Pigmented Villonodular Synovitis and Hemophilia . Synovial Chondromatosis . . . . . . . . . . . . . . . . . . . . . . . . . Lipoma Arborescens . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Amyloid Arthropathy . . . . . . . . . . . . . . . . . . . . . . . . . . . . Adhesive Capsulitis (Frozen Shoulder) . . . . . . . . . . . . .

3.3

Anatomy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 87

3.3.1 3.3.2

General Anatomy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 87 Specific Magnetic Resonance Anatomy and Variants . 87

3.10

Bone Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 124

3.10.1 3.10.2 3.10.3 3.10.4 3.10.5 3.10.6 3.10.7 3.10.8

Aseptic Osteonecrosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . Impression Fractures of the Humeral Head . . . . . . . . Avulsion Injuries . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Distal Clavicle Edema . . . . . . . . . . . . . . . . . . . . . . . . . . . . Shoulder Arthrosis (Omarthrosis) . . . . . . . . . . . . . . . . . Stress Reaction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Tubercle Cysts . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Congenital Malformations . . . . . . . . . . . . . . . . . . . . . . .

3.4

Disorders of the Rotator Cuff . . . . . . . . . . . . . . . . . . . 94

3.4.1 3.4.2

Impingement . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 94 Lesions of the Tendon Insertion (Insertion Tendinopathy, Rim Rent Lesions) . . . . . . . . . . . . . . . . . . 101

3.5

Disorders of the Proximal Biceps Tendons . . . . . 102

3.5.1 3.5.2 3.5.3 3.5.4

Tendinitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Tears . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Pulley Lesions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Chondromatosis and Osteochondromatosis . . . . . . . .

102 104 105 106

3.11

Disorders of the Acromioclavicular Joint . . . . . . . 129

3.12

Disorders of the Sternoclavicular Joint . . . . . . . . . 130

3.6

Disorders of the Remaining Muscles (Including the Sequelae of Nerve Compression Syndrome) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 107

3.13

Tumors of the Shoulder . . . . . . . . . . . . . . . . . . . . . . . . 130

3.14

Post-Therapy Findings . . . . . . . . . . . . . . . . . . . . . . . . . 131

3.6.1 3.6.2 3.6.3 3.6.4

Atrophy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Insertion Tendinopathy . . . . . . . . . . . . . . . . . . . . . . . . . . Fibrosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Muscle Fiber Tear . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

3.14.1 Injection . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 131 3.14.2 Shock Wave Lithotripsy . . . . . . . . . . . . . . . . . . . . . . . . . . 131 3.14.3 Surgical Procedures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 131

3.7

Disorders of the Bursae . . . . . . . . . . . . . . . . . . . . . . . . 109

3.7.1 3.7.2

Subacromial-Subdeltoid Bursa . . . . . . . . . . . . . . . . . . . . 109 Subcoracoid Bursa . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 110

3.8

Disorders and Instability of the Glenoid Labrum and Capsular Ligaments . . . . . . . . . . . . . . . . . . . . . . . 110

3.8.1 3.8.2 3.8.3

Traumatic Lesions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 110 Habitual Shoulder Dislocation . . . . . . . . . . . . . . . . . . . . 121 Labral Cysts . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 122

4.

The Elbow . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 146

84 84 84 85

107 108 108 109

3.15 3.15.1 3.15.2 3.15.3 3.15.4 3.15.5

124 125 127 127 127 128 129 129

Pitfalls in Interpreting the Images . . . . . . . . . . . . . 136

Misinterpretation of Increased Signal Intensity . . . . . Misinterpreting Normal Variants . . . . . . . . . . . . . . . . . . Misinterpretation of an Effusion . . . . . . . . . . . . . . . . . . Misinterpretation of Bone Marrow Distribution . . . . Misinterpretation of a Persistent Acromion Ossification Center . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3.15.6 Misinterpretation of Muscle Insertions into Bone . .

3.16

122 123 123 124 124 124

136 136 137 137 137 138

Clinical Relevance of Magnetic Resonance Imaging . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 138

M. Vahlensieck and M. D’Anastasi

vi

4.3.5 4.3.6 4.3.7

Recess and Bursae . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 155 Nerves . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 155 Blood Vessels . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 156

Patient Positioning . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 146 Coils . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 146 Planes and Sequences . . . . . . . . . . . . . . . . . . . . . . . . . . . . 146

4.4

Epicondylitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 158

4.4.1 4.4.2

Epicondylitis of the Radial Humerus . . . . . . . . . . . . . . . 158 Epicondylitis of the Ulnar Humerus . . . . . . . . . . . . . . . 158

4.3

Anatomy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 149

4.5

Lesions of the Collateral Ligaments . . . . . . . . . . . . 159

4.3.1 4.3.2 4.3.3 4.3.4

Ligaments . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Muscles and Tendons . . . . . . . . . . . . . . . . . . . . . . . . . . . . Bones . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Joint Cartilage . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

4.5.1 4.5.2 4.5.3

Ulnar Collateral Ligament . . . . . . . . . . . . . . . . . . . . . . . . 159 Radial Collateral Ligament . . . . . . . . . . . . . . . . . . . . . . . . 160 Annular Ligament . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 161

4.1

Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 146

4.2

Examination Technique . . . . . . . . . . . . . . . . . . . . . . . . 146

4.2.1 4.2.2 4.2.3

149 152 154 155

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3.1

4.6

Distal Biceps Tendon Rupture . . . . . . . . . . . . . . . . . . 161

4.13

Cartilage Damage . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 168

4.7

Rupture of the Triceps Tendon . . . . . . . . . . . . . . . . . 161

4.14

Plicae . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 168

4.7.1 4.7.2

Insertion Tendinopathy of the Triceps Tendon . . . . . 161 Snapping Triceps . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 161

4.15

Bursitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 168

4.8

Traumatic Lesions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 162

4.16

Neuropathies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 168

4.9

Arthrosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 163

4.17

Neoplasms and Neoplasmlike Changes . . . . . . . . 171

4.10

Apophysitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 165

4.18

Posttherapy Findings . . . . . . . . . . . . . . . . . . . . . . . . . . 173

4.11

Osteochondritis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 166

4.19

4.11.1 Osteochondritis Dissecans . . . . . . . . . . . . . . . . . . . . . . . . 166 4.11.2 Panner’s Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 167 4.11.3 Loose Joint Bodies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 168

Potential Sources of Mistakes When Interpreting Images . . . . . . . . . . . . . . . . . . . . . . . . . . . 173

4.20

Clinical Relevance of Magnetic Resonance Tomography . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 173

4.12

Radioulnar Synostosis . . . . . . . . . . . . . . . . . . . . . . . . . . 168

5.

The Wrist and Fingers . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 182

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Contents

M. Vahlensieck and M. Richter

5.1

Examination Technique . . . . . . . . . . . . . . . . . . . . . . . . 182

5.1.1 5.1.2 5.1.3

Patient Positioning . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 182 Coil Selection . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 182 Sequences and Parameters . . . . . . . . . . . . . . . . . . . . . . . 182

5.2

Anatomy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 182

5.2.1 5.2.2

General Anatomy of the Carpal Rows . . . . . . . . . . . . . . 182 Special Magnetic Resonance Anatomy . . . . . . . . . . . . 186

5.3

Spontaneous Avascular Necrosis . . . . . . . . . . . . . . . 191

5.3.1

Avascular Necrosis of the Lunate (Kienböck’s Disease) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 191 Spontaneous Avascular Necrosis of the Scaphoid (Preiser’s Disease, Köhler-Mouchet’s Disease) . . . . . . 194

5.3.2

5.4

Ulnocarpal Impaction Syndrome . . . . . . . . . . . . . . . 194

5.5

Ulnar Impingement Syndrome . . . . . . . . . . . . . . . . . 196

5.6

Hamatolunate Impingement . . . . . . . . . . . . . . . . . . . 197

5.7

Arthrosis (Osteoarthritis) . . . . . . . . . . . . . . . . . . . . . . 197

5.8

Carpal Coalition . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 198

5.9

Traumatic Lesions of the Carpal Bones . . . . . . . . . 199

5.9.1 5.9.2 5.9.3 5.9.4

Bone Contusion (Bone Bruise) and Occult Fracture . Fracture . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Dislocation and Subluxation . . . . . . . . . . . . . . . . . . . . . . Traumatic Lesions and Findings of the Postoperative Scaphoid . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

5.10

200

Diseases of the Ligaments . . . . . . . . . . . . . . . . . . . . . 205

5.10.1 Interosseous (Intrinsic) Ligaments . . . . . . . . . . . . . . . . 5.10.2 Capsular Ligaments of the Wrist (Extrinsic Ligaments) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5.10.3 Collateral and Annular Ligaments of Fingers . . . . . . . 5.10.4 Triangular (Ulnar) Fibrocartilage Complex . . . . . . . . .

5.11

199 200 200

205 206 208 208

Nerve Compression Syndrome . . . . . . . . . . . . . . . . . 209

5.11.1 Carpal Tunnel . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 209

5.11.2 Guyon’s Canal . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 211 5.11.3 Bowling Thumb . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 212 5.11.4 Wartenberg’s Syndrome . . . . . . . . . . . . . . . . . . . . . . . . . . 212

5.12

Tumors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 212

5.12.1 Subungual Tumors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 212 5.12.2 Giant Cell Tumors of the Tendon Sheath . . . . . . . . . . . 213 5.12.3 Rheumatoid Nodules . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 214

5.13

Ganglion Cysts and Other Cysts . . . . . . . . . . . . . . . . 214

5.13.1 Ganglion Cysts . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 214 5.13.2 (Pure) Cysts . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 216

5.14

Disorders of the Synovial Membranes Including Chronic Polyarthritis . . . . . . . . . . . . . . . . . . . . . . . . . . . 217

5.15

Disorders of Tendons . . . . . . . . . . . . . . . . . . . . . . . . . . 218

5.15.1 5.15.2 5.15.3 5.15.4 5.15.5

The Radial Wrist . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . The Dorsoradial Wrist . . . . . . . . . . . . . . . . . . . . . . . . . . . . Distal Dorsoradial Forearm . . . . . . . . . . . . . . . . . . . . . . . The Ulnar Wrist . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Flexor Tendons . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

5.16

Palmar Fibromatosis (Dupuytren’s Disease) . . . 220

5.17

Examples of Vascular Diseases . . . . . . . . . . . . . . . . 220

5.18

Pitfalls in Interpreting Images . . . . . . . . . . . . . . . . . 221

5.18.1 Incorrect Positioning of the Wrist . . . . . . . . . . . . . . . . . 5.18.2 Vascular Variants . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5.18.3 Accessory Muscles and Muscles of Variant Locations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5.18.4 Chemical Shift Artefact . . . . . . . . . . . . . . . . . . . . . . . . . . . 5.18.5 Magic Angle Phenomenon . . . . . . . . . . . . . . . . . . . . . . . 5.18.6 Bone Variants . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5.18.7 Carpe Bossu . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5.18.8 Dorsal and Palmar Entry Points for Nutrient Vessels in the Carpal Bones . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5.18.9 Flexor Tendon Sheaths of the Wrist and Hand . . . . . .

5.19

219 219 219 220 220

221 221 223 224 224 225 225 225 226

Clinical Relevance of Magnetic Resonance Imaging . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 226

vii

Contents

6.

The Hip and Pelvis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 234 M. Notohamiprodjo and M. Vahlensieck

6.1

Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 234

6.13

Early-Onset Osteoarthritis and Arthrosis . . . . . . 261

6.2

Examination Technique . . . . . . . . . . . . . . . . . . . . . . . . 234

6.14

Inflammatory Diseases . . . . . . . . . . . . . . . . . . . . . . . . 262

6.2.1 6.2.2 6.2.3

Patient Positioning . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 234 Coil Selection . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 234 Sequences and Parameters . . . . . . . . . . . . . . . . . . . . . . . 234

6.14.1 Osteomyelitis and Septic Arthritis . . . . . . . . . . . . . . . . . 262 6.14.2 Rheumatoid Arthritis . . . . . . . . . . . . . . . . . . . . . . . . . . . . 264

6.3

Anatomy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 236

6.4

Avascular Necrosis of the Femoral Head . . . . . . . 238

6.15.1 Synovial Osteochondromatosis . . . . . . . . . . . . . . . . . . . . 266 6.15.2 Synovial Folds (Plicae and Retinacula) . . . . . . . . . . . . . 266

6.5

Transient Osteoporosis . . . . . . . . . . . . . . . . . . . . . . . . 242

6.16

Amyloid Arthropathy . . . . . . . . . . . . . . . . . . . . . . . . . . 267

6.6

Perthes’ Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 243

6.17

Insertional Tendinopathy (Enthesopathy) . . . . . . 267

6.7

Slipped Capital Femoral Epiphysis . . . . . . . . . . . . . 246

6.8

Hip Dysplasia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 251

6.8.1 6.8.2

Hip Dysplasia in Neonates and Small Children (Congenital Hip Displacement) . . . . . . . . . . . . . . . . . . . 251 Hip Dysplasia in Adults . . . . . . . . . . . . . . . . . . . . . . . . . . . 251

6.9

Trauma, Stress, and Fatigue Fractures . . . . . . . . . 251

6.9.1 6.9.2

Posttraumatic Fractures . . . . . . . . . . . . . . . . . . . . . . . . . . 251 Stress and Fatigue Fractures . . . . . . . . . . . . . . . . . . . . . . 252

6.10

Impingement . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 254

6.11

Lesions of the Acetabular Labrum . . . . . . . . . . . . . 257

6.11.1 Anatomic Variants . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 258 6.11.2 Labral Tears . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 259

Diseases of the Capsule and Synovial Membranes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 266

6.17.1 Insertional Tendinopathy of the Gluteal Tendons . . 268 6.17.2 Insertional Tendinopathy of the Tendons of the Knee Flexor Group of Muscles . . . . . . . . . . . . . . . . . . . . 269 6.17.3 Rare Types of Hip Enthesopathy . . . . . . . . . . . . . . . . . . 270

6.18

Snapping Hip (Coxa Saltans) . . . . . . . . . . . . . . . . . . . 270

6.19

Neurovascular Compression Syndrome . . . . . . . . 270

6.20

Tumors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 270

6.21

Pigmented Villonodular Synovitis . . . . . . . . . . . . . . 270

6.22

Pitfalls in Interpreting the Images . . . . . . . . . . . . . 271

6.22.1 6.22.2 6.22.3 6.22.4 6.22.5

Hematopoietic Bone Marrow . . . . . . . . . . . . . . . . . . . . . Transcortical Synovial Herniation . . . . . . . . . . . . . . . . . Supra-acetabular Fossa . . . . . . . . . . . . . . . . . . . . . . . . . . Bursitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Accessory Iliacus Tendon . . . . . . . . . . . . . . . . . . . . . . . . .

6.23

Clinical Relevance of Magnetic Resonance Imaging . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 276

271 271 272 272 272

6.12

Degenerative Ligamentum Teres of the Femoral Head . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 261

7.

The Knee . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 282 M. Vahlensieck and A. Horng

viii

7.1

Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 282

7.2

Examination Technique . . . . . . . . . . . . . . . . . . . . . . . . 282

7.2.1 7.2.2

Patient Positioning and Coil Selection . . . . . . . . . . . . . 282 Sequences and Parameters . . . . . . . . . . . . . . . . . . . . . . . 282

7.3

Anatomy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 282

7.3.1 7.3.2

General Anatomy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 282 Specific Magnetic Resonance Imaging Anatomy . . . . 284

7.4

Meniscal Lesions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 290

7.4.1 7.4.2 7.4.3 7.4.4 7.4.5 7.4.6

Degenerative Changes and Tears . . . . . . . . . . . . . . . . . . Postoperative Changes . . . . . . . . . . . . . . . . . . . . . . . . . . . Variant Discoid and Ring Meniscus . . . . . . . . . . . . . . . . Parameniscal Cysts . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Meniscal Ossification and Calcification . . . . . . . . . . . . Meniscal Subluxation (Extrusion) . . . . . . . . . . . . . . . . .

7.5

Cruciate Ligament Injuries . . . . . . . . . . . . . . . . . . . . . 301

290 297 298 299 300 301

7.5.1 7.5.2 7.5.3

Anterior Cruciate Ligament Acute Tear . . . . . . . . . . . . 301 Posterior Cruciate Ligament . . . . . . . . . . . . . . . . . . . . . . 306 Postoperative Changes to the Cruciate Ligaments . . . 307

7.6

Collateral Ligament Injuries . . . . . . . . . . . . . . . . . . . 310

7.6.1 7.6.2

Medial Collateral Ligament Injuries . . . . . . . . . . . . . . . 310 Lateral Collateral Ligament Injuries . . . . . . . . . . . . . . . . 311

7.7

Lateral Capsular Ligament Injuries, Including Popliteus Injuries . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 311

7.8

Iliotibial Tract (Band) Syndrome . . . . . . . . . . . . . . . 311

7.9

Dyskinesia of the Femoropatellar Joint and Patellar Dislocation . . . . . . . . . . . . . . . . . . . . . . . . . . . . 312

7.9.1 7.9.2

Impaired Gliding Function . . . . . . . . . . . . . . . . . . . . . . . 312 Patellar Dislocation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 314

7.10

Patellar and Quadriceps Tendonitis . . . . . . . . . . . 315

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6.10.1 Cam Impingement . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 254 6.10.2 Pincer Impingement . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 254 6.10.3 Other Types of Impingement . . . . . . . . . . . . . . . . . . . . . . 256

6.15

Contents 7.11

Chondropathy, Early-Onset Osteoarthritis, Arthrosis, and Cartilage/Chondral Damage . . . . 317

7.17.1 Synovial Popliteal Cysts . . . . . . . . . . . . . . . . . . . . . . . . . . 336 7.17.2 Bursitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 339

7.11.1 7.11.2 7.11.3 7.11.4

Chondropathy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Early-Onset Osteoarthritis and Arthrosis . . . . . . . . . . Chondral (Cartilage) and Osteochondral Damage . . Treatment of Cartilage Damage and Posttreatment Follow-Up with Magnetic Resonance Imaging . . . . . .

7.18

Lesions of Hoffa’s Fat Pad and Other Fat Pads . 340

7.19

Ganglion Cysts (apart from Meniscal Ganglion Cysts/Parameniscal Cysts) . . . . . . . . . . . . . . . . . . . . . 341

320

Bone Trauma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 322

7.12.1 Bone Bruises . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 322 7.12.2 Fractures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 322

7.19.1 Intra-articular Ganglion Cysts . . . . . . . . . . . . . . . . . . . . . 342 7.19.2 Extra-articular Ganglion Cysts . . . . . . . . . . . . . . . . . . . . 342

7.20

Nerve Compression Syndrome and Periarticular Neuropathy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 342

Transient (Regional) Migratory Osteoporosis and Shifting Bone Marrow Edema of the Knee . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 324

7.21

Vascular Diseases . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 343

7.22

Special Features in Children . . . . . . . . . . . . . . . . . . . . 344

Osteochondritis Dissecans and Avascular Necrosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 324

7.23

7.14.1 Osteochondritis Dissecans . . . . . . . . . . . . . . . . . . . . . . . . 324 7.14.2 Spontaneous Idiopathic Osteonecrosis of the Femoral Condyle (Ahlbäck’s Disease) . . . . . . . . . . . . . . 325 7.14.3 Other Forms of Osteonecrosis in the Knee Region . . 328

Common Tumors and Tumorlike Lesions in and around the Knee . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 344

7.24

Pitfalls When Interpreting the Images . . . . . . . . . 345

7.13

7.14

7.24.1 Increased Signal Intensity at the Meniscus Periphery . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7.24.2 Pulsatile Flow Artefacts of the Popliteal Artery . . . . . 7.24.3 Line Artefacts . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7.24.4 Bi-, Tri-, and Multipartite Patella . . . . . . . . . . . . . . . . . . 7.24.5 Dorsal Defect of the Patella . . . . . . . . . . . . . . . . . . . . . . . 7.24.6 Accessory Posterior Sesamoids . . . . . . . . . . . . . . . . . . . . 7.24.7 Calcification . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7.24.8 Meniscomeniscal Ligament . . . . . . . . . . . . . . . . . . . . . . . 7.24.9 The Articularis (Muscle) . . . . . . . . . . . . . . . . . . . . . . . . . . 7.24.10 Absorption Cysts at the Insertion of the Cruciate Ligaments on the Tibial Plateau . . . . . . . . . . . . . . . . . . . 7.24.11 Asymmetry of the Epiphyseal Plate . . . . . . . . . . . . . . .

345 347 347 347 347 347 348 348 349

7.15

Changes to the Synovial Membrane and Joint Capsule, Sarcoidosis, and Gout . . . . . . . . . . . . . . . . . 328

7.15.1 7.15.2 7.15.3 7.15.4 7.15.5 7.15.6 7.15.7 7.15.8

Rheumatoid Arthritis . . . . . . . . . . . . . . . . . . . . . . . . . . . . Pigmented Villonodular Synovitis . . . . . . . . . . . . . . . . . Hemophiliac Arthropathy . . . . . . . . . . . . . . . . . . . . . . . . Sarcoidosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Lipoma Arborescens . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Amyloid Arthropathy . . . . . . . . . . . . . . . . . . . . . . . . . . . . Chondromatosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Gout . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

7.16

Synovial Plicae (Folds) . . . . . . . . . . . . . . . . . . . . . . . . . 334

7.17

Synovial Popliteal Cysts and Bursitis . . . . . . . . . . 336

8.

The Lower Leg, Ankle, and Foot . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 358

328 329 331 332 332 333 333 334

7.25

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7.12

317 317 318

349 349

Clinical Relevance of Magnetic Resonance Imaging . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 350

M. Vahlensieck, A. Sikorski, and C. Glaser

8.1

Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 358

8.4.9 Tarsal Coalitions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 376 8.4.10 Cartilage Deformity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 379

8.2

Examination Technique . . . . . . . . . . . . . . . . . . . . . . . . 358

8.5

Disorders of the Tendons . . . . . . . . . . . . . . . . . . . . . . 379

8.2.1 8.2.2 8.2.3

Patient Positioning . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 358 Coil Selection . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 358 Magnetic Resonance Imaging Protocols with Regard to Sequences and Parameters . . . . . . . . . . . . . . 358

8.3

Anatomy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 359

8.5.1 8.5.2 8.5.3 8.5.4 8.5.5

Achilles Tendon . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Plantaris Tendon . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Peroneal Tendons . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Deep Flexor Tendons . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Anterior Muscle Group (Extensor Group) . . . . . . . . . .

8.3.1 8.3.2

General Anatomy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 359 Specific Magnetic Resonance Imaging Anatomy . . . . 361

8.6

Ligament Injuries and Impingement Problems following Ligament Damage . . . . . . . . . . . . . . . . . . . 395

8.4

Disorders of Bones . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 367

8.4.1

Osteochondral Injuries, Osteochondritis Dissecans, and Osteonecrosis of the Talus . . . . . . . . . . . . . . . . . . . . Apo- and Epiphysitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Sesamoids and Accessory Bones . . . . . . . . . . . . . . . . . . Stress Reactions, Stress Fractures, and Occult Fractures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Bone Marrow Edema Syndrome of the Foot and Transient Osteoporosis . . . . . . . . . . . . . . . . . . . . . . . . . . . Osteomyelitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Shin Splint Syndrome . . . . . . . . . . . . . . . . . . . . . . . . . . . . Pediatric Fractures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

8.6.1 8.6.2 8.6.3

Talocrural Joint . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Lisfranc Injury . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Sinus Tarsi Ligament Injuries and Sinus Tarsi Syndrome . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Plantar Calcaneonavicular Ligament . . . . . . . . . . . . . . Impingement Syndrome . . . . . . . . . . . . . . . . . . . . . . . . . .

8.4.2 8.4.3 8.4.4 8.4.5 8.4.6 8.4.7 8.4.8

367 370 370

8.6.4 8.6.5

382 387 388 390 394

395 398 398 399 399

371

8.7

Diseases of the Plantar Fascia (Plantar Aponeurosis) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 400

374 374 375 375

8.7.1 8.7.2

Plantar Fasciitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 401 Plantar Fibromatosis (Ledderhose’s Disease) . . . . . . . 401

ix

Contents Diseases of the Fat Pads of the Feet and Plantar Vein Thrombosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 402

8.9

Disorders of the Nerves and Compression Syndrome . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 402

8.9.1 8.9.2

Tarsal Tunnel Syndrome . . . . . . . . . . . . . . . . . . . . . . . . . . 403 Other Compression Syndromes of the Foot . . . . . . . . 406

8.10

Osteoarthritis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 406

8.11

Arthritis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 406

8.17

Typical Foot Tumors . . . . . . . . . . . . . . . . . . . . . . . . . . . . 411

8.17.1 8.17.2 8.17.3 8.17.4 8.17.5 8.17.6 8.17.7 8.17.8

Xanthomas . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Ganglion Cysts . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Bone Tumors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Calcaneal Tumors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Giant Cell Tumors of the Tendon Sheath . . . . . . . . . . . Malignant Soft Tissue Tumors . . . . . . . . . . . . . . . . . . . . . Subungual Tumors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Epidermal Inclusion Cysts . . . . . . . . . . . . . . . . . . . . . . . .

8.18

Disorders of the Toes . . . . . . . . . . . . . . . . . . . . . . . . . . 414 Trauma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Sesamoids . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Gout . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Hallux Valgus and Metatarsalgia . . . . . . . . . . . . . . . . . .

Pitfalls in Interpreting Images . . . . . . . . . . . . . . . . . 415

8.12

Other Form of Synovitis . . . . . . . . . . . . . . . . . . . . . . . . 406

8.18.1 8.18.2 8.18.3 8.18.4

8.13

Diabetic Foot Syndrome . . . . . . . . . . . . . . . . . . . . . . . 406

8.19

8.13.1 Diabetic Neuro-Osteoarthropathy . . . . . . . . . . . . . . . . . 406 8.13.2 Nondiabetic Neuropathy . . . . . . . . . . . . . . . . . . . . . . . . . 409

411 411 411 412 412 413 413 413

414 415 415 415

8.19.1 Signal Patterns of Anatomic Structures . . . . . . . . . . . . 415 8.19.2 Accessory Bones and Sesamoids . . . . . . . . . . . . . . . . . . 416 8.19.3 Accessory Muscles . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 416

8.14

Hemophilic Osteoarthropathy . . . . . . . . . . . . . . . . . 409

8.15

Bursitis and Haglund’s Heel . . . . . . . . . . . . . . . . . . . . 409

8.16

Pseudobursae . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 411

9.

The Temporomandibular Joint . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 426

8.20

Clinical Relevance of Magnetic Resonance Imaging . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 417

S. Robinson and R. Fischbach 9.4.3 9.4.4 9.4.5

Disk Adhesion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 434 Disk Perforation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 434 Malpositions of the Condyle . . . . . . . . . . . . . . . . . . . . . . 434

9.5

Arthritis and Other Synovial Disorders . . . . . . . . . 435

9.5.1 9.5.2

Arthritis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 435 Other Synovial Disorders . . . . . . . . . . . . . . . . . . . . . . . . . 436

9.6

Bone Disorder . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 436

9.6.1 9.6.2

Osteoarthritis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 436 Trauma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 437

9.7

Treatment Outcomes . . . . . . . . . . . . . . . . . . . . . . . . . . 438

9.8

Clinical Relevance of Magnetic Resonance Imaging . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 439

9.1

Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 426

9.2

Examination Technique . . . . . . . . . . . . . . . . . . . . . . . 426

9.2.1 9.2.2 9.2.3 9.2.4 9.2.5

Patient Positioning . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Coil Selection . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Sequences and Parameters . . . . . . . . . . . . . . . . . . . . . . . Special Examination Techniques . . . . . . . . . . . . . . . . . . Dynamic Studies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

9.3

Anatomy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 428

9.3.1 9.3.2

General Anatomy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 428 Special Magnetic Resonance Imaging and Variants . 428

9.4

Disorders of the Articular Disk . . . . . . . . . . . . . . . . . 430

9.4.1 9.4.2

Abnormal Changes in the Structure and Shape of the Disk . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 430 Disk Displacement . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 431

10.

The Muscles . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 444

426 426 426 427 427

A.J. Hoeink, T.-U. Niederstadt, and M. Vahlensieck

10.1

Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 444

10.6

Muscular Dystrophy . . . . . . . . . . . . . . . . . . . . . . . . . . . 456

10.2

Examination Technique . . . . . . . . . . . . . . . . . . . . . . . 444

10.7

Inflammatory Myopathy . . . . . . . . . . . . . . . . . . . . . . . 457

10.2.1 Magnetic Resonance Imaging . . . . . . . . . . . . . . . . . . . . 444 10.2.2 Special Magnetic Resonance Spectroscopy of the Muscles . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 444

10.3

Anatomy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 446

10.3.1 General Anatomy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 446 10.3.2 Specific Magnetic Resonance Imaging and Functional Anatomy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 453

x

10.4

Neuropathy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 455

10.5

Myotonic Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . 456

10.7.1 Polymyositis, Dermatomyositis, and Inclusion Body Myositis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10.7.2 Viral and Bacterial Myositis . . . . . . . . . . . . . . . . . . . . . . . 10.7.3 Pyomyositis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10.7.4 Sarcoidosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

10.8

457 458 458 458

Muscle Changes after Radiotherapy and Local Chemotherapy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 460

10.8.1 Radiotherapy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 460 10.8.2 Local Chemotherapy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 460

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8.8

Contents 10.9

Traumatic Myopathy . . . . . . . . . . . . . . . . . . . . . . . . . . . 461

10.14 Muscle Tumors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 468

10.9.1 Acute Muscle Overload . . . . . . . . . . . . . . . . . . . . . . . . . . . 461 10.9.2 Chronic Overload . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 464

10.15 Pitfalls in Interpreting the Images . . . . . . . . . . . . . 468

10.10 Muscle Fibrosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 465 10.11 Compartment Syndrome . . . . . . . . . . . . . . . . . . . . . . 467 10.12 Rhabdomyolysis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 467

10.15.1 Signal Variations in Superficial Muscles . . . . . . . . . . 468 10.15.2 Inversion Recovery Sequences . . . . . . . . . . . . . . . . . . . 468 10.15.3 Misinterpretation of Findings in Association with Denervation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 468

10.16 Clinical Relevance of Magnetic Resonance Imaging . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 469

10.13 Secondary Myopathy . . . . . . . . . . . . . . . . . . . . . . . . . . 467

11.

Bone Marrow . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 474 M. D’Anastasi, M. Vahlensieck, and A. Baur-Melnyk

Examination Technique . . . . . . . . . . . . . . . . . . . . . . . . 474

11.2

Anatomy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 475

11.2.1 General Anatomy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 475 11.2.2 Specific Magnetic Resonance Imaging Anatomy . . . . 476

11.3

Generalized Disorders . . . . . . . . . . . . . . . . . . . . . . . . . 478

11.3.1 Reconversion and Hyperplasia . . . . . . . . . . . . . . . . . . . . 11.3.2 Cell Infiltration, Displacement, Uncontrolled Hyperplasia, and Skeletal Dysplasia . . . . . . . . . . . . . . . 11.3.3 Sclerotic Skeletal Dysplasia . . . . . . . . . . . . . . . . . . . . . . . 11.3.4 Hypoplasia and Fatty Replacement . . . . . . . . . . . . . . . . 11.3.5 Bone Marrow Fibrosis . . . . . . . . . . . . . . . . . . . . . . . . . . . .

12.

479 481 492 492 493

11.3.6 Serous Atrophy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 493 11.3.7 Storage Diseases . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 494 11.3.8 Posttransplant Bone Marrow Changes . . . . . . . . . . . . . 495

11.4

Focal Diseases . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 496

11.4.1 11.4.2 11.4.3 11.4.4 11.4.5

Edema . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Ischemia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Postradiation Changes . . . . . . . . . . . . . . . . . . . . . . . . . . . . Inflammation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Trauma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

11.5

Clinical Relevance of Magnetic Resonance Imaging . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 509

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11.1

496 497 497 500 504

Bone and Soft Tissue Tumors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 516 M. Vahlensieck and A. Baur-Melnyk

12.1

Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 516

12.2

Examination Technique . . . . . . . . . . . . . . . . . . . . . . . . 516

12.3

Tumors: General Information . . . . . . . . . . . . . . . 516

12.3.1 12.3.2 12.3.3 12.3.4 12.3.5 12.3.6

Comparison of Benign and Malignant Tumors . . . . . Characteristic Signal Intensity Patterns . . . . . . . . . . . . Staging . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Biopsy Planning . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Monitoring the Response to Chemotherapy . . . . . . . . Tumor Recurrence and Postoperative Fibrosis and Edema . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

13.

516 518 520 527 527

12.3.7 Effects of Radiochemotherapy on Healthy Bone . . . . 528

12.4

Tumors: Specific Section . . . . . . . . . . . . . . . . . . . . . . 529

12.4.1 12.4.2 12.4.3 12.4.4 12.4.5

Bone Tumors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Soft Tissue Tumors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Solid Tumors with Cyst-Isointense Signal Pattern . . . Metastases . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Pseudotumors and Tumorlike Substance Deposits, Paget’s Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 12.4.6 Extramedullary Hematopoiesis . . . . . . . . . . . . . . . . . . . 12.4.7 Chloroma (Granulocytic Sarcoma) . . . . . . . . . . . . . . . .

529 549 564 566 567 568 568

528

Osteoporosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 574 S. Grampp, M. Vahlensieck, and H. K. Genant

13.1

Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 574

13.2

Examination Technique . . . . . . . . . . . . . . . . . . . . . . . . 574

13.2.2 Relaxation Time Measurements and Spectroscopy . . 579

13.3

Clinical Relevance of Magnetic Resonance Imaging . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 581

13.2.1 Magnetic Resonance Imaging . . . . . . . . . . . . . . . . . . . . . 574

14.

The Sacroiliac Joints . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 586 M. Bollow, J. Braun, and K.-G. Hermann

14.1

Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 586

14.2

Examination Technique . . . . . . . . . . . . . . . . . . . . . . . . 586

14.2.1 Patient Positioning and Coil Selection . . . . . . . . . . . . . 586 14.2.2 Imaging Planes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 586 14.2.3 Sequences . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 586

14.3

Anatomy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 587

14.3.1 14.3.2 14.3.3 14.3.4

General Anatomy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Special Magnetic Resonance Imaging Anatomy . . . . Variants . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Enthesis Organ . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

14.4

Causes of Sacroiliitis . . . . . . . . . . . . . . . . . . . . . . . . . . . 595

587 588 590 590

xi

Contents 14.5

Inflammatory Rheumatoid Disorders of the Sacroiliac Joints . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 595

14.5.1 Spondyloarthritis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 14.5.2 Juvenile Spondyloarthritis . . . . . . . . . . . . . . . . . . . . . . . . 14.5.3 Magnetic Resonance Imaging Findings for Inflammatory Rheumatoid Sacroiliitis . . . . . . . . . . . . . 14.5.4 Staging and Scoring . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

14.6

595 598 598 608

Osteoarthrosis Deformans and Juxta-Articular Pneumatocysts . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 611

14.8

Osteitis Condensans Ilii and Sacri as well as Triangular Hyperostosis Ilii and Sacri . . . . . . . . . . 613

14.9

Osteomalacia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 619

14.10 Pyogenic, Septic Sacroiliitis . . . . . . . . . . . . . . . . . . . . 619 14.11 Tuberculous Sacroiliitis . . . . . . . . . . . . . . . . . . . . . . . . 621 14.12 Traumatic Changes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 621

14.7

Disseminated Idiopathic Skeletal Hyperostosis . 611

15.

The Jaws and Periodontal Apparatus . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 634

14.13 Tumor and Tumorlike Conditions of the Joint . . 621

S. Robinson

Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 634

15.2

Examination Technique . . . . . . . . . . . . . . . . . . . . . . . . 634

15.2.1 Equipment and Coils . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 634 15.2.2 Imaging Plane . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 634 15.2.3 Sequences . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 635

15.3

Anatomy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 635

15.3.1 General Anatomy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 635 15.3.2 Special Magnetic Resonance Imaging . . . . . . . . . . . . . . 635

15.4.1 Periodontitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15.4.2 Osteitis and Osteomyelitis . . . . . . . . . . . . . . . . . . . . . . . . 15.4.3 Osteoradionecrosis and Bisphosphonate-Induced Osteonecrosis of the Jaw . . . . . . . . . . . . . . . . . . . . . . . . . 15.4.4 Dentogenic Sinusitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15.4.5 Pulp Vitality . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15.4.6 Implantology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15.4.7 Differentiation between Solid and Cystic Changes . .

15.5

636 637 638 639 640 640 640

Clinical Relevance of Magnetic Resonance Imaging . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 643

15.4

Special Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 636

16.

Appendix . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 648 M. Vahlensieck

16.1

Other Disorders and Diagnoses . . . . . . . . . . . . . . . . 648

16.1.1 Differential Diagnosis of Swollen Extremities on Magnetic Resonance Imaging . . . . . . . . . . . . . . . . . . . . . 648 16.1.2 The Skin, Subcutaneous Tissues, and Fascia . . . . . . . . 648 16.1.3 Chronic Sports Injuries . . . . . . . . . . . . . . . . . . . . . . . . . . 652

16.2

16.2.1 16.2.2 16.2.3 16.2.4 16.2.5

Magic Angle Phenomenon . . . . . . . . . . . . . . . . . . . . . . . . Use of Dedicated Systems . . . . . . . . . . . . . . . . . . . . . . . . Use of 3 Tesla Systems . . . . . . . . . . . . . . . . . . . . . . . . . . . Use of Open High Field Systems . . . . . . . . . . . . . . . . . . . Use of Open Spinal Systems for Upright Imaging . . .

654 656 656 657 658

Other Aspects of Magnetic Resonance Imaging of the Musculoskeletal System . . . . . . . 654

Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 661

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15.1

Preface The second edition of this book contains a lot of new content. Nowadays, 3 Tesla scanners are used on a large scale, and open high-field systems have advantages for claustrophobic patients. There are also several technical aspects relating to sequence acquisition and technical innovations, such as MRI neurography and MRI prosthesis sequences, which had to be taken into account. Besides, some of the older classification systems have now been superseded by the continually more accurate imaging processes. For example, the aim of meniscus diagnostic imaging is no longer to characterize increases in signal intensity but rather to classify ruptures, in terms of the implicated type of tear and its extension, or to detect even the most minute ligament injuries, for example, of the fingers. Reflecting on that aspiration, we have introduced a myriad of new

graphics and reference sources, and have replaced and added several illustrations. In many places, we have referred to internet sites deemed useful by our contributing authors for those readers who wish to obtain more information. Likewise, research tips on more effective use of internet search terms for specific topics are also given. The sections on the clinical relevance are presented as a Clinical Interview in which we sought the opinions of clinical radiologists on the performance of MRI. This should help foster a better understanding among radiologists of any discrepancies with respect to the “clinician.” Professor Martin Vahlensieck, MD Professor Maximilian Reiser, MD Downloaded by: Collections and Technical Services Department. Copyrighted material.

Dear Readers,

xiii

Editors Martin Vahlensieck, MD Professor of Radiology Practice for Radiology and Nuclear Medicine Bonn, Germany

Contributors Andrea Baur-Melnyk, MD Professor of Radiology Department of Clinical Radiology Großhadern Clinic Munich, Germany

Harry K. Genant, MD Professor of Radiology and Orthopaedics Department of Radiology University of California San Francisco, California, USA

Matthias Bollow, MD Professor of Radiology Clinic for Diagnostic and Interventional Radiology and Nuclear Medicine Augusta-Kranken-Anstalt-Bochum Bochum, Germany

Juergen Gieseke Department of Radiology University Hospital Bonn Bonn, Germany

Juergen Braun MD Professor of Radiology Rheumazentrum Ruhrgebiet Herne, Germany Martin Breitenseher, MD Professor of Radiology Department of Radiology and Interventional Radiology Landesklinikum Waldviertel Horn Horn, Austria Melvin D’Anastasi, MD Department of Clinical Radiology Klinikum Großhadern Munich, Germany Roman Fischbach, MD Professor of Radiology Department of Interventional Radiology Asklepios Klinik Altona Hamburg, Germany Klaus M. Friedrich, MD Associate Professor Department of Neuroradiology and Musculoskeletal Radiology Medical University of Vienna Vienna, Austria

xiv

Christian Glaser, MD Radiology Center Munich-Pasing Munich, Germany Stephan Grampp, MD Private practice Stockerau, Austria Kay-Geert A. Hermann, MD Associate Professor Department of Radiology Charité University Hospital Berlin, Germany Anna Janina Hoeink, MD Department of Clinical Radiology University Hospital Münster Münster, Germany Annie Horng, MD Department of Clinical Radiology University Hospital LMU Großhadern Munich, Germany Thomas-U. Niederstadt, MD Department of Clinical Radiology University Hospital Münster Münster, Germany

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Maximilian Reiser, MD, FACR, FRCR Professor of Radiology Chairman of the Department of Clinical Radiology and Dean of Medicine Ludwig Maximilians University Munich, Germany

List of Acronyms Mike Notohamiprodjo, MD Associate Professor University Radiology Clinic University Hospital Tübingen Tübingen, Germany Christian W. A. Pfirrmann, MD Professor of Radiology University Hospital Balgrist Zurich, Switzerland Martin Richter, MD Hand Surgery Clinic Malteser Hospital Bonn/Rhein-Sieg Bonn, Germany

Alexander Sikorski, MD Eifel Foot Center Eifel Clinic Saint Brigida Simmerath, Germany Frank Traeber, MD Department of Radiology University Hospital Bonn Bonn, Germany Volker Vieth, MD Department of Clinical Radiology University Hospital Münster Münster, Germany

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Soraya Robinson, MD Associate Professor Urania Diagnostic Center Vienna, Austria

xv

AAOS ABER ACL ADC ADP ALPSA ARA ARCO ASAS ATP BMD BOLD CEST CHESS CID CM CNS COX-2 CRMO CRP CRPS CSF CT DESS dGEMRIC DISI DOMS DRESS DSA DVT DWI DWIBS ECG ED EMG ETL FAI FAS FISP FLAIR FOV FSE GAGL GARD G-CSF Gd-DTPA GLAD GLOM GM-CSF GRAPPA GRE HAGL HF HIV HLA

xvi

American Academy of Orthopedic Surgeons abduction and external rotation anterior cruciate ligament apparent diffusion coefficient adenosine diphosphate anterior labroligamentous periosteal sleeve avulsion American Rheumatism Association Association Recherche Circulation Osseous Assessment of SpondyloArthritis International Society adenosine triphosphate bone mineral density blood oxygenation level–dependent chemical exchange saturation transfer chemical-selective saturation concealed interstitial delamination contrast media central nervous system cyclooxygenase 2 chronic recurrent multifocal osteomyelitis cross-reactive protein chronic regional pain syndrome cerebrospinal fluid computed tomography double-echo steady state delayed gadolinium-enhanced magnetic resonance imaging of cartilage dorsal intercalated segment instability delayed-onset muscle soreness depth-resolved surface-coil spectroscopy digital subtraction angiography digital volume tomography diffusion-weighted imaging diffusion-weighted body suppression electrocardiogram echo distance electromyogram echo train length femoroacetabular impingement flip angle sweep fast imaging with steady precession fluid-attenuated inversion recovery field of view fast spin echo glenoid avulsion glenohumeral ligament glenoid articular rim divot granulocyte colony-stimulating factors gadolinium with diethylenetriamine penta-acetic acid glenolabral articular disruption glenoid labrum ovoid mass granulocyte macrophage colony-stimulating factor generalized autocalibrating partially parallel gradient echo humeral avulsion glenohumeral ligament high frequency human immunodeficiency virus human leukocyte antigen

ISIS IV LCL MAVRIC MCL mDixon MIP MRA MRI MRS MTC NAD nr-axSpA OPG PASTA PCL PDw PET PISI POLPSA PRESS PVNS RHAGL ROI SAPHO SCFE SCIWORA SE SEMAC SENSE SI SLAC SNAC SNR SPAIR SPIR STEAM STIR STT T1w T2w TE TF TFCC THRIVE TI TIRM TMJ TNF TR TSE TSH VOIs

image-guided in vivo spectroscopy intravenous lateral collateral ligament Multiacquisition Variable Resonance Image Combination from GE Healthcare medial collateral ligament modified Dixon maximum intensity projection magnetic resonance angiography magnetic resonance imaging magnetic resonance spectroscopy magnetization transfer contrast nicotinamide adenine dinucleotide nonradiographic axial spondyloarthritis orthopantomography partial articular-sided supraspinatus tendon avulsion posterior cruciate ligament proton density–weighted positron emission tomography palmar intercalated segment instability posterior labroligamentous periosteal sleeve avulsion point-resolved spectroscopy pigmented villonodular synovitis reverse humeral avulsion glenohumeral ligament region of interest synovitis, acne, pustulosis, hyperostosis, and osteitis slipped capital femoral epiphysis spinal cord injury without radiographic abnormality spin echo Section Encoding for Metal Artifact Correction from Siemens Healthcare sensitivity encoding signal intensity scapholunate advanced collapse scaphoid nonunion advanced collapse signal-to-noise ratio spectrally adiabatic inversion recovery spectral presaturation with inversion recovery stimulated echo acquisition mode short-tau inversion recovery scaphotrapeziotrapezoid T1-weighted T2-weighted echo time turbo factor triangular fibrocartilage complex T1w high-resolution isotropic volume excitation inversion time turbo inversion recovery magnitude temporomandibular joint tumor necrosis factor repetition time turbo spin-echo thyroid-stimulating hormone volumes of interest

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List of Acronyms

1.1

Introduction

2

1.2

Spin-Echo Sequence

2

Relevant Magnetic Resonance Imaging Techniques

1.3

Turbo/Fast Spin-Echo Sequence

2

1.4

Gradient-Echo Technique

4

1.5

Ultrafast Magnetic Resonance Imaging Techniques

6

1.6

Fat Suppression

6

1.7

Contrast Media and Contrast Dynamic Enhancement

9

1.8

Magnetic Resonance Arthrography

9

1.9

Cartilage Imaging and Parameter Maps (Quantitative Magnetic Resonance Imaging)

11

1.10

Magnetization Transfer Contrast

11

1.11

Diffusion-Weighted Imaging and Diffusion-Weighted Body Suppression

13

1.12

Magnetic Resonance Angiography

13

1.13

Relaxometry

14

1.14

Three-Dimensional Reconstruction

14

1.15

Multiplanar Reformatting

15

1.16

Radial Acquisition

16

1.17

Spectroscopy and Spectroscopic Imaging

16

1.18

Cinematic Examinations

21

1.19

Magnetic Resonance Myelography

21

1.20

Magnetic Resonance Neurography

21

1.21

Magnetic Resonance Imaging of Prostheses

21

References

24

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Chapter 1

Relevant Magnetic Resonance Imaging Techniques

1 Relevant Magnetic Resonance Imaging Techniques M. Vahlensieck, F. Traeber, and J. Gieseke

1.1 Introduction

1.1.4 Sequence

In this chapter, we will discuss the most important principles of the magnetic resonance imaging (MRI) techniques of relevance to the musculoskeletal system, focusing in particular on the practice-oriented implications of the following: ● Image contrast. ● Signal-to-noise ratio (SNR). ● Application and practicability of the various techniques.

Different sequences are used in MRI, which, depending on the specific task definition, will place more or less emphasis on the relaxation times or on proton density. For example, if an MRI sequence is sensitive for detection of different T1 relaxation times, the resultant image will be referred to as a T1-weighted (T1w) sequence or a T1 contrast sequence or image.

1.1.1 Longitudinal and Transverse Magnetization To generate an MR signal, the patient is placed in a strong external magnetic field (B0). Because of the external magnetic field, the protons in the tissue, which can be viewed as small magnets whose intrinsic magnetic fields are randomly oriented, will align parallel with the longitudinal axis of the strong external magnetic field (longitudinal magnetization). If a suitable high-frequency (HF) pulse is now applied to the tissue (90-degree pulse), this results in a change in the direction of the intrinsic magnetic fields of the protons for the duration of the pulse. This change in the direction of the magnetic fields can be measured as the transverse magnetization. When the HF pulse is turned off, the magnetic fields of the protons return to their original orientation parallel to the external magnetic field.

1.1.2 Measurement Time The transverse magnetization can be measured only for a certain period of time. The time during which the transverse magnetization is measurable will depend on the homogeneity of the external magnetic field and on the nature of the tissue, and is known as the effective T2 or T2* time. If a suitable pulse is radiated into the tissue in this situation (180-degree pulse), further signals will be generated (spin echo [SE]). The time typically needed for decay of this SE signal intensity is called the spin–spin or T2 relaxation time. Likewise, the time after which complete longitudinal magnetization is reached again differs according to tissue types and is known as the spin– lattice or T1 relaxation time. Inside a suitable scanner, the aligned protons induce a measurable HF (MR) signal. The intensity of that signal in different tissues will depend on, in addition to the relaxation times, the concentration of the protons (proton density).

1.1.3 Spatial Assignment The spatial position of the signals received from a tissue sample is determined through frequency and phase encoding of the MRI signal. A grayscale matrix can then be produced following spatial location of the MRI signal.

2

1.2 Spin-Echo Sequence 1.2.1 T1 Contrast Thanks to its T1 contrast with a TR (repetition time) that is shorter than the T1 relaxation time of the imaged tissue (TR of around less than 700 ms), and short TE (echo time; TE of around less than 20 ms), the SE imaging sequence is the cornerstone in MR diagnostic imaging of the musculoskeletal system. Fat and paramagnetic substances manifest as hyperintense signals, whereas muscles, cortical bone, calcifications, and most pathologic changes are hypointense. This sequence is not very susceptible to artefacts and has a high SNR. It is therefore used for anatomic orientation and for identification of blood. Every examination protocol should contain a T1w SE sequence in at least one plane.

1.2.2 Proton Density–Weighted Image Contrast SE sequences with a TR much longer than the T1 relaxation time (TR = around 1,800–3,000 ms) and short TE (TE = around 10– 20 ms) will produce proton density–weighted (PDw) image contrast. This type of image contrast has no relevant role in MRI of the musculoskeletal system.

1.2.3 T2 Contrast T2-weighted (T2w) SE sequences are produced by long TR and long TE (TE = around 80–120 ms). This means that fat and muscles appear somewhat more hypointense than on the T1w image. Conversely, fluid and most pathologic changes are hyperintense. Until recently, this sequence was the most important imaging sequence for diagnosis of pathologic findings. However, it is very susceptible to motion or pulsation artefacts, and is very time consuming. However, this important T2 image contrast can also be achieved with other less time-consuming techniques. Of these modalities, the turbo spin-echo (TSE) sequence has now largely supplanted conventional technology.

1.3 Turbo/Fast Spin-Echo Sequence The TSE sequence, which is also known as a “fast spin-echo sequence,” is a more advanced development of the rapid

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For a more in-depth description of the physics and technical principles involved, please refer to the literature.

1.3 Turbo/Fast Spin-Echo Sequence

TEeff ¼ ED


●

●

●

ðETL þ 1Þ 2

The ETL is usually chosen such that ED is between 9 and 15 ms. However, it must be pointed out here that the maximum ETL possible (and hence also the minimum acquisition time) is not selected for all examinations (e.g., for imaging the bone marrow), since, unlike in the conventional SE sequences, fat would exhibit unusually high signal intensity because of spin coupling and effective rephasing due to the short ED. This effect is more pronounced with shorter ED and lower field strengths. For imaging fatty tissue, the ETL is chosen such that the ED is between 13 and 15 ms. For a T2w image with, for example, TEeff = 90 ms, an ETL between 10 and 14 is used. The enormous time saved can be partially used to increase the resolution and/or the SNR, while, at the same time, an acceptable acquisition time is maintained. Using a conventional sequence, this can only be achieved with a considerably longer acquisition time (25 minutes or longer). TSE images have a number of particular features that are especially important in MRI of the musculoskeletal system: ● High fat signal: For example, fat has markedly higher signal intensity on TSE images; this can interfere with identification of

●

pathologic processes in the immediate vicinity of fat (▶ Fig. 1.2), as seen, in particular, in the extremities. However, depending on the respective task, this potentially unwanted side effect can be reduced by shortening the effective ETL, with correspondingly greater ED and less time saving, or through frequencyselective fat suppression (▶ Fig. 1.3).52 Susceptibility effects: Another special feature of the TSE sequence is its lower sensitivity to susceptibility effects. Magnetization transfer effects: These are seen increasingly in the image contrast with short ED, making the muscles, connective tissue, fibrous tissue, etc., appear increasingly darker. This effect can be exploited to program special fast band sequences. Edge and contour enhancement: Depending on the parameters selected for TSE sequences, in particular those with T2 and proton density contrast, the poor edge and contour enhancement is noticeable (this is known as blurring). Such artefacts occur when the high-order encoding steps important for spatial resolution are only read out late in the excitation cycle. These can be reduced by taking the following measures: ○ Increasing the receiver bandwidth (e.g., ±32 kHz at 1.5 T [Tesla], albeit at the expense of the SNR; this permits shorter ED, e.g., less than 10 ms). ○ Shorter echo length train (e.g., less than 120 ms). ○ Fewer echoes. ○ Special k-space sampling (e.g., asymmetrical). ○ Fat–water shift not greater than 2.5 pixels. Acquisition profile: Acquisition in the k-space must be changed depending on whether a T1w, T2w, or PDw TSE sequence is to be programmed. For a short TE in T1w sequences, an acquisition profile with earlier readout of the low-order (“low-high”) steps is available, and for longer TE, a profile with linear readout is available. Newer acquisition profiles also permit asymmetrical readout, which, in turn, provides for a shorter measurement time.

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acquisition relaxation-enhanced technique19 and of the multiecho multi-slice technique.27 It is similar to a multi-echo SE sequence within a TR interval. The echoes are generated by a train of 180-degree pulses (echo train; ▶ Fig. 1.1). The major difference between this and the multi-echo SE image sequence is that in this technique each echo is separately phase encoded so that multiple profiles can be acquired for spatial assignment from a single excitation pulse. This is repeated until all phase values needed for the required resolution have been acquired. This means that, compared with a conventional SE sequence, the acquisition time is reduced by a factor corresponding to the number of 180-degree pulses per excitation (echo train length [ETL], turbo factor). The distance between the 180-degree pulses is called the “echo spacing” or “echo distance” (ED). The ETL can be set to any number between 3 and 128, and for imaging the musculoskeletal system is typically between 3 and 16. The image contrast of the images generated is determined by the echoes produced by the low-order phase-encoding steps; the term “TEeff,” denoting the effective echo time, is used here. The relationship between TEeff, ED, and ETL can be expressed as follows:

In a study of disorders of the musculoskeletal system, the TSE sequence produced results comparable with those achieved with the conventional SE sequence.55

First slice

Second slice Fig. 1.1 TSE sequence. Simplified diagram. Several echoes with a constant echo distance (ED) are generated by 180-degree pulses during a TR interval (TR) after the 90-degree pulse. The TE determining the contrast lies in the middle of the echo train and is referred to as the TEeff (effective echo time). On using a multi-slice technique, several slices can be read out at different times (here, e.g., two slices).

Fig. 1.2 TSE sequences of a fat–water phantom. TR = 3,000 ms; TEeff = 100 ms. Fat above, NaCl solution (saline solution) below. Same window setting. The signal intensity from fat increases sharply in line with rising ETL. Upper left: ETL = 3; upper right: ETL = 6; lower left: ETL = 9; lower right: ETL = 12.

3

Fig. 1.3 TSE sequences of a knee joint. (a) TR = 3,000 ms; TEeff = 100 ms; ETL = 12. (b) ETL = 3, same window setting. Large Baker’s cysts, joint effusion. With ETL of 3, the fluid-to-fat contrast is greater.

1.4 Gradient-Echo Technique

●

In the gradient-echo (GRE) technique, the imaging signal is not induced by a rephasing pulse (180-degree pulse) as in the SE sequence; instead, this is done by gradient reversal. Furthermore, smaller excitation angles are used, thus changing the resultant image contrast. Hence, the following three parameters have to be considered when using a GRE sequence: ● TR. ● TE. ● Flip angle. Markedly shorter acquisition times can be achieved with GRE sequences than with SE sequences. In principle, four GRE techniques are distinguished (▶ Fig. 1.4)10: ● Basic form: The basic GRE technique (see ▶ Fig. 1.4a) is largely similar to an SE sequence apart from the fact that it does not contain any 180-degree pulse. This is one of the oldest GRE sequences and is often prone to artefacts. It is hardly used anymore. ● Steady-state GRE: In the steady-state GRE sequence (see ▶ Fig. 1.4b), longitudinal and transverse magnetization of tissue are in a steady state. The transverse magnetization is maintained through the use of a rewinder gradient. This gives rise to image contrast determined by the relationship between T2 relaxation time and T1 relaxation time (mixed weighted). However, that applies only when using an intermediate flip angle (10–40 degrees), short TR (TR less than 250 ms), and short TE. However, if, on the other hand, very small flip angles (less than 5 degrees) are selected, a PDw sequence will be obtained regardless of the GRE sequence used. Large flip angles (larger than 40 degrees) result in T1 contrast, and long TE leads to T2* contrast (effective T2), that is, contrast based on decay of the early MRI signal (free induction decay).

4

●

Spoiled GRE: This GRE sequence is based on destruction of the residual transverse magnetization by spoiler gradients or HF pulse. This is therefore also called a “spoiled GRE sequence” (see ▶ Fig. 1.4c). Since transverse magnetization does not reach a steady state in this sequence, it will depend on the tissue parameter T1 relaxation time, and the sequence used is the T1w sequence. This is also associated with the drawbacks of an extreme flip angle and long TE, as mentioned earlier. If TR of more than 250 ms is used for steady-state GRE sequences, the image contrast will increasingly resemble that of the spoiled GRE sequence since the transverse magnetization can no longer reach a steady state. Contrast-enhanced GRE: In this GRE sequence, the echo induced by the second 90-degree excitation pulse is read out within an acquisition sequence. Hence, it is essentially an SE sequence with the difference that no separate 180degree HF pulse is applied and gradient reversal is used instead. Here, the nominal TE is longer than the TR. The sequence leads to strong T2 contrast and is thus called “contrast-enhanced GRE” (see ▶ Fig. 1.4d). Since SE is read out late in the contrast-enhanced GRE sequence, the SNR is very low. As such, this technique has not proved successful in routine applications.

A summary of the image contrast obtained with GRE sequences is given in ▶ Table 1.1. Different manufacturers use their own nomenclature for GRE techniques. The most important acronyms of four manufacturers are listed in ▶ Table 1.2. In all GRE sequences, unlike in SE sequences, phase shifts that are not induced by gradients are not rephased and, as such, contribute to image contrast. As the TE gets longer, interface artefacts (susceptibility artefacts), and also the sensitivity for different dephasing of fat and water protons, increase. The difference in the phases between fat and water protons is determined by the difference in the resonance frequency of these

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Relevant Magnetic Resonance Imaging Techniques

1.4 Gradient-Echo Technique

HF Signal Frequency Phase

Fig. 1.4 Circuit diagrams of the four basic GRE sequences. (a) Basic GRE sequence. (b) Steady-state GRE sequence. (c) Spoiled GRE sequence. (d) Contrast-enhanced GRE sequence. First line: exciting HF pulse; second line: signal to be received; third line: frequencyencoding gradient; fourth line: phase-encoding gradient; fifth line: slice gradient.

Slice a HF Signal Frequency Phase Rewinder

Slice

b

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HF Signal Frequency Phase Spoiler

c TR

Slice

TE HF Signal Frequency Phase Slice

d

Table 1.1 Simplified guidelines for generation of specific contrast with GRE sequences Contrast

Parameter changes

Rho

Small flip angle

T1

Large flip angle

T1

Contrast-enhanced GRE

Mixed (T2/T1)

Steady-state with short TE

T2*

Long TE

Note: Mixed = contrast that is dependent on T2/T1 quotient; Rho = proton density; T1 = T1 relaxation time; T2 = T2 relaxation time; T2* = effective T2 relaxation time; TE = echo time.

components (▶ Fig. 1.5). The phase of each component depends on TE; the following phases are distinguished: ● In-phase. ● Out-of-phase. ● Opposed-phase (▶ Fig. 1.6). In the first case, the signal intensities of the two components are added, while in the second case the component signal strengths are subtracted. Pixels containing a particular ratio of fat and water protons therefore exhibit TE-related oscillating signal intensities and can even be extinguished in a ratio 50:50 (etching artefact, chemical shift of the second kind).

The oscillation period between in-phase and opposed-phase TE is proportional to the difference in resonance frequencies, df, between fat and water (3.2–3.5 ppm) and, as such, also depends on the magnetic field strength (period in ms = 1,000/df ). The oscillation period values are around: ● 19.7 ms for 0.35 T (df = around 51 Hz). ● 13.8 ms for 0.5 T (df = around 72 Hz). ● 6.9 ms for 1 T (df = around 144 Hz). ● 4.6 ms for l.5 T (df = around 217 Hz). ● 2.3 ms for 3.0 T (df = around 434 Hz). With longer TE, the oscillation period for fat and other composite tissues increasingly deviates from the theoretical values of the dual water–methylene complex because these tissues have additional small resonance peaks (e.g., protons in the vicinity of double bonds, methyl, and carboxyl groups) which cause these inaccuracies (▶ Fig. 1.7). Therefore, individual tests are needed to calculate optimum opposed-phase TE values for the various MRI systems. Opposed-phase GRE images have high sensitivity for visualization of hematopoietic bone marrow22 and pathologic lesions (▶ Fig. 1.8). Thanks to their high signal intensity, steady-state GRE sequences have proved useful for acquisition of three-dimensional (3D) datasets followed by multiplanar reformatting, in particular for diagnostic imaging of the joints. Spoiled GRE sequences with short TR (40–50 ms), short TE (5–10 ms), and

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Relevant Magnetic Resonance Imaging Techniques Table 1.2 Acronyms for four basic GRE techniques as used by different manufacturers Manufacturer

Basic GRE types

Spoiled GRE

Steady-state GRE

Contrast-enhanced GRE

Siemens

–

FLASH

FISP

PSIF

Picker

FE

PSR

FAST

CE-FAST

Philips

–

CE-FFE T1

FFE

CE-FFE T2

GE

MPGR

SPGR

GRASS

SSFP

Toshiba

PFI

–

FE

–

Elscint

–

SHORT

F-SHORT

E-SHORT

Subcutaneous fat

X

Y Interfaces

Out-of-phase

Opposed-phase

Muscles

Fig. 1.5 Proton spectra of subcutaneous fat and muscles. Schematic diagram. The pixels along the interface between fat and water show about equal portions of both constituents. –C=C–, double bonds predominate in unsaturated fatty acids; –CH2, –CH3, methylene and methyl groups.

intermediate flip angle (30–60 degrees) in combination with fat suppression are useful for visualizing cartilage. Spoiled or steady-state GRE sequences with long TR (450–600 ms), two TEs (short in-phase echo, long out-of-phase echo), and medium flip angle (25–30 degrees) have generally proved useful for diagnostic imaging of joints, soft tissues, and bones (double-echo GRE).51 The first short echo produces a high signal for anatomic orientation, while the second echo generates a strong T2* contrast for sensitive detection of pathologic changes. When interpreting images, the special features of the GRE technique must be borne in mind—for example, increased susceptibility effects, especially of the second echo, and dephasing effects that can cause apparent magnification of calcifications or intervertebral disk prolapses.

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Fig. 1.6 Signal vectors from fat and water in the xy plane in GRE sequences. Different phases of fat and water vectors with different TE. For pixels with fat and water portions, the following applies: for inphase, the signal intensities are added; for opposed-phase, signal intensities are subtracted.

1.5 Ultrafast Magnetic Resonance Imaging Techniques In recent years, numerous new sequences with very short acquisition times have been developed (▶ Table 1.3). Some of these imaging modalities are still at an experimental stage and are thus not yet widely available. These ultrafast MRI sequences are of interest for diagnostic imaging of the musculoskeletal system in that they permit cinematic motion analysis of the joints (see Chapter 1.18.2 ) as well as, if required, dynamic contrastenhanced imaging with high temporal resolution.

1.6 Fat Suppression The following methods can be used in MRI for suppression of the signal from fatty tissue.

1.6.1 Chemical-Selective Saturation Fat protons can be saturated selectively by applying a pulse immediately before the actual acquisition sequence so that they can no longer contribute to the image formation. This method is called CHESS (chemical-selective saturation, or also SPIR [spectral presaturation with inversion recovery]). Instead of the saturation pulse, a 180-degree inversion pulse can also

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In-phase

1.6 Fat Suppression

Fig. 1.7 Signal intensities of fat, muscles, and fat–muscle interface as a function of TE at 1.5 T with GRE technique. Muscles exhibit almost no signal oscillation, whereas fat exhibits low and the fat–muscle interface exhibits very strong signal oscillation with a somewhat different oscillation frequency. That difference can be explained by the spectra (see ▶ Fig. 1.6) since the spectrum of subcutaneous fat has several peaks from different groups (multicomponent system) and not just two main peaks (two-component system), as found, for example, in pixels along the interface. At a maximum signal, TE is known as “in-phase TE,” and at a minimum signal it is called “opposed-phase TE.”

be applied at the time when the longitudinal magnetization of fat protons is at zero (SPAIR [spectrally adiabatic inversion recovery]). This chemical-selective pulse can be combined with any sequence. This method is used for certain specific task definitions such as to delineate fatty tumors or tumor components from blood. Furthermore, good cartilage contrast can be achieved with this technique (▶ Fig. 1.9). It was possible to enhance the sensitivity for detection of rotator cuff tears of the shoulder joint by combining CHESS with direct MRI arthrography. However, routine use of selective fat suppression has not proved useful for demonstration of pathologic changes in soft tissues adjacent to joints.51 In recent years, the combination of selective fat suppression with a PDw TSE sequence (e.g., TR = 3,000 ms, TE = 45 ms) has proved useful as a routine sequence. This technique combines the advantages of high SNR and high contrast for pathologic lesions. The use of this sequence is therefore currently recommended in several planes when imaging all regions of the musculoskeletal system.

1.6.2 Chopper-Dixon Method This fat-saturated method takes advantage of the chemical shift between fat and water protons; hence, pure fat and pure water images can be acquired with different TE. This method is quite time consuming and has not become established in routine imaging. However, it can be used to quantify the fat and water content when investigating specific questions related to bone marrow disorders.

1.6.3 Modified Dixon Technique In modified Dixon (mDixon) technique, which is used to generate pure water and pure fat images, acquisition of a GRE sequence

with at least two echoes is needed but, unlike with the conventional method, it need not have an in-phase and opposed-phase TE. The TE can be selected as needed, thus permitting a shorter acquisition time. The water images acquired with the mDixon sequence can be used as fat-free images and are often superior to sequences with prepulses in terms of uniform fat suppression, in particular in the presence of strong magnetic fields. The mDixon technique can be used in combination with not only GRE sequences but also TSE sequences. One advantage is that these sequences are optimum for fat-free visualization. The mDixon–TSE sequence, too, permits fat-free and in-phase images without the use of an additional sequence. This ensures that all layers are identical in orientation and resolution and, when using contrast medium, also identical with regard to their contrast windows. Just as for conventional TSE sequences, PDw (▶ Fig. 1.10), T1w, and T2w images can also be generated with this method. Downloaded by: Collections and Technical Services Department. Copyrighted material.

Fat Muscle Interface

1.6.4 Short-Tau Inversion Recovery Short-tau inversion recovery (STIR) is based on the inversion recovery sequence with short TI (inversion time). In the inversion recovery sequence, the signal-generating 90- and 180-degree pulses are preceded by an inverting 180-degree pulse. The interval between the inverting 180-degree pulse and the signal-generating set of pulses is known as “t” (tau) or “TI.” The image contrast can be controlled by changing T. If a short t is selected (= STIR), an image contrast that is highly sensitive to long TI and T2 relaxation times is produced (additive T1/T2 image contrast). Here, the fat protons do not contribute to the signal since their longitudinal magnetization will have decayed (zero crossing; ▶ Fig. 1.11). Unlike the SPIR technique, the inversion pulse has no frequency-selective implications for the fat component, and hence the image contrast is determined by the TI selected. An MRI sequence that is sensitive to long TI and T2 times and in which fatty tissue appears as signal void or hypointense has better image contrast than other sequences for demonstrating pathologic changes, for example, edema or tumor.53 Numerous studies have attested to the superiority of this sequence, in particular, in detecting disorders of the musculoskeletal system. Bone marrow edema or soft tissue inflammatory processes can be delineated with excellent contrast. Therefore, an STIR sequence should be included in at least one plane when faced with diagnostic uncertainties. The acquisition time of a sequence can be shortened by modifying STIR, such as reducing TR and TI (fast STIR; ▶ Fig. 1.12)53 or combining it with a turbo sequence (TSE–STIR).

1.6.5 Water Excitation If only the water protons are selectively excited (water excitation), the fatty tissue will not contribute to the signal and will appear as hypointense or signal void. Selective water excitation can be combined with various types of sequences. The time saving of a few milliseconds is one advantage over selective fat suppression since incorporation of a selective fat saturation signal before the actual sequence is time consuming. However, a comparative study revealed that the images generated by sequences with selective water excitation were not as good as those produced by their fat-saturated counterparts.43

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Relevant Magnetic Resonance Imaging Techniques

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Fig. 1.8 Shoulder joint. TE values of 35 and 7 ms exhibit opposed-phase TE, where hematopoietic bone marrow is shown as hypointense signal and fat–muscle interfaces as signal void (etching artefact). With TE values of 14 and 28 ms, fat and water protons are in phase. (a) Oblique coronal SE sequence (0.5 T, TR = 600 ms, TE = 15 ms). (b) Oblique coronal GRE sequence (0.5 T, TR = 600 ms, TE=14 ms, flip angle = 30 degrees). (c) Obliquecoronal GRE sequence (0.5 T, TR = 600 ms, TE = 35 ms, flip angle = 30 degrees). (d) Oblique sagittal GRE sequence (0.5 T, TR = 600 ms, TE = 7 ms, flip angle = 30 degrees). (e) Oblique sagittal GRE sequence (0.5 T, TR = 600 ms, TE = 28, flip angle = 30 degrees).

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1.8 Magnetic Resonance Arthrography

Fig. 1.9 Knee joint. Sagittal SE sequence (1.5 T, TR = 600 ms, TE= 15 ms) with selective fat suppression. Cartilage exhibits particularly hyperintense signal. Fig. 1.10 mDixon technique. Plantar PDw TSE sequence of foot on mDixon technique (3 T, slice thickness = 2.5 mm, measurement time = 2:44 min). Good homogeneous visualization “without fat” in water image. (a) In-phase image. (b) Water image. Table 1.3 Fast MRI techniques Sequence

Acronym

Acquisition time per slice

Fast GRE

TFE Snapshot-GRE Turbo-FLASH

1–4 s

GRE and SE

GRASE

300–100 ms

Echo planar sequence

EPI

50–100 ms

1.7 Contrast Media and Contrast Dynamic Enhancement Intravenous administration of gadolinium-containing contrast media (CM) is not required for routine diagnosis of musculoskeletal system disorders. However, this is commonly used in the following cases: ● Investigation of inflammatory diseases. ● Delineation of fluid from solid, and edematous from infiltrative, components of primary and secondary musculoskeletal tumors.36,40 Dynamic contrast-enhanced investigations with fast GRE sequences can be useful in distinguishing malignant from benign tumors.11 However, its overall specificity is not particularly high.29 This technique has not become established for routine diagnosis of musculoskeletal neoplasms.

1.8 Magnetic Resonance Arthrography 1.8.1 Direct Magnetic Resonance Arthrography Direct injection of a diluted gadolinium solution into a joint has been able to enhance MRI sensitivity for a number of indications, for example, rotator cuff tears, avulsions of the glenoid labrum, or cartilaginous lesions of the knee.20,34 However, since this constitutes an invasive procedure, it should, on the whole, only be indicated subject to strict criteria. It is possible that certain diagnostic issues can also be clarified in future through the use of indirect MR arthrography.

1.8.2 Indirect Magnetic Resonance Arthrography Only recently was it discovered that following their intravenous administration, gadolinium-containing MRI contrast agents reached the joint cavity in a concentration that markedly increased signal intensity on T1w images. This produces an arthrographic effect without having to resort to intra-articular puncture. This method is also known as “indirect MR arthrography.” Diffusion of the contrast agent into the joint slowly increases over time and, in a resting state, reaches its maximum

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Fig. 1.11 STIR sequence. Schematic diagram of longitudinal magnetization (Mz) following 180-degree inversion pulse, as well as transverse magnetization (Mxy) of fat following 90-degree pulse, in tissue with short T1 and short T2 relaxation time (A) and in tissue with long T1 and long T2 relaxation time (B). At the time of the 90-degree pulse, fat has no longitudinal magnetization; hence, it does not produce any signal in the remaining course of the sequence. At the time of the 90-degree pulse, tissue A has lower longitudinal magnetization than B and also exhibits more rapid decay of transverse magnetization, giving rise to a higher signal intensity for tissue B compared with that of A. This contrast is known as “additive T1/T2 contrast.” It explains the high sensitivity of STIR sequences for detection of edema and other pathologic changes.

Fig. 1.12 Metastases to the femur from a bronchoalveolar carcinoma. Fast STIR sequence (0.5 T, TR = 1,000 ms, T1 = 100 ms, TE = 15 ms). In addition to the hyperintense signal from the intraosseous metastatic portion, an extraosseous portion as well as cortical erosion is demonstrated. The arrow denotes the hyperintense signal from the peritumorous reactive zone.

After exercise

At rest

Time (min) Fig. 1.13 Indirect MR arthrography of the upper ankle joint at rest and during exercise. Signal intensity in upper ankle joint following intravenous injection of gadolinium-containing MRI CM. Slow rise in signal at rest; rapid, intensive signal rise after joint exercise (half-hour walking).

concentration after 1 hour. Diffusion can be greatly expedited by exercising the joint (▶ Fig. 1.13).56 Contrast enhancement is particularly apparent in fat-suppressed sequences (▶ Fig. 1.14). The contrast agent is injected in a concentration of 0.1 mmol/kg body weight. So far, experiences have been gathered regarding the use of this method for the following joints: ● Knee joint.9 ● Ankle joint. ● Shoulder joint.56

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Fig. 1.14 Indirect MR arthrography of the upper ankle joint. The joint space exhibits hyperintense signal. Moderate signal intensity of cartilage. Discrete cartilage irregularities in the fibulotalar joint.

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Relevant Magnetic Resonance Imaging Techniques

1.10 Magnetization Transfer Contrast

1.9 Cartilage Imaging and Parameter Maps (Quantitative Magnetic Resonance Imaging) Cartilaginous lesions can be distinguished on the basis of four degrees of severity: ● Stage 1: no visible morphologic changes due to focal or extensive biochemical damage to proteoglycans and collagen fibrils (exploration with palpating hook shows softening and impressibility). ● Stage 2: cartilage damage to less than half of the normal cartilage thickness. ● Stage 3: cartilage damage to more than half of the normal cartilage thickness. ● Stage 4: cartilage damage to the entire cartilage thickness (reaching as far as the bone). Stages 2 to 4 are generally easy to detect, thanks to present-day enhanced MRI spatial resolution. However, that will always depend on the thickness of the cartilage layer; for example, in the case of finger joints, there is also a higher probability of error than with the knee (see Chapter 7.3.2). In the past, special GRE sequences were also used for contrast-enhanced visualization of cartilage. Stage 1 cartilage changes are difficult to identify with MRI modalities. The underlying biochemical changes in cartilage, in turn, lead to changes in the relaxation times as well as in the intensity of CM diffusion into the cartilage. This is the principle exploited by the MRI methods currently used for early detection of cartilage damage: ● T2 relaxation time: since the T2 relaxation time is prolonged in the early stages of cartilage damage, focal or extensive increase in signal intensity can occasionally be seen on PDw fat sat or T2w images. However, the results have to be interpreted carefully since there are also artificial inhomogeneities, for example, due to the “magic angle” (see Chapter 16.2.1). To quantify these effects, the damage can be visualized through relaxometry and generation of parameter maps (T2 map). T1rho relaxation time (relaxation in the rotating frame): By using a sequence with an additional HF pulse to “freeze” magnetization in the transverse plane (this is known as a spin-locking pulse),

the T1 relaxation times are measured. These T1rho times of early cartilage damage are prolonged and can therefore be demonstrated on T1rho parameter maps. ● CM diffusion (dGEMRIC [delayed gadolinium-enhanced magnetic resonance imaging of cartilage]): on MRI, intra-articular CM diffusion across the surface into the cartilage. This process unfolds slowly and, for example, on MRI arthrography results in apparent thinning of the cartilage because the signal intensities of the surface layers taking up the CM and the CM-enhanced joint fluid increasingly resemble each other. This effect is also exploited to image damage to cartilage since regions with impaired biochemistry exhibit greater contrast agent uptake. The contrast agent (CM) is injected intravenously, following which the patient should move around for 10 minutes (CM diffuses into the joint cavity). CM can continue to diffuse for around a further 80 minutes into the cartilage. Finally, a T1w parameter map is generated. ● Other modalities: Other modalities have been used (e.g., magnetization transfer), and are being used (ultrashort TE, gagCEST, DWI [diffusion-weighted MR imaging]) for cartilage assessment.26 Research is being carried out on a broad scale in the hope of coming one step closer to diagnosis and treatment of arthritis, an affliction that affects so many people. However, quantitative methods have no role so far in routine clinical practice for management of painful joints.

Internet Link

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This method has advantages over conventional MRI for assessment of joint cartilage, menisci, disks, labra, rotator cuff, etc.56 Superior contrast can also be achieved with this method when imaging the wrist.39 Extra-articular enhancement of bursae and tendon sheaths observed on indirect MR arthrograms should not be mistaken for CM escape from the capsule. Such misinterpretations can be avoided with experience and training, and bursa enhancement may even prove to be advantageous (e.g., for diagnostic assessment of the upper rotator cuff of the shoulder). Contrast enhancement of vascular structures is markedly less pronounced on delayed images compared with intra-articular enhancement. This method has become established particularly for preoperative diagnosis of shoulder instability as well as of rotator cuff tears, thanks to its noninvasive nature and high sensitivity.

●i

Further details can be found in the online journal Osteoarthritis and Cartilage.

1.10 Magnetization Transfer Contrast In addition to the resonance peak of the protons of free (unbound) water, the proton spectrum of biological tissues has a broad-based flat resonance generated by the protons bound to macromolecules. Conventional MRI uses the peak of the free protons. However, if the broad base of the bound protons is saturated, without directly impacting the free protons, it will nevertheless result in a change in the resonance peak of the free protons (▶ Fig. 1.15): ● Shortening of the longitudinal magnetization (magnetization transfer) of the water peak. ● To a lesser degree, reduction of the T1 relaxation time (cross relaxation) of the water peak.

Fig. 1.15 Saturation of the broad resonance signal. Saturation of the broad resonance signal from protons bound to macromolecules with resultant reduction in the resonance signal of the free protons by means of magnetization transfer contrast (MTC).

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Relevant Magnetic Resonance Imaging Techniques

The image contrast thus generated differs from the contrast based on the relaxation time and on differences in the proton density. Tissues with a strong MTC effect include: ● Muscles. ● Cartilage. ● Tendons. ● Brain substance.

visualization of superficial cartilage lesions (▶ Fig. 1.17). MTC suppresses the artificial increase in signal intensity (“magic angle phenomenon”) seen in tendons obliquely oriented (around 55 degrees) to the direction of the B0 field (▶ Fig. 1.18). MTC also produces high-contrast images for visualization of the anterior cruciate ligament. The MTC of cartilaginous tumors does not differ essentially from that of other tumors (▶ Fig. 1.19). Conversely, mature hyaline joint cartilage exhibits a much stronger MTC effect. MTC can enhance MR angiography (MRA) by suppressing the background signal.

This method is suitable for detection of early cartilage degeneration.54 By subtracting the MTC image from a non-MTC image, an image is obtained where the signal intensities are proportional to the MTC effect (MTC subtraction), and this is ideal for

Fig. 1.16 Chemical exchange and dipolar coupling. Chemical exchange (1) and dipolar coupling (2) between the protons bound to macromolecules (left) and free protons (right).

Fig. 1.17 Knee joint. MTC subtraction image of the knee joint. Good visualization of superficial cartilage lesions. Tissue without MTC effect is seen as black structures.

Fig. 1.18 Shoulder joint. Oblique-coronal section. Marked signal reduction in artificial signal increase in rotator cuff (magic angle phenomenon) due to MTC (arrows). (a) GRE sequence (TR = 600 ms, TE = 18 ms, flip angle = 30 degrees). (b) MTC sequence with otherwise the same parameters and same window setting.

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This technique is known as “magnetization transfer contrast” (MTC) due the reduction in the longitudinal magnetization. The visible changes in the water peak can be attributed to the chemical exchanges occurring at the interface of mobile (free) and restricted (bound) protons (▶ Fig. 1.16). The MTC effect can be generated in two ways: ● Frequency-saturating MTC method. ● Frequency-remote MTC method.

1.12 Magnetic Resonance Angiography

1.11 Diffusion-Weighted Imaging and Diffusion-Weighted Body Suppression Diffusion-weighted imaging (DWI) is a noninvasive imaging modality that was already established in routine neuroradiology as early as the 1990s. It is also commonly used, in the meantime, in MR diagnostic imaging of the prostate gland, liver, etc. Studies have revealed that in some cases DWI was able to evaluate the dignity of bone marrow processes of the musculoskeletal system, in particular in the case of pathologic vertebral body fractures (see Chapter 2.5.2), where malignancies tend to be associated with a lower diffusion coefficient. The choice of b value is crucial for a good image quality. In one study, it was demonstrated that at 1.5 T, b values of around 300 s/mm2 produced an acceptable signal with good diffusion effect.45 Diffusion-weighted body suppression (DWIBS) is a specific form of DWI, where an STIR pulse is integrated into the DWI sequence, with signal inversion seen in the resultant image (“PET-like”; PET = positron emission tomography). One potential application is the largely isolated visualization of lymph nodes.44

1.12 Magnetic Resonance Angiography The inflow of unsaturated blood into the image slice introduces higher signal intensity than that of the surrounding stationary tissue. This effect is known as the time-of-flight method and is utilized for angiographic visualization. The intravascular signal can be altered by turbulent flow as well as by magnetic susceptibility and spin saturation. At certain sites (e.g., bifurcations), flow separation can lead to circular flow with a longer residence time in the vascular volume. This phenomenon produces undesirable partial spin saturation in this region and a secondary decrease in signal intensity.15 The visualization of vascular malformations and of tumorfeeding vessels is a relatively rare indication for MRA. With few

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Fig. 1.19 Femur chondroma. (a) Axial GRE sequence (TR = 600 ms, TE = 9 ms, flip angle = 30 degrees). (b) MTC sequence with the same parameters and same window setting. Marked signal reduction in muscles with contrast reversal relative to fatty tissue; moderate signal reduction of tumor.

exceptions, the vessels of the extremities can be well visualized on MRA. The blood flow is pulsatile with an extreme velocity range to the point of flow reversal and with subsequent signal losses in small confined regions. Since the total diameter of all individual vessels together is so great, the flow in small caliber vessels might be too slow and be obscured in the image by saturation effects. This problem can only be overcome by improving the resolution at the expense of reduced signal intensity and a considerably prolonged acquisition time. While surface coils can somewhat offset the problem of reduced signal, they cannot eliminate it. Likewise, pulsatility often gives rise to vascular dislocation and local turbulence, and in turn to signal loss. This highlights the risk of misinterpreting such artefacts as stenoses or thrombi.

1.12.1 Gated-Inflow Technique The gated-inflow technique is an elegant way to circumvent pulsatility-induced attenuation of image quality.8,17 Here, data acquisition is synchronized with the cardiac cycle, where an electrocardiogram (ECG) is used to choose a suitable gate within the RR interval (interval between two R wave peaks), corresponding to an area of lower pulsatility, which is thus less susceptible to artefacts. Here, data are acquired in a special order (but only during the selected gate) until the entire data matrix (all phase encodings) is recorded. Depending on the vascular region, the optimum gate delay will vary in accordance with the R wave peak. The length of the gate also plays a crucial role in the image quality (▶ Fig. 1.20). To assure low-artefact visualization of the carotid arteries, the gate may be, for example, 70 to 80% of the RR interval, whereas for the lower leg arteries 25 to 50% of the RR intervals should be selected. Hence, the gated-inflow technique is a combination of cardiac gating and the inflow method, which strictly limits data acquisition to one interval of the cardiac cycle.41 In this way, artefacts induced by retrograde or pulsatile flow are suppressed and also the peripheral vascular regions are better delineated.

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Fig. 1.20 Arterial MRA with ECG-gated inflow. TR = 23 ms, TE = 6.9 ms, flip angle = 60 degrees, signal averages = 1, matrix = 128 × 256, FOV (field of view) = 161 mm × 230 mm, slice thickness 4 mm overlapping by 0.5 mm, caudal saturation, heart rate between 55 and 60/min. Marked reduction in artefacts through gating. With smaller gate (c), less pronounced pulsation artefacts but longer measurement time. (a) Without ECG gating; measurement time = 2:18 min. (b) With ECG gating; data acquisition 50 ms with delay of 150 ms after the R wave peak; measurement time = 5:07 min. (c) As in (b), but with smaller gate of 250 ms; measurement time = 8:07 min.

1.12.2 Phase Contrast Angiography

1.13 Relaxometry

Phase contrast angiography is used for MRA without contrast agent and exploits the phase shift between flowing blood and stationary tissue. However, this imaging modality has no role in visualization of the extremity vasculature due to the relatively long measurement time and poor separation between venous and arterial vessels.

In general, measurement of the relaxation times (relaxometry) does not enhance MRI specificity. Hence, this modality has no role in routine diagnostic imaging of the musculoskeletal system. For follow-up examination of diffuse infiltrative disorders, measurement of the T1 times may help identify any early changes because measurable changes in the relaxation times often do not yet translate into visible signal intensity changes. The relaxation times can also be displayed in the image, with the degree of brightness proportional to the relaxation time. Such displays are referred to as relaxation time maps or Tl or T2 maps.

1.12.3 Contrast Angiography CM-enhanced angiography is established as a routine diagnostic modality for demonstration of the extremity vasculature and has supplanted digital subtraction angiography (DSA) in 90% of cases when indicated for purely diagnostic purposes. Following peripheral injection of a single (0.1 mmol/kg body weight) or double dose (0.2 mmol/kg body weight) of a T1shortening, gadolinium-containing CM, a T1w 3D GRE sequence is initiated, mainly as a coronal image. The data thus acquired are displayed using maximum intensity projection (MIP). This assures excellent image quality that in some cases equates with that achieved with intra-arterial DSA. It is able to completely supplant venous DSA. Thanks to the development of a mechanism for automated table movement during the examination and the use of sequences that permit temporal adaptation of the contrast-generating profiles to the CM bolus, the entire vascular bed of the pelvis and legs can be visualized with a single CM injection (▶ Fig. 1.21 and ▶ Fig. 1.22).

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1.14 Three-Dimensional Reconstruction 3D reconstruction of 2D images can be useful for identifying certain disorders of the musculoskeletal system.49 These conditions include comminuted fractures and fractures in regions of complex anatomy such as the base of the skull or facial bones. This facilitates planning of surgical reconstruction. Other applications include volumetric rendering of tumors to monitor the effects of radio- or chemotherapy. Two 3D reconstruction techniques can be distinguished: ● Surface rendering: a virtual light source illuminates the surface of the object. ● Volume rendering: a virtual light is transmitted through the object (▶ Fig. 1.23).

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Relevant Magnetic Resonance Imaging Techniques

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1.15 Multiplanar Reformatting

Fig. 1.21 Peripheral arterial occlusive disease. Contrast-enhanced MRA. Visualization with MIP, anteroposterior (A/P) projection. Three planes visualized in single examination thanks to automated table movement. (a) Pelvis. (b) Thigh and knee. (c) Lower leg and feet.

visualization (segmentation) of MRI data is much more onerous since the signal intensities can be very inhomogeneous and tissues not intended to be displayed can exhibit signal intensities similar to the object of interest to be visualized in 3D reconstruction. For example, subcutaneous fat exhibits signal intensity similar to that of fatty bone marrow. Hence, thresholding alone would not be adequate for segmentation of MRI data. A combination of segmentation by thresholding and manual selection is generally used.43 This means that the object to be visualized in 3D reconstruction must be manually extracted from each MRI image dataset. This is a very timeconsuming and error-prone process; hence, to date it is not routinely used for 3D visualization of MRI data for the musculoskeletal system.

1.15 Multiplanar Reformatting

Fig. 1.22 Arteriovenous shunt in dialysis patient. MRA, MIP visualization in A/P projection.

A combination of these two techniques (hybrid rendering) produces the best 3D impression.49 3D presentation of computed tomography (CT) data uses a threshold classification system by setting a density value of a pixel (e.g., bone) for 3D display. Pixel extraction for 3D

The datasets of an MRI sequence can be reformatted as in the case of CT data to obtain images in other planes (multiplanar reformatting). While reformatting does not alter the image contrast, the spatial resolution of the reformatted images is determined by the parameters of the original dataset (slice thickness × pixel resolution). Any inequality in the voxel edge lengths of the original datasets (anisotropic dataset), if present, must be taken into account in the reformatted images. To generate relevant resolution in all spatial orientations, voxels with equal edge lengths are chosen (isotropic dataset); the pixel resolution of the reformatted image will have the same, or virtually identical, resolution as the original image. Computing isotropic datasets at high resolution from a large field of view, for example, in the case of a knee joint, is still very time consuming even when using 3D GRE sequences. Moreover, T1w and T2w images are needed to resolve most clinical questions. Therefore, routine generation of isotropic

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Fig. 1.23 Knee joint. 3D display of MRI data. (a) Surface rendering. (b) Volume rendering.

datasets with subsequent reformatting has not been recommended so far for MRI of the musculoskeletal system. Newer sequences used in combination with special coils and parallel imaging help to generate high-resolution images within an acceptable time frame. Further clinical studies are needed to demonstrate whether these sequences will supplant multiplanar imaging modalities. Reformatting of anisotropic datasets of conventional sequences with lower resolution of the reformatted images can be used for visualization of large tumors and for follow-up of treatment.

1.16 Radial Acquisition Radial acquisition is the term used to denote a radial sequence of images programmed to rotate at increments of several degrees around a central axis (▶ Fig. 1.24).30 The use of radial acquisition in studies conducted on the knee and shoulder joints did not show any advantage over conventional image sections. Hence, this technique has not found a place in routine MRI of the musculoskeletal system.

1.17 Spectroscopy and Spectroscopic Imaging Magnetic resonance spectroscopy (MRS) in human medicine is a relatively time-consuming and complicated technique and, as such, is rarely used in routine diagnostic imaging. However, since it can yield specific information on metabolic processes, it may find a role in clinical applications in the future. Intensive research is being carried out in this area and the results achieved are very promising.

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Fig. 1.24 Knee joint. Axial slice. Visualization of slices with radial acquisition.

Therefore, further details of this technique will now be presented in the following, in particular in relation to spectroscopy with hydrogen (1H) and phosphor (31P).

1.17.1 Hydrogen Spectroscopy Shielding of the static magnetic field by the electrons in the atomic shell gives rise to a chemical shift in the proton

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Relevant Magnetic Resonance Imaging Techniques

1.17 Spectroscopy and Spectroscopic Imaging

The area beneath the respective MRI spectral line is proportional to the concentration of the substance of interest. This permits noninvasive quantitative determination of the relative fat–water content, and is particularly useful in the case of bone marrow diseases24,38 and for staging degenerative myopathy disorders.4 ▶ Fig. 1.25 illustrates a number of examples with increased lipid components and massively reduced water portions on a T1w TSE image, on an STIR fat-suppressed coronal image, and in a color-coded map of the fat percentage as well as the proton spectrum of a lipoma on a 3-T scanner. With enhanced homogenization of the static magnetic field above the region of interest (shimming) during MRI examination, a linewidth of around 0.2 to 0.5 ppm can be obtained depending on the region and the volume size selected; this is generally adequate for spectral separation of the peaks of the molecular groups mentioned. Due to the very short T2 times of 30 to 40 ms already at 1.5 T for the H2O component in muscles and bone marrow, the theoretical resolution limit of around 10 Hz (corresponding to 0.15 ppm at 1.5T) is almost reached. It will be more difficult to observe other biologically interesting molecules in the proton spectrum because of the narrow chemical shift range of in vivo hydrogen compounds (only 8 ppm); interference is common already in the 1 to 4 ppm range (referred to the chemical shift of tetramethylsilane, set at = 0 ppm). Whereas the spectral resolution of 1H-MRS for the musculoskeletal system can be further enhanced only to an extent even with stronger magnetic fields, the detection sensitivity for metabolites can be markedly increased in the 1 to 10 mmol/L concentration range through suppression of the water resonance. In principle, this also permits identification of metabolic changes or enzyme defects with proton spectroscopy. The suppression techniques that can potentially be used include: ● Selective inversion of the H2O component through application of a preliminary 180- and 90-degree excitation pulse at the zero crossing of the longitudinal magnetization of the tissue water portions.35 ● Narrow-band presaturation through adiabatic or gaussian HF pulses (CHESS technique)18 or by means of binominal composite pulses. Additional fat suppression is needed to detect the CH3 duplet of lactate (the two possible spin orientations of the adjacent C–H protons result in a fine structure of cleavage into two smaller subpeaks = duplet) since otherwise this spectral line

would be obscured by the methyl resonance of fatty acids. A drawback of some of these modalities, as well as of various filter procedures used for postprocessing of spectra, derives from the fact that they modulate line amplitudes, thus not only eliminating the interfering components but also impairing signals from the metabolites of interest. As opposed to 1H spectroscopy of the central nervous system, which is used almost exclusively with suppression of the water signal, to date the various MRS suppression methods used for the musculoskeletal system have not proved successful and are only used in isolated cases. Besides, the use of MRS with other atomic elements, in particular phosphorus, is better at resolving most diagnostic issues. In terms of the coil technology, 1H-MRS of the musculoskeletal system is generally not a problem since the clinical issues to be resolved often relate to regions close to the body surface; hence, the surface coils used for MRI can also be employed. For relatively large volumes of interest (VOIs) or to compare the extremities on the right and left sides of the body, the standard body coil can also be used for spectroscopy.

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resonance frequency that is dependent on the molecular structure. This effect is exploited in the methods described earlier for selective fat suppression (see Chapter 1.6 ) or for generation of water and fat images (see Chapter 1.6.5 ). However, it can also be used for direct visualization of the tissue concentration of various hydrogen-containing compounds (MRI spectrum). The predominant signals in the 1H spectra of muscles, fatty tissue, and bone marrow are as follows: ● H2O peak. ● Signals from saturated and unsaturated fatty acids (–CH3–, –CH2–, –CH2–HC=, –CH2CO–, and –HC= molecule groups) in triglycerides.

Volume Selection Techniques The volume selection techniques that have proved most successful in proton spectroscopy are the dual SE (point-resolved spectroscopy [PRESS]) and STEAM (stimulated echo acquisition mode) techniques12: ● PRESS technique: Here, a slice-selective 90–180–180-degree pulse sequence is applied in which for each of the three HF pulses one of the spatial encoding gradients Gx, Gy, or Gz is switched. Only those spins within the rectangular intersection of the three planes selected by the gradients are in resonance for all HF pulses and yield a second SE. ● STEAM technique: In this modality, three slice-selective 90degree pulses are radiated into the tissue at intervals of TE/2 and TM (mean interval), and after a further interval TE/2, xy magnetization is rephased at the time of the stimulated echo (▶ Fig. 1.26). However, only 50% of the spins in the slice volume of the gradients contribute to the signal, with the other half being dephased during TM. Hence, the STEAM method has a relatively low SNR. Its main advantages are observed with short TE since all dephasing gradients can be switched in TM and do not contribute to TE. Data acquisition is performed in the second half of the echo signal. For both of the aforementioned techniques, the precision of gradient switching is of paramount importance for the localization quality. Firstly, it must assure rephasing of the second SE (stimulated echo) and, secondly, guarantee complete dephasing of all free induction decay signals and primary echoes, in particular for short TE. Postprocessing of spectra entails the following measures: ● Filter procedures for the time signal to improve SNR. ● Data interpolation through what is known as “zero filling.” ● Phase correction of Fourier transform signal.

Spectroscopic Imaging Spectroscopic imaging (also called chemical shift imaging) is an imaging modality similar to MRI for simultaneous acquisition of

17

(CH2)n

Glyc-H2

–CH3 CH2–CH2–CO

c

=CH–CH2–HC=

HC=

CH2–CO CH2–HC=

H2O

d Fig. 1.25 Lipoma in right calf muscles. 25-year-old female patient. (a) Axial T1w TSE image (TR = 505 ms, TE = 15 ms), showing volume selected for spectroscopy. (b) Coronal section with fat suppression in STIR technique (TR = 3,239 ms, T1 = 210 ms, TE = 20 ms). (c) Quantitative color map of relative fatty portion, from mDixon sequence (TE = 1.2/2.4 ms). Fat proportion of lesion 63% (posterior oval region of interest [ROI]). (d) 1H spectrum without water suppression (TR = 2,500 ms, TE = 20 ms, 8 signal averages); below: vertical axis magnified.

spectra from several volume elements (voxels).25 Before the sliceselective excitation pulse is radiated into the tissue, phaseencoding gradients are prepared in 1D or 2D spectroscopic imaging. For 2D spectroscopic imaging with, for example, 16 phase-encoding steps, the number of Nex signal excitations (Nex = number of signal averages) needed is 256 Nex. This generally results in relatively long acquisition times, but provides detailed information on the regional distribution of metabolites. In proton spectroscopy, this technique is often used in combination with H2O suppression pulses and the volume selection

18

methods described earlier for improved suppression of unwanted signals (▶ Fig. 1.27). So far, the prospects of using spectroscopic imaging in the musculoskeletal system appear slim.

Relaxometry The spectral acquisition methods described can also be applied as a dynamic sequence using different parameters. For example, the T2 relaxation times in tissue can be measured on using a sequence of spectra where the TE is varied and the line integrals

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Relevant Magnetic Resonance Imaging Techniques

1.17 Spectroscopy and Spectroscopic Imaging TE/2

TM

TE/2

HF Gz

TE Signal 180° HF

90°

180°

180°

Gx Gy

Gy Gz

Gx

Fig. 1.26 1H-MRS with volume selection in STEAM technique. HF pulse train and gradient switching. Gx,y,z = 90-degree pulses.

tailored to the relaxation curve. Similarly, the T1 relaxation times can be determined by first applying a 180-degree inversion pulse and changing the T1 delay with respect to the 90-degree excitation pulse. This method of chemical selective relaxometry has been successfully used especially in 1H spectroscopy of the vertebral and peripheral bone marrow.14,37,47

1.17.2 Phosphorus Spectroscopy Due to the pivotal role played by phosphorus compounds in energy metabolism and as constituents of the cell membrane, 31P spectroscopy is a potentially useful diagnostic modality, especially for metabolic diseases and tumors of the musculoskeletal system. Relatively large volumes or a high number of signal average measurements must be chosen because phosphorus compounds are present in low concentrations (approximately 10 mmol/L) and exhibit lower MRI sensitivity compared to 1H. The chemical shift of phosphorus metabolites is around 25 ppm; hence, most spectral lines can be easily separated from each other. However, the two lines representing adenosine diphosphate (ADP) are obscured by the resonance of the peripheral phosphorus atoms of adenosine triphosphate (ATP); hence, the important task of measuring the ADP:ATP ratio, and thus the phosphorylation potential, can only be accomplished indirectly. Phosphocreatine is the most important constituent, in particular, in the musculoskeletal spectrum; the inorganic phosphate line is also shown (▶ Fig. 1.28a). The pH value in tissues can be measured directly from the difference in the chemical shift between phosphocreatine and inorganic phosphates. In other soft tissues, phosphomonoester and phosphodiester compounds are also found as products of phospholipid metabolism of the cell membrane. High concentrations are interpreted as an indicator of increased proliferation in the presence of tumor changes. To improve SNR in 31P spectra, a second HF system based on 31P–1H dual resonance excitation as provided by the nuclear Overhauser effect can be exploited.3,32 Here, magnetization is transferred from the 1H spin system to the 31P nuclear spin through dipole relaxation, which, theoretically, yields maximum signal amplification by a factor of 2.24. Values in the 1.3 to 1.6 range are found in vivo.

Phase encoding

Fig. 1.27 1H-2D spectroscopic imaging with water suppression through frequency-selective inversion pulse and with additional SD volume selection in PRESS technique. HF pulse train and gradient switching. Gx,y,z = 90-degree pulses. Downloaded by: Collections and Technical Services Department. Copyrighted material.

Data acquisition

Whereas in 1H-MRS, even small amounts of subcutaneous fatty tissue in the selected volume will interfere with the signals from metabolites present in a low concentration, the phosphorus spectra are less susceptible to interference. Therefore, localization techniques with less sharply defined VOI limits can also be used in 31P-MRS, especially when high temporal resolution is needed for 31P-MRS during muscle exercise. The PRESS and STEAM techniques are not suitable since they call for acquisition of echo signals and several phosphorus metabolites have only very short T2 relaxation times. In the simplest case, a rough volume selection can be made on the basis of the mainly hemispherical detector design of a surface coil. This method can be refined by varying the transmission power so that only spins within a particular distance from the coil center receive a 90-degree excitation pulse and spectra can be acquired from different tissue depths (B1 or rotating frame technique). Due to the inhomogeneity of the B0 outside the VOI, the localization can also be determined by using additionally mathematical methods to filter out of broad spectral lines from adjacent regions (B0 or topical-magnetic resonance technique).16

Depth-Resolved Surface-Coil Spectroscopy Among the selection techniques with gradient switching, depthresolved surface-coil spectroscopy (DRESS) localizes a cylindrical volume with sharply defined upper and lower margins as well as, due to the coil sensitivity, limited lateral expansion.21 Signal subtraction is effected from a measurement with and without spatial encoding gradients; to accomplish that, the gradient should be oriented vertically to the coil plane. This method eliminates the intensive signal from subcutaneous fatty tissue between the coil and VOI and permits acquisition of images of a good quality with a temporal resolution of around 10 s for the 31P spectra localized. It therefore lends itself in particular to dynamic MRS during muscle exercise.

Adiabatic High-Frequency Pulses The selected VOIs can be evenly excited almost regardless of distance when using frequency-modulated (adiabatic) HF pulses.5

19

Relevant Magnetic Resonance Imaging Techniques Fig. 1.28 Calf muscles of healthy subject. 31P spectroscopy (with 14-cm surface coil). (a) 31P spectrum at rest (TR = 3,000 ms, 64 signal averages, acquisition time 3 min, volume selection with ISIS technique [image-guided in vivo spectroscopy]). (b) Axial T1w SE image showing ISIS-selected volume of 3.6 cm × 5 cm × 8 cm (A/ P/left/right/craniocaudal, TR = 500 ms, TE = 15 ms). (c) Dynamic 31P spectroscopy during muscle exercise (spectrum 2–5) and in the recovery phase (spectrum 6–8, TR = 3,000 ms, in each case 4 signal averages, acquisition time 12 s/spectrum, volume selection with DRESS technique [depth resolved surface coil spectroscopy]). PCr, phosphocreatine; Pi, inorganic phosphates.

PCr

b ATP

γ

10.0

α

0

δ (ppm)

a

β

–10.0

–20.0

PCr

ATP Pi

γ

α

β 17 min 12–24 s 0–12 s recovery Exercise stopped (after 13 min) 36–48 s 12–24 s 0–12 s exercise Before exercise

c

10.0

0

δ (ppm)

–10.0

–20.0

Image-Guided In Vivo Spectroscopy Image-guided in vivo spectroscopy (ISIS) is a more time-consuming technique33 but, like the STEAM and PRESS modalities, permits 3D localization of rectangular volumes (▶ Fig. 1.28b). The spin signals from the VOI are obtained only through complex addition and subtraction calculations based on eight individual measurements, using in each case various combinations of three frequency-selective inversion pulses and switching the three spatial encoding gradients. If the number of signal averages is equal, this will result in a much poorer SNR than, for example, that obtained with the DRESS technique. However, the ISIS technique is the most suitable method for localization of discrete focal lesions.

20

Two-Dimensional Spectroscopic Imaging Technique The 2D spectroscopic imaging technique already described embodies a novel approach for acquisition of volume-selected phosphorus spectra. The slice excited by the frequency-selective HF pulse is further broken down by the two phase encoded gradients into, for example, 8 × 8 voxels. There is no need here for additional suppression of interfering signals as in the case of 1H-MRS. This technique can also be implemented without slice selection as a 3D spectroscopic imaging modality with phase encoding of all three spatial directions, but in such cases very long measurement times are needed. Spectroscopic imaging is

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Pi

1.21 Magnetic Resonance Imaging of Prostheses

Dynamic Phosphorus Spectroscopy The use of dynamic phosphorus spectroscopy during muscle exercise permits direct monitoring of the biochemical processes involved in energy metabolism. When loaded, healthy muscles typically exhibit a rapid decline in phosphocreatine concentration and a rise in the inorganic phosphate peak, often observed with expression of a sugar phosphate component, with relatively rapid resumption of resting values during the recovery time (▶ Fig. 1.28c).46 Prolonged recovery times and anomalies in the maximum and minimum concentration of metabolites are an indicator of enzyme defects or of reduced mitochondrial oxidative potential.6 To date, there is really no morphological correlate to permit identification of such defects on MRI. Changes observed already during the resting phase in metabolites tend to be suggestive of inflammatory or degenerative muscle disorders with concomitant edema or conversion to fatty tissue.

1.17.3 Carbon Spectroscopy The main drawback of in vivo 13C-MRS is the rare natural abundance of this isotope (1.1%), together with a relative MRI sensitivity of only 0.016. Hence, despite the high concentration of carbon compounds in the body tissues, long measurement times are needed to obtain acceptable spectra. 13C-MRS provides detailed information on carbohydrate, fat, and protein metabolism; subcutaneous fat and muscles in close proximity to the coil are the most suitable for acquiring spectra with natural 13C.2 To date, in vivo 13C-MRS has been used in only very few specialist centers in view of the technical challenges it presents. Details of its potential applications can be found in the study by Boesch.7

1.18 Cinematic Examinations Several painful joint disorders are triggered by movement and can only be visualized when the joint is in certain positions. Conventional radiography can identify such conditions by obtaining functional views. Functional MRI of the joint offers the advantages of sectional imaging together with functional assessment of the joint. Concurrent evaluation of the soft tissues assuring joint stability is particularly useful. Two different techniques are used for cinematic functional MRI.

published articles report on experiences gathered with self-made devices.42 Since joint movement is somewhat restricted within closed MRI machines, only a small range of joint motion can be assessed. Open machines permit a considerably wider range of motion, and are also very suitable for imaging the shoulder, elbow, and hip joints.28

1.18.2 Very Fast Sequences Real-time functional MRI can be performed using very fast sequences such as echo planar methods, spectroscopic imaging, and helical imaging. These modalities are still in the developmental stage but are expected to revolutionize cinematic imaging of the joints. They can be used for MR fluoroscopy imaging of joints.

1.19 Magnetic Resonance Myelography

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advantageous when exploring the composition and extension of complex lesions and infiltration of the surrounding tissue.

On using very powerful T2w sequences (TE more than 120 ms), the contrast of fluid-containing organ structures can be enhanced to such an extent as to equate with selective visualization. This is exploited to examine various organ systems (MR cholangiography, MR sialography, MR urography, and MR myelography). However, it should be borne in mind that, on MR myelography, stenoses will appear somewhat more aggravated. Otherwise, this modality is a useful adjunct to the armamentarium available for spinal diagnostic imaging. Normally, using MIP several projections are made from a dataset (▶ Fig. 1.30). The technique is equally adept as conventional myelography at demonstrating spinal canal stenosis and nerve root sheath amputations. The usual artefacts seen on MRI must be taken into account when interpreting the images.

1.20 Magnetic Resonance Neurography The thickness of many peripheral nerves is such that they can be well visualized thanks to the continually enhanced MRI resolution. Nerves have relatively high water content, thus assuring good visualization on T2w, STIR, and fat-suppressed PDw or T2w sequences. The term MR neurography is also sometimes used for imaging aimed at demonstrating a nerve, plexus, or fascicle. MIP techniques can be used to gather interesting insights into nerves thickening and edema-induced changes.57

1.18.1 Cine Mode Static images are obtained with the joint in various positions and are then reviewed in cine mode. With this technique, retainer devices are used to restrict movement to a single defined plane. MR images are then obtained with the joint retained by the device in a defined position (▶ Fig. 1.29). In general, conventional SE or GRE sequences are selected, thus necessitating relatively long acquisition times. Experience is now available on most major joints and on the cervical spine. However, nonferromagnetic retainer devices are not readily commercially available for the various joints, such as the temporomandibular joint, knee, hand, or ankle joints, and most

1.21 Magnetic Resonance Imaging of Prostheses If certain technical parameters are taken into account, MRI can also be used to examine patients with hip and knee joint prostheses. The parameters to be observed to reduce metal artefacts are as follows: ● Lower magnetic field strength (recommended: midfield system at 0.5T). ● Short TE. ● No GRE sequences.

21

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Fig. 1.29 Femoropatellar joint. MRI cinematography. Axial MR images from motion study during flexion and extension 0 to 30 degrees. (a) Increased lateralization of patella during strong flexion as sign of lateral maltracking. (b) Increased medialization and strong tilting of patella during strong flexion as sign of medial maltracking. grad = degrees.

1.21 Magnetic Resonance Imaging of Prostheses

● ●

Increased receiver bandwidth (recommended: 10–20 kHz). TSE sequences with low ED.

Selective methods cannot be used for fat suppression, but an STIR technique can be used instead.48 Intravenous CM are also commonly used (with subtraction technique). The frequency-encoding direction is oriented, if possible, longitudinally to the prosthetic device. Wherever possible, prosthetic devices should not be positioned transversely to the direction of the B0. The following should be borne in mind as regards the prosthesis material: titanium or zirconium prostheses are less susceptible to major artefacts compared with stainless steel or cobalt chromium.

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Fig. 1.30 A/P projection of MIP of strong T2w MRI sequence of spinal canal of lumbar spine (a) as well as cervical spine (b). MR myelography. (a) Spinal canal of lumbar spine. (b) Spinal canal of cervical spine.

Using such prosthesis sequences (▶ Fig. 1.31), pathologies such as infections, granulomas, cysts, arthrofibrosis, tendon and muscle injuries, bone infarction, and synovitis, as well as loosening, may be visualized with relatively good sensitivity.31 To improve visualization of joint prostheses, certain manufacturers are supplying special packets or sequences that are less susceptible to metal artefacts (SEMAC [Section Encoding for Metal Artifact Correction from Siemens Healthcare] or MAVRIC [Multiacquisition Variable Resonance Image Combination from GE Healthcare]).1,13

23

Fig. 1.31 Patient with knee prosthesis. Optimized parameters at 0.5 T (prosthesis MRI). Relatively few metal artefacts around shaft and joint. (a) T1w TSE sequence. (b) T2w TSE sequence. (c) STIR sequence.

[16] Gordon RE, Hanley PE, Shaw D, et al. Localization of metabolites in animals

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weighted whole body imaging with background body signal suppression

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tion 3D display. Radiat Med. 2004; 22(4):275–282

Gelenkschäden am oberen Sprunggelenk. Fortschr Röntgenstr. 1995;

[45] Tang G, Liu Y, Li W, Yao J, Li B, Li P. Optimization of b value in diffusionweighted MRI for the differential diagnosis of benign and malignant vertebral fractures. Skeletal Radiol. 2007; 36(11):1035–1041

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[33] Ordidge RJ, Connelly A, Lohman J. Image-selective in-vivo spectroscopy (ISIS).

162:338–341 [57] Wadhwa V, Thakkar RS, Maragakis N, et al. Sciatic nerve tumor and tumorlike lesions - uncommon pathologies. Skeletal Radiol. 2012; 41(7):763–774

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2.1

Imaging

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2.2

Anatomy and Physiology

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The Spine

2.3

Degenerative Conditions of the Spine

41

2.4

Spondylitis and Spondylodiscitis

49

2.5

Posttraumatic Spinal Changes

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2.6

Postoperative Spinal Changes

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2.7

Tumors of the Spine

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2.8

Clinical Significance of Magnetic Resonance Imaging

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References

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Chapter 2

The Spine

2 The Spine K.M. Friedrich and M. Breitenseher

2.1 Imaging

2.1.3 Examination Protocols

2.1.1 Indications

Planes Sagittal Plane

MRI is also the primary imaging modality of choice for the following: congenital anomalies of the spine; diagnosis of tumors, inflammation, and infection of spinal structures; atlantoaxial subluxation; persistence or increase of treatment-refractory low back pain; acute nontraumatic spinal paralysis; and spinal cord diseases (tumors, inflammation, and multiple sclerosis). MRI can be used as a supplementary imaging modality to investigate cervical spine and neck pain, brachialgia (in particular radicular pain radiating into the arm), and thoracic spinal pain in the absence of trauma and spinal claudication. This attests to the paramount importance of this modality in the management of spinal patients.1

2.1.2 Hardware Spinal imaging calls for excellent detail and contrast resolution as well as for, as far as possible, uniform acquisition of all spinal segments. MRI with the use of phased-array surface coils provides for an optimum combination of these features. When using 3 T scanners, with their corresponding highresolution phased-array coils, it is possible to increase detail resolution compared with 1.5 T scanners, but with identical scan times. This is also true for MRI of the spine. For the postoperative spine with metallic hardware, preference is often given to 1.5 T scanners over their 3.0 T counterparts for safety reasons and to reduce metallic artefacts.

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The sagittal plane is the most commonly used plane for MRI of the spine. It gives an overview of several segments while permitting simultaneous acquisition of images of the vertebrae, intervertebral disks, spinal canal, and neural foramina. Lesions extending in a craniocaudal or posteroanterior direction can be well delineated.

Axial Plane The axial plane is the second most commonly used plane. It enables exact assessment of a lesion in terms of its axial extension. It is especially useful for visualizing spatial relationships to the dural sac and spinal cord as well as the shape of the spinal canal and vertebral joints. In higher grade stenosis, it can evaluate whether there is complete or partial loss of the cerebrospinal fluid (CSF) column or of the epidural fatty tissue. Likewise, deformation or signal changes of the spinal cord, conus medullaris, or cauda equina can be detected.

Coronal Plane The coronal plane can provide valuable additional information on scoliosis, pronounced unilateral osteochondrosis, and lateral disk herniations. Visualization of paraspinal abscesses or other spaceoccupying lesions (e.g., neurogenic tumors) constitutes another indication. In particular for imaging the lumbar spine, the use of the coronal plane for the routine short-tau inversion recovery (STIR) sequence has the advantage that the sacroiliac joints can also be imaged and evaluated for any signs of active arthrosis or sacroiliitis activity.

Important Sequences Spin-Echo and Turbo/Fast Spin-Echo Sequences T1-weighted (T1w) and T2-weighted (T2w) imaging spin-echo (SE) sequences are the basic sequences used for MR diagnostic imaging of the spine. In principle, these two sequences should, as far as possible, be performed in one plane since lesion characterization is one of the main functions of MRI, and this is done by assessment of the signal pattern in both weightings. Therefore, virtually every MRI examination of the spine begins with a T1w and T2w SE sequence. The T2w SE sequences currently used are generally turbo spin-echo (TSE) or fast spin-echo sequences (echo time [TE] of less than 10 ms). Advantages of these sequences: ● Contrast enhancement. ● Shorter scan time. ● Fewer motion artefacts. Disadvantages of these sequences: Decrease in signal-to-noise ratio (SNR).

●

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Although primary diagnostic imaging is not recommended for acute nonspecific low back pain, with and without radiation into the legs, or for chronic low back pain (longer than 12 weeks, psychosocial causes), magnetic resonance imaging (MRI) is the primary imaging modality indicated for specific low back pain. Specific low back pain is defined on the basis of the presence of at least one of the following warning symptoms (“red flags”). ● Onset before age 20 years or after 55 years. ● Neurologic deficits, including saddle anesthesia and sphincter or gait disorders. ● Extensive neurologic deficit. ● Previous tumor disease. ● General malaise. ● HIV infection (infection with the human immunodeficiency virus). ● Unintentional weight loss. ● Intravenous (IV) drug abuse. ● Use of corticosteroids. ● Recent injury. ● Diagnosed inflammatory disease or osteoporosis. ● Increasing load-dependent pain or at-rest pain. ● Simultaneous chest pain. ● Persistent severe impairment of lumbar flexion. ● Severe structural deformities. ● Fever.

2.1 Imaging

● ●

Increase in edge blurring. Edge enhancement artefact. Truncation artefacts.

The ultrafast SE sequence differs from the TSE sequence in that the turbo factor (TF) is higher and the TE shorter. This gives rise to effects that partially oppose and partially supplement those generated by the higher TF. However, in routine practice, increased edge blurring and reduced SNR do not result in any diagnostic limitation.11 The most important difference in the image quality is a further increase in the signal intensity of fatty tissue; hence, fluid or high-signal intensity lesions in the fatty marrow cannot be differentiated. Special care must be taken in the case of small medullary lesions since they can go undetected on the ultrafast SE sequence. However, these limitations are outweighed by the advantages of a faster sequence. On the other hand, T1w TSE sequences have not become established since contrast declines already at TF of 2 to 4. TSE sequences with a variable flip angle are also being increasingly used. These are three-dimensional (3D) sequences with high TF and, as such, high speed. This, in turn, permits acquisition of high-resolution 3D datasets which, in particular in the case of isotropic voxels, are also suitable for image reconstruction in any plane without loss of quality.

Gradient Echo Sequences In the past, gradient echo (GRE) sequences were commonly used thanks to their shorter examination time. However, they have been largely supplanted with the introduction of TSE technology. Special indications for GRE include the following: ● It can be used for acquisition of thin axial slices of the cervical spine. ● Detection or exclusion of blood breakdown products (deoxyhemoglobin, hemosiderin) with susceptibility artefacts are possible on T2w GRE images. ● The precessional time of protons bound to fat differs slightly from that of water protons; hence, the signal intensity is enhanced for the parallel vector (in-phase imaging), and it is attenuated for the antiparallel vector (opposed-phase imaging). Due to a decline in signal intensity in the opposed-phase technique (see Chapter 1.4), this method is very sensitive for detection of dispersed intracellular fat, which is generally found in benign, but not malignant, tissue. As such, this method can be useful in distinguishing benign from malignant vertebral body lesions.

Fat Suppression Sequences Since fat accounts for the image components with very high signal intensity/bright areas on T1w and T2w images, fat suppression can be used to visualize this tissue with a signal intensity ranging from hypointense to signal void. There are three ways of doing this: ● STIR sequence: Fat suppression is achieved during this sequence through readout of the fat signal in the zero crossing. This sequence exhibits intermediate signal intensity in the muscles, thus providing good anatomic information. The sequence has the advantage of bestowing highest sensitivity

●

●

for visualization of edema, with least susceptibility to artefacts, and is thus commonly used as a robust routine sequence. The comparatively somewhat poorer SNR is not a relevant limitation since, for diagnostic purposes, the sequence is mainly used only for assessment of signal intensity (edema). Fat presaturation pulse: Here, either T1w or T2w can be used for SE and GRE sequences. Using these fat suppression techniques, fatty lesions, for example, in the bone marrow, can be detected with high sensitivity. One drawback is that sometimes no reference can be established to the implicated fat; all lesions appear to have very high signal intensity, and a T2w sequence without fat suppression is needed for tissue characterization. Dixon’s method: This method of fat suppression is based on a simple spectroscopic imaging technique. Over the past two decades, it has become established as a potentially alternative routine method. It provides for short scan times with, at the same time, superior image quality.

Conducting a fluid-sensitive (T2w, PDw [protein density weighted]) fat suppression sequence is highly recommended since, among other things, important causes of pain can be better visualized. For example, the simultaneous presence of fatty and edematous (Modic II and Modic I) changes along the vertebral body end plates can mask clinically relevant edematous changes. These can be detected only by using fluid-sensitive, fat-suppressed sequences. These sequences are also very useful for detection of soft tissue and bone marrow edema of the zygapophysial joints as seen in active arthrosis.

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●

Diffusion-Weighted Sequences Diffusion-weighted imaging (DWI) sequences can provide valuable additional information for distinguishing osteoporotic from pathologic vertebral body fractures. However, to date this modality has only been used routinely in specialist centers since there are no generally valid “cut-off values.” Instead, only a relative distinction can be made by individual scanners.15

In-Phase and Opposed-Phase Imaging In-phase and opposed-phase imaging is able to visualize small amounts of fat in tissues. Healthy hematopoietic bone marrow has a fatty and an aqueous portion. Malignant neoplasms infiltrate the bone marrow and replace the fatty portion of the bone marrow. This can be assessed in vivo and noninvasively using inphase and opposed-phase imaging.94

Cinematographic Magnetic Resonance Imaging Motion MRI of the spine, in particular in open high-field MRI scanners, is not a routinely used imaging modality, and is only employed in isolated cases worldwide. Its main purpose is to visualize or reassess the extent of neural foramen stenosis or areas tangential to neural structures which cannot be easily demonstrated in a neutral position and when the patient is lying down.

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The Spine

In general, IV administration of gadolinium compounds as contrast media (CM) is not required for degenerative and traumatic lesions. However, they are routinely used in inflammatory and tumor diseases for enhanced delineation of pathoanatomic structures and to get a better insight into the nature of their structure. Besides, (semi-) quantitative signal intensity time curves can provide information on the perfusion activity of an inflammatory process or a blastoma. From this, conclusions can be drawn about the biological activity of such a process. In cases where CM is administered, an identical comparative T1w sequence must be performed prior to CM administration. Minimal CM enhancement can be detected using fat presaturation sequences. Conducting a dynamic CM series will make it much easier to distinguish between normal minimal CM enhancement and pathologic enhancement as seen in diffuse myeloma.6

Biochemical Magnetic Resonance Imaging In addition to information on morphology, the diffusedweighted imaging (DWI) and in-phase and opposed-phase imaging modalities described earlier also provide valuable insights into the biochemical composition of the tissues. Apart from these two techniques, there are myriad other MRI modalities which are able to do so and are thus collectively subsumed under the term “biochemical MR imaging.” That group of techniques also includes dGEMRIC (delayed gadolinium-enhanced magnetic resonance imaging of cartilage), TE mapping, T2* mapping, sodium MRI, and CEST (chemical exchange saturation transfer) imaging. The ability of each modality to clearly visualize the different biochemical components of tissue varies, and each has its pros and cons. These imaging techniques have been used to conduct several studies of the spine, including investigation of the biochemical composition of the intervertebral disks as well as of the articular cartilage of the zygapophysial joints.35,55,76,82 But to date only DMI and in- and opposed-phase imaging, at most, are routinely used, with the other techniques being largely confined to the research setting. However, from a current perspective, a more widespread use of biochemical imaging in routine diagnostic procedures in the future seems inevitable.

Examination Protocols for Common Diseases The basic protocol used in MR diagnostic imaging of the spine consists of the sagittal T1w SE, sagittal T2w TSE, axial T2w TSE sequence, and a sagittal or coronal STIR sequence. The slice thickness is up to 3 mm in the cervical vertebral area and up to 4 mm in the lumbar vertebral area. The field of view is 280 to 300 mm in the sagittal cervical spine and lumbar spine, and 180 to 210 mm in the axial cervical spine and lumbar spine. Various additions can be made to these protocols in accordance with the individual indication (▶ Table 2.1).

2.2 Anatomy and Physiology 2.2.1 Bone Marrow and Osseous Elements Bone Marrow MRI is the modality of choice for assessment of the bone marrow. The bone marrow is composed of the following two constituents: ● Hematopoietic (red) bone marrow. ● Fatty (yellow) bone marrow. The ratio of these two constituents is age related (▶ Fig. 2.1): In childhood and adolescence, hematopoietic bone marrow predominates. ● In adulthood, the ratio shifts toward a mixed bone marrow. ● In older age, the ratio shifts toward a predominance of fatty or fibrous marrow. ●

From the age of 30 years onward, the posterior spinal segments are completely composed of fatty marrow, whereas the vertebral bodies have a mixture of fatty and hematopoietic marrow (▶ Fig. 2.2). Normal hematopoietic bone marrow is of intermediate signal intensity on T1w images, and of intermediate to high signal intensity on T2w sequence. On fat-suppressed T2w sequences, it does not exhibit signal void; rather, it is of moderate to intermediate signal intensity because of its hematopoietic marrow component. With advancing age, and greater fatty marrow content, the signal intensity shows a marked increase on T1w images; it drops sharply on fat-suppressed T2w sequences, while

Table 2.1 MRI spine protocols for standard indications Indications Basic protocol (the following indications are additions to the basic protocol)

Sagittal T1w SE, sagittal T2w TSE, axial T2w TSE, sagittal/coronal STIR sequences

General postoperative disk herniation

+ Axial T1w SE sequence If differential diagnosis “recurrent/epidural fibrosis” is uncertain, then at least 6 months after surgery axial (+ sagittal) T1w SE sequence following CM administration

Spondylitis, tumor

+ CM series: axial T1w SE sequence with fat suppression, and sagittal T1w SE sequence without fat suppression

Trauma

+ Axial T1w SE sequence; if spinal cord changes blood-sensitive T2w GRE sequence (acute) + axial T1w SE sequence (chronic)

Abbreviations: SE, spin-echo; STIR, short-tau inversion recovery; T1w, T1-weighted; T2w, T2-weighted; TSE, turbo spin-echo.

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Contrast Media

2.2 Anatomy and Physiology

Fig. 2.2 Normal, age-related distribution pattern of active and inactive bone marrow in the vertebral bodies. (a) Predominantly hematopoietic marrow with fatty marrow around the basivertebral vessels in childhood. (b) Focal deposits of fatty marrow in adulthood. (c) Fatty marrow beneath the superior and inferior end plates in senescence.

in sequences without fat suppression it changes only slightly. Even with its greater portion of hematopoietic marrow, the bone marrow signal in healthy individuals is hyperintense to the intervertebral disk signal on T1w sequences (see ▶ Fig. 2.1). If the intervertebral disks appear iso- or hyperintense to bone marrow on T1w sequence, the “bright disk sign” is also interpreted as an indicator of a pathologic bone marrow process (▶ Fig. 2.3). Whereas up to age 2 years, the bone marrow exhibits marked CM enhancement, and slight CM enhancement up to age 7 years, there is generally no visual evidence of CM enhancement in middle and advanced age.78 The structure of the bone marrow is normally homogeneous to “fine grained” or mottled. But even more pronounced and coarse grained structural inhomogeneities are within the normal range provided that fat signals can be detected in at least some of the remaining sections. Such inhomogeneities are seen in advanced age with, in addition to fatty marrow, formation of fibrous marrow constituents, which typically produce a coarse grained or coarse meshed pattern. Occasionally, a more or less pronounced bandlike sagittally oriented structure, exhibiting fluidlike signals, is found in the posterior half of the vertebral body, median and parallel to the end plates. This corresponds to the basivertebral veins

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Fig. 2.1 Age-related signal intensity of bone marrow and intervertebral disks. Schematic diagram. Signal intensity continues to increase in bone marrow on T1w and T2w sequences. With advancing age, the intervertebral disks exhibit increasing signal loss on T2w sequence. Schema I and II show additional evidence of cartilaginous plates in infancy and childhood. (a) T1 weighting. (b) T2 weighting. I, infancy (0–2 y); II, childhood (2–10 y); III, young adulthood (10–30 y); IV, middle adulthood (30–60 y); V, advanced age (over 60 y).

Fig. 2.3 Bright disk sign. MRI, sagittal T1w SE image, section. The visualized intervertebral disks are hyperintense compared to the vertebral bodies, indicating diffuse bone marrow disease.

(Hahn-Furchen) and is therefore a normal finding, and should not be mistaken for a fracture line. Apart from this intraosseous vein, which is well visualized on MRI, there are other veins draining the vertebral bodies anteriorly and laterally. They terminate in Batson’s valveless venous plexus, which on both sides runs anterolaterally and posteriorly parallel to the spinal column. The arterial blood supply is provided by the segmental arteries whose intraosseous anastomoses are increasingly obliterated between the ages of 4 and 14 years. Several terminal arteries arise in the center (equator) and on the periphery (metaphysis) of the vertebral bodies.

Osseous Elements Vertebral Arches The vertebral arches enclose the spinal canal. Epidural fat surrounds the dural sac in the lumbosacral spine. It contains several small veins (epidural venous plexus). The dimensions of the bony spinal canal can be accurately determined on computed tomography (CT), whereas MRI can only give a rough estimate of these. However, thanks to the high image contrast, the extent of narrowing of the CSF space as well as changes in the spinal cord or cauda equina can be readily and effectively evaluated on MRI

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The Spine

Cauda equina

Nerve root ganglion Zygapophysial joint

Ligamentum flavum

Epidural vessels Ligamentum flavum Intraforaminal fat Disk

Basivertebral veins

Epidural fat

b

a

Cerebello medullary cistern

Os odontoideum

Lateral mass Dens

Atlantoaxial joint Vertebral body

Posterior atlantal arch Intervertebral disk

Vertebral body

Vertebral artery

Uncovertebral joint b

Posterior longitudinal ligament

Vertebra prominens (C7) Supraspinous ligament

Anulus fibrosus

Dens

Transverse ligament of atlas Cervical spinal cord

Lateral mass

Cerebrospinal fluid

a

c

Fig. 2.5 MRI anatomy of the cervical spine. (a) Sagittal T2w TSE sequence, section. There is slight posterior displacement of the os odontoideum. (b) Coronal T2w TSE sequence, section. (c) Axial T1w SE sequence, section.

(▶ Fig. 2.4, ▶ Fig. 2.5, ▶ Fig. 2.6, ▶ Fig. 2.7, and ▶ Fig. 2.8). The high contrast of epidural fatty tissue is of diagnostic benefit in intervertebral disk diseases.

Joints From each vertebral arch, an articular process extends upward and downward on both sides. Reflecting the range of motion required, the articular surfaces have different shapes in the various segments of the spine. For example, the articular surfaces in the cervical spine are flat and slope from the upper front backward and downward at an angle of 45% in relation to the

32

horizontal plane, while in the thoracic spine the articular surfaces are positioned virtually anteriorly. In the upper lumbar spine, the articular surfaces are oriented in a sagittal direction and in the lower lumbar spine in an oblique direction. The zygapophysial joints are synovial joints with hyaline joint cartilage. Hyaline joint cartilage manifests, at most, only slightly hyperintense on T2w TSE images. The subchondral region contains fatty marrow, and the joint capsule appears as a delicate hypointense structure on T1w and T2w images.81 On the dorsal aspect of the joint is a fibrous joint capsule, which, on the ventral aspect, merges with the ligamentum flavum.92 Axial and sagittal images are best for optimum visualization.

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Fig. 2.4 Normal MRI anatomy of a spinal section. Schematic diagram of vertebral body, intervertebral disk, neural foramina, dural sac with epidural fatty tissue, CSF, and cauda equina. (a) Median sagittal slice. (b) Parasagittal slice.

2.2 Anatomy and Physiology

Supraspinous ligament Spinal cord Epidural fatty tissue Cerebrospinal fluid

Fig. 2.6 MRI anatomy of the thoracic spine. Sagittal T2w TSE sequence, section.

When imaging the vertebral bodies, the first two cervical vertebrae are different in that the first cervical vertebra, the atlas, has no vertebral body and its absence is partially substituted by the dens of the second cervical vertebra. While the high joint density comprising six small joints with the atlas, axis, and occipital bone permits a broad range of motion, it also increases susceptibility to diseases such as rheumatoid arthritis. The cervical spine also features segments C2–C7 with their uncovertebral joints. These half joints develop during early childhood and are formed by the uncinate process at the upper lateral margins of the cervical vertebra below, the lateral margins of the inferior end plate of the vertebral body above, and the intervertebral disk of one segment, and are best imaged in a coronal plane (see ▶ Fig. 2.5b).

Congenital Spinal Anomalies There are a number of congenital spinal anomalies which have different designations reflecting their pathologic significance; a distinction is made between a variant, dysplasia and malformation.

Variant This is a form that differs from the standard but does not impact function and has no pathologic significance. Examples of such variants are cranial variants (e.g., cervical rib or sacralization of the fifth lumbar vertebral body) and caudal variants (lumbar rib, lumbarization of the first sacral vertebra). This entails assimilation of L5 to the shape of the sacral vertebra (sacralization of L5) and, conversely, assimilation of S1 to the shape of L5

Lumbarization of S1 typically manifests as a rectangular vertebral body in a sagittal slice, with a fully developed intervertebral disk of almost normal height in segment S1/S2. Sacralization of L5 can be recognized from the cone-shaped, caudal tapered, vertebral body of L5 and from the intervertebral disk in segment L5/S1, identifiable only as a residual structure of markedly reduced height. Most of these forms seen on MRI correlate with complete lumbarization or sacralization (uni- or bilateral) as demonstrated on conventional radiographs, and rarely with a bilaterally incomplete form. The incomplete transitional forms are rarely identifiable on MRI. At most, MRI will detect slight narrowing of the intervertebral disk and absence of horizontal degeneration. Nonetheless, some lumbosacral transitional vertebra cannot be classified on MRI. Hence, if precise segment assignment is not possible on MRI, a plain radiograph must be taken of the entire vertebral column prior to elective surgery56 since precise numbering of the vertebral bodies can be done only by counting downward from C2.

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Spinous process

(lumbarization of S1). If precise segment numbering is not possible, the term “transitional vertebra” is used. These transitional vertebrae can be unilateral or bilateral, asymmetric or symmetric, with different degrees of expression ranging from an assimilation tendency through coalescence to complete synostosis. Such variants per se can exhibit clinical symptoms. Since today MRI is used at an early stage and often as the sole imaging modality, including for preoperative diagnostic investigation, radiologists are expected to recognize such variants and be able to number the segments. Two criteria are important when interpreting the MRI results: ● The structure of the intervertebral disk. ● The shape of the vertebral body.56

Dysplasia This refers to congenital inferiority of a skeletal segment with potential pathologic significance if it results in physiologic stress or disease, as in the case of, for example, spondylolisthesis vera, that is, vertebral slippage (olisthesis) with gap formation in the region of the vertebral arch; this can be either congenital or caused by overloading. Spondylolisthesis falsa (= pseudospondylolisthesis), that is, vertebral slippage without gap formation, is mainly due to degeneration (severe arthrosis of the zygapophysial joints) and only rarely due to dysplasia. Displacement of the vertebral body without displacement of the spinous process is thus suggestive of gap formation and accordingly of spondylolisthesis vera, whereas displacement of the vertebral body with simultaneous displacement of the spinous process in the same direction points toward spondylolisthesis falsa. On the MRI, as in the projection radiography, the extent of vertebral slippage is generally classified using the Meyerding grading system, where the definition employed is based on the degree of slippage of the vertebral body above in respect of its counterpart below. The Meyerding grading system divides the superior end plate of the vertebra below into four segments of equal sizes and specifies in which quarter the anticipated extension of the posterior border of the vertebral body above lies. Hence, for example, anterolisthesis of L4, Meyerding grade I, means that the posterior border of the vertebral body L4 is displaced anteriorly by a maximum of one-quarter of the superior end plate of the vertebral body L5.50

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The Spine

Conus medullaris

Basivertebral veins

Posterior anulus fibrosus

Vertebral arch Perineural intraforaminal fatty tissue Intervertebral foramen Zygapophysial joint

Anterior anulus fibrosus

Nucleus pulposus

a

b

Conus medullaris

Vertebral arch Spinal ganglion Psoas Cauda equina Basivertebral vein

Psoas Lumbar vein Lumbar artery Intervertebral disk

c

Transverse process

d

Fig. 2.7 MRI anatomy of the lumbar spine. (a) Sagittal median T2w TSE sequence, section. (b) Sagittal foraminal T2w TSE sequence, section. (c) Coronal T2w TSE sequence, vertebral body level, section. (d) Coronal T2w TSE sequence, spinal canal level, section.

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Nerve root ganglion

Cauda equina fibers

2.2 Anatomy and Physiology

L4 root ganglion

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Fig. 2.8 MRI anatomy of the lumbar spine. (a) Sagittal median T2w TSE sequence, section. (b) Sagittal foraminal T2w TSE sequence, section. (c) Coronal T2w TSE sequence, vertebral body level, section. (d) Coronal T2w TSE sequence, spinal canal level, section.

L4 spinal nerve

L5 root

a

Psoas

Cauda equina fibers Spinal ganglion Zygapophysial joints Transverse spinous muscles Erector spinae Spinous process

b

Malformations These have their origin in embryonic development and involve the vertebral bodies and vertebral arches. Their pathologic significance ranges from insignificant to “incompatible with life”: ● Spinal dysraphia. ● Vertebral body malformations: ○ Block vertebra.

○ ○

Wedged vertebra. Half vertebra.

The term “spinal dysraphia” denotes a heterogeneous group of spinal anomalies with incomplete fusion of mesenchymal, bone, and neural structures. The simplest form of gap formation, that is, median division of the spinous process, is an incidental finding of no clinical relevance. The conus medullaris is situated as normal

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The Spine

Fig. 2.9 Lipomyelocele. Sagittal T1w SE sequence, section. Intraspinal growth of a structure (asterisk), isointense to fat, through a posterior bony vertebral defect with known lipomyelocele diagnosis.

at level L1/L2. The term “spina bifida” is often employed as a synonym for “spinal dystrophy” despite the former term referring to impaired fusion of the posterior bone segments of the spine. Spinal dysraphia conditions are divided into open and closed spinal dysraphia. In open spinal dysraphia, the nerve tissue is exposed on the outside, whereas in closed dysraphia it is covered in skin: ● Closed spinal dysraphia: If a subcutaneous mass is identified, mainly at the lumbosacral transitional level, the following forms of closed spinal dysraphia must be borne in mind: lipomyelocele or lipomyelomeningocele, or much less commonly meningocele or terminal myelocystocele: ○ Lipomyeloceles: These can be recognized from the fact that a lipoma has extended through the bony spina bifida defect into the spinal canal and is attached here to the neural plate (▶ Fig. 2.9). ○ Lipomyelomeningoceles: As opposed to lipomyeloceles, in the case of lipomyelomeningoceles there is extension of the subarachnoid space with displacement of the neural plate out of the spinal canal. ● Open spinal dysraphia: In open spinal dysraphia, a distinction is made between myelomeningoceles and myeloceles, with the latter rarely seen compared with the former. In both conditions, the neural plate is exposed because of the midline defect in the back: ○ Myelomeningocele: A myelomeningocele is present if the neural plate is raised above the level of the normal skin because of extension of the subarachnoid space (▶ Fig. 2.10). ○ Myelocele: A myelocele is present if the neural plate is situated at the level of the skin.66 In diastematomyelia, there is a sagittal gap formation splitting the spinal cord into two halves, with each hemicord enclosed in its

36

Fig. 2.10 Myelomeningocele. Sagittal T2w TSE sequence, section. Structure, isointense to fluid, emerging from the spinal canal through the bony vertebral defect, consistent with the markedly extended subarachnoid space in the presence of a myelomeningocele.

Fig. 2.11 Diastematomyelia. Axial T2w TSE sequence, section. The spinal cord is split in diastematomyelia.

own skin and separated by a septum but positioned within the same bony spinal canal (▶ Fig. 2.11). Among the spinal malformations, the block vertebra is the most common. Congenital fusion can be complete or incomplete, affecting one or several segments, in particular in the cervical spine and lumbar spine. The congenital block vertebra is recognizable from the continuous, bridging, bone marrow or residual intervertebral disk as well as often from narrowing in the region of the absent or residual disk (“wasp-waist” appearance). Conversely, the acquired block vertebra exhibits, in addition to the

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*

2.2 Anatomy and Physiology

a

b

Fig. 2.12 Differentiation between congenital and acquired block vertebra. Schematic diagram. (a) Congenital: diameter (sagittal) is reduced in the region of the blocked segment (“wasp waist”). The vertebral body contour is concave. (b) Acquired: diameter (sagittal) is increased in the region of the blocked segment (elephant foot–like). Residues of the underlying can still be recognized.

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typical double concavity of the anterior vertebral body, irregular bone and bone marrow bridging as persistent sequelae of the underlying disease (▶ Fig. 2.12). Klippel–Feil syndrome is a special form of the congenital block vertebra involving fusion of one or several vertebrae of the cervical spine or at the transitional level of the lumbosacral spine, possibly with a rudimentary disk (▶ Fig. 2.13). Congenital hemivertebrae and wedged vertebrae are comparatively less common (▶ Fig. 2.14). The hemivertebra constitutes a typical example of a minus variant, leading to congenital scoliosis. It is a severe malformation necessitating early surgical repair.

Bone Malformations or Changes Remnants of the (Embryonic) Notochord Cortical bone is hypointense on all sequences, exhibiting a uniform frame shape in the vicinity of the vertebral bodies. This uniformity of the bony frame may be interrupted by remnants of the notochord. These manifest as even, cone-shaped indentations at the end plates on the posterior aspect of the vertebral body; when several are present, they are typically seen on the opposite side at the end plates of a segment as well in a line in a mediansagittal slice.70 They are mechanical weak links where intraspongious intervertebral disk herniation tends to occur. Another diagnostic pointer for identifying a remnant of the notochord is its uniform conelike or hemispherical shape, with no changes in the perifocal bone marrow.

Fig. 2.13 Klippel–Feil syndrome. Sagittal T2w TSE sequence, section. Incomplete fusion of vertebral bodies C5 and C6 with rudimentary disk and typical concave configuration of the common anterior border of the vertebral body (“wasp waist”). Disk herniation of the adjacent segments as seen in connection degeneration.

Spongy Bone Spongy bone (also called cancellous or trabecular bone) is likewise markedly hypointense on all routine sequences, but because of limited MRI resolution and due to the excessively strong signal emitted by the fatty bone marrow, it is generally only faintly visualized. Only in the presence of pathologic changes, such as those seen in association with hemangioma vertebra, Paget’s disease, or osteoplastic metastases, can trabecular bones be clearly identified on MRI thanks to the volume increase. In research settings, the trabecular structure of bone can be demonstrated using high-resolution GRE sequences in high-field and ultra-high-field MRI scanners; however, these do not fully lend themselves for routine diagnostic purposes.

2.2.2 Neuroforamina Between every pair of vertebrae, there is an opening on each side called the intervertebral foramina or neuroforamina.

Fig. 2.14 Congenital wedged vertebra. Sagittal T2w TSE sequence, section. Sagittal-triangular configuration of vertebral body L1 with ensuing kyphotic kinked axis and spinal canal stenosis with known diagnosis of congenital wedged vertebra.

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The Spine

Fig. 2.15 Normal variant: conjoined nerve root. Typical protruding dural sac, here on the left in each case, in conjoined nerve root. (a) Axial schematic diagram. (b) Axial T1w sequence, section.

These are predominantly bounded by bone, cranially and caudally by the bony pedicles, posteriorly by the osseous joint processes of the zygapophysial joint, anteriorly in the cranial section by the vertebral body edge, and caudally by the intervertebral disk (see ▶ Fig. 2.4). The foramina have an almost longitudinal oval shape. There are several pathologic processes that result in distension, constriction, or deformation of the foramen. Each neuroforamen contains an emerging nerve root, epidural vessels, and fatty tissue. The nerve root is round to oval in shape, exhibits signal intensity isointense to that of the spinal cord, and is enclosed in protective perineural fatty tissue (isointense to fat). The ganglia of the nerve roots in the cervical spine are situated outside the neuroforamen, and in the lumbar spine they are at the level of the foramen. The ganglion of a nerve root varies in size, ranging in the lumbar spine from 6 mm at the level of L1 to 15 mm at S2. A conjoined nerve root, with two roots sharing a common sheath which only later separate, occurs as a normal variant (▶ Fig. 2.15). It is important to demonstrate its course in several slices since sequestered disk herniation can mimic such a normal variant. Just as the degree of reduction in the CSF demonstrates the extent of spinal canal stenosis, the reduction in perineural fatty tissue is indicative of the extent of neuroforaminal stenosis. Furthermore, nerve-root sheath cysts (Tarlov’s cysts) are commonly observed in the neuroforamina. These are cystic extensions of the nerve root sheath seen within the neuroforamina; on MRI, they are isointense to fluid, roundish perineural structures that do not take up contrast agent. Most nerve-root sheath cysts are asymptomatic, but there are also reports of symptomatic cases (involving, in particular, larger cysts; ▶ Fig. 2.16).

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Fig. 2.16 Nerve-root sheath cysts. (a) Sagittal T2w STIR sequence, section. Discrete structure, isointense to fluid, in the region of neuroforamen T12/L1 with reaction-free deformation of adjacent vertebral body T12; a similar structure at the level of S2 here with deformation of vertebral body S2. (b) Sagittal T1w sequence following CM administration, section. There is no CM uptake by the depicted structures at the level of T12/L1 and S2; these are consistent with nerveroot sheath cysts with pressure-mediated vertebral body deformation.

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a

2.2 Anatomy and Physiology

Each intervertebral disk is composed of a gelatinous core, the nucleus pulposus, which is surrounded by a ring of fibers (anulus fibrosus) as well as by the cartilaginous end plates. The anulus fibrosus is firmly anchored to the hyaline cartilage intercellular substance of the superior and inferior vertebral end plates (synchondrosis). The nucleus pulposus is under constant pressure and tries to drive the vertebral bodies apart. That is prevented by the anulus fibrosus and by the posterior and anterior longitudinal ligaments, which are located anteriorly and posteriorly to the spine. The height of the intervertebral disks increases from cranial to caudad, with only the disks of segment C7/T1 and L5/S1 being of reduced height compared with the disk above. The posterior border of the disk is flat or slightly convex (lumbar).57 The nucleus pulposus is composed of collagen and proteoglycans. The proteoglycans are responsible for the high water binding capacity of the nucleus pulposus. A very high positive pressure prevails within the nucleus pulposus which causes pretensioning of the associated ligaments. This pretensioning is responsible for the high elasticity of the vertebral column. Local incorrect loading and overloading of disks and subchondral structures occur in the absence of pretensioning. Due to the high water content, the intervertebral disk has moderately low signal intensity on T1w images and high signal intensity on T2w images. The water content declines with increasing age, as does the signal intensity on a T2w sequence. The initial sign of aging or of incipient degeneration is seen as a horizontal bandlike hypointense line at the center of T2w images. Such a change can be observed from age 30.93 Aging of the intervertebral disk manifests unevenly on MRI. The anulus fibrosus has a higher collagen and lower proteoglycan content compared with the nucleus pulposus and is thus hypointense on all MRI sequences. The third anatomic component of the intervertebral disk is the hyaline cartilaginous end plate with its interspersed pores. It bounds the intervertebral disk in the middle section of the end plate and is thus directly adjacent to the subcortical region of the vertebral body. It is isointense to the nucleus pulposus on MRI and cannot be delineated in routine imaging. In older adolescents and adults, the intervertebral disk receives its nutrients through diffusion. The subcortical region of the vertebral bodies plays a pivotal role in the functioning and pathophysiology of the intervertebral disk; the disks and subcortical region must be viewed as a single functional entity. Accordingly, repair mechanisms following inflammation and degeneration are initiated in the subchondral region. In children, as in adults, it is possible to distinguish between the nucleus pulposus and anulus fibrosus on T2w, but not on T1w, images. The cartilaginous end plate manifests as low signal intensity on T1w and T2w images compared with the nucleus pulposus. Another difference is seen in infancy: the nucleus pulposus, anulus fibrosus, and cartilaginous end plate are of moderate signal intensity on T1w images and cannot be distinguished from each other. On T2w images, the nucleus pulposus and anulus fibrosus are hyperintense, while the cartilaginous end plate exhibits a much lower signal.37

2.2.4 Ligaments The anterior and posterior longitudinal ligament reinforces the anulus fibrosus at the front and back. Normally, the anterior longitudinal ligament cannot be distinguished from the anulus fibrosus or the cortex layer of the vertebral bodies since it is isointense to these structures. This may also be true for the weaker posterior longitudinal ligament. Since the posterior longitudinal ligament is adherent in the region of the intervertebral disk but not at the level of the vertebral bodies, it can be identified because of the fat or veins interposed between the ligamentous structure and the posterior vertebral body cortex. In the presence of pathologic changes, for example, disk herniation, the posterior longitudinal ligament is disrupted and bathed in fluid, making it visible at disk level.32,57 The anterior and posterior longitudinal ligament, the ligamenta flava, and interspinous ligaments are pretensioned by the “bulging” nucleus pulposus with its high water content. This is responsible for the inherent elasticity of the vertebral column. The ligamenta flava, which are predominantly composed of elastic fibers and whose name derives from their yellow appearance, stretch out between the vertebral arches.57 At its lateral end, the ligamentum flavum extends over the anterior border of the zygapophysial joints. On T1w images, it is more hyperintense than other ligamentous structures. On CT, the ligamentum flavum has a maximum width of 4 mm in axial slices; pathologic thickening is seen from 5 mm.21 These are rough guide values which are also applied to MRI. The spinous processes are linked to each other by the supraspinous ligament and the interspinous ligaments. At the craniocervical junction, the transverse atlantal ligament emerges from the posterior longitudinal ligament and functions to border and stabilize the dens posteriorly against the spinal canal (see ▶ Fig. 2.5c). From the tip of the dens, the alar ligaments course in a virtually coronal plane to the clivus. In addition, the tectorial membrane serves as important anterior, and the posterior atlanto-occipital membrane as posterior, landmarks in demarcating the spinal canal between the base of the skull, the occiput, and the atlas (C1).

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2.2.3 Intervertebral Disks

2.2.5 Dural Sac, Spinal Cord, and Spinal Nerves The dural sac contains CSF, the spinal cord, conus medullaris, cauda equine, and nerve roots. The spinal cord is of moderate signal intensity on T1w and T2w images; on high-resolution fluid-sensitive sequences (especially GRE), it is also possible to occasionally distinguish, in particular, in the cervical spine, the butterfly-shaped, slightly hyperintense gray matter from the surrounding white matter (Fig. 2.17). Any higher signals emitted from the spinal cord must be interpreted as pathologic findings. The spinal cord is of uniform width in sagittal slices, with only the distalmost section of the spinal cord, the conus medullaris, being somewhat thicker. In infants, the conus medullaris terminates at the level of the third lumbar vertebra, and in most adults at the first lumbar vertebra. When the conus medullaris terminates distal to the second lumbar vertebra, the term “low-level conus” is used, as seen in tethered cord syndrome.

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Distal to the conus medullaris are the cauda equina fibers. By force of gravity, these can be identified when imaging patients in a supine position in the posterior sections of the dural sac where they are evenly distributed.88 Conversely, in the case of the mainly postinterventional spinal arachnoiditis, adhesions of the cauda equina fibers to the dural sac can be identified, leading to thickening of the dural sac wall, septation, and strand formation. The spinal cord is divided into 8 cervical, 12 thoracic, 5 lumbar, and 5 sacral segments with the correspondingly named spinal nerves. With 7 cervical vertebrae, 12 thoracic vertebrae, and 5 lumbar vertebrae, this means that the first cervical spinal nerve emerges from the spinal canal between the occiput and the first cervical vertebra and the eighth spinal nerve between the seventh cervical vertebra and the first thoracic vertebra. The spinal nerves in the cervical spine are numbered according to the vertebra below of the respective segment (e.g., segment C3/C4, spinal nerve C4) and the spinal nerves in the lumbar spine are numbered according to the vertebra above of the respective segment (e.g., segment L4/L5, spinal nerve L4). In healthy subjects, it is generally not possible to identify the central canal of the spinal cord on MRI. Dilation of the central canal is known as hydromyelia. The term syringomyelia is often used to denote cystic intramedullary cavitation. This is localized outside the central canal and does not communicate with the latter. Since often it is difficult to distinguish between these two entities, the term syringohydromyelia, a combination of “hydromyelia” and “syringomyelia,” is frequently employed (▶ Fig. 2.18). On MRI, cavitation manifests as intramedullary structures isointense to CSF, possibly with adjacent gliosis but without any contrast agent enhancement (differential diagnosis: cystic tumors). Often, the genesis is unclear but possible causes include posttraumatic, inflammatory, or vascular damage to the spinal cord and/ or postinflammatory adhesions, space-occupying lesions, or congenital changes to the subarachnoid space. The subarachnoid space surrounding the spinal cord is filled with CSF. The CSF appears isointense to fluid, that is, of low signal intensity on T1w images and of maximum signal intensity on

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Fig. 2.18 Syringohydromyelia. Sagittal T2w sequence, section. Spindle-and oval-shaped changes in signal intensity, isointense to CSF, in the central cervical spinal cord at the level of C4–C5 and C5–C7, with no evidence of blockage.

T2w images. The dural sac consists of the outer dura and of the loosely attached arachnoid mater on the inside, which extends as far as S2 and is hypointense on T1w and T2w images. Multiple sclerosis is a chronic inflammatory demyelinating disease that is mainly first diagnosed in the brain, but often also manifests in the spinal cord, in particular in the cervical spine (▶ Fig. 2.19). On MRI, mainly focal posterior or lateral lesions are seen, with CM enhancement only in the active stage. These lesions are hypo- to isointense on T1w images and hyperintense on T2w images, and in the axial plane, they often appear wedgeshaped. Less commonly seen are also diffuse patterns of involvement with concurrent swelling of the spinal cord, affecting a long section of the spinal cord. Differential diagnosis should also include acute transverse myelitis. On the MRI, this inflammatory demyelinating disease manifests as swelling of the thoracic or, less commonly, of the cervical spinal cord, and as central lesions that are lightly hypo- to isointense on T1w images and hyperintense on T2w images, affecting more than two-thirds of the spinal cord cross section and extending over more than two vertebral segments. Following CM administration, highly variable but mainly peripheral enhancement is observed. Onset of the disease is rarely idiopathic and is generally seen as a secondary sequela, for example, to collagenosis, infections, or radiation therapy. Acute inflammatory demyelinating polyradiculoneuropathy, known as Guillain–Barré syndrome, typically manifests clinically as ascending paralysis. Diagnostic imaging reveals, in particular, diffuse and preferentially anterior CM enhancement of the conus medullaris and the cauda equina. Without CM, at most discrete

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Fig. 2.17 “Butterfly” in cervical spinal cord (normal result). Axial T2w GRE sequence, section. The gray matter of the spinal cord appears slightly hyperintense compared with the surrounding white matter, with a shape suggestive of a butterfly.

2.3 Degenerative Conditions of the Spine end plates (e.g., superior end plates) appear to be wider on one side and narrower on the other side (inferior end plates). On the narrow side, the bone marrow interface is bandlike and markedly hyperintense due to overlapping of the fat and water signals. The chemical shift artefact is dependent on the magnetic field strength.

Motion Artefact The term “motion artefacts” is understood to mean not only distorted images caused by movement of the patient or the region of interest, but also false images originating from physiologic organ movements, such as vascular pulsations, breathing movements, and intestinal peristalsis. These artificial images (ghost images) project onto the region of interest and can be prevented by correctly selecting the phase-encoding direction and blanking out the interfering region through saturation and, in particular, by shortening the scan times.

CSF Flow Artefact

Fig. 2.19 Multiple sclerosis. Sagittal T2w sequence, section. Poorly defined, moderately hyperintense signal changes and slight swelling of the cervical spinal cord at the level of C2–C3; with a known diagnosis of intracerebral foci, these are consistent with plaques as seen in multiple sclerosis.

thickening of the affected cauda equina fibers can be identified. Spinal meningitis, in contrast, exhibits a partially hyperintense spinal cord and baked cauda equina fibers on T2w images. Here, CM enhancement is also partially nodular and much more extensive. In addition to epidural and subdural abscesses, intermedullary abscesses also occur secondarily to myelitis. On MRI, these, like intracerebral abscesses, are associated with swelling of the spinal cord, with a central melted down area, appearing hypointense on T1w images and markedly hyperintense on T2w images, with limited diffusion (reduced apparent diffusion coefficient [ADC] values) and pronounced marginal enhancement. Spinal cord infarction is rare, but when it does occur, it often manifests clinically as radicular pain, but typically also as acute paralysis. On MRI, hyperintense, rounded focal lesions in the anterior gray matter of the spinal cord (“owl sign”) are seen on T2w images. CM enhancement is also observed in the subacute phase.12

2.2.6 Imaging Artefacts The following artefacts are common and hamper MR diagnostic imaging of the spine.

Chemical Shift Artefact The fat signal is spatially shifted in the phase-encoding direction so that one side of the fat interface appears darker and the opposite side is brighter. At the level of the spine, the small spatial shift in the fat signal gives rise to the typical effect whereby the vertebral

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Spinal signal intensity is normally homogeneous; inhomogeneities are caused by CSF flow artefacts. They are mainly found in the upper segment of the spine. On sagittal T2w images, they can be seen as bandlike, tubular areas of signal void, and on axial sections as rounded oval areas of signal void. There is a risk of misinterpreting them as pathologic subarachnoid vessels.

Truncation Artefact Truncation artefacts are seen at tissue interfaces where there is a marked difference between the signal intensity of the respective tissues, for example, between the spinal cord and CSF. They manifest as parallel bands or semicircular lines along anatomic contours.

2.3 Degenerative Conditions of the Spine Degenerative conditions of the spine result in changes in the intervertebral disks, subcortical bone marrow, and the uncovertebral and zygapophysial joints. The main difference between such changes and those induced by physiologic aging is seen in the altered metabolic processes. Degeneration is associated with high metabolism, while aging is accompanied by a lower metabolism.

2.3.1 Bone and Bone Marrow Changes along the Vertebral Body End Plates Based on the large number of studies carried out, in particular the investigations undertaken by Modic et al,54 three fundamental types of changes can be distinguished (▶ Fig. 2.20).

Type I Type I changes are associated with pseudoinflammatory reactions involving bone marrow edema and hypervascularization. Bandlike or discrete hypointense signal changes are seen on T1w MR images, and hyperintense signal changes on T2w and STIR images. Following IV injection of gadolinium CM, there is marked

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T2w

Gd-DTPA

Type I degeneration

Fig. 2.20 Differential diagnosis of degenerative and inflammatory changes of vertebral bodies and interposed disk. Schematic diagram based on the classification proposed by Modic et al.53

Type II degeneration

Type III degeneration

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Spondylodiscitis

Fig. 2.21 Modic stage I. Active degenerative changes in the end plates (bone marrow edema). Sagittal MR images, sections. (a) T1w sequence. Hypointense bandlike signal changes along the end plates of L2/L3. (b) T2w sequence. Hyperintense bandlike signal changes along the end plates of L2/L3. (c) T2w STIR sequence. Hyperintense bandlike signal changes along the end plates of L2/L3.

contrast enhancement along the vertebral body end plates (▶ Fig. 2.21). These changes are consistent with “recent” pseudoinflammatory processes and constitute one of those morphologic alterations best correlated with pain radiating from the spine.22 In principle, such changes can regress without sequelae or they can progress to type II changes.

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Type II Type II changes are characterized by bandlike or discrete subcortical fatty marrow conversion along the vertebral body end plates. These are interpreted as a chronic bone marrow “stress reaction.” Progression from type I changes takes at least 6 to 9 months.

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2.3 Degenerative Conditions of the Spine

Fig. 2.22 Modic stage II. Chronic degenerative changes in the end plates (fatty marrow conversion). Sagittal MR images, sections. Lumbosacral transitional vertebra with partial lumbarization of S1. (a) T1w sequence. Hyperintense bandlike signal changes along the end plates of L2/L3. (b) T2w sequence. Hyperintense bandlike signal changes along the end plates of L2/L3. (c) T2w STIR sequence. Hypointense bandlike signal changes along the end plates of L2/L3.

Fig. 2.23 Modic stage III. Chronic degenerative changes in the end plates (sclerosis). Sagittal MR images, sections. (a) T1w sequence. Hypointense bandlike signal changes along the end plates of L3/L4. (b) T2w sequence. Hypointense bandlike signal changes along the end plates of L3/L4.

Typical characteristics of these are the bandlike hyperintense signal changes seen along the vertebral body end plates on T1w and T2w sequences (▶ Fig. 2.22).

Type III Type III changes have been well known for decades from conventional X-rays, and manifest as (reactive) bandlike or discrete sclerosis along the vertebral body end plates. Their onset period is probably between one and several years (▶ Fig. 2.23). Type III

changes are seen as bandlike hypointense signal changes along the vertebral body end plates on T1w and T2w MR images.

Mixed Forms There are, of course, also mixed or transitional forms of the three types. In that respect, particular attention must be paid to the simultaneous presence of type I and type II changes, since type I changes can be masked by type II changes on T1w and T2w sequences because of the predominance of the fat signal.

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Normal

Pathologic

Fig. 2.25 Intervertebral disk structure. Schematic diagram of the nucleus pulposus, anulus fibrosus, and cartilaginous end plates (with pores). The arrows show the pressure exerted on the intervertebral disk in a normal (cranial arrows) and a degenerative state (caudal arrows). At the margins, the disk abuts the vertebral body (= “exposed zone” of disk). 1, anulus fibrosus (“exposed bone”—route for spondylodiscitis); 2, nucleus pulposus (cartilaginous end plate—route for osteoporotic break).

However, a glance at the fluid-sensitive STIR sequence will help to definitively identify the Modic type I changes, which are probably the source of the patient’s pain (▶ Fig. 2.24).

2.3.2 Intervertebral Disk Changes The disk is composed mainly of proteoglycans and has thus a high propensity to bind water. Situated in the center of the disk is the nucleus pulposus. This is under positive pressure and is surrounded by the anulus fibrosus as well as the cartilaginous end plates, which contain pores. The structure of the anulus fibrosus is much more prominent anteriorly. In the middle section of the disk, the cartilaginous end plates act as a partial barrier between the nucleus pulposus/anulus fibrosus and vertebral body (▶ Fig. 2.25).4,13

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From the fourth year of life, the disk receives its nutrients through diffusion from the adjacent tissues (vertebral bodies, ligaments, etc.). Up to the fourth year of life, the disk is vascularized, something that has important implications for the spread of, for example, inflammatory processes.44 Degenerative disk changes can be well visualized, and even classified, on MRI. It is possible to evaluate both the signal intensity and the quality of delineation of the various disk constituents as well as the height of the disk. As degeneration progresses, the nucleus pulposus loses its signal that formerly had exhibited a homogeneously hyperintense or isointense signal relative to CSF on fluid-sensitive sequences. The signal is now more inhomogeneous and the nucleus pulposus can no longer be well demarcated from the anulus fibrosus. At this stage of degeneration, the height of the disk is invariably decreased. Disk revascularization can occur in the course of degenerative or traumatic processes. Onset of revascularization is generally first noted in the posterior or anterior part of the disk. Growth of more or less unresisted fibrovascular repair tissue into the anulus fibrosus can be seen at such sites, whereas the middle sections are “protected” by the end plates.

Anulus Fibrosus Tears Probably due to the changes in the subcortical perfusion and to the age-mediated decline in the nucleus pulposus internal pressure, lack of ligament pretensioning can often result in punctiform (incorrect) overloading of the anulus fibrosus. This, in turn, causes increasingly more tears and, because of the continuing enormous “positive pressure” (up to 800 kPa) prevailing within the nucleus pulposus, results in displacement of nucleus pulposus tissue into the annular tears. Tears and fissures in annular tissue can in principle extend in any direction. Of particular clinical significance are tears in the posterior anulus fibrosus. These can be detected as “high signal intensity zones” on fluid-sensitive MRI sequences, and are not necessarily accompanied by pain (▶ Fig. 2.26).

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Fig. 2.24 Modic stage I and II. Active and chronic degenerative changes in the end plates (bone marrow edema and fatty marrow conversion). Sagittal MR images, sections. (a) T1w sequence. Hyperintense bandlike signal changes along the end plates of L4/L5. (b) T2w sequence. Hyperintense bandlike signal changes along the end plates of L4/L5. (c) T2w STIR sequence. Hyperintense bandlike signal changes along the end plates of L4/L5.

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2.3 Degenerative Conditions of the Spine

Fig. 2.26 Anulus fibrosus tear. Sagittal T2w STIR sequence, section. Discrete punctiform signal changes (arrow), which are isointense to fluid and markedly hyperintense on T2w images, in the posterior anulus fibrosus of disk L4/L5, but no evidence of disk herniation.

Disk Herniation In the ensuing course, displacement of nucleus pulposus material into the anulus fibrosus leads to the formation of extensions in the outer disk contour. The term “bulge” denotes extensions of more than 180 degrees (occupying more than 50% of the entire vertebral circumference) (▶ Fig. 2.27). The term “herniation” is used for disk extensions of less than 50% (less than 180 degrees). Disk extensions of less than 25% (corresponding to less than 90 degrees) are known as “focal,” while extensions of between 25 and 50% of the circumference are called “broad-based herniations.” Herniations are furthermore classified according to their shape as protrusions and extrusions, where the presence of a “neck” serves to distinguish an extrusion from a protrusion. This means that, at least in one image plane (axial or sagittal), the width of the displaced disk material is greater than the width of the adjacent intervertebral space (▶ Fig. 2.28, ▶ Fig. 2.29, and ▶ Fig. 2.30). Diffuse adaptive changes in the disk contour due to adjacent deformities (scoliosis, spondylolisthesis) do not constitute a herniation. Based on axial sections, the location of the herniated disk material can be described as being central, subarticular, foraminal, or extraforaminal/lateral (▶ Fig. 2.31). Using sagittal sections, the craniocaudal location can also be accurately defined: ● At disk level. ● Infrapedicular. ● Pedicular. ● Suprapedicular.

Fig. 2.27 Intervertebral disk “bulging.” (a) Symmetrical bulging (schematic diagram). (b) Asymmetrical bulging (schematic diagram). (c) Axial T2w TSE sequence, section. Symmetrical bulging; in addition, arthrosis of the zygapophysial joints, hypertrophy of the ligamenta flava, and secondary spinal canal stenosis.

Once the nucleus pulposus material has extended as far as the posterior longitudinal ligament, but has not torn the ligament, the term “subligamentous herniation” is used. Accordingly, a tear in the ligament is called a “transligamentous herniation.” The former term “prolapse” is no longer used in conventional international nomenclature since the aim is to eliminate unclear definitions. Nonetheless, it is important that radiologists understand the terminology employed by the referring physicians and reach agreement on the nomenclature used. The term “sequester” is used to denote herniated disk tissue where continuity with the disk of origin is completely lost. In principle, it can be located either cranial or caudal to the respective disk. The term “migration” describes disk herniation where part of the disk material is displaced away from the site of extrusion, that is, the annular tear (generally in a cranial or caudal direction). Migration thus describes the localization of the displaced disk tissue and, unlike “sequestration,” does not give any insight into whether or not continuity with the parent disk is preserved (▶ Fig. 2.32). The condition whereby disk tissue protrudes through the vertebral end plate into the subcortical bone of the adjacent vertebral body is known as Schmorl’s node. Schmorl’s nodes may be an

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The Spine

Protrusion

Extrusion

a

c

b

d

e

Fig. 2.28 Disk herniation. (a) Axial schematic diagram of protrusion. The diameter of the herniated disk tissue is wider at the base of the hernia than at the periphery. (b) Axial schematic diagram of extrusion. The diameter of the herniated disk tissue is smaller at the base of the hernia than at the periphery. (c) Sagittal schematic diagram of protrusion. The diameter of the herniated disk tissue is wider at the base of the hernia than at the periphery. (d) Sagittal schematic diagram of extrusion. The diameter of the herniated disk tissue is smaller at the base of the hernia than at the periphery. (e) Sagittal schematic diagram of extrusion. While the shape of the herniated material is similar to that seen in protrusion (c), the diameter of the herniated disk tissue is smaller at the base of the hernia than at the periphery, hence this is a case of extrusion.

Fig. 2.29 (Focal) protrusion of the intervertebral disk. Posteromedial focal protrusion of disk L4/L5, with the diameter of the herniated disk tissue wider at the base of the hernia than at the periphery. (a) Sagittal median T2w TSE sequence, section. (b) Axial T2w TSE sequence, section.

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indicator of reactive bone marrow disorders (edema, fatty marrow conversion, sclerosis); adjacent bone marrow edema may cause pain (▶ Fig. 2.33). The most common localization for degenerative intervertebral disk processes is segments C5–C7 and L3–S1. Onset of degenerative changes at other sites is rare and generally of different etiology (trauma, inflammation, etc.). Lumbar disk herniation is typically seen in younger patients aged 25 to 45 years, and rarely among those below 20 years or above 65 years.43 However, in the majority of cases, disk herniation causes no, or only few, clinical symptoms and resolves after 9 to 12 months. On the other hand, there are many patients who report discogenic pain even though their radiology findings are unremarkable. Discogenic pain has various causes (e.g., abnormal blood levels of COX-2 [cyclooxygenase 2], prostaglandin, TNF [tumor necrosis factor]) and is only partially linked to mechanoreceptors.59 Hence, the radiology findings can only be interpreted in conjunction with the clinical results. Each diagnosis of disk herniation must include the following details: ● Form: ○ Protrusion. ○ Extrusion. ○ Intravertebral (Schmorl). ● Extension: ○ Focal. ○ Broad-based. ● Border (posterior longitudinal ligament). ● Continuity (sequester). ● Volume (axial diameter and sagittal extension). ● Structure (signal intensities). ● Localization (in horizontal and vertical plane; migration). ● Tangentation, compression, or displacement (spinal cord, cauda fibers, or nerve roots).

2.3 Degenerative Conditions of the Spine

Central

Subarticular

Suprapedicular

Foraminal

Extraforaminal

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Fig. 2.30 (Focal) extrusion of the intervertebral disk. (a) Sagittal median T2w TSE sequence, section. Posteromedial focal protrusion of disk L5/S1, with the diameter of the herniated disk tissue smaller at the base of the hernia than at the periphery. (b) Axial T2w TSE sequence, section. Right central or subarticular focal protrusion of disk L5/S1, with the diameter of the herniated disk tissue wider at the base of the hernia than at the periphery. Marked tangentation and displacement of the caudal fibers of S1, right.

Fig. 2.31 Anatomic localization of disk hernias. Schematic diagram. (a) Axial plain. (b) Sagittal plain.

Pedicular Infrapedicular Disk height

Fig. 2.32 Protrusion, migration, and sequester. Sagittal schematic diagram explaining terms. (a) Small subligamentous herniation (protrusion). (b) Subligamentous herniation with caudal migration. (c) Subligamentous herniation with caudal sequester.

2.3.3 Changes to the Zygapophysial Joints In general, the significance of the zygapophysial joints is underestimated, with diagnosis and treatment focusing mainly on the intervertebral disk. However, it should not be forgotten that the zygapophysial joints together with the intervertebral disk and the ligaments constitute a functional (spinal) unit known as the

Junghans motion segment. The zygapophysial joints are synovial joints, with synovial folds that compensate for incongruence of the articular surfaces, and extend over intra-articular structures that are not covered with cartilage, thus reducing joint friction and equalizing pressure within the joint. By virtue of their shape and function, these synovial folds are also called “meniscoids.” Some authors postulate that the meniscoids can directly or indirectly manifest symptoms because of incarceration between the cartilage layers or due to degenerative or posttraumatic changes. However, at present these intra-articular structures measuring only a few millimeters can only be visualized in research settings.29 Distortion of the zygapophysial joints due to left–right asymmetry, in particular at the thoracolumbar and lumbosacral junctions, must also be borne in mind. Distortion can be aggravated by degeneration and ultimately result in ischialgia as a sequela to active arthrosis or arthrosis-mediated neuroforaminal stenosis. This, too, highlights the interrelationship between the intervertebral disk and the zygapophysial joints since, for example, patients with lumbar disk herniation often exhibit asymmetry and sagittalization of the zygapophysial joints. This results, especially during rotation of the lumbar spine, in chronic excessive unilateral stress (▶ Fig. 2.34). This normal variant is thus a form of prearthrosis.

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Original axis

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Fig. 2.33 Active Schmorl’s nodules. Sagittal T2w STIR sequence, section. On T2w images, there is markedly hyperintense bone marrow edema of the superior end plate of vertebral body L5 in the presence of active Schmorl’s nodules (intraspongious herniation).

Degenerative changes include, as in any other synovial joint, cartilaginous and subchondral changes with symptoms of reactive synovitis. In terms of the pathophysiology involved, chronic overloading gives rise to the characteristic chondromalacia-related changes in cartilage with edema, defects, and fibrillation as well as “balding” and narrowing of the joint space. There is also evidence of subchondral microedema, minimal bleeding, and necrosis with minute reactive cyst formation, scleroses, or connective tissue formation. This severe damage, in turn, results in synovial effusion and development of osteophytes, deformation, and marked malpositioning of the joints (▶ Fig. 2.35 and ▶ Fig. 2.36).86 On MRI, subchondral bone marrow reactions, subchondral cysts, marginal osteophytes, and effusions can be identified in the cervical spine, especially in sagittal sections, and in the lumbar spine, in particular, in axial slices. It is important to characterize the bone marrow edema, soft tissue edema, and effusions in the vicinity of the zygapophysial joints on fluid-sensitive, fatsuppressed sequences (e.g., STIR) since these are all signs of active arthrosis and a reaction to overloading of the joints and can correlate with pain (▶ Fig. 2.37 and ▶ Fig. 2.38).28 Differential diagnosis should also consider the presence of seronegative spondyloarthropathy; however, in that case characteristic changes would be expected at the sacroiliac joints as well as a matching clinical picture and corresponding laboratory results. Occasionally, synovial cysts that have their origin in the zygapophysial joints are also seen on MRI as rounded, oblong, smooth, and sharply marginated structures that are isointense to fluid in

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Fig. 2.35 Changes in zygapophysial joint during degeneration. Schematic diagram. 1, subchondral cysts; 2, deformation, rolling; 3, osteophyte, sclerosed or containing fatty marrow; 4, synovial cyst; 5, synovitis; 6, effusion; 7, erosion; 8, destruction of subchondral cortex; 9, cartilage destruction; 10, subchondral sclerosis, fibrosis; 11, subchondral edema—granulation tissue.

relation to the respective joint and can give rise to tangentation, compression, or displacement of the spinal cord, cauda fibers, or nerve roots because of their space-occupying effect (▶ Fig. 2.39). In the late stages, vacuum phenomena may be observed, for example, in the disk; these manifest as markedly hypointense on all MRI sequences. Neuroforaminal narrowing and/or narrowing of the spinal canal can occur especially because of development of osteophytes during disk degeneration, but also due to arthrosis of the zygapophysial joints, reactive thickening of the ligamenta flava, or synovial cysts (▶ Fig. 2.40 and ▶ Fig. 2.41). In the presence of certain clinical conditions (e.g., acute overloading with reactive vascular dilation and concomitant tissue swelling), relative stenosis can lead to clinically symptomatic narrowing (“acute decompensation”

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Fig. 2.34 Movement of vertebral body and zygapophysial joint in rotation. Axial schematic diagram. Unilateral overloading of zygapophysial joint. In anisotropy, there is disproportionate overloading, that is, prearthrosis.

2.4 Spondylitis and Spondylodiscitis

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Fig. 2.36 Zygapophysial joint arthrosis. Pronounced zygapophysial joint arthrosis with deformation of the articular processes, cartilage balding, subchondral sclerosis, and effusions. (a) Sagittal T2w TSE sequence, section. (b) Axial T2w TSE sequence, section.

Fig. 2.37 Active zygapophysial joint arthrosis. On T2w images, there is marked hyperintense bone marrow edema and surrounding soft tissue edema as well as slight joint effusion in the region of the hypertrophic zygapophysial joints C4/C5, right. (a) Sagittal T2w STIR sequence, section. (b) Axial T2w TSE sequence with fat suppression, section.

secondary to chronic damage).22 This in turn leads to painful misalignment or malpositioning and to restricted motion. Once a diagnosis of absolute spinal canal, or neuroforaminal, stenosis is pronounced, on MRI, CSF can no longer be seen in the spinal canal on axial fluid-sensitive sequences to evaluate spinal canal stenosis, or no perineural fatty tissue can be detected around the nerve root on sagittal T1w sequences to evaluate neuroforaminal stenosis. Another reliable MRI sign of absolute spinal canal stenosis is the presence of proximal cauda redundancy, seen as an undulating course of the cauda equina fibers proximal to the stenosed segment. Likewise, epidural lipomatosis can cause spinal canal stenosis. This involves extradural hypertrophy or formation of new fatty tissue within the spinal canal, which is often seen in the presence of obesity, in long-term use of corticoids, or due to impaired corticoid metabolism, and which may or not be symptomatic (▶ Fig. 2.42). In status post lumbar fusion, the failure rate is between 30 and 46%, with failure rates of between 19 and 25% reported after microdiskectomy or open diskectomy.16 Therefore, surgery is indicated only subject to very stringent criteria. The reasons for failed back surgery syndrome are spinal canal stenosis in 70% of cases, recurrent herniation in 15%, and

arachnoiditis in 10% of cases. Following IV administration of a contrast agent, scars and recurrent hernias can be differentiated on MRI after postoperative month 6. There is typically homogeneous enhancement of scar tissue following contrast agent administration, while at most only slight or no enhancement of recurrent hernias is observed in marginal regions (▶ Fig. 2.43).

2.4 Spondylitis and Spondylodiscitis Spondylitis is a rare condition, with only 1 to 4% of all osteomyelitis cases occurring in the spine. Hematogenous spread is implicated in 40% of cases (originating from infections of the teeth, urinary tract, or other organs); in 30% of cases, there is continuous transmission from the immediate environment (e.g., the skin, a retropharyngeal abscess) or osteomyelitis occurs secondarily to trauma (postoperatively after disk operations), but nevertheless is of unknown origin in 30% of cases.86,87 In spondylodiscitis, as opposed to spondylitis, the intervertebral disk is also infected in addition to infection of the vertebral bodies.

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Both arterial and venous hematogenous spread can take place. Venous spread, which is a very contentious issue, is imputed to valveless connections between the veins of certain deep-seated organs (e.g., of the pelvis) and the paravertebral venous ring

Fig. 2.38 Active zygapophysial joint arthrosis. Sagittal T2w STIR sequence, section. On T2w images, there is marked hyperintense bone marrow edema and surrounding soft tissue edema as well as moderate joint effusion in the region of the hypertrophic zygapophysial joint L4/L5. Depicted is also minor superior end plate impression of vertebral body L5 with slight subchondral bone marrow edema pointing to a recent incident.

structures (Batson’s venous plexus). When the intra-abdominal pressure rises, the normal blood flow from the spinal column is reversed, thus granting pathogens from deep-seated organs direct access to the vertebral bodies. In terms of pathophysiology, a precondition for onset of bone marrow inflammation and subsequent bone inflammation is the presence of terminal arteries, and these can become infarcted because of bacterial embolism or sinusoids with slow-flowing blood. Bone marrow infection can occur in tissue regions damaged by infarction and ensuing inflammation, going on to spread more or less slowly to the bone tissue depending on host immunity and the virulence of the implicated pathogen.13 The localization of the terminal arteries within the vertebral bodies is the chief determinant of where inflammation will occur. The position of these arteries changes over the course of a lifetime: ● Up to the fourth year of life, the disk is vascularized and contains terminal arteries, whereas the vertebrae do not. ● From the fourth year of life, the disk vessels regress. Likewise, anastomotic connections between the metaphyseal and equatorial arteries in the vertebral bodies disappear. This gives rise to the formation of terminal arteries in the center and at the margin of the vertebral bodies (▶ Fig. 2.44). Accordingly, in children up to age 4 years, primarily spondylodiscitis with subsequent spread to the adjacent bones is observed; in contrast, in older children and adults, primary spondylitis typically occurs and can then spread to the disk. Due to the mainly degenerative revascularization of the intravertebral disks (▶ Fig. 2.45), in particular in the marginal regions, which occurs from age 40 years, bone inflammation can quickly spread to the intervertebral disk or even start concurrently with onset of bone inflammation.

Fig. 2.39 Synovial cyst in the region of the lumbar spine. (a) Sagittal T2w TSE sequence, section. Characteristic synovial cyst, whose contents are isointense to fluid, emerging from the right zygapophysial joint L4/L5. (b) Axial T2w TSE sequence, section. The depicted synovial cyst has a pronounced space-occupying effect, leading to compression and displacement of the cauda fibers.

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2.4 Spondylitis and Spondylodiscitis Fig. 2.40 Neuroforaminal stenosis. Moderate osteochondrosis of L5/S1 with moderate disk herniation, pronounced arthrosis of the zygapophysial joint resulting in complete disappearance of the perineural intraforaminal fatty tissue as seen in high-grade stenosis with marked tangentation or compression of nerve root L5. Moderate neuroforaminal stenosis in segment L4/L5, directly above it, with isolated punctiform tangentation of nerve root L4. (a) Sagittal T1w TSE sequence, section. (b) Sagittal T2w TSE sequence, section.

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Fig. 2.41 Spinal canal stenosis. Moderate chondrosis of L4/L5 with slight anterolisthesis of L4 (Meyerding I), slight broadbased disk herniation, marked arthrosis of the zygapophysial joints, hypertrophy of the ligamenta flava leading to absolute spinal canal stenosis. (a) Sagittal T2w TSE sequence, section. (b) Axial T2w TSE sequence, section.

Fig. 2.42 Spinal epidural lipomatosis. Increased amount of fat-isointense tissue in the epidural space, in particular in L5–S3, resulting in spinal canal stenosis in the presence of epidural lipomatosis. (a) Sagittal T1w SE sequence, section. (b) Axial T2w TSE sequence, section.

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● ● ● ● ● ●

The main pathogens implicated in pyogenic spondylitis are: Staphylococci (50%). Escherichia. Klebsiella. Pseudomonas. Streptococci. Viruses.

Specific spondylitis is caused mainly by tuberculosis pathogens (Pott’s disease), while infections caused by mycotic organisms (e.g., Candida, Aspergillus) as well as parasites (Echinococcus) are quite rare. Spondylitis is typically seen between the ages 50 and 70 years. Its distribution is 2:1 between men and women.

2.4.1 Pyogenic and Specific Spondylitis Pyogenic Spondylitis and Spondylodiscitis Diagnosis in the course of disease: ● Week 1: MRI and bone scintigraphy (technetium-99 m polyphosphate scintigraphy) permit early diagnosis (during the first week). On MRI, there is bone marrow edema (hypointense on T1w images, hyperintense on T2w images) along the end plates (▶ Fig. 2.46).38 This early form of spondylodiscitis can be distinguished from degeneration (Modic stage I) through the absence of degenerative changes in the disk or concurrent onset of disk edema. However, it is sometimes difficult to differentiate these conditions if the disk has already undergone degenerative changes, in particular in the early stage when there is so far no paravertebral soft tissue edema. ● Weeks 2–3: In the ensuing course, a demarcation zone composed of fibrovascular tissue develops. Concomitantly, bone marrow edema (and possibly soft tissue edema) resolves. This is typically apparent on T1w and T2w images as hypointense signal, in addition to pronounced enhancement following IV CM administration (▶ Fig. 2.47). In this stage, both the adjacent intervertebral disk and the surrounding soft tissue structures are generally affected. The intensity of CM enhancement is a measure of the acute nature of inflammation and the body’s counter-reaction. ● From week 4: From this week, increasing fibrosis and new bone formation at the margin of the lesion have a hypointense signal

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Fig. 2.44 Vertebral body arterial blood supply. Schematic diagram. Terminal arteries are formed following regression of anastomoses between the central (equatorial) and metaphyseal arteries between the ages of 4 and 11 years.

●

on T1w and T2w images, and enhancement is no longer seen after IV CM administration. From weeks 5–6: In normal healing, local bone marrow conversion takes place, with fatty marrow appearing at the margin of the lesion and, in some cases, also replacing this. To what extent fibrosis, bony bridging, or vertebral body fusion occurs will depend on the nature of the underlying infection as well as on its resolution.90

Abscess formation is one potential complication. Soft tissue abscesses typically show a space-occupying lesion with central fluid. Accordingly, on MRI there is a central homogeneous zone that is hypointense on T1w and hyperintense on T2w images with no enhancement after IV CM administration (▶ Fig. 2.48). In rare cases when the abscess fluid contains blood or has a particularly high protein content, it can also appear hyperintense on T1w images. Following IV CM administration, the abscess membrane, which can be of varying thickness, may exhibit intense enhancement depending on the severity of inflammation. Paravertebral abscesses are seen in particular in the

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Fig. 2.43 Status post disk operation of L4/L5 8 months previously. The patient now has recurrent symptoms. (a) Axial native T1w SE sequence. Hypointense left, paradural thickening; it is not possible to distinguish here between a scar and recurrent hernia. (b) Axial T1w SE sequence with CM. Strong enhancement of the entire left paradural tissue (arrow) is suggestive of postoperative scar tissue rather than a recurrent hernia.

2.4 Spondylitis and Spondylodiscitis Fig. 2.45 Revascularization of the intervertebral disk in the presence of degeneration. (a) Sagittal native T1w SE sequence, section. Striped fatty marrow conversion; the height of the intervertebral disk is reduced. The central section of the cortex is disrupted. (b) Sagittal T1w SE sequence with CM, section. Marked hyperintense enhancement in the part of the disk close to vertebral body because of fibrovascular tissue (= revascularization of intervertebral disk).

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Early signs of incipient healing of spondylitis or spondylodiscitis include: ● Resolution of edema in bone marrow and soft tissues. ● Less pronounced enhancement following IV CM administration. ● Local onset of fatty marrow conversion.45 In contrast, the increasing sclerosis and sintering of the vertebral bodies seen on plain radiographs and CT are relatively late signs of healing and present as discrete hypointensity on MRI.

c

Fig. 2.46 Spondylodiscitis. Schematic diagram of individual morphologic signs and signal pattern, such as spondylitis, diskitis, destruction of the end plates, epidural infiltration, and paravertebral abscess. (a) On T1w images. (b) On T2w images. (c) On T1w images following CM administration. 1, destruction of end plate; 2, spondylitis; 3, diskitis; 4, epidural abscess; 5, epidural infiltration.

retropharyngeal or psoas region. The spinal cord can become inflamed if the inflammatory process spreads to the spinal canal.

Specific Spondylitis and Spondylodiscitis The underlying pathophysiology is in principle the same for tuberculous and mycotic infections as for pyogenic infections. They tend to have an “insidious” course. Very often there are few clinical symptoms, whereas MRI already shows widespread involvement. Unlike pyogenic spondylitis or spondylodiscitis, the most common localization is the lower lumbar spine, lower thoracic spine, and the upper lumbar spine. The following signs point to the specific etiology: ● Multiple involvement of vertebral bodies. ● Often, pronounced soft tissue swelling with abscess formation. ● Concomitant calcification and sequestration (▶ Fig. 2.49). In rare cases, bone involvement is seen in echinococcosis. In 30 to 50% of cases, the thoracic or lumbar vertebral bodies, rarely the vertebral arches, are affected. A typical manifestation is the formation of multiple cysts, possibly with fluid–fluid levels, which are hyperintense on T2w and hypointense on T1w images. Because of their extensive growth, these cysts can destroy the cancellous bone and cortical bone, and even invade the surrounding soft tissues. A characteristic feature is also enhancement of the cyst wall and surrounding soft tissues following IV CM administration,83 attesting to active inflammation (▶ Fig. 2.50).

Differential Diagnosis Differential diagnosis during the early stage of spondylitis or spondylodiscitis must include degenerative changes (Modic stage I). In the majority of cases, differential diagnosis will be based on the degenerative changes often observed in the adjacent intervertebral disk with reduced disk height and hypointense signal seen on all MRI images, and possibly vacuum phenomena as well as the absence of reactive edema. If there is still doubt, ex juvantibus treatment can be administered, a tissue biopsy taken, or follow-up examination performed after a few weeks. Chronic dialysis patients with amyloidosis, or also hemophilia patients, may exhibit completely identical findings on plain radiographs and MRI. In such cases, differential diagnosis should take account of the patient’s medical history.

2.4.2 Rheumatoid Arthritis In rheumatoid arthritis, the spinal column may also be involved in around 60% of cases. Since rheumatoid arthritis is primarily a synovial disease, it requires the presence of a synovial membrane. Accordingly, the typical symptoms exhibited in the finger joints are seen in the vertebral bodies of the upper cervical spine, zygapophysial joints, and the sacroiliac joints.

Course of Disease Early signs with synovial thickening, edema, and effusion (best visualized as hyperintense signals on STIR sequences) as well as hypervascular proliferation (in both cases, there is strong enhancement following IV CM administration) can be identified on MRI. These changes can be detected before onset of the erosion typically seen on conventional radiographs. Reactive edema formation is generally observed in the adjacent bone marrow.3,9

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Fig. 2.47 Spondylodiscitis. (a) Sagittal T2w STIR sequence, section. Bilateral bone marrow edema along the vertebral body end plates with adjacent soft tissue edema in parts of the disk and early stage acute spondylodiscitis. (b) Sagittal T1w SE sequence following CM administration, section. Pronounced enhancement of the vertebral bodies close to end plates as well as enhancement of the disk and the preventral soft tissues in active acute spondylodiscitis with fibrovascular reaction.

Fig. 2.48 Para- and intraspinal soft tissue abscesses as well as intraosseous abscesses in tuberculous spondylitis. (a) Sagittal T2w STIR sequence, section. Extensive, moderate spindle-shaped formation in posterior spinal canal of upper thoracic spine in the presence of intraspinal soft tissue abscess. Soft tissue abscess also anterior to vertebral bodies at the thoracolumbar junction, but not affecting the disks, and with adjacent spondylitis and intraosseous abscesses. (b) Sagittal T1w SE sequence following CM administration, section. Strong enhancement of the abscess walls but no enhancement of the abscess contents of the depicted, partially intraosseous and partially prevertebral, abscesses in the region of the thoracolumbar junction.

In later phases, the characteristic pannus formation and subluxation can be identified. These changes are typically more pronounced at the level of the first and second vertebral bodies (dens) (▶ Fig. 2.51), and can give rise to severe clinical instability and

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spinal cord compression. Depending on how active the pannus tissue is, there will be more or less strong enhancement following IV CM administration. This variation in enhancement can be used as a semi-quantitative indicator of inflammatory activity (▶ Fig. 2.52).

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2.4 Spondylitis and Spondylodiscitis

Differential Diagnosis On MRI, juvenile chronic arthritis of the spinal exhibits similar morphology to that of adult rheumatoid arthritis. Often, there is

Fig. 2.49 Vertebral body sequester in tuberculous spondylitis. Axial CT image, section. Islandlike calcification areas at the center of the vertebral body in sequestered tuberculous spondylitis.

multisegmental cervical subluxation, vertebral body fusion, and bone erosion. Pannus formation is identical to the changes described earlier. Typically, cartilaginous changes can be detected before bone erosion.

2.4.3 Seronegative Spondyloarthropathy Seronegative spondyloarthropathies are a category of different clinical conditions which, however, have many common radiologic and genetic features. These comprise essentially the following diseases: ● Ankylosing spondylitis. ● Psoriasis. ● Reactive arthritis (formerly Reiter’s syndrome). ● Inflammatory intestinal diseases. ● Scleroderma. ● Dermatomyositis. ● Systemic lupus erythematosus. ● Mixed connective tissue disease. ● Sjögren’s syndrome. ● SAPHO syndrome (acquired hyperostosis syndrome with synovitis, acne, pustulosis, hyperostosis, and osteomyelitis).

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The morphologic changes to the intervertebral and sacroiliac joints exhibit essentially the same stage-related MRI findings. The clinical symptoms can be very pronounced despite the relatively few morphologic changes. Diagnosis can be compounded by the concurrent presence of different stages with different degrees of severity, as seen even within a single joint. This hampers severity assessment, staging, and follow-up. Such difficulties are not encountered in pyogenic arthritis. Osteoporosis and often multiple insufficiency fractures can be observed in rheumatoid arthritis, and are linked in some cases to treatment.

In most cases, distinctions can be made based on the gradual, but varying, involvement of the sacroiliac joints, vertebral column, and peripheral joints as well as concomitant changes to the skin. Various authors believe that this group of diseases first affects the soft tissues (connective tissue, tendons, tendon insertions, etc.), and only then spreading to joints, bones, and bone marrow.39 Several authors have reported early paravertebral thickening of the soft tissues with edema and vascular proliferation and spread to vertebral bodies and disk (▶ Fig. 2.53).61 A typical manifestation— in particular of ankylosing spondylitis—is Romanus’ and Anderson’s lesions which correspond to anterior spondylitis with “shiny corners” or spondylodiscitis (▶ Fig. 2.54). These changes apparently also give rise to syndesmophytes. Secondary manifestations include bone marrow edema that typically lead to vertebral body sclerosis and contour changes (“shiny” corners, barrel vertebrae, box-shaped vertebrae). As in rheumatoid arthritis, thickening of

Fig. 2.50 Echinococcosis. Multiple cystic changes within the spine, in bones and in the soft tissues with absolute spinal canal stenosis and compression of the spinal cord with known diagnosis of Echinococcus infection. (a) Sagittal T2w TSE sequence, section. (b) Axial T2w GRE sequence, section.

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The Spine the synovial membrane with edema, vascular proliferation, and effusion is seen in the joints—especially the sacroiliac joints. This is followed by bone marrow edema and chondrolysis leading in turn to synostosis. A salient feature, as seen in rheumatoid arthritis, is the concurrent presence of various stages (“mixed picture”). The level of inflammatory activity can be semi-quantitatively determined through IV CM administration (▶ Fig. 2.55).8 In the course of seronegative spondyloarthropathy, the bony elongated segments of the vertebral bodies and zygapophysial joints, as well as of spinous processes, can fuse together. This can result in biomechanical overloading of the unaffected spinal segments and is the cause of early, extensive degenerative changes or of atypically localized fractures. Such pathologies can be identified at an early stage on MRI as degeneration of an intervertebral disk, subcortical region, and zygapophysial joints or as incipient fracture of vertebral bodies.

Chronic recurrent multifocal osteomyelitis (CRMO) is a special type of disease. It is characterized by sterile (predominantly) plasma cell osteomyelitis which is mainly seen in adolescence (between the age of 10 and 30 years) and generally in women. It involves sterile inflammation (probably autoimmune mediated) and can resolve without any sequelae (bone marrow edema) or with pronounced sclerosis (Garré’s osteomyelitis). Many authors assign this to the SAPHO syndrome category of diseases. The vertebral column is implicated in 30% of cases. On MRI of the spine, typical inflammatory changes of all degrees of severity can be detected (bone marrow edema, destruction, sclerosis and fibrosis, and thickening of the soft tissues; ▶ Fig. 2.56).68 Unlike ankylosing spondylitis, which involves enthesitis, CRMO has all the typical manifestations of osteomyelitis.

In this chapter, we describe posttraumatic changes to the intervertebral disks, ligaments, and bones as well as posttraumatic changes to the spinal canal. ▶ Table 2.2 lists the imaging modalities recommended for diagnosing spinal injuries.

2.5.1 Posttraumatic Changes to the Intervertebral Disks and Ligaments Soft tissue and ligament injuries account for almost 90% of spinal trauma after cervical spine injury, of which only 4% are identifiable on plain radiographs. That highlights the paramount importance of MRI in this setting.

Intervertebral Disk Injuries

Fig. 2.51 Rheumatoid arthritis with pannus at C1/C2. Sagittal T2w TSE sequence, section. Hyperintense soft tissue between the atlas and dens suggestive of pannus tissue. Deformed, high-riding dens with distinct medulla oblongata impression.

Posttraumatic intervertebral disk herniation can present alone or, in 30% of cases, in combination with vertebral fractures.79 If it goes unnoticed, it can deteriorate in the course of treatment of a bone injury. Apart from the signs of disk herniation seen on MRI, the following can manifest additionally: ● (T2w) increased signal in the intervertebral disk itself as well as in the herniated material. ● Protrusion of disk material between the posterior border of the vertebral body and posterior longitudinal ligament. ● If the posterior longitudinal ligament is torn, herniation as far as the anterior epidural space.25

Fig. 2.52 Inactive rheumatoid pannus at C1/ C2. (a) Sagittal native T1 SE sequence, section. Hypointense soft tissue between atlas and dens. (b) Sagittal T1w SE sequence following CM administration, section. Only minimal enhancement of the soft tissue between the atlas and dens in inactive rheumatoid pannus.

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2.5 Posttraumatic Spinal Changes

2.5 Posttraumatic Spinal Changes

Fig. 2.53 SAPHO syndrome. Sagittal T2w TSE sequence. Partially hypointense and partially hyperintense prevertebral soft tissue thickening of L1–S1 and fatty marrow conversion along vertebral body end plates L2– S1 in SAPHO syndrome.

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Fig. 2.54 Ankylosing spondylitis of the spine. Sagittal T2w STIR sequence, section. Slight bone marrow edema at the anterior border of the vertebral body (arrows) and along the vertebral body end plates (asterisk), typical Romanus’ and Anderson’s lesions suggestive of ankylosing spondylitis.

However, it is often not possible to delineate existing degenerative changes from recent posttraumatic disk injuries in the absence of prior examinations.

Ligament Injuries

Fig. 2.55 Ankylosing spondylitis sacroiliitis. Paracoronal T1w SE sequence with fat suppression following CM administration, section. Enhancement of the sacroiliac joint spaces and of the contiguous subchondral regions as well as partially erosive, partially sclerotic subchondral changes in ankylosing spondylitis with signs of activity.

A healthy anterior longitudinal ligament, ligamenta flava, and the supraspinous ligament appear as hypointense structures on T1w images and contrast sharply with the hyperintense paraspinal fat. Thanks to the adjacent CSF, the posterior longitudinal ligament can be well visualized on T2w images. A torn ligament can be recognized on a T2w image, with or without fat suppression, since the ligament or ligament stumps are hypointense, whereas discontinuity sites are hyperintense. On examination of a series of cases of prevertebral swelling secondary to cervical spine trauma, a large number of torn anterior longitudinal ligaments were identified (▶ Fig. 2.57). In half of these cases, there was no bone damage or subluxation.74 In another series of studies, 30% of all thoracolumbar burst fractures were also associated with a tear of the posterior ligament.58 Direct and reliable visualization of ligament injury, in addition to the well-documented instability signs, is possible with MRI (▶ Fig. 2.58 and ▶ Fig. 2.59).

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Fig. 2.56 CRMO. (a) CT, sagittal reconstruction, section. Pronounced diffuse sclerosis of vertebral body L4 as well as slight diffuse sclerosis of the end plates of the adjacent vertebrae. (b) Sagittal T1w SE sequence, section. Marked hypointensity signal in vertebral body L4 as well as slight hypointensity signal of the end plates of the adjacent vertebrae. (c) Sagittal T2w STIR sequence, section. Pronounced inflammatoryedematous changes to vertebral body L4 as well as slight changes in the end plates of the adjacent vertebrae. (d) Sagittal T1w SE sequence with fat suppression following CM administration, section. Strong CM enhancement of vertebral body L4 as well as slight enhancement of the end plates of the adjacent vertebrae as well as of the center of disk L4/L5.

Whiplash injuries, with concomitant subligamentous hematoma, are likewise injuries typically associated with the anterior longitudinal ligament (▶ Fig. 2.60).

Vascular and Soft Tissue Injuries Magnetic resonance angiography (MRA), a noninvasive imaging modality, is able to detect 24% of cases of vascular changes in the

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vertebral artery which are often clinically silent when presenting unilaterally. However, bilateral vascular changes can have serious consequences. MRI signs include the following: ● Cannot be visualized: This is indicative of occlusion. ● Luminal constriction: This points to a spasm or dissection. ● Increase in the outer diameter: This can be caused by a vascular wall hematoma or a pseudoaneurysm.27 Multislice CT is used increasingly to diagnose such conditions.

2.5 Posttraumatic Spinal Changes Table 2.2 Correct use of imaging modalities for diagnosing spinal injuries1 Key questions: Injury to cervical spine?

CT: Method of choice; indication based on NEXUS and CCSPR criteria X-ray: Only indicated if there are no relevant neurologic symptoms and no further injuries MRI: If there is neurologic deficit

Injury to thoracic spine/ X-ray: Primary modality lumbar spine? CT: If there is suspected instability or relevant neurologic damage following considerable adequate bone injury MRI: If there is neurologic deficit MRI: To determine extent of injury and if there is intraspinal hemorrhage CT: To identify bone-related narrowing of the spinal canal and intraspinal hemorrhage Vertebral artery injuries?

CT angiography, MRA

Abbreviations: CCSPR, Canadian C-Spine Rule Study; CT, computed tomography; MRA, magnetic resonance angiography; MRI, magnetic resonance imaging; NEXUS, National Emergency X-Radiography Utilization Study.

2.5.2 Posttraumatic Bone Changes Recent bone injuries of the spine are first investigated on radiographs and/or CT. When the radiographic result is positive, CT is the method of choice for investigating the extent of the fracture as well as the bony spinal canal with respect to width and presence of any bone fragments. MRI is not as good as CT for demonstrating fresh fracture gaps or for imaging cortical bone. Nonetheless, MRI is indicated for certain specific aspects of fresh bone injuries (▶ Fig. 2.61).

Occult Injuries (Bone Marrow Contusion, Bone Bruise) MRI is able to visualize radiologically occult fractures and fissures as well as edematous bone marrow contusion. An incompletely displaced fracture or trabecular microfractures can be missed on radiography or CT. Thanks to its sensitivity for the concomitant edematous bone marrow changes, which are hyperintense on fluid-sensitive fat-suppressed sequences, MRI is able to diagnose bone injuries.42 Dislocated or locked facets, which are occult on projection radiography, can be demonstrated with both CT and MRI.18,20

Stress-Fracture Spondylolysis Stress fractures can be identified on MRI images due to the concomitant bone marrow edema. Based on present-day knowledge, spondylolysis is often thought to be a stress fracture resulting from overloading. Hence, in its early stage it can only be visualized on MRI on the basis of bone marrow edema. In most cases, but not always, spondylolysis can be directly identified on MRI. CT should be used if there is any doubt. The direct sign of

Fig. 2.57 MRI signs of acceleration trauma. Schematic median sagittal diagram. (a) Anterior tear in longitudinal ligament, superior end plate impression, bone bruise (1). Tear of the posterior longitudinal ligament, traumatic disk prolapse, anterior border fracture, hematoma of anterior longitudinal ligament (2). (b) Tear of interspinous ligament, ligamenta flava, supraspinous ligament, and hematoma neck muscles.

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Spinal cord injuries?

spondylolysis on MRI is the hypointense line, typically seen in the interarticular portion of the pedicle on T1w and T2w images (▶ Fig. 2.62). MRI diagnosis can be facilitated by bearing in mind the following indirect signs of spondylolysis: ● Large sagittal diameter of the spinal canal. ● Subtle wedge shape of posterior vertebral body segment. ● Reactive bone marrow changes in pedicle.85 The bone marrow changes in the pedicle can, like intervertebral disk–related bone marrow changes, be distinguished using the Modic I, II, and III classification system.84 Another typical localization of stress or insufficiency fractures is the lateral mass of the sacral bone. Bone marrow edema often results in vertical fracture lines (Honda’s sign; ▶ Fig. 2.63).

Compression Fracture Denis’ three-column model divides the vertebral column into the following three columns: ● Anterior column (comprising the anterior two-thirds of the vertebral body, anulus fibrosus, and the anterior longitudinal ligament). ● Middle column (comprising the posterior third of the vertebral body, pedicles, and the posterior longitudinal ligament). ● Posterior column (comprising the vertebral arch, zygapophysial joints, and the joint capsules and ligaments) between these structures. The model states that there is instability if at least two of the columns are completely damaged. A mainly stable compression fracture occurs if the anterior column has sustained injury but the middle and posterior columns remain intact. A traumatic compression fracture is caused by the impact of axial forces during flexion (▶ Fig. 2.64). There is little or no history of trauma in osteoporotic or blastomous compression fracture. On plain X-ray films, the compression fracture is characterized by the reduced height at the anterior

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The Spine Fig. 2.58 Full-thickness tear of anterior longitudinal ligament and anulus fibrosus. Sagittal T2w sequence, section. Signal and structural changes in the anterior longitudinal ligament and anulus fibrosus at the level of C6 with full-thickness tear of the anterior longitudinal ligament and adjacent anulus fibrosus. There is also posttraumatic edema of the spinal cord at the level of C5.

Spinal cord edema

Supraspinous ligament (disruption and tear) Interspinous ligament (tear)

Fig. 2.59 Tear of posterior dural sac, interspinous ligament, and disk C5/C6 as well as disruption and tear of supraspinous ligament. Sagittal T2w TSE sequence, section. Tear in disk at the level of C5/C6 and in anterior longitudinal ligament with subligamentous hematoma. Pronounced posterior soft tissue edema at the level of C1/C6; the supraspinous ligament is disrupted and torn; there is also a tear of the interspinous ligament and of the posterior dura at C5/C6 level. Spinal canal stenosis and myeloedema at the level of C5/C6.

Dural tear Spinal cord edema

Injury to anterior longitudinal ligament with subligamentous hematoma

Fig. 2.60 Whiplash injury. Injury to the anterior longitudinal ligament and subligamentous hematoma along C3/C4, bone damage to C5 with loss of height in anterior border of vertebral body and posttraumatic bone marrow edema, damage to interspinous ligaments and supraspinous ligament at the level of the middle cervical spine. (a) Sagittal T1w SE sequence. (b) Sagittal T2w SE sequence. (c) Sagittal T2w STIR sequence.

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Tear in anterior longitudinal ligament and anulus fibrosus

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2.5 Posttraumatic Spinal Changes

Fig. 2.61 Minor injury to 12th thoracic vertebral body in the form of minimal end plate compression fracture. The height of the anterior border of the vertebral body is only slightly reduced, the vertebral body inferior end plate is intact; the vertebral body superior end plate has a slightly flatarched impression. The bone marrow changes are suggestive of an injury, with bandlike bone marrow edema along the superior end plate of T12, which exhibits low signal intensity on T1w and high signal on T2w, in particular on STIR sequence. (a) Sagittal T1w SE sequence, section. (b) Sagittal T2w SE sequence, section. (c) Sagittal T2w STIR sequence, section.

Fig. 2.63 Insufficiency fracture of the sacrum. Paracoronal T2w STIR sequence, section. Pronounced bone marrow edema as well as a linear, vertical hypointense signal change due to recent fracture of the left lateral mass of the sacral bone. Fig. 2.62 Spondylolysis L5. Sagittal T1w SE sequence, section. Hypointense linear signal changes in the interarticular portion of vertebral body L5 (arrow) in spondylolysis with anterolisthesis of L5, neuroforaminal stenosis, and compression of nerve root L5.

border of the vertebral body, with the posterior border intact. MRI is the modality of choice for determining the age and cause of a compression fracture. Fresh fractures, unlike historic fractures, exhibit clear signs of bone marrow edema. It can be difficult in

some cases to distinguish osteoporotic from blastomous compression fractures but there are morphologic signs that facilitate this. ● The MRI signs pointing to osteoporosis as the cause of compression fracture include (▶ Fig. 2.65): ○ Multiple fractures. ○ Different-aged fractures (with fatty bone marrow attesting to a historic fracture and “bone marrow edema” as a sign of a fresh fracture).

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The Spine

In fresh fractures, bandlike “bone marrow edema.” Only partial obliteration of fatty bone marrow in “bone marrow edema.” ○ A fracture line running along the end plate and manifesting as a fluid-filled gap (high signal on T2w image = “fluid sign”). ○ Concave posterior vertebral body contour (▶ Fig. 2.66). The MRI signs pointing to a malignant cause of compression fracture include: ○ Multiple changes in vertebral bodies, but not all involving fractures. ○ Same-aged fractures. ○ Bone marrow changes are rounded, space-occupying, rather than bandlike, structures. ○ Complete obliteration of fatty bone marrow. ○ No fluid sign. ○ Convex posterior vertebral body contour. ○ Presence of soft tissue tumor portion. ○ Pedicle destruction. ○ ○

●

Apart from their ability to identify morphology on MRI, DWI sequences can help to distinguish between osteoporotic and blastomous vertebral body compression fractures (see Chapter 2.7.5).

Burst Fracture A burst fracture, which is often unstable, is caused by damage to Denis’ anterior and middle columns. The vertebral body is narrowed, with the fractured and height-reduced posterior border of the vertebral body curving dorsally, for example, in the shape of a fragment, against the spinal canal (▶ Fig. 2.67). In three-quarters

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of cases, this gives rise to neurologic symptoms. The posterior column may also be fractured. While radiography is the first diagnostic modality used, in 25% of cases it fails to properly identify fractures and dislocation of the posterior border of the vertebral body.2 It is very important to evaluate the stability of this fracture since in unstable fractures the vertebral body will continue to collapse, aggravating axis misalignment and possibly exacerbating spinal injury. If there are radiologic signs of an unstable fracture (plain radiographs and CT), MRI is not necessarily indicated, although it is excellent at visualizing the posterior longitudinal ligament, disk injuries, extent of spinal canal stenosis, and nature of the spinal cord injury. Burst fractures can be misinterpreted as stable fractures on using plain radiographs and CT without MRI. In this setting, MRI is able to distinguish stable from unstable fractures in that it is able to evaluate the posterior ligament complex comprising the posterior longitudinal ligament, ligamenta flava, supraspinous ligament, interspinous ligament, and joint capsules. Overall, in 28 to 47% of burst fractures, tears are seen in the posterior ligament complex.58,80

2.5.3 Posttraumatic Changes to the Spinal Canal Acute Spinal Cord Injury MRI is able to diagnose posttraumatic paralysis symptoms which are not, or not reliably, identified on CT. It is also able to

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Fig. 2.64 Compression fractures of the first and second lumbar vertebral body. The recent fractures can be recognized from the change in the shape (superior end plate impression) and of the adjacent signal change in bone marrow (edema) with intact posterior border of the vertebral body (asterisks). (a) Sagittal T1w sequence, section. (b) Sagittal T2w STIR sequence, section.

2.5 Posttraumatic Spinal Changes a Bandlike signal change “Fluid sign” Fat signal not altered

b

Concave contour Vertebral arch normal Fracture No destruction of terminal end plate

Diffuse signal change

Convex contour

Fat signal diminished

Vertebral arch affected Destruction of terminal end plate

Multiple similar signal patterns

Fig. 2.65 Differentiation of osteoporotic from blastomous vertebral body fractures based on MRI morphology. Schematic diagram. (a) Osteoporotic, benign vertebral body fracture. (b) Blastomatous, malignant vertebral body fracture.

differentiate between normal findings and spinal cord edema, cord hemorrhage, and/or spinal cord dissection: ● Spinal cord edema: Spinal cord edema is characterized by a change in the cord signal, which is hypointense on T1w and hyperintense on T2w images. This signal change is generally not well defined, is emitted from the center, and appears oval-shaped on transverse and spindleshaped on sagittal sections and may be associated with spinal cord thickening at this site. ● Spinal cord hemorrhage: Intramedullary bleeding can be diagnosed on MRI by virtue of the characteristic signal pattern of the blood breakdown products. The signal intensities of these blood breakdown products can be classified in chronological order, with the signal pattern mainly determined by the hemoglobin (▶ Fig. 2.68). The stages of clinical relevance in traumatology are as follows:

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Fig. 2.66 Osteoporotic vertebral body fracture. Height of vertebral body L2 reduced by up to 60%, hollow-shaped impression in the vertebral body superior end plate L2, gentle, linear hypointense signal change along the superior end plate L2, kinking and displacement of the upper third of posterior border of vertebral body L2 in a posterior direction, and pronounced bone marrow edema due to recent osteoporotic vertebral body fracture L2. (a) Sagittal T1w SE sequence, section. (b) Sagittal T2w STIR sequence, section.

Acute stage: The acute stage is characterized by the magnetic susceptibility effect of deoxyhemoglobin with a typical reduction in signal on T2w SE sequence, and which can be recognized more clearly on T2w GRE sequence. In this stage, there are additional signs of edema with perifocal increase in signal on T2w image. ○ Early subacute stage: The early subacute stage is reached when the patient has completed the initial treatment phase, for example, surgical stabilization, but there are no prospects of a more favorable prognosis. This early subacute stage is characterized by the presence of intercellular methemoglobin that typically has a high signal on T1w image. Spinal cord dissection: Often, it is not possible to distinguish clinically between complete disruption of the spinal cord, as seen, for example, in dislocated fractures of the middle thoracic spine, and intramedullary hemorrhage. ○

●

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Fig. 2.68 Intraspinal bleeding with spinal cord edema. Sagittal T2w STIR sequence, section. Hemorrhage at the level of C3 can be recognized from the reduced hyperintense signal in the central edema.

Fig. 2.67 Burst fracture with marked protrusion of the anterior and poster vertebral body border. Sagittal T2w TSE sequence, section. Fracture of the vertebral body inferior and superior end plate, displacement of the anterior border of the vertebral body in an anterior direction and of the posterior border of vertebral body in a posterior direction, leading to narrowing of the spinal canal, slight retrolisthesis of the vertebral body directly above it, and minor kyphotic kinking in the adjacent cranial segment.

MRI is important not only in diagnosing spinal cord lesions but also for assessing prognosis. With similar neurologic symptoms, the prognosis is much better for intramedullary edema than it is for hemorrhage, while for intramedullary hemorrhage it is better than for cord disruption (▶ Fig. 2.69). With the advent of titanium, the scope of MRI has expanded for diagnosis of postoperative spinal conditions.10,77

Chronic Spinal Cord Injury In the long term, MRI is able to distinguish between the following chronic injuries to the spinal cord: ● Posttraumatic syrinx: The syrinx appears as a spindle-shaped, isointense to fluid, area at the center of the spinal cord (see ▶ Fig. 2.18). Early diagnosis is important, and if neurologic symptoms persist, decompression should be indicated. ● Myelomalacia: Myelomalacia is a term referring to softening of the spinal cord with small cysts and gliosis, and with or without swelling. There is a marked rise in signal on water-sensitive FLAIR (fluid-attenuated inversion recovery), PDw, and T2w sequence. ● Spinal cord atrophy: Spinal cord atrophy can be seen as a discrete or longitudinal manifestation. Spinal cord injuries in children often do not show any sign of injury to the bony vertebral column. The acronym SCIWORA (syndrome)

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Fig. 2.69 Paralysis symptoms following dislocation with damage to all three columns. Sagittal T2w TSE sequence, section. Recent injury to cervical spine with involvement of all three columns and anterior dislocation; tear in disk C5/C6. There is high-grade damage to the spinal cord as well as edema. Distinct soft tissue edema and hematoma.

denotes spinal cord injury without radiographic abnormality. Such damage is caused by flexion, hyperextension, distraction, and ischemia in the very elastic juvenile vertebral column. MRI shows extraneural and neural lesions: the extraneural lesions relate to injuries of the posterior longitudinal ligament and intervertebral disk. Neural injuries involve spinal cord edema, hemorrhage, and damage to the spinal cord that can even include a tear of the spinal cord.

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The Spine

2.6 Postoperative Spinal Changes

Thanks to the sharp soft tissue contrast, MRI is able to distinguish the causes of spinal cord compression, such as disk prolapse, bone-related compression, or hematoma42,67: ● Posttraumatic disk herniation: This presents in the anterior portion of the spinal canal. ● Sequestration: The sequester can be displaced away from the respective disk in either a cranial or caudal direction and exhibit higher signal intensity also on T2w sequence. ● Bone fragment: This can be characterized by its sharply marginated shape secondary to fracture and, in particular, by its signal pattern, with signal void in the cortex. ● Hematoma: Unlike traumatic disk prolapse and dislocated bone fragment, this is half-moon to ring shaped in axial sections and appears longitudinally expanded in sagittal slices. For subacute and chronic courses of disease, differential diagnosis must also rule out epidural scar and arachnoiditis.

2.6 Postoperative Spinal Changes In this section, we describe the postoperative, surgery-related, changes seen in the intervertebral disk and the bony portion of the vertebral column.

2.6.1 The Postoperative Intervertebral Disk Normal Postoperative Images Following Surgery of the Intervertebral Disk The changes described in the following will vary because of the different techniques employed in disk surgery, ranging from laser decompression to the more classic forms of disk surgery. Edema formation, possibly with a space-occupying effect on the dural sac, is seen in the resected area of the disk or ligament. After 6 weeks to 6 months, this is replaced with granulation, and later scar, tissue. The anterior epidural edema, with disruption of the posterior anulus following disk curettage, can initially mimic recurrent disk prolapse because of the space-occupying effect. These, in some cases, very pronounced, changes resolve over a period of 2 to 6 months.7 Therefore, only in exceptional cases should MRI be performed within the first 6 weeks of surgery, and then only to rule out

significant postoperative hematoma at the laminectomy site, a pseudomeningocele, or infection of the disk space.

Postoperative Complications Following Disk Surgery In 20 to 40% of cases, the clinical symptoms will have remained unchanged following disk surgery. These symptoms are subsumed under the term failed back surgery syndrome. ● Principle causes: ○ Recurrent herniation. ○ Epidural fibrosis. ● More rare causes: ○ Diskitis. ○ Spondylodiscitis. ○ Arachnoiditis. ○ Abscesses. ○ Pseudomeningocele.

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Extradural Compressive Changes

As the postoperative course progresses, characteristic signs that can facilitate differential diagnosis are increasingly exhibited (▶ Table 2.3). The most reliable sign in distinguishing between recurrent herniation and epidural fibrosis is the response to contrast agent. With an accuracy of 70 to 80%, following IV CM administration CT is as accurate as MRI without CM administration in making that distinction. The most reliable differential diagnosis, “recurrent hernia versus scar tissue,” is provided by MRI on using IV CM (Gd-DTPA [gadopentetate dimeglumine]), with various studies reporting an accuracy of 96 to 100% (▶ Fig. 2.70, ▶ Fig. 2.71, and ▶ Fig. 2.72).23,62,64,65 However, it must be borne in mind that this distinction can only be made at the earliest 6 months after surgery. Three groups of signs can be distinguished on using CM MRI: ● Recurrent hernia alone. ● Epidural fibrosis alone. ● Combination of recurrent hernia and epidural fibrosis (see ▶ Fig. 2.70, ▶ Fig. 2.71, and ▶ Fig. 2.72).

Spinal Canal and Neuroforaminal Stenosis There are different mechanisms implicated in stenosis of the spinal canal. Removal of disk tissue results in narrowing of the intervertebral disk space and, in turn, in narrowing of the neuroforamina. Any ensuing segmental loosening can lead to

Table 2.3 MRI morphologic signs for differential diagnosis of recurrent prolapse versus epidural fibrosis MRI morphology

Recurrent prolapse

Epidural fibrosis

Signal intensity

As for disk

First T2w ↑, over time T2w ↓

Contact with intervertebral disk

Clear

Discrete/none

Border

Well defined

Poorly defined, irregular

Volume effect

Voluminous, space occupying

Slight to shrinking

Dural sac displacement

Away

Toward

CM enhancement

Slight and marginal

Distinct and uniform

Abbreviation: T2w, T2-weighted. Note: ↑, high signal intensity; ↓, low signal intensity.

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Fig. 2.70 Recurrent disk herniation. Discrete, central intraspinal space-occupying lesion in proximity to intervertebral disk and no CM uptake in recurrent disk herniation (arrows). (a) Axial native T1w SE sequence, section. (b) Axial T1w SE sequence following CM administration, section.

Fig. 2.71 Epidural fibrosis. (a) Axial native T1w SE sequence, section. Epidural fibrosis (arrows) with involvement of the right nerve root. (b) Axial T1w SE sequence following CM administration, section. Unmasking the nerve root. The arrows point to the epidural fibrosis.

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spondylolisthesis. Diskectomy stimulates the focal growth of osteophytes, while bone resection or fusion surgery results in bone proliferation with constriction of the spinal canal.14 The morphologic signs of postoperative spinal canal or neuroforaminal stenosis seen on MRI are consistent with degenerative spinal canal or neuroforaminal stenosis (see Chapter 2.3.3).

values or a signal pattern similar to CSF is seen posteriorly to the laminectomy site. In principle, the MRI signal characteristics are not specific for these fluid accumulations since MRI is not able to differentiate between benign postoperative fluid accumulation and a pseudomeningocele or abscess (▶ Fig. 2.74 and ▶ Fig. 2.75).

Postoperative Fluid Accumulation

Diskitis and Spondylodiscitis

A pseudomeningocele is caused by injury to the dura during surgery. It manifests as herniation of the arachnoid membrane through the dural gap and as proliferation into the arachnoid sac (true meningocele). But extravasation of CSF into the soft tissues leading to development of a fibrous capsule is commonly observed; this is known as a “CSF cushion” (▶ Fig. 2.73). On CT and MRI, a rounded structure with density

Diskitis or spondylodiscitis is seen in 1% of cases following lumbar laminectomy. On T1w MRI images, the intervertebral disk and adjacent vertebral bodies are visualized as a confluent hypointense area, while on T2w images this area is hyperintense. Following CM administration, enhancement of the disk and nearby peridiskal vertebral body segments can be observed.

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The Spine

2.6 Postoperative Spinal Changes Fig. 2.72 Combination of recurrent disk herniation and epidural fibrosis. Recurrent disk herniation without CM uptake, but with CM enhancement of the surrounding scar tissue. (a) Sagittal T2w TSE sequence, section. (b) Axial native T1w SE sequence, section. (c) Axial T1w SE sequence following CM administration, section. epidurale Epidural fibrosis Fibrose

Recurrent Recurrent disk diskherniation herniation

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a

Rezidiv einer DiskusRecurrent disk herniation

Epiduralepidurale fibrosis

herniation

Fibrose

epidurale Epidural fibrosis Fibrose

c

On comparing asymptomatic postoperative patients with their counterparts with postoperative diskitis, a minor difference is seen on MRI in the operated disk and in the peridiskal vertebral body end plate. CM administration is very beneficial here:

●

In patients with postoperative diskitis, edema and CM enhancement of the vertebral bone marrow is a characteristic manifestation on both sides of the implicated disk space.

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Fig. 2.73 Postoperative CSF cushion. CSFisointense, discrete fluid formation in surgical area and posterior to the spinous processes, reaching as far as T11 in a cranial, and L4 in a caudal, direction, against a background of an extensive CSF cushion following laminectomy of L2. (a) Sagittal T2w TSE sequence, section. (b) Axial T2w TSE sequence, section.

*

Fig. 2.74 Intraspinal abscess in status post hemilaminectomy. Central hypointense, discrete formation posterior to the vertebral body L4 and of disk L3/L4 (arrows), with strong peripheral CM enhancement, in the presence of epidural abscess as well as postoperative defect area and status post hemilaminectomy (asterisk). (a) Sagittal T1w SE sequence with fat suppression and following CM administration, section. (b) Axial T1w SE sequence with fat suppression and following CM administration, section.

●

●

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Enhancement of the disk space is suggestive of spondylodiscitis but is also seen in diskitis alone as well as in patients with an unremarkable postoperative course. CM enhancement of the posterior anulus can be identified in most asymptomatic patients and in all patients with diskitis.

The presence of all three signs serves as a diagnostic marker for spondylodiscitis, but one or occasionally two of these signs are also seen in asymptomatic patients. Epidural abscesses demonstrate significant marginal enhancement following IV CM administration. The extension of the abscess

2.6 Postoperative Spinal Changes

Empty dural sac Thickened dural sac

Fig. 2.76 Postoperative spinal arachnoiditis. Axial T1w SE sequence following CM administration, section. Image of an “empty” dural sac with thickened wall in the presence of adherent cauda equina fibers in postoperative arachnoiditis. Downloaded by: The University of Edinburgh. Copyrighted material.

Postoperative hematoma

Type I

Fig. 2.75 Postoperative epidural hematoma following posterior spondylodesis and disk replacement for bone fusion of L4/L5. Sagittal T1w SE sequence, section. Slight hyperintense space-occupying lesion posterior to disk L4/L5 and vertebral body L5 with extensive postoperative hematoma leading to narrowing of the dural sac.

can be precisely delineated with regard to the epidural space, paravertebral region, and any compression of the spinal cord.52,60

Arachnoiditis

Type II

Type III

Fig. 2.77 Spinal arachnoiditis. Schematic diagram. Asymmetrical distribution of the nerve roots in the lumbar dural sac due to adhesions in the presence of arachnoiditis. Due to inflammatory adhesions, this can manifest as displacement more toward the center (type I) or more toward the periphery (type II), or as extensive displacement of the dural sac (type III).

Arachnoiditis is a chronic inflammatory postoperative intrathecal pathology. On MRI, the central and peripheral adhesions of the nerve root are demonstrated as central stringlike agglutinated nerve roots or as adhesions to the dural sac circumference with ring-shaped thickening and signs of an “empty dural sac” on axial images (▶ Fig. 2.76 and ▶ Fig. 2.77).63 However, there is also the normal variant where the cauda fibers need to be distinguished from inflammatory adhesions (▶ Fig. 2.78).

2.6.2 The Postoperative Bony Spine The introduction of titanium and titanium alloys in spinal surgery has expanded the scope of application of MRI in the postoperative diagnostic setting. As such, assessment of the bone healing process now comes within the remit of MRI. There are, in principle, two mechanisms of bone healing: primary (per primam) and secondary (per secundam) bone healing: ● In per primam bone healing, two bone ends are fixed in place thanks to the dynamic properties of the osteosynthesis material, thus permitting primary bone healing without gap formation. On MRI, the bone marrow contiguous with the surgical

Fig. 2.78 Anatomic variants of the cauda fibers. Schematic axial image. Healthy lumbar spine at level L2–L5 (Modic). Visualized is the dural sac showing in each case three normal different forms of nerve root distributions. These must be distinguished from the asymmetrical distributions seen in association with inflammatory adhesions (see ▶ Fig. 2.77).

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Signs of an abnormal bone healing process include: ● Delayed or no CM enhancement, pointing to osteonecrosis. Table 2.4 Signal and CM patterns of regular bone healing (secondary/ per secundam) Weighting/CM

Days

Weeks

Months

Years

T1w

↓

↓

↑

↔ and/or ↓

T2w

↑

↑

↔

↔

CM

0

↑

↓

0

Abbreviation: T1w, T1-weighted; T2w, T2-weighted. Note: ↑, signal rise; ↓, signal decline; ↔, unchanging signal.

●

●

Strong involvement of the normal contiguous bone segments and soft tissues as a possible sign of osteomyelitis. Persistent bandlike signal alteration across the entire bone width or in the operated segment (Modic type I image), suggestive of instability or pseudarthrosis.53

Standard osteosynthesis materials that are properly fitted no longer constitute a contraindication to MRI examination. On using nonferromagnetic alloys or titanium, signal obliteration is, in the most favorable case, confined to the implant itself and of the same size (▶ Fig. 2.79). T1w and T2w SE sequences must then be used in cases where fat suppression sequences are not favorable and a GRE sequence is not advised because of major metal artefacts. It must also be borne in mind that metal artefacts manifest more strongly in line with increasing field strength, hence in such cases preference should be given to 1.0 T or 1.5 T MRI scanners over 3.0 T MRI scanners. MRI is not indicated for diagnosis of any loosening of prosthetic implants. However, MRI is beneficial in identifying inflammatory complications related to implants since it is able to visualize the extent of inflammation in bones and soft tissues and confirm or rule out abscesses. In the event of pain recurrence and a rise in the inflammatory parameters, the possibility of an epidural abscess must also be considered. MRI is the modality of choice here and will be able to visualize the characteristic features of an abscess. Vertebroplasty is a fluoroscopic or CT-based imaging procedure used to treat vertebral body fractures. This entails injection of polymethyl methacrylate, bone cement, through the pedicle directly into the fractured vertebral body. The injected bone cement exhibits a completely hypointense signal on all MRI

Fig. 2.79 Pedicle screws. The pedicle screws show a narrow metal artefact and provide for good assessment of the dural sac, bone marrow, soft tissues, and implant position on T2w TSE image. (a) Sagittal T2w TSE sequence, section. (b) Axial T2w TSE sequence, section.

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●

gap can over time appear reaction free and exhibit unchanging mixed bone marrow signal. Per secundam bone healing (▶ Table 2.4) normally occurs on using bone transplants, for example, following resection of benign bone tumor and focal filling or after filling the disk space during spondylodesis. The normal course of this bone healing process is first identified on MRI through the hypointense signal exhibited by the implant materials on T1w image and hyperintense signal on T2w image without CM enhancement. This is followed within a few weeks by strong CM uptake by the new growth of granulation tissue. The greater the implant material, the longer it will take for the granulation tissue to reach as far as the center. The intensity of CM enhancement declines over the ensuing course. After a number of months, fat deposition can be initially detected as a weak, and then as extensive, fatty marrow formation. This newly generated fatty marrow exhibits continuous bridging to its environment.36

2.7 Tumors of the Spine

In kyphoplasty, in contrast to vertebroplasty, before bone cement is injected, a balloon is introduced through a catheter to elevate the fractured vertebral body end plates. This helps to restore the original sagittal alignment of the vertebral column, conferring both cosmetic and functional benefits on patients. This can also be used for reduction of fractures of the adjacent vertebral bodies. The risk of bone cement extravasation is lower in kyphoplasty.

2.7 Tumors of the Spine Primary tumors of the spine account for only 3 to 9 % of all skeletal tumors (with the exception of hemangiomas and myelomas). Secondary tumors of the spine (metastases) are the most common type of spinal tumors in adults and children. MRI is used only as an adjunct to conventional radiography and CT for diagnosing primary spinal tumors. For benign primary tumors, MRI is mainly indicated to clarify any spread in the direction of the dural sac and/or paravertebral soft tissue structures. Conversely, MRI is the modality of choice for local staging and follow-up examination of malignant primary tumors. While for initial diagnosis of skeletal metastases technetium99 m phosphonate scintigraphy is the gold standard for initial whole-body screening for bone metastases, in the early stage small lesions can be missed because of no, or little, osteoblastic reaction. On the other hand, healing fractures or degenerative changes can also lead to false-positive results. Whole-body MRI

is superior to scintigraphy in terms of sensitivity and specificity for early diagnosis of skeletal metastases. In general, T1w TSE sequences, without CM, and STIR sequences are used to that effect (▶ Fig. 2.81). DWI sequences are also used in some places but, so far, not for routine purposes.91 PET (positron emission tomography)/CT is also employed as an alternative, or, in some cases, an adjunct, to whole-body screening for bone metastases. This has the advantage of providing information not only on morphology but also on metabolic processes. Many working groups worldwide have compared these two modalities and have concluded that both have their strengths and weaknesses and should be used accordingly.69

2.7.1 Development of Spinal Tumors There are different preconditions that must be met in order for primary and secondary spinal tumors to be able to develop and spread locally. One such requirement is adequate arterial vascularization. A particularly dense arterial network is found (in adults and children older than 4 years) in the anterior and subchondral vertebral bodies as well as in the pedicles. That mainly explains the frequent localization of metastases in these regions. Many authors also highlight the role in metastases to the spine played by the direct (valveless) venous connections between, on the one hand, the deep veins of the abdomen and breast and, on the other hand, the intra- and extraspinal venous plexus (Batson’s veins). Another recurring factor cited is the distribution of red (hematopoietic) bone marrow and fatty marrow. Over the course of a lifetime, this distribution changes in favor of the fatty marrow (see ▶ Fig. 2.2), but that process can be expedited by local “stress factors” (e.g., degeneration, resolved inflammation, trauma). Conversely, reconversion to red bone marrow can occur in particular in the presence of systemic diseases (e.g., anemia, lymphoma, diffuse metastases). Metastases, myeloma, lymphoma, Langerhans’ cell histiocytosis, and, less markedly, Ewing’s sarcoma are very closely associated with the presence of red bone marrow. Accordingly, they are found mainly in the region of the spine.26,46

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sequences (▶ Fig. 2.80). In status post vertebroplasty, the following complications can be identified on MRI: ● Infection. ● Spinal cord compression. ● Fracture of adjacent vertebral bodies. ● Fracture of the transverse process. ● Hematomas of the psoas muscle (in heparinized patients). ● Bone cement in the paravertebral soft tissues, peridural, intradiscal, or lumbar venous plexus.

Fig. 2.80 Status post vertebroplasty. T1w and T2w hypointense signal changes within vertebral bodies L3 and L4, suggestive of bone cement in status post vertebroplasty. Slight superior end plate impression of vertebral bodies L3 and L4 as well as marked superior end plate impression of vertebral body L2. There is also slight disk herniation at L3–S1. (a) Sagittal T1w SE sequence, section. (b) Sagittal T2w TSE sequence, section.

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2.7.2 Localization of Tumors Put simply, malignant and (pseudo)inflammatory processes are found more commonly in the vertebral bodies. In contrast, benign tumors tend to be localized in the posterior segments of the spine (vertebral arch, spinous process, transverse process, articular process—osteoblastoma, osteoid osteoma, aneurysmal bone cysts; ▶ Fig. 2.82).46

2.7.3 Common Benign Tumors and Tumorlike Lesions Hemangiomas are the most common benign primary spinal tumors and are found in all age groups. Around 10% of all people have hemangiomas, in particular in the thoracic and lumbar spine. Since these tumors are mainly clinically asymptomatic, they are often only discovered by chance. Many authors do not deem these to be genuine tumors, instead classifying them as a form of tissue dysplasia with accumulation of fatty tissue as well as (in particular venous) vessels and capillaries. Hemangiomas tend to be found mainly in the vertebral bodies and rarely grow in the direction of the vertebral arches. Their diagnosis has clinical implications, in particular if they become symptomatic, and in extreme cases—due to increasing compression—they cause narrowing of the dural sac or nerve roots. On MRI, a sharply demarcated lesion is generally seen, which, because of its fat content, is hyperintense on T1w and T2w images. On fat-suppressed images, hemangiomas may appear iso- or somewhat hyperintense to the surrounding bones (▶ Fig. 2.83). What are termed “aggressive” (symptomatic) hemangiomas have a more fibrovascular structure and therefore tend to be hypointense on T1w and T2w images. Marked enhancement is seen following IV CM administration.26

Aneurysmal Bone Cysts Aneurysmal bone cysts are the second most common type of benign bone tumors of the spine and are typically identified in

Fig. 2.81 Multiple skeletal metastases in patient with hypernephroma. T1w TSE sequence, whole-body MRI. Several rounded lesions, which are hypointense on T1w and hyperintense on T2w images, in both femurs with known diagnosis of metastases from renal cell carcinoma.

Furthermore, a number of other factors are important, for example, genes, cell division, local growth factors, cell and tissue mediators, but so far their role has not been fully elucidated. These are responsible for, among other things, onset of local clusters of tumors and, together with age and gender, play a crucial role in differential diagnosis.

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Fig. 2.82 Frequency distribution of tumors and tumorlike lesions in vertebral bodies and posterior spinal segments. AKZ, aneurysmal bone cysts; RT, giant cell tumor; H, hemangioma; LH, Langerhans’ cell histiocytoma; M, metastasis; MY, myeloma; OB, osteoblastoma; OO, osteoid osteoma.

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Hemangioma

2.7 Tumors of the Spine

Osteoid Osteoma and Osteoblastoma The majority of osteoid osteomas and osteoblastomas are found in the posterior segments of the spine. Whereas osteoid osteomas are most commonly identified during the second decade of life, osteoblastomas present especially in the second and third decade. Osteoblastomas measure more than 2 cm in diameter, while osteoid osteomas are smaller; hence, the osteoblastoma is seen as the “bigger brother” of the osteoid osteoma. In general, the characteristic clinical symptoms (salicylate-suppressed

nocturnal pain) and conventional radiography as well as CT findings mainly obviate the need for MRI examination. On MRI, the characteristic nidus exhibits a hypointense signal on T1w image and markedly hyperintense signal on T2w images and with strong CM enhancement as well as surrounding perifocal sclerosis (hypointense T1w and T2w images). A calcified nidus is naturally hypointense on T1w and T2w images. Another characteristic feature is the pronounced, and often extensive, bone marrow edema (▶ Fig. 2.85).95 For differential diagnosis, a Brodie’s abscess should be ruled out.

Langerhans’ Cell Histiocytosis (Eosinophilic Granuloma) In Langerhans’ cell histiocytosis, one or more vertebrae can be involved. The typical localization is the vertebral bodies and the most common age of onset is between 5 and 10 years. The characteristic osteolytic process can in 50% of cases lead to vertebral body collapse (vertebra plana) with swelling of the surrounding soft tissues (▶ Fig. 2.86). MRI shows (pseudo)inflammatory changes with edema and poorly defined borders but with strong enhancement following IV CM administration, in particular also in the surrounding

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the second decade of life. They occur in the posterior vertebral segments but the vertebral body is also often affected. There are primary and secondary aneurysmal bone cysts, with the latter also seen in association with osteoblastomas, giant cell tumors, and, very rarely, osteosarcomas. On MRI, aneurysmal bone cysts manifest as well-delineated, lobulated, expansive, in part solid, often multicystic periosteal lesions (▶ Fig. 2.84). Typically, the cysts contain fluid–fluid levels as well as blood breakdown products. While such changes will facilitate differential diagnosis, they are not pathognomonic. Calcification, which is often very thin (eggshelllike), can be observed as a mildly hypointense rim or septation.31

Fig. 2.83 Vertebral body hemangioma. Rounded, sharply and smoothly demarcated formation at the center of the vertebral body with coarse trabeculation and hyperintense signal on the visualized sequences in the presence of vertebral body hemangioma. (a) Sagittal T1w SE sequence, section. (b) Sagittal T2w TSE sequence, section. (c) Sagittal T2w STIR sequence, section.

Fig. 2.84 Aneurysmal bone cysts. Space-occupying lesion originating from vertebral body C6, sharply demarcated, multilobulated, with multiple fluid–fluid levels, only minor CM uptake by the wall, compression as well as displacement of the dural sac at the level of C5–C7 from dorsal and ensuing absolute spinal canal stenosis. (a) Sagittal T2w TSE sequence, section. (b) Sagittal T1w SE sequence with fat suppression and following CM administration, section.

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Fig. 2.85 Osteoid osteoma. (a) Sagittal T1w SE sequence with fat suppression and following CM administration, section. Strong CM uptake by the soft tissues at the level of C5–C7 paravertebral as well as by bony structures of zygapophysial joints C6/C7. (b) Axial T1w SE sequence with fat suppression and following CM administration, section. Moderate CM uptake by a rounded space-occupying lesion in the right pedicle at C6 with strong surrounding CM uptake by the adjacent bone as well as the adjacent soft tissues. (c) Axial CT, section. Rounded osteolysis of the right pedicle of C6 with discrete punctiform sclerosis at the center (nidus) in osteoid osteoma.

marginal zones. CM enhancement correlates with the activity stages (aggressiveness) of Langerhans’ cell histiocytosis.

Giant Cell Tumor This tumor typically manifests between the ages of 10 and 40 years and, when localized in the axial skeleton, is found in 70 to 80% of all cases in the sacral bone and less commonly in the vertebral bodies. It is an eccentric, characteristically relatively sharply marginated, often expansive osteolytic lesion. If found in a vertebral body, it can result in compression. On rare occasions, shell-like calcification is observed. MRI shows a solid tumor that exhibits a low signal intensity on T1w images and high signal intensity on T2w images (▶ Fig. 2.87). In particular following IV CM administration, a surprisingly large soft tissue tumor portion with strong homogeneous enhancement can be detected. Hence, MRI or CT is indicated preoperatively. This strong enhancement is also helpful when trying to diagnose recurrences. To what extent tumor aggressiveness is correlated with contrast agent enhancement intensity is unclear. In rare cases, fluid–fluid levels suggestive of secondary aneurysmal bone cysts can be identified. Occasionally, elevated hemosiderin content can generate uncharacteristically low signal intensity on all sequences.

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Fig. 2.86 Vertebra plana in the presence of eosinophilic granuloma. Sagittal T2w STIR sequence, section. The height of vertebral body T11 is greatly reduced, suggestive of vertebra plana with known diagnosis of eosinophilic granuloma.

2.7.4 Common Malignant Primary Tumors

Myeloma

The most common malignant primary tumors are myelomas and chordomas. Less common malignant primary tumors include chondrosarcomas, Ewing’s sarcomas (▶ Fig. 2.88), and osteosarcomas.

Myelomas are tumors that present at an older age, typically after the age of 50 years. The mainly multiple osteolytic, rarely expansive, lesions are found in vertebral bodies containing red bone marrow and often lead to fractures. However, the posterior

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2.7 Tumors of the Spine

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Fig. 2.87 Giant cell tumor. Space-occupying lesion of vertebral body S1 with marked inhomogeneous signal in giant cell tumor. Additional finding: osteochondrosis L5/S1 with slight Modic I changes as well as marked disk degeneration and herniation. (a) Sagittal T1w SE sequence, section. (b) Sagittal T2w TSE sequence, section. (c) Sagittal T2w STIR sequence, section.

Fig. 2.88 Ewing’s sarcoma. Tumor originating from vertebral body C2 with large soft tissue portion, strong CM uptake, leading to absolute spinal canal stenosis with known diagnosis of Ewing’s sarcoma. (a) Sagittal T2w TSE sequence, section. (b) Coronal T2w TSE sequence, section. (c) Axial T1w SE sequence with fat suppression and following CM administration, section.

vertebral segments can also be implicated in the event of reconversion of fatty to red bone marrow or because of direct infiltration. In around 3% of cases, the lesion is sclerotic and is mainly seen in association with POEMS syndrome (polyneuropathy, organomegaly, endocrinopathy, monoclonal gammopathy, skin disorders) whose pathogenesis is unknown. In some cases, there is complete diffuse involvement, with only osteopenia identifiable. MRI is endowed with 20 to 30% higher sensitivity for detection of myeloma foci compared with conventional radiographs. Since bone scintigraphy yields predominantly false-negative results, MRI is the modality of choice in particular also for diffuse involvement. The foci are characteristically hypointense on T1w and hyperintense on T2w images (▶ Fig. 2.89). A fat-suppression sequence (e.g., STIR) is recommended to distinguish hyperintense fatty marrow on T2w images. MRI can play a pivotal role in providing clinical, therapeutic, and prognostic insights. A clinically

symptomatic myeloma with unremarkable MRI results has in general an excellent prognosis. Besides, MRI is able in certain cases to assess the exact multiplanar extension of soft tissue tumors.47 The combined use of bone scintigraphy and MRI is very beneficial for the frequently employed differential diagnosis of myeloma, metastases, and osteoporosis. An unremarkable bone scan and pathologic MRI findings are suggestive of a myeloma, while, conversely, a pathologic bone scan and pathologic MRI findings are indicative of metastatic disease or osteoporosis, possibly with (micro)fractures.48,89 Involvement of the pedicles alone tends to point to metastatic disease and to rule out myeloma. However, myelomas can directly infiltrate the intervertebral disk and vertebral arch. To what extent metastases can be distinguished from osteoporotic vertebral body changes on DWI MRI sequences has not been fully elucidated. However, the fluid sign has proved to be a useful differential diagnostic sign (see ▶ Fig. 2.93).

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2.7.5 Common Malignant Secondary Tumors Metastases—with the exception of hemangiomas—are the most common spinal tumors. Metastases predominantly arise from the following carcinomas: ● Adults: ○ Mammary carcinoma. ○ Prostatic carcinoma. ○ Pulmonary carcinoma. ○ Renal carcinoma. ○ Carcinoma of the thyroid gland. ○ Carcinoma of the gastrointestinal tract. ● Children: ○ Neuroblastomas. ○ Leukemia. The most common localizations are: ● Vertebral bodies. ● Vertebral pedicles.

Fig. 2.89 Myeloma. (a) Sagittal T1w SE sequence. Multiple mottled signal changes in the entire spinal column; most are hypointense in the presence of myeloma; some are also hyperintense (example: L1)— suggestive of small hemangiomas. (b) Sagittal T2w STIR sequence. Multiple mottled hyperintense signal changes in the entire spinal column; most are suggestive of myeloma lesions (example: S2).

Chordoma Chordomas arise from the (remnants of the embryonic) notochord. Between 50 and 60% of all chordomas originate in the sacral bone or coccyx, and 30% in the region of the clivus. The typical age of onset is over 40 years. The implicated lesions are large and characteristically expansive and lytic, with, in 30% of cases, irregular, delicate calcified margins. In 10 to 40% of cases, the tumor matrix can exhibit central mottled calcification. In the rare cases where the cervical or thoracic spine is involved, the tumor has its origin in the vertebral body.

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Depending on how aggressive they are, the majority of metastases (75% of all metastases) are osteolytic with, more or less, sharply demarcated borders. Sclerotic halos are seen in slowgrowing metastases or as a response to treatment. Sclerotic (osteoblastic) metastases (15% of all metastases) have their origin in prostatic and mammary carcinomas, seminomas, and carcinomas of the uterus and ovary, as well as lymphomas. In exceptional cases, as in prostatic carcinoma, chondroma, and osteosarcoma, there is also new stromal bone formation. Around 10% of all metastases are a mixture of osteolytic and osteoblastic nature.26,46 Vertebral body fractures can occur secondarily to spinal metastatic disease. There can be infiltration of the intervertebral disk from the margin, especially in revascularization settings, but this is rarely seen (▶ Fig. 2.92). MRI is able to visualize metastases at an earlier stage than are bone scintigraphy, conventional radiography, or CT. Metastases manifest as hypointense on T1w and hyperintense on T2w images, while any sclerosis implicated can, but need not, reduce the high signal intensity. On fat-suppressed T2w images, metastases “light up” against the background of the spinal column. The fluid sign permits, with a high probability, the differentiation of osteoporotic from blastomous fractures. A characteristic finding is the high signal intensity seen in the fracture region on T2w images. This is indicative of an osteoporotic fracture (▶ Fig. 2.93). In cases where pathologic (edematous) hyperintensity is exhibited on T2w images, differential diagnosis can only be made through follow-up examination: resolution of the high signal intensity over a period of 4 to 8 weeks is suggestive of

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Metastases

2.7 Tumors of the Spine Fig. 2.90 Chordoma. Extensive tumor originating from vertebral body C2, hypointense on T1w and hyperintense on T2w images, with large soft tissue portion and absolute spinal canal stenosis as well as compression of the spinal cord with known diagnosis of chordoma. (a) Sagittal T1w SE sequence, section. (b) Sagittal T2w TSE sequence, section.

osteoporotic fracture. In contrast, unchanging or rising signal intensity is more likely to point to a metastatic fracture. Where fatty marrow is present, it is suggestive of an osteoporotic fracture and can facilitate differential diagnosis between metastatic and osteoporotic vertebral body fractures, which continues to pose a challenge despite how often it is done. An in-phase and opposed-phase quantification technique can be used for quantification to distinguish between osteoporotic and metastatic spinal anomalies. Accordingly, recent fractures that are hypointense on T1w sequences and exhibit a reduction in signal intensity of less than 20% on opposed-phase sequence are more suggestive of blastomous genesis of the fracture (▶ Fig. 2.94 and ▶ Fig. 2.95).94 The differences in signal can also be optically detected in the examples presented here (see ▶ Fig. 2.94 and ▶ Fig. 2.95). However, precise measurement of the signal intensities is generally

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Fig. 2.91 Chordoma. Large tumor originating from vertebral body S2/S3, hypointense on T1w and hyperintense on T2w images with distinct soft tissue portion and known diagnosis of chordoma (different patient from Fig. 2.90). (a) Sagittal T2w TSE sequence, section. (b) Sagittal T1w SE sequence with fat suppression and following CM administration, section.

needed. The routine use of MRI diffusion measurements based on ADC values for differentiation of metastatic from osteoporotic spinal anomalies is growing and significantly underpins diagnostic reliability. Bone metastases exhibit hyperintense signal on DWI sequences as well as low ADC values secondary to membrane damage and reduced bone marrow diffusion. In contrast, in fractured and inflammation-related bone changes, increased bone marrow diffusion with hypointense signal can be seen on DW sequences in addition to high ADC values.4,73

Secondary Lymphomas Primary lymphoma of bone is an extremely rare entity. Hence, the vast majority of bone lymphomas are secondary lymphomas, with onset between the ages of 20 and 60 years. Like myeloma,

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they are dependent on the availability of red bone marrow, which explains why the vertebral bodies are more often affected. The spine is implicated in 10 to 30% of cases in Hodgkin’s disease and in 5 to 25% of cases in non-Hodgkin’s lymphomas. The lesions are mainly aggressive, osteolytic, sclerotic, or mixed, with sclerotic changes occurring relatively often in Hodgkin’s lymphoma (= “ivory vertebra”). On MRI, the lesions exhibit homogeneous hypointense signal on T1w images and often appear as a mottled hyperintense mass on T2w images. A salient feature is the diffuse infiltration into the surrounding area (including the intervertebral disk), often extending beyond the normal tissue boundaries, with formation of a soft tissue tumor.26,31,61 IV CM injection results in, often mottled, enhancement. Central necrosis may be observed depending on the tumor size. There may be markedly low signal intensity on T2w images because of the highly sclerotic nature of the ivory vertebrae.

2.8 Clinical Significance of Magnetic Resonance Imaging Clinical interview

Fig. 2.93 Fluid sign. Sagittal T2w STIR sequence, section. Vertebral body fracture of L1 with marked reduction in height of vertebral body; involvement of the posterior border of vertebral body, spinal canal stenosis, distinct bone marrow edema and linear, fluid-isointense signal change (“fluid sign”; arrow) in the bone, parallel to fractured superior end plate in the presence of osteoporotic vertebral body fracture.

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●i

For the clinical interview, the authors were able to put questions to a renowned spinal specialist, Prof. Josef G. Grohs, Specialist for Orthopaedics and Orthopaedic Surgery in the Department of Orthopaedics at the Medical University of Vienna. Question: “For which clinical manifestations do you see false-positive MRI results more often?”

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Fig. 2.92 Vertebral body metastasis. Spaceoccupying lesion in posterior section of vertebral body L1, exhibiting marked CM uptake, hyperintense on T2w image, with infiltration of the posterior border of the vertebral body, large intraspinal soft tissue portion extending further in cranial and caudal direction, giving rise to high-grade spinal canal stenosis with compression of the conus medullaris in the presence of metastasis to the vertebral body from a renal cell carcinoma. While here the tumor is in contact with the contiguous disks, there is no evidence of clear infiltration. (a) Sagittal T2w STIR sequence, section. (b) Sagittal T1w SE sequence following CM administration, section.

2.8 Clinical Significance of Magnetic Resonance Imaging

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Fig. 2.94 Osteoporotic vertebral body fracture of L2. Use of in-phase and opposed-phase imaging for differentiation between osteoporotic and metastatic spinal anomalies. The signal is reduced by more than 20% within the region of interest (ROI) (oval-shaped marking) in vertebral body L2 on opposed-phase versus inphase sequence. (a) Sagittal T1w SE sequence, in-phase technique, section. (b) Sagittal T1w SE sequence, opposed-phase technique, section.

Fig. 2.95 Vertebral body metastasis of L2. Use of in-phase and opposed-phase imaging for differentiation between osteoporotic and metastatic spinal anomalies. The signal is not reduced (less than 20%) within ROI (oval-shaped marking) in vertebral body L2 on opposed-phase versus in-phase sequence. (a) Sagittal T1w SE sequence, in-phase technique, section. (b) Sagittal T1w SE sequence, opposed-phase technique, section.

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The Spine [5] Baur A, Stäbler A, Arbogast S, Duerr HR, Bartl R, Reiser M. Acute osteoporotic and neoplastic vertebral compression fractures: fluid sign at MR imaging. Radiology. 2002; 225(3):730–735 [6] Baur A, Bartl R, Pellengahr C, Baltin V, Reiser M. Neovascularization of bone marrow in patients with diffuse multiple myeloma: a correlative study of magnetic resonance imaging and histopathologic findings. Cancer. 2004; 101 (11):2599–2604 [7] Boden SD, Davis DO, Dina TS, et al. Contrast-enhanced MR imaging performed after successful lumbar disk surgery: prospective study. Radiology. 1992; 182 (1):59–64 [8] Bollow M, Braun J, Hamm B, et al. Early sacroilitis in patients with spondyloarthropathy. Radiology. 1995; 194:529 [9] Brandt KD, Doherty M, St. Lohmander L. Osteoarthritis. Oxford: Oxford University Press; 1998 [10] Breitenseher MJ, Gäbler C, Kukla C, Trattnig S, Imhof H. The traumatized and surgically treated spine. Current diagnostic imaging [in German]. Radiologe. 1994; 34(12):740–746 [11] Breitenseher M, Kontaxis G, Fleischmann D, Rand TH, Imhof H, Trattnig S. Ultrashort turbo-spin echo in comparison with turbo-spin echo. Possible applications in the musculoskeletal system [in German]. Radiologe. 1995; 35(12):981–983 [12] Breitenseher M. Der MR-Trainer Wirbelsäule. Stuttgart: Thieme; 2010 [13] Bullough PG, Boachie-Adjei O. Atlas of Spinal Diseases. New York, NY: Gower Medical Publishing; 1988 [14] Burton CV. Avoiding the “failed back surgery syndrome”. In: Cauther JC, ed. Lumbar Spine Surgery. Baltimore, MD: Williams & Wilkins; 1988:331–341 [15] Castillo M. Diffusion-weighted imaging of the spine: is it reliable? AJNR Am J Neuroradiol. 2003; 24(6):1251–1253 [16] Chan CW, Peng P. Failed back surgery syndrome. Pain Med. 2011; 12 (4):577–606 [17] Dagimanijian A, Schils J, McHenry MC. MRI imaging of spinal infections. MRI Clin N Am. 1999; 7:525 [18] Davis SJ, Teresi LM, Bradley WG, Jr, Ziemba MA, Bloze AE. Cervical spine hyperextension injuries: MR findings. Radiology. 1991; 180(1):245–251 [19] Denis F. The three column spine and its significance in the classification of acute thoracolumbar spinal injuries. Spine. 1983; 8(8):817–831 [20] Doran SE, Papadopoulos SM, Ducker TB, Lillehei KO. Magnetic resonance imaging documentation of coexistent traumatic locked facets of the cervical spine and disc herniation. J Neurosurg. 1993; 79(3):341–345 [21] Dorwart RH, Vogler JB, III, Helms CA. Spinal stenosis. Radiol Clin North Am. 1983; 21(2):301–325 [22] Eder M, Tilscher H. Schmerzsyndrome der Wirbelsäule. Stuttgart: Hippokrates; 1988 [23] Fandiño J, Botana C, Viladrich A, Gomez-Bueno J. Reoperation after lumbar disc surgery: results in 130 cases. Acta Neurochir (Wien). 1993; 122(1–2):102–104 [24] Fardon DF, Milette PC, Combined Task Forces of the North American Spine Society, American Society of Spine Radiology, and American Society of Neuroradiology. Nomenclature and classification of lumbar disc pathology. Recommendations of the Combined task Forces of the North American Spine

2.8.1 Acknowledgment We thank Dr. Maria Theresa Schmook for her assistance in researching figures (▶ Fig. 2.9, ▶ Fig. 2.10, ▶ Fig. 2.11, ▶ Fig. 2.59, ▶ Fig. 2.68, and ▶ Fig. 2.69).

Society, American Society of Spine Radiology, and American Society of Neuroradiology. Spine. 2001; 26(5):E93–E113 [25] Flanders AE, Schaefer DM, Doan HT, Mishkin MM, Gonzalez CF, Northrup BE. Acute cervical spine trauma: correlation of MR imaging findings with degree of neurologic deficit. Radiology. 1990; 177(1):25–33 [26] Freyschmidt J, Ostertag H, Jundt G. Knochentumoren. Berlin: Springer; 1998 [27] Friedman D, Flanders A, Thomas C, Millar W. Vertebral artery injury after

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acute cervical spine trauma: rate of occurrence as detected by MR angiography and assessment of clinical consequences. AJR Am J Roentgenol. 1995; 164 (2):443–447, discussion 448–449 [28] Friedrich KM, Nemec S, Peloschek P, Pinker K, Weber M, Trattnig S. The prevalence of lumbar facet joint edema in patients with low back pain. Skeletal Radiol. 2007; 36(8):755–760 [29] Friedrich KM, Reiter G, Pretterklieber ML, et al. Reference data for in vivo magnetic resonance imaging properties of meniscoids in the cervical zygapophyseal joints. Spine. 2008; 33(21):E778–E783 [30] Greenspan A. Orthopedic Radiology. Baltimore, MD: Williams & Wilkins; 2000 [31] Greenspan A, Remagen W. Differential Diagnosis of Tumors and Tumorlike Lesions of Bones and Joints. Philadelphia, PA: Lippincott-Raven; 1998 [32] Grenier N, Greselle JF, Vital JM, et al. Normal and disrupted lumbar longitudinal ligaments: correlative MR and anatomic study. Radiology. 1989; 171(1):197–205

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Answer: “False-positive MRI results are encountered more often in postoperative changes, in particular with regard to unclear recurrent prolapse and postoperative fluid accumulation, such as CSF cushions, seromas, or abscess formation.” Question: “For which clinical manifestations do you see false-negative MRI results more often?” Answer: “I encounter false-negative MRI results especially in the following two situations: Patients with persistent exertional radiculopathy for whom routine MRI is unable to detected any relevant foraminal stenosis at L3/L4 or L4/L5. I believe this is often due to position-related vertebral slippage. Conduct of MRI with the patient in a supine position leads to relaxation and loss of lordosis; hence, in patients exhibiting pronounced lumbar lordosis on lateral radiographs taken with the patient standing up, foraminal stenosis is missed on MRI when the patient is in a supine position. Similar problems can be seen in patients with Meyerding grade I spondylolysis or spondylolisthesis when they undergo MRI examination in a supine position.” Question: “For which clinical manifestations can MRI be dispensed with or for which is this modality being overused?” Answer: “MRI is only one aspect. Unfortunately, conventional radiography is often omitted for spinal patients. The reasons put forward for that range from ‘On MRI one sees everything more clearly’ to ‘An X-ray was carried out already five years ago, now I want to know what’s happening’. Another mistake in my opinion is that many people believe that a 3 T MRI scanner is needed for every patient. In most cases related to the spine, a 1.5 T MRI is adequate. Here, one should also bear in mind that increasingly more patients have several implants, for example, hip TEP [total endoprosthesis] and pedicle screws or active implantable medical devices; hence, here 3 T would be unsuitable and more metal artefacts could cause problems.”

2.8 Clinical Significance of Magnetic Resonance Imaging

Fischer; 1987 [34] Hackney DB. Magnetic resonance imaging of the spine. Technology and technique. Top Magn Reson Imaging. 1992; 4(2):7–11 [35] Haneder S, Apprich SR, Schmitt B, et al. Assessment of glycosaminoglycan content in intervertebral discs using chemical exchange saturation transfer at 3.0 Tesla: preliminary results in patients with low-back pain. Eur Radiol. 2013; 23(3):861–868 [36] Hilibrand AS, Dina TS. The use of diagnostic imaging to assess spinal arthrodesis. Orthop Clin North Am. 1998; 29(4):591–601 [37] Ho PS, Yu SW, Sether LA, Wagner M, Ho KC, Haughton VM. Progressive and regressive changes in the nucleus pulposus. Part I. The neonate. Radiology. 1988; 169(1):87–91 [38] Imhof H, Kramer J, Rand T, Trattnig S. Bone inflammation (including spondylitis) [in German]. Orthopade. 1994; 23(5):323–330 [39] Jevtic V, Rozman B, Kos-Golja M, Watt I. MR imaging in seronegative spondyloarthritis [in German]. Radiologe. 1996; 36(8):624–631 [40] Jevtic V, Rozman B, Kos-Golja M, Watt I. MR imaging in seronegative spondyloarthritis [in German]. Radiologe. 1996; 36(8):624–631 [41] Junghanns H. Die Wirbelsäule unter den Einflüssen des täglichen Lebens, der Freizeit, des Sportes. Stuttgart: Hippokrates; 1986 [42] Kalfas I, Wilberger J, Goldberg A, Prostko ER. Magnetic resonance imaging in acute spinal cord trauma. Neurosurgery. 1988; 23(3):295–299 [43] Kelsey JL, Golden AL, Mundt DJ. Low back pain/prolapsed lumbar intervertebral disc. Rheum Dis Clin North Am. 1990; 16(3):699–716 [44] Kramer J. Bandscheibenbedingte Erkrankungen. Stuttgart: Thieme; 1986 [45] Kramer J, Kainberger F, Stanisziewski K, Steiner E, Imhof H. Modern intervertebral disk diagnosis [in German]. Radiologe. 1993; 33(10):567–572 [46] Kricun ME. Imaging of Bone Tumors. Philadelphia, PA: Saunders; 1993 [47] Kusumoto S, Jinnai I, Itoh K, et al. Magnetic resonance imaging patterns in patients with multiple myeloma. Br J Haematol. 1997; 99(3):649–655

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nal bone marrow. Radiology. 1997; 204(1):201–205 [50] Meyerding HW. Spondylolisthesis. Surg Gynecol Obstet. 1932; 54:371 [51] Modic MT. Degenerative disc disease and back pain. Magn Reson Imaging Clin N Am. 1999; 7(3):481–491, viii [52] Modic MT, Feiglin DH, Piraino DW, et al. Vertebral osteomyelitis: assessment using MR. Radiology. 1985; 157(1):157–166 [53] Modic MT, Steinberg PM, Ross JS, Masaryk TJ, Carter JR. Degenerative disk disease: assessment of changes in vertebral body marrow with MR imaging. Radiology. 1988; 166(1, Pt 1):193–199 [54] Modic MT, Masaryk TJ, Ross RS. Magnetic Resonance Imaging of the Spine. St. Louis, MO: Mosby; 1994

(10):1079–1081 [78] Sze G, Bravo S, Baierl P, Shimkin PM. Developing spinal column: gadoliniumenhanced MR imaging. Radiology. 1991; 180(2):497–502 [79] Tarr RW, Drolshagen LF, Kerner TC, Allen JH, Partain CL, James AE, Jr. MR imaging of recent spinal trauma. J Comput Assist Tomogr. 1987; 11(3):412–417 [80] Terk MR, Hume-Neal M, Fraipont M, Ahmadi J, Colletti PM. Injury of the posterior ligament complex in patients with acute spinal trauma: evaluation by MR imaging. AJR Am J Roentgenol. 1997; 168(6):1481–1486 [81] Tournade A, Patay Z, Krupa P, Tajahmady T, Million S, Braun M. A comparative study of the anatomical, radiological and therapeutic features of the lumbar facet joints. Neuroradiology. 1992; 34(4):257–261

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3.1

Introduction

84

3.2

Examination Technique

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The Shoulder

3.3

Anatomy

87

3.4

Disorders of the Rotator Cuff

94

3.5

Disorders of the Proximal Biceps Tendons 102

3.6

Disorders of the Remaining Muscles (Including the Sequelae of Nerve Compression Syndrome)

107

3.7

Disorders of the Bursae

109

3.8

Disorders and Instability of the Glenoid Labrum and Capsular Ligaments

110

3.9

Disorders of the Synovial Lining and Joint Capsule 122

3.10

Bone Disorders

124

3.11

Disorders of the Acromioclavicular Joint

129

3.12

Disorders of the Sternoclavicular Joint

130

3.13

Tumors of the Shoulder

130

3.14

Post-Therapy Findings

131

3.15

Pitfalls in Interpreting the Images

136

3.16

Clinical Relevance of Magnetic Resonance Imaging 138 References

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Chapter 3

The Shoulder

3 The Shoulder M. Vahlensieck and C. Pfirrmann

As a ball-and-socket joint, the shoulder is a common site of chronic complaints. It is not unusual for young athletes to experience shoulder pain but have otherwise normal radiographic results. In addition to clinical diagnostic measures, there are a number of imaging procedures for further investigation of such complaints, with magnetic resonance imaging (MRI) playing a leading role. The increasing importance of MRI of the shoulder has been well documented in numerous review articles.9,53,63,76,105,129,133,142,161 In this chapter, we will present the anatomy and pathologic changes seen on the MRI scan and also discuss the relevance of MRI in diagnostic evaluation of the shoulder joint.

Internet link Further information with numerous images and texts can be found on the ShoulderDoc website.

●i

3.2 Examination Technique 3.2.1 Patient Positioning The patient is examined in a supine position, starting with the head. The patient should rest comfortably to avoid motion artefacts during examination. Supporting pillows, or similar, can be useful here. To avoid respiratory artefacts, the arm to be imaged should not be placed on the abdomen. It should be placed parallel to the body in a neutral position. Internal or external rotation of the arm should be avoided, as it could give rise to undesirable effects resulting from overlapping of the tendons of the rotator cuff with the surrounding soft tissues and hence to misinterpretations.23 The shoulder to be examined can be additionally stabilized with a sandbag to prevent minor movements. Suppression of respiratory artefacts is generally not needed. For patients with very broad shoulders, it may be necessary to position the patient somewhat obliquely by elevating the opposite shoulder. This will bring the respective side toward the isocenter of the magnetic field and improve the image quality.

field of view (FOV) and a body coil. The images thus obtained can help to select the higher resolution sequences for the respective shoulder and occasionally also to compare the distribution of the bone marrow signal of both shoulder joints.

Transverse (Axial) Plane The first high-resolution sequence is often performed in the transverse (axial) plane. It is important to ensure that the resolution is adequate and that the cranial sections include the acromioclavicular joint. For optimal resolution, the FOV should be adapted to the region of interest, as is the case for all higher resolution MRI examinations. Ideally, this is between 140 mm × 140 mm and 180 mm × 180 mm. Because of the signal-to-noise ratio (SNR), the value selected is determined by the magnetic field strength of the MRI scanner. The slice thickness should not exceed 4 mm. The most suitable sequences are proton density–weighted (PDw) TSE sequences with fat suppression. Transverse images are best suited for diagnosing disorders of the glenoid labrum and of the long head of biceps tendon.

Oblique Coronal Section The images obtained with these transverse sequences through the supraspinatus (muscle) are used to select the following two subsequent sequences (▶ Fig. 3.1): ● An oblique coronal T1-weighted (T1w) spin-echo (SE) or TSE sequence. ● An oblique coronal short-tau inversion recovery (STIR) or PDw fat-suppressed TSE sequence. This imaging plane is at an angle of around 45 degrees to the coronal plane and, as such, is parallel to the main axis of the supraspinatus. Using an SE sequence makes it easier to detect susceptibility artefacts, hemorrhage, and fatty marrow infiltration. Oblique coronal images are best suited for assessment of the rotator cuff and the subacromial-subdeltoid bursa. A frequency-selective, fat-suppressed PDw or T2-weighted (T2w) TSE sequence can be used as an alternative to the STIR sequence. Anterior

3.2.2 Coil Selection

Oblique sagittal

To obtain an adequate signal, the shoulder is examined using a dedicated shoulder coil. Alternatively, flexible or rigid ring coils as well as rectangular coils can be used. Various manufacturers currently offer multichannel shoulder coils.

3.2.3 Sequences and Parameters

Oblique coronal Posterior

Multiplane View The imaging protocol should ideally begin with a fast multiplane view (turbo spin echo [TSE] or gradient echo [GRE]) using a large

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Fig. 3.1 Transverse section of shoulder joint. Schematic diagram. Depiction of oblique sagittal and oblique coronal slices.

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3.1 Introduction

3.2 Examination Technique

Oblique Sagittal Section

Special Techniques

The oblique sagittal plane is perpendicular to the oblique coronal plane and lends itself to imaging the external rotator cuff as well as the supraspinatus outlet (see Coracohumeral and Glenohumeral Ligaments, p. 93). A fluid-sensitive sequence, such as an oblique sagittal TSE sequence (PDw fatsat TSE sequence), is suitable for, among other things, examination of the subacromial-subdeltoid bursa, deltoid, bony structures, and the rotator cuff. A non– fat-saturation sequence (T1w SE, T2w TSE) in this plane is suitable for detecting muscular atrophy and fatty degeneration and can be performed additionally, if necessary. This sequence should provide for widespread medial coverage of the soft tissues (at least half of the belly of the supraspinatus should be visualized medially) (▶ Fig. 3.2).

Special techniques, such as radial acquisition with radial rather than parallel acquisition,86 or 3D image depiction (3D rendering) which is even more time-consuming and error-prone, have not become established for routine MRI of the shoulder. Occasionally, it is easier to detect pathologic changes when the arm is in different positions because of the various tension forces applied to the soft tissue structures. One such position is the abduction and external rotation (ABER) position. Additional sections imaged in this position will help detect pathologies such as partial tear of the rotator cuff, thrower’s posterolateral impingement syndrome, or a horizontal tear component in partial rotator cuff rupture.66 However, such an additional time-consuming examination can generally be dispensed with in routine application.

3.2.4 Special Imaging Techniques Administration of intravenous contrast media (CM) can be helpful for detection of tumors with a soft tissue component.

Three-Dimensional Data Set with Subsequent Multiplanar Reformatting A technique involving acquisition of a three-dimensional (3D) data set with subsequent multiplanar reformatting has occasionally been advocated but has not yet become established for routine use, since, in such cases, only single-contrast images are available for image interpretation. Besides, the resolution in the reconstructed sections is identical with the original data set only for isotropic data sets (see Chapter 1.14). However, generation of an isotropic data set of the shoulder with good resolution is very time-consuming and, in the end, there is no time saving compared with conventional methods because of the additional long reconstruction times. One possible application of multiplanar reformatting of isotropic data sets is the visualization of anatomic structures that cannot be well evaluated in standard sections, such as the coracoacromial ligament. This permits selection of any planes with enhanced visualization of anatomic structures.

Fig. 3.2 Hook-shaped acromion with impingement of supraspinatus. Oblique sagittal slice. SE sequence (0.5 T, TR = 1,800 ms, TE = 20 ms).

Magnetic Resonance Arthrography MR arthrography, in particular when combined with fat suppression, can provide for significantly enhanced assessment of partial tears of the undersurface and internal surface of the rotator cuff.52,98 MR arthrography can also facilitate diagnosis of lesions in the biceps tendon, rotator interval (pulley), glenohumeral ligaments, and glenoid labrum.33,99 To perform this procedure, 10 to 15 mL of at least 1:250 (corresponding to 0.002 mmol/mL) diluted CM with some radiographic CM is injected into the joint under fluoroscopic guidance and then T1w images, ideally with fat saturation, are obtained (▶ Fig. 3.3). Alternatively, indirect MR arthrography131 can be performed. To that effect, 0.1 to 0.2 mmol/kg MRI CM is injected intravenously. The CM will be taken up by the internal joint space by exercising the joint for 10 to 15 minutes, if possible. To obtain arthrographic images, fat-suppressed T1w sequences are then obtained in the axial and sagittal planes. The sensitivity and specificity of indirect and direct MR arthrography are equally good.21,57,96,140 Ideally, the axial images should be obtained in internal and external rotation. MR arthrography, too, is performed with the arm in different positions for better detection of various pathologies (▶ Fig. 3.4). For example, it may be easier to identify lesions of the anterior labrum in external rotation, and posterior lesions in internal rotation, of the arm. This is particularly true for indirect MR arthrography. Because of the tension applied to the injured labrum, the torn area opens up more, resulting in CM uptake and better detection. Partial tears of the rotator cuff are best identified in indirect arthrography in the ABER position (discussed earlier).49 The sensitivity for diagnosis of SLAP (superior labral tear with anterior and posterior extension) lesions can be improved by carrying out MR arthrography under arm traction.19 Many of the additional positions explored hitherto are no longer used on a routine basis. The third way to obtain an MR arthrographic effect is to inject NaCl solution and generate T2w images. To that effect, around 10 to 15 mL NaCl solution is injected into the joint before examination. Compared with native MRI, this improves assessment of the labrum and glenohumeral ligaments.149 One drawback is the less favorable SNR resulting in poorer overall images (completeness of joint contrast, sharpness of the joint capsule, motion artefacts).155

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Contrast Media

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a

b

Fig. 3.3 Glenohumeral joint. Direct MR arthrography. (a) Axial slice. Medial glenohumeral ligament (arrow). (b) Oblique coronal sequence. Highcontrast visualization of the internal joint space. Inferior glenohumeral ligament (arrow).

Fig. 3.4 Shoulder joint in different arm positions. Indirect MR arthrography, axial plane. Different degrees of tension applied to capsule by the various rotation positions. The anterior labrum appears dilated and of rather homogeneous signal intensity (a, arrow). But a tear can definitely be ruled out. (a) Arm in internal rotation. (b) Arm in external rotation.

Cinematic Examination Cinematic examination of the shoulder girdle is possible with fast GRE sequences.11 On cinematographic investigation of rotational motion, the anterior labrum exhibits great mobility and deformability as well as marked signal variations. By contrast, the

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posterior labrum remains largely unchanged in shape and signal intensity.111 Open MRI scanners provide sufficient room for cinematographic imaging of the shoulder. Conversely, closed scanners permit only limited cinematographic exploration.

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The Shoulder

3.3 Anatomy

3.3.1 General Anatomy Within the shoulder girdle, the humerus and scapula (humeral glenoid joint) as well as the acromion and clavicle (acromioclavicular joint) articulate. The articular surface of the scapula covers only around one-third of the articular surface of the humerus. The area of contact within this joint is extended by a fibrocartilaginous rim, the glenoid labrum. The joint capsule is reinforced anteriorly by three ligaments (glenohumeral ligaments) that have two variable outpouchings for communication with the subscapularis bursa. The inferior glenohumeral ligament has two bundles, an anterior and a posterior bundle, between which lies the axillary recess formed by the capsule (▶ Fig. 3.5). The joint is surrounded by an envelope of connective tissue formed by the tendons of four muscles (rotator cuff). The multigastric subscapularis courses anteriorly, the digastric supraspinatus superiorly, and the infraspinatus and teres minor posteriorly. It was only recently that the structure of the supraspinatus, with its two segments, was identified more clearly thanks to MRI, among other things.136 The spatial relationship of the supraspinatus to the surrounding tissues is of great significance with regard to the pathologic changes seen in the rotator cuff. Horizontal connective tissue thickening on the undersurface of the rotator cuff of the supra- and infraspinatus muscles is also known as the “rotator cable” (semicircular humeral ligament).41,120 The arch formed by the acromion, coracoacromial ligament, and acromioclavicular joint is also called the “supraspinatus outlet” or coracoacromial arch.89 The tendon of the long head of biceps originates from the supraglenoid tubercle of the scapula and courses anteriorly through the joint to the bicipital groove (intertubercular sulcus) of humerus, where it is enclosed by a tendon sheath. The short head of biceps arises, together with the coracobrachialis, from the apex of the coracoid process. The large subacromial-subdeltoid bursa is situated between the deltoid surrounding the shoulder and the rotator cuff. It is the largest bursa in the human body and is composed of a subacromial portion and subdeltoid portion, often demarcated by an indentation. In 10% of cases, the subacromial-subdeltoid bursa communicates with the subcoracoid bursa deep to the coracoid process.

A wedge-shaped intra-articular disk, the articular disk, projects into the acromioclavicular from the upper part of the articular capsule.

3.3.2 Specific Magnetic Resonance Anatomy and Variants ▶ Table 3.1 assigns the most important anatomic structures to the planes most suitable for their visualization.

Transverse Plane Supraspinatus Muscle The supraspinatus, which courses at an angle of around 40 degrees to the coronal plane, is best demonstrated on transverse images (▶ Fig. 3.6). The centrally located tendon accepts fibers from the anterior and posterior muscle belly and assumes an eccentric course at an angle of 50 degrees within the muscle fibers (▶ Fig. 3.7). Both muscle bellies as well as the eccentric strong tendon insert at the greater tubercle. In over 80% of cases, the central tendon also inserts at the lesser tubercle as well as at the intertubercular ligament.136 Visualization of the supraspinatus on transverse images is useful for preparing the oblique coronal and oblique sagittal sections. It does not matter whether 40- or 50-degree angulation is selected for the oblique coronal sequences.135

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3.3 Anatomy

Glenoid Labrum The anterior and posterior parts of the glenoid labrum can also be well evaluated on transverse slices as signal void, mainly rectangular structures. They cap the cortical bone of the scapula as well as, to an extent, the high-signal hyaline articular cartilage. When interpreting the findings, it must be borne in mind that the labrum can have numerous variants and that in rare cases (up to around 8%) it cannot be visualized at all (▶ Fig. 3.8).70,71,92 The shape of the anterior labrum is more variable than that of its posterior counterpart, which is mainly triangular or rounded. Normal variants of the glenoid labrum are found in particular in the upper anterior portion (in up to 10% of cases) where the labrum can be separated from the bony glenoid fossa (sublabral foramen or subcoracoid recess) or may be completely absent (partial labral aplasia). Another normal variant where there is no labral attachment has been described for other labral zones as well as for the entire labrum. Partial aplasia is often associated with cordlike thickening of the medial glenohumeral ligament (Buford complex). Both normal variants can be mistaken for tears during arthroscopy and imaging investigation (▶ Fig. 3.9).

Table 3.1 Important anatomic structures of the shoulder joint, arranged according to the most suitable MRI plane Transverse ●

Fig. 3.5 Glenoid fossa. Schematic view from above of the three glenohumeral ligaments; insertion of the long biceps tendon as well as the remaining joint capsule. The axillary recess of the capsule lies folded between the anterior and posterior bundles of the inferior glenohumeral ligament.

● ● ●

●

Subscapularis Glenoid labrum Joint capsule Glenohumeral ligaments Biceps tendon

Oblique coronal ● ● ● ●

Supraspinatus Infraspinatus Subacromial bursa Acromioclavicular joint

Oblique sagittal ● ●

● ●

Rotator cuff Coracoacromial ligament Acromion Biceps tendon

87

The Shoulder

Deltoid

Clavicle Supraspinatus muscle Anterior belly Central tendon Posterior belly Spine of scapula Infraspinatus muscle

a

Short head tendon Greater tubercle

Coracoid process Pectoralis minor

Proximal humeral epiphysis Deltoid

Medial glenohumeral ligament Glenoid labrum

Normal epi- /metaphyseal step-off

Subscapularis

Proximal humeral metaphysis

Glenoid fossa

Lesser tubercle

Infraspinatus Teres minor

b

Biceps, long head tendon Biceps, short head

Humerus

Axillary artery and vein Coracobrachialis

Deltoid

Subscapularis

Triceps

Scapula Infraspinatus c Fig. 3.6 Anatomy of the shoulder. Transverse plane. GRE sequence (0.5 T, TR = 600 ms, TE = 14 ms, flip angle = 30 degrees). (a) Section 1. (b) Section 2. (c) Section 3.

Areas of increased focal and linear signal intensity within the labrum have also been reported in patients free of trauma and other complaints. It must therefore be assumed that, as seen on MRI of the knee menisci, there are also artificial

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signal variations within the glenoid labrum caused by the different orientation of the fiber cartilage in the main magnetic field or because of residual vascularization. These signals should not be mistaken for a tear.

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Biceps, long head tendon

3.3 Anatomy

Fig. 3.8 Glenoid labrum. Schematic diagram, transverse plane. Morphologic variants of the glenoid labrum with relative distribution in % of the anterior labrum. The posterior labrum is generally triangular or rounded. 1, triangular with line of basal increased signal intensity along the hyaline articular cartilage (50%); 2, rounded (20%); 3, comma-shaped, flattened (7%); 4, obliterated (3%); 5, cleaved (15%); 6, notched (8%); 7, central increase in signal intensity; 8, linear increase in signal intensity.

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Fig. 3.7 Supraspinous fossa. Schematic view from above. The supraspinatus consists of two muscle bellies and has a central, eccentrically located tendon.

Fig. 3.9 Normal variants of the superior anterior aspect of the glenoid labrum. Left: view from above of the glenoid fossa with the glenoid labrum and the three glenohumeral ligaments. Right: corresponding axial MRI of the upper portion of the glenoid fossa (level marked by line on depicted view). (a) Normal finding. (b) “Sublabral foramen” through the partially obliterated labral attachment to the glenoid fossa. (c) Partial labral aplasia. If this is accompanied by a thickened medial glenohumeral ligament, the term “Buford complex” is used to describe it. Caution: These normal variants must not be misinterpreted as labral avulsions.

Joint Capsule The joint capsule, too, is best demonstrated on transverse images. The insertion of the anterior capsule at the neck of scapula neck is variable and can be classified into three types (▶ Fig. 3.10 and ▶ Fig. 3.11).109 A recess between the scapula and anterior capsule should therefore not be hastily interpreted as capsular separation. The patient’s medical history and clinical examination results are decisive for the diagnosis. A proximal insertion at the neck of scapula (type III) is thought to be a predisposing factor for anterior shoulder dislocation.

Glenohumeral Ligaments The anterior joint capsule is reinforced by three glenohumeral ligaments. These fan out obliquely from the anterior glenoid margin to the head of humerus. Between the ligaments are two openings in the joint capsule assuring communication with the subscapularis bursa and the subcoracoid recess of the joint capsule (superior: Weitbrecht’s foramen; inferior: Rouviere’s foramen). The superior glenohumeral ligament is

small and thin, while, by contrast, the highly variable medial glenohumeral ligament is mainly strong and can often be identified as a signal-void, bandlike structure. Since it courses obliquely to the transverse plane, it is often only partially demonstrated (see ▶ Fig. 3.6b). The inferior glenohumeral ligament is composed of two bundles, between which is situated the axillary recess of the shoulder joint, into which parts of the ligaments radiate.115 The insertion of the medial and inferior ligaments at the glenoid is in close proximity to the glenoid labrum, creating a cleft between the labrum and ligament. This exhibits high signal intensity and should not be mistaken for a labral tear. There are anatomic variants of the ligaments ranging from nonformation of the medial and inferior ligaments, in up to 15% of cases,69 to variable courses (▶ Fig. 3.12). The variability in the course and thickness of the glenohumeral ligaments in turn results in differences in the synovial folds and recesses of the anterior joint capsule (six types according to DePalma25).

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Type I

Type II

Fig. 3.10 Variations in the insertion of the anterior joint capsule into the scapula. Schematic diagram, transverse plane. The capsule inserts at the base of the glenoid labrum in type I, more medially in type II, and farther along at the neck of the scapula in type III. Caution: Type III capsular insertion predisposes to shoulder dislocation and must not be misinterpreted as traumatic detachment of the capsule.

Fig. 3.12 Shoulder joint in view from behind after removal of humeral head. Schematic diagram to demonstrate the anterior glenohumeral ligaments which can only be seen from the inside. Constant view of the biceps tendon (superior ligament bundle) and of the superior glenohumeral ligament (ligament bundle beneath it; variable view of the medial and inferior glenohumeral ligaments. (a) Parallel ascending form (around 30% of cases). (b) Z-shaped configuration (around 55% of cases). (c) Parallel-horizontal form (around 15% of cases).

Fig. 3.11 Type I capsule inserts into the anterior glenoid labrum. Transverse plane, GRE sequence (0.5 T, TR = 600 ms, TE = 14 ms, flip angle = 30 degrees). The anterior glenoid labrum exhibits basal increased signal intensity along the hyaline articular cartilage (arrow). This finding must not be mistaken for a labral tear.

Tendon of the Long Head of Biceps The tendon of the long head of biceps as well as its sheath is also best delineated in the transverse plane. The tendon extends through the glenohumeral joint as well as through the bicipital groove, which is a bony groove in the anterior humeral shaft. Within the groove, the tendon is surrounded by the joint recess. Anteriorly, the groove is bounded by the transverse ligament. The tendon can be identified as a rounded, signal-void structure within the bicipital groove. Even in healthy individuals, it can be surrounded by a small amount of fluid.58

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Oblique Coronal Section Insertion of the Supraspinatus The oblique coronal plane (▶ Fig. 3.13 and ▶ Fig. 3.14) is particularly suitable for evaluating the insertion of the supraspinatus at the greater tubercle of the humerus. The fibrous connective tissue of the tendons generally manifests as signal void, and increased signal intensity is characteristic of pathologic changes. However, variable increased signal intensity is observed at the insertion of the supraspinatus in almost 80% of cases, and is particularly pronounced on T1w and PDw sequences, in the absence of any traumatic degenerative changes in the rotator cuff (see ▶ Fig. 3.13b). This increased signal intensity may be focal or longitudinal and observed at a superior, central, or inferior location within the tendon.94 This is thought to be related to early myxoid tendon degeneration, especially in view of the poor vascularity of this area (“critical zone”).108 These changes are not age related.

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Type III

3.3 Anatomy Acromioclavicular joint Clavicle Supraspinatus

Acromion

Subscapularis artery and vein Greater tubercle

Coracoid process Glenoid

Biceps, long head tendon

Subscapularis Deltoid Axillary artery and vein Coracobrachialis a Trapezius Fat pad

Fat pad of subacromial-subdeltoid bursa Supraspinatus tendon (“critical zone”) Greater tubercle

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Acromion Supraspinatus Glenoid labrum Subscapularis artery and vein Glenoid

Deltoid Glenoid labrum Axillary recess Biceps, long head tendon Subscapularis Axillary artery and vein Coracobrachialis b

Acromion Infraspinatus

Deltoid

Scapula Teres minor Posterior circumflex humeral artery and vein

Humeral diaphysis

Teres minor c

Fig. 3.13 Anatomy of the shoulder. Oblique coronal section. GRE sequence (1.5 T, TR = 550 ms, TE = 15 ms, flip angle = 25 degrees). (a) Section 1. (b) Section 2. (c) Section 3.

The following potential causes of this pseudolesion (“pseudogap”) have been ruled out: ● Interposition of tendon fibers with fat. ● Partial volume artefacts of muscle fibers. ● Special anatomic structure of the supraspinatus.135

It is therefore now thought to be a physical phenomenon related to the orientation of the tendon within the main magnetic field.29 It is well known that anisotropic tissue such as hyaline or collagen fibers change their relaxation times if their longitudinal fibrils are at a certain angle to the magnetic field. Experiments have demonstrated that this angle is 55 degrees and it is also referred to as

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the magic angle. This phenomenon also explains signal abnormalities found in other tendons and in cartilage (see Chapter 16.2.1) without any evidence of pathology.

Fig. 3.15 Fat stripe of subacromial-subdeltoid bursa. Oblique coronal T1w SE image (0.5 T, TR = 600 ms, TE = 20 ms). Visualization of the fat stripe as line of high signal (arrow).

Subacromial-Subdeltoid Bursa Another important structure to be evaluated in the oblique coronal plane is the subacromial-subdeltoid bursa. The bursa itself is normally not visible but it is surrounded by a layer of fatty connective tissues which can be identified on MRI in up to 70% of cases. The thickness of the peribursal fat plane (fat stripe) is positively correlated with the patient’s age and weight and negatively with athletic activity and muscle mass.78 It is visualized as a stripe of high signal intensity on T1w images (▶ Fig. 3.15). Displacement and obliteration of the fat stripe and fluid accumulation within the bursa serve as diagnostic criteria for various diseases.134

Acromioclavicular Joint The acromioclavicular joint is also best evaluated in the oblique coronal plane. The position of the articular disk and the width of the joint capsule are clearly delineated. Changes to the acromioclavicular joint have important implications for impingement syndrome of the supraspinatus. A thick layer of subacromial fatty tissue is normally seen on oblique coronal images (▶ Fig. 3.16). This fat pad is a fatty substance enclosed in a fascial sheath similar to Hoffa’s fat pad of the knee joint.138,144 It possibly plays a greater role than hitherto thought in the physiological movement of the shoulder girdle.

Labrum-Biceps Tendon Complex There is growing interest in the insertion site of the long head of biceps at the superior glenoid fossa and the superior glenoid labrum, known as the “labrum-biceps tendon complex.” Injuries to the superior labrum (SLAP lesions), which are relatively common, should be distinguished from the normal anatomic structures and normal variants. This is best done using oblique coronal MR images. The long biceps tendon inserts with 40 to 60% of its fibers at a bony projection of the neck of scapula (supraglenoid tubercle) and with the remaining fibers at the superior glenoid labrum over a width of several centimeters. If one compares this

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. Fig. 3.16 Subacromial fat pad. Schematic diagram to depict the location of the subacromial fat pad. The role of this fat pad in movement of the shoulder girdle is eliciting increasingly more interest. (a) Coronal plane. 1, acromioclavicular joint; 2, trapezius; 3, subacromial fat pad; 4, supraspinatus; 5, fat stripe of the subacromial-subdeltoid bursa; 6, fat stripe of the deltoid. (b) Axial plane. 1, subacromial-subdeltoid bursa; 2, acromion; 3, subacromial fat pad; 4, clavicle.

region with the face of a clock, the latter insert somewhat at the 11 to 1 o’clock position. Labral attachment variants have been identified and classified by Vangsness et al into four types141 depending on whether the majority of the fiber bundles are located posteriorly, bilaterally, or anteriorly to the 12 o’clock position. The most common type appears to be type II (strong posterior, weak anterior bundle), accounting for 33 to 50% of cases.5

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Fig. 3.14 Anatomy of the shoulder. Schematic diagram, oblique coronal section. 1, acromion; 2, supraspinatus tendon; 3, inferior glenoid labrum; 4, deltoid fat stripe; 5, fat stripe of the subacromialsubdeltoid bursa.

3.3 Anatomy

If this recess is located further anteriorly, it cannot be reliably differentiated from the normal variant of the sublabral foramen. The sublabral recess must be distinguished from tears of the glenoid labrum. The location of the recess correlates with variants of the biceps tendon attachment. The frequency with which a recess is detected increases with age, indicating that, in addition to the congenital normal variant, degenerative changes are also thought to play a role.45

Normal variants

Tear criteria

SLAP lesions

Fig. 3.17 Labrum-biceps tendon complex. Schematic diagram, oblique coronal section. (a) Normal variants: I, direct attachment of the glenoid labrum to the articular cartilage; II, small cleft between labrum and cartilage; III, gaping cleft. (b) Criteria for labral tear on MR images: I, irregular margins (unlike cleft); II, particularly wide cleft formation; III, change in direction of cleft formation. (c) SLAP lesions I–IV according to Snyder: I, frayed surface and/or small tears (fraying); II, tear reaching to biceps insertion; III, labral tear with separation or dislocation (bucket handle); IV, longitudinal tear of biceps tendon.

Oblique Sagittal Section Rotator Cuff The oblique sagittal plane (▶ Fig. 3.18 and ▶ Fig. 3.19) is important for assessment of the entire rotator cuff. Thanks to the characteristic arrangement of the four rotators around the glenoid process and the head of humerus, it is easy to identify the individual muscles and any tendon tears.

Coracoacromial Arch The coracoacromial arch can also be well evaluated in this plane. This arch is formed by the coracoid process, coracoacromial ligament, and acromion. The coracoacromial ligament is inconsistently visualized as a linear, signal-void structure. The ligament attachment to the acromion is variable, and four different insertion types have been identified (▶ Fig. 3.20).35 The ligament also varies in thickness (up to 3 mm). Thickness of up to 8 mm can result in considerable constriction of the subacromial space. The acromion, too, varies in shape and position, and these morphologic variants play an important role in impingement syndrome of the shoulder (▶ Fig. 3.21). For example, a hook shape (type III; see ▶ Fig. 3.21d) is more commonly associated with rotator cuff tear than a flat (type I; see ▶ Fig. 3.21b) or a concave shape that is curved versus the rotator cuff (type II; see ▶ Fig. 3.21c). This classification is based on radiographic demonstration of the bony shoulder axis in a special, oblique projection (“outlet view”)10 but can also be easily done after analyzing the entire stack of slices on oblique sagittal MRI sections. Farley et al additionally described an inferiorly convex acromion as type IV. According to Bigliani, that shape, like type II and III, does not cause significant narrowing of the subacromial space. A shallow slope is more often associated with a rotator cuff tear than a steep angle (see ▶ Fig. 3.2 and ▶ Fig. 3.21).4,8,60 The normal acromial slope seen in this plane is between 10 and 40 degrees.

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Noteworthy also in this context is the variable attachment of the superior glenoid labrum to the joint cartilage of the cavity. Only in around 25% of cases, this is a fixed, continuous connection; in the remaining cases, there is a cleft of variable depth and width between the labrum and cartilage, which is known as the “superior sublabral recess.” It can be up to 8 mm deep and located either posteriorly or more anteriorly, or can extend across the entire 11 to 1 o’clock position. Some authors classify the recess into different types depending on its depth (▶ Fig. 3.17)24: ● Type I: fixed (25% of cases). ● Type II: narrow (45%). ● Type III: deep (30%).

Coracohumeral and Glenohumeral Ligaments Occasionally, the coracohumeral ligament is visible in the oblique sagittal plane (▶ Fig. 3.22), and in the presence of joint effusions, the insertion of the glenohumeral ligaments at the glenoid labrum can be identified (▶ Fig. 3.23). A study aimed at improving visualization of the ligaments of the shoulder joint using individual angulation in the oblique sagittal plane was carried out. This was based on multiplanar reconstruction of a 3D data set from healthy volunteers. The evidence showed that the coracoclavicular ligament is best demonstrated when angled clockwise at 40 degrees with respect to the coronal plane, and the coracoacromial ligament when angled counterclockwise at 10 degrees with respect to the coronal plane.65 The coracohumeral ligament was hardly identifiable.

Subcoracoid Recess and Subcoracoid Bursa In the presence of joint effusions, the subcoracoid recess can be clearly identified in this plane superiorly and anteriorly to the subscapularis tendon. The subcoracoid bursa is located anteriorly

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Infraspinatus tendon Supraspinatus tendon

Deltoid

Deltoid Teres minor tendon

Subscapularis tendon

Teres minor Posterior circumflex humeral artery and vein

a

Acromioclavicular joint

Infraspinatus

Supraspinatus

Deltoid

Biceps, long head tendon Coracoid process Subscapularis

Teres minor

Biceps, short head and tendon Deltoid

Latissimus dorsi Teres major b

Spine of scapula

Clavicle

Supraspinatus Infraspinatus Coracoid process

Deltoid Glenoid fossa

Subscapularis Teres minor Coracobrachialis Pectoralis major

Teres major c

Fig. 3.18 Anatomy of the shoulder. Oblique sagittal section. GRE sequence (1.5 T, TR = 550 ms, TE = 9 ms, flip angle = 25 degrees). (a) Section 1. (b) Section 2. (c) Section 3.

to the subscapularis tendon, and if it is enlarged because of accumulated fluid, it cannot always be reliably differentiated from the joint process (▶ Fig. 3.24).117

3.4 Disorders of the Rotator Cuff 3.4.1 Impingement Narrowing and compression of tendons, bursae, cartilage, and/or other soft tissues often result in pain and restricted

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motion and are collectively subsumed under the term “impingement syndrome.” In the shoulder, such mechanisms are observed extra-articularly in the subacromial space (subacromial impingement) and at the coracoid process (coracoid impingement). As reported by several authors, they also often occur within the joint due to sweeping arm movements as associated with certain types of sport and because of repetitive microtrauma (posterosuperior and anterolateral impingement).

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Acromion

Coracoacromial ligament

3.4 Disorders of the Rotator Cuff

Fig. 3.20 Variations in the attachment of the coracoacromial ligament to the acromion. (a) Attachment at the apex of acromion (around 10% of cases). (b) Attachment at the base and undersurface of acromion (around 20% of cases). (c) Attachment at the base of acromion (around 50% of cases). (d) Attachment at the undersurface of acromion (around 20% of cases).

Fig. 3.21 Morphologic and positional variants of the acromion. Schematic diagram, oblique sagittal plane. A shallow slope and hook shape result in a markedly narrow supraspinatus outlet with risk of impingement syndrome. (a) Steep angle, flat-shaped acromion. (b) Shallow, straight-shaped acromion. (c) Curved shaped. (d) Hookshaped acromion.

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Fig. 3.19 Anatomy of the shoulder. Schematic diagram, oblique sagittal plane (corresponds somewhat to Fig. 3.18b). 1, acromion; 2, supraspinatus; 3, infraspinatus; 4, teres minor; 5, inferior glenohumeral ligament; 6, medial glenohumeral ligament; 7, subscapularis; 8, long biceps tendon; 9, superior glenohumeral ligament; 10, coracoid process; 11, coracoacromial ligament.

Fig. 3.22 Coracohumeral ligament. Oblique sagittal section. GRE sequence (0.5 T, TR = 600 ms, TE = 14 ms, flip angle = 30 degrees). Clear delineation of the coracohumeral ligament (arrow) beneath the coracoacromial ligament.

1 2

3 4 Fig. 3.24 Position of subcoracoid recess versus subcoracoid bursa when both are filled with fluid. Schematic diagram, sagittal plane. 1, coracoid process; 2, subcoracoid recess; 3, subcoracoid bursa; 4, subscapularis.

Subacromial Impingement

Fig. 3.23 Attachment of the inferior glenohumeral ligament. Oblique sagittal section. GRE sequence (1.5 T, TR = 550 ms, TE = 30 ms, flip angle = 25 degrees). Clear delineation of the attachment of the inferior glenohumeral ligament at the glenoid labrum (arrow).

According to Neer, restricted movement of the tendons of the rotator cuff in the subacromial space is subject to mechanical stress due to repetitive impingement of the tendon and mechanical stress. This in turn leads to mucoid degeneration and, later, a tear in the tendon.88,90 Neer distinguished three progressive stages of disease: ● Stage I: edema and microhemorrhage.

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●

Stage II: tendinitis and fibrosis. Stage III: tendon tears and reactive osteophytes.

The anterolateral segment of the supraspinatus tendon is most commonly affected. This constitutes a critical zone, a rounded area with reduced blood perfusion, which is located just a few centimeters away from where the tendon inserts into the bone.104 Today, numerous causes have been identified for such restricted motion of the rotator tendons, of which many can be clearly visualized on MRI.118 Examples of such causes include: ● Hook-shaped acromion (see ▶ Fig. 3.2). ● Shallow slope of the acromion (▶ Fig. 3.25). ● Osteophytes in the apex of acromion and acromioclavicular joint. ● Exostoses (▶ Fig. 3.26). ● Thickening of the coracoacromial ligament (▶ Fig. 3.27). ● Prominent acromioclavicular joint capsule in the presence of arthrosis. ● Probably the impact of the muscle tone, position within the shoulder girdle, and how such factors are affected by deterioration of the cervical spine. Signs of impingement on MRI: Indentation of the rotator cuff at the compression site. ● Thinning of the surrounding fat plane. ●

If these signs are manifested, the term “aggressive coracoacromial arch” is also employed.35 Since the MRI signs are not closely correlated with the clinical findings, the image results must be interpreted in the context of the clinical history.

Stage I (Degeneration) Constriction of the subacromial space results in inflammatory and degenerative reaction by the subacromial-subdeltoid bursa with fluid accumulation in the subacromial space as well as increased signal of variable intensity and possibly thickening of the rotator cuff tendon (generally the supraspinatus tendon). Neer also referred to this as “stage I impingement syndrome.” The bursal effusion also results in a relatively narrow fluid halo in the subacromial space. Bursitis as seen in association with rheumatoid disease of the shoulder joint often contains large amounts of effusion. Inflammatory reactions of the subacromial soft

Fig. 3.26 Cartilaginous exostosis. Oblique sagittal T1w sequence. Cartilaginous exostosis on the undersurface of the acromion with considerable narrowing of the subacromial space.

tissues can also be observed following trauma and embark on a chronic course (▶ Fig. 3.28).

Stage II (Partial Tear) If parts of the rotator cuff develop a tear secondarily to impingement syndrome or injury, focal discontinuity and/or increased signal intensity can be seen on T2w MR images (▶ Fig. 3.29). The partial tears can be graded on the basis of the lesion depth (according to Ellman): ● Grade 1: Defect smaller than one-quarter or 3 mm. ● Grade 2: Defect smaller than half or 3 to 6 mm. ● Grade 3: Defect greater than 6 mm. The following partial tears are distinguished in terms of the localization: ● Partial tears arising from the joint or cartilage side. ● Partial tears arising from the bursal side (▶ Fig. 3.30). ● Partial tears arising from both sides, with thinning of the tendon (▶ Fig. 3.31). ● Partial tears in the tendon substance (interstitial tears) or splitting of the tendon (delaminating), possibly with fluid accumulation in the muscle belly (▶ Fig. 3.32 and ▶ Fig. 3.33; see also ▶ Fig. 3.36).

Stage III (Full-Thickness Tear)

Fig. 3.25 Straight-shaped acromion. Oblique sagittal section. GRE sequence (1.5 T, TR = 600 ms, TE= 14 ms, flip angle = 30 degrees). Impingement of supraspinatus (arrow) through acromion with flat angle.

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A full-thickness tear of the rotator cuff results in a visible hole (discontinuity) in the tendon, and is most commonly seen in the supraspinatus (▶ Fig. 3.34). Tears are observed less often in the infraspinatus and subscapularis muscles. Subscapular lesions are seen secondarily to damage to the supraspinatus or, rarely, as isolated entities (▶ Fig. 3.35). MRI has proved to be a highly sensitive modality for detection of full-thickness tears. Its sensitivity is in the range of 80 to 100%

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●

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3.4 Disorders of the Rotator Cuff

Fig. 3.27 Thickened coracoacromial ligament. Apparent narrowing of the subacromial space as the most likely cause of impingement syndrome. The thickened ligament can be detected in several consecutive oblique coronal images as signal void point (arrows) and must be differentiated from osteophytic spurs at the apex of acromion. (a) Section 1. (b) Section 2.

Fig. 3.28 Tendinitis. Clinical impingement syndrome. Thickening and increased signal intensity of supraspinatus tendon as sign of grade 1 impingement with tendinitis. (a) Oblique coronal T1w image. (b) Oblique coronal PDw fatsat image.

and specificity is over 90%. As such, its results are on a par with those of arthrography.31,55,162 Thanks to the fact that it is able to visualize the entire rotator cuff, it is superior to ultrasound in terms of sensitivity (▶ Table 3.2).14 MRI is also valuable for preoperative assessment of full-thickness tears since it provides information on the state of the tendon endings, extension of tears, degree of muscle retraction, or the presence of any fatty atrophy. For localization of a tear, the rotator cuff can be divided into three zones (▶ Table 3.3).

The extension of a tear of the rotator cuff is an important criterion and as such constitutes the basis for arthroscopic grading of the disease. According to de Orio and Cofield as well as Bateman, four grades can be distinguished: ● Small: less than 1 cm. ● Medium: 1 to 3 cm. ● Large: 3 to 5 cm. ● Massive: greater than 5 cm.

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Fig. 3.29 Partial tear of supraspinatus. Oblique coronal section. Contrast increases with longer TE (more T2* weighting). (a) GRE sequence, first echo (1.5 T, TR = 600 ms, TE = 13 ms, flip angle = 25 degrees). (b) GRE sequence, second echo (TE = 30 ms). Partial tear of supraspinatus (small arrows), joint effusion (arrow), fluid in the subacromial-subdeltoid bursa (open arrow).

Fig. 3.30 Partial tear of the supraspinatus tendon on the bursal side. (a) Oblique coronal STIR sequence. Discrete fluid-isointense gap in the supraspinatus tendon (arrow) without complete discontinuity. (b) Oblique coronal T1w sequence. Signal-void foci on T1w and STIR contrast, consistent with calcifications (arrow).

Tendon retraction can also be graded (according to Patte) (▶ Fig. 3.36)12: ● Grade I: retraction of up to half the distance between the greater tubercle and middle of the humeral head. ● Grade II: up to the middle of the humeral head. ● Grade III: between the middle of the humeral head and glenoid. ● Grade IV: extending posteriorly to the glenoid process.

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Following dissection, the tear shape can be described using the Ellman’s arthroscopic classification system as C-, U-, and Lshaped or massive (▶ Fig. 3.37). The term “rotator interval” is used to denote the triangular space between the supraspinatus and subscapularis tendons as well as the base of the coracoid process. It is largely covered by the coracohumeral ligament and also contains the superior

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3.4 Disorders of the Rotator Cuff

Fig. 3.31 Partial rotator cuff tears. Indirect MR arthrography. (a) Oblique coronal section. Irregular thinning of rotator cuff in the region of the supraspinatus. On indirect MR arthrography, there is CM accumulation in the joint space and subacromial bursa with particularly clear delineation of the rotator cuff. (b) Oblique sagittal section. Partial tear of the supra- and infraspinatus muscles (arrows). (c) Oblique sagittal section. Partial tear of the subscapularis (arrow).

glenohumeral ligament and the long biceps tendon. Tears of the rotator cuff, in particular of the anterior portion of the supraspinatus and the superior portion of the subscapularis muscles, are often associated with changes to the structures in the rotator interval. Occasionally, the term “interval lesion” is used.82 Degeneration or tears are observed in the long biceps tendon, coracohumeral ligament, and superior glenohumeral ligaments. The deflection site of the long biceps tendon is situated within the rotator interval (see Chapter 3.5) and is generally also altered.100 Traumatic tears of the rotator cuff are generally seen in damaged tendons (mainly in elderly patients). If the healthy rotator cuff of a younger patient is exposed to the same accident mechanism (e.g., as happens when falling on an extended arm), this will most likely result in avulsion injury to the greater tubercle. The outcome of such injury ranges from avulsion edema through occult fracture to dislocated fracture (▶ Fig. 3.38).158,159

Stage IV (Chronic Tear) Chronic full-thickness tears of the rotator cuff give rise to various characteristic changes. Already within the space of a few months,

the affected muscle exhibits increasing signs ranging from hypoatrophy to atrophy, that is, the muscle mass is replaced with fat, as is also the muscle volume. Preoperative assessment of the extent of muscle atrophy in association with a complete rotator cuff tear is crucial prior to surgical reconstruction. There are a number of different criteria that can be used to grade muscle atrophy: ● Based on the volume: A healthy supraspinatus projects at a tangent from the spine of scapula to the coracoid process on sagittal images. Atrophy with shrinkage causes muscle retraction to beneath this line (▶ Fig. 3.39). Volumetry can also be performed by measuring the muscle diameter in this plane and comparing it with the diameter of the supraspinous fossa. This helps to calculate what is known as the “occupational ratio” based on the Thomazeau’s classification system. To that effect, the fossa volume is divided by the muscle volume. A ratio of 1 to 0.6 is normal, a ratio of 0.6 to 0.4 is indicative of moderate atrophy, and a ratio of less than 0.4 indicates severe atrophy. ● Based on signal intensity, semi-quantitatively (according to Goutallier): Atrophy leads to increasing fat deposition with rising signal intensity on T1w and TSE images: ○ Grade I: increased deposition of fatty streaks.

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Another typical change seen in chronic rotator cuff tears is the “high-riding” humeral head resulting from lack of soft tissue coverage and reduced muscular strength. The subacromial distance to the head of humerus declines increasingly (to less than 10 mm). Some authors specify this distance in millimeters; it can be used as a prognostic measure of the outcome of a surgical procedure. If there is direct contact between the head of humerus

and acromion, this will trigger reactive bone changes in the humerus and acromion undersurface (neoarthrosis). These changes produce characteristic radiographic and MRI findings. In this setting, shoulder arthrosis is then increasingly seen. The term “defect arthropathy” is used to denote these bone reactions. These changes progress slowly and can be graded according to different degrees of severity.43 A common classification (Hamada’s classification, modified according to Walch) is based on radiographic findings (▶ Table 3.4) but can also be applied to MR images. The high-riding humeral head as seen in chronic rotator cuff tear can cause damage, with partial or full-thickness tear, to the deltoid where it inserts into the acromion (▶ Fig. 3.40 and ▶ Fig. 3.41). Discontinuity at the myotendinous junction or directly at the attachment site as well as fluid accumulation in the remaining muscle belly may be observed.46,85 Chronic tears can result in compensatory hypertrophy of the remaining intact rotators. This has been reported, for example, for the teres minor, especially in the presence of tears of the subscapularis and infraspinatus muscles.74

Calcareous Tendinitis Calcification deposits in association with chronic tendinitis (calcareous/calcification tendinitis) are identified as signal void and, especially on GRE images with long TE, give rise to marked susceptibility artefacts. However, often the calcification deposits are not well visualized on MR. They can project from the tendon into the surrounding tissues, often causing severe pain (▶ Fig. 3.42). If these calcification deposits break away, they can migrate as loose bodies into the subacromial-subdeltoid bursa (▶ Fig. 3.43).

Subcoracoid Impingement Fig. 3.32 Partial tear of the supraspinatus tendon. Oblique coronal PDw fatsat sequence. Superficial oblique and longitudinal tears with delaminated split (in the tendon substance, longitudinal, arrow).

a

A prominent coracoid process and/or traction osteophytes of the short biceps tendon at the coracoid as well as the prominences of the lesser tubercle can cause coracoid impingement with damage to the subscapularis tendon (▶ Fig. 3.44).37 The distance between

b

Fig. 3.33 Partial tear of the supraspinatus tendon. Other patient. Deeper, mainly longitudinal tear (arrows). (a) Oblique sagittal PDw fatsat sequence. (b) Oblique coronal PDw fatsat sequence.

100

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Grade II: markedly increased fat deposition, exhibiting a signal of somewhat lower intensity than that of the muscle. ○ Grade III: fat signal intensity somewhat on a par with that of muscle. ○ Grade IV: predominantly fat signal. ○

3.4 Disorders of the Rotator Cuff

b

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a

Fig. 3.34 Full-thickness tear of the supraspinatus tendon with slight retraction. (a) Oblique coronal PDw fatsat sequence. The arrow marks the tear in the supraspinatus tendon. (b) Axial PDw fatsat sequence. It is sometimes possible to recognize the extension of the tear on axial images (arrow).

the coracoid process and lesser tubercle in symptomatic patients is often less than 5.5 to 10 mm. The long biceps tendon and medial glenohumeral ligament are also adversely affected.38 The clinical symptoms differ from those associated with subacromial impingement, with pain experienced at more anterior locations during adduction, internal rotation, and flexion in forward movements of the arm. The pathology spectrum is similar to the findings identified for the superior rotator cuff, ranging from tendinitis to tears (▶ Fig. 3.45 and ▶ Fig. 3.46).

Internal Impingement Another type of impingement mechanism has been reported in athletes, in particular those who frequently engage in throwing athletics, resulting in damage to the rotator cuff at the supra- and infraspinatus junction. Because of the extreme arm position adopted in abduction and external rotation (ABER position), pressure is applied by the posterosuperior labrum and glenoid on the rotator cuff. This condition is known as “posterosuperior glenoid impingement.”42,128

Fig. 3.35 Signs of lesions of the subscapularis. Schematic diagrams. In the presence of subscapularis tendinitis and/or tear, changes in signal intensity, as well as in the later stage, discontinuity can be clearly identified on axial (a) and sagittal images (b). Depending on the extent of damage to the reinforcing fibers, the biceps tendon can remain attached (1), be subluxed (2), or be displaced into the joint (5). Scarred fiber residues can be mistaken for a biceps tendon (1). In the case of full-thickness tears it may still be possible to detect within the defect linear signal-void residues or scarred fiber bundles (3). The tear is surrounded by effusion and in some cases free fluid. In the later stages, in particular on far medially sagittal sections, (c) fatty atrophy of the subscapularis can be detected. One reason for a degenerative subscapularis lesion may be impingement caused by osteophytic spurs originating in the apex of the coracoid process (4). (a) Axial plane. (b) Sagittal plane. (c) Sagittal plane, far medially positioned. Is, infraspinatus; Sc, subscapularis; Ss, supraspinatus.

3.4.2 Lesions of the Tendon Insertion (Insertion Tendinopathy, Rim Rent Lesions) Degenerative and traumatic changes at the tendo-osseous junction and tendon insertion (footprint) should be distinguished

Table 3.2 Sensitivity and specificity of various imaging modalities for evaluation of rotator cuff tears Sensitivity/specificity

Arthrography

Ultrasound

MRI

Direct MR arthrography

Indirect MR arthrography

Sensitivity (%)

71

60–90

66–99

100

100

Specificity (%)

71

50–70

75–88

100

86

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Zone Anatomic assignment A

Anterior sections with subscapularis tendon, rotator interval, and long biceps tendon

B

Cranial section in the region of the supraspinatus tendon

C

Posterior lesions in the region of the infraspinatus and teres minor muscles

a

b

c

d

e

from the changes associated with impingement. Overloading of the tendon insertion site appears to play a greater role here than does restriction of the range of motion. This leads to cystic remodeling in the greater tubercle, and may result in contact with the surface of the humeral head. Signs of insertion tendinopathy and of impingement are often exhibited concomitantly within the subacromial space. Damage to the tendon insertion area is often caused by avulsion mechanisms when engaging in sports involving sweeping arm movements or contact sports. A distinction is made between avulsions and partial tears (rim rent tear). Partial tears arise more often close to the articular side (PASTA [partial articular-sided supraspinatus tendon avulsion]) than from the bursal side (reverse PASTA). Central tears (CID [concealed interstitial delamination]; ▶ Fig. 3.47) must be distinguished from full-thickness tears (▶ Fig. 3.48 and ▶ Fig. 3.49).113 Partial tears can be graded based on the extent of tendon tapering: ● Grade I: 1 to 2 mm. ● Grade II: less than 50%. ● Grade III: more than 50%.

3.5 Disorders of the Proximal Biceps Tendons 3.5.1 Tendinitis

f

g

Fig. 3.36 Different lesions of the rotator cuff. Schematic diagram, oblique coronal section. (a) Normal finding. (b) Partial tear from articular side. (c) Partial tear from bursal side. (d) Partial tear from both sides with tapering. (e) Partial tear in tendon substance (longitudinal) with or without fluid accumulation in the muscle or at myotendinous junction. (f) Full-thickness, relatively small tear with grade I tendon retraction. (g) Full-thickness tear grade III tendon retraction.

Tendinitis (also called tendinopathy, tendinosis) of the long biceps tendon often manifests concomitantly with impingement syndrome, involving the intra-articular portion of the tendon immediately below the supraspinatus tendon. On MRI, swelling and increased signal intensity can be detected, in particular on oblique sagittal PDw fatsat images. Extensive tendinitis unrelated to impingement syndrome can also affect the entire tendon segment, that is, in addition to the intra-articular portion, also the (intertubercular) segment coursing within the bicipital groove. In such cases, there is also thickening of the tendon within the groove, and this is best evaluated on axial sections.

1 2

102

a

b

d

e

c

Fig. 3.37 Rotator cuff tears. Schematic diagram of rotator cuff from above. Cord-like thickening of the distal third of rotator cuff, probably due to tension forces applied, which is also known as the “rotator cable” (a). This configuration has a function similar to that of a suspension bridge. The remaining schematic diagrams illustrate various types of tears following dissection before suturing. (a) Normal finding. 1, suspension-bridge like portion of rotator cuff (suspension bridge); 2, cablelike thickening of rotator cuff (rotator cable). (b) C-shaped tear. (c) Ushaped tear. (d) L-shaped tear. (e) Massive tear.

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Table 3.3 Zonal distribution of rotator cuff according to Habermeyer for localization of rotator cuff tears

3.5 Disorders of the Proximal Biceps Tendons

a

b

c

d

Fig. 3.40 Chronic rotator cuff tear. Schematic diagram, oblique coronal slice. (a) Normal state. (b) Chronic rotator cuff tear with fatty atrophy of the supraspinatus and high-riding humeral head as well as reactive neoarthrosis towards acromion. (c) In addition, partial tear of the deltoid. (d) In addition, full-thickness tear of the deltoid.

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Fig. 3.38 Muscle fiber tear of infraspinatus muscle. Oblique sagittal PDw fatsat TSE sequence. Painful restricted motion following snowboard accident. Discrete defect at myotendinous junction of infraspinatus muscle (arrow) as well as subfascial fluid around infraspinatus muscle. Some fluid also in the subacromial-subdeltoid bursa.

Fig. 3.39 Atrophy of the supraspinatus. Oblique sagittal section. Schematic diagram illustrating increasing atrophy of the supraspinatus with chronic rotator cuff tear. In a healthy state, the muscle belly projects beyond the line between the spine of scapula and coracoid (gray muscle belly). With increasing atrophy, the contour of the increasingly brighter muscle is always below this line.

Table 3.4 Classification of “defect arthropathy” in the presence of massive tears of the rotator cuff according to Hamada and Walch Stage Finding I

Massive tear of rotator cuff but no high-riding humerus

II

High-riding humerus with acromion to humerus distance ≤ 5 mm

III

High-riding humerus and sclerotic concavity of undersurface of acromion (neoarthrosis)

IVa

High-riding humerus without neoarthrosis, but with signs of shoulder arthrosis (initially, joint space narrowing)

IVb

Neoarthrosis and shoulder arthrosis

V

Incipient collapse of humeral head

Often, an effusion is also observed within the biceps tendon sheath, but this is of limited specific diagnostic value since the

Fig. 3.41 Chronic rotator cuff tear with grade IVb defect arthropathy, according to Hamada, and deltoid tear. Sagittal T1w images. Shoulder arthrosis, neoarthrosis towards acromion with pronounced sclerosis and high-riding humerus, deltoid tear. Severe atrophy of the supra- and infraspinatus muscles (arrows).

biceps tendon sheath communicates with the joint and, in the event of joint effusion, it is also filled with fluid. At most, fluid accumulation confined to the sheath should be interpreted as a sign of inflammation. Disorders in the region where the biceps tendon attaches to the glenoid, that is, the biceps anchor, are observed secondarily to SLAP lesions or trauma. Other disorders frequently associated with inflammation of the biceps tendon include the following: ● Biceps tendon dislocation (subluxation tendinitis). ● Bone abnormalities and osteophytes of the bicipital groove (compression tendinitis).

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Fig. 3.43 Calcareous tendinitis. Axial PDw fatsat image. Signal void loose body in the subdeltoid portion of the subacromial-subdeltoid bursa, consistent with perforated and migrated calcification deposit (arrow).

● ●

Rheumatoid arthritis. Synovitis.

3.5.2 Tears If chronic tendinitis or injury leads to a tear of the biceps tendon, the tear will generally be located in the intra-articular segment. MRI findings include: ● Discontinuity on oblique coronal images. ● Inability to visualize the tendon at the expected site on oblique sagittal images. ● Increased signal intensity or ring shape (▶ Fig. 3.50 and ▶ Fig. 3.51).

104

If there are extensive tears with retraction of the tendon, an “empty groove” (sulcus) can also be identified, that is, the tendon cannot be delineated within bicipital groove on axial images (▶ Fig. 3.52). However, such severe forms of retraction rarely occur since they are generally prevented by adhesions within the biceps tendon sheath. Tears of the transverse ligament can be clearly identified on MRI if the resolution is adequate. Discontinuity of the ligament, which is normally seen as signal void, can then be identified in axial sections on all sequences. A torn transverse ligament can lead to medial dislocation of the long biceps tendon. An empty groove and subluxed tendon can then be identified at an uncharacteristic site anterior to the subscapularis tendon. If the subscapularis

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Fig. 3.42 Calcareous tendinitis. Large calcification deposit (a, arrow), within a segment of the supraspinatus tendon, exhibiting inflammatory changes, and to an extent projecting above this as a sign of mobilization or incipient perforation. (a) Oblique coronal T1w sequence. (b) Oblique coronal PDw fatsat sequence. (c) Axial PDw fatsat sequence.

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3.5 Disorders of the Proximal Biceps Tendons

Fig. 3.45 Coracoid impingement. Axial PDw fatsat image. Subscapularis tendinitis, Subdeltoid and subcoracoid bursitis as well as prominent coracoid process (arrow) with narrowing of the subcoracoid space as sign of coracoid impingement.

tendon, too, is torn, the biceps tendon may be dislocated deep in the glenohumeral joint (▶ Fig. 3.53).17,27 If biceps tendon subluxation is associated with shoulder dislocation, the subluxed biceps tendon may lie in such a position as to block reduction. Surgery is indicated in such cases.2

3.5.3 Pulley Lesions

Fig. 3.44 Coracoid impingement. With calcareous tendinitis of the subscapularis as well as perforation of the calcification deposits into the surrounding soft tissues. (a) Plain radiograph. Calcification deposit in projection to subscapularis tendon (arrow). (b) Axial GRE images. Tear of subscapularis tendon. Surrounded by edema and fluid accumulation, prominent coracoid process (arrow). (c) Axial GRE images, of a more caudal section. Signal-void calcification deposit (arrow), perforated from tendon, as well as traction osteophyte at apex of coracoid (open arrow).

The biceps pulley is the tendon structure situated at the entrance to the bicipital groove in the rotator interval between the supraspinatus and subscapularis muscles. This is a connective tissue sling formed by the coracohumeral ligament and the superior glenohumeral ligament which stabilizes the biceps tendon (▶ Fig. 3.54).145 This pulley would also have to be damaged for biceps tendon subluxation/dislocation to occur. Damage to this pulley can go unnoticed during open surgery or arthroscopy if not specifically sought. A preoperative diagnosis is therefore important, and is mainly based on indirect signs, in particular injury (increased signal intensity and enlargement) of the superior edge of the subscapularis tendon and biceps tendon subluxation/dislocation.145 In a series of 14 patients with pulley lesions (from a patient group who had undergone 522 operations on the shoulder), two specialist radiologists achieved a sensitivity of 86 and 93%, and a specificity of 100 and 80%.145 According to Habermeyer, pulley lesions can be divided into four categories (▶ Fig. 3.55). A good indirect sign of a pulley tear is pathologic approximation of the long biceps tendon to the superior edge of the subscapularis tendon on oblique sagittal images114 secondary to subluxation of the biceps tendon in a caudal direction

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b

Fig. 3.46 Coracoid impingement. Calcification of the subscapularis tendon at insertion site with focal signal obliteration (arrows). (a) Axial PDw fatsat sequence. (b) Oblique sagittal PDw fatsat sequence.

106

Fig. 3.47 Footprint tear. Oblique coronal PDw fatsat sequence. Central defect at insertion of supraspinatus tendon (arrow) because of partial tear.

Fig. 3.48 Rim rent tear. Oblique sagittal PDw fatsat sequence. Status post sports accident. Supraspinatus tear extending from greater tubercle (arrow; rim rent tear).

(▶ Fig. 3.56). In chronic cases, the biceps tendon exhibits inflammation-related thickening and a change in signal compared to fresh injuries. Increasing medialization of the long biceps tendon is seen on axial images (▶ Fig. 3.57; based on classification of long biceps tendon instability according to Bennett type 1 and 2). If the pulley ligaments and the transverse ligament of the biceps recess are torn but the insertion of the subscapularis tendon remains intact, this may lead to extra-articular dislocation of the biceps tendon (type 4 according to Bennett). Overloading of the

subscapularis may give rise to intra-articular dislocation of the biceps tendon (type 3 according to Bennett; ▶ Fig. 3.58).87,100

3.5.4 Chondromatosis and Osteochondromatosis As in other synovial compartments, metaplastic transformation can also occur in the synovial membrane, possibly giving rise to cartilage formation and later also to mature ossicles. Primary

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a

3.6 Disorders of the Remaining Muscles synovial chondromatosis or osteochondromatosis of unknown origin occurs also secondarily to, for example, arthrosis or trauma. In general, multiple changes are implicated and can be detected on radiography when calcified or ossified. They manifest differently on MRI depending on their histologic structure (▶ Fig. 3.59): they are hyperintense on fluid-sensitive sequences when the cartilage component is predominant, as well as on T1w

images when they are composed of fatty bone marrow; conversely, they are hypointense when they are calcified or composed of bone substance.

3.6 Disorders of the Remaining Muscles (Including the Sequelae of Nerve Compression Syndrome) 3.6.1 Atrophy Due to Inactivity

a

b

d

c

e

Fig. 3.49 Tears of rotator cuff insertion (rim rent tear). (a) Normal finding. (b) Partial tear of undersurface. (c) Partial tear of upper surface. (d) Central tear. (e) Tear.

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Muscle atrophy results in a decline in muscle mass as well as in fat deposition. This in turn leads to characteristic streaks of partially focal increased signal intensity in the muscle belly on T1w images. Such fatty atrophy can, very occasionally, develop because of muscle inactivity, in particular in the presence of obesity (▶ Fig. 3.60) and shoulder girdle dystrophy. It may be generalized or confined to individual muscles, for example, because of a torn tendon (▶ Fig. 3.61).

Due to Space-Occupying Lesions If individual muscles are involved, the possibility of a spaceoccupying lesion affecting the corresponding nerve must be considered. MRI is able to detect muscle edema within 24 to 48 hours of onset of acute denervation. Fatty atrophy develops several months after onset of chronic denervation. Depending on the muscles implicated, certain areas must be carefully explored for tumors13: ● Atrophy of the infraspinatus muscle, for example, can be caused by a space-occupying lesion in the posterior supraspinous fossa or infraspinous fossa or in the area between these two regions

Fig. 3.50 Intratendinous tears of long biceps tendon (longitudinal split). Increased signal intensity at center of slightly thickened long biceps tendon (arrows), intra-articular segment (a) and, in another patient, in the extra-articular portion (b). This lesion can be observed in association with isolated injuries to the biceps tendon, as a concomitant manifestation of impingement syndrome or, when located within the joint, in association with SLAP lesions. (a) Oblique sagittal PDw fatsat TSE sequence. (b) Axial TSE sequence.

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Compression of the axillary nerve can result in isolated atrophy of the teres minor and/or deltoid.68 Damage to the axillary nerve can occur typically between the teres minor (superior), deltoid (lateral), triceps (medial), and humeral shaft (inferior) (quadrilateral space). Possible causes include tumors or strands of connective tissue.

3.6.2 Insertion Tendinopathy Insertion tendinopathy (enthesopathy) can occur at the insertion site of the pectoralis major into the humerus because of overloading or even without any detectable cause. This can be accompanied by pain at rest or pressure pain as well as slight inflammation of the humerus. An erosion is seen at the characteristic site (outer margin of the bicipital groove at the level of the metaphyseal junction, crest of greater tubercle) and may or may not be accompanied by calcification of the insertion tendon. Computed tomography (CT) is better at identifying erosions and any calcifications present. On MRI, these changes appear more aggressive due to concomitant discrete bone marrow edema and surrounding soft tissue edema (▶ Fig. 3.64 and ▶ Fig. 3.65).26 These areas take up CM, and calcification is generally seen as signal void. This can be distinguished from a periosteal osteosarcoma since there is no infiltration of space-occupying extraneous tissue.

3.6.3 Fibrosis Fig. 3.51 Partial tear of biceps anchor. Oblique sagittal PDw fatsat image. Increased signal intensity at the center of biceps tendon, intraarticular segment, due to central partial tear (arrow).

Repetitive intramuscular injections can result in muscular contracture and fibrosis. Fibrotic changes appear as low signal or signal void on MRI and have a mainly strandlike arrangement within the muscle. If the deltoid is involved, tilting of the scapula is observed additionally.20

Fig. 3.52 Tear of long head of biceps. Transverse plane. (a) GRE sequence (1.5 T, TR = 600 ms, TE= 13 ms, flip angle = 30 degrees). Fluid in bicipital groove but biceps tendon not visualized (empty sulcus; arrow). (b) SE sequence (TR =1800 ms, TE = 80 ms). Retracted fragments of biceps muscle surrounded by hyperintense zone, consistent with hemorrhagic edematous changes (arrow).

108

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●

(based of the acromion) with involvement of the distal suprascapular nerve (▶ Fig. 3.62). Atrophy of the supraspinous and infraspinatus muscles can be caused by a space-occupying lesion in the anterior supraspinous fossa and/or the suprascapular notch (spinoglenoid notch) with damage to the proximal suprascapular nerve (▶ Fig. 3.63).34,154 Ganglia account for the majority of spaceoccupying lesions found in this region. They have low signal intensity on T1w images and, by contrast, have high signal intensity on T2w images, and may be septated. They do not take up CM and may be difficult to differentiate from dilated veins in the region of the suprascapular notch.

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3.7 Disorders of the Bursae

Fig. 3.53 Biceps tendon dislocation. (a) Axial GRE image. The bicipital sulcus (groove) is empty (arrow). The dislocated long biceps tendon can be recognized anteriorly to the anterior slip (open arrow). (b) Oblique coronal T1w image. The dislocated long biceps tendon courses atypically around the head of humerus (arrow).

4

5

3.7 Disorders of the Bursae 3.7.1 Subacromial-Subdeltoid Bursa

3 2

1

Fig. 3.54 Biceps tendon pulley mechanism. Sagittal section at the level of the lesser tubercle. The coracohumeral ligament as well as the superior glenohumeral ligament attach to the capsule between the supraspinatus and subscapularis (rotator interval) where they help to reinforce the long biceps tendon in the form of a reflection pulley. 1, Supraspinatus; 2, Biceps tendon; 3, Coracohumeral ligament; 4, Superior glenohumeral ligament; 5, Subscapularis.

3.6.4 Muscle Fiber Tear Muscle fiber tears often result in a subfascial intramuscular hematoma which is seen as a bright line on T2w images (▶ Fig. 3.66). The torn fiber itself can occasionally be identified as an intramuscular defect on the image.

Often, inflammation of the subacromial-subdeltoid bursa is seen as a concomitant manifestation of impingement syndrome, but can also occur on its own. Acute bursitis is accompanied by a bursal effusion that appears as low signal on T1w images and as high signal on T2w images (▶ Fig. 3.67). The configuration of the bursa and peribursal fat plane is determined by the amount of accumulated fluid and can be identified as high signal on T1w images (▶ Fig. 3.68). This fat plane is displaced laterally if the implicated effusions are small, as is frequently the case in impingement syndrome and isolated bursitis. With larger effusions, the inferior portions of the bursa are displaced laterally to the humeral shaft, causing the fat plane to assume a teardroplike configuration (▶ Fig. 3.69). Such large bursal effusions are commonly observed in association with inflammatory processes. If the latter spread to the peribursal connective tissue (peribursitis), the peribursal fat plane will be obliterated by the infiltration of fatty tissue. This diagnostic sign is often seen in association with rotator cuff tears. Extensive rotator cuff tears can also result in obliteration of the fat plane through mechanical destruction of the bursa. However, when evaluating this sign, one must bear in mind that the thickness of the peribursal fat stripe will depend on the patient’s body weight and is hardly identifiable in around 30% of healthy individuals.78 As such, obliteration of the fat plane is a reliable sign of rotator cuff lesions or bursitis only if it is newly detected in follow-up examinations.

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Normal findings

Type 1

Type 2

Type 3

Type 4

a

Fig. 3.55 Classification of pulley lesions of the biceps muscle according to Habermeyer. Schematic diagram. Types 2–4 generally exhibit inflammatory thickening and increased signal intensity of the biceps tendon. Damage to the undersurface of the subscapularis tendon (types 3 and 4) results in more inferoanterior displacement (subluxation) of the biceps tendon. Type 1 = tear of the superior glenohumeral ligament with slight dislocation of the long biceps tendon close to the subscapularis; type 2 = in addition, partial tear of the undersurface of the supraspinatus; type 3 = in addition to type 1 signs, partial tear of the undersurface of subscapularis; type 4 = ligament tear in addition to damage to the adjacent muscle undersurfaces. (a) Oblique sagittal sections at the level of the lesser tubercle. Left: Normal finding. (b) Axial images corresponding to the level indicator in the left image in a. Left: Normal findings.

The arrangement and pathologic changes to the peribursal fat plane of the subacromial-subdeltoid bursa can occasionally also be identified on native radiographs.147,148 Normally, the fatty tissue is asymmetrically distributed in the bursal wall and is more abundant in the wall distal to the joint. That accounts for the single fat stripe seen in healthy individual. Connective tissue proliferation secondary to chronic inflammation also results in increased fatty tissue in the wall proximal to the joint. If the bursa is distended because of an effusion, two fat planes are seen in oblique coronal sections (double-fat plane).134

In general, these are caused by traumatic dislocation, often giving rise to posttraumatic recurrent subluxation (instability). Following dislocation, the scapular neck capsule is often partially detached (capsular stripping; ▶ Fig. 3.70). Different types of labral lesions, of varying incidence, are distinguished in terms of their location and extension (▶ Fig. 3.71).

3.7.2 Subcoracoid Bursa

A Bankart’s lesion involves complete detachment of the anteroinferior labrum. It may be seen in association with a glenoid rim fracture (bony Bankart’s lesion) (▶ Fig. 3.72). Bankart’s lesions are classified surgically into small (type I), large (type II), degenerative (type III), and bony (type IV) forms. If there is degenerative damage, often a normal labrum can no longer be identified. Bony Bankart’s lesions are repositioned. Any chronic instability with an anteroinferior bone defect will be repaired by inserting a previously resected portion of the coracoid at the glenoid rim. If the glenoid bone is intact, the main focus is repair of soft tissue damage, which generally can be conducted as arthroscopic procedures to restore as far as possible the normal condition, for example, through repositioning the labrum and capsule or glenohumeral ligaments.

The subcoracoid bursa (see ▶ Fig. 3.24) may also be filled with fluid in the presence of joint effusion (communication with the joint). Fluid accumulation can also be observed in isolated cases secondarily to injections or subcoracoid bursitis.

3.8 Disorders and Instability of the Glenoid Labrum and Capsular Ligaments 3.8.1 Traumatic Lesions Traumatic lesions of the glenoid labrum include: ● Partial tears. ● Avulsions. ● Full-thickness tears. ● Full-thickness tears with labrum dislocation with or without involvement of the glenohumeral ligaments.

110

Anterior Labral Complex Bankart’s Lesion and Bony Bankart’s Lesion

ALPSA and Perthes’ Lesion The Bankart’s lesion must be differentiated from a labral tear with rupture of the scapular periosteum. In the former, the periosteum generally remains intact. The more chronic forms of this injury lead to labral medialization and scarring (ALPSA lesion [anterior

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b

3.8 Disorders and Instability of the Glenoid Labrum and Capsular Ligaments

b

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a

c

Fig. 3.56 Pulley lesion of biceps. (a) Oblique sagittal PDw fatsat sequence. Increased signal intensity at center of long biceps tendon as sign of a degenerative, inflammatory reaction (arrow). (b) Oblique sagittal PDw fatsat sequence adjacent to a. Thickening, increased signal intensity and migration in the direction of the subscapularis tendon (arrow) as sign of pulley lesion. (c) Axial PDw fatsat sequence. Thickening of the subscapularis attachment with increased contact with biceps tendon as sign of a subscapularis attachment lesion (arrow).

labroligamentous periosteal sleeve avulsion]; ▶ Fig. 3.73). If there is no dislocation, the condition is known as a Perthes’ lesion (▶ Fig. 3.74 and ▶ Fig. 3.75), an eponymous term attributed to the surgeon Perthes who first described this in 1906. Perthes’ lesions are more difficult to identify on MRI, but the images can be enhanced in various arm positions (▶ Fig. 3.76).150

GLAD Lesion A GLAD (glenolabral articular disruption) lesion is a partial tear of the labral base with associated articular cartilage damage but there is no full-thickness tear (▶ Fig. 3.77; see also ▶ Fig. 3.75).110

GARD Lesion A GARD (glenoid articular rim divot) lesion involves holelike damage to the cartilage in the glenoid fossa (▶ Fig. 3.78).

Andrews’ Lesion Injury to the inferior, posterior (▶ Fig. 3.79), entire anterior, or superoanterior labrum is less common (Andrews’ lesion). Andrews’ lesions must be distinguished from the normal anatomic variants found in this region (sublabral foramen, partial superior anterior labral aplasia).

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a

Fig. 3.57 Pulley lesion of biceps muscle. Axial PDw fatsat sequence. Medialization of the long biceps tendon at attachment of subscapularis tendon (arrow).

Fig. 3.58 Biceps tendon dislocation. Schematic diagram of classification according to Habermeyer. Left: tear of the superior glenohumeral ligament and of the undersurface of the subscapularis with complete dislocation of the long biceps tendon in intra-articular direction. Right: tear of the superior glenohumeral ligament, coracohumeral ligament and transverse ligament with complete extraarticular dislocation of the biceps tendon. (a) Oblique sagittal sections at the level of the lesser tubercle. (b) Axial images corresponding to the level indicator in the left image in a.

Fig. 3.59 Biceps chondromatosis. Distended biceps tendon sheath with fluid accumulation as sign of bicipital peritendinitis (no shoulder joint effusion). Signal-void nodular structures with hyperintense center as sign of multiple synovial chondromas or osteomas (can be differentiated on radiography). (a) Oblique sagittal PDw fatsat TSE sequence. (b) Oblique coronal STIR sequence.

Inferior Ligament Complex (HAGL and GAGL Lesions) Injury to the glenohumeral ligaments can also cause instability. In particular, the two-bundles of the inferior glenohumeral

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ligament play a pivotal role in stabilizing the shoulder girdle. Injuries are classified into the following types: proximal to the labrum, medial and proximal to the humerus. A distinction is also made between anterior and posterior lesions on the basis of the fibers involved. The term HAGL (humeral avulsion glenohumeral

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b

3.8 Disorders and Instability of the Glenoid Labrum and Capsular Ligaments

Fig. 3.61 Fatty atrophy of supraspinatus. Oblique coronal section. SE sequence (1.5 T, TR = 600 ms, TE = 20 ms). Markedly increased signal intensity of muscle due to fatty atrophy (arrows).

a

b

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Fig. 3.60 Intramuscular fat deposition in obesity. Oblique coronal section. SE sequence (1.5 T, TR = 600 ms, TE = 20 ms). Line of intramuscular increased signal intensity due to obesity. Cystoid absorption in head of humerus in the presence of supraspinatus enthesopathy (arrow).

Fig. 3.62 Atrophy of the infraspinatus muscle. Space-occupying lesion, characteristic of ganglion cyst, in the posterior supraspinous fossa (thin arrow). Weakness and uncharacteristic pain in external rotation. Denervation due to incipient atrophy and edema (thick arrows). (a) T1w sequence. The thin arrow marks the space-occupying lesion. Denervation pattern of the infraspinatus muscle with steep increase in signal intensity. (b) PDw fatsat sequence. The denervation pattern in this sequence, too, is associated with increased signal intensity.

ligament) lesion is used to denote anterior tears occurring close to the humerus.125 Based on this nomenclature, some authors make a further distinction between posterior tear (RHAGL [reverse HAGL]), tears of the anterior bundle close to glenoid (GAGL [glenoid avulsion glenohumeral ligament]) and of the posterior bundle close to glenoid reverse GAGL.44 Injuries to the glenohumeral ligaments are mainly observed in association with a labral tear. HAGL lesions are difficult to identify, but potential ways of doing so include the following: direct visualization of discontinuity of the implicated ligament (▶ Fig. 3.80); identification on oblique coronal images of deformation of the

axillary recess formed by the inferior glenohumeral ligament; and CM escape during arthrographic examinations.

Posterior Labrum Complex POLPSA, GLAD Lesion, etc. Posterior shoulder dislocation is less common and, like anterior dislocation, involves injury to the posterior labrum.44,112 The following lesions have been observed: ● Posteroinferior labral tear (reverse Bankart’s lesion) with or without bone involvement.

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Normal findings

Constellation 1

Constellation 2

Constellation 3

1

a

2

Fig. 3.63 Typical nerve compression constellations with denervation pattern of certain muscles of the shoulder. Schematic diagram. Constellation 1 = Ganglion cyst in anterior supraspinous fossa or scapular notch with denervation pattern of supra- and infraspinatus muscles; Constellation 2 = Space-occupying lesion at junction between posterior supraspinous fossa and infraspinous fossa with denervation of the infraspinatus muscle; Constellation 3 = Denervation of teres minor with or without involvement of the deltoid due to damage to axillary nerve or its branches on the undersurface of the teres minor (quadrilateral space). (a) Oblique sagittal section. Left: Normal finding. (b) Coronal section. Left: Normal finding. 1, Scapula; 2, Infraspinatus; 3, Teres minor; 4, Humerus; 5 = Deltoid; 6, Quadrilateral space.

3 5

b

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4

Fig. 3.64 Insertion tendinopathy of the pectoralis major. Schematic diagram of axial MRI of cortical erosion at crest of greater tubercle, with bone marrow edema beneath it. Soft tissue edema, increased signal intensity of inserting tendon.

●

● ● ●

Avulsion of the posterior capsule (POLPSA [posterior labroligamentous periosteal sleeve avulsion]). Labral tear with cartilage involvement (posterior GLAD lesion). Extensive posterior labral detachment (extensive lesion). Incomplete detachment of the posterior labrum (also known as “Kim’s lesion”).119

Impression fractures of the humeral head are less commonly observed in association with posterior shoulder dislocation than with anterior dislocation and are located in the anterior (anteromedial) head of humerus (reverse Hill–Sachs infraction or also McLaughlin’s fracture).

Bennett’s Lesion Bennett’s lesion is a special type of injury to the posterior labrum seen in professional throwing athletes. The throwing action

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Fig. 3.65 Insertion tendinopathy of the pectoralis in bodybuilder. Axial PDw fatsat image. Inflammatory thickening and increased signal intensity of the pectoralis major tendon, adjacent soft tissues and bone marrow. Cortical abnormalities (arrow).

results in chronic repetitive traction on the posterior labrum causing labral tears and/or traction osteophytes and calcification of the dorsal glenoid fossa.

Superior Labral Complex (SLAP Lesion) Injuries to the superior glenoid labrum often result from athletic activities involving overhead arm movements or from falling on an outstretched arm. Athletic activities involving overhead arm movements can damage this region due to increased traction or repetitive contusion trauma, leading to internal impingement

Fig. 3.66 Fibrous tear of deltoid. Oblique coronal STIR sequence. Fluid-isointense signal intensity in medial, subfascial segment of the deltoid (arrows) as sign of fibrous tear.

Fig. 3.67 Large effusion in the subacromial-subdeltoid bursa. Oblique coronal section. GRE sequence (1.5 T, TR = 600 ms, TE = 25 ms, flip angle = 30 degrees).

(see Internal Impingement, p. 94). Damage to the biceps anchor and to the superior glenoid labrum is seen increasingly also as a concomitant manifestation of rotator cuff lesions. Patients complain about nonspecific shoulder pain, stiffness, and instability, and occasionally report “clicking” or “snapping.”79,80 Injuries to the superior portion of the glenoid labrum (SLAP lesions) can be divided into four subtypes depending on their

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3.8 Disorders and Instability of the Glenoid Labrum and Capsular Ligaments

Fig. 3.68 Fat stripe of subacromial-subdeltoid bursa. Oblique coronal section. (a) Normal finding. The arrow marks the fat stripe. (b) Fat stripe displaced laterally due to small bursal effusion. (c) “Teardroplike” configuration of large effusion. (d) Obliteration in presence of inflammation or tear. (e) Double fat stripe in chronic inflammation.

extension and relation to the insertion of the biceps tendon, and these have different therapeutic implications (▶ Fig. 3.81)54: ● Type I: This lesion is confined to the insertion of the long biceps tendon at the glenoid fossa (10% of all SLAP lesions; ▶ Fig. 3.82 and ▶ Fig. 3.83). It manifests as a superficial irregularity caused by fraying and is often seen without associated trauma. Since it has a higher incidence with increasing age, it is also thought to be related to wear. Treatment is based on conservative measures or debridement. ● Type II: Detachment of the labrum and of the biceps anchor (40% of cases). Type II can be classified further according to Morgan et al83 into a more anterior (type IIa), a more posterior (type IIb), and a combined subtype (type IIc). The main therapeutic focus in stage II is on refixation. ● Type III: The torn labral rim is partially displaced into the joint (bucket-handle tear, 30% of cases; ▶ Fig. 3.84). ● Type IV: This is a bucket-handle tear that extends into the long biceps tendon, which is partially torn in a longitudinal direction (15% of cases; ▶ Fig. 3.85). In types III and IV, resection of the damaged labral segment may be needed in addition to surgical repositioning or refixation.

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Fig. 3.69 Omarthritis in rheumatoid arthritis with rotator cuff tear and large joint effusion. Oblique coronal section. (a) GRE sequence (TR = 600 ms, TE = 35 ms, flip angle = 30 degrees). The extensive effusion in the subacromial-subdeltoid bursa gives rise to a teardroplike configuration of the bursal fat plane (arrows). (b) T1w SE sequence (1.5 Tesla, TR = 600 ms, TE = 20 ms).

a

b

Fig. 3.70 Capsular stripping. Status post shoulder dislocation. (a) Axial PDw fatsat sequence. The glenoid labrum appears to be intact but the anterior capsule is greatly distended and seems to be detached from the neck of scapula in some places (arrow). (b) Oblique sagittal PDw fatsat sequence. Hill–Sachs lesion (arrow).

Further types of superior labral tears have been classified but this system is not used in clinical routine. However, these are mentioned here briefly only for the sake of completeness72,81: ● Type V: A tear extending far, from posteriorly to the biceps tendon insertion, in an inferoanterior direction (combination of Bankart’s lesion). ● Type VI: Type II with anterior or posterior tear of the superior labrum dislocated into the joint (flap). ● Type VII: Tear extending into the anterior capsule at the level of the medial glenohumeral ligament. Other authors even go on to type VIII to X tears: Type VIII: Tear extending in inferoposterior direction.

●

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●

●

Type IX: Partial or almost complete detachment of the labrum circumference. Type X: Extension of a SLAP II lesion into the rotator interval.

As for all labral lesions, direct or indirect MR arthrography is a very sensitive modality for SLAP lesions too (sensitivity: over 90%).48,56 However, specificity is markedly lower; hence, arthroscopy is generally needed for precise assignment of lesions to subtypes. Normal variants of the superior labrum insertion (see Chapter 3.15.2 ), such as superior sublabral recess (▶ Fig. 3.86), sublabral foramen, or the Buford complex, should not be mistaken for SLAP lesions.

3.8 Disorders and Instability of the Glenoid Labrum and Capsular Ligaments

SLAP lesions I–IV (13%) Andrews’ lesion (rare) Extensive anterior injury (rare)

Bennet’s lesion Other posterior injuries (15%)

Bankart’s, GLAD, ALPSA, HAGL lesions (65%) Inferior injury (6%) Fig. 3.72 Bankart’s lesion. Axial indirect MR arthrography. CM-filled defect at the base of the anteroinferior glenoid labrum (Bankart’s lesion: arrow, confirmed on arthroscopy).

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Fig. 3.71 Glenoid fossa with glenoid labrum. View from above. Designation and incidence or labral injuries. ALPSA = Anterior labroligamentous periosteal sleeve avulsion; GLAD = Glenolabral articular disruption; HAGL = Humeral Avulsion glenohumeral ligament; SLAP = Superior labrum tear with anterior posterior extension.

Fig. 3.74 Perthes’ lesion. Magnified axial section of indirect MR arthrogram. Tear of anteroinferior labrum but no major displacement. Capsule and periosteum are detached (Perthes’ lesion: arrows, confirmed on arthroscopy).

● ●

Fig. 3.73 Status post anterior shoulder dislocation. Axial T2w fatsat TSE sequence. Tear of anterior glenoid labrum with posteromedial displacement consistent with ALPSA lesion (arrow).

General Diagnostic Criteria for Magnetic Resonance Imaging Often, precise classification of a labral tear is not possible on native MR images. There are a number of signs that are suggestive of a lesion, and in some 57% of labral tears, the following MRI signs are exhibited: ● Increased basal linear signal intensity in the labrum. ● Deformation (in 24% of cases).

Labrum cannot be delineated (in 18% of cases). Ovoid low-signal mass at the level of the coracoid process (GLOM [glenoid labrum ovoid mass] sign; in 6% of cases).67

Additional signs include increased distance between the base of labrum and glenoid fossa (▶ Fig. 3.87) as well as fragment dislocation (▶ Fig. 3.88). An older system for classification of labral tears, which is hardly used anymore, is similar to the system used for meniscus injuries and distinguished four types of elevated signal intensity within the labrum and at the base of labrum: ● Stage I: In stage I, there is increased basal signal intensity with contact to the labral surface proximal to the joint as a sign of a partial tear. ● Stage II: In this stage, there is increased basal signal intensity with contact to the labral surface proximal and distal to the joint, but no labral dislocation, as a sign of a fullthickness tear. ● Stage III: In stage III, there is increased basal signal intensity with labral dislocation, but without capsular detachment from the scapula, as a sign of a full-thickness tear with dislocation.

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a

b

Fig. 3.76 Perthes’ lesion. Indirect MR arthrography. Status post shoulder dislocation. The torn glenoid labrum (arrows) is still apparently attached; this is seen in internal rotation. (a) Axial plane in internal rotation. (b) Axial plane in external rotation.

Fig. 3.77 GLAD lesion. Axial direct MR arthrogram of shoulder following anterior dislocation. Basal tear of anterior glenoid labrum with bone injury, but no evidence of capsular separation.

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Fig. 3.78 GARD lesion. Axial direct MR arthrography. Discrete cartilage damage in anterior glenoid.

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Fig. 3.75 Lesions of the anterior labral complex. Schematic diagram. Section of glenoid fossa, axial plane of the lowermost third. (a) Normal finding. (b) Labral tear without capsular detachment from scapula (Bankart’s lesion). (c) Labral tear with capsular detachment from scapula (Perthes’ lesion). (d) Labral tear with capsular detachment from scapula, medial dislocation and rotation of labrum (ALPSA lesion). (e) Basal tear with bone damage (GLAD lesion).

Fig. 3.79 Tear of posterior glenoid labrum with posttraumatic recurrent posterior shoulder dislocation (posterior instability). Indirect MR arthrography, axial plane. Broad line isointense to CM in posterior glenoid labrum (arrow).

a

b

c

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3.8 Disorders and Instability of the Glenoid Labrum and Capsular Ligaments

Fig. 3.80 HAGL lesion. Status post shoulder dislocation with discontinuity of the inferior glenohumeral ligament and capsule in proximity to humerus (arrow).

d

Fig. 3.81 SLAP lesions. Schematic view from above of glenoid fossa with insertion of the long head of biceps tendon. Types I–IV according to Snyder. (a) Tear in the region of biceps tendon insertion at the glenoid fossa and glenoid labrum. (b) Tear extending far in anterior (left) and posterior (right; type II) directions. According to Morgan, a tear with predominantly anterior localization is classified as type IIa, while a predominantly posterior localization is classified as type IIb, and complete extension as type IIc. (c) Bucket-handle tear (type III). (d) Bucket-handle tear with involvement of the biceps tendon (partial tear; type IV). Fig. 3.82 SLAP lesion. Oblique coronal indirect MR arthrography. Tear of superior labrum at biceps tendon insertion (SLAP lesion: arrow, confirmed on arthroscopy). Capsular tear in axillary recess. ●

Stage IV: In this stage, there is labral dislocation with capsular detachment from the scapula.

With this classification system, one must, however, bear in mind that often it is not possible to distinguish between stage I signal changes and increased basal signal intensity associated with normal variants. Besides, reliable differentiation from stages III and IV may not be possible because of the insertion variants of the anterior joint capsule. However, this can be easier when imaging a follow-up series of patients. Injuries to the anterior and posterior labrum are best seen on transverse images regardless of the sequence selected;

injuries to the superior and inferior labrum are best identified on oblique coronal images. The diagnostic accuracy of native MR images can be increased by reducing the slice thickness, for example, to 1 mm. There have been different reports on changes to arm positioning to improve detection of labral lesions. According to these reports, it was easier, for example, to evaluate the anterior labrum, anterior capsule, and inferior glenohumeral ligaments on MR arthrography when the arm was in abduction and external rotation (ABER position).64 In external rotation, it was also easier

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Fig. 3.83 SLAP lesion. Indirect MR arthrography, oblique coronal section. Broad cleft isointense to CM in superior glenoid labrum with horizontal orientation (arrow), characteristic of tear of superior labrum.

Fig. 3.84 SLAP III lesion. Direct MR arthrography. Fragment dislocation into the joint (arrow).

a

b

Fig. 3.85 Slap IV lesion. Wide areas of vertical and horizontal increased signal in the superior labrum complex (arrows) consistent with high grade SLAP lesion. (a) Sagittal T1w sequence. (b) Sagittal PDw fatsat sequence.

to assess the superior labrum in the region of the biceps tendon insertion and the superior glenohumeral ligament as well as, in some cases, to detect tears in the inferoanterior labrum. By contrast, on CT arthrography, it was easier in some cases to demonstrate anterior capsulolabral structures in internal rotation but detect tears in the posterior labrum in external rotation. Likewise, another study underlined the importance of conducting diagnostic imaging procedures in external rotation when investigating tears of the posterior labrum. These somewhat

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contradictory findings can be attributed to the heterogeneity of the patient group examined. In external rotation, tension is applied to the anterior portions of the capsule, causing any tears in this region to open wider and thus become more amenable to detection on arthrography. Conversely, if only avulsion injuries are involved (nondislocated Bankart’s lesion, Perthes’ lesion), the damaged portions will be more closely apposed, making it harder to detect them. Therefore, where there is diagnostic uncertainty, the authors recommend conducting indirect axial MR

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3.8 Disorders and Instability of the Glenoid Labrum and Capsular Ligaments

arthrography in both external and internal rotation to improve evaluation of labral injuries. Small tears will then be of variable width and easier to detect. However, when evaluating the results of such dynamic examinations, it is important to interpret the inherent deformability and changes in signal intensity, in particular in the anterior labrum and anterior capsuloligamentous complexes, as a normal finding.111 Apart from the inherent deformability and laxity of the capsuloligamentous structures, intra-articular displacement of parts of the anterior or posterior capsule and/or ligaments can also occasionally be observed in association with shoulder instability (▶ Fig. 3.89). Secondary to tears or partial tears of the subscapularis tendon, parts of this structure can migrate into the joint where they impede repositioning or cause persistent restricted motion (▶ Fig. 3.90). In one study, MRI sensitivity for detection of anterior lesions was 95%, for superior lesions 75%, for inferior lesions 40%, and for posterior lesions 8%.67 In other studies, the sensitivity of native MRI for detection of tears, regardless of the region of interest, was only between 45 and 85%.36,93 The advent of MR arthrography has greatly enhanced the sensitivity and specificity for assessment of lesions of the glenoid labrum, rivaling that of CT arthrography, the hitherto gold standard.7 For direct MR arthrography, Gd-containing CM in a dilution of up to 1:200 is injected into the joint under fluoroscopic control as a mixture with radiographic CM, and then a CM-sensitive sequence is used (▶ Fig. 3.91). For indirect MR arthrography, a dose of 0.1 mmol/kg of a commercially available MRI contrast agent is injected intravenously, the shoulder to be imaged is exercised for around 10 minutes, and then a fat-suppressed T1w sequence is acquisitioned. Both methods produced virtually comparable diagnostic results for the labrum (▶ Table 3.5).122,138

Fig. 3.87 Partial tear of the anterior glenoid labrum with deformation and increase in distance from the base. Transverse plane. GRE sequence (0.5 T, TR = 600 ms, TE = 9 ms, flip angle = 30 degrees). No dislocation. Labral base (long arrow), medial glenohumeral ligament (open arrow), hematopoietic bone marrow in the metaphysis (black arrows), normal rippled contour at metaphyseal junction (white arrows), no Hill–Sachs dent.

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Fig. 3.86 Sublabral recess. Indirect MR arthrography, oblique sagittal section. Pouch at base of labrum filled with CM (arrow), no horizontal orientation and close to glenoid. Hence not suggestive of SLAP lesion but consistent with pocket formation as seen in a normal variant.

Fig. 3.88 Tear of the anterior glenoid labrum with anterior dislocation. Transverse plane. GRE sequence (0.5 T, TR = 600 ms, TE = 35 ms, flip angle = 30 degrees). The arrow marks the anterior dislocation.

3.8.2 Habitual Shoulder Dislocation A distinction is made between posttraumatic recurrent shoulder dislocation and habitual shoulder dislocation or subluxation associated with ligamentous laxity resulting from either connective tissue defects or labral and shoulder dysplasia. MRI can also occasionally detect the cause and/or sequelae of recurrent dislocation. The anterior and posterior labrum may be deformed or the labrum completely absent. Other findings identified can include anlage-related

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Fig. 3.89 Herniation of parts of the capsule. Status post shoulder dislocation. (a) Indirect axial MR arthrography. Internal rotation. Slight posterior subluxation as well as intra-articular dislocation or herniation of the anterior capsuloligamentous structures. (b) Axial GRE image. Moderate external rotation. Dislocation or herniation of parts of the posterior capsule, including the teres minor.

case of posttraumatic recurrent shoulder dislocation secondary to the initial traumatic dislocation. For example, correction of multidirectional instability by anterior capsulorrhaphy alone can result in a high incidence of postoperative posterior dislocation.

3.8.3 Labral Cysts Just like meniscal cysts, labral cysts are thought to be of posttraumatic etiology or imputed to mucoid degeneration. This viewpoint is supported by their detection in association with labral tears.128 Labral cysts are hypointense on T1w contrast, and hyperintense on T2w contrast, images (▶ Fig. 3.92; also see ▶ Fig. 3.110). Lines of low signal intensity caused by septation are often observed. Labral cysts are found within the labrum, often causing ballooning of the labrum. However, the cysts can also prolapse through the labral fibers and manifest as large spaceoccupying lesions.128 These extralabral cysts are typically located in the posterosuperior, posteroinferior, and anterosuperior labrum (▶ Fig. 3.93), and are often identified on MRI from their connection to the parent cysts within the labrum or underlying labral tear. Fig. 3.90 Status post shoulder dislocation hampering repositioning. Axial PDw fatsat sequence. Damage to the anterior glenoid labrum with cartilage involvement (GLAD lesion, white arrow), subscapularis tear with migration or displacement of at least parts of the tendon into the joint (black arrow).

bone defects, for example, of the posterior glenoid,146 partial hypoplasia of the scapula and glenoid (see ▶ Fig. 3.110), and increased angulation of the articular surface of the glenoid fossa with respect to the longitudinal axis of the scapula. It is important to recognize the signs of multidirectional instability for preoperative assessment of habitual shoulder dislocation and also in the

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3.9 Disorders of the Synovial Lining and Joint Capsule 3.9.1 Arthritis Bony erosions manifest as a discontinued contour or substance defect and can be identified better on MRI compared with plain radiographs.60 Signal cysts are hypointense on T1w images and hyperintense on T2w images. Active pannus tissue also appears as low signal on T1w images and high signal on T2w sequences. Since the T2 relaxation time of

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3.9 Disorders of the Synovial Lining and Joint Capsule

Fig. 3.92 Hyperintense cysts in the posterior glenoid labrum. Axial GRE image.

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Fig. 3.91 Tear of the anterior glenoid labrum with lateral and posterior dislocation. Transverse plane SE sequence following CM injection into the joint (MR arthrography; 1,5 T, TR = 600 ms, TE = 20 ms).

Table 3.5 Sensitivity and specificity of various imaging modalities for detection of tears of the glenoid labrum Sensitivity/specificity

CT-arthrography

MRI

Direct MR arthrography

Indirect MR arthrography

Sensitivity (%)

90–95

45–85

92

91

Specificity (%)

90

80–90

92

91

fluid is longer than that of pannus, effusions can be clearly distinguished from active pannus on high-contrast T2w sequences. Besides, pannus enhances following CM administration. Inactive fibrous pannus exhibits a signal that ranges from hypointense to isointense to muscle on all sequences. Concomitant tears of the rotator cuff or tendon of the long head of biceps are commonly seen in rheumatoid arthritis. The MRI findings are similar to those observed for nonarthritic tears. Other changes concurrently seen include muscular atrophy, bursitis, and tendinitis.

3.9.2 Pigmented Villonodular Synovitis and Hemophilia Hemosiderin deposits, as seen in pigmented villonodular synovitis or hemophilic arthropathy, result in focal low signal intensity in the joint, which is best seen on T2w images.

3.9.3 Synovial Chondromatosis

Fig. 3.93 Paralabral cysts. Oblique sagittal STIR sequence. Fluid-intense, multilocular mass (arrow) in direct vicinity of inferior glenoid labrum.

Calcified or ossified loose joint bodies, as seen, for example, in association with synovial chondromatosis, can also manifest as low signal intensity or signal void on all sequences (▶ Fig. 3.94). Noncalcified chondromas appear as low signal intensity, often within a high signal intensity effusion; in their primary form, these are often seen in large numbers as rice grain–sized structures (▶ Fig. 3.95). Calcified chondromas appear as homogeneous signal void; osteomas exhibit characteristic layers of peripheral

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The Shoulder Often, signs of reactive synovitis with thickened, CM-enhanced synovial membranes are seen on MRI. Intraosseous amyloid deposits frequently give rise to multiple cystic bone erosions ranging in size from a few millimeters to 5 cm. These lesions appear as low signal intensity on T1w images and range from hypointense through inhomogeneous to hyperintense on T2w images. In the shoulder, they are found mainly in subchondral regions near the bicipital groove and the capsule insertion into the head of humerus.30

Fig. 3.94 Capsule chondromas or osteomas in the coracoid recess in association with shoulder arthrosis. Oblique sagittal PDw fatsat TSE sequence. The arrow marks the recess.

cortex and central fatty marrow. Secondary forms are seen in association with chronic synovitis, for example, arthrosis (▶ Fig. 3.96).

3.9.4 Lipoma Arborescens Just as in the knee joint, fat deposition can also be seen in the hypertrophied villi of the joints or subacromial-subdeltoid bursa secondary to chronic lipomatous proliferation of the synovial membranes of the shoulder joint. The term lipoma arborescens is also used to denote this condition (see Chapter 7.15.5). The fat-containing synovial villi are isointense to fat with massive thickening.95 Varying degrees of bone erosions are observed.18

3.9.5 Amyloid Arthropathy Complex articular and periarticular changes are seen following primary or secondary amyloidosis because of amyloid deposition. The changes related to ß2 microglobulin amyloid deposits following long-term dialysis in chronic kidney failure are relatively well known. The clinical symptoms include pain and restricted motion. At a relatively early stage, thickening of the joint capsule and of the tendons reinforcing the rotator cuff capsule is observed in such patients. The supraspinatus tendon can exhibit thickness of up to 1.3 cm (normal: 4–5 mm). The tendon appears as low signal intensity on all sequences; at most, slight inhomogeneity is seen. Concomitant joint and bursal effusions are invariably seen, some of which are loculated and of inhomogeneous distribution.

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Adhesive capsulitis (frozen shoulder) is a chronic inflammatory disease of the joint capsule of unknown etiology, which leads to fibrotic thickening of the capsule and shrinkage. It is seen most commonly in women aged 30 to 60 years.127 The clinical symptoms (especially at night) include painful and increasing loss of shoulder mobility lasting from months to a few years. The disease is generally self-limiting. When diagnosed at an early stage, it may be possible to restrict its course through physiotherapy and steroid injections. Occasionally, it may be necessary to mobilize the shoulder under anesthesia, or surgery may be needed. The condition is mainly diagnosed or ruled out on the basis of clinical symptoms. It cannot be identified on plain radiographs. On MRI, a thickened capsule with increased CM uptake is seen, in particular in the rotator cuff interval. In the ensuing course, the axillary recess is also affected, and is obliterated and thickened. The inferior glenohumeral ligament is relatively hyperintense on fat-suppressed PDw and T2w images (e.g., compared with the long biceps tendon) and may be surrounded by an edemalike halo. Obliteration of the subcoracoid fatty tissues,75 which also take up CM, is observed on imaging the rotator cuff interval. An area of low signal tissue thickening is observed at the biceps anchor.1,124

3.10 Bone Disorders 3.10.1 Aseptic Osteonecrosis Aseptic osteonecrosis of the humeral head is subject to the same diagnostic criteria as the femoral head necrosis (see Chapter 6.4). A focal or bandlike subchondral decrease in signal intensity is seen on T1w images. The bandlike low signal intensity often encloses a high signal intensity center suggestive of normal fatty marrow (▶ Fig. 3.97). On T2w sequences, bandlike reduced signal intensity is often observed in proximity to an area of bandlike high signal intensity. This is referred to as the double-line sign and is pathognomonic for bone marrow necrosis. The hypointense zone is indicative of sclerosis and the hyperintense zone of a reactive region between the viable and necrotic bone marrow. This disease is frequently bilateral. The risk factors include the following: ● Cortisone therapy. ● Alcoholism. ● Trauma (subcapital humerus fracture). ● Sickle cell anemia. Osteonecrosis is accompanied in over 50% of cases by a joint effusion. During the course of disease, the bony structures

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3.9.6 Adhesive Capsulitis (Frozen Shoulder)

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3.10 Bone Disorders

Fig. 3.95 Synovial chondromatosis. A 25-year-old patient with painful restricted motion. Numerous small hypointense (loose) joint bodies (like rice grains) in the joint recess. This causes synovitis and distension from effusion, a characteristic finding in synovial chondromatosis. (a) Oblique sagittal PDw fatsat sequence. (b) Oblique sagittal PDw fatsat sequence, other section. (c) Axial PDw fatsat sequence.

collapse (▶ Fig. 3.98) and there is onset of reactive fibrosis and sclerosis, appearing as reduced signal intensity on all sequences. MRI is considered the most sensitive imaging modality for detection of avascular osteonecrosis. The most common form of humeral head necrosis is posttraumatic necrosis, which is seen in particular secondarily to multifragmented, dislocated subcapital fracture. Less common pathogenetic forms (e.g., caisson disease, steroid therapy) occur bilaterally (as seen in up to 15% of cases of femoral head

necrosis). As a precaution, for such forms of necrosis the contralateral side should always also be imaged (▶ Fig. 3.99).

3.10.2 Impression Fractures of the Humeral Head Impression fractures of the humeral head secondary to shoulder dislocation can be identified on axial images. Depending on the

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Fig. 3.96 Shoulder arthrosis with secondary osteochondromatosis. Numerous layered joint bodies, some of which exhibit at their center signal isointense to fatty marrow, and of different sizes, as a sign of multiple capsular osteomas. (a) Oblique sagittal T1w sequence. (b) Oblique sagittal PDw fatsat sequence. (c) Axial PDw fatsat sequence.

extent of the fracture, a notch or only flattening on the humeral head is seen (▶ Fig. 3.100). For fresh impression fractures, concomitant bone marrow edema can be observed additionally on T2w images as increased signal intensity within the bone marrow (▶ Fig. 3.101). The following three grades can be distinguished in accordance with their angular involvement: ● Grade I: up to 30 degrees of the circumference. ● Grade II: between 30 and 60 degrees. ● Grade III: more than 60 degrees.

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The following impression fractures are differentiated: Superior impression fracture following inferior dislocation. ● Posterolateral impression (Hill–Sachs lesion) following anterior dislocation. ● Anteromedial impression (reverse Hill–Sachs lesion) following posterior dislocation (▶ Fig. 3.102). ●

On using the clock face as a reference when viewing the affected circumference of the humeral head on axial images, and with the bicipital groove at the 12 o’clock position, the location of the

3.10 Bone Disorders Hill–Sachs lesion ranges from the 3 to 5 o’clock position on the left, and from 7 to 9 o’clock position on the right, shoulder. With a slice thickness of 4 to 5 mm, the fractures can be seen on the two uppermost slices distal to the top of the humeral head. They must be distinguished from the anatomic indentation at the posterolateral portion of the humeral head at the epimetaphyseal junction, which can be visualized on more inferior slices (see ▶ Fig. 3.87).107 MRI has a sensitivity of 97% for detection of Hill– Sachs lesions.152 An equally good sensitivity can be achieved with conventional radiography only by resorting to special projections.

3.10.3 Avulsion Injuries Avulsion injury to the greater tubercle is a frequently encountered form of humeral trauma. It is not always possible to clearly identify this fracture on conventional radiographs. Thanks to its ability to visualize the associated bone marrow edema together with high-contrast depiction of the fracture lines of even nondislocated fractures, MRI confers advantages in detection of such injuries (▶ Fig. 3.103).73 Isolated avulsions of the lesser tubercle (▶ Fig. 3.104), teres minor, or the coracoid process (▶ Fig. 3.105) are relatively less common. Overall, CT is the imaging modality of choice for detection of avulsion fractures.

3.10.4 Distal Clavicle Edema

Fig. 3.97 Aseptic osteonecrosis. Oblique coronal section. SE sequence (1.5 T, TR = 600 ms, TE = 20 ms). Necrosis with hyperintense subchondral center surrounded by hypointense, bandlike zone (arrows).

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Changes occurring in the acromioclavicular joint following trauma or because of repetitive stress (e.g., weightlifters) can result in massive bone marrow edema of the distal clavicle and acromion (▶ Fig. 3.106). The capsule may be distended and swollen due to concomitant synovitis.28 These painful changes can persist for months, possibly leading to severe osteopenia of the distal clavicle. Osteolysis of the lateral clavicle is seen on conventional radiography. The underlying pathomechanism of this condition is not known; it is also called “posttraumatic osteolysis” (not to be confused with massive distal clavicle osteolysis).102 In most cases, there is complete resolution of edema during the repair phase, but there may be persistent enlargement of the joint space.

3.10.5 Shoulder Arthrosis (Omarthrosis) MRI is, to a certain extent, able to demonstrate the capsular damage occurring in association with arthrosis of the shoulder

Fig. 3.98 Humeral head necrosis. The necrotic zone is starting to fragment. Apart from subchondral osteonecrosis, metaphyseal bone marrow infarction is visualized as a line of geographic signal changes (a, arrow). Long-standing use of cortisone medication. (a) Oblique coronal T1w image. (b) Oblique sagittal PDw fatsat TSE image.

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Fig. 3.99 Bilateral humeral head necrosis. Coronal T1w overview sequence. On high resolution imaging of the symptomatic left shoulder, it was also possible to detect involvement of the asymptomatic contralateral shoulder thanks to this overview with reduced spatial resolution.

Fig. 3.101 Fresh Hill–Sachs compression fracture. Axial PDw fatsat TSE sequence. Compression of the lateroposterior humeral head circumference with concomitant edema as sign of fresh or “fresh” Hill–Sachs fracture.

girdle.40 It will also detect concomitant disorders such as rotator cuff lesions and osteonecrosis (▶ Fig. 3.107).

3.10.6 Stress Reaction Bone marrow edema or even stress fractures resulting from athletic activities (stress reaction) are relatively rarely seen

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Fig. 3.100 Posterolateral humeral head impingement following shoulder dislocation. Transverse plane. GRE sequence (0.5 T, TR = 600 ms, TE = 9 ms, flip angle = 30 degrees). Stage II Hill–Sachs lesion. The arrows mark the humeral head impingement.

Fig. 3.102 Reverse Hill–Sachs fracture. Axial PDw fatsat TSE sequence. Deep dent in the anteromedial humeral head circumference following posterior dislocation a few months previously. Absence of bone marrow edema as sign of historic reverse Hill–Sachs fracture.

in the shoulder region (▶ Fig. 3.108). Stress-mediated lesions of the proximal humeral epiphysis are often seen in adolescents who engage in pitching and throwing activities (little leaguer’s shoulder).47,123 MRI shows enlargement of the epiphysis with edematous signals in the epiphysis and adjacent bone regions.

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3.11 Disorders of the Acromioclavicular Joint

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Fig. 3.103 Avulsion fracture of greater tubercle. Oblique coronal section, indirect arthrography. Also partial tear of supraspinatus tendon (arrow).

3.10.7 Tubercle Cysts Cystic asymptomatic lesions are commonly observed at the insertion site of the infraspinatus on the posterior greater tubercle. These range in size from a few millimeters to a few centimeters. While the cysts are generally located in the subcortical region, they can also extend into the cortex. The etiology of such cysts is unknown but they are mainly of no significance and are not associated with tendinopathy. If the cysts are located in the anterior region, at the insertion of the supraspinatus, they will cause insertion tendinitis. These may be due to stress-associated absorption activities deep in the enthesis. On MRI, the characteristic signs of a bland cyst are seen, on rare occasions also surrounded by bone marrow edema (▶ Fig. 3.109). Such cysts are also found, though less often, in the lesser tubercle.151

3.10.8 Congenital Malformations Congenital malformations of the scapula associated with habitual shoulder dislocation (see Chapter 3.8.2), including hypoplasia or dysplasia of the glenoid fossa, can be visualized on MRI, and concord with the well-documented findings of conventional radiography. Congenital bone defects of the posterior shoulder socket are particularly common (dysplasia, hypoplasia) with compensatory hypertrophy of the posterior glenoid labrum. This predisposes to shoulder instability or habitual dislocation as well as a higher incidence of posterior labral tears (▶ Fig. 3.110).44 Please refer to Chapter 11.3 for MRI depiction of inflammatory and traumatic bone lesions.

3.11 Disorders of the Acromioclavicular Joint In addition to the capsule and the capsular ligaments, a ligamentous connection between the clavicle and coracoid process helps

Fig. 3.104 Avulsion fracture of lesser tubercle. Edema, contour level and slight dislocation of lesser tubercle after considerable trauma (arrows). Normal finding on conventional radiography. (a) Axial T1w sequence. (b) CT. (c) Oblique sagittal PDw fatsat TSE sequence.

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The Shoulder to stabilize the acromioclavicular joint. This consists of two portions (trapezoid and conoid) and can normally be visualized on MRI. The continuity of this ligamentous connection plays a pivotal role in classification of the severity of dislocation of the shoulder joint (▶ Table 3.6).3 Since ligament injuries can be directly visualized on MRI, this imaging modality also permits more precise classification than that afforded by plain radiographs.91

Often, the shoulder joint also exhibits widespread degenerative changes commonly implicated in onset of impingement syndrome (▶ Fig. 3.111).

3.12 Disorders of the Sternoclavicular Joint

3.13 Tumors of the Shoulder

Fig. 3.105 Avulsion fracture of coracoid process. Oblique sagittal PDw fatsat TSE sequence. Edematous changes along the insertion of short biceps tendon (short arrow), step deformity and edema in coracoid process (long arrow). The fracture was not detected on conventional radiography.

For tumor diagnosis, MRI is able to provide detailed information on the tumor size, infiltration into the joint soft tissues and any joint effusions. Diffuse infiltrative tumor entities can be recognized from the pathologic distribution of inactive fatty marrow and signal changes that are not isointense to fatty marrow, and these should not be misinterpreted as active bone marrow (▶ Fig. 3.113). MRI also helps the radiologist to become familiar with the normal distribution of active and inactive bone marrow. For example, hematopoietic marrow is still seen in the clavicle in late adulthood and should not be misinterpreted as a malignant infiltration (▶ Fig. 3.114). Please refer to Chapter 12 for details of the different tumor entities.

Fig. 3.106 Edema of the distal clavicle. Following historic injury, persistent pain in shoulder girdle, signal isointense to edema in the distal clavicle (arrows). No other pathology noted. (a) Oblique sagittal STIR sequence. (b) Oblique sagittal PDw fatsat TSE sequence.

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Disorders of the sternoclavicular joint often cause painful swelling of the superior margin of the sternum and often call for MRI investigation. Such complaints are often caused by arthrosis, as seen in association with or without synovitis (active arthrosis; ▶ Fig. 3.112). This joint can also be affected in the presence of spondyloarthropathy or SAPHO (synovitis, acne, pustulosis, hyperostosis, and osteitis) syndrome. Less commonly implicated here are tumors, in particular metastases, or arthritis. These latter diseases show a higher degree of osteodestruction, space occupying and CM uptake.

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3.14 Post-Therapy Findings

Fig. 3.107 Shoulder arthrosis. Severe osteophytosis (especially at caudal head of humerus). Subchondral cysts, asymmetrical narrowing of the joint space, subluxation-mediated defective position. (a) Oblique sagittal T1w sequence. (b) Axial PDw fatsat TSE sequence.

result in detection of focal increased signal intensity in the rotator cuff on MRI T2w images and must not be misinterpreted as focal inflammatory changes.59 Occasionally, injections are administered into the subacromial-subdeltoid bursa and can mimic a bursal effusion. Fluid accumulation along the fascia is also possible.153 MRI should not be performed earlier than 2 to 10 days after such injections.8

3.14.2 Shock Wave Lithotripsy In recent times, shock wave lithotripsy has been increasingly used to treat calcareous tendinitis of the rotator cuff. No changes in signal intensity were detected on T1w, T2w SE, or GRE images following shock wave therapy.116 It is possible that discrete edematous changes are seen on STIR images. Hence, shock wave lithotripsy is not thought to negatively impact interpretation of MRI images.

3.14.3 Surgical Procedures Fig. 3.108 Stress reaction in coracoid process. Oblique sagittal STIR sequence. Young patient with pain of unknown origin in particular during and after competitive sport (table tennis). Increased signal isointense to edema at base of coracoid process (arrow), consistent with stress reaction of overloading.

3.14 Post-Therapy Findings 3.14.1 Injection Steroids and/or analgesics are frequently injected for treatment or diagnosis of painful impingement syndrome. Such injections

Among the surgical procedures used to repair rotator cuff tears are tendon-to-tendon repair, tendon-to-bone repair, and closing the defect with autografts or allografts. Impingement syndrome can be treated surgically with acromioplasty, which can be combined with bursectomy or with incision of the coracoacromial ligament. Recurrent or persistent complaints following shoulder operations are common (in up to 25% of cases) and are caused by tendinitis, a new full-thickness or partial rotator cuff tear, persistent impingement, etc. These postoperative disorders must be distinguished from normal postoperative conditions. The normal postoperative MRI findings include obliteration of the normal periarticular soft tissues layers due to scarring or resection (▶ Fig. 3.115). The peribursal fat plane can no longer

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Fig. 3.109 Cysts in greater tubercle. Fluid-isointense cystic lesion in greater tubercle (b, arrow) with slight adjacent bone marrow edema. Cysts are often seen at this location and are thought to be associated with stress-induced absorption activities, as seen here at the insertion of the supraspinatus tendon into greater tubercle. Other cysts, presumably induced by stress, are found in the tibia (cruciate ligament insertion) or also in the calcaneus (changed static forces in the foot). (a) Oblique coronal T1w sequence. (b) Oblique coronal STIR sequence.

Table 3.6 Classification of dislocation injuries of shoulder joint according to Rockwood Type according to Injuries Rockwood

Fig. 3.110 Habitual shoulder dislocation. Axial PDw fatsat image. Marked hypoplasia of the posterior glenoid fossa with compensatory thickening of the posterior glenoid labrum (arrow). Large posterior labral cysts as sign of ensuing labral avulsion.

serve as a diagnostic pointer since the bursa may have been removed. A small bursal effusion frequently observed after shoulder operations should not be mistaken for bursitis or evidence of a recurrent rotator cuff tear.97 Besides, multiple focal areas of signal void are typically observed following surgery because of the susceptibility artefacts caused by bone and

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I

Distortion, partial injury to capsular ligaments

II

Capsular ligaments ruptured, moderate elevation of clavicle

III

As stage II plus coracoclavicular ligaments ruptured, marked elevation of clavicle

IV

As stage III plus trapezius ruptured, posterior clavicle displacement

V

As stage IV plus deltoid ruptured

VI

Inferior clavicle dislocation

abrasion of metallic implants. Such artefacts are most conspicuous on GRE sequences with long TE (▶ Fig. 3.116).

Surgical Repair of Rotator Cuff Tear Discrete defects of the rotator cuff may persist following surgical repair of rotator cuff tears because of the instruments used intraoperatively. Following fixation of the rotator cuff to the margin of the greater tubercle, there may be a residual defect at the insertion of the tendon (footprint) and this must not be misinterpreted as a recurrent tear.22 Hence, penetration of CM into the subacromial-subdeltoid bursa during postoperative arthrography is not a reliable sign of recurrent tear.106 Granulation tissue emits a fluid-isointense signal in the

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3.14 Post-Therapy Findings

Fig. 3.111 Severe shoulder arthrosis with significant narrowing of the subacromial space. Bone remodeling, subchondral cysts, synovitis, bone marrow edema, joint effusion. There are no signs of shoulder joint arthrosis. (a) Sagittal T1w sequence. (b) Sagittal PDw fatsat sequence. (c) Axial PDw fatsat sequence.

subacromial bursa which is virtually always present, even after surgical procedures with successful technical and clinical outcomes.160 Such changes should not be misinterpreted as bursitis. Likewise, abnormalities in the nature and intensity of signals in tendons tend to be more the rule than the exception and should not be overrated. In particular in the first 6 to

12 postoperative months, the operated tendon will be thinner and more hyperintense than usual. The graft transplant at the tendon insertion (footprint) appears diluted or incomplete for the first few months. The incidence of recurrent rotator cuff tears following rotator cuff repair reported in the literature varies and is higher for larger tears and higher patient age.22

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Fig. 3.112 Sternoclavicular arthrosis on left, right with signs of disease activity. Osteophytes, articular incongruence, bilateral subluxationmediated defective position. There are now clinical signs of more severe swelling of the painful right shoulder compared with the contralateral left, suggestive of active arthrosis with synovitis, periarticular thickening and bone marrow edema (b, arrows). No destructive process (metastasis, osteomyelitis, etc.). (a) Coronal T1w sequence. (b) Coronal STIR sequence.

Fig. 3.113 Leukemic infiltration. Extensive infiltration of the scapula and humerus with involvement of the epiphysis. Only a small amount of residual fatty marrow in the region of the greater tubercle remains unaffected (arrows). (a) Oblique coronal STIR sequence. (b) Oblique coronal T1w sequence.

Shoulder Instability Operation Surgery for instability-mediated recurrent shoulder dislocation is performed to restore stability of the shoulder joint. Various techniques are available to that effect: ● Labrum capsule reinsertion (Bankart’s procedure). ● Capsulorrhaphy (capsular shift).

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● ● ●

Coracoid transposition (Bristow–Helfet, Latarjet). Bone graft insertion (Eden–Hybbinette, Oudard). Subscapularis procedures (Putti–Platt, Magnuson–Stack).

In addition to open and arthroscopic surgical procedures, a minimally invasive combination of both techniques is also used.

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3.14 Post-Therapy Findings

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Fig. 3.114 Bone marrow of adult clavicle. Oblique coronal image of a sawn specimen of acromioclavicular joint and distal clavicle. Active hematopoietic (red) bone marrow seen in the clavicle. Inactive fatty (yellow) bone marrow in the distal clavicle epiphysis and acromion.

Fig. 3.115 Status post shoulder operation with resection of normal skin layers. Oblique coronal section. SE sequence (1.5 T, TR = 600 ms, TE = 20 ms). Subacromial-subdeltoid bursa partially resected. The arrow marks the resected skin layer.

Following successful surgical repair of shoulder instability, a rounded structure, similar to the labrum with altered signal intensity, is seen instead of the typical triangular hypointense labrum at the glenoid rim. The capsule and subscapularis tendon may be thickened because of scar tissue. If overcorrected, the anterior capsule space will appear narrower on MR arthrographic images. Following bone surgical procedures such as Bristow– Helfet or Latarjet, a bone graft can be seen at the anteroinferior glenoid rim, often accompanied by susceptibility artefacts and discrete scar formation (▶ Fig. 3.117). This scar tissue is presumably attributable to the bone graft and prevents recurrent anterior dislocation (“doorstop” sign).137,139

Acromioplasty Acromioplasty results in changes to the shape of the acromion and in reduced signal intensity on T1w and T2w images, thought to be due to sclerosis or fibrosis.

Tendon-to-Tendon Repair Following tendon-to-tendon repair, persistent increased signal intensity is observed on T1w and PDw sequences, while the

Fig. 3.116 Status post acromioplasty. Oblique sagittal section. (a) SE sequence (1.5 T, TR = 600 ms, TE = 20 ms). Step deformity in acromion (arrow). Smooth resection margin. (b) GRE sequence (TR = 600 ms, TE = 14 ms, flip angle = 30). Multifocal signal obliteration due to metallic and bone abrasion (arrows).

signal intensity remains unchanged, or is even higher, on T2w images.97 Hence, it is difficult to diagnose recurrent or partial tear.

Tendon-to-Bone Repair Following tendon-to-bone repair of the head of humerus, an area of low signal intensity at the humeral head is demonstrated on all sequences. Intraoperatively sustained nerve damage can result in persistent pain in the area innervated by the damaged nerve or in atrophy of the implicated muscle. For example, if a surgical access route through the deltoid is used, the anterior branch of the axillary nerve can be damaged and cause partial atrophy of the deltoid (▶ Fig. 3.118).81

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Fig. 3.117 Postoperative scarring of shoulder joint. Transverse plane. (a) SE sequence (1.5 T, TR = 600 ms, TE = 20 ms). Status post Eden–Lange– Hybbinette operation. Bone graft fused with the glenoid process (small arrow). Hypointense anterior scarred tissue (large arrow). (b) Schematic diagram of normal shoulder girdle (above) and following bone grafting with visualization of anterior scar (“doorstop” sign).

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An increased signal intensity on T2w or T2*w images is a reliable sign of rotator cuff lesions and should help to avoid misinterpretation (▶ Fig. 3.119). Physiologic increased signal intensity in muscles may be observed on T2w and fat-suppressed sequences in patients who engage in sporting activities involving the shoulder immediately prior to MRI examination. No changes in signal intensity are seen in the tendons after sporting activities, nor are there any notable changes in the fluid content of the bursae or joint space.16 Hence, any increased signal intensity in the supraspinatus tendon or effusion in the subacromial-subdeltoid bursa must be interpreted as a sign of pathology, even immediately after sporting activities.

4 Fig. 3.118 Course of axillary nerve and its branches in relation to deltoid. Schematic diagram, coronal view. Surgical lesions of the anterior branch of the axillary nerve may cause partial atrophy of the deltoid. 1 = Deltoid; 2 = Anterior branch of axillary nerve; 3 = Posterior branch of axillary nerve; 4 = Teres minor branch of axillary nerve (through quadrilateral space); 5 = Axillary nerve; 6 = Posterior trunk.

3.15 Pitfalls in Interpreting the Images 3.15.1 Misinterpretation of Increased Signal Intensity Artificially increased signal intensity within the tendons of the rotator cuff, especially of the supraspinatus, must not be mistaken for tendinitis or a partial tear. This raised signal intensity is probably caused by the orientation of anisotropic tissue in the main magnetic field and is seen most clearly on T1w and PDw images.

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3.15.2 Misinterpreting Normal Variants It is important that the radiologist be aware of the wide spectrum of morphologic variants of the glenoid labrum to avoid mistaking them for a tear. Since the glenoid labrum caps the hyperintense hyaline articular cartilage which, in turn, lies above signal-void cortical bone, this normal anatomic configuration must not be misinterpreted as a basal labral tear. Besides, proximity to the medial glenohumeral ligament can lead to linear increase in signal intensity that should not be mistaken for a labral tear.52 Tears of the superior glenoid labrum (SLAP lesions) should be distinguished from normal variants of the superior labrum79: ● Superior sublabral recess: in the 11 to 1 o’clock position (partial labral detachment). ● Sublabral foramen: in the 1 to 3 o’clock position (complete labral detachment in this area). ● Buford complex: in the 1 to 3 o’clock position (focal obliteration of the labrum with compensatory cordlike thickening of the medial glenohumeral ligament).

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b

3.15 Pitfalls in Interpreting the Images

Unlike a recess, tear tends to have irregular margins, are wider (“gaping”), and may change direction.24 A recess with a depth of up to 1 mm between the labrum and cartilage has been reported as normal variability for all regions of the glenoid labrum.130 A recess with a depth of up to 3 mm is typically found as a normal variant in the anterior, anteroinferior, and posterosuperior labrum. On axial sections, a morphologic variant of the posterolateral contour of the humeral head can occasionally be observed and should not be misinterpreted as a Hill–Sachs lesion (see ▶ Fig. 3.87).50 There are a number of anlage variants of the biceps muscle that can present a diagnostic challenge. These include a three-, four-, or rarely five-headed biceps muscle with myriad other potential origins (on the brachialis, pectoralis, outer side of humerus, bicipital groove, greater tubercle, or joint capsule). In particular, the variant with double origin and insertion into the capsule where two tendons are seen in the bicipital groove (accessory biceps tendon) can be mistaken for a longitudinal tear (longitudinal split). In such cases, a double-bone anlage of the bicipital groove has been reported. It should be possible to recognize the second tendon from its flat shape and thus facilitate its differentiation from a longitudinal tear (▶ Fig. 3.119).143 Aplasia of the biceps heads has also been reported. An empty groove is not necessarily to be equated with a tear of the long biceps head, which, in rare cases, may not at all have been formed. This situation must not be mistaken for tears.62 When evaluating the shape and position of the acromion or assessing the acromioclavicular joint for arthrosis, it is important to take account of the normal variant of a variable acromioclavicular joint (▶ Fig. 3.120). In particular, there may be mimicking of osteophytic spurs on oblique slices of the joint.

3.15.3 Misinterpretation of an Effusion An effusion in the subcoracoid recess must not be mistaken for a capsular tear with fluid escape into the soft tissues (▶ Fig. 3.121). There may be excessive anterior projection of the subcoracoid recess. A small amount of fluid in the tendon sheath of the long head of biceps is normal and should not be mistaken for a

a

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c

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Fig. 3.119 Double biceps tendon. (a) Axial PDw fatsat image. (b) Oblique coronal PDw fatsat image. (c) Oblique coronal T1w image. There are two tendons in the bicipital groove and intra-articular segment (arrow).

Fig. 3.120 Normal variant of joint orientations of acromioclavicular joint. Schematic diagram of acromioclavicular joint viewed from the front. (a) Outer upper to inner lower oblique orientation (overriding type). (b) Vertical orientation. (c) Incongruent. (d) Inner upper to outer lower oblique orientation (underriding type).

pathologic joint effusion. Furthermore, one of the branches of the anterior circumflex humeral artery may mimic fluid accumulation in the bicipital groove on axial GRE images.58 Synovial ligaments may be manifested along the course of the proximal biceps tendon sheath as fine signal-void structures (vincula tendina) and should not be misinterpreted as pathologic changes (▶ Fig. 3.122). An increase in signal intensity in the rotator cuff or fluid accumulation in the subacromial-subdeltoid bursa following administration of injection should not be mistaken for pathologic findings.

3.15.4 Misinterpretation of Bone Marrow Distribution Hematopoietic bone marrow, which on T1w images has lower signal intensity than fatty bone marrow, is normally seen in the proximal humeral metaphysis. This normal bone marrow distribution must not be misinterpreted as an infiltrative process of the humerus (see ▶ Fig. 3.87).

3.15.5 Misinterpretation of a Persistent Acromion Ossification Center Another potential source of misinterpretation relates to a persistent acromion ossification center (acromial bone) (▶ Fig. 3.123). Persistent synchondrosis between the base of acromion and the center mimics a fracture line on axial MRI images (▶ Fig. 3.124a). Degenerative changes may lead to impingement syndrome.

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Fig. 3.121 Joint effusion with fluid in subcoracoid recess. Transverse plane. GRE sequence (0.5 T, TR = 600 ms, TE = 35 ms, flip angle = 30 degrees). The arrow marks the fluid in the recess. This finding must not be mistaken for capsular tear.

Fig. 3.122 Vincula tendina. Axial PDw fatsat image. Joint effusion and effusion in the biceps tendon sheath. The tendon sheath surrounding the biceps tendon exhibits fine, bandlike structures, which are a normal finding. These bandlike structures are the vincula tendina.

Inflammatory changes (synchondrosis of the acromial bone) occur in athletes (e.g., tennis), leading to increased CM uptake by the synchondrosis and this must not be misinterpreted as osteomyelitis (▶ Fig. 3.124b). Good visualization is assured by plain radiographs only if appropriate settings are used (▶ Fig. 3.124c).

study that could warrant criticism (e.g., MR arthrography is not universally available; the amendments to diagnosis and treatment were probably overestimated since the study was performed by a teaching hospital), there is evidence that MRI impacted essentially not just the diagnosis but also therapy decisions.

3.15.6 Misinterpretation of Muscle Insertions into Bone For physiological reasons, the sites of muscle insertion into bone can be associated with roughness and marked abnormalities that must not be misinterpreted as inflammatory processes or tumors. One typical site in the shoulder girdle is the insertion of the deltoid into the humerus (▶ Fig. 3.125).

3.16 Clinical Relevance of Magnetic Resonance Imaging It is not possible to dispense with conventional radiography for diagnosis of shoulder disorders. MRI and radiography are complementary imaging modalities, with each having its strengths and weaknesses.15 Radiographs are better than MRI at identifying, in particular, calcifications and cortical abnormalities. Zanetti et al158 investigated the effectiveness of MR arthrography in a prospective study with 73 patients. The referring physician submitted a questionnaire before and after examination, specifying the diagnoses and intended treatment. Following MRI, the diagnoses were withdrawn in around one-third of cases, and new diagnoses were added in 13% of cases. The treatment concept was amended in 49% of cases. Despite the different aspects of the

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Clinical Interview

●i

Clinical interview with Prof. Dr. Kurt Steuer and Dr. Christian Paul, Medical Directors of the Department of Trauma Surgery of the Evangelical Hospitals, Betriebsstätte Waldkrankenhaus, Bonn-Bad Godesberg, as well as with Dr. Alexander Lages, Orthopaedist in Sports Medicine and Chemotherapy, Klinik am Ring, Cologne: Question: “What do you think is the role of MRI in the routine practices of an orthopaedist or trauma surgeon with regard to the shoulder girdle? For which disorders does it confer major advantages?” Answer: “All interviewees believe that the main advantage of MRI resides in the indication, choice of procedure, and treatment monitoring. In particular, being able to evaluate rotator cuff tears in terms of their extension, shape, or any muscle atrophy means that strategies can be well planned. For evaluation of labral lesions following shoulder dislocation, conduct of MRI as early as possible has important surgical implications. Being able to directly evaluate the coracoclavicular and acromioclavicular ligaments for timely assessment of shoulder joint injuries and their classification according to the Rockwood or Tossy system is considered a major advantage.” Question: “For which disorders do you encounter false-positive MRI results most often?”

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3.16 Clinical Relevance of Magnetic Resonance Imaging

Fig. 3.123 Acromion ossification centers. Schematic view of the acromion. The broken lines demarcate the border between different ossification centers (from anterior to posterior: preacromion, mesoacromion, metacromion), which can persist as acromial bone in the event of nonfusion with the base.

Question: “For which disorders do you encounter false-negative MRI results most often and why were diagnostic measures continued in such cases?” Answer: “Conditions that are commonly overlooked relate to the superior labrum (SLAP lesions), disorders of the long biceps tendon, acromial bone, frozen shoulder, and tears of the subscapularis tendon. It is not uncommon to misinterpret the morphologic situation of the rotator muscles with regard to atrophy. Historic bony Bankart’s lesions, erosions of the anterior glenoid, and dysplasia of the glenoid in the presence of habitual and posttraumatic recurrent shoulder dislocation are also a problem. The size and depth of a Hill–Sachs lesion should be characterized.” Question: “For which disorders can MRI be omitted and for which is it being overly used?” Answer: “MRI can be dispensed with when treating open fractures. The ability to interpret images where there are implants is limited. [Note inserted by the authors: In such situations, sequences compatible with prosthetic devices should be used.] MRI can also be

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Answer: “Increased signal intensities in the rotator cuff can be overrated and misinterpreted as a tear. Likewise, edema surrounding calcification deposits can be mistaken for a tear.”

Fig. 3.124 Synchondritis of acromial bone. Pain when playing tennis. (a) Axial high-contrast, fat-suppressed MRI image. The synchondrosis which takes up CM can be mistaken for an oblique fracture line (arrow). (b) Oblique coronal contrast-enhanced, fat-suppressed MR image. The hyperintense synchondrosis, whose entire course cannot be evaluated here, should not be misinterpreted as an inflammatory process (arrows). (c) Plain radiograph. Sclerotic changes surrounding the synchondrosis (arrow).

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[144] Wagner UA, Vahlensieck M, Wiggert M, et al. Anatomische Studie des subakromialen Fettkörpers. Orthop Prax. 1997; 33:679–681 [145] Weishaupt D, Zanetti M, Tanner A, et al. Lesions of the reflection pulley of the long head of the biceps tendon. Invest Radiol. 1999; 34:463 [146] Weishaupt D, Zanetti M, Nyffeler RW, Gerber C, Hodler J. Posterior glenoid rim deficiency in recurrent (atraumatic) posterior shoulder instability. Skeletal Radiol. 2000; 29(4):204–210 [147] Weston WJ. The enlarged subdeltoid bursa in rheumatoid arthritis. Br J Radiol. 1969; 42(499):481–486 [148] Weston WJ. The subdeltoid bursa. Australas Radiol. 1973; 17(2):214–215 [149] Willemsen UF, Wiedemann E, Brunner U, et al. Prospective evaluation of MR arthrography performed with high-volume intraarticular saline enhancement in patients with recurrent anterior dislocations of the shoulder. AJR Am J Roentgenol. 1998; 170(1):79–84 [150] Wischer TK, Bredella MA, Genant HK, Stoller DW, Bost FW, Tirman PF. Perthes lesion (a variant of the Bankart lesion): MR imaging and MR arthrographic findings with surgical correlation. AJR Am J Roentgenol. 2002; 178 (1):233–237 [151] Wissman RD, Kapur S, Akers J, Crimmins J, Ying J, Laor T. Cysts within and adjacent to the lesser tuberosity and their association with rotator cuff abnormalities. AJR Am J Roentgenol. 2009; 193(6):1603–1606 [152] Workman TL, Burkhard TK, Resnick D, et al. Hill-Sachs lesion: comparison of detection with MR imaging, radiography, and arthroscopy. Radiology. 1992; 185(3):847–852

(3):769–773 [154] Yanny S, Toms AP. MR patterns of denervation around the shoulder. AJR Am J Roentgenol. 2010; 195(2):W157–63 [155] Zanetti M, Hodler J. Contrast media in MR arthrography of the glenohumeral joint: intra-articular gadopentetate vs saline: preliminary results. Eur Radiol. 1997; 7(4):498–502 [156] Zanetti M, Gerber C, Hodler J. Quantitative assessment of the muscles of the rotator cuff with MRI. Invest Radiol. 1998; 33:163 [157] Zanetti M, Weishaupt D, Gerber C, Hodler J. Tendinopathy and rupture of the tendon of the long head of the biceps brachii muscle: evaluation with MR arthrography. AJR Am J Roentgenol. 1998; 170(6):1557–1561 [158] Zanetti M, Jost B, Lustenberger A, Hodler J. Clinical impact of MR arthrography of the shoulder. Acta Radiol. 1999; 40(3):296–302 [159] Zanetti M, Weishaupt D, Jost B, Gerber C, Hodler J. MR imaging for traumatic tears of the rotator cuff: high prevalence of greater tuberosity fractures and subscapularis tendon tears. AJR Am J Roentgenol. 1999; 172(2):463–467 [160] Zanetti M, Jost B, Hodler J, Gerber C. MR imaging after rotator cuff repair: full-thickness defects and bursitis-like subacromial abnormalities in asymptomatic subjects. Skeletal Radiol. 2000; 29(6):314–319 [161] Zlatkin MB, Reicher MA, Kellerhouse LE, McDade W, Vetter L, Resnick D. The painful shoulder: MR imaging of the glenohumeral joint. J Comput Assist Tomogr. 1988; 12(6):995–1001

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subtle diagnoses. AJR Am J Roentgenol. 2012; 199(3):534–545

[162] Zlatkin MB, Iannotti JP, Roberts MC, et al. Rotator cuff tears: diagnostic performance of MR imaging. Radiology. 1989; 172(1):223–229

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4.1

Introduction

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4.2

Examination Technique

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The Elbow

4.3

Anatomy

149

4.4

Epicondylitis

158

4.5

Lesions of the Collateral Ligaments

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4.6

Distal Biceps Tendon Rupture

161

4.7

Rupture of the Triceps Tendon

161

4.8

Traumatic Lesions

162

4.9

Arthrosis

163

4.10

Apophysitis

165

4.11

Osteochondritis

166

4.12

Radioulnar Synostosis

168

4.13

Cartilage Damage

168

4.14

Plicae

168

4.15

Bursitis

168

4.16

Neuropathies

168

4.17

Neoplasms and Neoplasmlike Changes

171

4.18

Posttherapy Findings

173

4.19

Potential Sources of Mistakes When Interpreting Images

173

4.20

Clinical Relevance of Magnetic Resonance Tomography 173 References

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Chapter 4

The Elbow

4 The Elbow M. Vahlensieck and M. D’Anastasi

Common indications for magnetic resonance imaging (MRI) of the elbow relate to traumatic and posttraumatic changes. These include, in particular, the following changes: ● Fractures and their sequelae (arthrosis, loose joint bodies). ● Osteochondritis dissecans. ● Disorders of tendons (in particular of the distal biceps tendon), muscle origins, and collateral ligaments. Other indications include the following: Space-occupying lesions and their differential diagnosis. ● Inflammatory processes. ● Nerve disorders (especially of the ulnar nerve). ●

The elbow joint is not one of the main regions featured in MR diagnostic imaging of the musculoskeletal system.

Internet Links and Internet Research

●i

There is a lot of information available on the topic “elbow” on the homepages of the American Shoulder and Elbow Surgeons, the British Elbow and Shoulder Society, the European Society for Surgery of the Shoulder and the Elbow, and the Musculoskeletal Radiology Working Group of the German Society of Radiology (AG Radiologie in der Deutschen Röntgengesellschaft). The following search terms can be useful when conducting internet searches: ● “elbow anatomy” ● “elbow MRI” ● “elbow mri,” etc.

4.2 Examination Technique 4.2.1 Patient Positioning The prone position with the arm above the head is one of the patient positions often used.91 This position has the advantage of bringing the arm into the isocenter of the magnet. There is little propagation of respiratory motions to the elbow. However, this arm position can lead to significant impingement symptoms in the shoulder joint, even in the shoulders of asymptomatic patients. Besides, there is little control of internal and external rotation. There are special coils that permit the elbow to be placed along the side of the body (e.g., flexible surface coils55 or dedicated transmitter–receiver coils). This position tends to reflect more the natural anatomic position56 and makes it easier to plan the imaging planes. However, this position may not be suitable for very muscular or obese patients due to the lack of space. Besides, since the elbow is at the periphery of the magnetic field, there may be deterioration of the image quality. Placing the forearm on the abdomen is not recommended because propagation of respiratory motions would cause motion artefacts.

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The patient is generally examined with the elbow extended; elbow flexion is recommended for certain indications only (e.g. snapping elbow, nerve compression, biceps tendon).48,84

4.2.2 Coils There is a range of coils that can be used to image the elbow, for example, dedicated rigid coils designed for the shoulder or cervical spine,73 Helmholtz coils,86 flexible coils, or sender-receiver coils (knee or hand coil). The ultimate choice will depend on the type of MRI scanner available (including the strengths and weaknesses of the various manufacturers with regard to certain components and sequences) as well as on patient mobility.

4.2.3 Planes and Sequences Several localization sequences are often needed because of the patient positioning problems described. In particular, axial sequences must be available to avoid planning sagittal and coronal sequences that are oblique with respect to the joint axis. There is no single strategy for choosing the sequences and planes to be used for the elbow region. In principle, the elbow, like other joints, should be imaged in three spatial planes (sagittal, axial, and coronal): ● The sagittal plane gives an overview of the elbow joint and is especially suitable for assessment of cartilage surfaces, the joint recess and its content (effusion, joint bodies), and the biceps and triceps tendon (▶ Fig. 4.1, ▶ Fig. 4.2, and ▶ Fig. 4.3). ● The coronal plane is particularly suitable for assessment of the collateral ligaments and the muscle origins at the epicondyles (▶ Fig. 4.4, ▶ Fig. 4.5, and ▶ Fig. 4.6). Angled coronal planes are recommended for visualization of the collateral ligaments,17 in particular images obtained in a paracoronal plane that is posteriorly tilted by 20 degrees with respect to the humeral shaft and with the elbow extended. Alternatively, with respect to the humerus, a coronal plane can be used with the elbow joint flexed at 20 to 30 degrees. However, these oblique planes are rarely used. ● The axial plane (▶ Fig. 4.7, ▶ Fig. 4.8, and ▶ Fig. 4.9) is best for evaluation of the anatomic relationships between the nerves and vascular structures (e.g., evaluation of the course of the ulnar nerve) and normal adjacent structures and disorders such as an enlarged bursa or a neoplasm. When designing the axial sequences, the very distal location of the radial tuberosity and hence of the radial insertion of the right biceps brachii must be taken into account (rule of thumb: 3 cm distal to the joint space).

Standard Magnetic Resonance Tomography Turbo spin-echo (TSE) sequences form the cornerstone of MRI, using both T1-weighted (T1w) and proton density–weighted (PDw) fat-suppressed sequences. Fat-suppressed sequences are endowed with high sensitivity for visualization of bone marrow and soft tissue processes. The following sequences are used:

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4.1 Introduction

4.2 Examination Technique Triceps brachii

Biceps brachii

Brachialis

Cephalic vein

Anconeus

Supinator

Radius

Brachioradialis

Extensor carpi ulnaris

Extensor carpi radialis longus Extensor digitorum

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Humerus Lateral epicondyle of humerus Humeroradial joint Radial head

Fig. 4.1 Sectional anatomy of the elbow joint. Sagittal plane. (a) T1w SE image. (b) Diagram for illustration of the imaging plane (left) and schematic diagram of the (anatomic) structures (right).

Triceps brachii

Biceps brachii Humerus Brachialis

Olecranon Lateral epicondyle of humerus Flexor digitorum profundus

Biceps tendon Cephalic vein Biceps tendon Radial tuberosity Supinator Extensor carpi radialis longus

Ulna

Brachioradialis

Fig. 4.2 Sectional anatomy of the elbow joint. Sagittal plane. (a) T1w SE image. (b) Diagram for illustration of the imaging plane (left) and schematic diagram of the structures (right).

● ●

Short-tau inversion recovery (STIR) sequences.91 Frequency-selective, fat-suppressed PDw TSE sequences.

When these sequences are used in the coronal plane, all the collateral ligaments can be demonstrated concurrently. A standard examination can consist of, for example, a coronal T1w and PDw fatsat sequence as well as a sagittal and axial PDw fatsat sequence. Intravenous contrast media (CM) is administered to enhance visualization of synovial and infectious processes as well as of tumors, often in combination with fat-suppressed T1w spin-echo (SE) sequences. The selected plane is tailored to the indication.

For example, the sagittal plane is best for displaying the entire synovial space in rheumatoid arthritis, whereas the axial plane is best for delineating a space-occupying lesion in the region of vascular nerve bundles.

Magnetic Resonance Arthrography Direct Magnetic Resonance Arthrography Direct MR arthrography is used less often in the elbow region than for shoulder examination. However, MR arthrography has benefits when exploring lesions of the ulnar collateral ligament13,18,61,78 and, of course, for detection of intra-articular processes, such as synovial

147

The Elbow Triceps brachii

Biceps brachii Humerus Triceps brachii tendon Humeral trochlea Olecranon Humeroradial joint

Brachialis Olecranon fossa Cephalic vein Bicipital tendon

Ulnar coronoid process Brachioradialis Ulna Extensor carpi radialis longus

Fig. 4.3 Sectional anatomy of the elbow joint. Sagittal plane. (a) T1w SE image. (b) Diagram for illustration of the imaging plane (left) and schematic diagram of the structures (right).

Biceps brachii Triceps brachii

Triceps brachii Brachialis

Humerus Brachioradialis Pronator teres Medial epicondyle of humerus Humeroradial joint Ulna Biceps brachii Bicipitis radii aponeurosis Flexor digitorum superficialis (ulnar and humeral head) Flexor digitorum profundus Flexor pollicis longus

Extensor carpi radialis longus Lateral epicondyle of humerus Humeroradial joint Radial head Bicipital tendon Supinator Radial tuberosity Extensor digitorum

Fig. 4.4 Sectional anatomy of the elbow joint. Coronal plane. (a) T1w SE image. (b) Diagram for illustration of the imaging plane (left) and schematic diagram of the structures (right).

folds4,18,22,79,89 and loose joint bodies, as well as for improved visualization of superficial cartilaginous lesions.98 Elbow joint puncture can be performed with the patient sitting or standing; this is best done under fluoroscopic control. If the patient is sitting, the flexed elbow is placed on the X-ray table. If the patient is in the prone position, imaging should be conducted with the patient’s arm placed above the head and the elbow in flexion. In general, a 24-G needle (0.55 mm) measuring 2.5 cm in length is adequate. After local anesthesia of the skin and periosteal surfaces, the needle is advanced between the radial head and humerus. There are also reports in the literature of puncture without

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local anesthesia.61 Occasionally, patients experience a vasovagal reaction to intra-articular injections. In such cases, the patient must be imaged while sitting down and must be continuously monitored. The CM used is 10-mL physiologic NaCl solution, and imaging is performed with SE sequences.61,89 Gadolinium-containing complexes are often used,18 typically with a gadolinium concentration of 2 to 2.5 mmol/L. The injected amount should be around 4 to 6 mL, depending on the joint volume. Physiologic NaCl solution is injected when the main focus is on T2-weighted (T2w) or fat-suppressed T2w sequences, whereas paramagnetic CM injection, whose main role is to shorten the T1 relaxation time, is used

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Flexor digitorum profundus

4.3 Anatomy Biceps brachii Triceps brachii Brachialis

Humerus Pronator teres

Brachioradialis

Medial epicondyle of humerus Humeroulnar joint

Extensor carpi radialis longus

Ulna Biceps brachii Bicipital radii aponeurosis

a

b

Flexor digitorum superficialis (ulnar and humeral head) Flexor digitorum profundus Flexor pollicis longus

Lateral epicondyle of humerus Humeroradial joint Radial head Bicipital tendon Radial tuberosity Supinator Extensor digitorum Downloaded by: Collections and Technical Services Department. Copyrighted material.

Triceps brachii

Fig. 4.5 Sectional anatomy of the elbow joint. Coronal plane. (a) T1w SE image. (b) Diagram for illustration of the imaging plane (left) and schematic diagram of the structures (right).

Triceps brachii

Triceps brachii

Humerus Olecranon

Lateral epicondyle of humerus Extensor tendon Supinator tendon Radial head Supinator

Flexor carpi ulnaris Ulna

a

Extensor digitorum Extensor carpi radialis

b

Fig. 4.6 Sectional anatomy of the elbow joint. Coronal plane. (a) T1w SE image. (b) Diagram for illustration of the imaging plane (left) and schematic diagram of the structures (right).

for standard or fat-suppressed T1w sequences, which in turn can be used in all three spatial planes. These sequences should be designed such that any extra-articular problems such as tumors are not overlooked; this can be assured, for example, by using a T2w sequence in at least one plane.

4.3 Anatomy The MR anatomy of the elbow joint is described in special publications, based on cadaver joints,10,19,55 in books28 and in various review articles29,30,89 (see ▶ Fig. 4.1, ▶ Fig. 4.2, ▶ Fig. 4.3, ▶ Fig. 4.4, ▶ Fig. 4.5, ▶ Fig. 4.6, ▶ Fig. 4.7, ▶ Fig. 4.8, and ▶ Fig. 4.9).

Indirect Magnetic Resonance Arthrography High contrast can be achieved for the elbow joint with indirect MR arthrography too (▶ Fig. 4.10). This modality can be used, for example, for monitoring osteochondral transplants.36

4.3.1 Ligaments ▶ Fig. 4.11 illustrates the collateral ligaments of the elbow joint.

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The Elbow

a

Median cubital vein Brachial artery Brachial veins Median nerve Median nerve Pronator teres Palmaris longus tendon Flexor carpi ulnaris Medial epicondyle of humerus Ulnar nerve

b

Cephalic vein Brachioradialis Radial nerve, radial collateral artery and vein Extensor carpi radialis Lateral epicondyle of humerus Anconeus Olecranon

Fig. 4.7 Sectional anatomy of the elbow joint. Transverse plane. (a) T1w SE image. (b) Diagram for illustration of the imaging plane (left) and schematic diagram of the structures (right).

a Bicipital tendon Median cubital vein Brachial arteries and veins Basilic vein Brachialis Medial epicondyle of humerus Pronator teres Flexor carpi radialis Ulnar nerve Flexor carpi ulnaris b

Flexor digitorum profundus

Cephalic vein Brachioradialis Extensor carpi radialis longus Radial nerve, radial collateral artery and vein Extensor carpi radialis brevis Extensor digitorum Extensor tendon Lateral epicondyle of humerus Anconeus Olecranon

Fig. 4.8 Sectional anatomy of the elbow joint. Transverse plane. (a) T1w SE image. (b) Diagram for illustration of the imaging plane (left) and schematic diagram of the structures (right).

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Bicipital tendon

4.3 Anatomy

Bicipital tendon Median cubital vein Brachial artery and vein Basilic vein

Brachioradialis Extensor carpi radialis longus

Brachialis

Radial nerve, radial collateral artery and vein Extensor carpi radialis brevis Radial head Common extensor tendon Proximal radioulnar joint

Pronator teres

b

Flexor carpi radialis Flexor digitorum superficialis Ulnar nerve Flexor carpi ulnaris Superficial ulnar collateral artery and vein Flexor digitorum profundus

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a

Anconeus Ulna

Fig. 4.9 Sectional anatomy of the elbow joint. Transverse plane. (a) T1w SE image. (b) Diagram for illustration of the imaging plane (left) and schematic diagram of the structures (right).

●

●

●

The anterior portion of the ligament is the most powerful and of greatest functional significance (anterior bundle).41,59 It extends from the ulnar epicondyle of humerus to the ulnar surface of the ulnar coronoid process. The posterior ligament courses toward the ulnar surface of the olecranon. The less powerful transverse or oblique ligament unites the ulnar portions of the anterior and posterior ligament.26

On MRI, these ligaments are identified as small hypointense structures. Situated between the ligaments and epicondyle of humerus is fat, with its characteristic high signal intensity on T1w images and which serves for internal demarcation of the ligament.61 Injuries to the ulnar collateral ligament are very common in pitching/throwing athletics.43

Radial Collateral Ligament

Fig. 4.10 Indirect MR arthrography of the elbow joint. Sagittal plane. The joint space exhibits strong CM enhancement.

Ulnar Collateral Ligament The ulnar or medial collateral ligament consists of three parts (▶ Fig. 4.12 and ▶ Fig. 4.13):

The triangular radial or lateral collateral ligament (▶ Fig. 4.14) is a more delicate structure than its ulnar counterpart. Its apex is situated at the radial epicondyle of humerus, while its base is at the annular ligament (see ▶ Fig. 4.11). A further radial ligamentary structure extends as a loop from the posterior radial epicondyle of humerus around the radial head to the ulna (lateral ulnar collateral ligament; ▶ Fig. 4.15). This ligament provides for posterolateral stabilization of the radius during varus stress,38,62,67 and in 90% of the population this ligament can be displayed on coronal images.88

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a

b

Fig. 4.11 Collateral ligaments of the elbow joint. The white arrow tips denote the radial collateral ligament (lateral collateral ligament) and the white arrows the anterior portion of the ulnar collateral ligament (medial collateral ligament). The tendons and common tendon insertion of the extensors (black arrow tips) and flexors (black arrows) course parallel to both ligaments. (a) Coronal PDw fatsat sequence. (b) Coronal T1w sequence.

Fig. 4.13 Ulnar (medial) collateral ligament of the elbow joint. Schematic diagram. Powerful anterior bundle (front), posterior bundle (middle), and transverse portion (back, distal).

Fig. 4.12 Elbow at the level of the ulnar nerve groove. Axial MR image. Joint-side boundary formed by capsule and posterior bundle of the ulnar collateral ligament (white arrow) and lateral boundary formed by the retinaculum of the ulnar nerve groove (also known as “Osborne’s ligament”; black arrow).

Annular Ligament of Radius The annular ligament is a cordlike thickening of the joint capsule which completely encompasses the radial head (▶ Fig. 4.16), thus providing for free motion and stabilization of rotational movement of the radioulnar joint.40

4.3.2 Muscles and Tendons The elbow muscles can be divided into the following groups: ● Posterior group. ● Anterior group. ● Medial (ulnar) group. ● Lateral (radial) group.

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Fig. 4.14 Radial (lateral) collateral ligament of the elbow joint. Schematic diagram. Radial collateral arrow (broad arrow), lateral ulnar collateral ligament (dotted arrow), and radial annular ligament (thin arrow).

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The Elbow

4.3 Anatomy

Posterior Group The posterior group comprises the triceps and anconeus. The triceps inserts at the olecranon. Depending on the arm position, the inserting triceps tendon can exhibit an undulating course and high signal intensity (▶ Fig. 4.17). The anconeus has probably evolved as part of the triceps and courses from the posterior radial epicondyle of humerus to the lateral (radial) surface of the olecranon and posterior surface of the distal humeral shaft.16

Anterior Group

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The anterior group of muscles comprises the biceps brachii and the brachialis. The brachialis is a powerful muscle that crosses the anterior aspect of the elbow joint and inserts at the ulna immediately distal to the coronoid process. The short head and long head of biceps brachii converge and form a connective tissue plate at the elbow, the bicipital aponeurosis, which extends to the ulnar forearm fascia and pronator teres.55 The distal biceps has additionally a tendinous portion that inserts at the radial tuberosity (▶ Fig. 4.18). With the arm in

Fig. 4.15 Lateral ulnar collateral ligament. Coronal PDw fatsat image of the elbow with view of the lateral ulnar collateral ligament, a loopshaped ligamentary structure running from the radial epicondyle to the ulna (arrow tips).

Fig. 4.16 Radial annular ligament. Axial PDw fatsat image. The annular ligament encircles the radial head (black arrow tip). At this level, partial images are obtained of the tendon of the brachialis (black arrow; courses to ulna), the biceps (white arrow tip; courses to radius), and parts of the bicipital aponeurosis of the biceps (white arrow). Fig. 4.17 Insertion of the triceps. Sagittal PDw fatsat image. The triceps insertion has an undulated course with physiologic changes in signal intensity in line with the elbow position (black arrow). Anterior joint capsule (white arrow).

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Fig. 4.18 Tendons of the biceps and of the brachialis. Axial PDw fatsat image at the level of the proximal forearm. The biceps tendon courses to the radius (white arrow) and the tendon of the brachialis to the ulna (black arrow). These two tendons should not be confused in the presence of inflammatory overloading syndrome or tears.

pronation, the biceps tendon is pulled posteriorly between the radius and ulna. The distal biceps tendon is best visualized on axial and sagittal sections. It must be ensured that the axial sections extend sufficiently distal to the radial tuberosity. Some authors have reported on the merits of the flexed abducted supinated view of the flexor tendons, with the arm above the head (▶ Fig. 4.19, ▶ Fig. 4.20, and ▶ Fig. 4.21).32

Medial Group The medial group of muscles comprises the pronator teres and the hand and finger flexors. It is very difficult to distinguish between the medial and lateral muscles at the level of the elbow.

Lateral Group The lateral (or radial) group of muscles comprises the supinator, finger and thumb extensors, and the powerful brachioradialis. The supinator arises from the posterolateral ulna and courses obliquely in a distal and lateral direction around the radius. With the forearm in pronation, the supinator completely encircles the radius. It is easy to delineate on all imaging planes. The remaining lateral muscles have a common origin at the lateral epicondyle of humerus.

4.3.3 Bones The elbow joint, formed by the humerus, radius, and ulna, is one of the bigger joints in the human body. Normal variants and overlapping effects can cause confusion on MR images, leading to false-positive diagnosis of joint step deformities and compression.73

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Fig. 4.19 Localizer for the sections to be imaged in flexed abducted supinated view.

Normal Variants One normal variant is a transverse groove in the synovial tunnel of the olecranon, in proximity to the trochlea of humerus which can simulate a cartilage defect.65,72 Another variant in the same region is a bony ridge that transverses the articular surface of the ulna but does not project above the joint cartilage. The ridge can be seen as a completely developed structure or manifest only on the radial or the ulnar aspect. It is generally 2 to 3 mm high.73 Such ridges were identified in 68 to 98% of cadaver ulnar specimens.73,95 On MRI, this finding can be mistaken for an intra-articular osteophyte or fracture residues.73

Overlapping Effect One overlapping effect that can be a diagnostic challenge relates to the sharp-angled junction between the capitulum of humerus and radial epicondyle of humerus: in the coronal and sagittal planes, it can simulate a genuine capitulum defect (▶ Fig. 4.22).65,73 Differential diagnosis of this pseudodefect must include a fracture, fracture sequelae, and an osteochondral defect. A correct diagnosis can be made by evaluating a series of MRI slices. Besides, there is the absence of the concomitant changes seen in the bone marrow (intra- and periosteal signal changes due to edema, hemorrhage, or bone repair activities) seen in acute trauma. In a study by Rosenberg et al,72 22 out of 32 patients and 14 out of 22 healthy volunteers exhibited a pseudodefect.

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The Elbow

a

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4.3 Anatomy

b

Fig. 4.20 Elbow in flexed abducted supinated view. T1w images. Good longitudinal view of the biceps tendon with insertion on the radial tuberosity (a; white arrow) and the brachialis tendon with insertion on the ulna (b; white arrow). Contusion edema of subcutaneous tissue (a; black arrow). (a) T1w image. (b) T1w image, another imaging plane.

4.3.4 Joint Cartilage Depending on its location, the joint cartilage ranges from 0.9 mm at the proximal ulna to 1.4 mm at the capitulum of humerus.86 While very variable, half of the cartilage volume tends to be found at the humerus and one-quarter at each of the radius and ulna. There is widespread variability in the size of the cartilage layer at the olecranon. In particular at the center, the cartilage is often missing or is seen, in some cases, also with a small bony notch or groove (trochlear notch, pseudodefect; ▶ Fig. 4.23). At the center of the joint surface of the olecranon, there is thus a notch that should not be mistaken for disease.

4.3.5 Recess and Bursae Recess The elbow joint has three principle recesses: ● Anterior recess. ● Posterior recess. ● Annular recess. The posterior recess is particularly voluminous with the elbow in extension. The annular recess encircles the radial head and is the distalmost recess. It has an extension running between the proximal ulna and the proximal radius, proximal to the radial tuberosity.87

MRI can sensitively detect fluid in the joint space, even a minute 1 mL quantity. Onset of fluid accumulation is first seen in the posterior recess. MRI is essentially more sensitive than conventional radiology (positive fat pad sign detected only after formation of 5–10 mL effusion) and possibly also than ultrasonography (positive signal after 1–3 mL).20

Bursae The bicipitoradial bursa (▶ Fig. 4.24) and the interosseous bursa are located on the cubital aspect of the elbow. Both have an anatomic relationship with the biceps insertion on the radial tuberosity, the bicipitoradial bursa on the radial aspect, and the interosseous bursa on the ulnar aspect, and, as such, can communicate with each other. As in other body regions featuring subcutaneous bony protuberances without muscle padding (the best-known example being the prepatellar bursa), the olecranon bursa can be found above the elbow (▶ Fig. 4.25).

4.3.6 Nerves Three principle nerves and their branches are important for the elbow region: ● Ulnar nerve. ● Radial nerve. ● Median nerve.

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a

b

Fig. 4.21 Biceps tendon tear. Elbow in flexed abducted supinated view. A 54-year-old patient with lifting injury. Biceps tendon tear with retraction of the tendon (a; arrow) and tendon stump of wavy appearance on radius (b; arrow). (a) T1w image. (b) T1w image, adjacent imaging plane.

Because of their signal patterns (medium to low signal intensity on T1w images, somewhat more hyperintense than muscles on T2w images50), it is not easy to delineate nerves from their surroundings except when they are enclosed in fatty tissue.48

Ulnar Nerve The ulnar nerve is easy to identify (see ▶ Fig. 4.7). It courses within the ulnar groove, a bony channel in the ulnar epicondyle (▶ Fig. 4.26 and ▶ Fig. 4.27). On the joint side, this groove is bounded by the capsule and the posterior bundle of the ulnar collateral ligament. The groove is covered by a retinaculum (ulnar nerve retinaculum, also known as Osborne’s ligament). This nerve is best evaluated on axial images; it can be identified anteriorly to the triceps on sagittal images of the ulna.71

Radial Nerve The radial nerve courses anteriorly between the brachialis, brachioradialis, and extensor carpi radialis. At the level of the humeroradial joint, it divides into a more delicate sensory branch (superficial branch) and a stronger motor branch (deep branch).71

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Median Nerve The median nerve runs anteriorly between the pronator teres and brachialis. This nerve can be identified distal to the joint and between the two heads of the pronator teres.

4.3.7 Blood Vessels The anteriorly located brachial artery courses along the brachialis and medial biceps. It divides into the ulnar artery and the radial artery. The bifurcation site varies but is generally 1 to 2 cm distal to the elbow joint. The radial artery runs between the brachioradialis and pronator teres, and the ulnar artery courses deep to the pronator teres. Both arteries give off recurrent branches that run along the radial nerve and ulnar nerve.55 The posterior recurrent ulnar artery arises from the ulnar artery immediately inferior to the elbow. This artery and its concomitant veins run posteriorly to the medial (ulnar) epicondyle, together with the ulnar nerve. Dilated veins can simulate a pathologic process of the ulnar nerve. A distinction can be made on the basis of the signal pattern: ● Veins are homogeneous and hyperintense on T2w images. ● By contrast, a damaged ulnar nerve is inhomogeneous.71

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4.3 Anatomy

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Fig. 4.23 Trochlear notch. Sagittal PDw fatsat image. At the center of the articular surface of the olecranon, a normal variant notch with no cartilage lining can be identified (arrow); this should not be misinterpreted as a pathologic lesion.

Fig. 4.24 Cubital synovial cyst. Axial schematic diagram at the level of the elbow joint. As a diagnostic aid in delineating cystic masses in the elbow, an effusion of the bicipitoradial bursa as seen in acute or chronic bursitis (often associated with rheumatoid arthritis) surrounds the biceps tendon and shows a thickened wall with CM uptake. 1, biceps tendon; 2, radius; 3, bicipitoradial bursa.

Fig. 4.22 Pseudodefect in capitulum of humerus. In the capitulum of humerus, there is a slight hollow at the junction between the cartilage layer and the cortex which could be mistaken for contusion injuries secondary to posterior dislocation or instability (arrows). This hollow can be identified in particular on sagittal and coronal images. However, the absence of edema, in particular on STIR images, tends to rule out fresh injury. It is not possible to reliably distinguish between an impression resulting from historic trauma and the hollow. (a) Sagittal T2w TSE sequence. (b) Coronal STIR sequence.

From lateral Fig. 4.25 Olecranon bursa. The olecranon bursa encloses the olecranon and extends to the insertion of the triceps tendon. 1, humerus; 2, triceps brachii tendon; 3, joint capsule; 4, radial collateral ligament; 5, radial annular ligament; 6, biceps brachii tendon, 7, radius; 8, ulna; 9, bursa subcutanea olecrani.

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Fig. 4.26 Ulnar nerve groove. Schematic diagram of the elbow joint, viewed from the ulna. The ulnar nerve courses on the epicondyle of ulnar humerus through a bony channel (ulnar nerve groove) that is covered by a ligament, the retinaculum of ulnar nerve groove (epicondyle-olecranon ligament or Osborne’s ligament), and far distal by parts of both heads of the flexor carpi ulnaris (aponeurosis of the flexor carpi ulnaris or arcuate ligament). The compartment thus formed is called the “cubital tunnel.” 1 = ulnar nerve; 2, retinaculum of ulnar nerve groove; 3, aponeurosis of flexor carpi ulnaris; 4, ulnar head of flexor carpi ulnaris; 5, humeral head of flexor carpi ulnaris.

In addition to the superficial basilic and cephalic veins, there are several anastomoses and collateral branches, some of which course in parallel to the arteries.

4.4 Epicondylitis 4.4.1 Epicondylitis of the Radial Humerus MRI plays a key diagnostic role in differentiating between epicondylitis and ligament lesions, muscle lesion, or bursitis, and serves to underpin therapy decisions as well as preoperative planning. As in the case of all joints, a number of potential pitfalls must be avoided. For example, steroid injections can give rise to changes in signal intensity that would overestimate the extent of epicondylitis. Therefore, MRI scans should always be carried out prior to such injections. Another drawback is the field inhomogeneity, in particular at the periphery of the coil, which is more pronounced when the elbow is placed along the side of the body. However, it is possible to distinguish these artefacts from genuine disorders on the basis of their shape, position, and signal pattern. Epicondylitis of the radial humerus is a type of overloading injury to the radial insertion of the extensor tendons. While often called “tennis elbow,” this disorder is also seen in association with other activities involving repetitive trauma. These include occupational repetitive activities with the forearm in rotation, as occurring, for example, in carpenters.65 Concomitant bone disorders are rarely seen in epicondylitis of the radial humerus but calcification of the soft tissues is common. Histology reveals epicondylitis with vascular proliferation and focal hyaline degeneration.69 Steinborn et al90 identified fatty degeneration. Other histology findings reported in the literature relate to the tendon origin (necrotic zones, calcification, scarring, discontinuity of collagen fibers, mucoid degeneration, infiltration

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Fig. 4.27 Ulnar nerve groove. Axial schematic diagram of the elbow joint at the level of the ulnar nerve groove. 1, retinaculum of ulnar nerve groove; 2, joint capsule; 3, superior collateral ulnar artery and vein; 4, ulnar nerve; 5, common flexor tendon; 6, humerus; 7, common extensor tendon; 8, ulnar olecranon.

of round cells, histiocytes and fibroblasts, granulation tissue, neovascularization, periostitis, and bursitis66,69), affecting especially the extensor carpi radialis brevis. On MRI examination, an increase in signal intensity is seen at the origin of the extensors as well as swelling on most sequences (▶ Fig. 4.28 and ▶ Fig. 4.29). In later stages, a partial tear occurs, or even a full-thickness tear with involvement of the collateral ligaments and adjacent soft tissues is seen. Calcifications can be identified in particular on gradient-echo (GRE) sequences.65 Noteworthy is that signal changes can also be observed increasingly at the origin of the extensors on the asymptomatic contralateral side (can be detected in 55% of patients on T1w images and in 27% of patients on T2w images). Such signal alterations were rarely found in bilaterally asymptomatic volunteers.90 Enhancement following intravenous CM administration is determined by the histologic nature of the changes: fibrovascular proliferation promotes CM uptake, while fibrosclerotic degeneration does not.90 The anconeus is thought to often also react to epicondylitis of the radial humerus, with diffuse hyperintensity signal seen on STIR images.16 The implications of this MRI finding, in particular its sensitivity, are unclear.66 Epicondylitis of the radial humerus can also impact the ulnar continuation of the lateral collateral ligament (lateral ulnar collateral ligament). The extent of changes occurring will depend on the severity of epicondylitis.8,46,47

4.4.2 Epicondylitis of the Ulnar Humerus Epicondylitis of the ulnar humerus results from irritation of the medial epicondylar apophysis following repetitive flexor traction on the pronator teres.88 This disorder is known as little leaguer’s elbow, pitcher’s elbow (baseball), or golfer’s elbow since it is seen predominantly in association with such types of sports.9 Other risk factors are American football (quarterbacks), tennis, or volleyball.88 Juvenile MRI shows discrete bone marrow edema and a slight abnormality of the apophyseal line. Besides, this leads to delayed closure of the apophysis. In adults, the apophyseal plate is fully developed and there tends to be thickening and signal alteration of the common muscle origin, as seen in disorders of the radial

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4.5 Lesions of the Collateral Ligaments

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Fig. 4.28 Epicondylitis of the radial humerus. Tennis player with painful radial epicondyle of humerus. The tendon of the common finger extensors on the epicondyle is thickened and exhibits increased signal intensity (arrows) as a sign of epicondylitis of the radial humerus. (a) Coronal T1w sequence. (b) Coronal PDw fatsat sequence.

aspect.43 Following intramuscular injections, increased signal intensity persists for up to 1 month postinjection and must be distinguished on differential diagnosis.70

4.5 Lesions of the Collateral Ligaments 4.5.1 Ulnar Collateral Ligament Lesions of the ulnar collateral ligament are caused by valgus stress during elbow flexion. These are not uncommon in throwing athletes. Clinical signs include the following: ● Ulnar joint space pain. ● Valgus instability.56,96

Fig. 4.29 Epicondylitis of the radial humerus. Coronal STIR sequence of the elbow joint. The patient reported severe pain of the radius, in particular when engaging in sport. No accident. The tendon of the wrist extensors exhibits a diffuse increase in signal intensity as well as discontinuity (arrow). There is discontinuity of the radial collateral ligament. As such, late-stage epicondylitis of the radial humerus presents in association with a tear of the radial collateral ligament.

The following signs are seen on MRI in the presence of lesions of the ulnar ligament: ● Discontinuity. ● Laxity. ● Ill-defined margins. ● Increased signal intensity.56 ● Concomitant injury to the adjacent muscle origin. The lesions are mainly found in the anterior segment, that is, in the middle to proximal portions (▶ Fig. 4.30). In the presence of changes due to repetitive trauma, the ligament and its surroundings are more hyperintense than usual. This finding is due to microtears, degeneration, hemorrhage, and edema.88 Nakanishi et al61 observed obliteration of the fatty tissue deep to the ligament in association with lesions of the collateral ligament.

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Some authors advocate the use of MR arthrography to distinguish such full-thickness tears from a partial tear.61,78 Uptake of contrast agent by the surrounding soft tissues can be observed for a full-thickness tear.61 MR arthrography has high sensitivity for ulnar collateral ligament lesions: in a study by Schwartz et al, 95% of full-thickness and 86% of partial tears were detected.78 MRI is also able to obtain additional findings. In acute lesions of the ulnar collateral ligament, bone contusions are occasionally observed in the radial elbow compartment.81,88 Out of 63 symptomatic elbows, Sugimoto et al91 detected 34 full-thickness tears and 5 partial tears of the ulnar collateral ligament. Furthermore, a total of 30 loose joint bodies in 14 elbows and cartilage damage in 21 elbows were detected. The MRI findings for the loaded ulnar collateral ligament change in line with patient age. In the immature elbow, the ulnar periosteum is displayed as a continuation of the collateral ligament. The insertion site, at least on GRE images, is slightly hyperintense in the growing body compared with adults. In young patients whose bones are not yet fully mature, the transition zone between the bony apophysis and

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ligament is, to some extent, particularly susceptible to injury, more so than the collateral ligament itself. The apophyseal center may appear segmented.92 Bone avulsion of the ulnar insertion of the anterior bundle of the ulnar collateral ligament has been reported in a small group of 20- to 22-yearold patients.33

4.5.2 Radial Collateral Ligament Among the lesions of the radial aspect, research has focused primarily on lesions of the ligament portion coursing in the direction of the ulna (lateral ulnar collateral ligament) since these result in posterolateral instability.62 Clinical diagnosis is difficult because patients experience severe pain during the instability provocation test (combination of supination, valgisation, and compression).62 Ligament lesions are seen mainly secondarily to complex injuries to the elbow joint in combination with fractures of the radial head (▶ Fig. 4.31). A reliable diagnosis should be possible on using 3D GRE sequences and corresponding thin coronal reconstructions.67 Lesions of the radial collateral ligament are

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Fig. 4.30 Tear of the ulnar collateral ligament. Status post trauma. Tear of the anterior bundle of the ulnar (medial) collateral ligament (a, b; white arrows) as well as straining of the common finger flexors (b, c; black arrows). (a) Coronal T1w sequence. (b) Coronal PDw fatsat sequence. (c) Sagittal PDw fatsat sequence.

4.7 Rupture of the Triceps Tendon

occasionally observed in association with avulsion of the common origin of the extensors.89

seen around the distal tendon in the bicipitoradial bursa (▶ Fig. 4.36).

4.5.3 Annular Ligament

4.7 Rupture of the Triceps Tendon

If the annular ligament is insufficient or torn, the proximal radius becomes detached from the ulna. This disorder occurs in adults only secondarily to massive trauma; hence, it must be viewed as a separate entity from its more common juvenile counterpart.63 MRI appears to have only a limited role in this setting, and there is a paucity of reports on this in literature.

Rupture of the triceps tendon is relatively rare. A tear can occur following forced overloading in extension (falling on extended arm) or from a direct blow to the tendon.93 Other causes include repetitive trauma (bowling, throwing, weightlifting) and the usual systemic risk factors or use of steroid medications. Bursitis of olecranon can be observed in association with, or mimic, a triceps tear.88 MRI is able to identify the extent of the tear and its location.60,94

4.6 Distal Biceps Tendon Rupture Distal biceps tendon rupture occurs, in particular, following forced flexion against strong resistance (lifting heavy objects).65 Distal rupture is generally caused by a single injury, typically following abrupt overloading by 40 kg or more in elbow flexion (▶ Fig. 4.32).88 The bicipital aponeurosis (▶ Fig. 4.33) often remains intact and prevents complete proximal retraction of the biceps. Hence, on clinical examination the most salient finding is supination weakness, and any partial or full-thickness tear can be clinically overlooked during examination. Insertion tendinopathy of the distal biceps tendon frequently occurs during overloading in occupational or sporting settings (▶ Fig. 4.34). Overlooked lesions can, in the long term, result in reduced flexion and supination strength and endurance.1 In addition to its diagnostic role in differentiating partial and full-thickness tears,25,27 MRI is also used to identify the extent of retraction of the biceps tendon. Fitzgerald et al27 confirmed the good correlation between MRI and surgical findings for 21 patients in differentiating between tendinitis as well as partial and full-thickness tears of the biceps tendon. Overloading trauma often gives rise to bicipital bursitis (▶ Fig. 4.35). With a partial tear of the biceps tendon, thickening or thinning of the tendon with excessively high signal intensity is observed. Fluid is also

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Fig. 4.31 Radial head fracture and tear of the radial collateral ligament. Coronal T1w image. Radial head fracture (black arrow) as well as tear of the radial collateral ligament and injury to insertion of extensor tendon (white arrow) with instability and malposition (gaping of the radial joint space).

4.7.1 Insertion Tendinopathy of the Triceps Tendon Insertion tendinopathy of the triceps tendon on the olecranon results in signal homogeneity of the tendon as well as in signal changes isointense to edema in the insertion region (▶ Fig. 4.37). Bursitis of olecranon may be observed additionally.

4.7.2 Snapping Triceps Findings related to snapping in the elbow region are generally caused by subluxation or dislocation of the ulnar nerve over the epicondyle of ulnar humerus during elbow flexion. This is thought to occur in up to 16% of the normal population.15 However, apart from that, snapping may also result from subluxation of the ulnar portion of the triceps tendon over the epicondyle.84 Spinner et al83 examined a series of 22 elbows. Out of the 22 elbows, 2 showed clinical signs of pain-free snapping phenomenon, 5 painful snapping, 3 ulnar nerve symptoms, and 6 a combination of painful snapping with ulnar nerve symptoms; the

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Fig. 4.32 Distal biceps tendon tear. Status post acute painful event with flexion weakness and elbow pain. Pain point in the proximal forearm. (a) Sagittal PDw fatsat image. Discontinuity of the distal biceps tendon with retraction and undulating course (arrow). (b) Axial PDw fatsat image of upper arm. Retracted, thickened tendon (arrow). (c) Axial PDw fatsat image of forearm. Biceps tendon (white arrow) absent but brachialis tendon preserved (black arrow).

remainder had no clinical symptoms (enrolled in the study during screening). On the whole, this disorder is uncommon. It is overlooked in half of cases, is often painful, and may occur in association with ulnar neuropathy. Medial displacement can be demonstrated with the elbow in maximum flexion on axial MRI planes with respect to the humeral axis. It is of crucial clinical importance to recognize the triceps involvement in medial snapping phenomenon. Failure to repair the triceps at the time of surgical repositioning of a subluxed ulnar nerve can result in persistent symptoms.83 Less common than snapping of the medial triceps head is its lateral variant, which has only been reported in isolated cases.85

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4.8 Traumatic Lesions Traumatic lesions of the elbow joint include fracture, bone contusion, occult fracture, subluxation, and dislocation. If on initial radiology examination an effusion without fracture is detected, in 17% of cases a fracture is subsequently identified on conventional radiology during follow-up examination.21 In another series, with positive fat-pad sign but no fracture identifiable on conventional radiology, in three-quarters or even more of cases an occult fracture was detected, virtually always in the region of the radial head.53,63 Other studies have also attested to the superiority in diagnosing fractures in the region of the head of radius

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4.9 Arthrosis

(▶ Fig. 4.38).24,65 In up to one-quarter of these patients, soft tissue injuries and, rarely, loose joint bodies, were detected additionally on MRI examination.11,63 To what extent MRI impacts therapy decisions was unclear. According to O’Dwyer et al,63 MRI had only a minor impact. MRI is thought to be superior to conventional radiology in diagnosing fractures, in particular in children with as yet incomplete ossification of the epicondyles.7,37,65 However, in this age group, too, it has only a limited influence on therapy despite the superiority of MRI in visualizing epiphyseal plate injuries.35,42 Direct application of force to bones as happens in impact trauma can cause painful or painless bone marrow edema even before the bone breaks. A diffuse reduction in signal intensity is observed on T1w, and increased signal on T2w, images, in particular on STIR contrast-enhanced sequences. Edema of the surrounding soft tissues is also often present. It is possible that such bone bruises will not require any specific treatment.53,63 Like other parts of the body, stress fractures also occur at the elbow and can be sensitively visualized on MRI, for example, on the olecranon.38 Occult fractures cannot be identified on conventional radiology, but on MRI they produce changes in signal intensity characteristic of fractures. Often, these consist of all sequences of a hypointense line as well as of other poorly demarcated concomitant changes (often subsumed under the collective term bone marrow edema). The predilection sites for fractures are those reported in the traumatology literature (▶ Fig. 4.39). As for other regions of the body, treatment of occult fractures ranges from conservative measures to immobilization with a cast, as used for classic fractures. MRI can play a crucial role in the case of dislocations and subluxations for detection of any concomitant injuries to bone, ligaments, or capsules (▶ Fig. 4.40 and ▶ Fig. 4.41). The typical sites where fractures, occult fractures, or bone bruises manifest as concomitant injuries secondarily to posterior subluxation or dislocation of the forearm versus the humerus, as

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Fig. 4.33 Bicipital aponeurosis. Schematic diagram. The distal biceps inserts at the radial tuberosity and on the plate of connective tissue plate on the forearm (bicipital aponeurosis). 1, biceps brachii; 2, biceps tendon; 3, pronator teres (humeral head); 4, radial flexor carpi radialis; 5, bicipital aponeurosis; 6, brachial artery; 7, median nerve.

occurs mainly after falling on the extended arm, are the coronoid process, radial head, and posterior margin of the capitulum of humerus.74 Concurrent ligament injuries, such as tears of the collateral ligaments, can result in instability. A characteristic muscle injury seen secondarily to posterior dislocation is straining or fibrous tears of the brachialis. Typical combinations of capsular and ligament injuries are seen in association with posterior dislocation or subluxation depending on the force applied and can serve for staging (▶ Table 4.1).

4.9 Arthrosis As for all joints, MRI is well suited to detection of early signs of arthrosis (early osteophytes, cartilage damage) (▶ Fig. 4.42). It is not uncommon for MRI to be able to identify early arthrosis as the cause of complaints which could not be identified on radiography. Arthrosis of the elbow joint (cubital arthrosis) is less common than arthrosis of the other joints of the lower extremities. Elbow arthrosis is caused by previous injury, overloading in occupational or sporting settings (e.g.,

Table 4.1 Staging of posterior elbow joint dislocation or subluxation in terms of concomitant soft tissue damage Stage Soft tissue damage and extent of defective position I

Radial collateral ligament partially or completely torn, posterolateral subluxation

II

As in stage I + capsular tear, incomplete displacement following dislocation

III

As in stage II + partial (stage IIIa) or full-thickness tear (stage IIIb) of the ulnar collateral ligament, possibly also detachment of the extensor or flexor tendons from the epicondyles, complete displacement following dislocation

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Fig. 4.34 Insertion tendinopathy of the distal biceps tendon. Painful proximal forearm. Thickened, inflammatory changes to the insertion of the distal biceps tendon on the radial tuberosity (white arrows), with normal appearance of brachialis tendon (d, black arrow). (a) Sagittal T1w image. (b) Sagittal PDw fatsat image. (c) Coronal PDw fatsat image. (d) Axial PDw fatsat image.

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4.10 Apophysitis

Fig. 4.35 Bicipital bursitis. Patient with painful proximal forearm because of overloading after lifting heavy loads in occupational setting. Inflammation of biceps tendon insertion on the radial tuberosity as well as bicipital bursitis with space-occupying lesion isointense to edema in elbow (arrows). There is strong CM enhancement due to chronic synovial proliferation. (a) Sagittal PDw fatsat image. (b) Coronal PDw fatsat image. (c) Axial PDw fatsat image. (d) Axial contrast-enhanced T1w image.

handball), or congenital malformations. Protracted courses of disease can lead to secondary chondromatosis and/or osteochondromatosis because of metaplastic thickening of the villi. The implicated joint bodies are well visualized on MRI (▶ Fig. 4.43). Secondary arthrosis as seen in hemophilia is often associated with small osteophytes and severe cartilage damage, even in young patients (▶ Fig. 4.44).

4.10 Apophysitis Repetitive stress at the epicondyles of patients can, as in all apophyses of the body, result in painful irritation. The ulnar (medial) epicondyle of young throwing athletes (little leaguer’s elbow) is often affected. On MRI, a change in signal isointense to edema can sometimes be observed at the apophysis and/or apophyseal plate.54

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Fig. 4.36 Insertion tendinopathy of the biceps. Axial schematic diagram of the forearm at the level of the insertion of the biceps tendon on the radius (radial tuberosity). Insertion tendinopathy of the biceps on the radius can give rise to changes in signal intensity at a characteristic location in the region of the radial tuberosity and/or the inserting biceps tendon. Besides, there may be concomitant or isolated bursitis of the adjacent bicipitoradial bursa. 1, biceps tendon; 2, bicipitoradial bursa; 3, ulna; 4, radial tuberosity; 5, radius. Fig. 4.37 Insertion tendinopathy of the triceps tendon. Sagittal PDw fatsat image. Pain above the olecranon, especially in bodybuilders. Inflammation-related rise in signal intensity at the triceps enthesis on the olecranon (arrow) secondary to insertion tendinopathy.

Fig. 4.38 Radial head fractures. Status post fall resulting in multifragment of the radial head (a, arrow). (a) Sagittal T1w image. (b) Sagittal PDw fatsat image.

4.11 Osteochondritis 4.11.1 Osteochondritis Dissecans Osteochondritis dissecans of the elbow, in particular of the capitulum, is not all that uncommon. Its prevalence is around one-quarter of that seen in the knee.88 Throwing sports, tennis, or gymnastics gives rise to repetitive compression and shearing motion between the radial head and the capitulum of humerus. This can cause osteochondritis dissecans in adolescents, with the peak age seen between 9 and 15 years. The dominant arm is

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normally affected.88 Apart from the injury itself, an ischemic component is also implicated.29,65 Left untreated, loose joint bodies will develop, causing joint blockade and, in the long term, arthrosis. On MRI, as in osteochondritis dissecans of the knee (see Chapter 7.14.1), a subchondral, osteochondral focal lesion is identified, which, depending on its stage, can be more or less well delineated from healthy bones. The increasing presence of fluid-isointense signals around the focal lesion is indicative of a poorer prognosis for spontaneous resolution, with increasing greater instability.45 In the final stage, the desiccated material is released from the bone and goes on to form loose joint bodies (▶ Fig. 4.45).

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Fig. 4.39 Radiologically occult radial fracture. Status post trauma. Bandlike edema zone in proximal radius (arrows). (a) Coronal T1w image. (b) Coronal PDw fatsat image.

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Fig. 4.40 Concomitant trauma following dislocation. Schematic sagittal view of the elbow (summary). Predilection sites for bone injuries (contusion, occult fracture, fracture), defective joint position, and common soft tissue damage following posterior elbow dislocation or subluxation. 1, capitulum of humerus; 2, malposition; 3, coronoid process; 4, radial head; 5, capsule; 6, brachialis.

4.11.2 Panner’s Disease Osteochondritis (juvenile osteonecrosis) of the capitulum of humerus (Panner’s disease) is often viewed as a separate entity from osteochondritis dissecans, although they appear similar on conventional radiology (▶ Fig. 4.46). This disease affects younger patients (5–10 years). In the course of disease, the capitulum epiphysis undergoes changes similar to those observed in the femoral epiphysis in Perthes’ disease, with epiphyseal “fragmentation” and slight hypertrophy (▶ Fig. 4.47).28 In the long term, it can lead to incongruence of the elbow joint. However, there are fewer residues than in osteochondritis dissecans. On rare occasions, loose joint bodies develop.

Fig. 4.41 Concomitant trauma following subluxation. Sagittal PDw fatsat image. Status post severe elbow trauma, possibly involving subluxation mechanism. Major joint effusion with capsular damage to proximal segment (arrow).

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4.11.3 Loose Joint Bodies

4.14 Plicae

Loose joint bodies68 may be formed secondarily to osteochondritis dissecans, but are also observed in association with arthrosis or synovial chondromatosis, and in posttraumatic settings (▶ Fig. 4.48). They can often be identified on T2w SE images because they are seen in association with a joint effusion which serves as an innate contrast agent. Joint bodies are particularly common in the olecranon fossa and in the triangle between the humerus, radius, and ulna (▶ Fig. 4.49). Quinn et al68 identified an MRI sensitivity of 100% and a moderate specificity of 67% for loose joint bodies. Indeed, synovial folds, blood clots, and similar hypointense structures can produce false-positive results.18 MR arthrography is probably not needed for detection of loose joint bodies since they are normally accompanied by a joint effusion which generates an arthrographic effect on T2w images. It is thought that there exists a congenital accessory, intra-articular, bone element that manifests as a secondarily, acquired, loose joint body (posterior supratrochlear bone). This bone element can grow to a considerable size and is located superior to the olecranon (▶ Fig. 4.50).

Plicae or synovial folds are often seen in autopsy specimens.97 They are the residues of embryonic septa that have regressed to varying degrees and can become symptomatic, for example, as in the knee joint (see Chapter 7.16).79 On clinical examination, symptomatic synovial plicae can mimic loose joint bodies or be mistaken for epicondylitis,14,79 causing impaired extension77 or leading to snapping.2 Symptomatic synovial folds are 2 to 5 mm in diameter and are thought to arise from the region of the posterior fat pad.40,75,79 The term radiohumeral meniscus of the elbow joint is also used to denote large radial plicae (▶ Fig. 4.52). This is located between the radial head and capitulum of humerus, and is manifested as a hypointense triangle on MR images. It has been demonstrated that these radiohumeral folds are regularly observed in the human body, but, because of the widespread variability, only in around 20% of cases are they displayed on MRI (▶ Fig. 4.53).97 They extend to varying degrees posteriorly, which explains the commonly employed term radioposterior plica (▶ Fig. 4.54).14 Symptomatic plicae are identified on MRI on the basis of their characteristic clinical signs as well as the presence of isolated radiohumeral effusions, a thickened plica, and discrete synovial irritation of the radiohumeral capsular ligament apparatus (▶ Fig. 4.55). Local cartilage damage or even arthrosis can develop following protracted courses of disease. The clinical symptoms may resolve on resection of a thickened plica.

4.12 Radioulnar Synostosis Fusion of the proximal third of the radius and ulna can result from embryonic malformation. Symptoms are normally manifested in infancy through restricted functional mobility of the elbow. Rarely, fusion of the distal and medial thirds is also seen. Four forms can be distinguished100: ● Fibrous synostosis. ● Bony synostosis. ● Associated posterior subluxation of the radius. ● Associated anterior subluxation of the radius. Besides, the length of the synostotic segment of both forearm bones can vary. The extent and shape of proximal radioulnar synostosis can be evaluated using radiography, computed tomography (CT), or MRI (▶ Fig. 4.51). There are divergent views about whether surgery should be indicated, and this will depend on the extent of the malformation and on the resultant disability. Secondary synostosis, such as bridging of the two bones by an osteochondroma34 or posttraumatic ossification of the interosseous membrane, must be distinguished from the congenital form.

4.13 Cartilage Damage When the elbow is subjected to a valgus force in extension, the ulnar margin of the olecranon is pressed against the olecranon fossa, giving rise, in the ensuing course, to chondropathy, arthrosis, and finally formation of loose joint bodies at the implicated site. Such disorders are observed, for example, in baseball pitchers.31,76 In general, arthrosis, as seen here, is a secondary form, occurring following trauma, osteochondritis dissecans, or in association with general inflammation or hemophilia.23 At most, MRI is able to directly visualize the cartilage damage or the location of loose joint bodies.

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4.15 Bursitis A bicipitoradial bursa may be observed in association with various processes, such as repetitive trauma, infection, systemic inflammation, hemophilia, synovial chondromatosis, and rarer disorders. Severe bursitis may be clinically palpable. The enlarged bicipitoradial bursa may be in communication with the superficial and deep branches of the radial nerve, giving rise to corresponding symptoms. However, the median nerve generally courses too far medially to cause compression80 but can occasionally be compressed by a greatly enlarged interosseous bursa or scar tissue.52,88 Bursitis of the bicipitoradial bursa and interosseous bursa is rare.52 The volume of the olecranon bursa can increase in the presence of systemic inflammatory processes (e.g., rheumatoid arthritis or gout). However, bursitis can also be caused by mechanical pressure, direct trauma, or direct infiltration of a pathogen. Often, traumatic damage can result in severe hemorrhage and ensuing bursitis (▶ Fig. 4.56). On rare occasions, radiohumeral bursitis deep to the tendon of the extensor brevis may be associated with epicondylitis of the radial humerus or clinically mimic that condition.64

4.16 Neuropathies Lesions are encountered most often in the exposed ulnar nerve, which, unlike the median nerve and radial nerve, is not covered by muscles. In a series of 15 patients with neuropathy in the elbow region, the ulnar nerve was affected in 11 cases, the median nerve in 3 cases, and the radial nerve in 1 case.71 These disorders manifested on MR images as nerve thickening,

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4.16 Neuropathies

Fig. 4.42 Arthrosis. Various patients with signs of arthrosis. (a) Coronal T1w image. Early osteophyte (arrows) in handball player. (b) Axial PDw fatsat image. Large osteophyte and effusion in active cubital arthrosis (arrows). (c) Coronal T1w image. Subchondral cysts (arrow) and marked cartilage narrowing in association with posttraumatic secondary arthrosis and deformed radial head. (d) Sagittal PDw fatsat image. Active cubital arthrosis with joint effusion, cartilage damage, and subcortical reactive bone marrow edema.

increased signal intensity on T2w images or changed position secondary to repetitive pressure, space-occupying lesion, or spontaneous subluxation or dislocation.3 The changes reported in the MRI literature include compression (osteophytes, neoplasm, ganglion cyst), scarring, and nerve subluxation.71,99 There may be

an increase or reduction in the volume of the implicated or increased signal intensity (▶ Fig. 4.57). There is no pathogenetic explanation for subluxation or dislocation of the ulnar nerve. Among the causes posited are laxity, nonanlage of the arcuate ligament, abnormal position of the

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Fig. 4.43 Secondary osteochondritis. Sagittal PDw fatsat image. Moderate cubital arthrosis. Numerous joint bodies in the proximal recess with stratification evidencing osteomas (arrows) as seen in association with secondary osteochondritis.

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ulnar epicondyle, an excessively flat bony indentation of the groove, trauma, valgus or varus deformity of the elbow, capitulum of humerus, or triceps hypertrophy.15 In a series of 27 patients, subluxation or dislocation of the ulnar nerve was identified in 4 cases (15%). The arcuate ligament was absent in two out of four patients, but none of the four patients exhibited any symptoms with respect to the ulnar nerve. Caution must be exercised on randomly discovering subluxation.73 Intra-articular nerve entrapment, for example, as seen in association with dislocation fractures, is a repositioning impediment and can be detected on MRI within the joint space.3 Other forms of nerve damage may be seen in the presence of scarring or compression (entrapment) in narrow anatomic passages (▶ Fig. 4.58). Damaged nerves may appear hyperintense on T2w images.82 However, slight hyperintensity of the ulnar nerve, in the region of the cubital tunnel, is also observed in a large proportion (60%) of asymptomatic individuals.39 More marked and extensive hyperintensity is seen in neuropathy as well as thickening.6 In one study, the nerve area identified on axial images for asymptomatic individuals was 0.06 cm2, while it was on average 0.12 cm2 for symptomatic patients (sensitivity: 95%, specificity: 80%).44 Damaged nerves as well as the surrounding tissue layers often take up CM. However, nerve symptoms related to a spaceoccupying lesion are better visualized on MRI, for example, those caused by a nerve tumor, such as a neurinoma or malignant schwannoma,71,82 a neoplasm in the vicinity of a nerve, hematoma, or enlarged bursa. Imaging the elbow in flexion can help to demonstrate compression and deformation of the ulnar nerve in the cubital tunnel which would otherwise go unnoticed (▶ Fig. 4.59; see also ▶ Fig. 4.26 and ▶ Fig. 4.27).48

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Fig. 4.44 Secondary arthrosis in hemophilia. A 26-year-old patient with hemophilia A. Massive cartilage narrowing, osteophyte, and effusion in active secondary arthrosis in the presence of hemophilic osteoarthritis. (a) Coronal PDw fatsat image. (b) Sagittal PDw fatsat image.

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4.17 Neoplasms and Neoplasmlike Changes

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Fig. 4.45 Osteochondritis dissecans, late stage. An 11-year-old girl. (a) Coronal T1w image. Osteochondral defect in capitulum of humerus (arrow). (b) Coronal PDw fatsat image. Empty joint mouse bed (arrow). (c) Sagittal PDw fatsat image. Loose joint bodies (arrow).

Fig. 4.46 Osteochondritis dissecans of capitulum of humerus. Sagittal T2w TSE image through the capitulum of humerus and radius. An 11-year-old boy. Defect of capitulum of humerus (arrow).

4.17 Neoplasms and Neoplasmlike Changes Primary bone neoplasms are rare in the elbow region.53 The following neoplasms are found in proximity to the elbow: ● Osteochondromas (2%). ● Enchondromas (2%). ● Solitary cysts (2%; although 62% of such changes are seen in the proximal and middle humerus). ● Aneurysmatic bone cysts (4%). ● Giant cell tumors (3%). ● Chondrosarcomas (1%). ● Osteosarcomas (fewer than 1%).

Fig. 4.47 Panner’s disease (juvenile osteonecrosis of the capitulum of humerus). Coronal T1w image. Onset of fragmentation and incongruence of overlying cartilage (arrow).

● ● ● ●

Plasmocytomas (1%). Ewing’s sarcoma (virtually never). Fibrous dysplasia (3%). Paget’s disease (virtually never).

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As regards soft tissue neoplasms, the following percentages of important neoplasms are found in the upper extremities (not including the wrist and hand): ● Benign neoplasms: ○ Lipomas (7%). ○ Fibrous histiocytomas (14%). ○ Nodular fasciitis (29%). ○ Hemangiomas (11%). ○ Fibromatosis (5%; ▶ Fig. 4.60). ○ Neurofibromas (11%). ○ Schwannomas (12%).50 ● Malignant neoplasms: ○ Malignant fibrous histiocytomas (14%; but this diagnosis now appears less common compared with the figures given in the literature). ○ Liposarcomas (5%). ○ Leiomyosarcomas (5%). ○ Malignant schwannomas (12%). ○ Synovial sarcomas (14%).

Fig. 4.48 Loose joint bodies. Transverse plane. (a) T1w SE sequence. Two fragments of the lateral epicondyle of humerus can be delineated at the level of olecranon (arrows). (b) 2D-FLASH sequence (see ▶ Table 1.2). A joint effusion can be identified close to the fragments (arrows).

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Fig. 4.49 Loose joint bodies. Depiction of a predilection site for loose joint bodies. (a) Schematic diagram of a sagittal MR image at the level of the ulnohumeral joint. (b) Schematic diagram of a sagittal MR image at the level of the radiohumeral joint. 1, anterior recess (coronoid); 2, posterior recess (olecrani); 3, semilunar trochlear notch; 4, annular recess (periradial or sacciform).

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Fig. 4.50 Posterior supratrochlear bone. Large bone element exhibiting characteristic layered structure of osteoma in proximal posterior joint recess proximal to the olecranon (arrows). In the absence of joint bodies and if there is only minor signs of arthrosis and no chronic synovitis, this is likely to be a posterior supratrochlear bone. (a) Coronal T1w image. (b) Axial PDw fatsat image. (c) Sagittal PDw fatsat image.

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4.20 Clinical Relevance of Magnetic Resonance Tomography

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Fig. 4.51 Radioulnar synostosis. A 7-year-old girl with increasing restriction of rotational and other movements. (a) Anteroposterior radiograph showing deformation of the elbow joint because of developmental malformation with radioulnar synostosis. Depression in the ulna (arrow). (b) Coronal T1w MRI image with corresponding deformities. (c) Sagittal STIR image. Bone synostosis. (d) Axial GRE sequence at the level of the synostosis (upper line in c marks the level). (e) Axial GRE sequence at the level of the synostosis (lower line in c marks the level).

4.19 Potential Sources of Mistakes When Interpreting Images

Fig. 4.52 Plica. Coronal schematic diagram. Plica formation at the radial joint capsule with development of a meniscuslike invagination. This plica can cause entrapment complaints that resolve on resection.

○ ○

Fibrosarcomas (13%). Epithelioid sarcomas (19%).51

As in other body regions, ganglia arising from different structures (e.g., periosteum, muscles, joint capsule) are also found in the elbow region (▶ Fig. 4.61).

4.18 Posttherapy Findings MRI of the elbow is often used following unsuccessful interventions for epicondylitis. The aim here is to identify any scarring and also rule out any additionally hitherto missed diagnosis. MRI is also able to demonstrate the outcome of conservatively or surgically treated fractures, including cartilage damage, loose joint bodies, and other interpositions. Another indication for MRI is follow-up examination of conservatively or surgically treated osteochondritis dissecans, where ingrowth of fragments and release from the joint mouse bed can be shown.

On rare occasions, a mature bone is observed in the triceps tendon close to the olecranon. Analogously to the knee joint, the term cubital patella is employed here. Signals isointense to fatty marrow are seen within this bone, surrounded by a signal-void cortex. Because of its shape, this can generally be distinguished from a fracture, while the signal pattern helps to differentiate it from a tumor or inflammatory process. This must not be mistaken for a tumor or inflammatory tendon changes, in particular when comparing the findings with those of a plain radiograph. The olecranon can contain an accessory or persistent bone center (supratrochlear bone). This must not be mistaken for a fracture or a loose joint body (see Chapter 4.7). A cartilage-free ridge of varying incidence and extension is seen in the semilunar trochlear notch of olecranon and must not be misinterpreted as an osteochondral defect (see Chapter 4.11.1).

4.20 Clinical Relevance of Magnetic Resonance Tomography In the majority of cases, diagnostic imaging of the elbow begins with conventional imaging in two planes. This provides information especially on axes and relationships between bones and bone-related details such as fractures, osteophytes, and loose joint bodies. Often, MRI is the next and final diagnostic step carried out for the elbow region. However, it is used much less here than for other body regions. It is used, in particular, when trying to

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Fig. 4.53 Humeroradial plica. (a) In dissection specimen. (b) On coronal T1w image in asymptomatic patient. (c) On coronal STIR image in symptomatic patient with isolated effusion on the radial aspect and prominent plica. The patient’s complaints resolved following arthroscopic resection of the plica and joint irrigation.

detect osteochondral lesions and loose joint bodies. MRI is also thought to be the best modality for direct visualization of cartilage. No consensus has been reached on whether MRI is superior to CT arthrography when seeking to identify loose joint bodies. However, one clear advantage of MRI is its noninvasive nature, which can be exploited for imaging ligaments and tendons as well as for diagnosis of neuropathy. MRI is eminently suitable for characterization and topographic classification of space-occupying lesions, such as swollen bursae,

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hematomas, and neoplasms. Compared with MRI, ultrasonography is generally a less cumbersome and less expensive imaging modality for diagnosing benign space-occupying lesions. However, matters are different for staging and followup of malignant neoplasms where undoubtedly MRI is the gold standard. Occasionally, CT may be a more appropriate adjunct to conventional radiology than MRI for purely bone-related processes (e.g., radioulnar synostosis, fractures).

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Fig. 4.54 Various locations of the humeroradial plica. Different patients. (a) Coronal PDw fatsat image. Radial location of the humeroradial plica is common (arrow). (b) Sagittal PDw fatsat image. Rare posterior location (arrow). (c) Sagittal PDw fatsat image. Likewise, rare anterior location (arrow).

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Fig. 4.55 Plica syndrome. Different patients with plica syndrome. (a) Coronal T1w image. Thickening and blurring of the humeroradial plica (arrow). Already, slight cartilage damage can be detected. (b) Coronal T1w image, different imaging plane. Linear and focal rise in signal intensity (arrow) within the humeroradial plica. (c) Sagittal PDw fatsat image. Likewise, linear and focal rise in signal intensity (arrow) within the humeroradial plica.

Fig. 4.56 Bursitis of olecranon. Status post impact injury with major swelling of olecranon over previous 6 weeks. Fluidisointense ballooning of the olecranon bursa (arrows) due to posttraumatic bursitis. (a) Sagittal PDw fatsat image. (b) Axial PDw fatsat image.

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Fig. 4.57 Neuritis of the ulnar nerve. Wheelchair user with increasing paraesthesia and numbness of the ulnar fingers as well as elbow pain. Marked thickening and increased signal of ulnar nerve in and around the ulnar nerve groove (arrows) due to neuritis. (a) Axial PDw fatsat image. (b) Sagittal PDw fatsat image.

Fig. 4.58 Entrapment of the median nerve. Status post surgery of the elbow region, now with scarred thickening of the cubital aponeurosis (bicipital aponeurosis; a, c; arrow) and postoperative susceptibility artefacts, leading to compression of the median nerve (b, arrow). Clinical symptoms of median neuropathy. (a) Axial contrast-enhanced T1w image. (b) Adjacent axial contrast-enhanced T1w image. (c) Sagittal GRE sequence.

Clinical Interview

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Clinical Interview with the Medical Director of the Center for Orthopaedics and Traumatology of Bonn Community Hospital (Gemeinschaftskrankenhauses Bonn), Dr. Jochen MüllerStromberg: Question: “What do you think is the role of MRI in the everyday routine practices of an orthopaedist or trauma surgeon for the elbow? For which clinical manifestations do you see the greatest advantages?”

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Answer: “It has a major role. The main advantages are in looking for occult fractures in children following trauma. Often a positive fatpad sign is detected on an X-ray but the fracture is not seen. MRI is very useful in such cases. I also think it has major advantages in distinguishing chronic epicondylitis from other disorders.” Question: “For which clinical manifestations are false-positive MRI results most commonly encountered?”

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4.20 Clinical Relevance of Magnetic Resonance Tomography

Fig. 4.59 Claw hand. (a) Damage to the ulnar nerve at the level of the elbow causes the following: claw hand with hyperextension especially of the fourth and fifth fingers at the metacarpophalangeal (MCP) joint; slight flexion at the interphalangeal joints because of damage to the interosseous muscles; slight abduction of these fingers and hyperextension of the thumb at the MCP joint; and hypothenar and interosseous atrophy. More distal nerve damage at the level of the wrist affects the deep branch with more severe muscle atrophy of the first space but no hypothenar atrophy. (b) The claw position of the fourth and fifth finger may be absent (other patient).

Fig. 4.60 Fibromatosis. (a) Native T1w image. Fibromatosis of the forearm in a 5-year-old boy. Infiltration of fibromatous tissue into the skin and muscle fascia. (b) Contrast-enhanced T1w image. Strong CM enhancement, also in the adjacent, irritated cubital soft tissues.

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Fig. 4.61 Extensive ganglion cyst of the elbow. A 48-year-old female patient. A ganglion cyst was identified on the radiodorsal elbow of this 48-year-old secretary; this rapidly increased in size within the space of a few weeks. In (a) and (b), fluid-isointense ganglion cyst with connection to joint and multiple septa. (a) Axial T2w sequence. (b) Coronal STIR sequence. (c) Axial T1w sequence. (d) Irritation synovitis on high-contrast CM image.

Answer: “Tears of the distal biceps tendon are occasionally misdiagnosed as false positive. In these cases, there tends to be only inflammation or a partial tear of the biceps tendon or a disorder of the adjacent brachioradialis tendon. I believe that incorrect positioning of the elbow in flexion can explain why the biceps tendon cannot be optimally evaluated. Another disorder that occasionally produces a false-positive result is a tear of the collateral ligaments. [Note by the authors: Following severe trauma, there may also be changes to the signal intensity exhibited by the collateral ligaments because of straining or edematous imbibition, thus masking them.] What is important in such cases is the correlation with the findings of clinical examination—tears of the collateral ligament lead to considerable joint instability which can be identified during clinical examination.”

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Question: “For which disorders do you encounter false-negative MRI results most often and why were diagnostic measures continued in such cases?” Answer: “Synovial plicae and loose joint bodies are sometimes missed. Patients complain about entrapment problems and, because of this, are referred for MRI arthroscopy even when false-negative results are obtained.” Question: “For which clinical manifestations can MRI be omitted and for which is the modality overly used?” Answer: “In most cases, MRI can be omitted when treating classic fractures when there is no evidence of soft tissue complications. In my opinion, MRI is requested too often for acute epicondylitis that has a typical clinical picture and history (sport, etc.).”

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ment injury in the throwing athlete: evaluation with saline-enhanced MR arthrography. Radiology. 1995; 197(1):297–299 [79] Schweitzer ME, Marone P, Cho C, et al. Elbow synovial fold syndrome. Radiology. 1999; 213(P):414 [80] Skaf AY, Boutin RD, Dantas RW, et al. Bicipitoradial bursitis: MR imaging findings in eight patients and anatomic data from contrast material opacification of bursae followed by routine radiography and MR imaging in cadavers. Radiology. 1999; 212(1):111–116 [81] Sonin AH, Fitzgerald SW. MR imaging of sports injuries in the adult elbow: a tailored approach. AJR Am J Roentgenol. 1996; 167(2):325–331 [82] Sonin AH, Tutton SM, Fitzgerald SW, Peduto AJ. MR imaging of the adult elbow. Radiographics. 1996; 16(6):1323–1336 [83] Spinner RJ, Goldner RD. Snapping of the medial head of the triceps and recurrent dislocation of the ulnar nerve. Anatomical and dynamic factors. J Bone Joint Surg Am. 1998; 80(2):239–247 [84] Spinner RJ, Hayden FR, Jr, Hipps CT, Goldner RD. Imaging the snapping triceps. AJR Am J Roentgenol. 1996; 167(6):1550–1551 [85] Spinner RJ, Goldner RD, Fada RA, Sotereanos DG. Snapping of the triceps ten-

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231(3):797–803 [60] Murphy BJ. MR imaging of the elbow. Radiology. 1992; 184(2):525–529 [61] Nakanishi K, Masatomi T, Ochi T, et al. MR arthrography of elbow: evaluation of the ulnar collateral ligament of elbow. Skeletal Radiol. 1996; 25 (7):629–634 [62] O’Driscoll SW, Bell DF, Morrey BF. Posterolateral rotatory instability of the elbow. J Bone Joint Surg Am. 1991; 73(3):440–446 [63] O’Dwyer H, O’Sullivan P, Fitzgerald D, Lee MJ, McGrath F, Logan PM. The fat pad sign following elbow trauma in adults: its usefulness and reliability in suspecting occult fracture. J Comput Assist Tomogr. 2004; 28(4):562–565 [64] Osgood RB. Radiohumeral bursitis, epicondylitis, epicondylalgia (tennis elbow). Arch Surg Chic. 1922; 4:420 [65] Patten RM. Overuse syndromes and injuries involving the elbow: MR imaging findings. AJR Am J Roentgenol. 1995; 164(5):1205–1211 [66] Potter HG, Hannafin JA, Morwessel RM, DiCarlo EF, O’Brien SJ, Altchek DW. Lateral epicondylitis: correlation of MR imaging, surgical, and histopathologic findings. Radiology. 1995; 196(1):43–46 [67] Potter HG, Weiland AJ, Schatz JA, Paletta GA, Hotchkiss RN. Posterolateral rotatory instability of the elbow: usefulness of MR imaging in diagnosis. Radiology. 1997; 204(1):185–189 [68] Quinn SF, Haberman JJ, Fitzgerald SW, Traughber PD, Belkin RI, Murray WT. Evaluation of loose bodies in the elbow with MR imaging. J Magn Reson Imaging. 1994; 4(2):169–172 [69] Regan W, Wold LE, Coonrad R, Morrey BF. Microscopic histopathology of chronic refractory lateral epicondylitis. Am J Sports Med. 1992; 20 (6):746–749 [70] Resendes M, Helms CA, Fritz RC, Genant H. MR appearance of intramuscular injections. AJR Am J Roentgenol. 1992; 158(6):1293–1294 [71] Rosenberg ZS, Beltran J, Cheung YY, Ro SY, Green SM, Lenzo SR. The elbow: MR features of nerve disorders. Radiology. 1993; 188(1):235–240 [72] Rosenberg ZS, Beltran J, Cheung YY. Pseudodefect of the capitellum: potential MR imaging pitfall. Radiology. 1994; 191(3):821–823 [73] Rosenberg ZS, Beltran J, Cheung Y, Broker M. MR imaging of the elbow: normal variant and potential diagnostic pitfalls of the trochlear groove and cubital tunnel. AJR Am J Roentgenol. 1995; 164(2):415–418 [74] Rosenberg ZS, Blutreich SI, Schweitzer ME, Zember JS, Fillmore K. MRI features of posterior capitellar impaction injuries. AJR Am J Roentgenol. 2008; 190(2):435–441 [75] Ruiz de Luzuriaga BC, Helms CA, Kosinski AS, Vinson EN. Elbow MR imaging findings in patients with synovial fringe syndrome. Skeletal Radiol. 2013; 42 (5):675–680

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5.1

Examination Technique

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5.2

Anatomy

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5.3

Spontaneous Avascular Necrosis

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5.4

Ulnocarpal Impaction Syndrome

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5.5

Ulnar Impingement Syndrome

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5.6

Hamatolunate Impingement

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5.7

Arthrosis (Osteoarthritis)

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5.8

Carpal Coalition

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5.9

Traumatic Lesions of the Carpal Bones

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Diseases of the Ligaments

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5.11

Nerve Compression Syndrome

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5.12

Tumors

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5.13

Ganglion Cysts and Other Cysts

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5.14

Disorders of the Synovial Membranes Including Chronic Polyarthritis

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Disorders of Tendons

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Palmar Fibromatosis (Dupuytren’s Disease)

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Examples of Vascular Diseases

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Pitfalls in Interpreting Images

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Clinical Relevance of Magnetic Resonance Imaging 226 References

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Chapter 5

The Wrist and Fingers

5 The Wrist and Fingers M. Vahlensieck and M. Richter ●

5.1.1 Patient Positioning The wrist is generally imaged with the patient in the prone position and the arm extended. This position has the advantage of bringing the wrist into the isocenter of the magnet and, in most cases, improves the quality of fat suppression. However, it is not a very comfortable position for the patient, and there is additionally the risk of the images being blurred. Alternatively, the patient can be placed in the supine position and the arm placed along the side of the body for examination. However, this results in “off-center imaging” and inhomogeneous fat suppression.

5.1.2 Coil Selection Surface coils with a small diameter as well as volume coils can be used. Volume coils provide for higher signal-to-noise ratio but are expensive. In general, they are not part of the standard magnetic resonance imaging (MRI) equipment and must be procured separately.

5.1.3 Sequences and Parameters An established protocol for the wrist will include coronal T1weighted (T1w) turbo spin-echo (TSE) and short-tau inversion recovery (STIR) or proton density–weighted (PDw) fatsat, sagittal as well as axial PDw fatsat sequences. Modern MRI scanners permit a slice thickness of between 2 and 3 mm and in-section resolution of 0.5 to 0.7 mm2. For diagnostic considerations related to the entire hand, for example, rheumatoid arthritis, a larger field of view is selected to visualize the hand in its entirety. A larger circular coil is needed to that effect. The maximum reasonable imaging resolution is used to image the fingers; suitable sequences include sagittal T1w and PDw fatsat as well as axial and coronal PDw fatsat sequences. Gradient-echo (GRE) sequences are generally no longer routinely used because of their susceptibility to artefacts. Most diagnostic queries can be clarified with the help of (unenhanced) native images. Injection of contrast media (CM) can provide additional insights into inflammatory and tumor processes. MR arthrography, whether as a direct or indirect technique, can in most cases be dispensed with for diagnostic imaging of the hand and wrist. However, it is useful for visualizing the intrinsic ligaments and the triangular fibrocartilage complex (TFCC).

5.2 Anatomy 5.2.1 General Anatomy of the Carpal Rows The eight wrist bones can divided functionally into the following carpal rows: ● Proximal carpal row: ○ Scaphoid. ○ Lunate. ○ Triquetrum.

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Distal carpal row: ○ Trapezium. ○ Trapezoid. ○ Capitate. ○ Hamate.

The pisiform articulates with the triquetrum and can be considered to be a sesamoid in the flexor carpi ulnaris tendon. Functionally, it is an exception in that it does not contribute to direct transmission of forces in the wrist. The articulation between the distal articular surface of the radius, distal ulna, and triangular disk and proximal carpal row is known as the radiocarpal joint. It communicates in around 15% of cases with the pisotriquetral joint. The midcarpal joint is formed by the proximal and distal carpal rows. The carpometacarpal joints constitute the bases of the metacarpals and the distal carpal row. Because of the strong ligamentous connection, no joint motion is permitted between the distal carpal bones and the second and third metacarpals (amphiarthrosis), whereas a certain amount of extension and flexion are possible in the fourth carpometacarpal joint, and this is more pronounced in the fifth carpometacarpal joint. The articulation between the metacarpal bases is also referred to as the intermetacarpal joint. The first carpometacarpal joint (saddle joint of thumb) and the distal radioulnar joint are independent joint compartments. On the ulnar aspect, the articular surface of the distal radius is concave, forming a notch (ulnar notch/sigmoid notch) for the head of ulna.

Ligaments ●

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The anatomic relationships between the ligaments of the wrist are very complex. The following ligaments are distinguished: interosseous (intercarpal) ligaments that partially compartmentalize the internal joint space and, as such, are intrinsic ligaments. The extracarpal (extrinsic) ligaments reinforcing the joint.

Intrinsic Ligaments The proximal carpal row is linked together by the interosseous ligaments between the scaphoid and lunate (scapholunate ligament) and between the lunate and triquetrum (lunotriquetral ligament) (▶ Fig. 5.1), forming a single functional unit. These ligaments prevent communication between the radiocarpal and midcarpal joints. Both ligament structures are composed of three segments: each has a dorsal and palmar taut portion as well as a thinner proximal (membranous) part. In the case of the scapholunate ligament, the dorsal segment is of greatest importance for stability and functionality; the reverse is true for the lunotriquetral ligament. The ligaments enclose the bones in a U- and C-shaped manner (▶ Fig. 5.2). Like all fibrous and ligament structures of the human body, these ligament structures, too, are often subject to degenerative processes, with defects of the scapholunate and lunotriquetral ligaments seen in around 30% of asymptomatic elderly patients. The distal carpal row is also interconnected by interosseous ligament structures (see ▶ Fig. 5.1).

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5.1 Examination Technique

5.2 Anatomy

Extrinsic Ligaments

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Fig. 5.1 Coronal section through the wrist. Schematic diagram showing compartmentalization of the wrist into five joint compartments based on the interosseous ligaments and the triangular disk according to Greenspan. 1, first carpometacarpal joint compartment; 2, common carpometacarpal compartment; 3, midcarpal compartment; 4, radiocarpal joint; 5, scapholunate ligament; 6, distal radioulnar joint; 7, triangular disk; 8, ligament between lunate and triquetrum; 9, space between pisiform and triquetrum; 10, intermetacarpal compartment.

Fig. 5.2 Scapholunate ligament. Axial PDw fatsat image showing the palmar and dorsal portions of the scapholunate ligament (arrows).

Based on the configuration of the interosseous ligaments as well as of the ulnar disk, different joint compartments can be distinguished (see ▶ Fig. 5.1). Familiarity with these compartments is of paramount importance for conduct of arthrography and interpretation of the arthrograms. On MRI, the distribution patterns of fluid accumulation and effusions within the various compartments can help to pinpoint the site of a pathologic process.

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The entire carpal region is enveloped in a strong connective tissue capsule, partially reinforced by powerful ligaments (▶ Fig. 5.3). On the palmar aspect, the radiocapitate ligament, which is part of the palmar radiocarpal ligament, extends from the radial styloid process across the waist of the scaphoid to the capitate. Pursuing a similar diagonal course, the palmar radiotriquetral ligament, which is also part of the palmar radiocarpal ligament, inserts on the ulnar aspect of the radial styloid process. It crosses the lunate, to which it is connected through fiber bundles. Since there are carpal fiber bundles on the ulnar aspect which, in the TFCC, radiate from the ulnar styloid process into the carpal region giving rise to a V-shaped configuration with the radial palmar ligaments, these ligaments are also called proximal and distal V ligaments. On the dorsal side, there are two powerful ligament bundles, each of which courses diagonally. The proximal ligament bundle extends from the dorsal radius across the lunate to the triquetrum (dorsal radiotriquetral ligament) and is also referred to as the “dorsal component of the carpal sling,” with the triquetrum being the “stone” in the sling. From the triquetrum, broadly fanshaped fibers extend over the distal carpal row to the trapezium (dorsal intercarpal ligament). Radial and ulnar collateral ligaments are found on the respective sides of the carpal region. The ulnar triangular disk (▶ Fig. 5.4) is composed of fibrocartilage and is situated between the distal ulna and triquetrum and lunate. It has a flat, triangular configuration, radiates into the hyaline joint cartilage of the distal articular surface of the radius, and fuses imperceptibly with a complex structure of fibers and ligaments between the ulnar styloid process and the proximal carpal row (triangular ligament). Two fiber bundles of the triangular ligament are distinguished: ● One fiber bundle extends to the ulnar styloid process. ● One fiber bundle extends to the base of the distal ulna (ulnar fovea). This is the bony attachment of key importance for the stability of the distal radioulnar joint; it is also known as the “subcruentum ligament.” With its undersurface, the ulnar triangular disk glides over the head of the distal ulna, which is covered with hyaline joint cartilage. The ulnar-sided compartment of the radiocarpal joint is distal to the triangular disk. The central and radial portions of the disk are not vascularized, hence they exhibit poorer spontaneous healing following injury compared with the ulnar portion. The ulnar portions have higher signal intensity on MRI due to vascularization. Since even on imaging it is difficult to clearly distinguish between the multiple ligament structures on the ulnar aspect, the disk and this ligament complex are known as the triangular fibrocartilage complex (TRCC) (▶ Fig. 5.5). In addition to the ulnar disk, this complex includes the following structures: ● Dorsal and palmar radioulnar ligament. ● A variable ligament structure between the triquetrum and ulna (known as the “ulnocarpal meniscus” or “meniscal homologue”; ▶ Fig. 5.6).12

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Fig. 5.4 Ulnar triangular disk. Coronal T1w image showing the anatomy of the disk (arrow).

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Ulnar collateral ligament. Two ulnocarpal (extrinsic) ligaments on the volar aspect (ulnolunate ligament and ulnotriquetral ligament).

Internet Research

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The search term TFCC can be useful for internet research related to the “triangular fibrocartilage complex.”

The ulnocarpal meniscus can sometimes contain an accessory ossicle (os triquetrum secundarium or os triangulare). The opening to the prestyloid recess (also referred to as the ulnar recess; ▶ Fig. 5.7), which is an extension of the joint capsule measuring a few millimeters, is located between the disk and meniscus. The shape of this extension varies (it is saccular in 38% of cases,

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Fig. 5.5 Triangular fibrocartilage complex. 3D diagram showing the anatomy of the triangular fibrocartilage complex. 1, tendon sheath of extensor carpi ulnaris; 2, ulnotriquetral ligament; 3, ulnolunate ligament; 4, palmar radioulnar ligament; 5, articular disk; 6, dorsal radioulnar ligament; 7, extensor carpi ulnaris; 8, ulna; 9, radius; 10, lunate; 11, triquetrum.

tubular in 18%, or tapered in 13%) and should not be mistaken for injuries or ganglion cysts.

Tendon Sheaths Both the radiocarpal and midcarpal joints contribute to flexion and extension as well as to radial and ulnar abduction. Flexion is more pronounced in the radiocarpal joint, while extension largely takes place in the midcarpal joint. The scaphoid undergoes the most conspicuous changes between radial and ulnar abduction of the wrist. Its normally 45- to 50-degree palmar inclination relative to the longitudinal axis of the radius rotates palmarly with radial abduction, while it extends upright and fills the space between the distal radius, trapezium, and trapezoid.

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Fig. 5.3 Extrinsic ligaments of the wrist. (a) Dorsal view. (b) Palmar view. 1, radius; 2, triquetrum. Ligaments between forearm and carpal bones: 3, ulnar carpal collateral ligament; 4, radial carpal collateral ligament; 5, palmar radiocarpal ligament; 6, dorsal radiocarpal ligament; 7, palmar ulnocarpal ligament. Ligaments between the carpal bones: 8, radiate carpal ligament; 9, pisohamate ligament; 10, palmar intercarpal ligaments; 11, dorsal intercarpal ligaments. Ligaments between carpal bones and metacarpals: 12, pisometacarpal ligament; 13, palmar carpometacarpal ligaments; 14, dorsal carpometacarpal ligaments. Ligaments between the metacarpals: 15 and 16, metacarpal ligaments.

5.2 Anatomy After passing through the openings and channels of the wrist, the muscle tendons are surrounded by tendon sheaths arranged in several tendon sheath compartments (▶ Fig. 5.8, ▶ Fig. 5.9, and ▶ Fig. 5.10). Finger flexion is mediated by a superficial (flexor digitorum superficialis) and a deep flexor tendon (flexor digitorum profundus). The deep tendon inserts at the base of the distal phalanx;

the superficial tendon divides into two parts at the level of the proximal phalanx and inserts laterally to the deep tendon at the base of the intermediate phalanx. The tendons are routed through several ligaments on the bone (annular and cruciate ligaments; ▶ Fig. 5.11).

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Fig. 5.6 Meniscal homologue. Coronal schematic diagram showing the anatomy of the meniscal homologue of the triangular fibrocartilage complex. 1, fifth metacarpal bone; 2, hamate; 3, triquetrum; 4, lunate; 5, entrance to prestyloid recess; 6, articular disk; 7, ulnar attachment; 8, ulna; 9, styloid attachment; 10, meniscal homologue with central area of increased signal intensity due to increased perfusion, with styloid and triquetral attachment; 11, ulnar collateral ligament; 12, extensor carpi ulnaris tendon.

Fig. 5.7 Ulnar recess. Coronal PDw fatsat image. High-contrast demonstration of the markedly fluid-filled ulnar recess (arrow).

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Fig. 5.8 Anatomy of the tendons and tendon sheaths of the hand. (a) Anterior (palmar) view of the flexor tendons. (b) Posterior (dorsal) view of the extensor tendons. 1, extensor retinaculum; 2, retinaculum septa; 3, flexor retinaculum; 4, cruciate ligaments; 5, annular ligaments. Some predilection sites of tendinitis: distal circle, tendinitis of third extensor tendon compartment at the intersection of extensor pollicis longus and second extensor tendon compartment; proximal dashed circle, myotendinitis of the extensor pollicis brevis and abductor pollicis longus at the crossover point of the second extensor tendon compartment; arrow, de Quervain’s tenovaginitis; dashed arrow, tenovaginitis of extensor carpi ulnaris.

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Extensor retinaculum

Extensor digitorum and indicis muscles

Fourth tendon compartment

Extensor pollicis longus Extensor carpi radialis brevis

Extensor digiti minimi

Extensor carpi radialis longus

Fifth tendon compartment

Third tendon compartment

Second tendon compartment

Extensor pollicis brevis

First tendon compartment Extensor carpi ulnaris

Sixth tendon compartment

Abductor pollicis longus Radius

Ulna

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Tendons of the flexor digitorum superficialis and flexor digitorum profundus in the ulnar tendon sheath

Palmar carpal ligament

Median duo Median nerve Flexor carpi radialis tendon Flexor pollicis longus tendon in the radial tendon sheath

Radial trio

Second tendon quartet

Ulnar artery Ulnar nerve

Radial artery

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Pronator quadratus Simplified method for illustrating how the superficial finger flexor tendons of the wrist are arranged

Radius

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Fig. 5.10 Anatomy of the tendons and tendon sheaths of the hand. Schematic cross-section showing the flexor tendons.

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Fig. 5.11 Flexor tendons of the fingers and their reinforcing ligaments. Schematic diagram. A1–A5, annular ligaments (pulleys); C 1–C 3, localization level of cruciate ligaments; FDP, flexor digitorum profundus; FDS, flexor digitorum superficialis; intersecting line, approximate level of ▶ Fig. 5.27.

Finger extension is mediated by extensor tendons and interosseous and lumbrical muscles. The extensor tendon inserts at the dorsal base of the intermediate and distal phalanges. In doing so, it

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divides into various strands (medial and lateral tract) at the level of the proximal phalanx, forming henceforth an aponeurosis of complex anatomy (▶ Fig. 5.12). Extension of the index and little finger is mediated by two extensor tendons: the extensor digitorum as well as the extensor indicis and extensor digiti minimi; ▶ Fig. 5.13.

5.2.2 Special Magnetic Resonance Anatomy Coronal Plane The coronal plane is the standard plane for visualizing the wrist. The bone marrow space of the carpal bones, in particular of the lunate and scaphoid, can be well evaluated showing homogeneous bright signal intensity on T1w SE sequences (▶ Fig. 5.14, ▶ Fig. 5.15, and ▶ Fig. 5.16). Discrete punctate decreases in signal

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Fig. 5.9 Anatomy of the tendons and tendon sheaths of the hand. Schematic cross-section showing the six extensor tendon compartments.

5.2 Anatomy

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Fig. 5.12 Anatomy of the finger extensors and flexors. Schematic diagram. (a) Posterior view. (b) Lateral view with extended finger. 1, triangular zone of dorsal aponeurosis (triangular ligament); 2, insertion of extensor tendon at the base of intermediate phalanx (intermediate tract); 3, extensions of the long extensor tendon to the lateral tract; 4, palmar extensions of the dorsal aponeurosis (interosseous bundle); 5, extensor tendon; 6, interosseous muscles; 7, metacarpal bone; 8, segment of interosseous muscle tendon running to base of proximal phalanx and the joint capsule; 9, lumbrical; 10, insertion of interosseous muscle at the lateral tract; 11, lateral tract of dorsal aponeurosis; 12, insertion of extensor tendon at the base of the distal phalanx (lateral tract); 13, tendon of flexor digitorum profundus; 14, tendon of flexor digitorum superficialis; 15, vincula longa; 16, vinculum breve; 17, collateral ligaments. Downloaded by: Collections and Technical Services Department. Copyrighted material.

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Fig. 5.13 Tendons and ligament structures at the level of the metacarpal bones. Schematic diagram of axial section. MC, metacarpal (bone). 1, extensor digitorum; 2, extensor indicis; 3, collateral ligaments; 4, intermetacarpal fibers; 5, extensor digiti minimi; 6, palmar plate; 7, sagittal ligament; 8, flexor digitorum superficialis; 9, flexor digitorum profundus; 10, deep transverse metacarpal ligament; 11, first lumbrical muscle; 12, first dorsal interosseous muscle.

intensity may be indicative of bone islands, small cysts, or nutrient channels. The homogeneously high signal intensity is attributed to the absence of hematopoietic bone marrow in the distal extremities. The interosseous scapholunate and lunotriquetral ligaments can be visualized reliably only in the coronal plane. The lunotriquetral ligament is somewhat smaller and thus not as readily identifiable as its scapholunate counterpart. These ligament structures do not occupy the entire intercarpal spaces but are somewhat more located in the peripheral contact zone; hence, in the coronal plane these ligaments are demonstrated at the radiocarpal rather than at the midcarpal joint (▶ Fig. 5.17). As in other intercarpal joints, the interspaces are filled with hyaline cartilage of the respective carpal bones. The somewhat stronger scapholunate ligament exhibits variations in its attachment to the hyaline joint cartilage of the scaphoid and lunate. A broad attachment zone along the proximal articular surface of the lunate is the most

Fig. 5.14 Sectional anatomy of the wrist. Coronal T1w SE image. The bone marrow space of the carpal bones exhibits homogeneously high signal. The interosseous ligaments (scapholunate: black arrow; lunotriquetral: white arrow) have low signal intensity. H, hamate; K, capitate; L, lunate; S, scaphoid; Ti, triquetrum; Tr, trapezoid.

common finding. Like the capsular ligaments and fibrocartilaginous triangular disk, the interosseous ligaments have low signal intensity on all sequences (▶ Fig. 5.18). Conversely, when these fibrocartilaginous structures are in certain joint positions, an artificial increase in signal may occasionally be observed on T1w, T2*w, and PDw images. This should not be misinterpreted as a pathologic increased signal; see the magic angle phenomenon (see Chapter 5.18.5).

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Fig. 5.15 Sectional anatomy of the wrist. Coronal T1w SE image, showing the carpal tunnel with hypointense flexor tendons. The more hyperintense central linear structure is a segment of the median nerve (arrows). Situated between the hamulus of hamate and pisiform is Guyon’s canal. H, hamulus of hamate; P, pisiform; S, palmar scaphoid pole; T, trapezium.

Fig. 5.17 Scapholunate and lunotriquetral ligaments. Coronal 3D GRE image of a healthy volunteer. Scapholunate (thick arrow) and lunotriquetral (thin arrow) ligaments have a triangular shape, with central area of somewhat inhomogeneously increased intensity. The hyperintense cartilage can be identified at the bases. The ulnar ligament complex, comprising the ulnar disk with hyperintense radial attachment through the cartilage layer of the radius, is well delineated. Ulnar-sided signal increase due to highly vascularized connective tissue. Distal and ulnar to this is the ulnocarpal meniscus, and ulnar to the latter is the ulnar carpal collateral ligament.

Moreover, in recent years, there have been increasing reports of various patterns of increased signal intensities, particularly in thin sections, in the scapholunate and lunotriquetral ligament of asymptomatic patients, attributed to degenerative changes (▶ Fig. 5.19). These increases in signal intensity may be punctate

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Fig. 5.16 Sectional anatomy of the wrist. Coronal T1w SE image, showing the radial aspect of the proximal and distal V ligament (radiocapitate ligament, radiotriquetral ligament, arrows).

Fig. 5.18 Scapholunate and lunotriquetral ligaments. Coronal PDw fatsat image showing the membranous portion of the intrinsic ligaments. The scapholunate ligament can be seen as a homogeneous triangle (white arrow). The lunotriquetral ligament manifests as a more linear structure (black arrow).

and more linear both along the course of the ligament and directly at the bone attachment. Besides, morphologic variants, triangular, linear, or amorphous forms, were also identified on thin MRI sections. In the ulnar disk, degenerative changes can be observed already in the third decade of life; these also result in increased signal intensity and should not be mistaken for acute tears or inflammatory processes. On histology, these areas are

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The Wrist and Fingers

5.2 Anatomy

shown to have a reduced chondrocyte count as well as an altered fibrous matrix. On MRI, focal as well as linear increased signal intensity is observed on T1w and T2w images (see ▶ Fig. 5.19). The linear increased signal intensity may extend to the surface and in most such cases is suggestive of already chronic full-thickness tears. While these degenerative changes progress with age, they are rarely symptomatic. In the majority of all healthy wrists, no fluid or effusions can be detected in the carpal joints or joint recess, although identification of a small amount of fluid on T2w, STIR, or GRE sequences may also be normal. An effusion measuring more than 1 to 1.5 mm must be viewed as pathologic. The coronal plane is also used to evaluate the triangular disk. On 3-mm sections, the disk can only be clearly delineated in one to two sections; therefore, a thinner slice (1.5–2 mm) should be selected in the vicinity of the triangular disk. On the ulnar aspect, the hypointense fibers of the disk radiate into the hyaline joint cartilage of the distal radial articular surface where they form a broad-based attachment along both the radiocarpal joint and more proximally along the distal radioulnar joint.

Sagittal Plane Images in the sagittal plane demonstrate the axial relationships between the carpal bones. In particular, the axes of the radius, lunate, capitate, and scaphoid can be measured as on a lateral radiograph but without any overlapping (▶ Fig. 5.20, ▶ Fig. 5.21, and ▶ Fig. 5.22). Palmar or dorsal subluxations can be accurately visualized only in the sagittal plane. Even minor subluxations as well as discrete sites of incipient cartilage degeneration can be identified. Therefore, the sagittal plane is necessary for diagnosis of instability and degenerative changes.

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Fig. 5.19 Ulnar triangular disk and intrinsic ligaments. Variable schematic MR image of the ulnar triangular disk and intrinsic ligaments between lunate and scaphoid and between lunate and triquetrum. (a) The fibrocartilaginous ulnar triangular disk is mainly demonstrated as an area of low signal intensity to signal void (left). With advancing age, degenerative increased signal intensity, which (from left to right) is initially focal, and linear in more advanced stages, and which can also extend as far as the surface. (b) The intrinsic ligaments of the proximal carpal row generally exhibit low signal intensity to signal void and have a triangular shape (around 60% of cases). Morphologic variants (upper row) may result in a more linear (around 30% of cases) or amorphous depiction (over 10%). Signal deviations include (from left to right) focal signal increase at the center, at the tip (around 5%), or at the base (around 3%); in addition, central (around 10%), uni- or bilateral linear signal increase close to the attachment site as well as areas of diffuse increased signal intensity.

Fig. 5.20 Sectional anatomy of the wrist. Sagittal T1w SE image, showing parts of the scaphoid and STT joint (joint between scaphoid, trapezium, and trapezoid). On the palmar aspect, the radiocapitate and radiotriquetral ligaments are diagonally transected (arrows). Illustrated also are the longitudinal axis of the wrist (vertical line along the radiolunate–capitate–metacarpal axis) and the scaphoid axis which is angled 30 to 60 degrees. K, capitate; S, scaphoid; Tr, trapezoid.

The sagittal plane is also able to demonstrate structural changes in the lunate in patients with avascular necrosis (lunate malacia).

Transverse Plane The axial or transverse plane displays the carpal tunnel and its contents. The retinaculum, which extends between the distal scaphoid pole, tubercle of the trapezium, and the hamulus of hamate, can be identified as hypointense structures (▶ Fig. 5.23). Immediately beneath this lies the median nerve, which, because of its water and lipid content, exhibits higher signal intensity on all sequences compared with the flexor tendons. Positional variants of the median nerve can be easily detected on transverse images and should not be mistaken for pathologic dislocations. This plane is also suitable for assessment of the ulnar nerve channel, Guyon’s canal. The tendons of the deep and superficial finger flexors can be clearly delineated (▶ Fig. 5.24), thus helping to identify any inflammatory changes to the tendon sheaths or effusions on T2w images. Likewise, palmar and dorsal capsular ligaments can be demonstrated on transverse images, in particular in the presence of pathologic changes. The precise anatomic position of the radioulnar joint can be evaluated only on transverse images. Even minor palmar or dorsal subluxations can be identified (▶ Fig. 5.25).

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Fig. 5.21 Sectional anatomy of the wrist. Sagittal T1w SE image, showing the normal alignment of the radius, lunate, and capitate. On the palmar aspect, the flexor tendons have low signal intensity. K, capitate; L, lunate; R, radius.

Fig. 5.22 Sectional anatomy of the wrist. Sagittal T1w SE image, showing the pisotriquetral joint and ulnar styloid process. H, hamate; P, pisiform; Ti, triquetrum.

Fig. 5.23 Sectional anatomy of the wrist. Transverse T1w SE image, showing the flexor retinaculum as a hypointense ligament (curved arrow). The superficial and deep finger flexor tendons are also seen as areas almost devoid of signal. The median nerve lies relatively far toward the radius and has an oblique oval shape and high signal intensity compared with the flexor tendons (arrow). H, hamate with hamulus; K, capitate; T, trapezium; Ti, trapezoid.

Magnetic Resonance Anatomy of the Fingers Ligament structures and tendons, such as the collateral ligaments, flexor and extensor tendon, and annular ligaments,

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appear as signal void (▶ Fig. 5.26). In most cases, all three imaging planes can be successfully used to evaluate pathologic changes in the fingers. MRI is able to visualize increasingly more complex details (▶ Fig. 5.27).

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Fig. 5.24 Sectional anatomy of the wrist. Transverse T1w SE image at the level of the scapholunate joint space. The palmar-sided capsular ligaments are better developed than their dorsal counterparts. L, lunate; S, scaphoid.

5.3 Spontaneous Avascular Necrosis MRI has become established as a very sensitive imaging modality for diagnosis of avascular necrosis, thanks to its ability to directly identify pathologic processes unfolding within the bone marrow space. Scintigraphy is endowed with similarly high sensitivity but lower specificity. Conventional radiographs and even CT produce negative results in the early stages of avascular necrosis. The most common forms of spontaneous avascular necrosis of the wrist are as follows: ● Spontaneous avascular necrosis of the lunate (Kienböck’s disease, lunate necrosis). ● Spontaneous avascular necrosis of the scaphoid (Preiser’s disease; less common). There are a few case reports on spontaneous avascular necrosis of the other carpal bones: ● Spontaneous avascular necrosis of the trapezoid (Agati’s disease). ● Osteochondritis dissecans of the pisiform (Schmier’s disease). ● Spontaneous avascular necrosis of the triquetrum (Witt’s disease). ● Multiple avascular necrosis involving the capitate, trapezium, and hamate (Brainard’s disease).

5.3.1 Avascular Necrosis of the Lunate (Kienböck’s Disease) Lunate avascular necrosis (formerly known as “lunate malacia”) is a disease of the lunate, leading to its progressive collapse and to carpal dislocation and instability as well as to secondary arthrosis. Men are affected around three to four times more often than women. The disease is mainly unilateral but bilateral

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5.3 Spontaneous Avascular Necrosis

Fig. 5.25 Sectional anatomy of the wrist. Transverse T1w SE image at the level of the distal radioulnar joint. The radial tubercle (also known as Lister’s tubercle) can be identified on the dorsal aspect of the radius (arrow). The lines connecting the dorsal and palmar corners of the radius are also shown to help measure ulnar dislocations. The ulna should not project beyond these lines by more than half a shaft width. R, radius; U, ulna.

involvement is also possible, with different stages of disease affecting each wrist. Onset of symptoms is often between the age of 20 and 40 years, but there are also cases arising only after age 50 years. Disease onset is generally of an insidious nature. Radiating wrist pain can persist for years, leading to increasing active and passive restricted motion and declining gripping strength. The time to progression to more advanced stages varies greatly from one person to another and can range from a few months to years. There is a sensation of local pain pressure over the dorsum of the hand, with swelling seen mainly only in advanced stages. Characteristically, passive dorsal extension of the middle finger is painful. The cause and pathophysiologic mechanisms at work here have not been fully elucidated to date. Various factors have been posited, such as historic trauma, repetitive mechanical strain, and incongruence of the radiocarpal articular surface. Most cases of early-stage disease appear to involve bone marrow edema with no avascular necrosis so far, possibly as a stress reaction to the continuing high pressure exerted on the lunate. Over the course of months to years, bone marrow edema progresses to fibrosis and sclerosis of the medullary cavity. By this stage, there appears to be increased perfusion of the lunate with raised bone metabolism on scintigraphy. The blood supply is restricted only by progressive fibrosis and sclerosis of the medullary cavity. Any microfractures occurring in areas of raised pressure—in particular in the subchondral spongious region proximal to the radius—will result in discrete avascular necrosis because of mechanical bone destruction. Initial fragmentation seen in stage IIIa occurs mainly in the proximal subchondral region close to the articulation with the distal radius. This zone of the radial lunate pole exhibits relative hypovascularity and is thus thought to be the source of necrosis in the majority of cases

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(▶ Fig. 5.28). Only by this stage is there histologic evidence of avascular necrosis, albeit only in discrete fractured areas of the lunate, whereas, despite reduced signal intensity on MRI T1w images, viable bone is detected in the remaining bone marrow regions. MRI is very sensitive in detecting even the earlier stages, whereas radiographs produce positive results only from stage II when there is increased sclerosis. The disease is generally classified today in four stages in accordance with Lichmann (▶ Fig. 5.29): ● Stage I (early stage): Here, low-grade reduction in signal intensity affecting the entire lunate or only the proximal portion is seen on MRI T1w images (▶ Fig. 5.30), while increased signal intensity is observed on T2w images. Homogeneous, moderate to intensive CM enhancement is observed following gadolinium (Gd) administration. Enhancement is best visualized on frequency-selective fat-suppressed sequences. On plain radiographs, the lunate appears normal in this stage. ● Stage II: Increasing sclerosis and focal cystic necrosis generally originating from the radius and proximal subchondral space are seen in stage II. Hence, increasing density with isolated cysts is observed on plain radiographs. On MRI, declining signal

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Fig. 5.26 MRI anatomy of the fingers. T1w SE sequences. (a) Coronal plane. Signal-void collateral ligaments (upper arrow) and flexor tendon (lower arrow). (b) Axial plane. Nail bed (left arrow) and annular ligament (right arrow). (c) Sagittal plane. Flexor tendon (arrow).

Fig. 5.27 MR anatomy of the finger flexors. Axial T1w sequence at the level of the base of the intermediate phalanx (see ▶ Fig. 5.11). Illustrated are both bundles of the superficial flexor tendon in the insertion region at the intermediate phalanx beside and beneath the deep flexor tendon, which extends to the distal phalanx (arrow).

●

intensity is seen on all sequences, as well as reduced CM enhancement and cysts. Stage III (late stage): The lunate undergoes structural changes with loss of height, fragmentation, and extension seen in the sagittal plane (▶ Fig. 5.31). Fragmentation often begins in the proximal, radial-sided subchondral region, later followed by complete collapse with increasing dorsopalmar extension.

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5.3 Spontaneous Avascular Necrosis

Fig. 5.28 Stage II avascular necrosis of the lunate (Kienböck’s disease). Zonal arrangement of changes in signal intensity showing distal edematous pattern and signal void in the proximal portion (arrows). The proximal segment of the lunate is relatively poorly vascularized. Necrosis and fragmentation are thought to often originate from here. (a) Coronal T1w SE sequence. (b) Sagittal T1w SE sequence. (c) Coronal STIR sequence.

Stage

Radiography

MRI

I

Unremarkable

Diffuse or proximal edema pattern with CM enhancement

II

Complete or partial sclerosis, increasing cystoid components

Inhomogeneous signal intensity, increasingly hypointense on T2w images, patchy CM enhancement

IIIa

Height reduction, fragmentation

IIIb

Increasing carpal collapse

T1w and T2w hypointensity, mainly no CM enhancement anymore

IV

Sintering, secondary arthrosis

Graphic synopsis of MRI findings (T2w fatsat sequences)

Fig. 5.29 Staging of avascular necrosis of the lunate (Kienböck’s disease). Modified according to Lichtman et al,33 based on radiography and MRI criteria.

Normal

Secondary arthrosis

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The Wrist and Fingers Arthrodesis or denervation operations can help alleviate symptoms in stage IV. MRI may be indicated if there are persistent or progressive postoperative complaints as well as unclear results on clinical examination and conventional radiography. Precise knowledge of the surgical procedure employed is crucial for interpretation of the postoperative images. The viability of the transplanted pisiform bone grafts can be verified using contrast-enhanced MRI.69

Fig. 5.30 Avascular necrosis of the lunate, MRI stage I. Coronal T1w SE image. Homogeneous diffuse signal reduction in lunate (edema), no deformation. Slight negative ulnar variance. The radiograph was unremarkable, no evidence of sclerosis. The PDw fatsat sequence (not illustrated) shows diffuse signal increase (stage I).

●

Areas of discrete or disseminated hyperintense or fluid-isointense signal can be observed on T2w images between the necrotic bone areas. CM uptake, if seen at all, is confined to the peripheral zones or to punctate areas in the repair granulation tissue. The term stage Mb is used to denote the additional onset of insufficiency of the scapholunate ligament leading to rotary subluxation of the scaphoid. Stage IV (chronic avascular necrosis of the lunate): The instability caused by the fragmented lunate is consistent to an extent with scapholunate insufficiency. This leads to degenerative changes, manifesting initially at the radial styloid process and going on to affect the midcarpal joint (secondary arthrosis; ▶ Fig. 5.32). Proximalization of the capitate ultimately results in wrist collapse and in onset of generalized arthrosis of the radiocarpal and midcarpal joints.

Treatment options include, depending on the stage of disease, conservative therapy (immobilization in stages I and II) or surgical restoration of joint congruence through lengthening the ulna or shortening the radius (stage II level surgery). In recent years, revascularization of the lunate has also been implemented in stages I and II by transplanting vascularized bone grafts from the radius. Occasionally, stage II procedures can also be used for stage IIIa. Because of the fractures and altered shapes seen in stage Mb, the most common therapeutic approach is removal of the lunate with intercarpal arthrodesis (scaphotrapeziotrapezoid [STT] arthrodesis) or resection of the entire proximal carpal row (proximal row carpectomy). In the past, lunate resection with implantation of a plastic replacement was used to prevent secondary arthrosis and wrist collapse in stage III, using tendon interposition, silicone (Swanson prosthesis), Vitallium, or even acryl. Today, due to complications such as wrist collapse and silicone synovitis, the options currently used include intercarpal arthrodesis (e.g., STT arthrodesis) or an extended resection procedure with additional resection of parts of the adjacent carpal bones (proximal row carpectomy). Other surgical options include transplantation of the pisiform to the lunate compartment or free transplantation of vascularized osseocartilaginous femur grafts.

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In 1910, Preiser was the first to describe a disorder of the scaphoid which, like avascular necrosis of the lunate, led to spontaneous collapse of this carpal bone. This disease affects adults and causes progressive painful wrist weakness and pressure pain of the anatomic snuff box. The dominant hand is more often affected. As in Kienböck’s disease, its etiology has not been fully elucidated. It may be a type of stress reaction of the bone involving ischemia. Many case histories point to recent or historic trauma. Discrete sclerotic and cystic bone changes are seen on radiographs in the early stages of disease. As the disease progresses, the scaphoid undergoes deformation and loss of height, eventually leading to its complete fragmentation. On MRI, there is initially a multifocal edema pattern with reduced signal intensity on T1w images and increased signal intensity on T2w or fat-suppressed contrast-enhanced sequences (▶ Fig. 5.33). In the ensuing course, the entire bone exhibits reduced signal intensity, followed by discontinuous signal patterns attesting to fragmentation.

5.4 Ulnocarpal Impaction Syndrome Ulnocarpal impaction syndrome is a disorder where there is impaction of the ulnar head of the relatively long ulna on the TFCC and the ulnar wrist. The ulnar aspect of the lunate, in particular, is exposed to high pressure, leading to destruction of the joint cartilage on the ulnar lunate and the interposed triangular disk. This is eventually followed by rupture of the disk as well degenerative bone changes in the radial-sided distal ulna and the ulnar-sided proximal lunate (▶ Fig. 5.34, ▶ Fig. 5.35, and ▶ Fig. 5.36): ● Erosion of the joint cartilage. ● Progressive subchondral sclerosis. ● Cyst formation affecting especially the ulnar-sided proximal lunate as well as bone marrow edema in this region. In elderly patients, cartilage degeneration, on its own, in the region of the radial head on the proximal radius can result in relative lengthening of the distal ulna, in turn causing ulnocarpal impaction syndrome. Similar sequelae can result from congenital positive ulnar variance. On MR images, perforation of the triangular disk is seen in the majority of cases, while rarely only degenerative changes without complete disk perforation are observed (▶ Fig. 5.37; see also ▶ Fig. 5.36).

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5.3.2 Spontaneous Avascular Necrosis of the Scaphoid (Preiser’s Disease, Köhler-Mouchet’s Disease)

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5.4 Ulnocarpal Impaction Syndrome

Fig. 5.31 Avascular necrosis of the lunate, MRI stage III. Different patients. (a) Coronal T1w SE image. Inhomogeneous signal reduction as well as reduction in height of the lunate. (b) Coronal CM-enhanced image of another patient. Generally, no CM uptake. (c) Sagittal T1w SE image. Inhomogeneous reduction in signal intensity, fragmentation of the lunate as well as incipient carpal collapse with caudate dislocation of the capitate. (d) Radiographic image of a different patient with avascular necrosis of the lunate, of the same stage. The lunate is fragmented, showing negative ulnar variance.

Ulnocarpal impaction syndrome occurs in 18% of all patients secondarily to distal radial fracture and serves to explain recurrence of symptoms following an initially normal healing phase after fracture of the distal radius. On the whole, cases of ulnocarpal impaction syndrome are associated with a benign clinical course. In the event of a slight posttraumatic excess length, increased abrasion and ongoing deformation in the region of the disk and adjacent cartilage layer can lead to “self-healing” with reduction of the impaction pressure. This also leads to resolution of bone marrow edema. For the remaining cases, ulnar cauterization osteotomy or distal intraarticular resection of the distal ulna proximal to the disk—also the use of arthroscopy—is indicated. Distal radial fracture is

initially followed by formation of arched spurs and extension of the disk over the relatively distally displaced ulna. In 87% of cases, there are cystic changes and bone marrow edema in the area affected by lunate impaction, and in 43% of cases in the region of the triquetrum.14,18,27 Unlike avascular necrosis of the lunate, bone marrow edema and cystic changes are seen in the ulnar-sided portion of the lunate. Localized edema formation in this segment of the proximal and ulnar-sided lunate should not be misinterpreted as avascular necrosis.64,65 The cysts typically seen in the presence of ulnocarpal impaction syndrome are subchondral cysts, and these must be differentiated from ganglion cysts. Intact hyaline joint cartilage is needed for ganglion cysts.

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Fig. 5.32 Avascular necrosis of the lunate, MRI stage IV. (a) Overview image. Fragmented lunate of reduced height, with sclerosis of the fragments. (b) T1w SE image. Lunate showing a decrease in signal intensity and reduced height. Secondary arthrosis of the radiocarpal joint with subchondral sclerosis of the radial styloid process and osteophytes (arrow) can, in most cases, be better evaluated on this sequence than on conventional radiographs. (c) T2w SE image. Effusions on the radial styloid process and increased signal intensity between the lunate fragments. This is probably consistent with reparative fibrovascular granulation tissue.

The changes associated with ulnocarpal impaction syndrome must also be distinguished from fibrous lunotriquetral coalition and from avascular necrosis of the lunate on differential diagnosis.

5.5 Ulnar Impingement Syndrome In contrast to ulnocarpal impaction syndrome, which is caused by a relatively too long ulna, ulnar impingement syndrome generally results from a posttraumatically shortened ulna. Because of this, the palmar and dorsal capsular ligaments of the distal radio-

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ulnar joint embark on a diagonal course that is no longer vertical to the rotation axis of the distal radioulnar joint but now runs from the distal radial aspect to the proximal ulnar aspect. In turn, this results in relative shortening of these ligaments and restricted pro- and supination of the distal radioulnar joint. During rotational motion, the relatively too short capsular ligaments give rise to impaction of the distal ulna on the ulnar aspect of the distal radius. In chronic cases, this is followed by absorption changes in the region of the ulnar-sided distal radius (▶ Fig. 5.38 and ▶ Fig. 5.39).3,14 This type of impingement syndrome can also

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5.7 Arthrosis (Osteoarthritis)

Fig. 5.33 Avascular necrosis of the scaphoid (Preiser’s disease). (a) Coronal T1w SE image. (b) STIR sequence. Inhomogeneous edematous pattern in scaphoid.

result from congenital shortening of the ulna, as seen in Madelung’s deformity, with radial displacement of the longitudinal axis. However, this is only one of the manifestations of this complex deformity. Painful ulnar impingement is seen most commonly secondarily to resection procedures on the cubital head and following Kapandji–Sauvé operation.

5.6 Hamatolunate Impingement In some half of cases, the lunate has a separate articular surface from the hamate. This facet is thought to contribute to arthrosis due to static disbalance. The term hamatolunate impingement is used to denote this condition. Even at an early stage, telling signs of incipient arthrosis can be recognized on MRI, with bone marrow edema in the joint region.

Internet Research

●i

More information can be found on the internet using the search term hamatolunate impingement.

5.7 Arthrosis (Osteoarthritis) Arthrosis (arthrosis deformans) is a common disorder of the hand with myriad different forms seen, for example, Heberden’s and Bouchard’s arthrosis, rhizarthrosis, and STT arthrosis, as well as pisotriquetral, intercarpal (e.g., between the hamate and lunate: hamate tip syndrome), radiocarpal, or radioulnar arthrosis. Here, only a few examples of active (synovial) arthrosis are given. In general, diagnosis is based on appropriate X-ray examination. In some cases, it may be difficult to establish whether it is the arthrosis identified on radiography which is causing the clinical symptoms or whether there is another underlying cause not detected on X-ray. In such an event, MRI will be able to distinguish cartilage damage, symptomatic synovitis, and/or associated bone marrow edema from other diseases, for example, avascular necrosis. The corresponding signs on MRI can be applied in general to other regions (▶ Fig. 5.40, ▶ Fig. 5.41, and ▶ Fig. 5.42). On rare occasions, synovial proliferation with formation of loose joint bodies is seen in association with chronic arthrosis, accompanied by synovitis. The predilection sites of such loose joint bodies include, as in the case of all joints, the “capsular sheaths” (recess), for example, in areas proximal and distal to the pisotriquetral joint.

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Fig. 5.34 Ulnocarpal impaction syndrome. A/P radiographic image of the wrist in the presence of ulnar compression syndrome. Relative ulnar displacement and lytic–sclerotic changes to the ulnar base of the lunate.

Fig. 5.35 Ulnocarpal impaction syndrome. (a) Image of a sawn crosssectional specimen of the wrist showing ulnocarpal impaction with torn triangular disk and defect in the joint cartilage on the proximal, ulnar-sided lunate. (b) The radiographic image of the specimen also shows sclerosis of the ulnar-sided lunate.

Arthrosis progression in the presence of carpal instability eventually leads to impairment and destruction of the arched architecture of the wrist, with increasing deformation and collapse. This ultimately gives rise to carpal collapse (SLAC wrist [scapholunate advanced collapse], if the scapholunate ligament is torn, or SNAC wrist [scaphoid nonunion advanced collapse] if there is scaphoid pseudarthrosis).

5.8 Carpal Coalition Coalition of carpal bones is a rare anatomic anomaly resulting from failure of segmentation of a common cartilaginous carpal anlage. A distinction is made between coalitions involving bone, incomplete bone, cartilage, and connective tissue bridging, presenting with or without other anomalies (classification according to Minaar); see also Chapter 8.4.9. Carpal coalition occurs most often between the lunate and triquetrum, and occasionally between the hamate and capitate. Other forms, such as coalition between the pisiform and hamate, between the capitate and trapezoid, and between the scaphoid and trapezium, are rare. Lunotriquetral coalition is particularly common in African populations, with an incidence of up to 10%. While the bony coalition between the carpal bones is not significant, there is a genetic predisposition to impaired segmentation. Bony

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Fig. 5.36 Ulnocarpal impaction syndrome. Schematic diagram, coronal section, fat-suppressed T2w MRI image. Congenital or acquired ulnar displacement relative to the radius causes cartilage damage to the ulna, lunate, and triquetrum, as well as damage (narrowing or tear) to the ulnar disk, bone marrow edema, and absorption and subchondral cysts in the lunate and triquetrum.

lunotriquetral coalitions are almost always symptomatic.55 Pfitzner53 reported on incomplete lunotriquetral fusion with manifestations similar to pseudarthrosis and used the term coalescence to denote this condition. Coalitions must be differentiated from posttraumatic or postinflammatory

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5.9 Traumatic Lesions of the Carpal Bones

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Fig. 5.38 Ulnar impingement syndrome. Schematic diagram, coronal section, T1w MR image or, in principle, radiograph. Traumatic, postoperative, or congenital shortening and dislocation of the ulna results in painful absorption processes on the radius as well as in sclerosis of the radius and ulna (neoarthrosis).

Fig. 5.37 Ulnocarpal impaction syndrome. Coronal PDw fatsat image. A relatively excessively long ulna and low-grade degenerative changes to the articular disk due to impingement disorder.

arthrodesis. On radiography, complete bony forms of bone fusion and incomplete or also cartilaginous forms can be seen as irregular joint gaps, in some cases accompanied by reactive changes. On MRI, continuous bone marrow can be identified in the bony forms, while cartilaginous forms manifest as narrowed joint gaps with different degrees of irritation of the adjacent bony segments (similar to pseudarthrosis; ▶ Fig. 5.43).

5.9 Traumatic Lesions of the Carpal Bones 5.9.1 Bone Contusion (Bone Bruise) and Occult Fracture In general, MRI is not the primary imaging modality indicated to detect or rule out a fracture. Conventional radiography and CT are used to that effect. However, MRI is adept at demonstrating the precursor stages of a fracture (contusion and occult fracture) as well as concomitant soft tissue injuries (▶ Fig. 5.44).

Bone Bruise MRI is able to reliably identify bone bruises, thanks to its high sensitivity for detection of posttraumatic diffuse bone marrow edema, including in the wrist.

Fig. 5.39 Ulnar impingement syndrome. Coronal T1w SE sequence. Shortened ulna, ulnar axis displacement, absorption activity at radius (arrow).

Occult Fractures Occult fractures are fractures seen on MRI but not on plain radiographs. In the pre-MRI era, such fractures were detected on serial radiographic examinations due to the fact that after a period of 2 to 5 days the fracture line opened wider because of absorption processes, thus rendering it visible on radiographs. Occult fractures can also be detected on follow-up

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The Wrist and Fingers scintigraphic examination, which yields a positive result after a certain period of time following injury. In the modern era, MRI is able to diagnose an “occult fracture” immediately after the traumatic event. The characteristic signs, as for fractures visible on plain radiographs, are: ● Linear bone marrow edema with signal reduction on T1w, and signal increase on T2w, contrast images. ● A central area of reduced signal intensity to signal void on both contrast sequences (▶ Fig. 5.45 and ▶ Fig. 5.46).9

5.9.2 Fracture The scaphoid fracture is the most common type of fracture of the carpal bones (see Chapter 5.9). Fractures are often accompanied by bony ligament avulsions of the dorsal aspect of the triquetrum. Since avulsion fractures generally do not cause any significant bone marrow edema, such fractures are easily missed on MRI. CT is much more sensitive at identifying these. Fractures of the hamulus of hamate often go undetected on conventional radiographs (▶ Fig. 5.47).

Occult fractures should not be mistaken for bone bruises.

Subluxations in the region of the wrist can be visualized on sectional imaging of the relatively dislocated adjacent articular surfaces. Dislocations frequently occur in combination with fractures; several forms of wrist dislocations are distinguished. Chronic subluxation of the pisiform can cause reactive synovitis.

Fig. 5.40 Active, isolated radioulnar arthrosis. Schematic diagram, T2w fat-suppressed MR image. Cartilage damage to the radius and ulna at the level of the radioulnar portion of the joint, synovial effusion of the radioulnar recess, early osteophytes of radius. The ulnar disk is unremarkable.

5.9.4 Traumatic Lesions and Findings of the Postoperative Scaphoid Because of their high incidence and potentially relevant clinical complications, such as pseudarthrosis and necrotic fragmentation, details of trauma, posttraumatic complications, and

Fig. 5.41 Active distal radioulnar arthrosis. Joint incongruence, effusion of the radioulnar recess, early osteophytes (arrow). The ulnar disk is unremarkable. (a) Coronal T1w SE sequence. (b) Coronal STIR sequence.

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5.9.3 Dislocation and Subluxation

5.9 Traumatic Lesions of the Carpal Bones

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Fig. 5.42 Active rhizarthrosis. Joint effusion, dislocation, osteophytic spur at the base of the first metacarpal bone; subchondral bone marrow edema (b, arrow). (a) Coronal T1w SE sequence. (b) Coronal STIR sequence.

Fig. 5.43 Fibrous lunotriquetral coalition. A 31-year-old man with ulnar-sided pain 1 week following heavy work. (a) The lunotriquetral joint space is narrowed and the borders of the lunate and triquetrum are unremarkable in this region. (b) Coronal T1w GRE image. Reduction in signal intensity in almost the entire lunate and the adjacent triquetrum. (c) Coronal STIR image. In these regions, there is bright signal due to marked bone marrow edema as well as effusion in the radiocarpal joint.

postoperative findings of the scaphoid will now be addressed separately here.

●

Fractures

Surgery is indicated for unstable fractures in accordance with the Herbert classification. MRI signs include: ● Bone marrow edema. ● Hypointense to signal-void fracture line. ● Edema of the surrounding soft tissues with edematous infiltration of the parascaphoid fat (▶ Fig. 5.48).

Between 60 and 70% of scaphoid fractures occur in the middle third (the waist). The tubercle (5–10%), distal (5–10%), and proximal poles (15–20%) are less often involved. The fracture line may be oriented in a more horizontal or more vertical direction. The signs of instability7 include the following: ● Opening of the fracture line by more than 1 mm. ● Step deformities exceeding the cortical thickness.

●

Widening of the fracture line. Carpal ligament instability.

MRI is less reliable at identifying the width of the fracture line compared with CT.

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Fig. 5.44 The median nerve is partially severed following a sharps injury. (a) Sagittal T2w TSE sequence. Discontinuity of the median nerve (arrow). (b) Axial PDw fat-suppressed TSE sequence. Fluid-isointense defect (arrow) with areas of inhomogeneity (possibly due to the fibrous remnants of the nerve). (c) Axial PDw fat-suppressed TSE sequence. The morphology of the nerve within the carpal tunnel appears normal (arrow).

Fig. 5.45 Occult fracture of the pisiform following a fall. Edematous pattern and hypointense line in pisiform (arrow). Unremarkable radiograph. (a) Coronal T1w SE sequence. (b) Coronal STIR sequence.

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5.9 Traumatic Lesions of the Carpal Bones

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Fig. 5.46 Radiologically occult scaphoid fracture. Fracture line in the edematous zone. (a) Coronal T1w image. (b) Sagittal PDw fatsat image.

Fig. 5.47 Fracture of the hamulus of hamate. Status post fall. Unremarkable radiograph; a tangential image was not produced. MRI shows the transverse fracture at the base of the hamulus of hamate (c, arrow). The coronal images show the edematous pattern of the hamulus (a, b, arrow). (a) Coronal T1w image. (b) Coronal PDw fatsat image. (c) Axial PDw fatsat image.

Pseudarthrosis, Fibrous Union, and Partial Union Pseudarthrosis Nonunion of a fracture 3 months after injury is referred to as “delayed bone healing,” and nonunion after more than 6 months

is called “pseudarthrosis.” The more proximal the fracture location and the more displaced the fragments, the greater the probability of delayed bone healing, not least due to the specific nature of scaphoid vascularization. Other factors implicated in occurrence of pseudarthrosis include: ● Initially overlooked scaphoid fractures. ● Inadequately immobilized scaphoid fractures.

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a

b

Fig. 5.48 Questionable scaphoid fracture. Trauma 5 days previously; unclear radiographic results. (a) Coronal T1w image. Edema and line (arrow) in scaphoid as fracture sign. (b) Coronal PDw fatsat image. No edema of the proximal fragment (arrow), possibly indicative of impaired viability. Highcontrast examination would have been helpful here.

The postfracture incidence of pseudarthrosis is estimated at 5 to 10%. On radiography, a persistent fracture line and dense areas of signal inhomogeneity of the adjacent bone fragments and cysts are observed in association with pseudarthrosis. Based on the conventional radiographic signs, pseudarthrosis of the scaphoid can be assigned to four stages, for each of which a different therapeutic option is recommended: ● Stage I: Absorption stage with widening of the fracture line. ● Stage II: Cyst formation. ● Stage III: Sclerosis of the fragments with increased (hypertrophic form) or only few osteophytes (atrophic form). ● Stage IV: Secondary arthrosis, with onset at the radial styloid process, increasing carpal dislocation, and instability even leading to wrist collapse. On MRI, the pseudarthrosis line manifests as an inhomogeneous structure, with generally increased signal intensity on T2w images and with varying degrees of bone marrow edema seen in the contiguous fragments of reduced signal intensity on T1w sequences, and increased signal intensity on T2w and fatsuppressed images. Cysts presenting in the ensuing course have low signal intensity on T1w images, while they appear rounded and have very high signal intensity on T2w contrast images. Sclerosis results in a slow progressive reduction in signal intensity on all contrast images. CM administration can provide valuable insights into the viability of the fragments.

Fibrous Union Fibrous union of a fracture must be distinguished from pseudarthrosis. The former case is characterized by union and stabilization of the fracture with, to a large extent, restoration of the loadbearing ability based on nonossified fibrous tissue. This fibrous callus cannot be reliably identified on radiography. At most, it is

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thought to appear somewhat more dense than the surrounding soft tissues. Detection of persistent instability of the fragments in fluoroscopy-guided motion studies is suggestive of pseudarthrosis. By contrast, MRI is much more adept at detecting a fibrous union since the bridging connective tissue has low signal intensity on all sequences. Besides, fatty bone marrow without any evidence of bone marrow edema is seen in the adjacent bone fragments.

Partial Union Since partial union of a scaphoid fracture is also observed, before issuing a diagnosis of pseudarthrosis the corresponding line should be identifiable across the entire bone thickness.

Posttraumatic Avascular Necrosis The majority of the blood vessels supplying the scaphoid enter the bone via the scaphoid waist in the region of the lateral tubercle. Most of the proximal scaphoid pole is completely covered in hyaline cartilage and receives its blood supply from the distal pole. Fractures of the middle third scaphoid, and increasingly fractures at the transition to the proximal third scaphoid, sever the proximal scaphoid fragment blood supply, thus often causing necrosis of the proximal fragment. Less commonly, depending on the accident mechanism, necrosis of the distal fragment is observed, too. Necrosis can also present at a later stage, in particular, in association with delayed healing and pseudarthrosis. On conventional radiographs, posttraumatic avascular necrosis manifests as a relative increase in the density of the affected fragment since, because of absent or impaired perfusion following posttraumatic immobilization, there is no or only slow demineralization of the fragment compared to the surrounding bone. This is later followed by increased intramedullary sclerosis, deformation, and fragmentation of the necrotic fragment.

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5.10 Diseases of the Ligaments

●

●

●

On MRI, the following are detected: No necrosis, viable fragments: To a large extent, normal bone marrow signal in both fragments, slight edema pattern in both fragments. If such a pattern is seen, there is no need to administer CM for further diagnostic purposes. At a later stage, the signal on native images may be reduced because of sclerosis, hampering diagnosis based on MRI alone (▶ Fig. 5.49). No necrosis, impaired viability of the proximal fragment: Moderate hypointensity of the proximal fragment on T1w contrast images, heterogeneous signal on PDw fatsat images, and low CM uptake compared with the distal fragment. Partial necrosis: Parts of the proximal fragment exhibit no CM enhancement. Complete necrosis: Marked hypointensity on T1w images, heterogeneous signal on T2w contrast images, and largely no CM enhancement of the proximal fragment (▶ Fig. 5.50). The intensity of CM enhancement decreases in line with declining viability, as seen on CM images and in the CM dynamics on comparing both fragments.48 Persistence of signal change for over 6 weeks after injury in one of the two fragments, with normalization of signal in the other fragment, is highly suggestive of avascular necrosis and impaired viability. No CM uptake by one fragment compared with CM uptake by the other fragment, as well as persistent edema of both fragments, is a relatively reliable sign of necrosis. In one study, it was easier to detect declining viability by investigating the dynamics of CM uptake (▶ Table 5.1). In complex exceptional cases, this technique can thus facilitate diagnosis. Depending on the age of the fracture or pseudarthrosis, viable, nonviable, and sclerotic (callused) bone can be seen in the proximal fragment on histology, thus explaining the heterogeneous results obtained when evaluating viability.17

Postoperative Findings When interpreting the MRI findings after surgical repair of pseudarthrosis of the scaphoid, it should be borne in mind that bone marrow edema can persist for several months to a year after surgery, in particular on STIR images. Besides, when evaluating an

a

b

osseous or a fibrous union, the radiologist should know which surgical technique was used (▶ Fig. 5.51). The success rate of the Matti–Russe graft is 87 to 95%. Modern osteosynthesis materials (e.g., titanium Herbert screw) permit limited assessment of the viability of the proximal fragment and the former pseudarthrosis gap despite susceptibility artefacts. CT is better at evaluating the extent of union.

5.10 Diseases of the Ligaments 5.10.1 Interosseous (Intrinsic) Ligaments Wrist arthroscopy based on radio cinematography continues to be the diagnostic gold standard for dynamic investigation of the wrist. Three-compartment arthrography, with initial injection of the midcarpal joint, is another tried and tested method for detection of tears of the interosseous ligaments between the scaphoid and lunate (scapholunate ligament) and between the lunate and triquetrum (lunotriquetral ligament). The ability to demonstrate these ligaments on MRI is between 70 and 95% and very variable. Thanks to enhanced resolution, the diagnostic accuracy of MRI at detecting such ligament tears has improved in recent years. MR arthrography also confers advantages in certain complex situations. In addition to full-thickness tears, partial tears, which are more difficult to identify, may be observed, affecting the dorsal, palmar, or central (membranous) segment (▶ Fig. 5.52). ● Direct signs of a tear: ○ Discontinuity. ○ Signal increase. ● Indirect signs of a tear: ○ Focal fluid accumulation. ○ Increased distance between the affected carpal bones at rest or in certain joint positions, possibly with subluxation (▶ Fig. 5.53).

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●

If there is a full-thickness or partial tear of an interosseous ligament, infiltration of vascularized granulation tissue into the residual ligament structures can be observed. While intravenous

c

Fig. 5.49 Pseudarthrosis of the scaphoid. Irregular signal reductions in both fragments (a, arrow) due to sclerotic processes. Nonetheless, there is good viability with strong, homogeneous CM enhancement by both fragments (b, c). (a) Native coronal T1w image. (b) Coronal T1w image following CM administration. (c) Subtraction image.

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T1w

PDw fatsat

CM

CM dynamics Signal

Viable fragments

Fig. 5.50 Avascular necrosis. Schematic diagram showing varying viability of the proximal fragment in the presence of a scaphoid fracture or pseudarthrosis. The signal intensity on native MR images depends on the age of the fracture or the pseudarthrosis (variable edematous pattern, increasing sclerosis, etc.).

Time Signal

Reduced viability of proximal fragment

Time Signal

Time Signal Complete necrosis of proximal fragment (nonviable) Time

Table 5.1 Sensitivity, specificity, and accuracy of native MRI, CM-enhanced MRI, and dynamic CM-MRI showing reduced viability and necrosis of the proximal fragment of pseudarthrosis of the scaphoid in 35 patients.48 The gold standard is intraoperative inspection (punctate bleeding after exploration with palpating hook and osteotomy). Following CM administration, in particular the specificity of necrosis detection can be improved. No pathognomonic signs are seen Viability

Sensitivity/specificity/accuracy (%)

Native MRI

CM-MRI

Dynamic CM-MRI

Reduced viability

Sensitivity

25

25

67

Specificity

74

73

96

Accuracy

69

68

93

Sensitivity

67

60

67

Specificity

76

93

92

Accuracy

74

88

87

Necrosis

tear, and a severe degenerative process with this technique either.

5.10.2 Capsular Ligaments of the Wrist (Extrinsic Ligaments) Fig. 5.51 Surgical technique for pseudarthrosis of the scaphoid. Schematic diagram. (a) Inlay cancellous bone graft (Russe technique). (b) Inlay cancellous bone graft with two additional corticocancellous chips (Matti–Russe). (c) For small proximal fragments, replacement of the proximal fragment with corticocancellous graft (Russe II); this inevitably results in severing of the intercarpal ligaments. (d) Osteosynthesis with double zinc plate (Ender) or Herbert screw with cancellous bone graft.

administration of Gd-DTPA results in enhancement, it is not possible to reliably distinguish between a full-thickness tear, partial

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Multiple discrete ligament structures are seen embedded for reinforcement into the palmar and dorsal joint capsule of the wrist. Even on the anatomic specimen, these ligaments are difficult to visualize as separate entities. On MRI, these discrete ligament structures are delineated only in around 50 to 70% of cases. The probability of a reliable diagnosis is even lower; hence, the extrinsic capsular ligaments cannot be reliably demonstrated on native MR images. Capsular ligament insufficiency and tears can cause instability that is usually well visualized on conventional radiographs as well as on MRI. The zigzag deformities on dorsal rotation of the lunate and axial displacement of the capitate in a dorsal direction (DISI [dorsal intercalated segment instability]) and the variants

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Partial necrosis of proximal fragment

5.10 Diseases of the Ligaments

a

b

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Fig. 5.52 Tear of scapholunate ligament. (a) Coronal PDw fatsat image. Slight increase in distance between lunate and scaphoid as well as inability to demonstrate the membranous portion (arrow). (b) Axial PDw fatsat image. Discontinuity of the dorsal portion of the ligament (arrow). Whether the palmar ligament segment is still intact cannot be clearly elucidated.

Fig. 5.53 Scapholunate diastasis (rotational subluxation of the scaphoid) in association with a torn scapholunate ligament. (a) Conventional radiographic image. Unremarkable findings. (b) Radiographic image obtained on application of ulnar stress in patient after a “click” was felt. Distance of more than 2 mm between scaphoid and lunate (Terry Thomas sign) as well as ringlike structure in the distal scaphoid corresponding to projection of the waist over the palmarly titled scaphoid (“signet ring sign” scaphoid). (c) Coronal T1w SE image of a different patient. Increased distance between the scaphoid and lunate as well as signal increase and questionable disruption of the contour of the scapholunate ligament (arrow).

with palmar rotation of the lunate and axial displacement of the capitate in a palmar direction (PISI [palmar intercalated segment instability]) can be identified on MRI sagittal sections. An overview of the dislocations seen secondarily to ligament injuries is given in ▶ Table 5.2. These dislocations may be associated with fractures, resulting in numerous different types of combinations. If a dislocation is accompanied by a fracture, the term used to denote it begins with the prefix “trans,” followed by the name of the fractured bone, and then by the type of dislocation, for example, “trans scaphoid perilunate dislocation.” In addition, there are rare types of dislocation related to the mechanism of trauma. These findings are based

on radiographic images but can also be applied to the corresponding MRI images. On lateral images of healthy subjects, the lunate is normally angled 0 to 30 degrees relative to the longitudinal axis (radius–lunate–capitate–metacarpals). Normally, the scaphoid is angled 30 to 60 degrees relative to the longitudinal axis (see ▶ Fig. 5.20). It can generally be assumed that palmar or dorsal perilunate dislocations, palmar or dorsal midcarpal dislocations, and palmar or dorsal dislocations of the lunate are really different manifestations of the same perilunate injury. Axial images on which the radioulnar joint space appears narrowest are used when determining ulnar dislocation on the basis of the well-established CT criteria. The

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The Wrist and Fingers Table 5.2 Relatively common dislocation and instability of the wrist Dislocation/instability

Injury

Signs

I Scapholunate dissociation and scaphoid rotational subluxation

Scapholunate ligament Radioscaphoid ligament Palmar radiocapitate ligament

Scapholunate distance > 2 mm, provoked by ulnar stress (Terry Thomas sign) Ring structure of the scaphoid (signet ring sign) Palmar tilting of the scaphoid

II Perilunate dislocation

Radiocapitate ligament

Dorsal and proximal displacement of the capitate versus the lunate

III Midcarpal dislocation

Lunotriquetral ligament Radiotriquetral ligament Ulnotriquetral ligament

As II + lunate subluxation with slight tilting of the axis in palmar direction

IV Lunate dislocation Ulnar (sub)luxation

All lunate ligaments Triangular fibrocartilage complex (ulnar disk complex: radioulnar ligaments)

Palmar tilting of the lunate Triangular appearance of the lunate and disruption of the second (carpal) arch

DISI

Scapholunate ligament Palmar radioscapholunate ligament Pseudarthrosis of the scaphoid

Dorsal tilting by more than 30 degrees

PISI

Triquetrohamate ligament

Palmar tilting of the lunate by more than 30 degrees, often also dorsal tilting of the capitate by more than 30 degrees

Dislocations

measuring lines used are those connecting the palmar corner of the radial articular surfaces and the outer corner of the radius as well as the dorsal corner of the radial articular surfaces and outer dorsal corner. Normally, the ulna should not project beyond these lines by more than half a shaft width (see ▶ Fig. 5.25). Other methods of measurement have been described by Wechsler et al.74

5.10.3 Collateral and Annular Ligaments of Fingers The collateral ligaments, which are used to stabilize joints, and their injuries are well visualized on MRI. Pathologic criteria include thickening in association with spraining or scarred healing of a tear as well as partial or complete discontinuity of the damaged ligament (▶ Fig. 5.54). Joint subluxation/dislocation is a common sign of instability (▶ Fig. 5.55 and ▶ Fig. 5.56). The finger flexor tendon sheath is reinforced on the finger bones by a complex ligamentary apparatus which binds the tendons to the bone. The annular ligaments (ring pulleys) are part of this ligamentary apparatus and, depending on their localization, are designated from A1 pulley (at the level of the proximal interphalangeal joint) to A5 (at the level of the distal interphalangeal joint). Three further oblique ligament structures are known as the cruciate ligaments. An injury to the annular and cruciate ligaments (e.g., as sustained during ring or climbing sports accidents) can result in discrete pathologic increased distance between the bone and flexor tendon (▶ Fig. 5.57), often seen in the region of the proximal phalanx (A2 pulley; ▶ Fig. 5.58).

5.10.4 Triangular (Ulnar) Fibrocartilage Complex Pain in the region of the ulnar aspect of the proximal wrist can be caused by pathologic changes to the triangular disk and the

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surrounding capsuloligamentous apparatus, the TFCC (see Extrinsic Ligaments, p. 183), also referred to as the “ulnocarpal complex.” Based on the clinical symptoms, differential diagnosis of a torn disk includes injury to the lunotriquetral ligament, the extensor carpi ulnaris tendon, pisotriquetral joint, and the distal radioulnar joint. The triangular disk may be completely torn, thus allowing communication between the radiocarpal and distal radioulnar joint, or there may only be partial distal (radiocarpal) or proximal (undersurface of disk) tears. Chronic irritation and tears with infiltration of vascularized granulation tissue are seen during repair processes. Synovial irritation with synovial proliferation can also trigger secondary vascularization of the fibrocartilage complex. Negative ulnar variance gives rise to an anlage-mediated strong triangular disk; hence, negative ulnar variance largely preempts disk rupture. Conversely, positive ulnar variance frequently predisposes to defects and tears in the already developmentally very thin triangular disk. In later years, because of the relatively increasing ulnar length, this can cause ulnocarpal impaction syndrome affecting the lunate. Previously, arthrography was the only imaging modality for detecting pathologic changes and tears in the triangular disk. Following injection into the radiocarpal joint, the contrast agent penetrates into the distal radioulnar joint. There are disk tears that allow the contrast agent to spread only in one direction; therefore, if a negative result is obtained following radiocarpal injection, a second injection can be administered into the distal radioulnar joint to reliably detect a torn disk. On MRI, the triangular disk exhibits low signal intensity on all sequences. The signal intensity increases toward the ulna at the transition to the adjacent fibrous complex. In the presence of disk tears, areas of discrete high signal intensity are seen on T2w or STIR sequences. There are generally minor effusions in the distal radioulnar joint, thus attesting to the highly positive correlation between fluid detection in this joint and disk rupture. Secondary vascularization due to infiltration of synovial pannus or of

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Instability

5.11 Nerve Compression Syndrome

a

c

Fig. 5.54 Status post contusion trauma with tear of ulnar collateral ligament and the sagittal ligament. Discontinuity of the ulnar-sided collateral ligament as well as the capsular ligament structures of the third metacarpophalangeal joint (a, c, arrow). (a) Coronal T1w image. (b) Coronal PDw fatsat image. (c) Axial PDw fatsat image.

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Fig. 5.55 “Ski thumb.” Status post skiing accident. Thickening and discontinuity of the proximal third of the ulnar collateral ligament (a, arrow) as well as subluxation/dislocation. Collateral ligament injuries are common in ball sports injuries or skiing accidents (ski thumb: tear of the ulnar collateral ligament of metacarpophalangeal joint D1). (a) Coronal T1w image of the proximal metacarpophalangeal joint. (b) Coronal PDw fatsat image of the proximal metacarpophalangeal joint.

a

vascularized granulation tissue following stress-induced damage or degenerative chronic processes of the TFCC can be sensitively demonstrated on T1w images following intravenous administration of Gd-DTPA. Frequency-selective, fat-suppressed images are also useful here. Coronal native T2w GRE sequences are suitable for detection of disk tears. The majority of tears of the triangular disk occur secondarily to degenerative changes, with a triangular disk tear or defect identified already in some 8% of patients aged 30 to 40 years and in more than 50% of patients aged over 60 years. Since tears of the triangular disk are seen increasingly with advancing age and the majority of such tears are not clinically symptomatic, caution is needed when interpreting the MRI results while bearing in mind the patient’s medical history. Degenerative tears are mainly found at the center of the disk and tend to have a rounded shape (▶ Fig. 5.59). Secondary vascularization as seen in the wake of chronic degenerative damage appears to be positively correlated with the clinical complaints. Ulnar-sided tears are more difficult to detect on MRI compared with their radial-sided counterparts. Most acute traumatic tears of the disk occur in the radial-sided thin disk region, where the hyaline joint cartilage extends from the distal radius, and typically run vertically from surface to surface (▶ Fig. 5.60). Traumatic lesions are also seen in the region of the ulnar attachment. Apart from increased signal on T1w and T2w images, and in particular on fat-suppressed images, another sign of

a lesion is discrete fluid accumulation especially in the distal radioulnar joint as a sequela of the communication created between the radiocarpal recess and the distal radioulnar compartment. Based on the classification into degenerative and traumatic injuries of the ulnar fibrocartilage complex as well as on the concomitant and subsequent manifestations, Palmer classified the lesions into nine types and proposed various treatment concepts that are being increasingly implemented (▶ Table 5.3).49,50 When taking all diagnostic criteria into account, MRI is thought to have a sensitivity of over 90% at detecting disk lesions.83 However, other authors have not obtained such good results, something that depends essentially on the sequences, hardware, and magnetic field used.

5.11 Nerve Compression Syndrome 5.11.1 Carpal Tunnel The median nerve and finger flexor tendons (flexor digitorum profundus, flexor digitorum superficialis, and flexor pollicis longus) pass from the distal forearm to the palm of the hand through an anatomic tunnel. This tunnel is bordered dorsally by the carpal bones and palmarly by the flexor retinaculum, a broad fibrous

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Fig. 5.56 “Ski thumb.” Status post sports accident. Coronal T1w image of metacarpophalangeal D1. Discontinuity of the distal segment of the ulnar collateral ligament (arrow).

band. The median nerve is normally located palmarly to the flexor tendons, but there are developmental variants where the nerve lies within the dorsal aspect of the tunnel. Wrist flexion causes minor displacement and deformation, in particular flattening of the median nerve. Disorders involving compression of the median nerve within the carpal tunnel cause carpal tunnel syndrome, neuropathy with pain, paresthesia of the radial 2½ fingers, weakness, and possibly atrophy of the thenar muscles, in particular at night. This disorder typically affects patients aged 30 to 60 years and presents bilaterally in up to 50% of cases. Carpal tunnel syndrome may be caused by space-occupying lesions within the carpal tunnel, for example: ● Tumors. ● Ganglion cysts. ● Muscular hypertrophy. ● Rheumatoid arthritis. ● Excessive fatty deposits. ● Tendinitis. ● Peritendinitis. ● Amyloid deposits. ● Edema (pregnancy). ● Processes that constrict the carpal tunnel from the outside (e.g., in the presence of fractures or exuberant callus formation). Congenital anomalies such as a persistent thrombosed median artery or dystopia of the lumbrical muscles can also cause carpal tunnel syndrome. The median artery is a vascular variant with persistence of an embryonic forearm artery.60

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Fig. 5.58 Annular ligament injury. Axial T1w image of a patient who sustained sports injury a few weeks previously, with increasing pain at flexor aspect of index finger. The increased distance between the flexor tendon and the phalanx and discontinuity of the ulnar-sided annular ligament (arrow) are suggestive of a tear of the reinforcing ligaments of the flexor tendon. Reactive inflammation of the surrounding soft tissues with swelling and signal alteration.

Fig. 5.59 Central tear in triangular disk. Coronal PDw fatsat image. The arrowhead points to the tear.

Carpal tunnel syndrome diagnosis is normally based on clinical signs and electrophysiology measurements, such as measurement of nerve conduction speed, and electromyography. Since most cases of carpal tunnel syndrome are idiopathic, more in-depth diagnostic measures are needed only in clinically suspicious

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Fig. 5.57 Increased distance between the flexor tendon and proximal phalanx D3 following injury to annular ligament. Schematic diagram, axial plane. Results of adjacent index finger normal.

5.11 Nerve Compression Syndrome

Fig. 5.60 Radial-sided, vertical tear in triangular disk. Coronal PDw fatsat image. The arrowhead points to the tear.

T1w and T2w sequences as well as occasionally as signal reduction in the nerve on T1w and T2w images, probably due to fibrosis. Postoperative MRI shows discontinuity of the retinaculum as well as postsurgical susceptibility artefacts (▶ Fig. 5.62). In the event of persistent or recurrent symptoms of carpal tunnel syndrome following surgical repair, MRI will be able to directly identify potential causes such as incomplete incision of the retinaculum and postoperative scarring or neuromas.

5.11.2 Guyon’s Canal The ulnar nerve passes together with the ulnar artery from the distal forearm to the palm of the hand through an anatomic tunnel called Guyon’s canal (▶ Fig. 5.63). This canal extends from the pisiform as far as the hamulus of hamate and is bordered by the flexor retinaculum, abductor digiti minimi (hypothenar), pisiform, and the hamulus of hamate. The palmar border is formed by the palmar aponeurosis, which is reinforced proximally by the palmar carpal ligament (proximal hiatus) and distally by the palmaris brevis tendon as well as the connective tissue origin of the flexor digiti minimi brevis (distal hiatus). Constriction of the canal can cause ulnar nerve neuropathy, similar to carpal tunnel syndrome of the median nerve. Depending on the localization and extent of damage, the clinical symptoms manifested include paresthesia of the hypothenar portion of the hand and ring and little fingers and/or motor disorders of the muscles innervated by the ulnar nerve (▶ Fig. 5.64 and ▶ Fig. 5.65). There are numerous conditions that can cause narrowing of Guyon’s canal, of which some can be visualized on MRI, for example: ● Ganglion cysts (▶ Fig. 5.66). ● Tumors. ● External pressure, for example, cycling (in particular mountain biking), certain occupational activities. ● Aneurysms of the ulnar artery. ● Muscular anomalies. ● Thickening of the flexor carpi ulnaris tendons.

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cases. Conventional radiography and CT are able to detect any bone-related causes. MRI can directly visualize myriad soft tissue– and bone-related causes. For example, an increase in the volume of the carpal tunnel causes bulging of the flexor retinaculum, and this can be determined by measuring the distance between the flexor retinaculum and an imaginary line running between the hamulus of hamate and trapezium. Besides, changes can be detected in the nerve itself, manifesting as increased signal intensity on T2w images (▶ Fig. 5.61), as well as increased thickness. The rise in signal intensity is probably due to edema. Neural swelling is usually most pronounced at the level of the pisiform. Occasionally, nerve flattening is observed, especially at the level of the hamulus of hamate. In the late stages of chronic courses of disease, atrophy of the thenar muscles manifests as increased signal intensity on

Table 5.3 Classification of injuries of the ulnar triangular fibrocartilage complex according to Palmer50 Stage I (traumatic)

II (degenerative)

Lesions

Therapy

Ia

Central tear

Poor spontaneous healing: debridement

Ib

Ulnar-sided tear, often with avulsion of the ulnar styloid Good spontaneous healing, acute → immobilization or process and radioulnar instability due to torn radioulnar repositioning ligaments

Ic

Torn ulnocarpal ligaments

Debridement/ligament suture

Id

Disk avulsion from the radius, possibly with concomitant avulsion fracture

Debridement

IIa

Thinning disk but no tear

Debridement, possibly, ulnar shortening

IIb

IIa + chondromalacia

As IIa

IIc

Central, mainly oval-shaped tear

As IIa

IId

IIc + torn lunotriquetral ligament with secondary instability

Debridement, lunotriquetral arthrodesis

IIe

Ulnocarpal arthrosis

Ulnar head hemiresection, Kapandji–Sauvé operation, ulnar head prosthesis

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● ● ● ●

Dupuytren’s disease. Arthrosis of the pisotriquetral joint. Fractures of the hamulus of hamate or pisiform. Fractures of the metacarpal bases.

5.11.3 Bowling Thumb Damage sustained to the ulnar palmar nerve of the thumb during bowling can cause compression syndrome with thickening at the pressure site (ulnar aspect of thumb) and corresponding paresthesia and pain. While imaging is generally not indicated, MRI is able to demonstrate thickening of the ulnar-sided nerve with edema of the surrounding soft tissues.40

5.11.4 Wartenberg’s Syndrome Damage to the superficial branch of the radial nerve, for example, due to (de Quervain’s) tenovaginitis/tenosynovitis of the first extensor tendon compartment or also following puncture, causes paresthesia of the thumb. There have also been reports of more proximal damage to this nerve branch.34 Tenovaginitis or, in rare cases, space-occupying processes, can also be clearly identified on MRI as the cause of this damage.

Fig. 5.62 Status post carpal tunnel operation. Axial PDw fatsat image. Discontinuity of the flexor retinaculum (arrow), median nerve, susceptibility artefacts.

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2

5.12.1 Subungual Tumors A number of soft tissue tumors, which exhibit specific clinical symptoms and features on MRI, occur in the region of the fingertips beneath the nails (subungual region) (▶ Fig. 5.69).

Glomus Tumors Glomus tumors are benign hamartomas originating from glomus bodies in the human organism (from thermoregulatory connective tissue and arteriovenous tangled anastomoses enclosed in neural networks). Glomus bodies are found in all parts of the

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5.12 Tumors Tumors of the bone and soft tissues are discussed in Chapter 12.3. Only the tumor entities specific to the hand and wrist region are described here (▶ Table 5.4 and ▶ Table 5.5) while mentioning a number of special features (▶ Fig. 5.67 and ▶ Fig. 5.68). Because of their high incidence and unclear pathogenesis, ganglion cysts will be discussed separately in the next section.

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9 7 8

Fig. 5.63 Guyon’s canal. Schematic diagram of an axial section through the hand at the level of pisotriquetral joint illustrating the layout of Guyon’s canal. 1, flexor retinaculum; 2, Guyon’s canal; 3, palmar aponeurosis; 4, ulnar nerve; 5, abductor digiti minimi; 6, pisiform; 7, triquetrum; 8, capitate; 9, lunate; 10, scaphoid; 11, median nerve in carpal tunnel.

skin, in particular in the acral skin regions (fingertips, thenar and hypothenar eminences, sole of the foot, tip of the coccyx, nose, back of the tongue, and genital cavernous bodies). Accounting for 75% of all such tumors, the predilection site of glomus tumors is the hand, especially the subungual region (65%). The clinical symptoms include sudden attacks of severe pain (in particular

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Fig. 5.61 Carpal tunnel compression syndrome. Bulging of the flexor retinaculum (a, straight arrow) as well as increased signal intensity of the median nerve on both sequences (a, curved arrow). (a) Axial PDw SE image. (b) Axial T2w SE image.

5.12 Tumors when touched), cold sensitivity of the tumor region, sensitivity to pressure and shock as well as often bluish discoloration seen through the nails, and impaired nail growth. The extent of destruction seen at the tip of the distal phalanx varies greatly. Occasionally, a sharply marginated osteolytic structure can be observed on radiographs at the unguicular process. On MRI, the highly vascularized tumor exhibits low signal intensity on T1w and high signal intensity on T2w images, with strong CM enhancement (▶ Fig. 5.70).

Epidermal Cysts Epidermal cysts (synonyms: epithelial cysts, epidermis cysts, epithelioid cysts) are cystic space-occupying lesions found in

subcutaneous tissue or also in bone and arising from proliferation of skin cells (squamous epithelial cells). One possible explanation for their occurrence is the dislocation of epidermal cells through injuries and trauma (hence the term inclusion cyst). The cyst contains a paste made of protein, fat, and a keratinlike substance. This space-occupying lesion can present anywhere in the body, but predilection sites are the hands and feet, in particular the phalanges and subungual region. Clinical symptoms include pain, pressure sensitivity, and swelling. On radiographs, an erosion of variable size can be seen in the distal phalanx. On MRI, a cystoid structure, ranging from muscleisointense to slightly hyperintense, is observed on T1w and T2w images, as well as moderate marginal CM enhancement. Based on these signal properties, this tumor can generally be delineated from other tumors.

Other Tumors of the Subungual Regions

Type 4 Type 2 Pisiform

Deep branch (motor)

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Superficial branch (sensory)

Other tumors of the subungual region include1: ● Mucoid cysts. ● Exostoses. ● Soft tissue chondroma. ● Keratoacanthoma. ● Hemangioma. ● Squamous epithelioma. ● Malignant melanoma.

5.12.2 Giant Cell Tumors of the Tendon Sheath

Type 3

Type 1 Hamulus of hamate

Ulnar nerve

Fig. 5.64 Different forms of damage to ulnar nerve depending on localization. Schematic diagram. Type 1, sensory disruption and paresis of all intrinsic hand muscles innervated by the ulnar nerve; type 2, isolated paresis of all intrinsic hand muscles innervated by the ulnar nerve; type 3, isolated paresis of intrinsic hand muscles innervated by the ulnar nerve (apart from the abductor digiti minimi); type 4, isolated sensory disruption.

These synovial tumors are composed of histiocytes, giant cells, and xanthomatous cells (also called “xanthoma”). They constitute an entity that is histologically related to that seen in pigmented villonodular synovitis, with both conditions showing hemosiderin deposition which is crucial for detection on imaging. Nodular or more diffuse growth is observed in the region of the tendon sheaths, presenting initially without pain or impairment of tendon function. The flexor tendons are often implicated. MRI shows a localized or more multifocal to diffuse tumor in the region of the tendon sheath with low signal intensity on T1w images, and heterogeneous signal intensity ranging from high to muscle-isointense on T2w images, variable CM enhancement and characteristic areas of focal signal void due to hemosiderin

Fig. 5.65 Ganglion cyst at the exit from Guyon’s canal. Patient with weakness of the ulnar-sided fingers. Ganglion cyst on the ulnar-sided palm of hand (arrow). Finding consistent with type 3 lesion of ulnar nerve due to ganglion cyst at exit from Guyon’s canal. (a) Coronal PDw fatsat image. (b) Axial PDw fatsat image. a

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The Wrist and Fingers deposition (see ▶ Fig. 5.68).42 Bone erosions are present in 20% of cases (▶ Fig. 5.71).35

5.12.3 Rheumatoid Nodules Inflammatory pseudotumors (rheumatoid nodules) are seen in association with certain rheumatic diseases and manifest as tumors because of their focal nodular shape. They may

have a central area of necrosis. Rheumatoid nodules may be a precursor to a joint disorder and are found mainly in the subcutaneous fatty tissue of the dorsum of hand, but they can also affect bursae, joints, tendons, tendon sheaths, and ligaments.73 On MRI, a space-occupying lesion with low signal intensity is seen on T1w images and inhomogeneously high, and partially low, signal intensity is seen on T2w images, as well as often pronounced marginal enhancement on contrastenhanced images.

5.13 Ganglion Cysts and Other Cysts

Fig. 5.66 Ganglion cyst in Guyon’s canal. Axial T2w TSE image at the level of lunate, also showing the scaphoid and triquetrum (palmar = below). On the left (ulnar) side is an extremely hyperintense spaceoccupying lesion with displacement of the ulnar neurovascular bundle (arrow).

Ganglion cysts are gelatinous masses originating from ligamentous, osseous, or tendinous structures and occurring in proximity to joints. They can also be found within bones (▶ Fig. 5.72 and ▶ Fig. 5.73). They constitute the most common type of soft tissue mass found in the hand, of which two-thirds are observed in the dorsum of hand. The most common localization for intraosseous ganglion cysts is the lunate close to the scapholunate joint space. The most frequent site of origin for ganglion cysts in the wrist region is the scapholunate ligament and the radioscapholunate ligament. Ganglion cysts are a common disorder of the wrist region, giving rise to pressure-related complaints.

Table 5.4 Bone tumors of the hand and wrist, classified in terms of dignity and incidence (e.g., 37% of all enchondromas observed [90 out of 245] were in the hand and wrist region). The entire collection comprised 8000 tumors51 Dignity

Entity

Total number

Number and percentage in hand and wrist region

Benign

Enchondroma

245

90 (37%)

Giant cell tumor

425

63 (15%)

Osteoid osteoma

245

18 (7%)

Osteochondroma

727

28 (4%)

Aneurysmal bone cyst

134

6 (4%)

Osteoblastoma

63

2 (3%)

Chondromyxoid fibroma

39

1 (2.6%)

Hemangioma/lymphangioma

80

0

Chondroblastoma

79

0

Hemangioendothelioma

60

6 (10%)

Chondrosarcoma

634

14 (2.2%)

Periosteal osteosarcoma

56

1 (2%)

Osteosarcoma

1,274

13 (1%)

Ewing’s sarcoma

402

5 (1%)

Lymphoma

469

4 (0.9%)

Fibrosarcoma

207

1 (0.5%)

Metastases

3,000

2 (0.1%)

Myeloma

556

0

Malignant

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5.13.1 Ganglion Cysts

5.13 Ganglion Cysts and Other Cysts Table 5.5 Common soft tissue tumors of the hand and wrist and some of their features Features

Epidermoid

Often posttraumatic subcutaneous infiltration of dermal tissue into the distal phalanx, with painful swelling

Glomus tumor

Subungual, very painful space-occupying lesion of the neuromyoarterial glomus < 1 cm

Giant cell tumor of the tendon sheath

Relatively common, often on the flexor aspect, mainly painless; often manifests as low signal intensity on T1w and T2w contrast sequences due to hemosiderin deposition

Lipoma

Often large lobulated space-occupying lesion, often in thenar

Hemangioma, lymphangioma

Often diffuse extension; often with phleboliths; extremely hyperintense on T2w contrast images

Ganglion cyst

See section on “ganglion cysts and pure cysts” (Chapter 5.13)

Primary chondromatosis

Multiple, partially calcified, rice grain–like chondromas in tendon sheaths or joints

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Tumor

Fig. 5.67 Osteoid osteoma of the second metacarpal bone. (a) Coronal T1w SE sequence. Cortical thickening due to osteoid tumor (low signal to signal void on all sequences; arrow). (b) Coronal STIR sequence. (c) Axial contrast-enhanced sequence. Reactive bone marrow and edema of the surrounding soft tissues, tumor core (nidus) with CM uptake (arrow).

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Fig. 5.68 Giant cell tumor of the tendon sheath. A hypointense space-occupying lesion of the ring finger, directly adjacent to the flexor tendon sheath, which appears hypointense with CM uptake on T1w contrast sequences and manifests as an inhomogeneous structure on T2w contrast images. Giant cell tumors of the finger tendon sheath are the most common type of soft tissue tumor of the hand. They may contain more or less connective tissue and hemosiderin and accordingly often exhibit slightly high to low signal intensity on T2w images.10 (a) Coronal T1w SE sequence. (b) Coronal STIR sequence. (c) Axial contrast-enhanced sequence. Dorsal marking ball.

On MRI, ganglion cysts exhibit characteristic signal intensity, with low signal on T1w and particularly high signal intensity on T2w images. Often, septation manifests as lines of signal-void structures within the ganglion cyst (▶ Fig. 5.74). Furthermore, funnel-shaped tapering of the cyst can often be detected, consistent with a stem originating from the parent cyst (▶ Fig. 5.75). Depending on its localization and size, a ganglion cyst may be loculated and have a rounded, oval, or longitudinal shape.

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5.13.2 (Pure) Cysts Pure cysts containing serous fluid can be distinguished from ganglion cysts and, like the latter, may be intra- or extraosseous. They are thought to be of different pathomechanical etiology

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Fig. 5.69 Subungual space-occupying lesion. Schematic diagram. 1, matrix; 2, nail sinus; 3, subungual lesion; 4, nail bed; 5, fingertip; 6, nail bed (sterile matrix); 7, distal phalanx.

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5.14 Disorders of the Synovial Membranes Including Chronic Polyarthritis Fig. 5.70 Painful glomus tumor beneath thumb nail. Subungual tumor with high signal intensity on PDw fatsat image and strong CM enhancement. The thumb nail manifests as signal void (b, arrow). (a) Native axial T1w image. (b) CM-enhanced axial T1w image. (c) Oblique sagittal PDw fatsat image.

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c

from the ganglion cysts, that is, they are probably linked to synovial inclusions or synovial proliferation. Chronic synovitis (arthritic or arthrotic) can give rise to cystic ballooning of joint recesses (e.g., pisotriquetral recess). In most cases, it is not possible to distinguish between pure cysts and ganglion cysts on the basis of the clinical manifestations. Differentiation on MRI is also challenging since their signal intensities are identical, but detection of septation and a stalk tend to discount the presence of pure cysts. On magnetization transfer contrast images, ganglion cysts exhibit markedly lower signal intensity than pure cysts. Marginal contrast enhancement can be observed following CM administration, either through a pseudocapsule in the ganglion cyst or due to the presence of a wall in synovial cysts. On the whole, there is little clinical benefit in making a distinction between ganglion and pure cysts since the same treatment is used for their symptoms. Ganglion cysts and pure cysts can rupture, following which diffuse swelling, a change in signal intensity due to tissue irritation, and the leaked fluid can be demonstrated on MRI.19

5.14 Disorders of the Synovial Membranes Including Chronic Polyarthritis As in other joints, MRI is able to directly visualize proliferation of the synovial membranes based on their thickened appearance. There is now a rise in signal intensity on T2w images and strong CM uptake. On native images, it is often not possible to differentiate between an effusion and active pannus, but that difficulty can be circumvented through CM injection. Chronic scar/pannus tissue exhibits somewhat lower signal intensity on T2w images. Incipient bone erosions can also be well visualized on MRI. MRI is very sensitive at demonstrating erosions, tendinitis, and peritendinitis (▶ Fig. 5.76 and ▶ Fig. 5.77). Peritendinitis can be typically seen in association with psoriatic osteoarthropathy, but is also an early sign of chronic polyarthritis.45 Arthritic and synovial changes can be detected at an early stage on MRI. It has been

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Occasionally, the arthritic joint can exhibit pathologic CM enhancement even before onset of clinical symptoms. The MRI subtraction technique followed by maximum intensity projection (MIP) is very sensitive at detecting such CM enhancement (▶ Fig. 5.78).66 In one study on using this method, a positive diagnosis was made for 6 out of 26 patients with chronic polyarthritis at a much earlier stage than would have been possible on the basis of the ARA (American Rheumatism Association) criteria alone.66 The authors recommend incorporating this MRI modality into a decision-making tree when trying to diagnose unclear cases of rheumatic disease.

5.15 Disorders of Tendons Fig. 5.71 Giant cell tumor of tendon sheath. Tumor close to the extensor tendon sheath with erosion of the second metacarpal bone. (a) Coronal T1w and PDw image. (b) Axial PDw fatsat image.

Tendinitis and tenosynovitis of the wrist, distal forearm, and hand are a common disorder. Tendinitis and peritendinitis in these regions are caused by various types of overloading when engaging in athletic or occupational activities (including writing

b

Fig. 5.72 Intraosseous ganglion cyst. Atypical wrist pain. Cystic space-occupying lesion in the region of the scapholunate joint space with intraosseous component (b, arrow). Edema of the surrounding bone marrow of lunate. (a) Coronal T1w image. (b) Coronal PDw fatsat image.

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possible over time to differentiate between these changes, and they have been classified by Scheck et al58 into the following stages: ● Stage 0: Normal joint, no inflammatory changes. ● Stage I: Synovitis but no signs of intra-articular space-occupying soft tissue pannus, no cartilage or bone destruction (exudative proliferative stage). ● Stage II: Stage I + intra-articular pannus lesion with or without indirect signs of cartilage involvement, no bone changes. ● Stage III: Stage I or II + bone lesion (at most one discrete area of fat signal loss and signal increase on T2w or STIR sequence (early destruction stage). ● Stage IV: Stage I and II, in addition several areas of discrete pannus tissue infiltration into bone (marked destruction stage). ● Stage V: Over 50% of articulating joint destroyed (mutilation stage).

5.15 Disorders of Tendons or typing), but these conditions may also be of rheumatic or traumatic etiology. Wrist fractures can also cause tendinitis and peritendinitis (▶ Fig. 5.79). Apart from stress-related pain, there is generally focal, longitudinal, or more diffuse swelling. A characteristic finding is pain radiating into the proximal forearm or also in a distal direction, in particular when loading against resistance. In chronic courses of disease, especially rheumatic processes, there is involvement of the adjacent bones with erosions visible on radiographs (e.g., ulnar styloid process in tendinitis of the sixth extensor tendon compartment). MRI can be used to distinguish this disorder from tumors and for diagnosis in unclear clinical situations through detection of the characteristic signs. In the majority of cases, the unenhanced images alone are able to

provide reliable signs. Tenosynovitis results in increased signal intensity, and tendon thickening is mainly seen additionally (▶ Fig. 5.80). In longer courses of disease or tendinitis of traumatic onset, there are often signs of a partial tear with partial discontinuity of the tendon or with central splitting and a central area of focal increased signal intensity. On PDw fatsat images, tenosynovitis exhibits a ring-shaped peritendinous increase in signal intensity of variable thickness (with corresponding low signal intensity on T1w images). In particular, in peritendinitis of rheumatic etiology, very large tendon sheath effusions with focal reduced signal due to synovial proliferations and villi are seen. There are certain predilection sites with a high incidence of tendinitis and tenosynovitis; these are discussed in the following.

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Inflammation of the tendons of the abductor pollicis longus and extensor pollicis brevis (known as the first extensor tendon compartment) at the level of the radial styloid process is a commonly observed form of tenosynovitis (de Quervain’s tenovaginitis stenosans; ▶ Fig. 5.81 and ▶ Fig. 5.82). Chronic courses with stenosis are common.

5.15.2 The Dorsoradial Wrist The extensor pollicis longus tendon courses from the third extensor tendon compartment to the thumb. In doing so, it crosses the second extensor tendon compartment distal to a bony prominence on the distal radius (dorsal radial [Lister’s] tubercle). This intersection is a predilection site of tendinitis and peritendinitis, hence the term distal (second) intersection syndrome.51

5.15.3 Distal Dorsoradial Forearm

Fig. 5.73 Intraosseous ganglion cyst in lunate. Cystic defect in radialsided lunate with marginal sclerosis.

On the distal forearm, around 5 cm proximal to the dorsal radial tubercle, the tendons and myotendinous junctions of the extensor pollicis brevis and abductor pollicis longus of the first extensor compartment intersect with the tendons of the second extensor compartment. This region is prone to stress leading to tendinitis and peritendinitis, probably due to increased repetitive friction stress intersection syndrome, also known as Oarsman’s wrist or forearm). Examples of the types of stress giving rise to this clinical picture include canoeing, weightlifting, or agricultural activities.31

b

Fig. 5.74 Radial volar septate wrist ganglion cyst. The arrowheads in (b) and (c) point to the ganglion cyst. (a) Coronal T1w image. (b) Coronal PDw fatsat image. (c) Axial PDw fatsat image.

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b

c

Fig. 5.75 Ganglion cyst on dorsum of hand. Large multiloculated ganglion cyst (a, black arrows) on dorsum of hand and stalklike spur in the direction of the scapholunate ligament (b, arrow). The blood vessels mainly exhibit a central area of reduced signal intensity because of obliteration of flow due to laminar flow (a, white arrow). Marking ball on dorsum of hand. (a) Axial PDw fatsat image. (b) Sagittal PDw fatsat image. (c) Coronal PDw fatsat image.

5.15.4 The Ulnar Wrist Inflammatory processes of the flexor or extensor carpi ulnaris tendon are also commonly observed (▶ Fig. 5.83). Overloading at the attachment site of the flexor carpi ulnaris tendon on the pisiform can cause pain of the pisiform and, because of irritation of the ulnar nerve, paresthesia of the ring and little finger. Occasionally, calcification of the pisiform is seen on radiographs or CT. On MRI, edematous, inflammatory thickening can be identified at the tendon attachment site (enthesopathy) to the pisiform.

5.15.5 Flexor Tendons The flexor tendons commonly affected include the flexor carpi ulnaris and flexor carpi radialis tendons. Tenosynovitis in association with psoriasis can affect one branch, with peritendinitis as well as inflammatory swelling of the remaining soft tissues (▶ Fig. 5.84). Increased CM uptake is exhibited by reactive inflammatory tissue.

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A specific type of chronic tenosynovitis, often seen along the course of the flexor tendons of the fingers, can lead to stenosis of the tendon sheath with impaired gliding capacity. Sometimes, only jerky finger movement is possible (trigger and snapping finger— tenovaginitis stenosans, annular ligament stenosis; ▶ Fig. 5.85). The predilection site is at the level of the first pulley (A1). Tendon tears occur mainly secondarily to injury. Retraction of the proximal tendon stump in a more proximal direction is seen in longstanding tears (▶ Fig. 5.86). MRI is adept at visualizing tendon tears.

5.16 Palmar Fibromatosis (Dupuytren’s Disease) Slowly progressing fibrosis, later accompanied by nodular thickening of the palmar aponeurosis and/or of the subcutaneous fatty tissue, causes increasing flexion contracture mainly along the course of the middle, little, and ring fingers due to shrinkage. This

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5.18 Pitfalls in Interpreting Images

Fig. 5.76 Chronic polyarthritis. (a) Coronal T1w SE sequence. Numerous erosions (dashed arrows) as well as tendinitis of the flexor carpi ulnaris with erosion of the ulnar styloid process (arrow). (b) Contrast-enhanced sequence. CM uptake by inflammatory pannus tissue (arrow).

condition, known as Dupuytren’s disease, often manifests bilaterally. MRI initially shows increased signal intensity on PDw fatsat images, later followed by demonstration of the pain-free subcutaneous nodules as focal or confluent, multi-stranded space-occupying lesions arranged parallel to the flexor tendon. These lesions exhibit signal of varying intensity depending on their connective tissue content. Variations are also seen in CM uptake in line with cellular composition, ranging from slight to strong enhancement.73 This disorder can manifest concomitantly with other diseases of the connective tissues such as Ledderhose’s disease of the plantar aponeurosis (see Chapter 8.7). In this regard, there have also been reports of nodular indurations over the dorsal aspect of the dorsal interphalangeal joints (“knuckle pads”) and induratio penis plastica, also as a hereditary disease (hereditary polyfibromatosis).

5.17 Examples of Vascular Diseases Repetitive (“hammering”) pressure on the hypothenar in the region of the hamulus of hamate (in occupational or athletic settings or following injury) can cause damage to the ulnar artery with stenosis, occlusion, and/or aneurysm formation (hypothenar hammer syndrome). The clinical picture includes pain, Raynaud’s

phenomena, numbness, ischemia of the ring and little fingers, and pressure-sensitive swelling of the hypothenar. On MRI or MR arthrography, damage to the ulnar artery manifests as thickening, aneurysms, and/or segmental occlusion with or without collateral circuits (▶ Fig. 5.87).6 Hemangiomas ( p. 549 ) and lymphangiomas ( p. 558 ) are commonly found in the region of the hand.

5.18 Pitfalls in Interpreting Images 5.18.1 Incorrect Positioning of the Wrist Incorrect positioning of the wrist can result in mimicking of subluxations and instability. Radial abduction and/or palmar flexion can masquerade as palmar rotation dislocation of the scaphoid. If the wrist is imaged in hyperflexion, the lumbrical muscles in the carpal tunnel can also simulate a tumorous space-occupying lesion. Ulnar abduction of the wrist causes dorsal tilting of the lunate axis, and this should not be mistaken for dorsal instability. It should be possible to distinguish between instability and malpositioning on the basis of the relative position of the lunate versus the capitate: if the wrist is incorrectly positioned toward the ulna, this will lead to palmar displacement of the lunate, but the latter is not seen in cases of instability. Pronation causes slight dorsal displacement of the ulna versus

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Fig. 5.77 Rheumatoid arthritis. Coronal PDw fatsat images. (a) Multifocal bone marrow edema, asymmetrical erosion, erosions of the wrist, and the second and third metacarpophalangeal joints as a sign of polyarthritis. (b) Massive peritendinitis (arrow).

Fig. 5.78 Suspected chronic polyarthritis. MRI with subtraction technique and MIP performed to rule out hand involvement following unclear clinical findings. Both hands placed in head coil (prone position). The hand blood vessels can be well evaluated. No evidence of articular hyperemia. Chronic polyarthritis of the hand can be rule out. (a) Coronal T1w sequence before CM injection. (b) Subtraction images (native series minus contrast-enhanced series), shown as coronal MIP.

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5.18 Pitfalls in Interpreting Images Fig. 5.79 Status post distal radial fracture and tear of the articular disk. Trauma 5 days previously. (a) Coronal PDw fatsat image. (b) Axial PDw fatsat image. Posttraumatic tendinitis and peritendinitis of tendon of the pollicis longus in third extensor tendon compartment (arrow).

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b

Fig. 5.80 Tenovaginitis of the flexor tendon. Marked thickening and increased signal intensity of the tendon sheath, enclosing a largely normal tendon. (a) Coronal STIR sequence. (b) Axial STIR sequence. (c) Axial STIR sequence, of other region.

the radius, while supination leads to slight palmar displacement. These normal positional changes should not be mistaken for ulnar subluxation.

median nerve. In rare cases, this variant can be the cause of carpal tunnel syndrome.

5.18.2 Vascular Variants

5.18.3 Accessory Muscles and Muscles of Variant Locations

Vascular variants such as a persistent median artery can also lead to diagnostic pitfalls. In the latter case, a variant vessel is seen inside the carpal tunnel beside a proximally divided duplicated

These muscles can mimic tumors and cause compression syndrome of the median or ulnar nerves. The following variants have been described:

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b

Fig. 5.81 de Quervain’s tendinitis and peritendinitis. Painful swelling at the level of the radial styloid process, radiating into the forearm. Marked thickening and increased signal intensity of the tendons of the first extensor tendon compartment (a, b, arrows) as well as inflammation of the surrounding soft tissues secondary to de Quervain’s tendinitis and peritendinitis. (a) Coronal T1w image. (b) Axial PDw fatsat image. (c) Coronal PDw fatsat image. Additional findings: vertical tear in articular disk (arrow).

● ●

●

●

●

Variable development and insertion of the lumbrical muscles. Accessory radial and palmar abductor digiti minimi of the pisiform. Dorsal extensor digitorum brevis manus of the second and third metacarpals. Prominent belly of the flexor digitorum superficialis in the carpal tunnel. Variants of the palmaris longus, for example, palmar to Guyon’s canal.

Muscle variants can be detected on the basis of their muscle-isointense signals on MRI (▶ Fig. 5.88).

5.18.4 Chemical Shift Artefact Visualization of the thickness of the hyaline joint cartilage may vary in accordance with the frequency-encoding direction because of chemical shift artefacts. This is seen in particular in the case of the interosseous joint space between the lunate and scaphoid and triquetrum as well as the radio- and midcarpal joint. It may be necessary to change the direction of frequency encoding and select sequences with a greater bandwidth.

5.18.5 Magic Angle Phenomenon An artificial increase in the signal intensity of tendons depending on how they are positioned in respect of the magnetic field has

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5.18 Pitfalls in Interpreting Images been reported for sequences with short TE (T1w and PDw) and is known as the “magic angle phenomenon” (see Chapter 16.2.1).

●

●

5.18.6 Bone Variants The following bone variants can also lead to diagnostic pitfalls on MRI10: ● Fusion (often lunotriquetral). ● Accessory bones.

● ●

Absent or incomplete fusion of ossification centers (in particular of the scaphoid, capitate, and hamulus of hamate). Dysplasia. Aplasia. Bone islands.

Where there is failure of fusion of ossification centers, it may be difficult to distinguish such variants from fractures. In the case of a fracture, MRI is generally able to identify the concomitant fracture edema, and where there is division it demonstrates the intact cartilage layer and/or the intact amphiarthrosis and synchondrosis between the ossification centers. In fusions, bridging with fatty bone marrow can be detected.

5.18.7 Carpe Bossu

Fig. 5.82 Peritendinitis. The patient had reported swelling and pain, of several months’ duration, over the ulnar styloid process. The radiograph shows erosion of the ulnar styloid process (arrow) as well as soft tissue swelling.

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Situated on the radial-sided base of the third metacarpal is a more or less well-developed process (styloid process) which projects into the gap between the base of the second metacarpal, trapezoid, and capitate.59 The term carpe bossu is used to designate this entity if there is a visible projection, which may or not be painful; ▶ Fig. 5.89). If this process is very well developed, it can be palpated through the skin and can cause painful swelling. If the process is not fused with the base of the metacarpal bone, an accessory bone element can manifest at this site. There may be inflammatory swelling of the adjacent tissues and focal arthrosis. This condition was first described by the French physician J. Foille in 1931 who coined the term carpe bossu (from the French word bossu = hunchbacked). The terms carpal boss or carpal bossing73 are also used. Soft tissue swelling and possibly arthrosis at characteristic sites can be detected on MRI.

5.18.8 Dorsal and Palmar Entry Points for Nutrient Vessels in the Carpal Bones These entry points vary and can be identified on conventional radiographs as radiolucent structures of different sizes and

b

Fig. 5.83 Massive tendinitis and peritendinitis of the extensor carpi ulnaris tendon. Axial PDw fatsat images. Rheumatoid arthritis patient. (a) There is a central area of discontinuity due to partial tear (stage II; arrow). (b) Massive bulging of the tendon sheath because of synovial proliferation (arrow).

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Fig. 5.85 Stenosing tenovaginitis of the finger tendon sheaths at the level of pulley A2. “Trigger finger.” Schematic diagram.

surrounded by sclerosis.10,59 On MRI, they manifest at different locations as small foci of a few millimeters in diameter which are hypointense on T1w images and hyperintense on T2w contrast and, in particular, on GRE and fat-suppressed images. These nutrient channels should not be mistaken for bone cysts, for example, as seen in incipient avascular necrosis of the lunate (▶ Fig. 5.90).71,72

5.18.9 Flexor Tendon Sheaths of the Wrist and Hand The anlage of the flexor tendons is highly variable (▶ Fig. 5.91). Accordingly, there is broad interindividual variability in the magnitude of increase in signal intensity exhibited by patients with tenosynovitis and peritendinitis on T2w images.

5.19 Clinical Relevance of Magnetic Resonance Imaging Clinical Interview

●i

Clinical interview with Dr. Martin Richter, Medical Director of Hand Surgery, Malteser Krankenhaus, Bonn: Question: “What do you think is the role of MRI in the everyday routine practices of a hand surgeon? For which clinical manifestations do you see the greatest advantages?

226

Answer: “MRI has greatly expanded the diagnostic horizons also in hand surgery. What is crucial for the validity of the conclusions drawn from MRI findings, too, is the quality of the images, which is essentially determined by the equipment used, for example, hand coils, and the experience of the physician interpreting such images. On MRI, we are able to visualize just about all anatomic structures more or less well. But that should not result in the uncritical application of that modality, since not all changes are best diagnosed or followed up on MRI. One important advantage of MRI is its ability to diagnose circulatory disorders in the region of the carpal bones. Previously, it was not possible to diagnose or follow up early-stage avascular necrosis of the lunate. Nor was it possible hitherto to evaluate the proximal scaphoid pole in the presence of scaphoid pseudarthrosis in cases with a small proximal fragment or recurrent pseudarthrosis. MRI supported by CM administration has expanded the diagnostic spectrum here and is of clinical relevance for treatment and prognosis, making it indispensable for modern-day treatment of such diseases. MRI also confers major advantages for assessment of soft tissue tumors. Here, too, this imagining modality should not be deployed in an uncritical manner for each and every soft tissue tumor (clinically straightforward ganglion cyst or discrete giant cell tumor). For larger tumors, such as hemangiomas, lymphangiomas, and more deep-seated tumors, for example, intramuscular, or where there is suspected malignancy, MRI bestows a diagnostic advantage since it is generally good at showing the extent, infiltration, or involvement of blood vessels and nerves. That has important implications for the type of technique used (incision biopsy or complete resection?) as well as for the surgical procedure strategy (what must be resected, how can the tumor be resected, and what structures may have to be reconstructed?). MRI is the only imaging modality able to visualize the TFCC or the ulnocarpal disk. But that ability does not imply that it has no limitations. With a sensitivity of 0.75 and a specificity of 0.81, a positive result is not proof of a torn disk, nor does a negative result necessarily rule this out. In everyday routine practice, outside study settings, the results obtained appear to be markedly worse [Note by the authors20]. It is therefore important to always take into account the findings of clinical examination to ensure that MRI of the wrist is not viewed as a conditio sine qua non for wrist arthroscopy in highly suspicious clinical cases. However, in unclear cases MRI can be used as an additional component for evaluation and treatment of TFCC.”

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Fig. 5.84 Tendinitis, peritendinitis, and cellulitis of the thumb in a patient suffering from psoriasis. “Sausage finger.” Fluid-isointense bulging of the tendon sheath. Increased signal intensity of the flexor tendon on T2w contrast images; there is also fluid-isointense bulging of other soft tissues. (a) Sagittal STIR sequence. (b) Axial T2w TSE sequence.

5.19 Clinical Relevance of Magnetic Resonance Imaging

a

c

d

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b

e

Fig. 5.86 Status post recurrent tear of the flexor pollicis longus tendon. Axial T1w images at various levels. (a) Distal phalanx level. The flexor tendon can be identified (arrow). (b) Proximal phalanx level. Die flexor tendon is not demonstrated. (c) Metacarpus level. The tendon is not demonstrated (arrow). (d) Wrist level. Massively thickened (retracted) tendon stump (arrow). (e) Distal forearm level. Retracted tendon stump at the myotendinous junction with layered pattern (arrow).

b

Fig. 5.87 Hypothenar hammer syndrome. Pain in hypothenar region. Repetitive occupational stress in this region reported in the patient’s medical history. (a) MR arthrography. Segmental occlusion of ulnar artery (arrow) and also damage to overlying vein. (b) Axial T1w image. Hyperintense thickening (arrow) along the vessels, consistent with thrombosed vessel.

a

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*

c

Fig. 5.88 Suspected space-occupying lesion of wrist. The examination involved placement of a marking ball on the swollen region (asterisk). Muscle-isointense swelling can be seen on all sequences, which proved to be a distal variant segment of the flexor carpi ulnaris (a, c, arrow). (a) Axial T1w image. (b) Axial PDw fatsat image. (c) Coronal STIR image.

Fig. 5.89 Carpe bossu. Schematic diagram of the hand skeleton, dorsal view. Pronounced styloid process at the radial base the fifth metacarpal bone (arrow).

228

Question: “For which clinical manifestations are false-positive MRI results most commonly encountered?” Answer: “Smaller fluid collections in the region of the wrist are often diagnosed as small ganglion cysts even when there are actually no ganglion cysts or corresponding symptoms. The same applies for orthograde sections of vessels imaged in proximity to joints. Degenerative changes in the TFCC are often diagnosed as tears but cannot be identified as such on arthroscopy (see the previous answer for sensitivity and specificity). Tears of the ulnar collateral ligament of the thumb diagnosed on MRI often turn out to be only partial injury or capsular damage, and assuming that the stability is preserved, these could already be ruled out on clinical examination and hence there is no need for surgical repair.” Question: “For which disorders do you encounter false-negative MRI results most often and why were diagnostic measures continued in such cases?”

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a

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5.19 Clinical Relevance of Magnetic Resonance Imaging

Fig. 5.90 Nutrient channels in the wrist. (a) Schematic diagram of frequent locations of “cystoid” lesions representing nutrient channels in the wrist. (b) Coronal T1w SE image. Several nutrient channels can be identified as hypointense dots. (c) The nutrient channels exhibit high signal intensity on T2w image (coronal GRE image). (d) Coronal 3D GRE image of a different patient. A relatively large area of focal hyperintensity, consistent with a nutrient channel, can be detected. (e) Macerated lunate. Broad variability of the vascular nutrient channels is demonstrated.

Fig. 5.91 Flexor tendon sheaths of hand. Schematic diagram. Examples of common developmental variants as well as communication of the flexor tendon sheaths of the hand. Accordingly, there is broad interindividual variability in fluid distribution seen in association with tenosynovitis on T2w MR image.

Answer: “Like false-positive results, false-negative results are also obtained for the TFCC. If the ends of the triangular disk are closely juxtaposed or if the slice thickness or imaging section does not

include the entire tear, the MRI findings will be normal despite the tear.” Question: “For which clinical manifestations can MRI be omitted and for which is the modality overly used?” Answer: “In routine practices, one notices that MRI is used as the primary diagnostic modality for the following clinical manifestations: MRI is not needed for the classic hand surgery clinical manifestations of an arthrotic nature, such as rhizarthrosis or SLAC or SNAC wrist. Diagnosis, including of severity, and treatment can be made using only properly produced radiographs. In general, a diagnosis of de Quervain’s tenovaginitis stenosans can be made through clinical examination with a positive Finkelstein test, and MRI is not needed for diagnosis of unclear wrist pain. Likewise, a scapholunate ligament tear should first be investigated on the basis of stress test radiographs and in unclear cases with radio cinematography. Fluoroscopy-guided motion analysis is best at investigating questions related to intercarpal ligament tears or midcarpal instability.

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For diagnosis of an unclear scaphoid fracture, I prefer CT of the scaphoid axis since on such images I am best able to detect the fracture type, extent of dislocation, and any debris zones. That is important for decision making and planning. If an ulnar collateral ligament tear is suspected, MRI can be dispensed with. In general, X-rays to rule out a fracture and clinical stability testing, possibly under local anesthesia, are often enough for diagnosis. The radiographs or sonography images obtained during a stress test help to measure the degree of instability (extent of opening on lateral view).”

wrist: indirect MR arthrography versus unenhanced MR imaging. Radiology. 2003; 227(3):701–707 [22] Herold T, Lenhart M, Held P, et al. Indirekte MR-Arthrographie des Handgelenks bei TFCC Läsionen. Fortschr Röntgenstr. 2001; 173(11):1006–1011 [23] Hofmann-Preiss K, Grebmeier J, Reichler B, Flügel M, Lenz G. A comparison of arthrography and magnetic resonance tomography in painful limited movements of the hand [in German]. Radiologe. 1990; 30(8):380–384 [24] Hooper G. Kienböck’s disease. J Hand Surg [Br]. 1992; 17(1):3–4 [25] Horcajadas AB, Lafuente JL, de la Cruz Burgos R, et al. Ultrasound and MR findings in tumor and tumor-like lesions of the fingers. Eur Radiol. 2003; 13 (4):672–685 [26] Imaeda T, Nakamura R, Miura T, Makino N. Magnetic resonance imaging in Kienböck’s disease. J Hand Surg [Br]. 1992; 17(1):12–19 [27] Imaeda T, Nakamura R, Shionoya K, Makino N. Ulnar impaction syndrome: MR imaging findings. Radiology. 1996; 201(2):495–500

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6.1

Introduction

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6.2

Examination Technique

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The Hip and Pelvis

6.3

Anatomy

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6.4

Avascular Necrosis of the Femoral Head

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6.5

Transient Osteoporosis

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6.6

Perthes’ Disease

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6.7

Slipped Capital Femoral Epiphysis

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6.8

Hip Dysplasia

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6.9

Trauma, Stress, and Fatigue Fractures

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6.10

Impingement

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6.11

Lesions of the Acetabular Labrum

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6.12

Degenerative Ligamentum Teres of the Femoral Head

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6.13

Early-Onset Osteoarthritis and Arthrosis

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6.14

Inflammatory Diseases

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Diseases of the Capsule and Synovial Membranes

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6.16

Amyloid Arthropathy

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6.17

Insertional Tendinopathy (Enthesopathy) 267

6.18

Snapping Hip (Coxa Saltans)

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6.19

Neurovascular Compression Syndrome

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6.20

Tumors

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6.21

Pigmented Villonodular Synovitis

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6.22

Pitfalls in Interpreting the Images

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6.23

Clinical Relevance of Magnetic Resonance Imaging 276 References

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Chapter 6

The Hip and Pelvis

6 The Hip and Pelvis 6.1 Introduction Magnetic resonance imaging (MRI) is a well-established modality for imaging the pelvis and, in particular, the hip. It is especially suitable for demonstration of incipient inflammatory and degenerative changes since it can detect pathologic lesions at an earlier stage than, for example, conventional radiography. Thanks to the ongoing advances in MRI technology, differentiated visualization of even small anatomic structures is now possible. For the musculoskeletal system, these developments have translated into improved spatial resolution and shorter imaging times. Today, MRI is often used early on, possibly with intra-articular contrast media (CM) injection, if the radiographic findings are inconclusive or symptoms persist and cannot be explained by the radiographic results. As is the case for all other regions of the body, an MRI indication for exploring disorders of the bony pelvis and hips should be based on a meticulous examination technique and an understanding of the correlation between the patient’s medical history and imaging results.37

Internet Links and Internet Research

●i

Information on the topic of the “hip and pelvis” can be found on the homepages of the American Academy of Orthopedic Surgeons (AAOS), the Association Recherche Circulation Osseous (ARCO), and the Musculoskeletal Radiology Working Group of the German Society of Radiology.

6.2 Examination Technique 6.2.1 Patient Positioning The patient is examined supine with the hips in a neutral position. External rotation should be avoided to assure as far as possible standard positioning. Supporting pillows can be placed beneath the patient’s legs and knees for greater comfort.

6.2.2 Coil Selection Planning and overview images of the entire pelvis are acquired with body or phased-array coils (e.g., “cardiac,” “body array” coils). Then the side of the body to be imaged is shown in high resolution. To that effect, for example, a surface ring coil, combination of several surface coils, or the phased-array coil already used for the overview images can be selected.

of view that includes both hips. Comparison of the two sides of the body on these overview images helps increase the diagnostic certainty as well as, in cases of avascular necrosis of the femoral head, confirm or rule out involvement of the contralateral side. Next, to get a high-resolution image of the affected hip, an oblique coronal image is obtained parallel to the femoral neck (▶ Fig. 6.1), with a STIR or PDw fatsat and a T1w TSE sequence. For certain diagnostic explorations, it may also be beneficial to obtain oblique sagittal and axial images perpendicular to the axis of the femoral neck. For good soft tissue contrast for the PDw fatsat sequences, an echo time (TE) of 28 ms is recommended for 1.5 T and 34 ms for 3 T.39 Oblique coronal plane sections allow optimum demonstration of the superior labrum, suprafoveal femoral cartilage, and cartilage superior to the lateral acetabular dome (roof). It also enables examination of the hip adductors, short external rotators, attachment site of the iliopsoas, and the origins of the hip abductors and the iliofemoral ligament. The sagittal plane is especially suitable for imaging the anterior labrum and the femoral joint cartilage. The axial plane is particularly suitable for demonstrating the anterior and posterior acetabular cartilage as well as the anterior and posterior labrum. This plane also allows good visualization of the iliopsoas tendon, including the bursa, as well as of the femoral and sciatic nerves.

Special Sequences To mitigate partial-volume effects when evaluating the acetabular labrum, some authors recommend incorporating a batch of sequential radial sections as a special additional sequence, for example, in combination with MR arthrography. First of all, a planning image is generated, with parallel intersection of the acetabulum or acetabular opening (en face image). As the acetabulum is spatially tilted in two planes, an oblique axial image and an oblique coronal image are needed (▶ Fig. 6.2). These images are then used to plan the batch of sequential radial sections, with the sections rotating around a central intersection point.90 The labral portions to be evaluated can be designated using the clockface system (▶ Fig. 6.3). On using radial image acquisition, an area of low signal is generated at the center of each image (“cross talk”); this permits only limited assessment. No consensus has been reached on whether this imaging plane improves sensitivity for detection of labral tears.127

6.2.3 Sequences and Parameters Routine Sequences To gain an overview, imaging starts with a coronal T1-weighted (T1w), short-tau inversion recovery (STIR), or proton density– weighted (PDw) fatsat sequence and an axial T2-weighted (T2w) turbo spin-echo (TSE) sequence using a 512 matrix and large field

234

Fig. 6.1 Imaging planes of the hip. Schematic diagram. A, coronal section; B, oblique coronal section parallel to axis of the femoral neck; C, oblique sagittal section perpendicular to B.

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M. Notohamiprodjo and M. Vahlensieck

6.2 Examination Technique

3 o’clock position

Axial planning image

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Coronal planning image

9 o’clock position 4 o’clock position

En face image

Radial images

12 o’clock position

11 o’clock position

6 o’clock position Fig. 6.2 “Radial” MRI of the hip. To acquire “radial” MR images of the hip, first an en face image (view from above of the acetabulum [“bird beak image”]) is generated with double angulation on the coronal and axial images planned parallel to the acetabulum (lines). From the resultant image, a batch of sequential radial images is then planned. Next, using the clock-face system, the labral portion can be evaluated from the images thus generated.

Direct and indirect MR arthrography (see Chapter 1.8) is better at evaluating the acetabular labrum, joint capsule, and the internal joint structures128,130: ● Direct MR arthrography has the advantage of distending the capsule in patients who have no joint effusion, thus increasing the detection rate for labral tears. ● Indirect MR arthrography, by contrast, is easier to perform and improves assessment of periarticular concomitant reactions.

Of importance for MR arthrography is the use of fat-suppressed sequences (see ▶ Fig. 6.45 and ▶ Fig. 6.47). Ideally, oblique coronal, oblique sagittal, and especially also oblique axial sequences should be used (oriented along the femoral neck, in particular for assessment of the femoral neck thickness in impingement syndrome). Applying traction to the leg will help to slightly open the joint space and facilitate evaluation.87 Pain reduction or resolution following additional analgesic injection can be interpreted as an important clinical test.47

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The Hip and Pelvis

1 2

Fig. 6.3 The “acetabular clock face.” Schematic view from above of the acetabulum. The various segments of the acetabular labrum and transverse acetabular ligament can be designated using the clockface system. 1, semilunar cartilage; 2, acetabular labrum; 3, acetabular fossa with fat pad; 4, transverse acetabular ligament.

12 o’clock position

9 o’clock position

3 o’clock position

3 4

a

b

Fig. 6.4 Status post total hip replacement. Pain in the right hip following total hip replacement. Periarticular fluid collection with thickened, CMenhanced capsule (a, arrow), consistent with an abscess. Relatively few implant-related artefacts on using prosthetic sequences. (a) Axial CM sequence. (b) Subtraction image.

MRI can also be used for patients with prosthetic hip implants (see Chapter 1.21). However, certain technical requirements must be met to minimize artefacts. It is also suitable for evaluation of the surrounding soft tissues, any muscular atrophy, granulomas, synovitis, etc. (▶ Fig. 6.4 and ▶ Fig. 6.5).

6.3 Anatomy The pelvis has to transmit the weight of the body to both feet and at the same time allow a large range of motion of the hips. The sacroiliac joint and the symphysis pubis are capable only of minimal movement. The hip bone (coxal bone) is formed by the ilium, ischium, and pubis. These bones converge to form the acetabulum. In infants and small children, the acetabulum is united by a Yshaped cartilage.

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The hip is a ball-and-socket joint composed of the articulation of the spherical femoral head with the acetabulum. The hyaline cartilage covering the semilunar surface of the acetabulum is shaped like an inverted horseshoe (▶ Fig. 6.6 and ▶ Fig. 6.7). It contains a nonarticulating central depression (acetabular fossa). Within the acetabular fossa (▶ Fig. 6.8), MRI is able to demonstrate the fatty tissue and ligamentum teres of the femoral head, which has low signal intensity. This ligament often has several bands (up to three bands have been characterized) running from the insertion at the superior margin of the fovea of head of femur (fovea for ligament head) to the insertion of the transverse ligament, which is really a ligamentous portion of the acetabular labrum at the base of the acetabular fossa. In rare cases, it may be absent. It is innervated and has blood vessels leading to the femoral head (branch of the obturator artery, which, however, is often

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6 o’clock position

a

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6.3 Anatomy

b

Fig. 6.5 Status post total hip replacement. Fluid collection (arrows) lateral to the greater trochanter following total hip replacement, consistent with bursitis. Relatively few implant-related artefacts on using prosthetic sequences. (a) Oblique coronal T1w TSE sequence. (b) STIR sequence.

1 2

14 13

2

3

12

4

11

5 6 10

10 9 8 7

1 3 4 5

7

6 7

9

8

Fig. 6.6 Anatomy of the hip. Schematic 3D diagram. 1, iliofemoral ligament (transected); 2, anterior inferior iliac spine; 3, acetabular labrum; 4, acetabular fossa fat pad; 5, transverse acetabular ligament; 6, pubofemoral ligament (transected); 7, obturator membrane; 8, ligament of head of femur (transected) (also known as ligamentum teres of the femoral head); 9, ischiofemoral ligament (transected); 10, iliofemoral ligament (transected); 11, zona orbicularis; 12, femoral head; 13, joint cartilage; 14, semilunar surface of the acetabulum.

Fig. 6.7 Anatomy of the adult hip. Schematic diagram. 1, ligament or foveal plica (fold); 2, acetabular fossa fat pad; 3, ligament of head of femur; 4, transverse ligament; 5, inferior plica (fold); 6, inferomedial retinaculum (Weitbrecht’s ligament); 7, zona orbicularis; 8, fovea of femoral head (central hollow in femoral head); 9, superior labral plica; 10, acetabular labrum.

obliterated in adults). The femoral head is almost completely coated by hyaline cartilage, sparing only the insertion area of the ligamentum teres of the femoral head at the fovea of head of femur. The femoral neck separates the femoral shaft from the pelvis, thus allowing a greater range of motion of the leg.

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The Hip and Pelvis the femoral neck. The joint capsule is reinforced by various ligaments: ● The iliofemoral ligament arises from the anterior inferior iliac spine and extends posteriorly in a fan shape before inserting at the greater trochanter and the intertrochanteric line. ● The pubofemoral ligament arises from the superior pubic ramus and radiates laterally and anteriorly into the joint capsule of the hip, continuing to the inferior aspect of the intertrochanteric line. ● The ischiofemoral ligament is located dorsally. It arises from the ischium, runs almost horizontally, and inserts at the superior aspect of the intertrochanteric line. The sacroiliac joints are only capable of limited movement. The articulating surfaces of the sacrum and ilium serve to transmit weight. The articular surfaces are covered by hyaline cartilage and bound together by strong ligaments: the anterior, interosseous, and posterior sacroiliac ligaments. ▶ Fig. 6.9 and ▶ Fig. 6.10 illustrate the sectional anatomy of the hip in the axial plane.

6.4 Avascular Necrosis of the Femoral Head

Fig. 6.8 Sectional anatomy of the hip. Coronal T1w SE image. 1, fold; 2, femoral neck; 3, gluteus minimus; 4, gluteus medius; 5, obturator internus; 6, iliacus; 7, acetabulum; 8, acetabular fossa; 9, acetabular labrum; 10, obturator externus.

Avascular (ischemic) necrosis of the femoral head can present in association with myriad diseases and trauma. The common etiologic factor implicated here is thought to be ischemia and anoxia of the bone marrow of the femoral head. The main causative factors are believed to be extraosseous arterial factors, for example, trauma, vasculitis, or vasospasms as seen in caisson disease (decompression sickness). Since large areas of the femoral head are covered by hyaline cartilage preventing vessels from entering the bone marrow, the vascular supply to the femoral head is highly vulnerable and largely dependent on the deep branch of the medial circumflex femoral artery and the artery of the ligamentum teres of the femoral head. In the event of (medial intracapsular) femoral neck or acetabular fractures and hip dislocations, the arterial blood supply to the femoral head will be severed. There may also be intra-arterial impairment

Fig. 6.9 Sectional anatomy of the hip. Axial T1w SE image at the level of both femoral heads. 1, obturator internus; 2, gemellus inferior; 3, obturator internus tendon; 4, gluteus maximus; 5, acetabulum; 6, femoral head; 7, iliopsoas; 8, rectus femoris and tendon; 9, sartorius; 10, gluteus medius; 11, urinary bladder; 12, vagina; 13, rectum; 14, rectus abdominis.

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The femoral neck is anteriorly angulated in relation to the femoral shaft (antetorsion). The joint capsule arises from the bony rim of the acetabulum. Anteriorly, it encloses the entire femoral neck and inserts at the intertrochanteric line. Posteriorly, it covers around two-thirds of

6.4 Avascular Necrosis of the Femoral Head

of the blood supply because of microembolisms, for example, in sickle cell anemia or fat embolism. Furthermore, there is virtually no way to release pressure from the head of femur in the event of a space-occupying lesion or intra-articular rise in pressure. This can hinder venous drainage in the long term. Such a rise in pressure can be caused by fat cell hypertrophy following corticosteroid treatment or Gaucher’s disease. Likewise, repetitive microfractures and cytotoxic factors, for example, alcohol consumption, pancreatitis, or steroid therapy, can increase the intraosseous pressure. Besides, hemarthrosis of the hip can raise the intra-articular pressure, thus adversely affecting venous drainage. In infants and young children, purulent joint effusions can also cause avascular necrosis of the femoral head epiphysis. Since often there is no history of trauma or of an underlying disease that might predispose to avascular necrosis of the femoral head, this condition is referred to as idiopathic or primary avascular necrosis of the femoral head. Avascular necrosis of the femoral head may present secondarily to the following disorders: ● Trauma: ○ Femoral head fractures. ○ Slipped capital femoral epiphysis (SCFE). ○ Dislocation of the femoral head. ○ Vascular damage. ● Elevated cortisol levels: ○ Corticoid therapy. ○ Cushing’s disease. ● Hemoglobinopathy: ○ Sickle cell anemia. ○ Polycythemia vera. ● Local infiltration diseases: ○ Gaucher’s disease. ○ Infections. ○ Neoplasms. ● Autoimmune diseases: ○ Lupus erythematosus. ○ Other collagen disorders. ○ Giant cell arteritis.

●

●

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Fig. 6.10 Sectional anatomy of the hip. Axial T1w SE sequence at the level of the femoral necks. 1, femoral artery; 2, femoral vein; 3, urinary bladder; 4, vagina; 5, rectum; 6, pubis; 7, ischium; 8, femoral head; 9, femoral neck; 10, greater trochanter; 11, obturator internus; 12, gemellus inferior; 13, gluteus maximus; 14, pectineus; 15, iliopsoas; 16, sartorius; 17, rectus femoris; 18, tensor fasciae latae; arrow, iliofemoral ligament.

Congenital and embryonic disorders: ○ Legg–Calvé–Perthes disease. ○ Congenital hip dysplasia. ○ Ehlers–Danlos syndrome. ○ Hereditary dysostosis. Other diseases: ○ Barotrauma (caisson disease). ○ Pancreatitis. ○ Hyperlipidemia. ○ Diabetes mellitus. ○ Alcohol abuse. ○ Hyperuricemia.

The ratio of male to female involvement is 4:1. Onset of avascular necrosis of the femoral head is most common between the ages of 30 and 50 years. Both hips are affected in around 30 to 70% of cases, with either synchronous or metachronous involvement of the contralateral hip. Early diagnosis of avascular necrosis of the femoral head is crucial so that symptoms can be properly classified and, in particular, treatment specific to the respective stage initiated. The main focus is on prevention of collapse of the roof of the femoral head, since this is quickly followed by severe degenerative joint changes. Various classification systems have been proposed for staging avascular necrosis of the femoral head. The most common system continues to be that devised by Ficat and Arlet (▶ Table 6.1),35 which was initially applied only to conventional radiography. Hungerford and Lennox expanded that classification system to include MRI and hence stage 0: ● Stages 0 and 1: In these stages, necrosis is already histologically visible, but the radiographic findings are still normal. The patient has no symptoms (stage 0), or may complain of pain and restricted motion of sudden onset despite the unremarkable radiographic results. MRI is particularly valuable in these early stages of disease since it often permits a conclusive diagnosis. ● Stage 2: MRI is also extremely useful in this stage of avascular necrosis of the femoral head. From the changes seen on the radiographs in this stage, it is still often not possible to make a

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The Hip and Pelvis Table 6.1 Staging of avascular necrosis of the femoral head according to Ficat Stage

Symptoms

Radiography

Morphologic changes

0

None

Normal

Histologic necrosis in bone marrow

1

Pain, restricted motion

Normal

Necrosis

2

Pain, restricted motion

Sclerosis, radiolucency

Necrosis

3

Increasing complaints

Flattening of the femoral head, subchondral Necrosis and subchondral fracture fracture (crescent sign)

4

Increasing complaints

Arthrosis, joint destruction

Steinberg et al112 and Ohzono et al88 developed this staging system further. Other aspects taken into account for classification and evaluation of necrosis and the resultant prognosis related to the following two parameters: ● Localization (A = lateral; B = central; C = medial). ● Extension (A: less than 25% of the femoral head circumference; B: 15–30% of the femoral head circumference; C: more than 30% of the femoral head circumference). In addition, the ARCO classification was introduced (classification by the Association Research Circulation Osseous); this is a combination of the Ficat–Arlet classification, Hungerford–Lennox modification, Steinberg quantification, and the Ohzono localization systems (▶ Table 6.2). Noteworthy is that only moderate interobserver variability was found for both the Ficat–Arlet and the ARCO classification systems.102 That should be borne in mind when comparing different studies. MRI is the most precise diagnostic modality for detection of avascular necrosis of the femoral head. Bone scintigraphy (skeletal scintigraphy, bone scan) is more sensitive at detecting avascular necrosis of the femoral head than radiography but is less sensitive than MRI. As mentioned earlier, MRI is particularly suitable for sensitive detection and specific characterization of avascular necrosis of the femoral head already during stage 1.75,123 For example, avascular necrosis of the femoral head was diagnosed in between 6 and 7.6% of asymptomatic kidney transplant patients on steroid therapy, who are at particularly high risk for that condition38,82,116: ● Necrotic zone: On follow-up of kidney transplant patients at various intervals for 24 months, 14 out of 104 patients were found to have avascular necrosis of the femoral head, which in some cases spontaneously resolved. The sensitivity of the various cellular components of the bone marrow to anoxia and ischemia varies. Hematopoietic cells become necrotic already after 6 to 12 hours and osteoblasts and osteoclasts after 12 to 48 hours, whereas fat cells die off only after 2 to 5 days. The bone marrow signal detected on MRI is determined by its macroscopic composition, especially its fat cell content.70,121 In particular, edema or biochemical changes in the bone marrow fatty tissue result in marked changes in signal intensity. It is therefore no surprise that, in the absence of other changes, anoxic necrosis of osteocytes and

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Table 6.2 ARCO classification of avascular necrosis of the femoral head Stage

Histology and imaging

0

Normal findings on radiographs, MRI, and bone scan Signs of necrosis on histology

1

Normal findings on radiographs/CT Signs of disease on MRI and bone scan, in respect of implicated part of femoral head, lateral, central, or medial involvement of femoral head circumference: ● 1a: 15% ● 1b: 15–30% ● 1c: 30%

2

On radiographs, structural changes in bone but no change in contour of femoral head; still no changes in joint space On MRI, specific findings related to avascular necrosis of the femoral head with involvement of the femoral head circumference: ● 2a: 15% ● 2b: 15–30% ● 2c: 30%

3

On radiograph, structural changes in bone with subchondral fracture manifesting as areas of sickle-shaped radiolucency (crescent sign); flattening of contour of femoral head; still normal joint space Crescent sign: ● 3a: crescent sign—15% of the articular surface and femoral head flattened by 2 mm ● 3b: crescent sign—15–30% of the articular surface and femoral head flattened by 2–4 mm ● 3c: crescent sign—30% of the articular surface and femoral head flattened by 4 mm

4

Progression to arthrosis deformans with flattened femoral head and joint space narrowing No further subclassification or quantification

osteoclasts cannot be detected on MRI either. Nadel et al83 conducted experimental studies with dogs after complete devascularization of the entire femoral head. During the first hours after complete anoxia, no signal changes were detected on SE and STIR images. However, dynamic contrastenhanced (Gd-DTPA) scans revealed the absence of perfusion and CM enhancement. In the vast majority of cases, the necrotic zone was confined to the cranial portion of the femoral head, mainly the anterosuperior segment, and was generally hemispherical, lentil- or dome-shaped (▶ Fig. 6.11). In most cases, the necrotic zone was delineated from the healthy bone marrow on the basis of the hypointense linear zone. The central necrotic zones can exhibit a variety of signal patterns, which were assigned to four

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definitive diagnosis or the referring physicians from other disciplines fail to understand the radiologist’s diagnosis. By contrast, on MRI there is compelling evidence of avascular necrosis of the femoral head.20

Necrosis, arthrosis

6.4 Avascular Necrosis of the Femoral Head

Unless prosthetic hip replacement is scheduled, MRI is eminently suitable for planning surgical procedures. The location and extent of necrosis can be exactly determined on sagittal and coronal

a

images (▶ Fig. 6.13). Beltran et al4 and Lafforgue et al62 found that core decompression of the femoral head was especially promising if less than 25% of the femoral head was necrotic. MRI is indicated for avascular necrosis of the femoral head in the following cases: ● Suspected avascular necrosis of the femoral head but with negative or inconclusive radiographic findings. ● Exclusion or confirmation of contralateral involvement in unilateral avascular necrosis of the femoral head. ● Determination of the localization and extension of the necrotic zone. ● Inconclusive differential diagnosis of a hip disorder. ● Treatment monitoring (▶ Fig. 6.14).

Table 6.3 Signal pattern of the central necrotic regions according to Mitchell Class

T1w

T2w

Tissue/fluid

A

↑

–

Fat

B

↑

↑

Subacute hemorrhage

C

↓

↑

Fluid

D

↓

↓

Fibrosis

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●

different categories by Mitchell et al80 (▶ Table 6.3). However, the variation in the necrotic constituents has no prognostic relevance since the chief prognostic determinant is the size of the necrotic zone. In that respect, a distinction is made between a mild (less than 15% of the femoral head affected), moderate (15–30% of the femoral head affected), and severe form. According to Steinberg et al, the severe form had a much poorer prognosis compared with its milder counterpart.112 Often, an inhomogeneous signal pattern that cannot be assigned to any of the categories listed in ▶ Table 6.3 is observed. Double-line sign: In around 80% of cases, a highly specific doubleline sign is identified on T2w images.80,114 The sign is characterized by a hyperintense line along the necrotic side and a hypointense line along the healthy bone marrow (see ▶ Fig. 6.11). This double-line sign reflects the hypervascular peripheral region of the necrotic area surrounded by a fibrotic and sclerotic zone (▶ Fig. 6.12). The hypervascular peripheral zone seen in avascular necrosis of the femoral head can exhibit marked CM enhancement on MRI.

b

Fig. 6.11 Avascular necrosis of the right femoral head. (a) Sagittal T1w SE image. The necrotic zone has the same signal intensity as that of normal bone marrow on the T1w image. In the anterosuperior segment, the necrotic zone is demarcated by a line of low signal (arrow). (b) Sagittal PDw image. On the T2w image, the typical double-line sign (arrows) considered pathognomonic for vascular necrosis of the femoral head can be identified.

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b

Fig. 6.12 Avascular necrosis of the left femoral head. (a) Coronal T1w sequence. (b) PDw fatsat sequence. Incipient fragmentation and double-line sign (arrow). Moderate osteoarthritis; small joint effusion.

6.5 Transient Osteoporosis Transient osteoporosis is a relatively rare clinical manifestation whose etiology has not been conclusively determined. It is generally seen in young and middle-aged men with a history of infection or trauma. In recent years, transient osteoporosis has also been increasingly reported in pregnant women during the third trimester. Differential diagnosis of transient osteoporosis versus other diseases, in particular septic and tuberculous arthritis as well as inflammatory rheumatoid arthritis, is of crucial importance since very different treatment measures are needed. Transient osteoporosis is not confined to the femoral head and can affect all other body regions, for example, the foot, ankle, or even the spine. Conventional radiographs often show asymmetrical demineralization of the femoral head and femoral neck with poor delineation of the cortex. In general, spontaneous resolution of the clinical symptoms and regression of the radiographic changes take place after 6 to 12 months. Bone scintigraphy demonstrates markedly increased radionuclide enrichment, while the histopathologic manifestations of transient osteoporosis include increased bone remodeling and inflammatory changes. Signs of low-grade chronic inflammation are seen in the synovial membrane. On MRI, transient osteoporosis exhibits a largely specific constellation of findings. Diffuse signal changes are identified in the femoral head and femoral neck and can spread to the femoral shaft (▶ Fig. 6.15). A marked decline in signal intensity of the bone marrow is observed on T1w images, while there is a sharp rise in signal intensity on fat-saturated T2w images and, in particular, on STIR images (▶ Fig. 6.16). The

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signal changes seen in transient osteoporosis are thought to be due to edema of the bone marrow.125 Follow-up examinations have revealed that this edematous pattern resolves after 6 to 10 months.12 As transient osteoporosis resolves, subchondral changes are often identified and these are classified as subchondral fractures and thought to have played a causative role in onset of the condition.81 Various authors have posited a possible etiologic link between transient osteoporosis/bone marrow edema and avascular necrosis of the femoral head.42,85,124 For example, following detection of bone marrow edema in the femoral head and femoral neck on MRI, changes suggestive of early avascular necrosis of the femoral head were identified at the time of histologic processing of the core decompression specimen.45 From these findings, it has been concluded that bone marrow edema represents a potentially reversible intermediate stage in the development of overt avascular necrosis of the femoral head and that there are interindividually different repair mechanisms at work that determine whether bone marrow edema resolves or progresses to avascular necrosis of the femoral head. Kramer et al60 reported on nine pregnant women who experienced severe treatmentrefractory pain in one or both hips during the last trimester of pregnancy. Out of a total of 11 pathologically altered hips, bone marrow edema was detected in 8 cases and avascular necrosis of the femoral head in 3. Core decompression was performed for the patients with bone marrow edema, resulting in rapid pain relief and regression of the signal changes on MRI. By contrast, conservative treatment was associated with a protracted healing course of 4 to 6 months. Intramedullary pressure was markedly high in all cases of bone marrow edema.

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The Hip and Pelvis

6.6 Perthes’ Disease Fig. 6.13 Avascular necrosis of both femoral heads. Whereas on the right, there is extensive necrosis with marked changes in signal intensity, cysts, and fracture (c, arrow), on the left there is only a small necrotic area in the superior segment of the femoral head, demarcated by a band of low signal intensity (a, arrows). (a) Coronal T1w image. (b) Coronal STIR image. (c) Overview image of the pelvis.

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a

c

6.6 Perthes’ Disease Perthes’ disease (synonyms: Legg–Calvé–Perthes disease, juvenile osteochondrosis deformans) is seen predominantly in children aged 2 to 12 years, and more often in boys than girls. Its etiology has not been fully elucidated; it is thought to be an idiopathic juvenile form of avascular necrosis of the femoral head. Three stages have been distinguished, mainly lasting for years: ● Initial stage: The epiphysis stops growing probably because of ischemic damage. The cartilage receives its nutrients from the synovial fluid, continues to grow normally, and often appears thicker. Patients generally have severe complaints. Radiographs are initially mainly unremarkable but in the ensuing course show increasing homogeneous thickening of the epiphyseal ossification center. On MRI, an edematous

●

pattern can be identified in parts or the entire epiphyseal ossification center (low signal intensity on T1w images, and high signal intensity on T2w images; ▶ Fig. 6.17). The metaphysis may also be partially implicated (▶ Fig. 6.18).33 Often, there is concomitant synovitis with effusions and thickened synovial membranes.100 Revascularization stage: Already a few weeks after onset of necrosis revitalization with neovascularization, absorption processes and formation of initially fibrous bones are observed (condensation phase). During this phase, marked thickening of the epiphyseal ossification center is seen on radiographs. MRI shows regression of the edematous pattern, with low signal intensity on T1w and T2w images (increasing sclerosis and fibrosis; ▶ Fig. 6.19; see also ▶ Fig. 6.18). Declining stability in this phase can result in fractures and fragmentation of the epiphyseal

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The Hip and Pelvis

Fig. 6.14 Avascular necrosis of the femoral head. Resolution after core decompression. (a) T1w SE sequence before treatment. Characteristic subcortical necrotic focus in the femoral head, demarcated by a line of low signal intensity. (b) T1w SE image. There is complete resolution of findings 6 months after core decompression, with line of low signal intensity along the decompression channel. (c) STIR image. Decompression channel identified as area of high signal intensity.

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6.6 Perthes’ Disease Fig. 6.15 Transient osteoporosis of the left hip. Comparison of both hips on conventional radiographs reveals osteopenia of the left femoral head with less clear delineation from the cortex (a, arrow). On MRI, pronounced bone marrow edema can be identified, reaching into the left intertrochanteric region. (a) Overview image of the pelvis. (b) Coronal T1w image. (c) Coronal PDw fatsat image.

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a

ossification center (fragmentation phase). On radiographs, patchy and/or linear radiolucencies (e.g., subchondral fracture) are identified in the sclerotic epiphysis. MRI also shows a

fragmented inhomogeneous epiphyseal ossification center. Flattening or other deformities as well as lateral subluxation may occur in this stage.

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The Hip and Pelvis Fig. 6.16 Transient osteoporosis in postpartum patient. On both sides, marked bone marrow edema of the femoral heads can be seen extending into the intertrochanteric region. No double-line sign. The markedly hypertrophic postpartum uterus with placental remnants can still be seen (arrows). (a) Coronal PDw fatsat image. (b) Coronal T1w image.

b

●

Repair stage with restoration of the epiphysis. Depending on the severity of disease and response to treatment, the epiphysis may be more or less completely restored or there may be a residual deformity with coxa vara, lateral subluxation, and an enlarged, mushroom-shaped femoral head. This may predispose to early development of arthrosis of the hip (prearthrotic deformity). MRI shows normalization of signal intensity, with detection of a signal that is isointense to fatty marrow in the epiphyseal ossification center and in the metaphysis.

The severity of this disease can be classified on the basis of the extent of epiphyseal involvement61: ● Cattarall classification: ○ Group I: Involvement of less than 25% of the epiphysis of the anterior quadrant. ○ Group II: Involvement of less than 50% of the epiphysis; the metaphysis is rarely involved. ○ Group III: Involvement of more than 50% of the epiphysis; in most cases, there is also involvement of the metaphysis. ○ Group IV: Involvement of the entire epiphysis and also of the metaphysis. ● Salter and Thompson classification: ○ A: Involvement of less than 50% of the epiphysis. ○ B: Involvement of more than 50% of the epiphysis.

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As in adult avascular necrosis of the femoral head, bilateral involvement is seen in more than one-third of cases, with either synchronous or metachronous onset. For Salter and Thompson class A, ongoing monitoring is recommended, whereas for class B different forms of active treatment are indicated (treatment for synovitis symptoms, offloading of the hip, hip centering, corrective surgery, etc.). MRI is suitable for early detection of Perthes’ disease and at a stage when radiographs and bone scintigraphy are still normal.14,21,104 Already in the early phase, diffusion-weighted imaging (DWI) shows markedly higher diffusion in the affected femoral head compared to the contralateral hip (see ▶ Fig. 6.17).126

6.7 Slipped Capital Femoral Epiphysis SCFE is a condition seen during puberty when, for unknown reasons, displacement of the proximal femoral epiphysis occurs. It is thought to be attributable to reduced epiphyseal stability occurring secondarily to hormonal dysfunction with fragmentation of the growth plate close to the metaphysis; other potential etiological factors include malnutrition,

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6.7 Slipped Capital Femoral Epiphysis Fig. 6.17 Early Perthes’ disease, on the left. So far, there are no changes in the shape of the left femoral head epiphysis. Only a discrete reduction in signal intensity (a, arrow) on the T1w SE image and increase in signal intensity on PDw fatsat image. Cartilage thickening (b, arrow) leading to slight lateral displacement of the left femoral head. Increased diffusiveness seen on the apparent diffusion coefficient (ADC) map in the left femoral head (c, arrow). (a) Coronal T1w SE image. (b) Coronal PDw fatsat image. (c) ADC map (b = 0 and 600).

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b

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endocrine disorders, overweight, or hip dysplasia. In addition, mechanical factors, for example, a fall, may be implicated in SCFE.117 There have also been reports of familial clustering. The predilection age is 9 to 15 years, but later onset, independently of age, has been observed in association with skeletal developmental disorders, uremia, or following radiotherapy, etc. Bilateral involvement is seen in 20 to 35% of cases, with various stages often observed. The incidence is given as 1 to 4 per 100,000 inhabitants per year.

The clinical manifestations include hip pain (50% of patients) and a slight limp. However, often only pain in the knee region (25% of cases) or thigh is reported. Depending on the stage, there may also be restricted internal rotation or even displaced external rotation with leg shortening. The following forms have been distinguished: ● Acute form (acute SCFE). ● Chronic form (chronic and slow SCFE). ● Prodromal form (preslip SCFE).

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Fig. 6.18 Perthes’ disease with fragmentation, left. The predominantly hypointense epiphyseal ossification center is collapsed and fragmented at its center, causing considerable deformity of the femoral head as well as lateral subluxation. Subluxation and deficient coverage are also seen on radiographs. (a) Radiograph. (b) Coronal PDw fatsat image. (c) Coronal T1w image.

Fig. 6.19 Perthes’ disease in revascularization stage (condensation phase). A change in signal intensity is observed in over half the epiphyseal ossification center (mainly reduced signal intensity). There is slight, especially lateral, thickening of the cartilage. Irritative synovial effusion. Incipient lateral subluxation. (a) Oblique coronal T1w SE sequence. (b) STIR sequence.

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6.7 Slipped Capital Femoral Epiphysis

Semiquantitative classification is based on the extent of epiphyseal displacement relative to one-third of the metaphysis diameter: ● Mild: less than one-third of the metaphysis diameter. ● Moderate: between one- and two-thirds of the metaphysis diameter. ● Severe: more than two-thirds of the metaphysis diameter. Increased pain on loading is a sign of instability. On radiography, the prodromal preslip manifests as widening and irregularity of the epiphyseal growth plate. As medial and dorsal displacement of the epiphysis progresses, the following signs become apparent: ● A metaphyseal step-off can be identified on the anteroposterior (A/P) radiograph; the femoral neck tangent then no longer intersects the lateral epiphysis: pathologic line of Klein. ● Projection of the affected epiphysis on the A/P radiograph is less than on the contralateral side. ● The epiphyseal–diaphyseal angle (Southwick head-shaft angle) is diseased compared with the contralateral hip (▶ Fig. 6.21).

Fig. 6.20 Slipped capital femoral epiphysis. STIR sequence. The oblique sagittal plane accentuates the dorsal displacement seen in slipped capital femoral epiphysis.

●

Lateral projections (Lauenstein, Imhäuser, Gekeler, or Engelhardt radiographs) show a pathologic epiphyseal torsion angle (synonyms: metaphyseal–epiphyseal angle, angle of metaphyseal tilt; normally less than 10 to 12 degrees; see ▶ Fig. 6.21).16

In slow chronic courses of disease, reactive periosteal bone spurs are formed on the medial aspect of the femoral neck as well as osteophytes on the medial epiphyseal-sided metaphysis. On MRI, the prodromal SCFE form manifests as an irregular and widened epiphyseal growth plate with surrounding bone marrow edema (▶ Fig. 6.22).63 MRI is much more sensitive at detecting prodromal SCFE than are radiographs. MRI thus plays a leading role in decision-making regarding prophylactic pinning of the contralateral hip in manifest SCFE.28 In the manifest forms, displacement of the epiphysis can be identified on MRI as on radiographs (▶ Fig. 6.23), but MRI is more precise at determining the angle of displacement.110,117 The epiphyseal–diaphyseal angle and the line of Klein can be determined on coronal sections. A correlation between the epiphyseal torsion angle on lateral radiographs can be established on sagittal slices (displacement angle = angle between the anterior tangent at the femoral neck and the perpendicular line on the tangent at the epiphyseal base; see ▶ Fig. 6.21).110 In healthy individuals, this angle is on average 24 degrees. Often, an effusion secondary to irritative synovitis is identified on radiographs, with periarticular swelling and demineralization. On MRI, the effusion, periphyseal bone marrow edema, and CM-enhanced, thickened synovial membrane

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Occasionally, there is sudden exacerbation of the chronic form with marked displacement (acute-on-chronic). The degree of displacement (▶ Fig. 6.20) can be classified as follows: ● Mild slip (10–15-degree epiphyseal torsion angle). ● Moderate slip (15–40-degree epiphyseal torsion angle). ● Severe form (40–90-degree epiphyseal torsion angle).

Fig. 6.21 Sipped capital femoral epiphysis. Various methods for measuring the extent of slipped capital femoral epiphysis (see text; schematic diagrams). Bilateral evaluation of the measurement results is performed. (a) A/P radiograph or oblique coronal MR image to determine the epiphyseal–diaphyseal angle (left) and the femoral neck tangent (right). (b) Radiographs after Lauenstein or oblique sagittal MR images to determine the epiphyseal–diaphyseal angle (left) as well as the epiphyseal torsion angle (right).

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Fig. 6.22 Slipped capital femoral epiphysis, left. Oblique coronal STIR image. Slight medial and dorsal displacement of the epiphysis as well as the edematous signal intensity of the enlargement of the epiphyseal growth plate. Concomitant effusion and synovitis. In prodromal slipped capital femoral epiphysis, where there is still no evidence of displacement, edematous enlargement of the epiphyseal may occasionally be the only diagnostic sign identifiable.

can be clearly identified. Besides, MRI is able to visualize any associated avascular necrosis of the femoral head, as seen in 15% of cases.53 Treatment is tailored to the respective stage and comprises the following options: ● Nail fixation for prodromal and mild displacement. ● Intertrochanteric osteotomy for the moderate form. ● Subcapital osteotomy for the severe form. In addition, epiphyseal repositioning with screw fixation can be performed within the first few days for acute displacement. SCFE complications: ● Diffuse acute chondrolysis: This is seen in 7 to 10% of cases. It manifests as massive, uniform thinning of the cartilage with loss of up 50% of the original cartilage layer. Chondrolysis can present spontaneously in the course of disease, in particular following surgical procedures. Complications occur especially if there is cartilage penetration by nails. Chondrolysis progresses from months to years often resulting in ankylosis of the hip.73 ● Avascular necrosis of the femoral head (see Chapter 6.4): This can manifest following surgery. ● Cam impingement (see Chapter 6.10.1): SCFE is also associated with cam impingement, with an elevated α-angle and anterior and anterosuperior cartilage damage.76 Functional techniques

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Fig. 6.23 Slipped capital femoral epiphysis, left. Complete displacement of the femoral epiphysis. Reactive irritative synovial effusion. (a) Coronal T1w sequence. (b) Axial PDw fatsat sequence. (c) Coronal PDw fatsat sequence.

such as dGEMRIC or measurement of the T2 and T2* time may help identify early degenerative changes to the joint cartilage secondary to SCFE.77,129

6.9 Trauma, Stress, and Fatigue Fractures

6.8.1 Hip Dysplasia in Neonates and Small Children (Congenital Hip Displacement) Ultrasonography has proven very useful in diagnosis of hip dysplasia, and is the modality of choice in the first year of life. It is able to demonstrate the anatomic relationship between the femoral head and acetabulum. Since it is especially important for infants and small children to avoid ionizing radiation, ultrasound is also suitable for hip screening. After the age of 1 year, radiography of the hips is needed. While this is able to visualize the relationship between the femoral head and acetabulum, including in particular any cranial and lateral displacement of the femoral head, it is unable to show the complex anatomic changes underlying hip dysplasia, especially the A/P spatial relationship between the femoral head and acetabular roof. It is also not able to directly demonstrate the joint capsule, ligaments, or muscles. Obviating the need for ionizing radiation, MRI is able to visualize also the nonosseous components of the femoral head and acetabulum, joint capsule, and labrum, with MRI multiplanar slices producing excellent 3D impressions of the anatomic topography. The cartilage of the femoral head epiphysis exhibits intermediate signal density on T1w images and high signal intensity on GRE sequences (▶ Fig. 6.24 and ▶ Fig. 6.25). The fibrocartilaginous acetabular labrum is seen as a triangular area of signal void at the acetabular rim on T1w and T2w SE images.53 In congenital hip displacement, dislocation, infolding, and hypertrophy of the acetabular labrum as well as of the joint capsule may be a contraindication to conservative surgical reduction.20 Likewise, the ligamentum teres of the femoral head, which can be identified on

MRI as a triangular bandlike structure that is devoid of signal, often exhibits thickening and is thus an impediment to reduction of the femoral head. MRI also allows evaluation of the cartilaginous portions of the acetabulum and femoral head as well as the acetabular labrum. Coronal and transverse T1w sections show the exact position of the femoral head epiphysis in the acetabulum, something that is often not possible on conventional radiography. Another advantage conferred by MRI, apart from visualization of any impediment to reduction surgery, is its enhanced sensitivity in detecting recurrent hip dislocations even when the patient is wearing a cast.122 Associated changes, for example, ischemic necrosis or joint effusions, can be detected on T2w sequences.

6.8.2 Hip Dysplasia in Adults The structure, size, and depth of the acetabulum are highly variable (▶ Fig. 6.26). Apart from pronounced congenital hip displacement, a broad spectrum of other forms of neonatal dysplasia is seen, ranging from deficient bony coverage of the femoral head to increased coverage. Overcoverage can give rise to pincer-type impingement syndrome (see Chapter 6.10.2). Reduced coverage is a form of prearthrosis causing labral degeneration even in young adults (labrum syndrome) and cartilage damage, including osteochondral lesions (▶ Fig. 6.27). To demonstrate the extent of dysplasia resulting from deficient femoroacetabular bone coverage, MRI (additional coronal sections), too, is able to measure an angle between the lines between the center of the femoral head, edge of the acetabular roof, and the longitudinal axis of the body (Wiberg’s center edge angle; ▶ Fig. 6.28).5 This angle should not be less than 25 to 30 degrees in adults.43 With advancing age, the angle increases because of bone apposition. MRI can help detect early degeneration of the labrum and cartilage.49

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6.8 Hip Dysplasia

6.9 Trauma, Stress, and Fatigue Fractures 6.9.1 Posttraumatic Fractures

Fig. 6.24 Bilateral dorsal hip dislocation. Axial GRE sequence, examination performed with 0.5 T. Six-month-old male patient. High signal intensity in the cartilaginous portions of the acetabulum and femoral heads. The arrowheads point to bilateral hip dislocation. A, acetabulum; H, femoral heads.

In most cases, fractures of the femoral neck, roof of femoral head, and acetabulum can be conclusively diagnosed on conventional radiography, using, if necessary, computed tomography (CT) as an adjunct. CT is particularly useful for complex pelvic fractures, which often involve injury to the sacroiliac joint too, since it allows detailed analysis of the fracture line and position of the bony elements. MRI is able to sensitively demonstrate posttraumatic soft tissue reactions, for example, following avulsion injuries (▶ Fig. 6.29 and ▶ Fig. 6.30) and soft tissue damage (▶ Fig. 6.31). MRI may be indicated for diagnostic imaging of occult fractures as well as stress and fatigue fractures.40 The term occult fractures is used to denote injuries that are not detectable even on properly performed and evaluated radiographic examinations and which generally involve a discrete, undisplaced fracture. In clinically suspected cases, MRI has proved able to conclusively confirm or rule out such fractures of the proximal femoral shaft.29,68 Numerous studies34,41,94 have shown that where an occult fracture of the hip or pelvis is suspected, MRI should be performed immediately after conventional radiography. MRI is especially helpful in osteoporosis patients since, due to the greatly reduced bone

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Fig. 6.25 Bilateral hip dysplasia and dislocation, left. The ossification centers of the femoral head manifest as hypointense oval structures. The cartilaginous components of both hips exhibit high signal intensity. (a) Before reduction. The arrowheads point to the hip dislocation. (b) After reduction. Restoration of the normal position of the femoral heads to the acetabulum.

density, occult fractures can be missed. Occult pelvic fractures are often found in the sacrum as well as in the superior and inferior pubic rami. Apart from occult fractures, there may also be soft tissue injuries, in particular tears, hematomas, and muscle contusions, especially involving the adductors, quadratus femoris, and pectineus.15 The study authors therefore advise against using an abridged examination protocol suitable only for detection of occult fractures of the femoral neck. While, on the whole, bone scintigraphy is endowed with high sensitivity, it has poor specificity and precision of anatomic assignment of the findings. On T1w images, occult fractures are mainly seen as indistinct bands or lines of low signal in the bone marrow extending to the cortex. This hypointense zone reflects the actual fracture line, surrounding edema, and hematoma in the bone marrow. A bandlike zone of increased signal intensity can be seen on T2w images, in particular with fat saturation, and is even more clearly visible on STIR images (▶ Fig. 6.32). The fracture line itself may appear as an even more intense signal or as a linear decrease in signal intensity. Such a decrease in signal intensity is thought to be caused by trabecular compression. Extensive areas of markedly decreased signal intensity can be observed on T2*w GRE sequences. False-positive findings can be caused by degenerative joint changes and ligament avulsions. False-negative results are obtained predominantly in elderly patients and patients with chronic renal insufficiency, local synovitis, or on steroid therapy. False-negative findings may also be encountered in the immediate posttraumatic phase (24 hours). Several authors have focused on whether MRI can yield prognostic insights into the likelihood of development of avascular necrosis of the femoral head secondary to femoral head fractures. After conducting native MRI sequences, Speer et al108 found no signal changes in the femoral head of 15 patients 48 hours after subcapital femur fracture. In view of the high incidence of avascular necrosis of the femoral head associated with such injuries, is it

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quite probable that unenhanced MRI is not able to detect the early signs of posttraumatic avascular necrosis of the femoral head. Lang et al64 used contrast-enhanced MRI to image 10 patients with fresh femoral neck fracture and compared the findings with those of selective angiography of the femoral head. In those cases where angiography revealed intact hip vessels, CM uptake similar to that of the healthy contralateral hip was also seen on contrastenhanced MRI. Conversely, where angiography showed disruption of the vessels of the femoral head, no CM uptake was observed on contrast-enhanced MRI. These findings could have therapeutic implications as to whether internal fixation or primary hip replacement should be performed.

6.9.2 Stress and Fatigue Fractures MRI can also help clarify suspected stress fractures. The following two types of stress fractures are distinguished: ● Fatigue fractures. ● Insufficiency fractures.27 Insufficiency fractures are caused by normal strain acting on weakened bone (osteoporosis, osteomalacia, status post radiotherapy, rheumatoid arthritis, steroid therapy; ▶ Fig. 6.33), while fatigue fractures occur in normal bone subjected to increased strain (e.g., march fracture). On radiographs, the stress fracture is seen as a fracture line perpendicular or oblique to the longitudinal axis of the respective bone, often surrounded by marked perifocal sclerosis and possibly also periosteal new bone formation. However, in the absence of these characteristic signs, diagnosis of a stress fracture may prove challenging. In particular, during the initial 10 to 14 days before visible endosteal and periosteal callus formation, there are generally no definitive signs that can be identified on radiographs.

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6.9 Trauma, Stress, and Fatigue Fractures

Fig. 6.26 Hip dysplasia with high dislocation, left, and neoarthrosis. The left acetabulum is almost completely absent. This leads to high hip dislocation following valgus deformity and to articulation with the ilium. There are marked degenerative changes. (a) Coronal T1w image. (b) Coronal PDw fatsat image. (c) Overview image of the pelvis.

MRI can be valuable in such cases and can contribute to differential diagnosis. On T1w images, the stress fracture manifests as a bandlike zone of reduced signal intensity in the bone marrow with extension into the cortex. On T2w images, in particular with fat saturation and on STIR images, extensive zones of high signal intensity can frequently be identified. These are caused by edema and hemorrhage into the bone marrow; this phenomenon was already discussed in Chapter 2.5.2 and Chapter 3.10.6. Pelvic fatigue fractures are commonly observed in the sacrum (often also bilaterally) and the supra-acetabular region of the ilium. Whereas the fatigue fractures of the ilium run parallel to the acetabulum and horizontally, those of the sacrum are mainly oriented perpendicular and parallel to the sacroiliac joint (▶ Fig. 6.34). A subchondral fracture line in the femoral head is generally diagnosed as a stress fracture in young patients and as an insufficiency

fracture in older patients. On high-resolution T1w and PDw sequences, an ultra-discrete hypointense line can occasionally be identified beneath the subchondral plate, in some cases surrounded by characteristic extensive edema. On low-resolution sequences, the discrete fracture cannot be identified and the bone marrow edema can be misinterpreted as avascular necrosis of the femoral head or as transient osteoporosis (▶ Fig. 6.35).46 Blomlie et al13 examined 18 patients who had undergone radiotherapy for malignant tumors of the pelvis and later experienced radiation-induced insufficiency fractures of the sacrum. They alerted to the risk of misinterpreting the MRI findings as metastases. In the vicinity of insufficiency fractures, extensive zones of decreased signal intensity were observed on T1w images and increased signal intensity on STIR images. In 16 patients, both sacral alae were affected. Fatigue fractures of the medial and

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6.10 Impingement

6.10.1 Cam Impingement

Fig. 6.27 Hip dysplasia, left. Oblique coronal PDw fatsat image. Considerable labral degeneration, basal labral tear, secondary arthrosis, and synovitis especially of the craniolateral portion.

Teardrop figure

Fig. 6.28 Measurement of Wiberg’s center edge angle on MR images. Midcoronal overview image, schematic diagram, highlighting the acetabular “teardrop figure.” From the line connecting the center of the femoral heads (following overprojection in each case of an imaginary circle), a perpendicular line is drawn upwards and a line drawn from the center of the femoral head to the bony acetabular rim. The angle is measured between these two lines.

supra-acetabular portion of the ilium, pubis, and lumbar vertebral bodies, which were also within the radiation field, were detected concurrently in some patients. Bone scintigraphy is also endowed with high sensitivity, but low specificity, for detection of stress fractures. The combination of clinical pain symptoms and focally increased nuclide enrichment on scintigrams is often interpreted as bone metastasis, especially in elderly patients followed up for tumor surveillance. Here, MRI is adept at making a correct diagnosis. CT is also very useful for evaluation of insufficiency fractures of the sacrum. MR arthrography, that is, MRI examination after intra-articular injection of diluted contrast agent, is indicated for detection of

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Cam impingement is caused by a nonspherical configuration of the femoral head at the femoral head–neck junction (▶ Fig. 6.36). Decreased offset of the lateral femoral neck (pistol grip deformity; ▶ Fig. 6.37) causes impingement on the acetabulum, with corresponding changes to the joint cartilage and labral defects, typically in the anterosuperior region (▶ Fig. 6.38). While the degenerative changes are often missed on conventional radiographs, they can be reliably identified on MRI. The α-angle has been used by some authors as a quantitative measure of femoral waist deficiency. Initially, that angle was only used for anterior manifestations of femoral waist deficiency, but, in the meantime, thanks to radial sequences, it is applied to the entire circumference. A limit value of 55 degrees is established in the literature; however, more recent studies show widespread interinvestigator variability in measurements, with manifest overlapping of the α-angle value of healthy volunteers and symptomatic patients. While this attests to high sensitivity, it implies correspondingly low specificity. Therefore, there is a risk of obtaining false-negative results for cam impingement in borderline cases. For that reason, other authors continue to view clinical examination as a more important diagnostic criterion.72 Often, a bump can be identified on the anterolateral femoral neck in the presence of cam impingement. It remains unclear whether this constitutes a primary deformity or a change presenting secondarily to chronic mechanical stress. That increased osteogenic cell recruitment was observed in surgically resected bumps by Jäger et al48 lends credence to the latter possibility. Chronic mechanical stress results in degenerative changes to the labrum, cartilage, and bone, in particular in the anterosuperior region of the joint. These changes resemble those seen in earlyonset osteoarthritis of the hip (see Chapter 6.14.1). Surgical treatment involves timely repair of the labral tears and tapering of the enlarged femoral neck. On MRI, in addition to the degenerative changes outlined, focal bone marrow edema can occasionally be detected in the region subjected to mechanical stress as a reliable sign of symptomatic impingement (▶ Fig. 6.39).

6.10.2 Pincer Impingement In pincer impingement, overcoverage by the acetabulum causes restricted hip motion and results in greater contact

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Femoroacetabular impingement (FAI) has elicited increasing attention in recent decades. Often, symptoms are manifested already between the ages of 20 and 30 years, leading to early degenerative changes. FAI is caused by abnormal contact between the proximal femur and the acetabulum. Timely diagnosis will pave the way for corrective surgery and thus prevent early-onset osteoarthritis of the hip. The most important determinant of the postoperative outcome is the extent of preoperative degenerative changes to the hip. Hence, the radiologist’s main role is to determine the degree of such degenerative changes at the time of diagnosis.

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6.10 Impingement

Fig. 6.29 Acetabular avulsion fracture. Football injury 3 weeks prior to examination. The initial radiographs were unremarkable. Increasing pain on exertion. Shell-like bone damage (a, arrow) resulted in periosteal and soft tissue irritation with strong CM uptake (b, c, arrows). (a) Coronal T1w SE sequence. (b) Coronal STIR sequence. (c) Coronal CM-enhanced T1w SE sequence.

between the acetabulum and femur (see ▶ Fig. 6.36). A bony bump is seen less often than in cam impingement and the αangle is generally not pathologically enlarged. On axial

sections, a much deeper acetabulum is seen compared with cam impingement.92 There may be either general, as seen in protrusio acetabuli, or localized overcoverage as occurs with

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acetabular retroversion. Pincer impingement, like cam impingement, is associated with anterosuperior joint degeneration but also with a much higher incidence of severe cartilage damage resulting in delamination of the posterior and posteroinferior portion of the joint. There is also extensive peripheral ossification, in turn augmenting acetabular overcoverage. An accessory ossicle is often detected at the acetabular rim in patients with FAI; this is thought to have resulted from the increased mechanical stress.57 Treatment of pincer impingement involves corrective surgery to reduce overcoverage. Often, a combination of both mechanisms—cam and pincer impingement—is seen (▶ Fig. 6.40). In patients who engage in sporting activities that require extreme hip movements, for example, ballet or martial arts, changes are frequently identified, that is, labral and cartilage lesions as seen in pincer impingement but without any evidence of acetabular overcoverage. It is thought that the extreme hip movements will have caused hip subluxation, permitting linear contact between the superior or posterosuperior acetabulum and the femoral head–neck junction.58

6.10.3 Other Types of Impingement Apart from the commonly encountered FAI, there are other rare intra-articular and extra-articular factors that cause hip impingement. Since the symptoms are often nonspecific, diagnostic imaging plays a pivotal role. A number of atypical forms of impingement syndrome have only been reported in small case series and must be further validated. Subspine impingement is caused by a protruding, deep-set anterior inferior iliac spine, for example, following apophyseal avulsion (▶ Fig. 6.41). Those affected are typically male adolescents. The deep-set anterior inferior iliac spine can cause movement conflict with the lateral femoral neck, in particular, in flexion. The bony prominence can often be identified on radiography but in some cases only CT or MRI are able to give a clearer picture of the anatomic relationships. Imaging the hip in flexion is advantageous here.66 Ischiofemoral impingement is caused by the close spatial relationship between the lesser trochanter and the ischial tuberosity, as well as by the resulting constriction and possibly atrophy of the quadratus femoris. It is more prevalent in women. This

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Fig. 6.31 Status post dislocated fracture of the hip. (a) Oblique coronal STIR sequence. MRI is better at evaluating the capsular damage, periarticular hematoma, and the internal joint space. (b) Coronal reconstruction CT image. The acetabular avulsion fracture (arrow) can be identified more clearly on CT.

condition was first reported in patients following total hip replacement or femur osteotomy52; in recent years, it has also been increasingly reported in patients who had not had previous surgery.89,118,119 In ischiofemoral impingement, the distance between the lesser trochanter and the greater trochanter is significantly reduced (13 ± 5 mm; control: 23 ± 8 mm), but patient positioning, especially rotation of the affected hip, is of paramount importance. MRI is able to additionally detect moderate edema or fatty atrophy of the quadratus femoris. Differential diagnosis should include lesions of the quadratus femoris. A detailed medical history may help to clarify this. Besides, injuryrelated edema tends to be seen more at the myotendinous junction, whereas edema secondary to impingement has a diffuse appearance.

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Fig. 6.30 Avulsion fracture of the rectus femoris from the anterior inferior iliac spine, left. Axial PDw fatsat image. The arrowheads point to the avulsion fracture.

6.11 Lesions of the Acetabular Labrum

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Fig. 6.33 Stress fracture in dialysis patient. Coronal PDw fatsat image. Pain in both proximal upper thighs in dialysis patient. Stress fracture, right (arrow), with bone marrow edema and low signal fracture line at typical location and fatigue reaction, left.

In iliopsoas impingement, there is a direct spatial relationship between the iliopsoas tendon and the anterior labrum. Recent studies have demonstrated that patients with such a configuration often sustain injury to the anterior labral region contiguous with the muscle tendon but exhibit no signs of FAI. The labral tears associated with iliopsoas impingement are typically found in the 3 o’clock position; tears seen in the presence of FAI are generally in the 11:30 to 1 o’clock position.11 The mechanical etiology of labral changes has not been fully elucidated to date.

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Fig. 6.32 Occult fracture of the femoral neck, left. This elderly female patient complained of pain in the left hip. (a) Coronal CT. A fracture of the acetabulum was detected on CT (arrow). (b) Coronal STIR image on following day. Discrete fracture line (arrow) in the lateral femoral neck which was not visible on CT. (c) Coronal CT on subsequent day. Fracture dislocation occurred when moving the patient.

Fig. 6.34 Stress fractures in pelvic–hip region. Schematic diagram of the coronal plane, showing the predilection sites of stress fractures in the pelvic–hip region. A conclusive diagnosis of stress fracture can be made based on the medical history as well as on detection of the typical signs of edema and a line of reduced signal intensity. In atypical cases, it is more difficult to diagnose early stress reactions in the absence of the bandlike areas of low signal intensity. Familiarity with the typical locations and orientation of stress reactions (running parallel to the sacrum and/or perpendicular to the sacroiliac plate, extending along the ilium, oriented perpendicular to the pubis and ischium, oriented horizontally to the acetabulum) may be very useful in such cases.

6.11 Lesions of the Acetabular Labrum In recent years, there has been a greater awareness of the significance of injuries and degenerative lesions of the acetabular labrum, in particular those related to FAI. Labral injuries have been identified in 25 to 55% of patients with hip and groin pain,74 and 90% of patients with labral tears experience pain in the anterior hip or inguinal region.84 Thanks to the improved imaging

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b

Fig. 6.35 Insufficiency fracture of the sacrum, right. (a) CT images shows discontinuity of the anterior contour of the cortex and discrete sclerosis of the right sacrum (arrow). (b) Axial STIR image. Diffuse increased signal intensity in the right sacrum with low signal fracture line (arrow). (c) Axial T1w SE image. Extensive decrease in signal intensity in the lateral portions of the sacrum.

6.11.1 Anatomic Variants

a

b

c

d

Fig. 6.36 Cam, pincer, and mixed-type hip impingement. Schematic diagram. (a) Normal finding. (b) Cam impingement: decreased offset of the femoral neck, in particular of the anterior segments. (c) Pincer impingement: pathologic overcoverage of the femoral head. (d) Mixed form of impingement: combination of cam and pincer impingement.

afforded by MRI, hitherto undiagnosed hip complaints are being increasingly imputed to a labral tear. High-resolution techniques are needed to that effect. Unenhanced MRI is not able to conclusively diagnose tears of the acetabular labrum since the joint cavity is not distended and labral variants may be visualized. Higher sensitivity can be achieved with direct and indirect MR arthrography.128,130 Oblique sagittal and, especially, oblique axial sections are useful.

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The appearance of the acetabular labrum varies on the MR image and is also dependent on the patient’s age. A triangular labrum of homogeneously low signal intensity is seen in around 70% of young persons. In 16% of cases, the labrum has a rounded, flat, or irregular shape, and in some 14% of cases it cannot be demonstrated at all. The labral thickness is greater in the superior and posterior portions, varying by around 2 to 3 mm.7 On comparing both hips, a difference in the shape was seen in 15% and a difference in thickness was seen in 25% of asymptomatic patients.2 With advancing age, the triangular shape is increasingly replaced by a poorly demarcated form. The labrum exhibits homogeneously low signal intensity in around 65% of young persons. Areas of focal, linear, or diffuse increased signal intensity are observed in 22% of cases, with the areas of linear hyperintensity extending to the labrum surface in around 13% of cases. On native MRI, the latter cannot be distinguished from labral tears. The percentage of patients with increased signal intensity of the labrum continues to grow with increasing patient age (▶ Fig. 6.42, ▶ Fig. 6.43, and ▶ Fig. 6.44).67 These changes in the shape and signal intensity of the acetabular labrum seem to be dependent not only on patient age but also on the particular location within the labrum. For example, in the anterosuperior labrum, significant differences are discerned

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a

6.11 Lesions of the Acetabular Labrum

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Fig. 6.37 Pistol grip deformity. Coronal PDw fatsat sequence. The hip is shaped like a pistol grip as a result of decreased offset of the femoral neck (arrow).

6.11.2 Labral Tears Tears of the acetabular labrum can present immediately following trauma, often after dislocations or degenerative changes to the hip. Typical predisposing disorders include: ● Femoroacetabular or iliopsoas impingement. ● Hip dysplasia. ● Perthes’ disease.

Fig. 6.38 Cam impingement. Paraxial PDw fatsat image. Decreased offset of the anterior femoral neck. Changes in signal intensity in the anterior labrum.

versus the signal-void triangular shape of the posterior labrum1; these differences are typically attributed to cam impingement. For MR arthrography, it must be noted that the joint capsule inserts at the base of the labrum, thus giving rise to a normal longitudinal recess (perilabral sulcus), which should not be mistaken for the, mainly, diagonal tears (▶ Fig. 6.45). On native MRI, this recess manifests only as an effusion. In up to 25% of cases, a sublabral sulcus is also identified, that is, a groove situated between the cartilage and labrum (▶ Fig. 6.46 and ▶ Fig. 6.47). Studier et al113 demonstrated that anterior sublabral sulci have a linear configuration, do not fully infiltrate the labrum, and are not associated with any perilabral manifestations such as ganglion cysts or cartilage damage. In that study, sublabral sulci were mainly found in the anteroinferior labrum. However, Saddik et al identified 48% of the sulci in the posterosuperior and 44% in the anterosuperior labrum.101 These locations, in particular, can be mistaken for labral tears, and in principle CM uptake by the superior portions of the labrum is suggestive of a tear.

Clinical symptoms include, apart from pain, signs of compression or clicking sounds. The pain may derive from an anterior tear sustained during internal rotation and adduction of the extended hip, or from a tear of the posterior labrum in external rotation and abduction of the flexed hip. Labral tears are caused either by detachment of the labrum from the acetabulum or because of intrinsic defects (▶ Fig. 6.48 and ▶ Fig. 6.49). On MRI, diagonal lines of increased signal intensity, mainly extending to the surface, are detected in the signal-void triangular labrum (▶ Fig. 6.50). In severe cases, a fragment of the labrum may be dislocated. Labral detachment is more common than tears but both may occur in the same labrum. On MR arthrography, CM is taken up by the tear, thus providing for high-contrast delineation and increasing the diagnostic accuracy of conventional MRI from 36 to 91%.25 However, arthroscopy continues to be the gold standard. Blankenbaker et al designed a system where the labral tears are classified in terms of their clock-face position (see ▶ Fig. 6.3).8 Analogously to the shoulder, it is very difficult to differentiate traumatic, symptomatic labral tears from physiologic spaces at attachment sites,113 in particular in the absence of concomitant manifestations. Degenerative changes can occasionally be identified as areas of increased signal intensity within the labrum (▶ Fig. 6.51). These can progress to full-thickness tears. A distinction must be made between the increased signal intensity of the labrum resulting from degenerative changes and the physiologically increased signal intensity identified at the base of the labrum attributable to the presence of blood vessels (transition zone).

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a

Fig. 6.39 Cam and pincer impingement. Oblique coronal PDw fatsat images of two patients. Focal bone marrow edema in the region of mechanical damage (arrows). (a) Patient with cam impingement. Marked labral degeneration. (b) Patient with pincer impingement.

Fig. 6.40 Arthrosis in mixed-type impingement. Sagittal 3D SSFP sequence (see ▶ Table 1.2). In this 40-year-old patient, there is overcoverage of the right hip and waist deficiency of the femoral neck. Pronounced degenerative changes to cartilage with subchondral cysts in the anterior and posterior portions of the joint.

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Fig. 6.41 Subspine acetabular impingement. Coronal PDw fatsat sequence. This 37-year-old female patient most probably exhibits posttraumatic acetabular damage with a prominent acetabulum (arrow). There is evidence of restricted motion with marked osteophytic spurs of the femoral neck. Pronounced degenerative changes are also seen in the inferomedial portions of the joint.

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6.13 Early-Onset Osteoarthritis and Arthrosis a

70% age↓

16%

14% age↑

b

65% age↓

22% age↑

Fig. 6.42 Variability of the acetabular labrum. Schematic diagram (coronal plane) of variability of MRI morphology and signal intensity of the acetabular labrum in healthy volunteers (n = 200). (a) Morphology: triangular (70% of younger persons, less common with advancing age), round or flat (16%), cannot be identified (14% of younger persons, more common in older persons). (b) Signal intensity: homogeneously low signal intensity (65% of younger persons, less common with advancing age), focal, linear, or diffuse increased signal intensity (22%, more common in older persons), line of increased signal intensity extending to the labral surface (13%, more common with advancing age).

13% age↑

Fig. 6.43 Labral syndrome. Oblique coronal schematic diagram. Degenerative changes in the region of the external superior hip with moderate dysplasia of the acetabulum and basal tear of the acetabular labrum, subchondral bone marrow edema of the external superior acetabulum and in the contralateral femoral head, soft tissue edema, synovitis, deformity, and altered signal intensity in the labrum. Painful flexion, internal rotation, and adduction, in some cases with clicking phenomenon.

Cysts can also be seen in association with degenerative changes or following trauma (▶ Fig. 6.52). Cysts of the acetabular labrum may range from a few millimeters to 2 to 3 cm. Like other cysts, they are hypointense on T1w and hyperintense on T2w images, and are found most often in the posterosuperior region.103 Patients with labral cysts often report historic trauma and exhibit signs of hip osteoarthritis. Pain is typically experienced in internal rotation and flexion.

6.12 Degenerative Ligamentum Teres of the Femoral Head There is growing awareness of the pivotal role of the ligamentum teres of the femoral head in underpinning the functions of the hip, which is now seen to equate with that of the anterior cruciate ligament of the knee. The prevalence of tears identified on arthroscopy was 4 to 15%. Disorders such as ruptures, partial tears, and degeneration are now thought to be the third most common

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cause of hip complaints among professional athletes.22 Evaluation of findings on conventional unenhanced MRI is often a challenge but this situation can be greatly remedied with MR arthrography. The standard criteria for classification of ligament tears are used to distinguish full-thickness from partial tears (▶ Fig. 6.53)10: ● Partial and complete discontinuity. ● Undulating course. ● Focal pseudotumorous thickening. ● Effusion. ● Synovitis. ● Foveal bone marrow edema. In the presence of degenerative and inflammatory changes, ligament thickening and changes in signal intensity, possibly with elongation and an irregular contour (fraying) and often with edema, are observed in the fovea for the ligament of head of femur.22

6.13 Early-Onset Osteoarthritis and Arthrosis MRI is not the primary imaging modality for chronic degenerative and inflammatory rheumatoid joint disorders. Its main application is in differential diagnosis of complex cases in addition to scientific research. Using standard examination techniques, especially T1w and T2w SE sequences, advanced stages of hip arthrosis can be clearly identified, including joint space narrowing, subchondral sclerosis, osteophytes, and subchondral cysts. Morphologic details that are missed on radiographs can also be visualized, thanks to the fact that sectional images of the hip can be flexibly chosen and depicted without overlap, in particular in the coronal plane. Rosenberg et al98 conducted MRI examination of patients who then received prosthetic hip implants. This allowed for correlation of the MRI results with the macroscopic and histopathologic findings on investigation of the explanted femoral heads. Good concordance with the macroscopic and histopathologic findings was achieved on using T1w 3D GRE sequences. Occasionally, bone marrow edema of the femoral head and/or acetabulum can be observed in active arthrosis of the hip (▶ Fig. 6.54). In such cases, joint effusion and thickening of the synovial membrane can also be detected. This synovial proliferation should not be mistaken for chronic rheumatoid joint changes.

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Fig. 6.44 Labral syndrome. Raised signal intensity in the deformed superior acetabular labrum, synovial irritation with focal effusions, edema of superior acetabulum and surrounding soft tissues. (a) Oblique coronal T1w sequence. (b) Oblique coronal STIR image.

b

Fig. 6.45 Perilabral recess. Injection of CM during MR arthrography causes distension of the joint capsule. A physiologic perilabral recess is seen between the labrum and joint capsule (b, arrow). (a) Fluoroscopy image for control of CM injection. (b) MR arthrography, coronal plane.

6.14 Inflammatory Diseases 6.14.1 Osteomyelitis and Septic Arthritis MRI is endowed with high sensitivity for diagnosis of septic and tuberculous infections. A conclusive diagnosis can be made from the morphologic changes seen on MRI only after also taking

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account of the clinical symptoms and the laboratory test results. Arthritis originating from the surrounding bone is generally accompanied by extensive bone marrow edema and joint effusion in the early stages of disease. This helps to differentiate this condition from inflammatory rheumatoid disease where there are typically no, or less pronounced, changes in the signal intensity of the bone marrow. Joint space narrowing and widespread osteoporosis are often seen on radiographs in both rheumatoid

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6.14 Inflammatory Diseases

Fig. 6.47 Sublabral recess. Coronal PDw fatsat sequence following arthrography. A smoothly marginated groove can be seen between the cartilage and the unremarkable labrum, corresponding to a sublabral recess.

b

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Fig. 6.46 Acetabular labrum. Schematic diagram of the acetabular labrum in the coronal plane. (a) Labral recess due to capsular attachment to the external base of labrum. Normal findings on MR arthrogram or on native MRI in association with joint effusion. (b) Basal labral tear. Tear oriented perpendicular to labrum surface (unlike recess).

arthritis and tuberculous arthritis. While this characteristic sign is not identifiable on MRI, confirmation or exclusion of changes to the bone marrow constitutes an important criterion for differential diagnosis. Infections confined to the joint cavity and not arising from a hematogenous focus in the bone marrow of the surrounding bones can present a differential diagnostic challenge. In such cases, a septic joint effusion whose signal characteristics do not differ from those of a serous joint effusion can be identified (arthrographic effect on T2w sequences). Joint puncture is needed to isolate the causative pathogen (▶ Fig. 6.55). Bacterial arthritis not involving osteomyelitis can cause impaired perfusion in the femoral head, with 2- to 4-minute delay in signal increase on contrast-enhanced dynamic MRI and photopenia in bone scintigraphy.55 For differentiation between septic arthritis and transient synovitis, dynamic MRI was found to have a sensitivity of 85.7%, specificity of 72.7%, a positive predictive value of 66.7%, and negative predictive value of 88.9%. This disease can often involve elevated intra-articular hydrostatic pressure or septic thrombosis and higher risk of avascular necrosis of the femoral head. The sacroiliac joint and the parts of the sacrum and ilium bounded by the joint are also often susceptible to tuberculous and other bacterial infections. Detection of a focal bone abscess or extraosseous extension of an abscess is an important indicator of bacterial infection, thus ruling out spondyloarthropathy. In arthritis patients, MRI is able to demonstrate cartilage changes and subchondral erosions. More discrete cartilage degeneration can only be identified on high-resolution techniques, possibly with traction application. For treatment planning, especially in a preoperative setting, MRI is able to determine the exact extent of infection. In particular, it can show to what degree bones, soft tissues, and the joints are affected.24 Fat-saturated T2w SE sequences and contrastenhanced T1w images with fat saturation are especially useful to that effect.

c

Fig. 6.48 Extensive longitudinal tear of left labrum. (a) Coronal STIR image of pelvis. In the absence of intra-articular CM uptake, the left labral lesion is hardly visible. But there is a joint effusion of the left hip. (b) Sagittal T1w image taken during MR arthrography. A longitudinal labral lesion with CM uptake can be identified in the 11 to 1 o’clock position (arrow). (c) Coronal PDw fatsat sequence. The longitudinal tear can be detected in the center of the labrum (arrow).

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For rheumatoid arthritis of the hip and other rheumatoid diseases, MRI is able to detect various morphologic changes not seen at all, or only partially identifiable, with other imaging modalities.105 On PDw sequences, incipient thinning of the joint cartilage and discrete erosions can be detected before they are apparent on radiographs. Because of the corticosteroid treatment frequently prescribed, rheumatoid arthritis patients are at high risk for avascular necrosis of the femoral head (see Chapter 6.4 p. 238), which can be reliably detected on MRI. An arthrographic effect is achieved on T2w images, allowing joint effusions to be

Fig. 6.49 Complete detachment of the labrum. Sagittal PDw fatsat sequence carried out during MR arthrography of the left hip. Complete detachment of the labrum to 2 o’clock position (arrow) without any associated cartilage damage. Unlike the sublabral recess, here the labrum is completely detached from the cartilage.

visualized with high signal intensity so that even small amounts of liquid, bursal effusions, and synovial extensions can be clearly identified. However, contrast versus the surrounding fatty structures is rather poor on TSE sequences. Conversely, good contrast in respect of surrounding fatty structures is achieved on fatsaturated T2w SE and STIR sequences. In contrast-enhanced images, synovial proliferation seen in association with inflammatory rheumatoid diseases shows marked and rapid CM uptake, facilitating its delineation from joint effusions and contiguous soft tissue structures. Fat-saturated T1w sequences are particularly suitable here. Dynamic contrastenhanced MRI examinations are able to quantitatively determine the speed and extent of enhancement of synovial proliferation. Certain authors point out that the speed and magnitude of CM uptake are correlated with the activity of the inflammatory rheumatoid process. The same applies for other functional techniques such as DWI.19 These techniques, which are still in their infancy,

Fig. 6.50 Complex tear of the acetabular labrum with vertical and horizontal components (arrow). Oblique coronal PDw fatsat image. The arrowhead points to the tear.

Fig. 6.51 Mucoid degeneration of the labrum. The anterior portions of the labrum (arrows) exhibit highgrade raised signal intensity secondary to mucoid degeneration. There is also incipient perilabral cyst formation. (a) Axial PDw fatsat sequence during MR arthrography. (b) Sagittal PDw fatsat sequence during MR arthrography.

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b

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6.14.2 Rheumatoid Arthritis

6.14 Inflammatory Diseases

a

a

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Fig. 6.52 Perilabral cysts and subchondral acetabular cyst. Discrete perilabral cysts (a, b, white arrows) can be seen in the left hip on sagittal SSFP sequences (see ▶ Table 1.2), with labral degeneration and a subchondral cyst (a, black arrow) in the acetabulum. (a) Imaging plane 1. (b) Imaging plane 2.

b

b

Fig. 6.53 Pathologic visualization of the ligamentum teres femoris in two patients. (a) Axial PDw fatsat image. Pseudotumorous thickening and tortuous course of ligament (arrow), suggestive of a possible tear. (b) Oblique coronal PDw fatsat image. Thickening, increased signal intensity in the ligament (arrow) and perifoveal bone marrow edema suggestive of an inflammatory reaction, also seen following trauma (foveitis with ligament and synovial inflammation).

Fig. 6.54 Severe active osteoarthritis of the left hip, moderate osteoarthritis of the right hip. Coronal PDw fatsat image. Bilateral marked osteophytic spurs on the acetabulum and lateral acetabulum (arrows). Cartilage degeneration especially in the zone exposed to stress on the left (arrowhead) as well as diffuse bone marrow edema suggestive of active disease. There is also widespread reactive synovial proliferation.

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are expected to play a special role in investigating and predicting the response to antirheumatic drugs. It must, however, be stressed that synovial enhancement is not proof of an inflammatory rheumatoid joint process. Indeed, similar findings can be seen in severe arthrosis, posttraumatic changes, bacterial arthritis, and even tumor-related changes. This is particularly true for intracapsular osteoid osteoma of the femoral neck and femoral head. In such cases, there is no, or only limited, periosteal and endosteal new bone formation. Often, an extensive joint effusion and synovial proliferation that can mimic an inflammatory rheumatoid disease are detected.

6.15 Diseases of the Capsule and Synovial Membranes

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which is mainly seen in association with severe osteoarthritis of the hip. Detection of calcified joint bodies will facilitate diagnosis on conventional radiographs. MRI is able to additionally visualize cartilaginous joint bodies. On T2w images, these manifest as defects in the hyperintense joint effusion. The signal intensity of the joint bodies depends on their composition: if they are completely calcified, they will appear as signal void. Purely cartilaginous joint bodies exhibit intermediate signal intensity on T1w and T2w images. If ossified joint bodies contain bone marrow, a central area of fat-isointense signal intensity can be identified. Periarticular bursae, such as the iliopsoas bursa or obturator externus bursa, may be affected (extra-articular osteochondromatosis; ▶ Fig. 6.56).96

6.15.1 Synovial Osteochondromatosis

6.15.2 Synovial Folds (Plicae and Retinacula)

Synovial osteochondromatosis is characterized by the presence of loose joint bodies occurring secondarily to cartilaginous metaplasia and neoplasia of the synovial membrane. It presents most commonly in the knee and hip joints. Primary idiopathic osteochondromatosis must be distinguished from secondary osteochondromatosis,

As in other joints, connective tissue folds (synovial folds) covered by synovial membranes may be seen at characteristic sites in the hip. As the deployment of arthroscopic and arthrographic examination techniques becomes more common, such structures are increasingly reported.6,9,54 In some

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Fig. 6.55 Bilateral Salmonella arthritis of the hip. Moderate joint effusion, bone marrow edema, and strong CM uptake seen in both hips. The diagnosis was confirmed through aspiration of the joint effusion. (a) Coronal PDw fatsat sequence. (b) Axial T1w fatsat sequence following intravenous administration of CM.

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6.17 Insertional Tendinopathy (Enthesopathy)

Fig. 6.56 Chronic synovitis in bilateral hip osteoarthritis. The main finding in this patient was inguinal swelling of unknown origin, more pronounced on the left than on the right. MRI demonstrated bilateral iliopsoas bursitis with fluid-isointense signal, CM-enhanced halo as well as central defects due to debris and synovial proliferation and cartilaginous-osseous metaplasia (secondary osteochondromatosis). (a) Axial T2w TSE sequence with fat saturation. (b) CM-enhanced T1w sequence. (c) Coronal T2w TSE sequence with fat saturation.

cases, plicae (folds) are thought to be the remnants of an embryonic joint compartment that failed to be fully absorbed during fetal development and are thus not invariably present. Apart from joint fluid production, plicae help to stabilize the joint. They also contain neurovascular structures. Typically, three hip plicae are distinguished (▶ Fig. 6.57; see also ▶ Fig. 6.7): ● Plica arising from the superior paralabral capsule (labral or superior plica; seen in around 95% of cases). ● Plica surrounding the ligament of head of femur and arising from the acetabular fossa (ligamentous or middle plica; seen in around 78% of cases). ● Plica originating from the inferior paralabral capsule (present in around 75% of cases.36 Plicae may become symptomatic and give rise to compression with inflammatory thickening, clicking sounds, snapping phenomena, and cartilage damage. The labral plica causes most complaints with compression of the labrum or transverse ligament.32 Plicae are not significantly correlated with labral tears, FAI, or degenerative joint changes.6 A number of fibers from the capsular ligament apparatus extend from the femoral capsule insertion along the inferior femoral neck to the femoral head and were designated by Weitbrecht as the “inferior (or medial) retinaculum” (Weitbrecht’s ligament). On arthrography or on images with joint effusion, this

retinaculum can be identified as a signal-void band running parallel to the femoral neck (see ▶ Fig. 6.7).

6.16 Amyloid Arthropathy Longstanding hemodialysis as seen in renal insufficiency can result in excessive deposition of ß2 microglobulin amyloid in the periarticular capsules, tendons, and bones. In the hip, this can cause thickening of the iliotibial tract, joint effusions, bursal effusions, in particular in the trochanteric and iliopsoas bursae, and amyloid pseudotumors in the femur (▶ Fig. 6.58).

6.17 Insertional Tendinopathy (Enthesopathy) Tendon insertion sites can become inflamed because of mechanical stress, for example, overloading during sporting activities or chronic displacement due to static changes (▶ Fig. 6.59). The tendon insertion site itself, the adjacent bone marrow, surrounding soft tissues, and the bursa may be involved in the inflammatory process. Damaged tendons are therefore at risk for full-thickness tears in the event of subsequent partial injury or in some cases can even develop spontaneous tears (▶ Fig. 6.60).

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Fig. 6.57 Hip plicae (folds). (a) Ligamentous plica (arrow) parallel to the ligamentum teres. (b) Labral plica (arrow) between labrum and joint capsule. (c) Femoral neck plica (arrow).

Fig. 6.58 Dialysis arthropathy and amyloidosis. Severe synovitis, erosions at capsule attachment, osteodestructive focal lesion on greater trochanter, and soft tissue swelling and signal changes consistent with massive amyloid deposits secondary to long-term dialysis. (a) Coronal T1w SE sequence. (b) Coronal fat-saturated TSE sequence.

6.17.1 Insertional Tendinopathy of the Gluteal Tendons Insertional tendinopathy of the gluteus muscle tendons at the greater trochanter (gluteus medius and minimus muscles) is a common form of hip overloading injury. It often affects elderly patients presumably because this patient group is more vulnerable to static changes in the bones of the axial skeleton and the foot. A typical

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symptom is pain at rest and on exertion, which is also aggravated by the application of pressure to the greater trochanter. On MRI, edema is observed in the soft tissues surrounding the greater trochanter, in particular on STIR images (▶ Fig. 6.61). Concomitant bursitis gives rise to a fluid-isointense structure on the trochanter (then referred to as “trochanteric bursitis”). Three different potential types of bursa are distinguished: ● Bursa between the gluteus minimus and bones.

6.17 Insertional Tendinopathy (Enthesopathy) ● ●

7 6

5 4

1

3 2

Fig. 6.59 Examples of common types of insertional tendinopathy in the hip and pelvis. Schematic diagram.1, adductor group and gracilis on pubis close to symphysis; 2, knee flexors (hamstrings) on ischial tuberosity; 3, iliopsoas on lesser trochanter; 4, gluteus maximus on linea aspera of femur; 5, gluteus medius and minimus muscles on greater trochanter; 6, rectus femoris at the anterior inferior iliac spine; 7, iliotibial tract, sartorius, and tensor fascia latae at the anterior inferior iliac spine; 8, abdominal muscles at iliac crest.

Bursa between the gluteus minimus and medius muscles. Large bursa between the tendon insertion sites of the gluteus medius and gluteus minimus and the more distal gluteus maximus tendon.

The tendon insertion site at the greater trochanter is broad and divided into four zones or facets. In more protracted or severe cases of disease, concomitant bone marrow edema is identifiable in the greater trochanter. Furthermore, high-resolution MRI is able to detect small amounts of fluid in the trochanteric bursa (up to 2 mm wide). These are not indicative of disease and should not be misinterpreted as bursitis in the absence of other relevant symptoms. Surgery should be indicated for cases refractory to conservative treatment. Occasionally, edema of the soft tissues and bones can be seen for several months on postoperative follow-up images. Signal changes in the greater trochanter in status post trochanteric osteotomy need not necessarily be indicative of periostitis (▶ Fig. 6.62). Downloaded by: Collections and Technical Services Department. Copyrighted material.

8

6.17.2 Insertional Tendinopathy of the Tendons of the Knee Flexor Group of Muscles Another characteristic type of enthesopathy of the hip region relates to insertional tendinopathy of the flexor muscles of the

a

b

c

Fig. 6.60 Not quite fresh avulsion of knee flexors (semimembranosus, semitendinosus, and biceps femoris muscles, “hamstrings”) of ischial tuberosity. Left, coronal schematic diagram illustrating the levels indicated in (a), (b), and (c). (a) Axial T2w MR image through ischial tuberosity. The inserting tendon plate is largely absent on the corresponding right side (compare with left). (b) Axial T2w MR image through the myotendinous junction of the muscle group. Fluid collection and partially undulating course of tendon portions as well as fluid-filled gaps. (c) Axial T2w MR image through muscle group at the level of the proximal thigh. Muscle edema and incipient atrophy secondary to loss of function, showing it is not really an acute event. (d) Sagittal T2w image. Partially retracted muscles with undulating tendon portions and fluid or blood collections suggestive of tears.

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Fig. 6.61 Insertional tendinopathy of the gluteus medius and minimus at the greater trochanter. Edematous enlargement of the tendon attachment. (a) Coronal T1w image. (b) Coronal STIR image.

knee (knee flexor group of muscles: the semimembranosus, semitendinosus, and biceps femoris muscles, also known as the “hamstrings”) at the ischial tuberosity. A clear clinical sign of this disorder is the characteristic pressure pain at the ischial tuberosity. On MRI, the typical signs of insertional tendinopathy are seen at the tuberosity (▶ Fig. 6.63).

6.17.3 Rare Types of Hip Enthesopathy Rare types of enthesopathy affect the gluteus maximus enthesis at the proximal femur along the linea aspera (▶ Fig. 6.64), adductor insertion at the pubis (▶ Fig. 6.65), attachment of the iliotibial tract at the anterior superior iliac spine,106 etc. Occasionally, calcification as well as productive and absorptive changes to the cortex at the attachment site can be seen on radiographs (▶ Fig. 6.66); however, MRI is by far the most sensitive modality for detection of enthesopathy.

6.18 Snapping Hip (Coxa Saltans) Mechanical friction between the iliotibial tract or gluteus maximus and greater trochanter can cause soft tissue irritation with or without snapping hip phenomenon (see Snapping Phenomena, p. 652) (▶ Fig. 6.67). In some cases, the snapping sound is audible. Other extra-articular causes implicated in snapping hip phenomenon are: ● Interaction between the biceps femoris tendon and the ischial tuberosity. ● Interaction between the iliopsoas tendon and a bony prominence on the pelvis (iliopectineal eminence). Intra-articular causes include loose joint bodies or prominent plicae.

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6.19 Neurovascular Compression Syndrome The large periarticular nerve trunks are relatively often damaged by various pathologic processes. MRI can be used to elucidate the cause of nerve compression syndrome since it is able to confirm or rule out tumors or other space-occupying processes. MRI also plays an important role in diagnosis in that it detects any changes in the signal intensity and/or thickness of nerves as well as neuropathic raised signal intensity (T2w contrast) in the innervated muscles (▶ Fig. 6.68). ▶ Table 6.4 lists a number of examples of compression syndrome of the hip region.

6.20 Tumors The main tumors seen in the hip region are chondrogenic tumors, intra-articular osteoid osteoma (▶ Fig. 6.69), metastases, and synovial tumors. See also Chapter 12.3.

6.21 Pigmented Villonodular Synovitis Pigmented villonodular synovitis most commonly affects the knee but the hip may also be involved. While the etiology of pigmented villonodular synovitis has not been conclusively determined, there is a broad consensus that it is a condition with benign tumorlike lesions of the synovial membrane. The most conspicuous findings on radiographs include periarticular bone destruction attributable to tumorlike, intra-articular synovial proliferation. These areas of destruction are round and

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6.22 Pitfalls in Interpreting the Images

Fig. 6.62 Status post surgical repair of insertional tendinopathy at the greater trochanter. Persistent pain. Postoperative edematous soft tissue changes as well as contour irregularity and increased signal intensity in the surface of the greater trochanter suggestive of periosteal irritation. (a) Coronal T1w SE sequence. (b) Coronal STIR image.

content.50,59 Hemosiderin deposits can be identified very sensitively on T2w GRE sequences. In addition to the areas of low signal, cystic components and joint effusion are also observed in association with pigmented villonodular synovitis. Injection of CM is followed by conspicuous synovial enhancement. Unlike in osteoarthritis and rheumatoid arthritis, the cartilage and joint space width are typically preserved in pigmented villonodular synovitis.

6.22 Pitfalls in Interpreting the Images Fig. 6.63 Insertional tendinopathy of the knee flexors (hamstrings) at the ischial tuberosity. Axial T2w TSE sequence. Bilateral fluidisointense changes at the tendon insertion on the ischial tuberosity (arrows). Clinical symptoms: pain on exertion and characteristic pressure pain in ischial tuberosity.

surrounded by a sclerotic halo. With regard to the location of these areas, it must be noted that the joint capsule inserts distally at the femoral neck and, accordingly, any pigmented villonodular synovitis–mediated destruction can also extend along the femoral neck. Typically, the periarticular bony sections of the acetabulum and proximal femur are concurrently affected. But by no means are these changes detected on radiography, and also on MRI, invariably present. For example, intra-articular signs of pigmented villonodular synovitis may be exhibited but without any bone destruction. Here, MRI often allows a more specific diagnosis. Typically, pigmented villonodular synovitis has low signal intensity on both T1w and T2w images, thus differentiating this condition from virtually all tumor-related and inflammatory changes exhibiting high signal intensity on T2w images. The low signal intensity seen on T2w images derives from the variable hemosiderin

6.22.1 Hematopoietic Bone Marrow On axial images, in particular, for example, in the proximal femur, there is a risk of mistaking remnants of metaphyseal hematopoietic marrow for infiltrative processes. Chapter 11.3.4 gives details of the age-related distribution of hematopoietic and fatty bone marrow. Scarred remnants of the epiphyseal growth plate in adults manifest as lines of low signal and should not be misinterpreted as the linear signal changes seen in avascular necrosis of the femoral head.

6.22.2 Transcortical Synovial Herniation Bone defects of variable size, but typically measuring up to 3 cm and surrounded by a sclerotic halo, are seen in the femoral neck on radiographs in up to 5% of adults.17 These are thought to reflect transcortical synovial herniation of the joint capsule with erosion of the anterior femoral neck cortex affecting especially the zona orbicularis (▶ Fig. 6.70). These findings are characteristically observed in the anterosuperior quadrant of the proximal

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The Hip and Pelvis should not be mistaken for erosions caused by inflammatory synovial proliferation or tumors. These changes are mainly asymptomatic but in rare cases they can cause pain lasting from weeks to months. Occasionally, increased radionuclide enrichment can be observed in this region on bone scintigraphy. Recently formed lesions may be accompanied by more or less extensive bone marrow edema on MRI,26 making their differential diagnosis from tumors a challenge.

A supra-acetabular fossa is identified in around 10% of patients, hampering interpretation of radiographic results. It is one of numerous variants of the acetabular roof and can normally be identified on coronal sections in the 12 o’clock position. On MR arthrography, type I can be distinguished from type II in that it takes up CM, while the latter is filled with cartilage. Type I can progress to type II through bone remodeling. The supra-acetabular fossa may also be identifiable on conventional radiographs. On arthroscopic imaging, no cartilage defect is normally seen in this region; hence, the supra-acetabular fossa, like the dorsal patellar defect, is classified as a pseudolesion. However, extensive defects found at uncharacteristic locations may be interpreted as rare osteochondral lesions.30

6.22.4 Bursitis

Fig. 6.64 Insertional tendinopathy of the gluteus maximus. Edema in gluteus maximus enthesis at the linea aspera of femur (arrows). (a) Coronal STIR sequence. (b) Axial STIR sequence.

femoral neck and less commonly in the medial-caudal region. No consensus has been reached on the likelihood of a relationship between synovial herniation and FAI.56,69 The rationale for that viewpoint is the repetitive impingement of the femoral neck on the anterosuperior acetabulum, giving rise to (synovial) fluid herniation into the cortex. On MRI, similar-sized defects are seen in the characteristic locations. These predominantly fluid-filled lesions are hypointense on T1w and hyperintense on T2w images, while fibrous tissue lesions are mainly hypointense. The lesions are surrounded by a signal-void halo and are also known as herniation pits and

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Bursitis may present as a single entity or coincident with inflammatory joint diseases. Inflammation causes swelling that can be mistaken for a tumor, especially when not accompanied by other symptoms (▶ Fig. 6.71). Radiologists should therefore be familiar with the anatomic locations of bursae when interpreting crosssectional images (▶ Fig. 6.72). The iliopectineal (iliopsoas) bursa is the largest bursa in the hip region (3 × 4 to 72 × 4 cm) and is absent in only around 2% of cases. Congenital communication with the hip is seen in 15% of cases. Tears of the joint capsule following chronic abrasion of the iliopsoas tendon can also result in acquired communication between the bursa and the hip. Furthermore, inflammatory or mechanical changes, such as trauma, arthrosis, and aseptic avascular necrosis of the femoral head, can also result in secondary communication. Only rarely does the obturator externus bursa communicate with the joint and when inflamed can be seen as a fluid-filled structure along the course of the obturator externus (▶ Fig. 6.73).96 On MRI, inflamed bursae exhibit low signal intensity on T1w and high signal intensity on T2w image, with low signal inclusions occasionally observed in longstanding inflammation. The bursal lining is of variable thickness and takes up CM. Interpretation of such findings is compounded by their multifarious manifestations and possible communication with the joint cavity.

6.22.5 Accessory Iliacus Tendon An accessory iliacus tendon, which is part of the iliopsoas tendon complex, is identified on MR arthrography in up to 66% of cases (▶ Fig. 6.74).115 This accessory tendon’s narrow course can be seen within the lateral segment of the iliacus. It is normally asymptomatic but in a small anatomy study was found to cause compression of the femoral nerve.109 The accessory tendon is

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6.22.3 Supra-acetabular Fossa

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6.22 Pitfalls in Interpreting the Images

Fig. 6.65 Gracilis syndrome (insertional tendinopathy of gracilis on pubis close to symphysis). Pain when engaging in sports. Evidence of edema at gracilis insertion site (arrows). (a) Coronal STIR sequence. (b) Axial STIR sequence.

a

b

Fig. 6.66 Productive insertional tendinopathy of iliopsoas on lesser trochanter, right. (a) Radiograph. Longitudinal calcification in the projection to the tendon insertion of iliopsoas on lesser trochanter (arrow). (b) Coronal PDw fatsat sequence. Inflammatory-edematous signal intensity in and around the distal iliopsoas tendon and at the tendon insertion (black arrow) as well as the focal areas of signal void due to calcification (white arrow).

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Fig. 6.67 Hip tract syndrome. Young woman. Pain on exertion, in particular in the right greater trochanter, especially when dancing. Fluid-isointense signal intensity between iliotibial tract and greater trochanter (arrows; bursitis and pseudobursitis = fluid collection due to chronic inflammatory irritation). The medical history, localization of fluid, and absence of signal changes at the gluteus insertion on greater trochanter are suggestive of hip tract syndrome (mechanical irritation of soft tissues between tract and greater trochanter) and appear to discount gluteus insertional tendinopathy. (a) Coronal STIR sequence. (b) Axial STIR sequence.

separated from the main tendon by a thin fatty fascia and can be mistaken for a longitudinal iliacus tear. However, no muscle edema is detected on fat-suppressed T2w sequences. Fatsuppressed sequences also allow identification of the fatty fascia.

Fig. 6.68 Obturator neuropathy. Acute onset paresthesia and numbness of inside of thigh of right leg as well as muscular weakness. Status post multiple injections into the gluteus maximus. MRI shows isolated edema in the region of the adductors, consistent with an acute denervation pattern. The patient’s report of new onset of numbness sensation of the thigh is consistent with the sensory area innervated by the obturator nerve. Whether the injections into the gluteus maximus (e.g., edema in the gluteus maximus) are responsible cannot be fully elucidated. (a) Coronal STIR sequence. (b) Schematic diagram illustrating the course of the obturator neve and the muscles innervated by it. (c) Schematic diagram illustrating the sensory area innervated by the obturator neve.

Table 6.4 Compression syndrome of hip region Nerve

Potential causes of compression

Sciatic

Compression by the piriformis (piriformis syndrome)

Obturator Compression in obturator canal (e.g., by an obturator hernia, pubic osteitis) Femoral

274

Compression in the groin

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The Hip and Pelvis

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6.22 Pitfalls in Interpreting the Images

Fig. 6.69 Intra-articular osteoid osteoma of the hip. Young man with nocturnally pronounced pain that responds well to acetylsalicylic acid. Edema surrounding a low signal focus (nidus; a, c, arrows) of expansive nature in femoral neck. Reactive synovitis with effusion in hip. (a) Oblique coronal T1w SE sequence. (b) Oblique coronal STIR sequence. (c) Axial T2w SE sequence.

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The Hip and Pelvis

Clinical Interview

c

Fig. 6.70 Transcortical synovial herniation. (a) Schematic diagram in coronal plane. Characteristic location of the defects caused by transcortical synovial herniation in the external superior quadrant of the femoral neck (bold circles). Less commonly, these defects are also observed in the medial lower portion (thinly drawn circle). It is conceivable that pressure and erosions along the zona orbicularis of the joint capsule have perforated the cortex leading to synovial herniation. (b) Anterior view of anatomic specimen of the hip. Several round cortical defects are seen at the junction from the medial to the cranial third of the femoral neck, consistent with the lesions associated with transcortical synovial herniation. (Reproduced with permission from Prof. Dr. H. M. Schmidt, Anatomic Institute of the University of Bonn.) (c) Axial PDw fatsat sequence. Synovial herniation pits measuring several millimeters can be identified in the anterior femoral neck (arrow).

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●i

Clinical interview with Prof. Dr. Thomas Kälicke, Medical Director of the Department of Orthopedics, Traumatology, Hand and Reconstructive Surgery at the Betriebsstätte St. Josef Hospital of the GFO Kliniken Bonn, and Prof. Dr. Alfred Karbowski, Medical Director of the Clinic for Orthopedics, Specialist Orthopedics, and Sports Medicine at the Augustinian Hospital (Krankenhaus der Augustinerinnen), Severinsklösterchen Cologne: Question: “What do you think is the role of MRI in the routine practices of an orthopaedist or trauma surgeon with regard to the hip region? For which disorders does it confer major advantages?” Answer: “It plays a major role and provides good results in the case of avascular necrosis of the femoral head, occult fractures, and stress fractures. It is of great significance in clarifying hip pain of unknown origin, in particular for detection of labral tears, enthesopathy, and bursitis. MRI is also important for investigating suspected loosening of prosthetic implant devices as well as for detection of chronic synovitis in association with ‘particle disease’.” Question: “For which disorders do you encounter false-positive MRI results most often?” Answer: “Postoperative fluid collections can be mistaken for an abscess.” Question: “For which disorders do you encounter false-negative MRI results most often and why were diagnostic measures continued in such cases?” Answer: “Labral lesions may be missed on unenhanced MRI. MR arthroscopy has a greater role here.” Question: “For which disorders can MRI be omitted and for which is it being overly used?” Answer: “MRI is indicated too often for hip osteoarthritis.”

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6.23 Clinical Relevance of Magnetic Resonance Imaging

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6.23 Clinical Relevance of Magnetic Resonance Imaging

Fig. 6.71 Rheumatoid arthritis of the hip and visualization of the iliopsoas bursa. The arrows point to the iliopsoas bursa. (a) Coronal T1w SE image. The iliopsoas bursa has low signal intensity that hardly differs from that of muscles. The vessels are displaced medially by the bursa. (b) Axial T2w GRE image. High signal intensity in bursa which is consistent with the effusion in the hip. (c) Axial T2w GRE image. The axial section at the level of the hip demonstrates the communication (arrowhead) between the bursa and hip. The bursa extends upwards under the iliopsoas and can be identified anteriorly to the ilium.

Fig. 6.72 Location of bursae. Schematic diagram of the hip illustrating the location of normal (solid circles) and variant (dotted circles) bursae. (a) Anterior view of the hip. (b) Posterior view of the hip. 1, insertion of iliopsoas; 2, iliopectineal bursa (iliopsoas); 3, subcutaneous and subfascial trochanteric bursa of gluteus maximus; 4, trochanteric bursa of gluteus medius; 5, trochanteric bursa of gluteus minimus; 6, bursa of obturator internus (insertion zone; variable); 7, bursa of piriformis; 8, bursa of quadratus femoris (variable); 9, bursa of biceps femoris; 10, bursa of obturator externus; 11, sciatic bursa of gluteus maximus; 12, subcutaneous sciatic bursa.

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The Hip and Pelvis Fig. 6.73 Axial sectional anatomy of the pelvic hip region. Schematic diagram. On the left, small joint effusion (2) and fluid-filled distended bursa of obturator externus (1), separated by capsular parts (3). The bursa is situated along the course of the obturator externus, displacing it. On the right, normal appearance of muscle (4).

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Fig. 6.74 Accessory iliacus tendon, left. The accessory iliacus tendon is separated from the main tendon by a fatty septum.

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syndrome: what is it and where is it? Skeletal Radiol. 2011; 40(12):1553–1556 [107] Sobotta J. Atlas der Anatomie des Menschen, Band 2. 20. Aufl. München: Urban & Schwarzenberg; 1993 [108] Speer KP, Spritzer CE, Harrelson JM, Nunley JA. Magnetic resonance imaging of the femoral head after acute intracapsular fracture of the femoral neck. J Bone Joint Surg Am. 1990; 72(1):98–103 [109] Spratt JD, Logan BM, Abrahams PH. Variant slips of psoas and iliacus muscles, with splitting of the femoral nerve. Clin Anat. 1996; 9(6):401–404 [110] Stäbler A, Genz K, Seiderer M. MRT der Epiphyseolysis capitis femoris (ECF). Bildgebung. 1992; 59(3):133–135

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[113] Studler U, Kalberer F, Leunig M, et al. MR arthrography of the hip: differentiation between an anterior sublabral recess as a normal variant and a labral tear. Radiology. 2008; 249(3):947–954 [114] Sugimoto H, Okubo RS, Ohsawa T. Chemical shift and the double-line sign in MRI of early femoral avascular necrosis. J Comput Assist Tomogr. 1992; 16 (5):727–730 [115] Tatu L, Parratte B, Vuillier F, Diop M, Monnier G. Descriptive anatomy of the femoral portion of the iliopsoas muscle. Anatomical basis of anterior snapping of the hip. Surg Radiol Anat. 2001; 23(6):371–374 [116] Tervonen O, Mueller DM, Matteson EL, Velosa JA, Ginsburg WW, Ehman RL. Clinically occult avascular necrosis of the hip: prevalence in an asymptomatic population at risk. Radiology. 1992; 182(3):845–847 [117] Tins B, Cassar-Pullicino V, McCall I. The role of pre-treatment MRI in established cases of slipped capital femoral epiphysis. Eur J Radiol. 2009; 70(3):570–578 [118] Torriani M, Souto SC, Thomas BJ, Ouellette H, Bredella MA. Ischiofemoral impingement syndrome: an entity with hip pain and abnormalities of the quadratus femoris muscle. AJR Am J Roentgenol. 2009; 193(1):186–190 [119] Tosun O, Algin O, Yalcin N, Cay N, Ocakoglu G, Karaoglanoglu M. Ischiofemoral impingement: evaluation with new MRI parameters and assessment of their reliability. Skeletal Radiol. 2012; 41(5):575–587

[94] Quinn SF, McCarthy JL. Prospective evaluation of patients with suspected hip

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focal lesions. Radiology. 1989; 171(1):135–140 [122] Vahlensieck M, van Deimling U. Kernspintomographie bei Hüftdysplasie von Säuglingen im Fettweißgips. Z Radiol. 1994; 150:34 [123] Vande Berg B, Malghem J, Labaisse MA, Noel H, Maldague B. Avascular necrosis of the hip: comparison of contrast-enhanced and nonenhanced MR imaging with histologic correlation. Work in progress. Radiology. 1992; 182(2):445–450 [124] Vande Berg BE, Malghem JJ, Labaisse MA, Noel HM, Maldague BE. MR imaging of avascular necrosis and transient marrow edema of the femoral head. Radiographics. 1993; 13(3):501–520 [125] Wilson AJ, Murphy WA, Hardy DC, Totty WG. Transient osteoporosis: transient bone marrow edema? Radiology. 1988; 167(3):757–760 [126] Yoo WJ, Kim YJ, Menezes NM, Cheon JE, Jaramillo D. Diffusion-weighted MRI reveals epiphyseal and metaphyseal abnormalities in Legg-Calvé-Perthes disease: a pilot study. Clin Orthop Relat Res. 2011; 469(10):2881–2888 [127] Yoon LS, Palmer WE, Kassarjian A. Evaluation of radial-sequence imaging in detecting acetabular labral tears at hip MR arthrography. Skeletal Radiol. 2007; 36(11):1029–1033 [128] Ziegert AJ, Blankenbaker DG, De Smet AA, Keene JS, Shinki K, Fine JP. Com-

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[80] Mitchell DG, Rao VM, Dalinka MK, et al. Femoral head avascular necrosis:

7.1

Introduction

7.2

Examination Technique

The Knee

7.3

Anatomy

7.4

Meniscal Lesions

7.5

Cruciate Ligament Injuries

7.6

Collateral Ligament Injuries

7.7

Lateral Capsular Ligament Injuries, Including Popliteus Injuries

7.8

Iliotibial Tract (Band) Syndrome

7.9

Dyskinesia of the Femoropatellar Joint and Patellar Dislocation

7.10

Patellar and Quadriceps Tendonitis

7.11

Chondropathy, Early-Onset Osteoarthritis, Arthrosis, and Cartilage/Chondral Damage

7.12

Bone Trauma

7.13

Transient (Regional) Migratory Osteoporosis and Shifting Bone Marrow Edema of the Knee

7.14

282 282 282 290 301 310 311 311 312 315 317 322

324 Osteochondritis Dissecans and Avascular Necrosis 324

7.15

Changes to the Synovial Membrane and Joint Capsule, Sarcoidosis, and Gout

7.16

Synovial Plicae (Folds)

7.17

Synovial Popliteal Cysts and Bursitis

7.18

Lesions of Hoffa’s Fat Pad and Other Fat Pads

328 334 336 340

7.19

Ganglion Cysts (apart from Meniscal Ganglion Cysts/Parameniscal Cysts)

341

7.20

Nerve Compression Syndrome and Periarticular Neuropathy

7.21

Vascular Diseases

7.22

Special Features in Children

7.23

Common Tumors and Tumorlike Lesions in and around the Knee

7.24

Pitfalls When Interpreting the Images

7.25

Clinical Relevance of Magnetic Resonance Imaging References

342 343 344 344 345 350 351

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Chapter 7

The Knee

7 The Knee 7.1 Introduction The knee joint is one of the weight-bearing joints of the human body. The joint-moving levers of the tibia and femur are longer than those of any other joint. Furthermore, the knee joint permits complex and extensive movements involving numerous active and passive mechanisms. It is therefore no surprise that the knee is particularly susceptible to injury and degeneration. Recent controlled clinical trials have revealed that the power of clinical tests had been overrated in the past.120 This was particularly true with regard to the detection of meniscal damage. Magnetic resonance imaging (MRI) is a long-established valuable and reliable modality for diagnostic imaging of joints, especially the knee. Today, after the brain and the spine, the knee joint accounts for most MRI indications. It is often used to confirm or rule out the indication for arthroscopy, and when properly deployed, it should help reduce the diagnostic arthroscopy rate, while at the same time paving the way for well-targeted, therapy-oriented arthroscopy.10

7.2 Examination Technique 7.2.1 Patient Positioning and Coil Selection The patient is examined supine in the feet-first position, with the knee minimally flexed and the leg slightly in external rotation. As for all MRI examinations, the patient should be comfortable, in order to avoid movement. Even small bumps or a hard surface can cause pain within minutes, invariably resulting in undesired movement by the patient. The use of sandbags, for example, has proved beneficial in preventing vibrations or movements when imaging the extremities. All manufacturers offer a high-resolution volume coil for examining the knee. For very obese patients, it may also be necessary to use other surface coils such as a ring coil or a flexible rectangular coil. The knee joint space should be in the center of the coil. Often, the patella is placed in the center, causing undesirable loss of signal in structures of interest in the distal knee due to their being outside the optimum field of the receiver coil. Points of tenderness or palpable lesions can be marked my means of fat points or with a tube containing copper sulfate solution.

Although most pathologic conditions are already identifiable on native images, a contrast medium (CM)-enhanced sequence can confer additional diagnostic benefits in the presence of tumors or arthritis. Indirect MR arthroscopy can be advantageous for detection of meniscal tears. Numerous pulse sequences have been recommended for evaluation of hyaline joint cartilage. Fat-saturated 3D gradient-echo (GRE) sequences ensure high contrast between hyaline joint cartilage, intra-articular fluid, and fatty tissue. Recht et al158 achieved best results with a spoiled Gradient Recalled Acquisition in Steady State (GRASS) sequence (see ▶ Table 1.2), with TE (echo time) = 10 ms and a flip angle of 60 degrees. Eckstein et al60 obtained the best signal-to-noise ratio (SNR) and contrast-tonoise ratio using a 3D Fast Low Angle Shot (FLASH) sequence with fat saturation (TR [repetition time] = 60 ms, TE = 11 ms, flip angle = 60 degrees; see ▶ Table 1.2) compared with other pulse sequences (T1w and T2w spin-echo [SE] sequence, magnetization transfer contrast–fast imaging with steady precession [MTC-FISP; see ▶ Table 1.2], double-echo steady state [DESS]). These findings also showed the closest correlation with cartilage thickness and cartilage volume values based on anatomic measurements.60,61,77 Vahlensieck et al found MTC to be endowed with high sensitivity for detection of cartilage lesions.213

7.3 Anatomy 7.3.1 General Anatomy Menisci of the Human Knee The menisci are crescent-shaped laminae made of fibrocartilaginous tissue (▶ Fig. 7.1) that largely compensate for the incongruence between the articular surfaces of the femoral condyles and tibia, thus protecting against points of excessive pressure by distributing the weight uniformly over a wider area. The standing

7.2.2 Sequences and Parameters In most cases, injuries and disorders of the knee involve several anatomic structures. Therefore, the examination strategy should include a standard protocol that addresses most clinical questions as well as additional protocols tailored to specific clinical indications. Although there is a plethora of recommendations available on this topic, not all of them are based on empirical data. Currently, T1w turbo spin-echo (TSE) sequences are recommended in at least the sagittal plane and PDw fat-saturated (fatsat) TSE sequences in the three principle planes. The slice thickness should not exceed 3 to 4 mm. The in-slice resolution is 0.4 to 0.9 mm. The sequential slices should encompass the entire knee joint, including the peripheral meniscal regions.

282

Fig. 7.1 Meniscus. Sagittal T1w sequence at the level of the pars intermedia of the lateral meniscus.

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M. Vahlensieck and A. Horng

7.3 Anatomy

Posterior

LM

Anterior Cruciate Ligament The primary function of the ACL is to prevent anterior subluxation of the tibia. It arises from the posterior aspect of the inner surface of the lateral femoral condyle and inserts in the anterior intercondylar area of the tibia anterolaterally to the anterior intercondylar eminence (see ▶ Fig. 7.3). It is around 35 mm long and around 11 mm thick.104 The ACL consists of three components: ● Anteromedial bundle. ● Intermediate bundle. ● Posterolateral bundle. When the knee is extended, the entire ligament is uniformly taut; in flexion, the anteromedial bundle remains taut but the other bundles are relaxed. On MRI, the anteromedial bundle can be differentiated from the posteromedial bundle in over 90% of cases.

Posterior Cruciate Ligament

MM

Anterior

The PCL arises from the inner aspect of the medial femoral condyle and inserts at the posterior aspect of the tibia in the posterior intercondylar notch. It is much stronger than the ACL. It is around 38 mm long and around 13 mm thick. When the knee is extended, the PCL is relaxed and exhibits superoposterior convexity (“boomerang” configuration). When the knee is flexed, the PCL is taut and embarks on a straight course.

Medial Collateral Ligament

Fig. 7.2 View from above of the medial and lateral menisci. Schematic diagram. LM: lateral meniscus; MM: medial meniscus.

Medial MM anterior horn

collateral ligament (MCL). The anterior horns of both menisci are connected in around 60% of cases by the transverse ligament of knee, which in around 10% of cases is divided into several ligament strands. In 1 to 4% of the population, there is a posterior transverse ligament and in 1 to 4% also a transverse ligament connection between the posterior horn and the anterior horn of the other meniscus. Both menisci are connected on their outer aspect with the synovial membrane of the joint capsule. The menisci are composed of fibrocartilage, with a large proportion of collagen fibers containing individual cartilage cells. The majority of the stronger collagen fibers course externally in a longitudinal direction and are crossed on the inside by weaker, radially oriented fibers. In adults, the menisci are poorly vascularized. The capillary loops of the vascularized peripheral zone (“red zone”) supply the inner avascular meniscal regions (“white zone”). Downloaded by: Collections and Technical Services Department. Copyrighted material.

adult transmits 40 to 60% of the weight through the menisci, reducing compression of the joint cartilage. The menisci are 3 to 5 mm at the periphery, decreasing to less than 0.5 mm at the inner free border. Both menisci have an anterior horn and a posterior horn, as well as a pars intermedia, which constitutes the central two-thirds of the meniscus. Viewed from above, the lateral meniscus is largely round in shape. It is attached anteriorly and posteriorly to the intercondylar notch and is only loosely attached to the joint capsule elsewhere. The tendon of the popliteus courses freely through the joint capsule. The posterior horn of the lateral meniscus is unattached in the region where the popliteus tendon passes beneath it. The posterior horn of the lateral meniscus can send two ligaments to the medial femoral condyle, which course posteriorly (posterior meniscofemoral ligament of Wrisberg) or anteriorly (anterior meniscofemoral ligament of Humphrey) to the posterior cruciate ligament (PCL). One of these ligaments is found in 30 to 40% of cases, and both ligaments are found in around 10% of cases. The lateral meniscus is also fixed posteriorly by fascicles running between the posterior horn and the tendon or tendon sheath hiatus of the popliteus (posteromedial and anteroinferior popliteomeniscal fascicle), which can be well visualized on the MR image.152 In up to 15% of cases, the anterior horn is not normally attached to the tibial plateau, and in such cases, attachment is mediated by the transverse ligament to the anterior margin of the tibia (this should not be mistaken for meniscal subluxation) or through a ligament connection to the anterior cruciate ligament (ACL).48 The medial meniscus has a slightly larger radius and is longitudinal/oval or comma-shaped (▶ Fig. 7.2). It is wider in the region of the posterior horn than in the region of the anterior horn and pars intermedia. The anterior horn is attached to the anterior intercondylar area of the tibia (▶ Fig. 7.3). The pars intermedia is attached to the deep layers of the medial

The MCL plays a key role in assuring the stability of the knee joint. It is composed of a superficial and a deep layer. The deep

Lateral LM anterior horn

Anterior cruciate ligament

Tibial articular surface

MM posterior horn

LM posterior horn

Fig. 7.3 Attachment of the menisci and cruciate ligaments at the tibial plateau. Schematic diagram. LM: lateral meniscus; MM: medial meniscus.

Posterior cruciate ligament

283

The Knee layer is also termed the “medial capsular ligament” and attaches the medial meniscus to the femur (meniscofemoral ligament) and the tibia (meniscotibial ligament). The MCL arises from the medial femoral condyle and extends to the medial surface of the tibia, around 7.5 to 10 cm distal to the articular surface. The deep and superficial layers of the MCL are separated by fatty tissue and a bursa.

Lateral Collateral Ligament

The patellar tendon, together with the quadriceps muscle, quadriceps tendon, and patella, constitutes the “extensor mechanism” of the knee joint. The quadriceps tendon inserts at the superior pole of the patella. Some fibers of the quadriceps tendon continue anteriorly to the patella and insert as the patellar tendon at the tibial tuberosity. Most of the fibers of the patellar tendon originate from the rectus femoris.

7.3.2 Specific Magnetic Resonance Imaging Anatomy ▶ Fig. 7.4, ▶ Fig. 7.5, and ▶ Fig. 7.6 demonstrate the sectional anatomy of the knee joint.

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The lateral collateral ligament (LCL) extends obliquely from the lateral femoral condyle, running posteriorly and inferiorly to the fibular head. The popliteal tendon courses between the lateral meniscus and the LCL and inserts at the lateral distal femur.

Patellar Tendon

Fig. 7.4 Sectional anatomy of the knee joint. MRI, axial plane. (a) 1, iliotibial tract; 2, patellar ligament; 3, medial meniscus. (b) 4, transverse ligament of knee. (c) 5, semimembranosus bursa. (d) 6, lateral femoral condyle; 7, anterior cruciate ligament; 8, posterior cruciate ligament.

284

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7.3 Anatomy

Fig. 7.4 Sectional anatomy of the knee joint. (continued) (e) 9, lateral patellar retinaculum; 10: popliteus (tendon). (f) 11, medial alar plica.

285

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The Knee

Fig. 7.5 Sectional anatomy of the knee. MRI, coronal plane. (a) 1, iliotibial tract; 2, lateral meniscus. (b) 3, posterior cruciate ligament; 4, medial collateral ligament; 5, medial meniscus; 6, anterior cruciate ligament. (c) 7, lateral collateral ligament.

286

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7.3 Anatomy

Fig. 7.6 Sectional anatomy of the knee. MRI, sagittal plane. (a) 1, lateral meniscus anterior horn; 2, popliteus (tendon). (b) 3, lateral meniscus. (c) 4, posterior cruciate ligament; 5, anterior cruciate ligament. (d) 6, medial meniscus anterior horn. (e) 7, semimembranosus (tendon); 8, medial meniscus posterior horn; 9, pes anserinus.

287

The fibrocartilage of the menisci has only a small number of unbound protons and is therefore largely displayed as being devoid of signal, regardless of which pulse sequence is selected. However, it should be noted that the menisci exhibit higher signal intensity on GRE images, and this should not necessarily be attributed to a pathologic process. A somewhat undulating course of the pars intermedia can be normal, depending on how the knee is positioned and the degree of flexion (flounce). An artificial increase in signal intensity can also be observed on T1w and PDw sequences because of the magic-angle phenomenon.74 Globular and linear hyperintensities in the meniscus may be caused by mucoid degeneration or a meniscal tear. Since differentiation of these two entities is paramount, various classification systems have been devised and will be discussed later. On coronal and sagittal images, the peripheral layers of the menisci manifest as biconcave disks (“bow tie”) and the inner layers as signal-void triangles (▶ Fig. 7.7).26,160 Familiarity with a number of anatomic peculiarities is required to avoid misinterpreting them as pathologic findings. The anterior transverse ligament of the knee connects the anterior horns of both menisci (▶ Fig. 7.8). It is located posteriorly to Hoffa’s fat pad and anteriorly to the joint capsule. On sagittal sections, a hyperintense line can be identified in 22 to 38% of cases at this site, where the transverse ligament of the knee joins the anterior horn of the lateral meniscus.89,222 This hyperintense line should not be mistaken for a tear in the anterior horn of the lateral meniscus.

Fig. 7.7 Visualization of the meniscus on sagittal MR image in relation to the imaging plane. Schematic diagram.

a

b

By reviewing the sequential sagittal sections, it will be possible to clearly identify the various anatomic structures. Likewise, the anterior meniscofemoral ligament can masquerade as a tear where it inserts at the posterior horn of the lateral meniscus.208 However, it should not be mistaken for a “bucket handle” tear with a displaced fragment in the intercondylar notch (▶ Fig. 7.9 and ▶ Fig. 7.10). The tendon sheath of the popliteal tendon manifests as a vertical or slightly obliquely oriented zone of high signal intensity, bordered posteriorly by the posterior horn of the lateral meniscus. Unfamiliarity with this situation can result in it being misinterpreted as a vertical tear of the posterior horn of the lateral meniscus or as meniscocapsular separation. Finally, it must be borne in mind that the pars intermedia of the lateral meniscus is not attached to the LCL. Therefore, the hyperintense zone between the lateral meniscus and ligament should not be mistaken for meniscocapsular separation. On sagittal sections, the entire course of the ACL is visualized, provided that the knee is rotated externally by 15 to 20 degrees (▶ Fig. 7.11). The use of paracoronal slices angulated along the course of the ligament on sagittal slices is often a valuable addition to sagittal sections, since they also clearly visualize the femoral origin of the ligament. The ACL is demonstrated as a signal-void ligament, which can exhibit higher signal intensity, especially in the tibial portion, because of interposed fatty tissue between individual fiber bundles. The magic-angle phenomenon may also be responsible for the higher signal intensity along the ligament course. The PCL exhibits homogeneously low signal intensity and can be clearly identified on sagittal slices. It has an even, curved posterosuperior course. The entire course of the MCL can be demonstrated on midcoronal slices. It has low signal intensity on all pulse sequences. The tibial collateral ligament is composed of a superficial and a deep layer: ● The superficial layer extends from the medial femoral condyle to the inner aspect of the tibial metaphysis, 7.5 to 10 cm distal to the joint space. ● The deep layer of the MCL serves to reinforce the joint capsule and is separated anteriorly from the superficial layer. It is much shorter than the superficial layer and runs from the distal portion of the medial femoral condyle to the proximal tibia. It sends fibrous connections to the medial meniscus. The deep layer of the tibial collateral ligament is not normally discernible.

c

Fig. 7.8 Anterior transverse ligament of knee. The anterior transverse ligament (arrows) connects the anterior horns of the menisci and on sagittal images can mimic a meniscal tear at the insertion site (a, arrow). (a) Parasagittal T1w image. (b) Coronal PDw fatsat image. (c) Sagittal PDw fatsat image.

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7.3 Anatomy

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Fig. 7.9 View of the anterior and posterior meniscofemoral ligaments anterior and posterior to the posterior cruciate ligament on sagittal images. Schematic diagram. 1, anterior meniscofemoral ligament; 2, posterior meniscofemoral ligament.

Fig. 7.10 Meniscofemoral ligament. Coronal PDw fatsat image. Visualization of the meniscofemoral ligament (arrow).

Medial

Lateral

Fig. 7.11 View from above of the tibial plateau, with projection of cruciate ligaments. Schematic diagram. To improve assessment of the anterior cruciate ligament on sagittal images, it is best to image the leg in slight external rotation owing to the oblique orientation; otherwise, an angulated plane can be selected. 1, anterior cruciate ligament; 2, posterior cruciate ligament. Fig. 7.12 Marked undulation of the patellar tendon. Asymptomatic female patient with no reported history of knee trauma.

The superficial and deep layers of the MCL are normally separated by fatty tissue. The normal patellar tendon is devoid of signal on all MRI pulse sequences and is seen as a straight structure.30 It has a mean anteroposterior diameter of 0.5 cm. However, Schweitzer et al182 identified V-shaped discrete foci of hyperintensity in the patellar tendon of even asymptomatic patients. These hyperintense areas were located in 82% of patients in the proximal end and in 32% of patients in the distal end of the tendon. No further increase in signal intensity was seen in these foci on T2w images compared with PDw images. It is unclear whether these hyperintense foci

are suggestive of hitherto clinically silent tendon degeneration or are attributable to the complex structure of the patellar tendon. Even in 71% of asymptomatic patients, a more or less undulating course is identified, and in older and more obese patients, such findings are more common (▶ Fig. 7.12). A variety of pulse sequences have been recommended in this setting (see Chapter 7.2.2 p. 282).121,163,205 From anatomically correlated measurements, it has been concluded that fat-suppressed T1w 3D GRE sequences are able to reliably and reproducibly

289

The Knee

7.4 Meniscal Lesions 7.4.1 Degenerative Changes and Tears The menisci of the knee have various roles in the function of the knee joint and in protecting the joint cartilage. Damage to the menisci can result from injury or from insidious, degenerative changes, mainly occurring in the setting of cartilage erosion. Hence, meniscal tears can be classified as more degenerative and/or more traumatic forms. In addition to the medical history and patient age, MRI, based on signal and morphologic alternations, can facilitate classification. Other criteria used to describe tears include location, extension, fragment dislocation, and stability.

Posterior

b

Degeneration Degenerative Changes Focal increases in signal intensity in the menisci are generally a sign of degenerative (mucoid) changes and may appear as focal or linear areas of increased signal on MRI (▶ Fig. 7.13). The central meniscal regions are more highly vascularized in children and adolescents than in adults. Therefore, hyperintensity in the former group does not have the same implications as in the latter group and may be a sign of normal nutrition. Long-term follow-up observations have revealed that in the majority of cases, foci of increased signal intensity continue unchanged; they only rarely develop into tears or can resolve.56 Degenerative changes in the menisci result in a loss of elasticity of the collagen fibers, predisposing them to tears in the event of trauma. Small tears often occur at the periphery of the meniscus, creating a frayed contour. Besides, synovial fibrillation can also occur. Occasionally, this disruption of the peripheral meniscal contour can be visualized on MRI (fraying; ▶ Fig. 7.14). Pronounced meniscus degeneration can cause maceration but with no immediate evidence of a tear. In such cases, a normal meniscus shape can be seen on MRI, and occasionally, only a diffuse rise in signal intensity may be detected over the entire meniscus. Such findings can give rise to false-negative results on MRI. There are also reports by surgeons of the meniscus disintegrating on coming into contact with a palpating hook. Most other signs of meniscus degeneration, such as calcification, gas accumulation, and bone metaplasia, can be classified on radiographs and, at most, are seen on MRI as areas of abnormal reduced signal intensity or signal void.

Degenerative Tears Increased signal intensity extending into the cartilaginous surface of the meniscus is generally a sign of tears. Degenerative tears are typically horizontal or oblique–horizontal tears that run from the inner margin of the menisci and almost split the meniscus (cleavage tear; ▶ Fig. 7.15, ▶ Fig. 7.16, and ▶ Fig. 7.17). Linear hyperintensity extending into the peripheral superior and inferior surface of the meniscus, with declining signal intensity toward its apex, may be a sign of a tear in the meniscal substance (closed tear). The peripheral raised signal intensity is no longer consistent with a tear but rather suggestive of degeneration. Such tears can be identified on arthroscopy only by probing.

c Lateral d a e

Fig. 7.13 Normal menisci with no tears. Schematic diagram. (a) View from above. (b) Cross-section exhibiting homogeneously low signal intensity to signal void. (c) Increased signal intensity at the base due to nutrition. (d) Longitudinal central hyperintensity due to mucoid degeneration. (e) Focal central hyperintensity due to mucoid degeneration.

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a

b

Fig. 7.14 Degenerative, superficial meniscal damage with “fraying.” Schematic diagram. (a) View from above. (b) Cross-section.

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demonstrate the cartilage thickness and cartilage volume.59,61,62 On using this sequence to image patients, it was possible to accurately determine loss of cartilage and surface changes.190 However, heavily T2w TSE sequences are better at diagnosing structural changes to hyaline cartilage. MTC and MTC subtraction have proved superior for detection of superficial defects and lesions within the cartilage substance.213 Hyaline joint cartilage has intermediate signal intensity on T1w SE images. The basal calcified cartilage layers cannot be delineated from the subchondral bone. Hyaline joint cartilage normally exhibits low signal intensity on T2w SE images. On GRE sequences, the image contrast varies greatly in accordance with the respective imaging parameters. An intermediate flip angle (20–40 degrees) is generally recommended to display the hyaline joint cartilage. If there is a joint effusion, an “arthrographic effect” can be achieved with heavily T2w sequences and can be exploited for detection of discrete superficial lesions of the joint cartilage. The amount of joint synovial fluid within a healthy knee varies and increases after physiologic stress or athletic activities. A diagnosis of joint effusion should be issued only if the slice thickness of the visible fluid collection in the suprapatellar recess and/or posterior to the cruciate ligaments (posterior recess) is more than 10 mm on sagittal MR images.80

7.4 Meniscal Lesions

a

b

d

f

c

e

Fig. 7.16 Horizontal tear of lateral meniscus. Sagittal T1w sequence. Horizontal hyperintensity extending to meniscus surface (arrow) as a sign of a horizontal tear of the anterior horn of the lateral meniscus.

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Fig. 7.15 Horizontal meniscal tears. Schematic diagram. (a) Horizontal, peripheral gaping tear (fish-mouth tear; cross-section). (b) Oblique tear extending to undersurface. (c) Oblique tear extending to surface. (d) Displaced horizontal tear forming a “bucket handle” (view from above). (e) Displaced horizontal tear forming “flap” (view from above). (f) Displaced horizontal tear (cross-section). The inferior, anterior half of the meniscus is absent.

A tear may be very wide (“gaping”) and contain fluid (fishmouth tear; ▶ Fig. 7.18). In addition to segmental extensions, the entire meniscus may also be affected. Part of the meniscus can become detached and displaced into the joint (flap tear). The meniscus is then often deformed, with part of it missing, for example, the inferior anterior third (▶ Fig. 7.19). Dislodged portions, as in other dislocated tears, may have a “bucket-handle” appearance65 and come to rest anterior to other meniscal parts or even give rise to loose joint bodies. It may be difficult to detect such tears on arthroscopy, since the meniscus surface appears normal.

Traumatic Tears and Avulsions Traumatic incidents, often involving a combination of injuries, typically result in longitudinal or transverse tears. Basal avulsions are rarely seen at the meniscal attachment to the tibial plateau.

Longitudinal Tear Vertical longitudinal tears are often found in the more peripheral vascularized “red” zone, since they tend to follow the dominating longitudinal configuration of the peripheral fibers. They may be of variable length. On MRI, a cleft may be identified, depending on the location of the tear (▶ Fig. 7.20 and ▶ Fig. 7.21).

a

b

Fig. 7.17 Oblique tear of medial meniscus. Sagittal T1w sequence. Obliquely oriented hyperintensity extending to undersurface of the meniscus (arrow) as a sign of a horizontal tear in the posterior horn of the medial meniscus.

c

Fig. 7.18 Fish-mouth tear of medial meniscus. Horizontal meniscal tear in the posterior horn of the medial meniscus, with fluid accumulation in the gaping tear (fish-mouth tear). (a) Sagittal T1w sequence. (b) Sagittal PDw fatsat sequence. (c) Coronal PDw fatsat sequence.

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a

b

Fig. 7.19 Dislocation of the inferior anterior portion of a horizontal tear of the medial meniscus, with characteristic substance defect. The arrowheads point to the substance defect. (a) Sagittal T1w image. (b) Sagittal PDw fatsat image.

c a

f d

e b

g

h Fig. 7.20 Longitudinal meniscal tears. Schematic diagram. (a) Small longitudinal tear (view from above). (b) Large longitudinal tear. (c) Partial longitudinal tear extending from the surface (cross-section). (d) Partial longitudinal tear extending from the undersurface. (e) Full-thickness longitudinal tear. (f) Displaced longitudinal tear forming a “flap” (view from above). (g) Displaced longitudinal tear, with interiorly flipped fragment forming a “bucket handle.” (h) Displaced longitudinal tear, with interiorly displaced fragment forming a “bucket handle.”

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When tears occur at the outermost periphery, the meniscus may become fully detached from the joint capsule (meniscocapsular separation); in such cases, fluid can be detected between the meniscus and joint capsule. Dislocation may occur if a torn meniscal fragment becomes displaced. Displaced meniscal fragments may be found at the most diverse locations in the joint (▶ Fig. 7.22). Extensive longitudinal tears may result in intra-articular displacement of the central meniscal fragment, which, however, continues to be attached at the meniscal base. When viewed from above, such a tear has a bucketlike appearance with a large handle (bucket-handle tear). The following changes and signs can occasionally be seen on MRI (▶ Fig. 7.23):

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7.4 Meniscal Lesions

a

b

a

b

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Fig. 7.21 Longitudinal meniscal tears. Two patients. The arrowheads point to the longitudinal tears. (a) Sagittal T1w sequence. Longitudinal meniscal tear of the posterior horn of the medial meniscus. (b) Coronal PDw fatsat sequence. Meniscal tear in the pars horizontalis of the lateral meniscus.

c

Fig. 7.22 Displaced medial meniscal tear (most probably a longitudinal tear). Distorted posterior horn of medial meniscus (tip absent; a, arrow); meniscal fragment in the intercondylar notch (b, c, arrows). (a) Sagittal T1w image. (b) Coronal PDw fatsat image. (c) Axial PDw fatsat image.

Posterior cruciate ligament

Posterior cruciate ligament

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●

Displaced fragment a

Displaced fragment MM stump b

Fig. 7.23 MRI findings of bucket-handle tear of the medial meniscus. Schematic diagram. (a) Sagittal plane. (b) Coronal plane. MM: medialmeniscus.

●

Double PCL sign: Here, the medially displaced meniscal fragment is visualized as a hypointense bandlike structure on sagittal slices parallel to and beneath the PCL. In rare bucket-handle tears of the lateral and medial menisci, two fragments can be seen deep to the PCL, manifesting as a triple PCL sign (▶ Fig. 7.24).

Detection of a fragment in the intercondylar notch: oronal slices (▶ Fig. 7.25; see also ▶ Fig. 7.23b).223,225 Double meniscal anterior horn sign (▶ Fig. 7.26a): When seen immediately posterior to the anterior horn, the fragment is magnified and appears to be duplicated. Flipped meniscus sign: This sign is seen in association with anterior displacement of a detached meniscal fragment (see ▶ Fig. 7.26a).7 Narrowed, missing, deformed depiction of the pars intermedia or the detached meniscal part (▶ Fig. 7.26b and ▶ Fig. 7.26c): For example, shortening and enlargement of the triangular transverse surface or nonvisualization of this structure at its normal anatomic position. Normally, the posterior horn of the medial meniscus appears much larger than the anterior horn on sagittal slices. Failure to identify this as such is suggestive of a bucket-handle tear. On coronal slices, the pars intermedia of both menisci is normally of the same size.

Bucket-handle tears of the medial meniscus are much more common than those of the lateral meniscal. Small bucket-handle fragments are, naturally, harder to detect than their larger counterparts.

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a

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c

a

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Fig. 7.25 Bucket-handle tear of the medial meniscus. (a) Coronal PDw fatsat sequence. Detection of a meniscal fragment in the intercondylar notch (arrow). (b) Axial PDw fatsat sequence. Expansion of the meniscus (arrow).

Fig. 7.26 Bucket-handle tear of the lateral meniscus, with anterior displacement of the detached fragment. (a) Sagittal image. Double anterior horn sign (flipped meniscus sign; arrow). (b) Posterior coronal image. Mostly, nonvisualization of the meniscus. (c) Anterior coronal image, showing thickened meniscus.

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Fig. 7.24 Bucket-handle tears of the medial and lateral menisci with double anterior horn sign. (a) Sagittal T1w sequence. Bucket-handle tear with double anterior horn sign on the outside (arrow). (b) Sagittal T1w sequence. Bucket-handle tear with double anterior horn sign on the inside (arrow). (c) Sagittal T1w sequence. Bucket-handle tear with triple posterior cruciate ligament sign (arrow).

7.4 Meniscal Lesions

Transverse Tear

d

e b

f

g c Fig. 7.27 Transverse (radial) meniscal tears. Schematic diagram. (a) Small transverse tear (view from above). (b) Large transverse tear. (c) Transverse tear with longitudinal tear component (parrot-beak tear). (d) Displaced parrot-beak tear forming a “flap.” (e) Transverse tear with nonvisualization of the meniscus apex but with shimmering contour of parts of the adjacent healthy meniscus due to partial volume artefact (cross-section). (f) Absence of meniscus apex. (g) Shimmering contour of entire meniscus due to partial volume artefact (ghost meniscus).

a

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a

A “transverse” or “radial” tear is the term used to denote a deep vertical notch in the meniscus, running perpendicular to the margin (▶ Fig. 7.27 and ▶ Fig. 7.28). Such tears can be of a traumatic and/or degenerative nature and account for around 15% of meniscal tears, affecting mainly the posterior horn of the medial meniscus as well as the pars intermedia and the posterior horn of the lateral meniscus. On coronal MR images, a segmental cleft can be seen in the meniscus (cleft sign); on consecutive oblique images, this appears to have “marched” on each adjacent image (marching cleft sign). On sagittal images there is a loss of meniscus substance on the slices showing a tear, often with a well-defined boundary versus the healthy meniscus (truncated triangle sign), or there is a complete absence of meniscus substance on an image, showing the shimmering contour of the adjacent healthy meniscus due to partial volume artefact (ghost sign).86 On axial images, the entire cleft or V-shaped defect can sometimes be identified. Deep radial tears can inflict damage on the stabilizing longitudinal meniscal fibers to such an extent as to cause subluxation of the meniscus (see Chapter 7.4.6).48 If radial tears at the center of the meniscus continue along the longitudinal axis, a fragment of the meniscus body may become loose, causing a large cleft or fragment subluxation (parrot-beak tear; ▶ Fig. 7.29).

b

Fig. 7.28 Signs of radial tear of medial meniscus. (a) Coronal PDw fatsat sequence. Cleft sign (arrow). (b) Sagittal T1w sequence. “Marching cleft” sign (arrow).

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Fig. 7.29 Displaced tear, most probably a transverse tear that has progressed to a longitudinal tear with fragment displacement. Cleft in the medial meniscus (a, arrow); partially detached medial meniscus, with external inferior displacement of the detached meniscal fragment (b, c, arrows). (a) Sagittal PDw fatsat image. (b) Coronal PDw fatsat image. (c) Axial PDw fatsat image.

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The term complex tears denotes various types of differently oriented tears that cause meniscal fragmentation. Complex tears are often observed in menisci secondarily to trauma or degenerative changes.

Detachment Trauma can result in detachment of the menisci from their insertion (root tear; ▶ Fig. 7.30). Detachment of the posterior horn of the lateral meniscus is frequently seen in the setting of a torn ACL. It is often difficult to detect meniscal detachment on MRI, with only fluid-filled or hyperintense defects discernible at the tibial attachment53 or high signal thickening visible at the attachment of anterior horn of the lateral meniscus. Basal tears cause instability, with varying degrees of meniscal dislocation or subluxation (▶ Fig. 7.31 and ▶ Fig. 7.32).

for detection of lateral meniscus tears than for detection of medial meniscus tears. This is particularly true for detachment (root tears) as well as for tears of the posterior horn of the lateral meniscus, especially for longitudinal tears close to the meniscus base.49 Clinical tests (e.g., Steinmann-I and Steinmann-II tests, McMurray’s test, Apley’s compression and distraction test, and Payr’s test) have an accuracy of up to 75%, depending on the publication.90 Accuracy of MRI (see ▶ Table 7.1) is superior to that of clinical tests. Although arthroscopy is normally the reference standard invoked when evaluating MRI, it should be noted that arthroscopy with a diagnostic accuracy of 70 to 98% is not a perfect gold standard. Peripheral meniscal tears and those on the undersurface of the posterior horn of the medial meniscus can be missed.156 Tolin and Sapega200 pointed out that for meticulous and comprehensive examination of the posterior horn of the medial meniscus, posterior access was

Validity of Magnetic Resonance Imaging When evaluating the MRI findings, apart from direct evidence of the tear manifesting as linear hyperintensity and extending to the surface of the meniscus, morphologic changes not involving signal alterations, such as bucket-handle tears (see Longitudinal Tear, p. 291), must also be taken into account. A high level of diagnostic certainty can be achieved if type III signal alterations and the aforementioned morphologic findings are employed as diagnostic criteria (▶ Table 7.1). This certainty is even higher if a lesion is confirmed in two planes and is identifiable on more than one section of the same imaging plane. From the table, it can be seen that MRI sensitivity is poorer

Fig. 7.30 View from above of the lateral meniscus, with avulsion tear at the anterior attachment. Schematic diagram.

a

b

Fig. 7.32 Basal tear of the posterior horn of the medial meniscus. Coronal PDw fatsat image. Discontinuity of the meniscus at the attachment site (arrow) and subluxation of the meniscus.

c

Fig. 7.31 Status post injury leading to basal tear (root tear) at the attachment of the anterior horn of the lateral meniscus. Hyperintense area of partial discontinuity of the meniscal attachment and evidence of long-standing small cysts (a, c, black arrows); thickening of attachment (b, arrow); meniscus instability with subluxation or slight displacement dislocation (a, white arrow). Absorption cyst at tibial plateau (a, arrowhead). (a) Coronal PDw fatsat image. (b) Sagittal PDw fatsat image. (c) Axial PDw fatsat image.

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Complex Tear

7.4 Meniscal Lesions Table 7.1 Results of diagnosis of meniscal tears using magnetic resonance imaging Author

Sensitivity (%)

Specificity (%)

Accuracy (%)

MM

LM

MM

LM

MM

LM

Jackson et al95

98

85

89

99

93

97

Mink et al136

97

92

89

91

94

92

97

96

91

98

94

98

Fisher et al71

93

69

84

94

89

88

De Smet et al51

93

80

87

93

90

89

Justice and Quinn102

96

82

91

98

95

93

Boeree et

al18

Abbreviations: LM, lateral meniscus; MM, medial meniscus.

Whereas more false-negative results are obtained for the lateral meniscus, the incidence of false-negative and false-positive results is similar for the medial meniscus. Interpretation of the MRI findings for the menisci is also largely dependent on the SNR and hence on the magnetic field strength of the scanner used. For example, open low-field systems perform less well than medium- and high-field systems (sensitivity: 50–60 vs. 90–100%; specificity: 90 vs. 95%).211 A number of refinements and improvements to the imaging technique have been recommended to further enhance MRI performance, for example: ● Intravenous (IV)214,223 and intra-articular administration4 of paramagnetic CM. ● 3D reconstruction of 2D MRI data.57 Ultrathin axial slices using T2*w GRE sequences appear to be particularly suitable for detection of radial meniscal tears.5,122 It was not possible to significantly improve MRI diagnostic accuracy for detection of meniscal lesions using radial imaging as the primary modality.157

Therapeutic Relevance and Prediction of Outcome of Clinical Treatment Joint incongruence secondary to meniscal tear can soon give rise to hyperintense synovial irritation of the medial posterior capsule of the knee joint, which can be identified especially on fat-suppressed images; in all probability, this will have been the main source of the clinical symptoms manifested during periods of acutely painful flares. The resultant damage to the joint cartilage can be visualized for long-standing tears or also long after meniscus surgery. Damage resulting from meniscal tears can be treated with conservative or arthroscopic surgery. Persistent clinical symptoms following arthroscopic repair may be attributable to ongoing

synovitis, bone marrow edema, active arthrosis, infection, recurrent tear, persistent tear, etc. Factors conducive to a poor clinical outcome following arthroscopy include severe cartilage damage and bone marrow edema in the compartment to be operated.105

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needed in addition to the arthroscopic standard anterior portal. There are also possibly semantic differences in the terminology used to describe MRI and arthroscopy findings. For example, changes identified on MRI as “tears of a free meniscal rim” could possibly be interpreted on arthroscopy as merely “fraying.”102 Other reasons for false-positive MRI findings are as follows: ● Vacuum phenomena. ● Magic-angle phenomenon in lateral meniscus. ● Anatomic variants.

7.4.2 Postoperative Changes Meniscus surgical procedures include the following techniques: ● Meniscal suture. ● Partial resection. ● Meniscectomy.

Meniscal Suture In general, meniscal suture is used to repair only peripheral lesions, since only these lesions are likely to heal with ingrowth of granulation tissue. These are normally longitudinal and oblique tears. Grade III signal changes can persist in the long term following conservative treatment and meniscal suture, even if patients are free of symptoms. There is reason to suspect a recurrent tear only if corresponding changes are seen on follow-up examination. However, when signal changes consistent with grade III lesions are identified, it is not possible to differentiate healing processes involving granulation and scar tissue from a recurrent tear. In the event of renewed onset of symptoms, the possibility of a tear at another site must also be contemplated.

Partial Resection Most central and/or complex meniscal tears cannot be sutured and are repaired by careful resection of the damaged meniscal tissue. Such an approach is generally suitable for radial, horizontal, complex, and/or dislocated tears. Following partial meniscus resection, it must be borne in mind that an area of central hyperintensity that hitherto did not extend to the surface (type II hyperintensity) can manifest postoperatively as type III hyperintensity, extending to the surface (resection margin) due to resection of part of the meniscus. This should not be misinterpreted as a recurrent full-thickness tear, since it is indicative of meniscal degeneration, as seen in the preoperative setting. On the MRI scan, often only discrete deformity of the meniscal rim can be identified following partial resection. Such findings can easily be overlooked if the medical history is not known. Intra-articular CM injection can facilitate diagnosis of recurrent meniscal tear following partial resection or meniscal suture.4

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a

b

Fig. 7.33 Discoid meniscus, on the outside. Tissue proliferation and thickened lateral meniscus covering the entire lateral condyle. Increased signal intensity at the center but not extending to the surface; this is thought to be more due to the specific fiber architecture than to high-grade degenerative changes (arrows). (a) Coronal PDw fatsat image. (b) Sagittal T1w image.

osteoarthritis or gradually progressive postoperative arthrosis may manifest as signal void and may be mistaken for meniscal remnants or postoperative loose joint bodies. Progression of osteoarthritis signs, such as cartilage lesions, osteophytes, subchondral cysts, and sclerosis, can often be observed during the postoperative course. As with all surgical interventions, corresponding skin defects and susceptibility artefacts are detected because of metal and bone abrasion following open meniscectomy.

7.4.3 Variant Discoid and Ring Meniscus

Fig. 7.34 Incomplete discoid form. Coronal PDw fatsat image. A thin segment of the lateral meniscus extends far into the joint space, pointing to an incomplete discoid form.

Whether indirect MR arthroscopy can be effectively deployed to that effect in future remains to be elucidated.

Meniscectomy Following total meniscectomy, the meniscus can no longer be visualized at its normal anatomic location. Cartilaginous calcification or vacuum phenomena in association with preexisting

298

Discoid menisci are morphologic variants in which the central parts of the meniscal disks are not, or not fully, absorbed during fetal development. The following forms are distinguished: ● Complete forms (▶ Fig. 7.33). ● Incomplete forms (▶ Fig. 7.34). ● Rare ring form. ● Deformed lateral meniscus with no posterior attachment (attached only by the meniscofemoral ligament; this is known as a Wrisberg variant, with painful blockage and snapping phenomena). The prevalence is around 3% for the lateral meniscus and 0.1 to 0.3% for the medial meniscus. In most cases, a snapping sound can already be heard in childhood; otherwise, a discoid meniscus does not cause any complaints. However, discoid menisci are at risk for tears that then do become symptomatic (▶ Fig. 7.35 and ▶ Fig. 7.36). Discoid menisci can be conclusively diagnosed in most cases on MRI by comparing the typical abnormalities with the normal

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7.4 Meniscal Lesions

7.4.4 Parameniscal Cysts Para- and intrameniscal cysts are fluid collections in the region of the meniscocapsular interface or within the meniscus and are observed more often in the lateral meniscus than in the medial meniscus. They are generally associated with horizontal or

a

complex meniscal tears. These cysts may be asymptomatic or cause pain because of inflammation and compression of the surrounding soft tissues. Depending on their size, they may present as palpable masses and can also give rise to snapping phenomena (▶ Fig. 7.37, ▶ Fig. 7.38, and ▶ Fig. 7.39). Medial meniscal cysts are frequently larger than lateral meniscal cysts and eccentric because of their attachment to the medial collateral ligament. This means that they are not exactly at the same level as the underlying tear. Meniscal cysts are prone to recurrence following resection. Fluid-isointense meniscal cysts and ganglion cysts are seen on MRI. A stalk leading to the meniscus can often be observed for parameniscal cysts, but meniscal ganglion cysts are not connected to the joint cavity.

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morphologic findings. Besides, the height of a discoid meniscus is often up to 2 mm more than that of the normal meniscus of the same knee joint.187 Discoid menisci commonly exhibit high signal intensity, which is currently thought to be more a manifestation of impaired fiber architecture than of degenerative changes, especially in young patients (see ▶ Fig. 7.35b).

b

Fig. 7.35 Incomplete discoid medial meniscus with signs of degeneration. Symptomatic 36-year-old patient. Irregular contours and thickening of the medial meniscus, blurred margin, indentation (arrows), and minor chondropathy with cartilage thinning. (a) Coronal PDw fatsat image. (b) Sagittal PDw fatsat image.

a

b

Fig. 7.36 Discoid meniscal tear. The entire discoid lateral meniscus has an irregular shape, with increased signal intensity extending to the surface, suggestive of underlying tears (arrows). (a) Coronal GRE sequence. (b) Sagittal T1w sequence.

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Fig. 7.37 Parameniscal cyst. Parameniscal cyst arising from a severely misshapen and hyperintense lateral meniscus, projecting as a distorted flap beneath the lateral collateral ligament and the patellar retinaculum. The parameniscal cyst exhibits high signal intensity (arrows). (a) Axial T2w SE sequence. (b) Coronal T2w SE sequence.

Fig. 7.39 Meniscal cyst. Coronal MRI slice. Painful outer swelling. Subluxed lateral meniscus and meniscal cyst manifesting as fluidisointense mass adjacent to the meniscus (arrow).

Fig. 7.38 Parameniscal cyst. Sagittal PDw fat-suppressed TSE sequence. Fluid-isointense, small structure (arrow) with stemlike connection to a tear in the anterior horn of the lateral meniscus.

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7.4.5 Meniscal Ossification and Calcification On rare occasions, a discrete ossicle can be identified in the meniscus (commonly in the posterior horn of the medial meniscus). Since this has fatty marrow at its center, it exhibits a bilayer structure characteristic of osteomas on MRI. Meniscal calcification in association with chondrocalcinosis or other diseases involving calcium deposition in synovial tissues is

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7.5 Cruciate Ligament Injuries

Fig. 7.40 Complete meniscal dislocation secondary to traumatic tear. Coronal PDw fatsat image. Medial collateral ligament tear.

generally easily identified on radiographs. A correlated finding seen on rare occasions on MRI, in particular on T2*w GRE sequences, is small punctate areas of signal void in the cartilage and menisci. Gas accumulation within the meniscus can result in a similar finding.

7.4.6 Meniscal Subluxation (Extrusion) Projection of the pars intermedia beyond the edge of the tibial plateau by more than 3 to 5 mm on coronal MR images is referred to as “meniscal subluxation” (extrusion) by some authors.23 This slight displacement of the meniscus in the region of the pars intermedia is commonly seen in association with arthrosis. Slight displacement may also result from joint effusions of different etiology. Unlike the posterior and anterior horns, the pars intermedia has no firm attachment and is therefore more mobile. Such fixation, as it exists here, is mediated via the longitudinal meniscal fibers. Severe subluxation of the posterior or anterior horn can also be observed following trauma, in particular in the presence of complex and radial meniscal tears, where the longitudinal meniscal fibers are severed (▶ Fig. 7.40), and in meniscal detachment (root tear).24,43

7.5 Cruciate Ligament Injuries 7.5.1 Anterior Cruciate Ligament Acute Tear Anterior cruciate ligament (ACL) injuries are often seen in the setting of tears of the MCL, medial meniscus, and joint capsule. In up to 80% of cases, there is discontinuity or inability to visualize the posterosuperior popliteomeniscal fascicle. However, isolated ACL tears are uncommon. The accuracy of clinical diagnosis is reported to be relatively high (sensitivity: 75–95%; specificity: 95–100%). Lee and Yao120 obtained a sensitivity of 87% and a specificity of 89% for clinical examination; clinical examination of fresh injuries is much more difficult.94

Fig. 7.41 Lesions in anterior cruciate ligament. Schematic diagram. (a) Normal finding. (b) Discontinuity of ligament. (c) Nonvisualization in the normal anatomic position. (d) Undulating course, with focal increase in signal intensity. (e) Focal increase in signal intensity. (f) Distension and diffuse signal intensity.

ACL tears exhibit a number of direct and indirect signs on MRI. The constellation of findings will depend largely on whether the lesions involve fresh or chronic, partial or full-thickness tears (▶ Fig. 7.41). Direct signs of ACL tear (▶ Fig. 7.42) include the following: ● Discontinuity of the ligament. ● Nonvisualization of the ACL at its normal anatomic position in the lateral intercondylar notch. ● Undulating ACL contour. ● Displacement of the tibial or femoral ligament segments. In most cases, the tibial ligament portion is almost horizontally positioned. Fresh injuries manifest on T2w images as diffuse or focal hyperintensity in the ligament and surrounding region, with poor delineation and bulging of the ligament.208 The direct signs of ACL tear are reported to have a sensitivity of 93% and specificity of 97%.3,120,162,165,216 High-contrast images of these changes are obtained, in particular, with fat-saturated T2w and short-tau inversion recovery (STIR) sequences. Delineation versus cruciate ligament fibers and edema can be improved by using MTC pulses. Increased signal intensity in the soft tissues posterior to the joint cavity may be manifested as a sign of concomitant capsular injury.

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b

c

Fig. 7.42 Status post skiing injury with proximal tear of the anterior cruciate ligament, tear of medial collateral ligament, tear of Hoffa’s fat pad, and popliteal injury. (a) Sagittal T1w sequence, with complete discontinuity and thickening of the anterior cruciate ligament (arrow). (b) Sagittal PDw fatsat image. Flat angulation of torn anterior cruciate ligament, rupture line in Hoffa’s fat pad (black arrow, “Hoffa fracture”), as well as popliteal injury (white arrow). (c) Coronal PDw fatsat image, with discontinuity of the anterior cruciate ligament (white arrow) and discontinuity of the superficial layer (arrowhead) and the deep layer (black arrow) of the medial collateral ligament.

Fig. 7.43 Changes in the posterior cruciate ligament as an indirect sign of torn anterior cruciate ligament. 1, reduction in posterior cruciate ligament angle (normal: around 123 degrees and with anterior cruciate ligament tear: around 106 degrees); 2, posterior cruciate ligament line does not intersect with the distal femur (in distal 5 cm).

●

●

Indirect signs of ACL tear include the following: Increased angulation or buckling of the PCL (▶ Fig. 7.43, ▶ Fig. 7.44, and ▶ Fig. 7.45). Posterior displacement of the lateral meniscus beyond the posterior boundary of the tibial plateau.

The changes attest to anterior instability and are essentially based on anterior displacement of the tibial plateau in relation to the femoral condyles.203 A distance of more than 5 mm between the vertical lines drawn tangentially to the posterior cortical margins of the lateral femoral condyle and tibial plateau is suggestive of a full-thickness ACL tear (▶ Fig. 7.46 and ▶ Fig. 7.47).

302

Fig. 7.44 Anterior cruciate ligament tear. Moderate increase in posterior cruciate ligament angle.

In acute ACL injuries, subchondral bone bruises are frequently observed in the middle portion of the lateral femoral condyle and posterolateral segment of the tibial plateau (▶ Fig. 7.48 and ▶ Fig. 7.49). These are caused by transient subluxation and impaction of the middle portion of the lateral femoral condyle at the posterolateral tibial plateau. Apart from subchondral bone bruises, osteochondral and chondral compression fractures can occur at the lateral femoral condyle. Subchondral bone bruises can be visualized with high sensitivity on fat-saturated T2w TSE and STIR sequences.170 Occasionally, focal bone edema can also be seen at the attachment and origin of the ACL (▶ Table 7.2 and ▶ Fig. 7.50).

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a

7.5 Cruciate Ligament Injuries

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Fig. 7.46 Anterior displacement of the tibial plateau as an indirect sign of an anterior cruciate ligament tear. x > 5 mm, suggestive of tear. Fig. 7.45 Anterior cruciate ligament tear. Sharp posterior cruciate ligament angle.

Fig. 7.47 Anterior cruciate ligament tear. Posterior displacement of the posterior horn of the lateral meniscus (arrowhead).

The patellar tendon, too, may exhibit foci of increased signal intensity in association with ACL tears; these tears are seen more often in the tibial than in the patellar ligament segments. The patellar ligament and the LCL may have a somewhat undulating course because of their instability. In the majority of cases, ACL tears can be diagnosed on the basis of direct signs. Only rarely are indirect signs the only indication of an ACL tear. Nevertheless, they can provide valuable confirmation of the diagnosis and increase diagnostic accuracy. Robertson et al170 analyzed a total of 22 different signs of ACL tears on MRI and established that the following signs had the highest predictive value (in descending order): ● ACL discontinuity. ● Discontinuity of individual fiber bundles.

Fig. 7.48 Anterior cruciate ligament tear. Sagittal T2w SE sequence with fat saturation. The cross-sectional view of the lateral femoral condyle shows bone bruises in the middle portion of the femoral condyle (arrowheads) as well as in the posterior portion of the tibial plateau (arrow) as an indirect sign of an anterior cruciate ligament tear.

●

● ●

Bone bruise (bone marrow edema) in the posterolateral tibial plateau. Buckled PCL. Positive sign of a PCL line.

Depending on the intensity of femoral impaction with respect to the tibia, the femoral bone bruise may be located more anteriorly (less force) or more posteriorly (more force),

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a

b

Fig. 7.49 Acute anterior cruciate ligament tear. Sagittal PDw fatsat sequences. (a) Discontinuity and hyperintense thickening of the anterior cruciate ligament (arrow). (b) Bone bruise in the lateral femoral condyle (white arrow). Additional finding: Popliteal trauma with steep rise in signal intensity (black arrow).

Table 7.2 Sensitivity of the indirect signs (see ▶ Fig. 7.50) of the anterior cruciate ligament tear78 Indirect sign

Normal

Acute

Chronic

ACL tear

Sensitivity (%) Acute

Chronic

ACL angle

55 degrees

30.7 degrees

27.2 degrees

87

100

ACL angle (Blumensaat’s line)

-1.6 degrees

26.6 degrees

27 degrees

87

100

Bone bruises

NA

NA

NA

76

100

PCL line

NA

NA

NA

45

76

PCL angle

123 degrees

109 degrees

95 degrees

42

84

Posterior displacement 0.5 mm of LM

2.1 mm

5.1 mm

30

76

Anterior drawer

5.4 mm

8.7 mm

27

61

2.2 mm

Abbreviations: ACL, anterior cruciate ligament; LM, lateral meniscus; NA = not applicable; PCL, posterior cruciate ligament. Note: ACL angle = angle between tangent at the anterior ACL and the tibial plateau; ACL angle (Blumensaat’s line) = angle between tangent at the anterior ACL and Blumensaat’s line; PCL line = line drawn posterior to the distal portion of the PCL; when the PCL is intact, it intersects the femur within 5 cm of the distal femur; PCL angle = angle between lines through the center of the proximal portion of the PCL; posterior displacement of the LM = extension of the posterior border of the lateral meniscus beyond the tibial plateau; anterior drawer = tangent at the posterior border of the lateral femoral condyle and the tibia.33

because it may also be associated with a slight compression fracture of the lateral femoral condyle in the region where, in any case, a slight notch can be identified. This depression then appears to be deeper, with surrounding edema (“deep lateral sulcus sign”; ▶ Fig. 7.51).39 In the event of ACL avulsion from the femoral insertion, discrete marrow edema may be identifiable in the lateral femoral

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condyle. The low signal ligament cannot be delineated in the intercondylar notch, with this replaced with edema. Often, these discrete signs can contribute to diagnosis in the case of lessretracted ACL avulsion; these signals can be demonstrated more clearly on axial images (▶ Fig. 7.52). In addition to sagittal slices with external rotation of the leg, oblique coronal sections in parallel to the ACL are very useful, especially

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7.5 Cruciate Ligament Injuries

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Fig. 7.50 Indirect sign of anterior cruciate ligament tear. (a) Tangents and angle. A: tangent at Blumensaat’s line; B: tangent at the anterior contour of the anterior cruciate ligament; C: tangent at the tibial plateau contour. 1, angle between the anterior cruciate ligament and Blumensaat’s line; 2, anterior cruciate ligament angle. (b) Anterior cruciate ligament tear. 1, the angle between the anterior cruciate ligament and Blumensaat’s line is normally around -1.6 degrees; in the presence of an ACL tear, it is positive (> 26 degrees). 2, the anterior cruciate ligament angle, which is normally around 55 degrees, is greatly reduced to around 30 degrees.

Fig. 7.51 Normal and hollowed-out depression of the femoral condyle. Schematic diagram of an MR image of the knee, sagittal plane. (a) Normal depression: both femoral condyles have a slight troughlike depression, extending from the anterior third to the posterior two-thirds. (b) Hollowed-out depression: in addition to contusion of the lateral femoral condyle, anterior cruciate ligament tears may also be associated with minor compression fractures, leading to hollowing out of the depression (deep lateral sulcus sign) and edema.

if other findings are inconclusive and a partial tear is suspected.91 Partial volume effects can produce false-positive or false-negative results on sagittal slices, in particular close to the femoral origin of the ACL, which can be ruled out on the oblique coronal slices.

Partial Tear Detection of partial ACL tears has important clinical implications, since they can progress to full-thickness tears and predispose to knee instability. Such detrimental sequelae can be prevented through timely surgical intervention.178 A distinction is made between transverse partial tears and transverse longitudinal tears (delamination or longitudinal splitting). On MRI, a partial ACL tear is associated with the following characteristic findings206: ● Hyperintensity in the ligament, with still-identifiable intact ligament fibers that can be traced from the femoral origin to the tibial insertion. ● Sausage-shaped thickened structure secondary to hemorrhage into the ligament sheath and edematous obliteration of the actual ligament structures. ● Bowing or undulating ACL contour. ● Nonvisualization of ACL on T1w images, but intact fibers still discernible on STIR or GRE images. ● Absence of secondary signs of ACL tear. Exclusion of anterior tibial subluxation of more than 5 mm is an important criterion for ruling out full-thickness ACL tear.34 However, experience has shown that MRI is not particularly adept at diagnosis of partial ACL tears, and with a sensitivity of

1

2

Fig. 7.52 Marrow edema. Schematic diagram of an MR image of the knee, axial plane. 1, discrete marrow edema with insertional tendinopathy or avulsion edema at the lateral femoral condyle at the attachment of the anterior cruciate ligament; 2, nonvisualization of the anterior cruciate ligament in the intercondylar notch and soft tissue edema pointing to avulsion of the anterior cruciate ligament from the lateral femoral condyle.

40 to 75% and specificity of 62 to 89%, it does not assure adequate diagnostic accuracy.206

Chronic Tear Historic ACL tears (chronic tears) are sometimes difficult to diagnose on MRI. There are no secondary signs such as edematous changes, and often the medical history is blank (“no recollection of trauma”). Nonvisualization of the cruciate ligament (absorption) as a relatively reliable sign can be expected in only around 50% of cases. In the other half of cases, the ligament stump, remnants of the synovial sheath, and scar tissue can mimic an intact ACL, even within the space of a few months (pseudoligament).193 In a study of 40 arthroscopy-confirmed historic ACL tears, no

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Thickening and Degeneration The ACL is particularly susceptible to mucinous degeneration. Occasionally, marked ligament thickening and diffuse hyperintensity can then be identified (▶ Fig. 7.54). However, thickening can also be caused by ganglion cysts within the ACL.

Fig. 7.53 Stump retraction with anterior entrapment following anterior cruciate ligament (ACL) tear. Schematic diagram. Low signal intensity identified at the tip of Hoffa’s fat pad, comma-shaped to nodular structure, consistent with the entrapped ACL stump surrounded by irritative edema. (a) Coronal plane. (b) Sagittal plane.

a

b

7.5.2 Posterior Cruciate Ligament Tears of the PCL are essentially less common than those of the ACL. The following trauma mechanisms have been reported (▶ Fig. 7.55): ● Direct force applied to the proximal and anterior portions of the tibia, with the knee in flexion, resulting in posterior displacement of the tibia (this injury usually causes a tear in the middle portion of the ligament and damage to the posterior joint capsule). ● Hyperextension (this often results in bony avulsion at the tibial PCL attachment). ● Severe abduction and adduction injuries involving rotation. ● Avulsion at the femoral insertion (peel-off lesion). Arthroscopic detection of PCL injuries via an anterior access can be challenging if the ACL is still intact.127 Such injuries are often seen in association with complex damage to other internal

Fig. 7.55 Injury mechanisms and findings in torn posterior cruciate ligament (PCL). Schematic diagram. (a) Force applied to the proximal tibia, with the knee in flexion (arrow). 1, tear of middle PCL segment; 2, posterior joint capsule tear; 3, bone bruises in the anterior portion of the tibial plateau and the (lateral) femoral condyle. (b) Hyperextension injury. 1, bone avulsion at PCL insertion on tibia; 2, bone bruises in the anterior portion of the tibial plateau and femoral condyle.

c

Fig. 7.54 Mucoid degeneration of the anterior cruciate ligament. A 44-year-old woman with inner aspect symptoms and no trauma. Diffuse thickening, edema-isointense signal changes, and partial CM uptake (c, arrow) by ACL, pointing to mucoid degeneration. (a) Sagittal T1w sequence. (b) Sagittal STIR sequence. (c) Sagittal CM-enhanced sequence.

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ligament stump was identifiable in 19 cases, discontinuous stump was seen in 14 cases, and continuous stump was seen in 7 cases, although elongated pseudoligaments were also observed.149 Scarred adhesions linking the torn ACL to the PCL were seen in six cases. Scarred adhesions can also spread to the roof and sidewall of the intercondylar notch. The distal fragment of a torn ACL can fold anteriorly and manifest as a fibrous scarred mass, possibly with signs of entrapment. On MRI, proliferation of hypointense to signal-void nodular tissue can then occasionally be observed at the tip of Hoffa’s fat pad between the condyle and the tibial plateau, in some cases surrounded by edema (pseudocyclops lesion; ▶ Fig. 7.53).93

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7.5 Cruciate Ligament Injuries

Fig. 7.56 Posterior cruciate ligament (PCL) tear. (a) Sagittal T1w SE sequence. Discontinuity of the tibial portion of PCL (arrow). (b) Sagittal T2w SE sequence. Marked rise in signal intensity at PCL insertion, in particular on T2w image (arrowhead).

Table 7.3 Findings associated with injuries of the posterior cruciate ligament Concomitant injury

Incidence (%)

Joint effusion

64

Bone bruises

36

Medial meniscus

32

Lateral meniscus

30

Medial collateral ligament

23

Anterior cruciate ligament

17

Lateral collateral ligament

6

of the preserved contour, with increased signal intensity on PDw images (over 7 mm; in one study it was 12–22 mm; ▶ Fig. 7.57).171 Bone bruises in the anterior portion of the tibial plateau often serve as indirect signs of fresh PCL tears (▶ Table 7.3).103 A prominent posterior meniscofemoral ligament (Wrisberg’s ligament) can masquerade as an intact PCL. Fig. 7.57 Posterior cruciate ligament (PCL) partial tear. Sagittal PDw fatsat sequence. Acute trauma. Marked thickening and hyperintensity of PCL. Some fiber strings appear to be still intact, suggesting an extensive partial tear.

ligamentous structures, especially the posterolateral capsular complex and collateral ligaments, giving rise to severe instability of the knee joint. In general, MRI is adept at diagnosing PCL tears, while essentially applying the same criteria used for tears of the ACL (▶ Fig. 7.56).82,193 However, one difference in ACL versus PCL tear criteria relates to (in over 50% of cases) thickening and continuity

7.5.3 Postoperative Changes to the Cruciate Ligaments Torn cruciate ligaments can be reconstructed using synthetic or autologous grafts. One potential donor site is the patellar tendon. The most common reconstruction technique involves drilling channels (bone tunnels) into the femoral condyle and tibial plateau. Bone plugs attached to each end of the graft are then inserted into these tunnels and secured with interference screws. Some surgeons have advocated the use of double-bundle

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a

b

a

b

c

d

e

Fig. 7.59 Signal changes in reconstructed anterior collateral ligament (ACL). Schematic diagram, sagittal plane. Initial rise in signal intensity from periphery to center. Restoration of low signal intensity after around 18 to 24 months (see text).

reconstruction in order to reflect the double-bundle anatomy of the ACL with different functional effectiveness. To this end, the anteromedial and posterolateral bundles are each reconstructed separately in two drilling channels.32,153 On MRI, multiple foci of signal void may be detected, caused by bone or metal abrasion as well as by metal screws. The drilling channels are displayed as signal void, and their orientation and angulation can be evaluated as on radiographs. The reconstructed ligament exhibits low signal intensity on all sequences. In addition, focal or linear areas of increased signal intensity are observed; these are thought to relate to fibrosis and, in some cases, also fatty tissue, and they should not be mistaken for a recurrent tear.35,177 Likewise, an undulating contour of the reconstructed ligament constitutes a normal postoperative finding. Any evidence of discontinuity is a reliable sign of a recurrent rupture. The reconstructed graft changes over time due to initial edema formation and secondary ingrowth of fibroblasts, as well as revitalization and formation of a new viable ligament within 18 to 24 months after surgery. This gives rise to a mixed constellation of findings on MRI181: an increase in signal intensity is observed within the first 6 months, especially on T1w and PDw, but also on T2w, images. At this stage, it may not be possible to delineate the reconstructed graft from the surrounding connective tissue or from effusions. The

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signal intensity declines again during the subsequent 6 to 24 months, until homogeneously low signal intensity is exhibited by the graft. Focal areas of low-grade hyperintensity can continue beyond this period (▶ Fig. 7.58).180 The changes begin at the margin and extend into the center, but the reverse is true as edema resolves, with more pronounced changes seen in the joint than in the bone tunnel (▶ Fig. 7.59).8 Currently, heavily T2w TSE sequences are recommended for evaluation of cruciate ligament reconstruction, because, first of all, heavily T2w sequences have lower sensitivity for detection of the normal signal changes seen postoperatively, and, second, TSE sequences are less prone to susceptibility artefacts. CM enhancement reflects the zonal remodeling processes, with initial peripheral ring-shaped enhancement and continuing decline in CM enhancement after up to 2 years.150 Complications associated with anterior cruciate reconstruction: ● Instability. ● Pain. ● Functional impairment. ● Absorption. ● Recurrent tear. ● Tunnel and graft cysts. ● Excessive scarring. Functional impairment with discrete inflammation or entrapment often results from improper positioning of the bone tunnels (drilling holes). The following requirements apply for the tibial bone tunnel (▶ Fig. 7.60): ● It should not begin anterior to the extension of Blumensaat’s line on the tibial plateau. ● It must lie within second quarter of the area anterior to the tibial plateau tangent. ● Its angulation should be similar to that of Blumensaat’s line. Placement of the tibial tunnel too far anterior will adversely affect graft function in the roof of the intercondylar notch (superior notch or roof impingement). The femoral bone tunnel should penetrate the lateral femoral condyle at the intersection of the posterior cortical tangent of the femur with Blumensaat’s line (▶ Fig. 7.6, see also ▶ Fig. 7.60, ▶ Fig. 7.61). Failure to observe this

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Fig. 7.58 Cruciate ligament reconstruction. Continuity of the reconstructed cruciate ligament demonstrated in two different patients. (a) Sagittal T1w image. (b) Sagittal PDw fatsat image.

7.5 Cruciate Ligament Injuries

position and placement of the tibial tunnel too far lateral can cause sidewall impingement of the graft in the intercondylar notch.159,201 Impingement syndrome in association with cruciate ligament reconstruction can lead to a discrete area of edematous bulging of the graft, with high signal intensity on T2w images. With continuing impingement, graft rupture may occur. Mechanical damage to the graft within the intercondylar notch can be repaired by means of notchoplasty to widen the roof of the intercondylar notch. Cortical defects are seen in the initial postoperative course, followed later by coverage of the defect with new cortical tissue and cartilage. These changes can be identified on MRI in over 90% of cases, and in the event of an excessive reaction, they will help pinpoint the cause of notchoplasty failure.133 Postoperative metal, synthetic, or bone abrasion within the joint may cause discrete inflammatory reactions. A predilection site where such focal synovitis, leading to fibrosis, is commonly seen is anterior to the tibial drilling hole on Hoffa’s fat pad. These discrete inflammatory nodules can grow to a considerable size and can cause impingement. On arthroscopy, a nodular mass similar to the eyes of a cyclops is seen, hence the term cyclops syndrome (localized anterior arthrofibrosis). On MRI, an inhomogeneous, poorly delineated mass of varying signal intensity can be identified on all sequences (▶ Fig. 7.62).22 Generalized fibrosis of the joint capsule (diffuse arthrofibrosis) results in widespread loss of motion and can be identified on MRI from the hypointense capsular thickening. Occasionally, ganglion cysts and general (pure) cysts can develop along the bone tunnels (tunnel and graft cysts). The cysts can grow to a very large size and infiltrate the surrounding soft tissues and manifest clinically as a palpable mass or swelling.79

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Fig. 7.60 Drilling channels (bone tunnels) for anterior cruciate ligament (ACL) reconstruction. Schematic diagram of sagittal plane with help lines to verify placement of the drilling channels for ACL reconstruction. The tibial bone tunnel should not start anterior to the extension of Blumensaat’s line on the tibial plateau or within the second quarter anterior to the tibial plateau tangent and should be angled similar to Blumensaat’s line. The femoral bone tunnel should penetrate the lateral femoral condyle at the intersection of the posterior cortical tangent of femur with Blumensaat’s line. 1, posterior cortical tangent of femur; 2, Blumensaat’s line; 3, tibial plateau tangent. Fig. 7.61 Status post anterior collateral ligament (ACL) reconstruction. Coronal fat-suppressed PDw TSE sequence. Good visualization of a strong graft at the entrance to the femoral bone tunnel. No sign of notch impingement.

Fig. 7.62 Status post anterior collateral ligament (ACL) surgery. Sagittal T1w sequence. Round scar tissue at the tip of Hoffa’s fat pad (cyclops lesion; arrow).

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7.6 Collateral Ligament Injuries Complex injuries to the knee often involve the collateral ligaments and the posterior portions of the joint capsule.92,101 On clinical examination, it is not possible to clearly distinguish between a medial meniscal tear and an isolated injury to the MCL. In terms of severity, collateral ligament injuries can be graded as follows: ● Grade I: Sprain with local tenderness; no instability. ● Grade II: Partial ligament tear, local tenderness, and moderate opening with valgus stress. ● Grade III: Full-thickness ligament tear; marked instability.

a

b

c

7.6.1 Medial Collateral Ligament Injuries MCL injuries are much more common than those involving lateral ligament structures. They are caused by excessive valgus stress during flexion. The vast majority of these injuries involve the femoral MCL portion and occasionally extend into the joint space. They are found less commonly in the tibial portion. Depending on the severity of the injury, the following findings may be observed183: ● Poorly delineated area of MCL hyperintensity (edema, hemorrhage), with fluid collection around the ligament and in the surrounding soft tissues. ● Thickening and partial discontinuity of the ligament. ● Ligament discontinuity, undulating ligament contours, and ligament detachment from the bone at its origin or insertion. ● Involvement and avulsion of the deep layer as well (meniscofemoral and meniscotibial ligaments; ▶ Fig. 7.63). ● The MCL can no longer be delineated from the subcutaneous fatty tissue. ● Bone marrow edema (bone bruise) in the medial femoral condyle or tibial region.

d-A

e

f

d-B

d-C Fig. 7.63 Medial collateral ligament (MCL). Schematic diagram. (a) Normal visualization, with superficial main portion of the ligament, the deep portion, and the interposed gliding layer mainly accommodating the MCL bursa. (b) Grade I lesion after sprain showing ligament continuity and an edematous fluid collection along the ligament and in the surrounding soft tissues. (c) Grade Il lesion (partial tear) with partial discontinuity, thickening, and edema. (d) Grade Ill lesion with complete discontinuity of the femur (A) or, less commonly, the tibia (B) and undulating course, with or without involvement of the deep layer (C). (e) Tears confined to the deep layer present, mainly in combination with other types of injuries (often ACL tears) rather than as single entities. (f) Chronic or historic tears cause fibrous thickening, calcification, or ossification of the overloaded ligament attachment (Pellegrini–Stieda syndrome).

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The screws and bone plugs can become loose and dislodged. This can generally be detected already on radiographs. Complete discontinuity of the graft is suggestive of recurrent rupture, whether secondary to trauma or degeneration. Laxity of the graft may be a sign of instability, as observed following a fresh (recurrent) tear (buckling of the PCL course with increased angulation and anterior displacement of the tibia).148

7.8 Iliotibial Tract (Band) Syndrome Table 7.4 Signs of medial collateral ligament injury on MRI168 Sensitivity (%)

Specificity (%)

Proximal discontinuity

7

98

Distal discontinuity

12

100

Increased signal intensity in ligament

31

98

Subcutaneous edema

57

96

Fascia edema

76

96

Bone bruise (medial)

53

95 Fig. 7.64 Lateral trauma. Schematic diagram of MRI scan of the knee (coronal plane) to demonstrate potential lateral capsular ligament injuries, mainly after varus injury. (a) More posterior section. 1, injuries to the popliteal tendon; 2, capsular tear and bone avulsion from the tibial plateau (Segond’s fracture); 3, lateral collateral ligament injuries; 4, fibular avulsion of the lateral collateral ligament. (b) More anterior section. 1, rare injury to iliotibial tract; 2, rare avulsion of tract from the tibial eminence (Gerdy’s tubercle).

It is also important to pay attention to concomitant injuries, such as tears of the ACL, meniscocapsular separation, and bone bruises in the lateral portion of the tibia and/or femur. MCL tears are often accompanied by tears of the ACL. Bone bruises on the medial aspect of the tibia and femur, that is, at the MCL attachment, are observed in around one quarter of patients. These are best recognized on fat-saturated T2w SE and STIR images. On comparing the clinical results with MRI grading of MCL injuries, Schweitzer et al183 reported an increase in pain, swelling, and instability from grade I to grade II but not from grade II to grade III. The authors imputed this to posttraumatic edema and muscular defense at the time of clinical examination and concluded that MRI did not lend itself to evaluation of the severity of MCL injuries. Conversely, Yao et al227 correctly graded severity of MCL injuries in 87% of cases (▶ Table 7.4).

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Signs

7.6.2 Lateral Collateral Ligament Injuries LCL injuries are much less common than those of the MCL and are caused by excessive varus stress. The MRI findings are similar to those encountered in MCL injuries.

7.7 Lateral Capsular Ligament Injuries, Including Popliteus Injuries As mentioned above, LCL injuries are much less common than MCL injuries. They are often encountered as combination injuries involving the collateral ligament and other structures (anterior and posterior lateral capsular ligament injury) secondary to varus trauma. The ACL is also often torn in such settings. Injuries to the iliotibial tract such as sprains, partial tears, and bony avulsions at the attachment to Gerdy’s tubercle are often seen in the anterior portion. In the posterior portion, the following findings may be observed (▶ Fig. 7.64, ▶ Fig. 7.65, and ▶ Fig. 7.66)21,217: ● LCL injuries. ● Bone avulsion of the collateral ligament from the fibular tip. ● Capsular tears and bony avulsions of the capsule from the tibial insertion (Segond’s fracture). ● Injury to the popliteus muscle or its tendon (avulsion from the femoral insertion, resulting in an empty popliteal recess). ● Injury to the myotendinous junction.

Fig. 7.65 Normal anatomy of the lateroposterior knee. Sagittal PDw fatsat image. Fabella (black arrow), superior meniscopopliteal fascicle (arrowhead), and popliteal tendon attached to lateral meniscus by inferior meniscopopliteal fascicle (white arrow).

● ● ● ●

Muscle belly injuries. Arcuate ligament injuries. Meniscopopliteal fascicle injuries. Popliteofibular ligament and fabellofibular ligament injuries.

7.8 Iliotibial Tract (Band) Syndrome Parts of the tendons of the tensor fasciae latae, gluteus maximus, and gluteus medius from the pelvic region form a narrow tendon plate that extends on the outer aspect of the thigh to the eminence on the proximal anterior tibia (Gerdy’s tubercle). This iliotibial tract (band) moves over the lateral femoral condyle during knee movements. When engaging in athletic activities, for

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a

b

c

a

b

Fig. 7.67 Iliotibial tract (band) syndrome. External pain, in particular when walking downhill. Thickened, hyperintense tissue between the iliotibial tract and the lateral femoral condyle, inflammatory pseudobursa (white arrows), and eccentric joint effusion (black arrow). (a) Coronal PDw fatsat image. (b) Axial PDw fatsat image.

example, as seen in distance runners, or even in persons with no history of sports involvement, this is often associated with palpable snapping and can cause mechanical irritation of the soft tissues around the lateral femoral condyle (iliotibial tract syndrome). Often, characteristic clinical symptoms are identified such as pain at rest and pressure point pain somewhat superior to and anterior to the joint space. Occasionally, it may be difficult to differentiate this condition from internal knee damage. MRI can help do so by identifying characteristic signs, for example, edema-isointense swelling of the soft tissues between the band and the lateral femoral condyle. Fluid-isointense structures of several centimeters in size, consistent with an inflamed iliotibial bursa or inflammatory fluid collection (pseudobursa), are also

312

sometimes observed.142 Besides, mechanical irritation can give rise to a conspicuous eccentric effusion in the lateral joint recess (▶ Fig. 7.67).

7.9 Dyskinesia of the Femoropatellar Joint and Patellar Dislocation 7.9.1 Impaired Gliding Function As a sesamoid bone, the patella glides over the trochlear groove of the femur. This gliding process is also known as “tracking.” Impaired gliding causes retropatellar pain (impingement,

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Fig. 7.66 Lateral trauma. Status post skiing accident with external pain. (a) Sagittal T1w image. Central area of increased signal intensity in the popliteal tendon (arrow) pointing to fine tear. (b) Sagittal PDw fatsat image. Edema at the myotendinous junction of the popliteus (black arrow) and avulsion of the inferior meniscopopliteal fascicle (white arrow). (c) Coronal PDw fatsat image. Lesion of arcuate ligament (white arrow) and fluid collection in popliteus pointing to fibrous tear (black arrow).

7.9 Dyskinesia of the Femoropatellar Joint and Patellar Dislocation

Fig. 7.68 Femoropatellar maltracking. Symptomatic patient, with no evidence, as yet, of cartilage damage. Marked flattening of the medial femoral trochlea (arrow) as predisposing factor for maltracking.

a

● ●

● ●

Horizontal dystopia (often lateralization). Vertical dystopia (high-riding patella/patella alta or low-riding patella/patella baja). Trochlear dysplasia (often flattening). Decentralized attachment of the patellar ligament at the tibial tuberosity (can be determined by measuring the distance between the trochlea and tibial tuberosity).55

These predisposing factors can be well visualized on radiographs and MR images (▶ Fig. 7.68). To some extent, the underlying abnormalities can be detected on tangential radiographs obtained at 30-, 60-, and 90-degree flexion. However, since subluxation or hyperpressure frequently occurs between 0- and 30-degree flexion, they are missed on radiographic examination. Impaired motion can be visualized as a film with cinematographic MRI. The following syndromes are distinguished: ● Lateral subluxations syndrome: The patella projects beyond the lateral facet of the femoral trochlea on minimal flexion. ● Lateral hyperpressure syndrome: The lateral facet of the patella moves toward the femoral condyle, without evidence of subluxation. ● Medial subluxation syndrome: The patella projects beyond the medial femoral trochlea. ● Lateral–medial patellar subluxation: With increasing flexion of the knee, the patella moves from lateral to medial direction, until it projects beyond the medial trochlea.

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hyperpressure), chondropathy (chondromalacia or patellar chondropathy) and, in the long term, leads to osteoarthritis (femoropatellar osteoarthritis). This condition is also referred to as “maltracking” or “abnormal tracking.” Adolescent and/or overweight women often report such complains, typically with pain and with or without cracking sounds when climbing stairs. Numerous morphologic and functional causes have been identified as the source of such impairment: ● Incongruence of the joint facets (which normally consist of a smaller medial and a larger lateral facet). ● Accentuated patellar tilt angle. ● Patellar dysplasia.

To evaluate the extent of subluxation, qualitative criteria such as the relative position of the patellar tip to the trochlea,186 and quantitative criteria (patellar tilt angle, bisect-offset ratio, and the extent of lateral displacement) can be applied.25,141 During the early symptomatic stages of this disease, MRI demonstrates discrete edema secondary to inflammatory reactions in Hoffa’s fat pad (often in the superolateral region; ▶ Fig. 7.69),198 in the anterior tibial fat pad, or along the

b

Fig. 7.69 Femoropatellar maltracking. Lateral femoropatellar maltracking, with pain on exertion, in particular when climbing stairs, but there is also pain at rest. Irritative edema in superolateral Hoffa’s fat pad (arrows) pointing to maltracking, with contusion of the fat pad. (a) Sagittal PDw fatsat image. (b) Axial PDw fatsat image.

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7.9.2 Patellar Dislocation Traumatic dislocation of the patella, in particular lateral dislocation, often occurs secondarily to impact injury sustained while engaging in contact sports. Depending on the implicated

injury mechanism, dislocation with a different orientation is very rarely observed. In the majority of cases, spontaneous repositioning of the dislocated patella occurs without patients having at all been aware of dislocation and ensuing repositioning. A characteristic constellation of findings suggestive of dislocation is identified on MRI. MRI is also the best imaging modality to identify when surgery is indicated for a cartilage flake fracture or an occult avulsion fracture. The characteristic signs of a complete lateral patellar dislocation include (▶ Fig. 7.70 and ▶ Fig. 7.71): ● Contusion edema of medial patellar pole. ● Corresponding bone bruise at the lateral femoral condyle.108,218 Other signs: ● Signal changes, with or without discontinuity of the medial patellar retinaculum. ● Concomitant soft tissue edema (sprain, partial tear, or fullthickness tear), with or without bony avulsion from the medial patellar aspect. ● Osteochondral lesions of the medial patellar facet or lateral femoral condyle. ● Misalignment of the patellar axis.

Fig. 7.70 Lateral patellar dislocation. Axial schematic diagram of the knee. Synopsis of changes possibly seen secondary to lateral patellar dislocation. 1, Bone or nonbone avulsion of the medial retinaculum from the medial patellar pole; 2, bone bruise of medial patella; 3, misalignment of the patellar axis; 4, flake fractures of patella or lateral femoral condyle; 5, bone bruise at lateral femoral condyle; 6, adductor magnus tendon; 7, adductor tendon; 8, avulsion of the medial patellar retinaculum (medial patellofemoral ligament) from the adductor tendon; 9, edema-isointense, torn or partially torn medial patellar retinaculum with altered signal intensity and edema of the surrounding soft tissue.

a

b

Because of the complexity of the anatomic structures involved, injuries to the retinaculum can have a broad range of manifestations. The patellar retinaculum (tendon) is composed of connective tissue plates between the lateral and medial patellar margins, fibers of the vastus lateralis and medialis (and the more distal obliquely oriented fiber bundles of the vastus medialis, also known as the “vastus obliquus”), collateral ligaments, capsule, and the menisci (referred to by some authors as the patellomeniscal ligament41), as well as the superior margin of the tibia.194 Thickened fiber bundles extending from the patella to the femur and to the superior margin of the tibia have been assigned specific names (patellofemoral ligament and medial and lateral patellotibial ligaments). The medial patellofemoral ligament

c

Fig. 7.71 Bilateral patellar dislocation. Young female patient status post skiing accident and injury to both knees. MRI, which was indicated to exclude internal injuries, showed bilateral patellar dislocation, with apparent spontaneous repositioning. (a) Axial PDw fatsat image. Contusion edema as a hallmark of resolved patellar dislocation at the medial patellar pole (black arrow) and the lateral femur condyle (white arrow) and injury to medial retinaculum on the patellar (black arrow) and femoral attachment (arrowhead). (b) Sagittal T1w sequence. Evidence of a substance defect in overlying cartilage of lateral femur condyle (arrow). (c) Sagittal T1w image. Evidence of detached osteochondral fragment (arrow), consistent with substance defect in (b).

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patellar ligament.36 In the later stages, patellar chondropathy with small areas of cartilage damage can be observed on high-resolution MR images. In the ensuing stage, femoropatellar arthrosis is detected. Dyskinesia can be treated conservatively (strengthening of the vastus medialis or lateralis) or surgically (retinaculum incision).

7.10 Patellar and Quadriceps Tendonitis The clinical symptoms of overuse injury at the inferior patellar pole exhibit the following signs, depending on their temporal course: ● Pain inferior to the patellar apex during athletic activities. ● Pain also after athletic activities. ● Point tenderness. ● Quadriceps atrophy. ● Partial or full-thickness tear of the patellar tendon with a palpable tendon gap. ● Impaired function of the quadriceps muscles. ● High-riding patella.

inserts at the adductor tubercle (insertion of the adductor magnus) of the femur (▶ Fig. 7.72). The patellar tendon serves to attach the patella and to facilitate knee extension. Injury to the medial retinaculum can include tears of the medial patellar margin, tears of the middle third, and avulsion of the medial patellofemoral ligament from the adductor tubercle. In one experimental study among 10 cases of lateral patellar dislocation identified on an MR image, there were 6 retinaculum tears, of which 3 were on the medial patellar margin, 2 on the adductor tubercle of the femur, and 1 located on both sides.31

7.10 Patellar and Quadriceps Tendonitis The patellar tendon is the ligamentous connection between the patella and the tibial tuberosity and is a continuation of the quadriceps tendon. Some anterior fibers extend over the patellar surface and are firmly attached to it. A posterior group of fiber bundles inserts directly at the patellar apex. Chronic overuse of the patellar and quadriceps tendon, as typically occurs among track and field athletes as well as in joggers, can cause quadriceps insertional tendinopathy at the superior patellar pole (around 10% of cases), of the patellar ligament at the patellar insertion (around 70% of cases; patellar apex syndrome, patellar tendinitis, and jumper’s knee), and of the patellar ligament at the insertion on the tibial tuberosity (around 20% of cases).

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Fig. 7.72 Patellar retinaculum. Schematic diagram of anterior knee joint to demonstrate the anatomy of the patellar retinaculum. 1, quadriceps tendon; 2, vastus medialis; 3, vastus obliquus; 4, medial patellofemoral ligament; 5, media retinaculum; 6, medial patellotibial ligament; 7, patellar ligament; 8, lateral patellotibial ligament; 9, lateral retinaculum; 10, lateral patellofemoral ligament; 11, vastus lateralis.

Diagnosis is generally based on the clinical symptoms and can, in most cases, be confirmed by ultrasonography. In the absence of specific clinical findings, MRI may be indicated to differentiate between this condition and other disorders such as femoropatellar arthrosis, chondromalacia, plica syndrome secondary to infrapatellar plica or prepatellar bursitis. On midsagittal MRI sections, the normal patellar tendon is demonstrated as a signal-void structure that increases somewhat in thickness in a caudal direction. Normally, the thickness of the tendon should not exceed 7 mm. Patellar tendinitis, including at its insertion (stage I), may exhibit the following signs: ● Thickness exceeding 7 mm immediately inferior to the patellar apex. ● Increased signal intensity of posterior portion of tendon on all sequences. ● Irregularity of posterior tendon. ● Decreased signal intensity of adjacent Hoffa’s fat pad on T1w images. ● Signal equalization on T2w and CM-enhanced images (concomitant Hoffa’s disease). Partial tears (stage II) or full-thickness tears (stage III) are manifested as partial or complete discontinuity of the tendon, undulating course of the remnant distal fibers as well as high-riding patella.17,63,130 Insertional tendinitis is often seen secondarily to injury (▶ Fig. 7.73). The patellar tendon is more likely to exhibit an undulating course in the presence of a joint effusion, and this is even more pronounced in patients with a torn ACL, since there is often anterior displacement of the tibia. This changes the insertion angle of the patellar tendon at the tibial tuberosity and the distance between the patella and tibial tuberosity.182 Painful juvenile avascular necrosis of the apophysis of the tibial tuberosity (Osgood–Schlatter’s disease) may be accompanied by distal patellar tendinitis. This manifests as an indistinct swollen distal tendon with increased signal intensity, especially on T2w and fat-suppressed images. Quadriceps tears can occur following severe trauma or, if already damaged, even after moderate injuries. The tendon stump may be displaced into the joint, causing impingement (▶ Fig. 7.74). Partial tears of the quadriceps tendon can involve one of the three layers of the quadriceps tendon (▶ Fig. 7.75): ● Superficial layer: rectus femoris. ● Middle layer: vastus medialis and lateralis. ● Deep layer: vastus intermedius.

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a

b

Fig. 7.73 Posttraumatic patellar tendinitis. Status post severe impact trauma 3 weeks prior to MRI examination. Infrapatellar pain and swelling. Massive thickening and edema-isointense signal changes of proximal patellar ligament at the inferior patellar pole. Mild bone marrow edema at the inferior patellar pole, and linear zone devoid of signal in the posterior third of the ligament, possibly suggestive of a posttraumatic partial tear (b, arrow). (a) Sagittal T1w image. (b) Sagittal PDw fatsat image.

Fig. 7.74 Avulsion of the quadriceps tendon at the superior patellar pole. Sagittal STIR sequence. Complete discontinuity and dislocation of the quadriceps tendon (arrow).

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Fig. 7.75 Insertion of quadriceps tendon. Sagittal PDw fatsat image. The normal trilaminate structure of the quadriceps tendon insertion at the superior patellar pole can be easily identified (black arrow). Some fluid in the deep infrapatellar bursa (white arrow).

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The Knee

7.11 Chondropathy, Early-Onset Osteoarthritis, Arthrosis, and Cartilage/Chondral

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Fig. 7.76 Various degrees of retropatellar cartilage damage. Sagittal view of three sawn patellar specimens.

7.11 Chondropathy, Early-Onset Osteoarthritis, Arthrosis, and Cartilage/Chondral Damage 7.11.1 Chondropathy The term chondropathy is used to describe cartilage damage, without any other signs of arthrosis. The improvements in spatial resolution afforded by MRI now increasingly permit better evaluation of the cartilage, even on routine images. Damage to the hyaline joint cartilage can be caused by: ● Degeneration. ● Trauma. ● Inflammatory joint diseases. ● Hemophilia.

Fig. 7.77 Grade III damage to deep cartilage at the medial femoral condyle. Coronal PDw fatsat image. The arrowhead points to the cartilage damage.

Cartilage damage is evaluated on the basis of different criteria by using numerous classification systems (▶ Fig. 7.76): ● According to Noyes and Stabler: shape, size, depth, and location. ● According to Outerbridge: depth. ● According to Ficat: depth. ● According to Bauer: shape. ● According to the International Cartilage Repair Society: size, depth, location, and condition of the corresponding surface area. The authors believe that classification of cartilage damage according to depth (modified after Outerbridge) has proved successful in describing the cartilage damage identifiable on MR images: ● Grade I: Superficial lesion (cannot often be detected on MRI). ● Grade II: Up to 50% of the cartilage thickness damaged. ● Grade III: Over 50% of the cartilage thickness damaged (▶ Fig. 7.77). ● Grade IV: Cartilage damage reaches to the bone, typically accompanied by subchondral bone marrow edema (▶ Fig. 7.78). The term chondropathy can be used to describe the early stages of degenerative joint diseases, where only cartilage damage is visible. This often involves the femoropatellar region, even in younger patients (see Chapter 7.9), when it is termed “chondropathy or patellar chrondromalacia” (▶ Fig. 7.79).

Fig. 7.78 Grade IV extensive cartilage damage with subchondral bone marrow edema at the medial retropatellar surface. Axial PDw fatsat image. The arrowhead points to the cartilage damage.

7.11.2 Early-Onset Osteoarthritis and Arthrosis In addition to cartilage damage, other signs of arthrosis can also be demonstrated at an early stage on MRI. Small osteophytic outer-edge reactions (early osteophyte) and cartilage damage are

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Fig. 7.79 Femoropatellar arthrosis. Femoropatellar arthrosis in association with patellar dystopia (lateralization), with thinning of the overlying cartilage and severe cartilage ulceration (grade III) as well as high-grade cartilage–bone ulcer manifestation (grade IV; can be recognized from the discrete subcortical edema, osteophytes, and subchondral sclerosis). (a) Axial T1w image. (b) Axial T2w image.

the changes typically observed during this stage, when the radiographs are still often normal (▶ Fig. 7.80). The term early-onset arthrosis or radiographically occult arthrosis is used to describe the condition at this stage. Other characteristic findings manifested in association with degenerative joint diseases are subchondral cysts. Such cysts may be quite large or only a few millimeters in diameter and are often seen already at an early stage, commonly at locations where bone edema had been observed a few months previously but the cartilage was normal.42 Such cysts are thought to result from absorption processes following incorrect static loading (absorption cyst) and are seen at certain predilection sites (intercondylar eminence as well as lateral and medial tibial plateau). As arthrosis progresses, the following classic signs predominate: ● Joint space narrowing. ● Subchondral sclerosis. ● Osteophytic outer-edge reactions. ● Subchondral cysts. These signs give rise to conspicuous changes on MRI as well as on radiographs. Chronic synovitis in association with degenerative joint diseases can lead to metaplastic changes in the thickened joint villi and formation of joint bodies, which can also manifest as loose joint bodies. Chondromas and/or capsular osteomas can be identified on MRI as layered intracapsular or intra-articular bodies (▶ Fig. 7.81).

7.11.3 Chondral (Cartilage) and Osteochondral Damage This damage occurs following exposure to strong shear, rotational, or tangential forces affecting only the hyaline joint

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Fig. 7.80 Early osteophytes on the knee. Axial PDw fatsat image. Degenerative changes to joint, with multiple small osteophytes at cartilage-bone junctions (arrows).

cartilage (chondral damage) or also the subchondral bone and overlying cartilage (osteochondral injury). The subchondral bone may be impacted or fragmented, with partial or complete detachment of the fragment (▶ Fig. 7.82). Chondral and osteochondral injuries are generally accompanied by changes to the subchondral bone marrow, termed bone

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The Knee

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7.11 Chondropathy, Early-Onset Osteoarthritis, Arthrosis, and Cartilage/Chondral

Fig. 7.81 Capsular osteoma. Detection of two large capsular osteomas in the medial recess and intercondylar notch exhibiting layered signal intensity (arrows). (a) Coronal PDw fatsat TSE sequence. (b) Axial PDw fatsat TSE sequence.

Fig. 7.82 Osteochondral compression fracture of the lateral femoral condyle. (a) Sagittal PDw SE sequence. Compression and thinning of the hyaline joint cartilage in the region of the lateral femoral condyle (arrows). (b) Sagittal fat-saturated T2w SE sequence. Subchondral bone marrow edema with low signal intensity on PDw (a) and high signal intensity on fat-saturated T2w image (arrowheads).

bruises (see Chapter 7.12.1), and may also be characterized in terms of their edema pattern. Traumatic chondral and osteochondral injuries are more sharply marginated than areas of degenerative cartilage damage

(▶ Fig. 7.83a and ▶ Fig. 7.84).194 Osteochondral lesions are often caused by shear forces (flake fracture; ▶ Fig. 7.83b). Larger cartilage “flakes” can be identified as loose cartilage-isointense joint bodies on cartilage sequences (▶ Fig. 7.85).

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I

II

III

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a

b

Fig. 7.83 Cartilage lesions. (a) Schematic diagram. 1, normal cartilage layer; 2, type IV degenerative cartilage damage with irregular boundary; 3, traumatic cartilage lesion with sharply marginated boundary (bone marrow edema may be present in both types [II and III]). (b) Status post sports injury, with osteochondral flake fracture of medial patellar facet (arrow).

Fig. 7.84 Traumatic cartilage lesion. Sagittal 3D GRE sequence. Visualization of medial femoral condyle. Sharply marginated discrete cartilage defect following sports accident. The previous examination 9 months earlier had been normal at this location. A less well-defined and abrupt boundary would have been expected in association with degenerative cartilage damage.

Fig. 7.85 Loose cartilage joint body in the medial recess of knee. (a) Axial fat-suppressed GRE sequence. Joint body manifests as cartilage-isointense structure (arrow). (b) Axial fat-suppressed T2w TSE sequence.

7.11.4 Treatment of Cartilage Damage and Posttreatment Follow-Up with Magnetic Resonance Imaging Since the ability of cartilage to regenerate itself is limited, cartilage damage usually leads to irreversible progressive joint incongruence, with associated painful synovitis and progressive

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7.11 Chondropathy, Early-Onset Osteoarthritis, Arthrosis, and Cartilage/Chondral

The more elaborate transplant techniques described in the orthopedic literature tend to be indicated for discrete lesions in younger patients. MRI has proved valuable for the follow-up of morphologic changes and of the graft healing process, thus obviating the need for arthroscopic follow-up.

Autologous Cartilage–Bone Grafts For this technique, one or several (mosaicplasty) small cartilage– bone cylinders are harvested from a non–weight-bearing region of a joint (e.g., inner lateral femoral condyle)—or a region with minimal weight-bearing function—and transplanted into the area

with cartilage damage. The following criteria are applied for follow-up with MRI (▶ Fig. 7.86): ● Cartilage congruence: Step deformities can cause mechanical problems in the immediate postoperative course or occur during the cylinder sintering processes. ● Cylinder healing: During the healing process, bone marrow edema is seen immediately after grafting at the boundary between the cylinder and the adjacent intramedullary cavity. This edema continues to be visible for several weeks, and there is increasing CM uptake by the cylinder and the contiguous intramedullary cavity.88 The boundary becomes increasingly less well delineated. Increased CM enhancement can persist for over 6 months or, in some cases, even up to 12 months,88 even when there is clinical evidence of stable healing after 6 to 14 weeks.202 Edema resolution and blurring of the boundary zone are accompanied by restoration of normal signal intensity in the intramedullary cavity, until, eventually, hardly any boundary can be identified. ● Complications: ○ Impaired healing. ○ Partial healing, with persistent boundary or cyst formation. ○ Osteonecrosis. ○ Graft dislocation.202

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arthrosis. Therapeutic options (in addition to symptomatic treatment)131 include: ● Increase gliding function (reduce friction) or induce enhanced regeneration or chondroprotection, based on injection therapy (e.g., with glucosamine, chondroitin sulfate, and hyaluronic acid). ● Induction of enhanced regeneration through invasive intramedullary procedures, followed by microbleeding through superficial abrasion (abrasion arthroplasty), drilling (Pridie drilling), or microfracturing. ● Cartilage, cartilage–bone cylinders, or periosteal transplants.

Often, edematous changes continue to be seen at the donor site for up to 12 months after surgery.88

Autologous Chondrocyte Implantation/ Transplantation

Fig. 7.86 MRI after cartilage–bone knee graft. Schematic diagram. Bone marrow edema surrounding the grafts whose boundary appear more or less well defined, depending on how well they are integrated. Incongruence of upper cartilage layer. Three grafts (b) are used to treat a large area (mosaicplasty). (a) Sagittal plane. (b) Axial plane.

For this technique, chondrocytes (around 200–300 mg) are harvested from a non–weight-bearing region, grown in cell culture, and then implanted into the cartilage defect, by means of either an injection of a carrier substance (then fixed with fibrin glue) or a pouchlike reservoir (periosteal flaps are first sutured). This procedure is indicated for large, isolated areas of cartilage damage in younger patients.132,140,199,202 On MRI examination, the implant initially exhibits increased (to fluid-isointense) signal intensity, which becomes similar to that of normal cartilage after 6 to 12 months. In most cases, marked signal inhomogeneity is observed within the implant. Ideally, the thickness of the implant corresponds to that of the surrounding cartilage (▶ Fig. 7.87).

Fig. 7.87 Status post autologous chondrocyte knee implant. Sagittal schematic diagram. Ideal healing during the immediate postimplant course (a–c) and complications (d–f). (a) The graft manifests as a hyperintense structure on enhanced T2w image. (b) Increasing normalization of signal in line with that of the surrounding healthy cartilage after 3 months. (c) Signal intensity largely in line with that of the surrounding healthy cartilage after 6 months. (d) Implant hypertrophy. (e) Incomplete defect filling. (f) Detachment.

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Osteochondral Allograft Implantation For this technique, the shell-like cartilage–bone graft was harvested from a cadaveric knee. The postoperative course can be well evaluated on MRI.188

7.12 Bone Trauma 7.12.1 Bone Bruises Bone bruises were first identified on MRI, and this has opened up new perspectives. Bone bruises, on the one hand, help explain unclear posttraumatic complaints and, on the other hand, lend credence to the suspicion of intra-articular lesions. Bone bruises are caused by trabecular microfractures, with edema and hemorrhage into the bone marrow. Histology is not normally performed to confirm this finding. However, in one case, a biopsy was taken during cruciate ligament reconstruction, showing edema with hemorrhage in the bone marrow. On MRI, the “edema pattern” can be identified: decrease in signal intensity on T1w images and increase in signal intensity on T2w images. Bone bruises can be visualized particularly well on fat-saturated T2w images and with STIR sequences.6,210,212 Strong CM enhancement can often be detected on fat-saturated T1w sequences. Edema-isointense changes may persist on MRI for up to 10 months in the case of severe bone bruises.20 Bone bruises can be caused by direct blunt trauma or complex traumatic mechanisms, with damage to the capsular ligament. Following blunt trauma, bone marrow edema is found in the region to which force had been applied. Bone bruises in association with capsular ligament injuries exhibit a characteristic distribution pattern. With fresh tears of the ACL, an edematous zone is observed in around half of all cases in the lateral femoral condyle and in the posterolateral portion of the tibial plateau.126,137,227 In acute injury to the PCL, bone bruises are seen in the anterior portion of the tibial plateau and in the femoral condyles. In the presence of acute patellar dislocation, Virolainen et al218 identified bone bruises in the lateral femoral condyle (100% of cases), in the medial portion of the patella (33% of cases), and in the lateral segment of the tibial head. Spraining of the medial patellar retinaculum and hemarthrosis were seen in all cases. Osteochondral and chondral lesions could not be demonstrated on MRI with sufficient clarity. Subchondral bone marrow edema is also identified in association with chondral and osteochondral injuries. Whereas geographic forms increasingly result in early arthrosis,215 most reticular changes resolved without any sequelae. Detection of bone bruises can have major implications when treating the

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patient. For example, effective decompression measures can prevent subsequent osteochondral damage or progression to manifest fractures. Bone bruises generally resolve within 6 to 8 weeks.

7.12.2 Fractures Occult fractures, that is, fractures that are not identifiable on radiographs even when using appropriate equipment and assessment techniques, can be reliably detected on MRI. In addition to linear fracture lines, here too the “edema pattern” can serve as an important diagnostic pointer. When evaluating the actual fractures on MRI, it should be borne in mind that avulsion fractures generally cause little bone marrow edema (▶ Fig. 7.88) and can often be better assessed on computed tomography (CT). Avulsed bone fragments exhibit a characteristic bilaminate structure on MRI (signal-void cortex with adjacent more hyperintense intramedullary portion) and are often greatly displaced (as seen on the radiographs) and/or twisted. Frequently, they cannot be identified so clearly on MRI because they are masked by surrounding hemorrhagic edematous swelling. Typical avulsion fractures encountered in the region of the knee (often seen in combination with other injuries) include the following81: ● Lateral capsular avulsion (Segond’s fracture). ● Medial capsular ligament avulsion (reverse Segond’s fracture). ● Capsular ligament avulsion from the intertubercular eminence. ● LCL avulsion or biceps femoris avulsion (fibular head avulsion, arcuate complex, or posterolateral corner avulsion). ● Quadriceps avulsion from the superior patellar pole. It is not uncommon for fractures to be first identified on MRI after no conclusive diagnosis could be made on radiography (▶ Fig. 7.89

Fig. 7.88 Partial medial collateral ligament tear (deep layer) with avulsion fracture from the tibial plateau. The arrow points to the avulsion fracture.

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Fluid-isointense defects can persist in the implant in the event of incomplete defect filling. Implant detachment due to poor integration gives rise to basal signal intensity and can result in complete detachment and generation of loose joint bodies. Implant thickening (hypertrophy) is seen in up to 25% of cases, but this rarely persists for longer than 1 year. Edema may be identified in the subchondral portions of the bone marrow, even during a normal healing course.

and ▶ Fig. 7.90). Nondisplaced avulsion fractures of the cruciate ligaments (ACL: intercondylar tubercle; PCL: posterior tibial plateau) are occasionally more easily identified on MRI than on

radiographs.134 Bone injuries involving the intramedullary cavity can give rise to characteristic reflections within the joint caused by bloody fluids of varying fat content (lipohemarthrosis; ▶ Fig. 7.91).

Fig. 7.89 Fracture of the tibial plateau. Sagittal T1w SE sequence. There are few changes seen in the cartilage layer overlying the fracture line.

Fig. 7.90 Transverse patellar fracture. Coronal STIR sequence. Horizontal hyperintense fracture line (arrow). A synchondrosis in association with bipartite patella embarks on different course (eccentric oblique, mainly external) exhibiting low signal intensity on fat-suppressed image.

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7.12 Bone Trauma

Fig. 7.91 Lipohemarthrosis secondary to patellar dislocation with fracture. Fluid–fluid levels in the knee joint, with fat component in the “superior” layer (a, arrow); patient in supine position. (a) Sagittal STIR sequence. (b) Axial T2w TSE sequence.

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Curtiss and Kincaid reported in 195945 on transitory demineralization of the hip in pregnancy, which could be identified on radiography. The etiology and pathogenesis of this transient hip osteoporosis have not been conclusively determined, but it is thought to be a form of reflex dystrophy. Occasionally, regional osteoporosis can be observed in this context or as an isolated entity in the region of the knee joint, typically affecting the femoral condyles and/or tibial plateau. Clinical symptoms include painful restricted motion, which may be accompanied by soft tissue swelling. As in the hip, MRI shows diffuse homogeneous bone marrow edema of a shifting nature and lasting from several weeks to a few months as well as a small joint effusion.221 The changes start in one of the condyles, with or without migration to the other condyle over a period of a few months (normally 2–8 months). If an edema pattern can be identified but with no radiographic evidence of osteopenia, it is termed transient (shifting) edema of the knee. Spontaneous resolution of this condition is generally seen.75,139

7.14 Osteochondritis Dissecans and Avascular Necrosis 7.14.1 Osteochondritis Dissecans The etiology of osteochondritis dissecans has not been conclusively elucidated. Among the possible causes posited are recurrent trauma, focal ischemia, and impairment of the normal ossification processes. However, timely diagnosis and treatment have important prognostic implications for osteochondritis dissecans, since otherwise, there is a risk of earlyonset arthrosis. Adolescents are by far the largest group affected by osteochondritis dissecans. The intercondylar portion of the medial femoral condyle is the predilection site within the knee.124 The condition of the hyaline joint cartilage and the stability of the osteochondral fragment are the chief determinants of the treatment regime initiated.135 The staging proposed by Clanton and DeLee38 has been modified by Kramer et al114 to incorporate the characteristic MRI findings (▶ Fig. 7.92 and ▶ Table 7.5):

●

●

●

Type I: Type I osteochondritis dissecans is demonstrated on MRI as a lentiform or oval subchondral decrease in signal intensity on T1w images. No changes are identifiable on arthroscopy, since the overlying joint cartilage remains intact. Radiographic findings are also normal at this stage. Type II: In type II osteochondritis dissecans, there is incipient demarcation of the displaced fragment, as manifested by a change in signal intensity (▶ Fig. 7.93). Type III: Only type III osteochondritis dissecans can be identified on arthroscopy from the circumscribed bone lesions and partial detachment of the fragment. Small cysts may be seen in the underlying subchondral bone. Synovial fluid and contrast agent are able to enter the gap between the necrotic fragment and the osseous crater (▶ Fig. 7.94).

If the displaced fragment has become fully detached from the osseous crater (type IV), it will be surrounded by fluid.50 Finally, the fragment has separated from the crater (type V) and can now be detected as a loose joint body within the joint cavity (▶ Fig. 7.95). Native MRI is endowed with a sensitivity of 92% and a specificity of 90% for differentiation between stable and unstable fragments. The signal intensity of the necrotic fragment differs from that of the normal bone marrow and is essentially determined by its content of fatty tissue, sclerotic material, and edema (▶ Fig. 7.96). In general, in the later stages, an increasing decline in signal intensity is observed, correlating with the increasing density seen on radiographs. Occasionally, extensive bone marrow edema can be identified on fat-saturated T2w SE and STIR images in the bone marrow regions surrounding the necrotic fragment. Some authors recommend examination with IV or contrast enhancement. If enhancement is observed at the boundary between the displaced fragment and bone crater after administration of IV CM, this is suggestive of fibrous bridging with fixation of the fragment.1 MR arthroscopy is able to reliably

Type I

Type II

Type IV

Type III

Type V

Fig. 7.92 Types of osteochondritis dissecans according to Kramer and Scheurecker. Schematic diagram.

Table 7.5 Staging of osteochondritis dissecans according to Clanton and DeLee and Kramer et al

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Type

MRI

Arthroscopy/arthrotome

Treatment

I

Subchondral decrease in signal intensity

Unremarkable

Decompression

II

Demarcation

Unremarkable

Drilling

III

Cartilage defect, partial separation, cysts

Cartilage defect, partial separation

Drilling, curettage, stabilization (pins)

IV

Cartilage defect, complete separation, cysts Cartilage defect, complete separation

Curettage, drilling, resection, transplantation

V

Loose joint body

Resection of joint body, transplantation

Loose joint body

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7.13 Transient (Regional) Migratory Osteoporosis and Shifting Bone Marrow Edema of the Knee

a

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7.14 Osteochondritis Dissecans and Avascular Necrosis

b

Fig. 7.93 Stage II osteochondritis dissecans. Incipient demarcation of fragment (b, arrow). (a) Sagittal PDw fatsat image. (b) Coronal PDw fatsat image.

addition, lack of CM uptake by the displaced fragment is viewed as a poor prognostic factor. In one study, all patients with evidence of CM enhancement by the necrotic fragment experienced remission during the 30-month observation period (9 out of 9 patients). In patients with no enhancement, the remission rate was only 40% (22 out of 55 patients).9

7.14.2 Spontaneous Idiopathic Osteonecrosis of the Femoral Condyle (Ahlbäck’s Disease)

Fig. 7.94 Stage III osteochondritis dissecans Coronal PDw fatsat image. Cartilage damage and partly fluid-isointense demarcation of fragment (arrow).

determine partial and complete detachment of the necrotic fragment, hence this modality is more accurate than native MRI for precise diagnosis of this stage (▶ Fig. 7.97).112 In

Spontaneous osteonecrosis of the femoral condyle mainly affects the medial femoral condyle, with onset generally in middle to old age.2 Patients complain of sudden attacks of severe pain, often long before changes can be identified on radiographs. As the diseases progresses, a subchondral radiolucent line that shows increasing flattening and arthrotic changes can be seen in the affected femoral condyle. Frequently, concomitant damage to the medial meniscus can be observed. MRI allows early diagnosis and precise evaluation of the extent of the necrotic zone (▶ Fig. 7.98).117 The prognosis is poor if the necrotic area exceeds 5 cm2 or occupies more than 40% of the condylar width.15 A bandlike or lentiform area of subchondral low signal intensity can be seen on T1w images. An extensive indistinctly demarcated area of increased signal intensity is seen in the surrounding bone marrow on T2w images, in particular on using a fat-saturated pulse sequence, as well as on STIR images. Extensive edematous zones are detected even in the soft tissues.

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Fig. 7.95 Stage V osteochondritis dissecans. (a) Sagittal T1w SE sequence. Large mouse bed (bone crater). (b) Sagittal STIR sequence. The implicated loose joint body can be seen in the superior recess of Hoffa’s fat pad (arrow) on a STIR image (arthroscopically confirmed).

Fig. 7.96 Corticoid-induced avascular necrosis of the femoral condyles, with secondary osteochondritis dissecans. (a) Sagittal T1w SE-image. The necrotic area of the femoral condyles manifests as an irregularly outlined zone of low signal intensity (arrows). The bone fragment exhibits normal fat-isointense signal intensity and is demarcated by a dark halo (arrowheads). (b) Sagittal T2w SE-image. The necrotic areas of the femoral condyle continue to exhibit low signal intensity. The fragment is surrounded by a halo of hyperintense fluid (arrowheads).

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7.14 Osteochondritis Dissecans and Avascular Necrosis

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Fig. 7.97 Atypical osteochondritis dissecans. Coronal PDw TSE sequence with fat suppression. The inner aspect of the medial femoral condyle is a predilection site for osteonecrosis of the distal femur. The lateral condyle is less commonly affected. On rare occasions, osteochondritis of the tibia is seen. Here, stage II and stage III osteochondritis in a 35-year-old marathon runner. Without arthrography, a clear distinction cannot be made between stages II and III.

Fig. 7.98 Ahlbäck’s disease. Linear demarcated subcortical focus at the medial femoral condyle, with adjacent edema in elderly woman. Additional finding: tibial absorption cyst at the level of the insertion of the anterior cruciate ligament. (a) Coronal GRE sequence. (b) Sagittal fat-suppressed PDw TSE sequence.

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The Knee Table 7.6 Juvenile avascular necrosis of the knee Proper name

Location

Predilection age

Köhler’s disease

Patella

Childhood

Sinding–Larsen’s disease

Secondary ossification center on patella underside

Adolescence

Caffey’s disease

Tibial intercondylar eminence

Adolescence

Blount’s disease

Medial tibial condyle

Infancy

Osgood–Schlatter’s disease

Tibial tuberosity

Infancy, adolescence

Juvenile Osteonecrosis During childhood and adolescence, painful disorders may present in various regions of the skeletal systems whose characteristic changes can be identified on imaging and which are collectively subsumed under the term juvenile osteonecrosis (summarized for the knee region in ▶ Table 7.6). The tibial tuberosity is relatively often implicated (Osgood– Schlatter’s disease). Children complain of pain and swelling at the insertion of the patellar ligament, even when not exercising the joint. The radiographs show a prominent tibial tuberosity, with fragmentation of varying severity. MRI demonstrates fragmentation, bone marrow and soft tissue edema, occasionally deep infrapatellar and/or superficial bursitis, as well as bulging and increased signal intensity at the insertion of the patellar ligament. The disease is generally self-limiting. In adulthood, a prominent fragmented tuberosity, but no edema, is seen. Similar MRI changes are observed for juvenile osteonecrosis in other body regions.

Bone Marrow Infarction Occasionally, MR images of section of the knee bone marrow also demonstrate areas of bone marrow infarction, mainly in the metaphysis but also in the epi- and diaphysis. These exhibit characteristic garlandlike signal alterations, with high signal intensity (also referred to as fibroblast halo) seen on T2w images and fat-isointense signal at the center. In most cases, these characteristic changes facilitate differential diagnosis (▶ Fig. 7.99).

Secondary Osteonecrosis The term osteonecrosis in the epiphyseal regions of the femur and tibia is used to describe ischemic damage to the bone marrow, with an edema pattern, attributable to various causative factors (e.g., cortisone medication, alcohol abuse, and postarthroscopy) (▶ Fig. 7.100).123,176 MRI displays extensive diffuse bone marrow edema, mainly in distal parts of the femur and/or tibia. In later stages, in addition to the diffuse edema pattern, subchondral lines and/or lentiform areas of subchondral sclerosis can be seen.

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7.15 Changes to the Synovial Membrane and Joint Capsule, Sarcoidosis, and Gout Normally, the synovial membrane cannot be identified on MR images, whereas the joint capsule is visualized as a linear structure of low signal intensity. Synovial membrane thickening and increased CM uptake, often accompanied by a joint effusion, are observed in association with a vast number of joint disorders. These changes are particularly conspicuous in rheumatoid arthritis, hemophilic arthropathy, and pigmented villonodular synovitis (PVNS).

7.15.1 Rheumatoid Arthritis Rheumatoid arthritis gives rise to hypertrophy and villous transformation of the synovial membranes. Synovial proliferation is an important pathogenetic factor in progressive joint destruction (synovial arthropathy). Hypervascular synovial proliferation is seen during the active phase of disease, whereas fibrotic synovial proliferation prevails in the chronic inactive phase. On unenhanced T1w MR images, areas of synovial proliferation exhibit low signal intensity and are hard to delineate from a joint effusion. On T2w images, they may manifest as areas of low, high, or mixed signal intensity. Zones of active hypervascular synovial proliferation are seen to exhibit high signal intensity on T2w images. A marked increase in signal intensity in areas of synovial proliferation is observed after IV injection of Gd-based contrast agent, providing strong contrast, versus the joint effusion. This enhancement is particularly pronounced on fat-saturated sequences (▶ Fig. 7.101). Dynamic, contrast-enhanced images showed a rapid rise in signal intensity in the zones of synovial proliferation. This increase was fastest in hypervascular active pannus, reaching its peak after around 60 seconds, whereas in fibrotic pannus, signal intensity reached its peak only after 120 seconds.109 The enhancement factor for hypervascular pannus was 145% and for fibrotic pannus was 25%. Several studies have also demonstrated that dynamic, contrast-enhanced MRI was able to effectively document the success of antirheumatic treatment. It remains unclear at present whether this modality can be effectively deployed for monitoring the response to treatment and whether the parameters used in dynamic, contrast-enhanced MRI can grant useful prognostic

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7.14.3 Other Forms of Osteonecrosis in the Knee Region

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7.15 Changes to the Synovial Membrane and Joint Capsule, Sarcoidosis, and Gout

Fig. 7.99 Bone marrow infarction. Patient with pain in medial aspect of knee. The causes identified were pes anserinus syndrome with anserine bursitis (a, arrow). There was also extensive infarction of the femoral shaft (b, c) and of the femoral condyles (d). Long-term cortisone treatment was given for bronchial asthma. The infarcts were asymptomatic. It was not possible to gain any conclusive insights into the age of the infarcts despite persistent edema (or the fibroblast zone; increased signal intensity in particular on STIR image). (a) Coronal T2w sequence. (b) T2w SE sequence. (c) STIR sequence at the level of the femoral shaft. (d) STIR sequence at the level of the femoral condyles.

insights into rheumatoid arthritis. However, one thing that is beyond doubt even at the present stage is that MRI is an extremely valuable tool for preoperative management of synovectomy and for resolving diagnostic dilemmas. MRI is also adept at identifying popliteal cysts, which often also have a synovial lining, as well as tendon sheath disorders and ligament tears and lesions.

7.15.2 Pigmented Villonodular Synovitis PVNS is characterized by villous and/or nodular synovial proliferation, which can be seen in large joints, bursae, and tendon sheaths. With an incidence of 60 to 80%, monoarticular involvement of the knee joint is very common. The etiology of PVNS is

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Fig. 7.100 Osteonecrosis. Acute knee pain in an alcohol-dependent patient. Bone marrow edema in the distal femoral epiphysis and in parts of the proximal tibial epiphysis with inhomogeneous signal intensity, in particular in the subchondral zone. These changes are consistent with acute secondary osteonecrosis. (a) Coronal PDw fatsat TSE sequence. (b) Sagittal STIR sequence.

Fig. 7.101 Arthritis. Patients with rheumatoid arthritis and acute painful swelling. Synovial thickening with strong CM uptake. (a) Sagittal T1w SE sequence before CM administration. (b) Sagittal T1w SE sequence after CM administration.

unclear, but neoplastic processes are thought to be implicated. Onset of the disease occurs mainly between the ages of 30 and 50 years. Synovial proliferations of PVNS are highly vascularized and

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have a tendency to bleed. PVNS infiltrates are seen in the hyaline joint cartilage and the subchondral bone of corresponding joint bodies, giving rise to polycyclic sclerotic bone destruction.

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7.15 Changes to the Synovial Membrane and Joint Capsule, Sarcoidosis, and Gout Depending on their extension, isolated nodular, multifocal nodular, and diffuse types can be distinguished. Nodular and multifocal nodular PVNS often exhibit characteristic findings on MRI: one or several different-sized synovial masses with strong CM are seen in the joint cavity (▶ Fig. 7.102 and ▶ Fig. 7.103). The term extra-articular PVNS is used to describe the involvement of bursae or tendon sheaths. Reflecting the variable hemosiderin content, signal inhomogeneity, including areas of signal void, is seen because of susceptibility effects, in particular on T2*w GRE sequences (▶ Fig. 7.104 and ▶ Fig. 7.105).100,111,196 The diffuse type (around 25% of cases) gives rise to extensive areas of often slight thickening of the synovial membranes. This type is difficult to diagnose. Bone erosions are seen in association with both types.145 Some studies have reported malignant transformation PVNS (3% of cases).145

Fig. 7.102 Pigmented villonodular synovitis. Sagittal CM-enhanced T1w SE sequence. CM-enhanced somewhat inhomogeneous tumor at the tip of Hoffa’s fat pad.

a

b

d

e

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7.15.3 Hemophiliac Arthropathy Depending on the implicated stage, hemophiliac arthropathy induces a variety of changes due to recurrent bleeding and microbleeding in bones, joint, and soft tissues (see, e.g., ▶ Fig. 4.44). After several years, extensive secondary arthrosis characterized by widespread cartilage damage (“cartilage balding”) and

c

Fig. 7.103 Pigmented villonodular synovitis with strong, diffuse, and multifocal growth. Strong CM uptake by parts of the thickened synovial membranes and nodular masses (c, e, arrows). (a) Axial native T1w image. (b) Axial T1w image following CM administration. (c) Axial subtraction image. (d) Sagittal T1w image following CM administration. (e) Sagittal subtraction image.

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a

b

Fig. 7.104 Focal pigmented villonodular synovitis. Patient with suprapatellar swelling and restricted motion. Space-occupying lesion in the suprapatellar recess (arrows), with multifocal reduced signal intensity on both T1w and T2w CM-enhanced sequences, consistent with hemosiderin deposits in association with focal pigmented villonodular synovitis. (a) Sagittal T1w sequence. (b) Sagittal PDw fatsat sequence.

Fig. 7.105 Pigmented villonodular synovitis of the knee, demonstrated in a Baker’s cyst. (a) Sagittal T2w TSE image. Effusion in the joint cavity, suprapatellar recess, and Baker’s cyst, which exhibits nodular changes. (b) Sagittal FLASH image (see ▶ Table 1.2) after CM injection. Intensive enhancement of the thickened synovial membrane (arrows). Baker’s cyst is devoid of signal because of susceptibility artefact caused by iron deposits (arrowheads).

large subchondral bone cysts can be detected (▶ Fig. 7.106). Areas of synovial proliferation often manifest as signal void because of blood breakdown products, especially on GRE images.

7.15.4 Sarcoidosis Sarcoidosis is also reported to affect the synovial membranes in addition to bones. MRI demonstrates uniform synovial

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thickening, with strong CM uptake.154 When the bones are affected, multiple foci of disease may be seen in the bone marrow of tubular bones (Jüngling’s disease; ▶ Fig. 7.107).

7.15.5 Lipoma Arborescens This is a rare condition that affects the synovial membranes and leads to villous hypertrophy with increased fat deposition. The macroscopic appearance of the hypertrophic villi is

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7.15 Changes to the Synovial Membrane and Joint Capsule, Sarcoidosis, and Gout

a

b

c

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Fig. 7.106 Hemophilic osteoarthropathy of the knee with secondary arthrosis, extensive cartilage damage, and large subchondral bone cysts. (a) Sagittal PDw fatsat image. (b) Coronal PDw fatsat image. (c) Axial PDw fatsat image.

Fig. 7.107 Sarcoidosis. Multiple round foci in the bone marrow of the tibia and femur in patient with sarcoidosis. (a) Sagittal T1w image. (b) Coronal GRE image.

a

b

similar to that of a tree with its arborized branching (Latin: arbor = tree). This entity of unknown etiology is not a real neoplasm. Hence, the term villous lipomatous proliferation of the synovial membranes has been proposed. In addition to the knee joint, lipoma arborescens can also present in the shoulder, hip, or elbow joints. Because of tissue proliferation, different-sized bone erosions may be observed, as in other conditions involving synovial proliferation or deposition of pathologic substances (PVNS, amyloidosis, and chrondromatosis). Swelling of the joint, mainly without pain, may persist from years to decades. Intermittent joint effusions are usually observed, but laboratory blood and effusion test results are normal.175 This condition presents bilaterally in up to 20% of cases. It is thought to occur more frequently in association with posttraumatic arthrosis, causing impingement of the affected joint, joint fatigue, as well as quadriceps atrophy. MRI is able to diagnose this disorder by detecting the almost pathognomonic garland- or frondlike distension of the joint capsule, which is manifested as high signal intensity on T1w images and as signal void on fat-suppressed sequences (▶ Fig. 7.108).

Unlike the hypertrophic villi, the inflamed hypertrophic synovial membranes do not take up CM. In the knee joint, the changes are most conspicuous in the suprapatellar recess.40 Treatment involves total synovectomy.69

7.15.6 Amyloid Arthropathy Long-term hemodialysis for kidney failure can result in excessive deposition of β2 microglobulin amyloid. Amyloid is deposited in the periarticular joint capsule, tendons, and bone, leading to thickening of the joint capsule and tendons, effusions, and intraosseous pseudotumors (see Chapter 3.9.5).

7.15.7 Chondromatosis Joint chondromatosis is associated with the formation of numerous rice grain–sized, nodular bodies within the synovial membranes as well as synovial tissue proliferation and, possibly, bone erosions. This condition is currently thought to be of neoplastic etiology. It mainly affects men between the ages of 30 and 50 years. The knee joint is a common predilection site for this

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The Knee

a

b

c

disease, involving swelling and, in some cases, painful restricted motion. Depending on the extent of their calcification, cartilaginous bodies can be detected already on radiographs. On MRI, numerous different-sized bodies of varying signal intensity are demonstrated within the thickened areas of synovial proliferation; these may be more pronounced at certain locations. Typically, these bodies exhibit low signal intensity on fatsuppressed PDw TSE images and intermediate intensity on enhanced T1w images. The areas of synovial proliferation take up CM, whereas the cartilaginous bodies generally do not, or only marginally, take up CM. In prolonged courses of disease, it may be possible to identify larger bodies as well as osseous bodies resulting from metaplastic transformation, with a characteristic cortical margin and central bone marrow-isointense signal. The term secondary chondromatosis is used to denote this condition when it occurs as a sequela of a different underlying condition (mainly arthrosis).144

7.15.8 Gout Pathologically increased deposition of uric acid crystals (urates) in various tissues can give rise to the clinical picture of gout. The disease progresses in stages from years to decades, often affecting, in particular, the large toe, sesamoid bones, feet, knee, hands and elbows, and, occasionally, also the axial skeleton. In principle, gouty tophi may be seen anywhere in the body. Arthritis with effusions and periarticular soft tissue swelling can be observed in the early stage. In the subsequent stage (rarely, also early on), granulomas are formed as a reaction to the deposition of crystals (gouty tophus), giving rise, in some cases, to characteristic radiographic findings. On MRI, tophi can manifest as osteolytic masses; as lesions in tendons, ligaments, and soft tissues; and also as extensive pannus thickening of the joint capsule or bursal walls. These exhibit low signal intensity on T1w images and predominantly inhomogeneously low signal on T2w images, with heterogeneous CM uptake. The tophi can range from a few millimeters to several centimeters in diameter. Relatively little perifocal reactive bone

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marrow edema is seen in association with osteolytic or erosive tophi.46

7.16 Synovial Plicae (Folds) During the embryonic period, the knee joint consists of three separate synovial compartments: one suprapatellar and two infrapatellar (lateral and medial) compartments. In the course of normal embryogenesis, the dividing septa regress, creating one large synovial cavity. Remnants of these embryonic membranes are normally visible in adults and are referred to as synovial folds or synovial plicae. These are found bilaterally beside the patella, extending to Hoffa’s fat pad (alar plicae; ▶ Fig. 7.109), and are also encountered between the intercondylar fossa and the tip of Hoffa’s fat pad, parallel to the ACL (infrapatellar plica). The alar plicae can be visualized on MRI, in particular in the presence of an effusion, as signal-void linear structures on axial and coronal images; the infrapatellar plica cannot normally be demonstrated on MRI. The incidence of persistent synovial plicae is estimated to be between 20 and 60%. Due to deviations from normal embryonic development, more or less well-pronounced septal remnants may persist. These can also be identified as synovial plicae and can be visualized on MR images, in particular in the presence of an effusion, as signal-void structures. Persistence of the septum between the infra- and suprapatellar compartments gives rise to the suprapatellar plica (▶ Fig. 7.110 and ▶ Fig. 7.111), which may be fully preserved and may also then divide the adult knee into two separate compartments. However, partially regressed forms with a central opening of varying size (porta) and peripheral remnants are more common. The suprapatellar plica is mainly asymptomatic and can be clearly identified on MRI, especially on sagittal sections. Persistence of complete embryonic knee compartments can predispose to infection and should be taken into account for preoperative management or as a possible explanation for asymmetrical joint effusions. They are best detected on arthrography. Persistence of the complete suprapatellar plica leads to creation of a

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Fig. 7.108 Lipoma arborescens. Marked fat-isointense villous hypertrophy of the knee joint, in particular the suprapatellar recess. Femoropatellar arthrosis and osteoarthritis. (a) Axial PDw fatsat sequence. (b) Coronal PDw fatsat sequence. (c) Sagittal T1w sequence.

7.16 Synovial Plicae (Folds)

Axial plane 2

1

3 Sagittal, paramedian plane

Sagittal, median plane

4 4

Fig. 7.110 Suprapatellar synovial plica. T2w SE sequence with fat saturation. High signal intensity of synovial fluid, with clear demarcation of the plica (arrow). Gross fragmentation in the region of the posterior horn of the medial meniscus, demonstrated as an incidental finding.

3 8 6 a

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5

7

b Fig. 7.109 Synovial plicae of the knee joint. Schematic diagram. (a) Normal visualization of the alar plicae on axial image (left). Persistent thickening of lateral patellar plica and medial patellar plica on axial image (upper right) as well as medial patellar plica on sagittal image (lower right). (b) Suprapatellar plica with small residual opening (porta) and infrapatellar plica on sagittal image. 1, alar plica; 2, lateral patellar plica; 3, medial patellar plica; 4, effusion; 5, suprapatellar plica; 6, Hoffa’s fat pad; 7, infrapatellar plica; 8, medial meniscus.

separate suprapatellar bursa, which, in the event of bursitis, can be identified as a palpable suprapatellar mass. In the absence of regression of the infrapatellar septum, the adult knee may continue to be divided into two infrapatellar compartments. However, in most cases, there is partial regression, leaving infrapatellar plicae of varying sizes (also referred to as ligamentum mucosum). In general, impaired regression of the infrapatellar plica is asymptomatic and cannot be demonstrated on MRI. A thickened infrapatellar plica can be mistaken for the ACL, thus making it more difficult to diagnose tears of the cruciate ligament. The infrapatellar plica may be completely absent in 5% of cases; impaired regression with the formation of a septum is seen in around 7% of sections. The exact function of the plica is not known, but it is thought to contribute to joint stability in flexion by reinforcing the adjacent alar plicae. Thickened plicae may also be observed in the medial and lateral knee joints with normal alar plicae. The medial patellar plica is encountered much more commonly than the lateral patellar plica. These plicae can be identified on axial and paramedian sagittal MR images, in particular in the presence of effusions. The

Fig. 7.111 Suprapatellar synovial plica. Coronal T2w SE image. The suprapatellar synovial plica (arrow) can be delineated from the hyperintense joint effusion.

medial patellar plica may become symptomatic (plica syndrome; ▶ Fig. 7.112), for example, medial pain and impingement are commonly seen following injury or overloading during athletic activities. In the ensuing course, even cartilaginous ulceration of the medial femoral condyle may be observed. Arthroscopic resection of the plica is possible if conservative treatment fails. An arthroscopic classification scheme distinguishes four types of medial patellar plicae76: ● Type A: Chordlike thickening of the capsule. ● Type B: Plica that does not extend to the femoral condyle. ● Type C: Plica extending to or covering the medial femoral condyle. ● Type D: Central defect (fenestration) in the plica.

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a

b

Fig. 7.112 Medial patellar plica. (a) Patient with no sign of knee compartment damage (arrow). (b) Patient with symptoms at the medial patellar margin, with third-degree cartilage damage at the medial patellar facet (black arrow) and scarred distortion of the medial alar plica (white arrow).

7.17 Synovial Popliteal Cysts and Bursitis 7.17.1 Synovial Popliteal Cysts Synovial popliteal cysts are cystic lesions with synovial lining, which are encountered in the popliteal fossa and normally communicate with the knee joint. Their etiology has not been fully determined. They are thought to represent discrete perforations in the joint capsule in the region of neighboring bursae, leading to communication between the bursa and the joint (▶ Fig. 7.113 and ▶ Table 7.7). The rise in pressure within the bursa can then result in cystic distention. This mechanism can also explain the higher incidence of popliteal cysts with advancing age as well in association with previous injuries (typically, meniscal tears and lesions of the ACL). Likewise, the higher incidence of such cysts among patients with rheumatoid arthritis can be imputed to an increase in intra-articular pressure secondarily to joint effusions. The bursa most commonly implicated is the gastrocnemius– semimembranosus bursa at the medial femoral condyle (▶ Fig. 7.114). The membranelike tissue layer between this bursa and the joint is very thin, thus possibly predisposing it to tears. The incidence of communication between the bursa and the joint is estimated to be 35 to 55%. A valvular (ball-valve) mechanism imposes one-way flow on the joint fluid, that is, the fluid can enter the bursa but its backflow is prevented, thus further contributing to cystic distention. The incidence of a disruptive mass in the bursa (Baker’s cyst) in association with an existing communication is 5% (▶ Fig. 7.115). Due to the persistently high pressure prevailing within the bursa or cyst because of a valvular mechanism or chronic

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Fig. 7.113 Bursae on and around the knee joint. Schematic diagram. (a) Midsagittal slice. (b) Medial sagittal slice. (c) Anterior view. (d) Posterior view. 1, prepatellar bursa; 2, deep infrapatellar bursa; 3, subcutaneous infrapatellar bursa; 4, bursae of the lateral collateral ligament; 5, iliotibial bursa; 6, pes anserine bursa; 7, bursae of the medial collateral ligament; 8, medial gastrocnemius bursa; 9, lateral gastrocnemius bursa; 10, gastrocnemius-semimembranosus bursa; 11, tibiomembranosa bursa.

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7.17 Synovial Popliteal Cysts and Bursitis Table 7.7 Overview of the bursae of the knee and associated inflammation69,71,128,158,210 Bursa

Location

Cause and clinical picture of inflammation / special features

Differential diagnosis

Prepatellar bursa

Between patella and subcutis

Kneeling activity

Tendinitis of the patellar ligament

Deep infrapatellar bursa and subcutaneous infrapatellar bursa

Around the tibial insertion of the patellar ligament

Jumping, running

Osgood–Schlatter’s disease

Medial gastrocnemius bursa

Between medial femoral condyle Communicates with the joint in and insertion of the medial gastro- around 50% of cases cnemius head

Gastrocnemius–semimembranosus bursa

Between semimembranosus tendon and medial gastrocnemius head at the level of the medial femoral condyle

Lateral gastrocnemius bursa

Between lateral femoral head and lateral gastrocnemius head

Tibiosemimembranosa bursa

At the level of the meniscus between semimembranosus tendon and tibia, comma-shaped, not always present158

Anserine bursa

Between pes anserinus (fanlike Joggers, pain on climbing stairs insertion of gracilis, sartorius, semimembranosus, and semitendinosus muscles) and medioanterior tibia71,210

Bursa of the lateral collateral ligament

Between meniscus and collateral ligament

Bursa of the medial collateral ligament

Between deep and superficial layer Arthrosis osteophytes of medial collateral ligament; not present in 7% of the population

Meniscal damage, collateral ligament injuries, meniscocapsular separation, meniscal ganglion cysts

Iliotibial bursa

Beneath the insertion of the ilioti- Joggers, varus stress bial tract at the lateral tibial condyle (Gerdy’s tubercle)128

See ▶ Fig. 7.125

Popliteal bursa

Capsular recess the level of the popliteal tendon

Often enlarged, really a Baker’s cyst, swelling of the medial popliteal fossa

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May be fused with the pes anserine Medial meniscus lesion or pes gastrocnemius–semimembranosus bursa, may communicate with the joint Ganglion cyst; see ▶ Fig. 7.119

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Fig. 7.114 Fluid in the gastrocnemius–semimembranosus bursa. Axial PDw fatsat image. Superficial posteromedial portion (white arrowhead), deep anterolateral portion (black arrowhead), gastrocnemius medialis tendon (black arrow), semimembranosus tendon (dotted arrow), and semitendinosus tendon (white arrow).

Fig. 7.115 Large Baker’s cyst. Axial PDw fatsat image. Fluid collection in semimembranosus semitendinosus bursa, with ballooning superficial portion and visible connection to deep portion of bursa (arrow).

Fig. 7.116 Dissected Baker’s cyst. Painful swelling in the calf. Large inhomogeneous, predominantly fluid-isointense mass between the gastrocnemius medialis and fascia caused by dissected Baker’s cyst. This inhomogeneity is characteristic and may be attributable to changes in protein concentration, loculation, synovial proliferation, and, possibly, hemorrhage. (a) Sagittal T2w sequence. (b) Axial PDw fatsat sequence.

a

b

arthritis, the bursa can extend deep into the soft tissues of the lower leg (known as dissection). Dissections can involve both the superficial and deep parts of the bursa, causing large masses in some cases. Accordingly, these manifest as superficial lesions between the gastrocnemius medialis and the lower leg fascia (▶ Fig. 7.116) or as deep masses between the gastrocnemius and the soleus (▶ Fig. 7.117). Dissections have also been reported in muscle bellies (intramuscular dissection); these appear to arise mainly from cranial extension into the vastus medialis and caudal spread into the gastrocnemius medialis.67

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A sudden rise in pressure can cause a tear. Differential diagnosis should take account of the following disorders: ● Gastrocnemius–semimembranosus bursitis. ● Popliteal artery aneurysm. ● Varicose veins. ● Hematoma. ● Tumors of the soft tissues and bone.

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7.17 Synovial Popliteal Cysts and Bursitis

a

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Fig. 7.117 Extensive intermuscular dissection of the deep portion of a Baker’s cyst between the gastrocnemius medialis and soleus. Fluid-isointense large intermuscular mass in the calf, with synovial proliferation and septa pointing to chronic activity. (a) Coronal T2w fatsat image. (b) Axial PDw fatsat image.

b

a

b

Fig. 7.118 Chronic prepatellar bursitis following impact trauma 6 months previously. Fluid collection in prepatellar bursa (a, arrow), with thickened wall (b, white arrow) and synovial proliferation (b, black arrow). Arthrosis, historic anterior cruciate ligament tear. (a) Sagittal PDw fatsat image. (b) Sagittal T1w image.

7.17.2 Bursitis Bursitis is caused by repetitive stress on the respective tendon or myotendinous junction, as experienced during athletic activities or encroachment of the synovial space, for example, by osteophytes. Chronic bursitis is often seen after direct impact trauma to the bursa and hemorrhage (▶ Fig. 7.118). The clinical symptoms include pain on exertion, pain at rest, and pressure point pain (▶ Fig. 7.119 and ▶ Fig. 7.120; see ▶ Table 7.7). Pain relief

after steroid injection into the bursa is indicative of bursitis. Infectious bursitis is diagnosed through aspiration and isolation of the causative pathogen. MRI is indicated to facilitate differential diagnosis if the clinical symptoms are not very specific.98,119 In the healthy knee, most bursae cannot be visualized on MR images. However, after exposure to stress, somewhat more fluid can be detected, in particular, in the deep infrapatellar bursa, the medial gastrocnemius bursa, and the gastrocnemius–semimembranosus bursa, and this

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Fig. 7.119 Anserine bursitis. Sagittal T2w sequence. The patient reported pain on exertion in the inner anterior knee, in particular when jogging. Fluid accumulation in anserine bursa as sign of anserine bursitis in association with pes anserine syndrome (arrows).

must be differentiated from symptomatic bursitis. In bursitis, a fluid-distended bursa of low signal intensity is seen on T1w images and high signal intensity on T2w images. In chronic bursitis, hyperintense thickening of the bursal wall as well as areas of signal-void defects in the effusion, caused by debris, can occasionally be seen on T1w images. Increased signal intensity may be observed already on T1w images because of the higher protein content associated with chronic bursitis. Unlike other forms of bursitis, prepatellar bursitis is typically associated with indistinct subcutaneous signal changes as a manifestation of the inflammatory response by the surrounding connective tissues. An isolated fluid collection between the deep and superficial layers of the MCL without any evidence of trauma or joint effusion is suggestive of MCL bursitis (▶ Fig. 7.121).

7.18 Lesions of Hoffa’s Fat Pad and Other Fat Pads The large triangular fat pad beneath the patella (Hoffa’s fat pad) is composed of structural fat that responds to nutritive effects only after a delay. It is interspersed with numerous stabilizing hypointense fibrous septa and is attached at the base to the meniscal anterior horns as well as to the tibial plateau. Its periarticular surface is covered with synovial lining, and at its apex is the transverse ligament, which connects the meniscal anterior horns. The infrapatellar plica extends from this apex to the inner aspect of the lateral femoral condyle. It merges with the alar plicae, located

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Fig. 7.120 Iliotibial bursitis Coronal T2w sequence. Fluid-isointense structure between iliotibial tract and lateral femoral condyle in a patient with lateral knee pain, consistent with iliotibial bursitis in association with iliotibial tract syndrome (arrow).

on the side of the fat pad. In around 10% of cases, the joint capsule extends in this transition region into the fat pad, forming a bump of up to 1.5 cm in size (Hoffa’s recess). This should not be mistaken for ganglion cysts. Another recess has been identified on the superior aspect of the fat pad, immediately beneath the superior patellar pole; loose joint bodies are common here. The fat pad underpins the function of the menisci in offsetting the incongruence between the tibia and the femur. Reflecting its position and function, Hoffa’s fat pad is prone to disease or is implicated in disorders of the knee joint. MRI is adept at demonstrating such conditions. The fat pad can tear following trauma, giving rise to both longitudinal and transverse “fracture lines”. These traumatic clefts are filled with fluid and blood and can be identified as hyperintense lines, especially on STIR sequences. Hoffa fractures are increasingly observed in association with tears of the ACL as well as with fractures of the tibial plateau. Discrete edema of the fat pad is seen secondarily to disorders of the patellar ligament (insertional tendinopathy at the tibia and patella) as well as in avascular necrosis or impaired growth of the tibial tuberosity (Osgood–Schlatter’s disease) and the inferior patellar pole (Sinding–Larsen’s disease). Discrete edema and later hypointense scar tissue are identified on all sequences around the arthroscopic access routes to the knee joint (typically, anterolateral, anteromedial, and central access routes). Infiltration by inflammatory pannus tissue that takes up CM with and without signal-void deposits of hemosiderin is seen in

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7.19 Ganglion Cysts (apart from Meniscal Ganglion Cysts/Parameniscal Cysts) Occasionally, a giant cell tumor of the tendon sheath originating from the patellar ligament can be identified in Hoffa’s fat pad; this has inhomogeneous signal intensity on MRI, with predominantly low signal intensity on both T1w enhanced T2w images, on strong CM uptake (▶ Fig. 7.122).107 Following surgical reconstruction of cruciate ligament tears, a discrete scar of varying signal intensity can be observed at the base of the fat pad (local arthrofibrosis, or cyclops lesion). Repetitive stress can cause recurrent impingement of the fat pad, in turn giving rise to diffuse inflammation, synovial proliferation on its superior aspect, and swelling (Hoffa’s disease/Hoffitis). Edema-isointense signal intensity, a space-occupying effect with distortion of the patellar ligament, and, in the late stages, chronic metaplasia with and without calcification are seen on MRI. There may also be real intracapsular chondromas. Joint diseases, such as tumors, lipoma arborescens, and synovial chondromatosis, may also extend into the fat pad. Other fat pads in and around the knee can exhibit inflammatory signal intensity, including increased CM uptake and swelling, then giving rise to complaints (obesity), mainly caused by mechanical irritation or compression: ● Suprapatellar (quadriceps) fat pad (▶ Fig. 7.123). ● Supracondylar anterior femur fat pad. ● Cruciate ligament fat pad.184,191

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the diffuse and local forms of PVNS, rheumatoid arthritis, and, to a lesser degree, also in nonspecific synovitis. In some cases, very large ganglion cysts are found, in particular, in the fat pad folds and recess, in addition to meniscal ganglion cysts that extend from the anterior horns into the fat pad.

7.19 Ganglion Cysts (apart from Meniscal Ganglion Cysts/ Parameniscal Cysts) Fig. 7.121 Medial collateral ligament bursitis. Coronal PDw fatsat image. Fluid between the deep and superficial layers of the medial collateral ligament (arrow) pointing to medial collateral ligament bursitis.

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Ganglion cysts are gelatinous masses that have their origin in tendons, ligaments, tendon sheaths, joint capsules, bursae, subchondral bone, menisci, or disks. These can cause pain because of compression of adjacent structures as well as nerve palsy and atrophy of the innervated muscles.

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Fig. 7.122 Giant cell tumor. Painful infrapatellar mass. Inhomogeneous mass almost occupying the entire Hoffa’s fat pad, with partially fluid-isointense and partially solid signal intensity; confirmed on histology as a giant-cell tumor. (a) Sagittal T1w sequence. (b) Sagittal PDw fatsat sequence.

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degeneration and ganglion cysts within cruciate ligaments are frequently overlooked on arthroscopy.12 Ganglion cysts of the tibiofibular joint capsule can cause peroneal nerve palsy. Meniscal ganglion cysts, unlike meniscal cysts (see Chapter 7.4.4), are not associated with tears. Intra-articular ganglion cysts can also arise from the alar plicae and are then found on the posterior aspect of Hoffa’s fat pad. Ganglion cysts have even been found within Hoffa’s fat pad.27 These may be large, almost occupying the entire fat pad as a loculated mass, and are thought to originate from ligament strands interspersed in the fat pad.

7.19.2 Extra-articular Ganglion Cysts Fig. 7.124 Intra-articular ganglion cysts of the cruciate ligaments. Schematic diagram. The classification is important for preoperative management of arthroscopic or arthrotomic resection. 1, ganglion cyst in cruciate ligament; 2, ganglion cyst between the cruciate ligaments; 3, ganglion cyst posterior to the cruciate ligaments.

On MRI, ganglion cysts exhibit low signal intensity on T1w images and homogeneously high signal intensity on T2w images. Often, a stalk to the anatomic parent structure as well as linear signal-void septation can be identified. These criteria help distinguish ganglion cysts from other masses.29,98

7.19.1 Intra-articular Ganglion Cysts The incidence of intra-articular knee ganglion cysts is 0.2 to 1%. Intra-articular ganglion cysts of the knee that have their origin in the cruciate ligaments may be found anterior or posterior to, or within, the cruciate ligament and can be removed by arthroscopy or arthrotomy when symptomatic (▶ Fig. 7.124). They are mainly found anterior to the tibial aspect of the ACL. Ganglion cysts are often associated with mucoid degeneration of the anterior cruciate, which now appears thickened and of higher signal intensity, possibly with increased CM uptake. Mucoid

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Extra-articular ganglion cysts are also common, in particular, at the femoral insertion of the gastrocnemius medialis (▶ Fig. 7.125).96

7.20 Nerve Compression Syndrome and Periarticular Neuropathy Diagnostic imaging, in addition to clinical examination and electrophysiology, plays an increasingly more pivotal role in exploring nerve compression syndrome and traumatic nerve lesions. MRI can be used in the following settings: ● Detection of a perineural mass with nerve compression (often ganglion cysts). ● Detection of a tumor of the nerve itself. ● Thickening (inflammatory swelling), tapering (atrophy or partial discontinuity), or discontinuity of a nerve (best visualized on high-resolution MR neurography). ● Atrophy denervation pattern (see Atrophy, p. 455) with longstanding damage to area innervated by the nerve Damage to the peroneal nerve in the knee at the level of the proximal fibula is relatively often caused by ganglion cysts, fractures,

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Fig. 7.123 Obesity of the suprapatellar fat pad. Suprapatellar pain without discernible cause. Thickening with edema-isointense signal changes in the suprapatellar fat pad, pointing to obesity of the suprapatellar fat pad (arrows). (a) Sagittal T1w sequence. (b) Sagittal PDw fatsat sequence. (c) Axial PDw fatsat sequence.

Fig. 7.125 Ganglion cyst in gastrocnemius medialis. Sagittal PDw fatsat image. Multicystic mass, characteristic of ganglion cyst, at the level of the gastrocnemius attachment on femur (arrow).

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7.21 Vascular Diseases

Fig. 7.126 Thrombosed varicose veins or thrombosed ostial aneurysm of the small saphenous vein in association with varicosis, confirmed on surgery. Axial TSE sequence with fat suppression. The patient reported a mass in the popliteal fossa. Basal varicosis of the small saphenous vein diagnosed years previously. Mass in the popliteal fossa of varying, layered signal intensity. Likewise, hyperintense halo suggestive of methemoglobin, observed on T1w image. Tortuous venous course surrounded by phleboedema.

compression at what is known as the soleal sling (fibrous insertion of the soleus).37,116

7.21 Vascular Diseases

Fig. 7.127 Cystic adventitious degeneration of the popliteal artery, confirmed on surgery. Multiple, different-sized cystic masses along the course of the popliteal artery, with septation in some cases.

lower-leg cast, contusion, tumors, varicose veins, and prolonged periods of knee immobilization.58 The clinical picture associated with paresis of the foot extensors includes the following: pain at the level of the fibular head and impaired sensory function of the lateral lower leg and posterior foot. Tibial nerve compression in the popliteal fossa can be caused by ganglion cysts, etc., or may also present secondarily to muscle

Diseases of the popliteal vessels can be a challenge for differential diagnosis, since it is difficult to identify changes, especially if the patient history and details of other diagnoses are not available. Aneurysms can be recognized from their location along the course of a normal vessel as well as from the inhomogeneous signal generated by the flowing blood. Venous thrombosis causes vascular distension as well as inhomogeneous signal intensity due to the presence of clot components of varying ages, with and without methaglobulin detection (▶ Fig. 7.126). Phleboedema secondary to thrombosis can be well visualized, especially on STIR sequences. Cystic adventital degeneration (also called “cystic adventitial necrosis”) is characterized by multiple gelatinous masses in the vascular wall; these range from a few millimeters to centimeters in diameter and may cause vascular constriction.68,195 These cysts resemble ganglion cysts and often also have a similar signal pattern, with low signal intensity on T1w and high signal intensity on T2w images (▶ Fig. 7.127). In terms of pathogenicity, they are thought to result from an embryological developmental anomaly or vascular extension of synovial cysts from an adjacent joint.73 The vascular lumen may be severely constricted. The popliteal artery is often affected (▶ Fig. 7.128). Because of its location within the popliteal fossa, differential diagnosis must also take account of a Baker’s

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Fig. 7.128 Cystic adventitious degeneration of the popliteal artery. Stenosis of the popliteal artery due to conglomerate of cystic masses (arrows) around the popliteal artery. (a) MR angiography. (b) Axial PDw fatsat image. (c) Sagittal PDw fatsat image.

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cyst, normally found in the medial region. Varicose veins rarely present a diagnostic challenge by virtue of the characteristic tortuous course exhibited. Malignant vascular tumors are very rare (e.g., leiomyosarcoma of the popliteal artery).106 Transient stenosis of the popliteal artery can present when engaging in certain activities (entrapment syndrome) because of muscle hypertrophy, muscle variants, and/or a variant course of the popliteal artery. Occasionally, this clinical picture can be visualized on MR angiography at rest and following provocation (▶ Fig. 7.129).

7.22 Special Features in Children Differences in ossification of the femoral condyles can present between the ages of 2 and 12 years, giving rise to foci of variable signal intensity of several millimeters in the subchondral bone marrow, especially in the posterior region.97 There is no evidence of bone marrow edema. This picture changes on follow-up, holding out good prospects for a normal

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ossification process and should not be misinterpreted as osteochondritis dissecans or a bone infarct.

7.23 Common Tumors and Tumorlike Lesions in and around the Knee Enchondromas are one of the most commonly encountered bone tumors in the femur-sided knee joint (see Chondromas [Enchondromas] p. 539). This tumor is often an incidental finding on using MRI to investigate other complaints. In some cases, the tumors may be very large by then. The tumor is typically identified as a chondrogenic matrix with a “popcorn” appearance and lobulated boundary, exhibiting a stippled, ring, or crescent-shaped pattern of CM uptake. The reported incidence is 3%.220 Enchondromas are also often found in the tibia- and fibula-sided knee joint.

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7.24 Pitfalls When Interpreting the Images

Fig. 7.129 Transient stenosis of the popliteal artery. Patient with transient ischemic symptoms of right lower leg. On provocation blood flow in the right popliteal artery (a, arrow) comes to a halt (b), and muscular compression of the arterial lumen. (a) Axial GRE sequence at rest. (b) Axial GRE sequence on provocation (forced plantar flexion). (c) Corresponding contrast angiography at rest. (d) Corresponding contrast angiography on provocation. The popliteal artery is completely compressed on provocation.

Often, a small focal lesion is found in the mediodorsal cortex of the distal (supracondylar) femur of adolescents, typically between the ages of 10 and 15 years. This varies in size from a few millimeters to 2 cm and exhibits muscle-isointense signal intensity on T1w and is slightly hyperintense on enhanced T2w images. The lesion takes up very little CM and may have a signalvoid boundary (▶ Fig. 7.130). This is a growth anomaly with infiltration of fibrous tissue into the cortex (fibrous cortical defect, nonossifying fibroma, cortical desmoid, and cortical irregularity). The lesion is self-limiting (“outgrows itself”), asymptomatic, and does not require treatment or biopsy.118 It is not uncommon for the lesion to be mistaken for a tumor and biopsied or subjected to unwarranted MRI scans once detected on radiographs. This lesion is often located at the insertion of the gastrocnemius medialis. Certain authors thus hypothesize that it is a transient manifestation of traction-induced damage to the cortex.

Cartilaginous exostoses are frequently seen in the knee region (see Osteochondromas p. 541). These may present as single entities or in association with hereditary diseases, when multiple lesions are observed (▶ Fig. 7.131).

7.24 Pitfalls When Interpreting the Images 7.24.1 Increased Signal Intensity at the Meniscus Periphery The increased signal intensity seen at the meniscus periphery, which is caused by fibrovascular bundles, must be distinguished from increased intrameniscal signal intensity. The latter increases in signal intensity are uniform, symmetrical, and radiate from the meniscal border. In one-third of cases, linear hyperintensity can be

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Fig. 7.130 Fibrous cortical defect. Incidental finding of fibrous cortical defect in distal femur in 24-year-old female patient. Small inhomogeneous, focal lesion surrounded by area of low signal (arrows) in the lateroposterior cortex of the distal femur. (a) Coronal PDw fatsat sequence. (b) Axial T1w sequence.

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Fig. 7.132 Artefacts in MRI knee scan. Pitfalls when evaluating the menisci. Schematic diagram. (a) Increased signal intensity at the superior margin of the anterior horns of the menisci because of transverse ligament of knee, at the posterior horn due to the posterior meniscofemoral ligament. (b) Line of increased signal intensity at the meniscal rim on sagittal image due to partial volume artefacts.

Fig. 7.131 Multiple cartilaginous exostoses in association with a hereditary disease (aclasis). Sagittal T1w image. Multiple bone outgrowths on the femur and tibia (arrows) caused by the exostotic bone.

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observed on sagittal images at the insertion of the transverse ligament into the anterior horn of the lateral meniscus and should not be mistaken for a meniscal tear. Less commonly, a similar rise in signal intensity is seen where the transverse ligament inserts at the anterior horn of the medial meniscus. These changes may stem from the accompanying branches of the lateral inferior geniculate artery or from the fat surrounding the ligament (▶ Fig. 7.132). In one-third of cases, the insertion of the meniscofemoral ligaments at the superior aspect of the posterior horn of the lateral meniscus can also masquerade as a tear on sagittal images. The pars intermedia of the lateral meniscus is not attached to the LCL. The popliteal tendon and popliteal sheath tendon run between the meniscus and joint capsule and can also mimic a

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7.24 Pitfalls When Interpreting the Images

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Fig. 7.133 Tripartite patella. Additional ossification centers at the upper outer edge (arrows). (a) Coronal T1w sequence. (b) Coronal PDw fatsat sequence.

vertical tear of the posterior horn of the lateral meniscus or meniscocapsular separation, in particular on coronal images.

7.24.2 Pulsatile Flow Artefacts of the Popliteal Artery Pulsatile flow artefacts of the popliteal artery can mimic fragmentation of the posterior horn of the lateral meniscus. In cases of doubt, by changing the window, the pulsatile flow artefacts can be identified as a ghostlike band across the entire image in the phase-encoding direction. Such an artefact can also be immediately detected on changing the phase-encoding direction.

7.24.3 Line Artefacts Line artefacts (truncation artefacts) known from other body regions can present when using a 128 × 256 matrix. These can mimic longitudinal meniscal tears204 but are now rarely encountered, since a higher-resolution matrix is normally used for meniscus diagnostic imaging.

7.24.4 Bi-, Tri-, and Multipartite Patella As in conventional radiography, persistent patellar fragmentation (bi-, tri-, and multipartite patella) can be mistaken for fractures (▶ Fig. 7.133). However, unlike fractures, anatomic fragmentation of the patella is not accompanied by edema and the connection between the patellar fragments can be identified as a hyperintense cartilaginous synchondrosis on T2w images. The overlying cartilage layer is intact. Besides, persistent patellar fragmentation —as opposed to a fracture—is seen at typical locations. For example, the small fragment of the bipartite patella is located at the

superolateral border of the patella (▶ Fig. 7.134). Bipartite patella is seen in 1% of the population and generally presents bilaterally. The second fragment may also be absent, causing indentation of the patella (patella emarginata). Such a morphologic variant should not be misinterpreted as an avulsion fracture. Occasionally, bipartite patella synchondritis can develop and manifest on MRI as edematous increased signal intensity of the synchondrosis and adjacent bone marrow edema.

7.24.5 Dorsal Defect of the Patella In around 1% of the population, a superolateral defect measuring 0.5 to 2.5 cm is detected in the posterior patella surface. Like a partite patella, this is thought to be imputable to an ossification anomaly and should not be misinterpreted as a pathologic lesion. Occasionally, only an irregular cartilaginous structure can be identified at this location on MRI (▶ Fig. 7.135).

7.24.6 Accessory Posterior Sesamoids Accessory posterior sesamoids (fabellae, “small beans”) should not be mistaken for loose joint bodies or fracture fragments. From their typical location and size of 5 to 20 mm, they can be easily identified already on radiographs. Between 10 and 20% of the population have a lateral fabella. This sesamoid is embedded in the lateral half of the gastrocnemius head and articulates with the lateral femoral condyle. It is found bilaterally in around 75% of cases. On rare occasions, a medial fabella can be found in the medial half of the gastrocnemius head or a distal fabella in the popliteal tendon, posterior and medial to the fibular head. Unlike loose joint bodies, fabellae are covered by a layer of hyaline cartilage on their articular surface with the femur; this can be identified on MRI.

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Fig. 7.134 Bipartite patella. Second patellar ossification center at the upper outer edge (b, c, arrows). (a) Coronal T1w sequence. (b) Coronal PDw fatsat sequence. (c) Axial GRE sequence.

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7.24.7 Calcification

7.24.8 Meniscomeniscal Ligament

In general, calcification manifests as signal void on all MRI sequences and causes major susceptibility artefacts. Under hitherto unknown circumstances, small concentrations of calcium precipitates lead to an increase in signal intensity, especially on T1w images. The implicated regions include the basal ganglia, intervertebral disks, the lungs, and menisci. Hence, meniscal chondrocalcinosis can give rise to increased signal intensity, which could be misinterpreted as a meniscal tear.30

In 1 to 4% of cases, there is a ligamentous connection between the anterior horn of a meniscus and the posterior horn of the contralateral meniscus. The ligament is named after the respective anterior horn; hence, a lateral and medial meniscomeniscal segment has been distinguished.178 This ligament runs obliquely through the intercondylar notch and can be mistaken for a bucket-handle tear (▶ Fig. 7.136).

7.24 Pitfalls When Interpreting the Images

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Fig. 7.135 Patellar defect. Cartilage anomaly on the superior retropatellar surface, suggestive of a developmental variant. (a) Sagittal T1w image. (b) Sagittal PDw fatsat image.

Fig. 7.136 Oblique meniscomeniscal ligament. Oblique meniscomeniscal ligament observed in up to 4% of cases (arrows). This ligament should not be mistaken for meniscus fragments in relation to bucket handle tears. PCR: posterior cruciate ligament. (a) Coronal section. (b) Sagittal section. (c) Axial section.

7.24.9 The Articularis (Muscle) The articularis is a small muscle that must be differentiated from the quadriceps, inserts at the distal femur, and extends from the superior pole of the suprapatellar bursa. It helps ensure tension of the joint capsule and suprapatellar bursa to facilitate movement. On MRI, it can be identified as a variable muscle mass deep to the rectus femoris. Reactive hypertrophy should not be mistaken as a tumorous mass.155

7.24.10 Absorption Cysts at the Insertion of the Cruciate Ligaments on the Tibial Plateau Occasionally, cystic focal lesions of a few millimeters to over 1 cm are seen at the tibial plateau, immediately below the insertion of the PCL and ACL. These are thought to reflect

Fig. 7.137 Absorption cysts in the proximal tibial plateau, directly below the insertion of the cruciate ligaments. Sagittal schematic diagram. These cysts are thought to be of mechanical etiology.

stress-related absorption processes similar to the absorption cysts observed in the greater tubercle of the shoulder, deep to the supraspinatus insertion,128 and should not be mistaken for cystic or other types of tumors (▶ Fig. 7.137 and ▶ Fig. 7.138; see also ▶ Fig. 7.98).

7.24.11 Asymmetry of the Epiphyseal Plate Ossification of the epiphyseal plate does not occur in a uniform manner, with delays often seen, in particular, in the lateral third. Any partial openings thus observed in the epiphyseal plate should not be misinterpreted as traumatic lesions.99

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Fig. 7.138 Cruciate ligament cyst. Coronal PDw fatsat image. Absorption cyst at the insertion of the anterior cruciate ligament (arrow).

7.25 Clinical Relevance of Magnetic Resonance Imaging In addition to conventional radiography, a large number of other radiologic imaging modalities have been used and, in some cases, continue to be employed for diagnostic evaluation of the knee: ● Single- and double-contrast arthrography. ● CT and CT arthrography. ● Ultrasonography. ● Stress views. However, these modalities are unsuitable or too laborious for differentiated and precise evaluation of internal structures of the knee. Although MRI, too, has certain limitations, it is the imaging modality of choice for noninvasive or minimally invasive diagnosis (MR arthroscopy63,78,80,82) of damage to internal structures of the knee. It is generally advisable to obtain conventional radiographs before MRI. For example, periarticular bone tumors or stress fractures, which might be clinically attributed to internal lesions, can be clearly identified on radiographs. It is completely unacceptable to perform several MRI scans to investigate an osteosarcoma of the distal femur even before obtaining the first radiographs. Conventional radiography is also indicated to detect or rule out periarticular bone fractures. A thorough clinical examination must also be advocated: it is not uncommon for pathologic changes of the hip to present with referred pain in the knee. Resorting to MRI before carrying out meticulous clinical examination will only have negative implications for the radiologist’s credibility and will possibly result in failure to initiate proper treatment. Arthroscopy, which has witnessed a dramatic increase in recent years, now clearly competes with MRI for diagnostic evaluation of the knee.

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Several studies have demonstrated that MRI is able to provide diagnostic insights into acute injuries and chronic damage to the knee, which clearly outperform clinical assessment. Its role in diagnosing chronic inflammatory joint diseases is less clear-cut, and its therapeutic relevance is not seen in a favorable light by all rheumatologists. However, the relevance of MRI in resolving diagnostic dilemmas is indisputable. The cost–benefit analysis studies hitherto published in the United States have attested to the cost-effectiveness of MRI. Ruwe et al174 performed MRI for 103 patients with acute knee injuries and hemarthrosis, of whom 44 patients were immediately referred for arthroscopy. A further six patients later underwent arthroscopy based on their clinical condition. Overall, over a 22month period, it was possible to dispense with arthroscopy in 51.4% of patients, resulting in savings of 103,700 US dollars. Of course, it may not be possible to extrapolate these findings to the health care systems of other countries. Besides, they do not take account of the implications of long-term incapacity to work or of the complications identified on arthroscopy. Therefore, in terms of the overall health care costs, selective deployment of MRI is likely to be even more advantageous, provided that its indication is based on a meticulous and expert approach and the findings are interpreted by experienced and discerning radiologists.

Clinical Interview

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Clinical interview with Dr Holger Haas, Medical Director of the Center for Orthopedics, Traumatology Surgery and Sports Medicine, Bonn Community Hospital (Gemeinschaftskrankenhaus Bonn). Question: “What do you think is the role of MRI in the routine practices of an orthopedist or trauma surgeon with regard to the knee? For which disorders does it confer major advantages?” Answer: “It has major advantages when it comes to diagnosing and treating space-occupying lesions, masses, and other types of tumors in the knee, in particular when using CM-enhanced sequences. It also provides valuable information for diagnostic investigation of osteochondritis dissecans, ligament and menisci disorders, as well as other soft tissue lesions and for casting light on unclear clinical pictures. I believe that specific MRI sequences hold out interesting prospects for cartilage imaging.” Question: “For which disorders do you encounter false-positive MRI results most often?” Answer: “For suspected meniscal tears (Note: bear in mind known pitfalls!) and ligament injuries. Often, when bone marrow and/or soft tissue edema is detected, too much emphasis is put on the underlying condition (e.g., stress fractures and tumors). Particularly in the case of ligament injuries, there is often a discrepancy between a clinically stable situation and detection of what is thought to be a tear on MRI.” Question: “For which disorders do you encounter false-negative MRI results most often, and why were diagnostic measures continued in such cases?”

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7.25 Clinical Relevance of Magnetic Resonance Imaging [17] Bodne D, Quinn SF, Murray WT, et al. Magnetic resonance images of chronic

Answer: “For suspected meniscal and ligament tears. Often, the discrepancy with regard to the clinical findings is noticed (e.g., entrapment, a typical clinical finding), and this is then investigated further.” Question: “For which disorders can MRI be omitted and for which is it being overly used?” Answer: “MRI should not be automatically used to investigate symptoms such as pain or clinical manifestations, for example, arthrosis, without a sound clinical indication. Nor should each and every minor sprain warrant MR imaging. MRI is not normally needed for preoperative management of a prosthetic implant. Likewise, conventional images (e.g., Rosenberg or stress views) are better for differential indication of uni- or bicondylar prosthesis.”

patellar tendinitis. Skeletal Radiol. 1988; 17(1):24–28 [18] Boeree NR, Watkinson AF, Ackroyd CE, Johnson C. Magnetic resonance imaging of meniscal and cruciate injuries of the knee. J Bone Joint Surg Br. 1991; 73(3):452–457 [19] Boks SS, Vroegindeweij D, Koes BW, Hunink MG, Bierma-Zeinstra SM. Follow-up of posttraumatic ligamentous and meniscal knee lesions detected at MR imaging: systematic review. Radiology. 2006; 238(3):863–871 [20] Boks SS, Vroegindeweij D, Koes BW, Bernsen RM, Hunink MG, BiermaZeinstra SM. MRI follow-up of posttraumatic bone bruises of the knee in general practice. AJR Am J Roentgenol. 2007; 189(3):556–562 [21] Bolog N, Hodler J. MR imaging of the posterolateral corner of the knee. Skeletal Radiol. 2007; 36(8):715–728 [22] Bradley DM, Bergman AG, Dillingham MF. MR imaging of cyclops lesions. AJR Am J Roentgenol. 2000; 174(3):719–726 [23] Breitenseher MJ, Trattnig S, Dobrocky I, et al. MR imaging of meniscal subluxation in the knee. Acta Radiol. 1997; 38(5):876–879 [24] Brody JM, Lin HM, Hulstyn MJ, Tung GA. Lateral meniscus root tear and meniscus extrusion with anterior cruciate ligament tear. Radiology. 2006; 239(3):805–810

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1991; 179(3):629–633

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8.1

Introduction

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8.2

Examination Technique

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The Lower Leg, Ankle, and Foot

8.3

Anatomy

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8.4

Disorders of Bones

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8.5

Disorders of the Tendons

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8.6

Ligament Injuries and Impingement Problems following Ligament Damage

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8.7

Diseases of the Plantar Fascia (Plantar Aponeurosis)

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8.8

Diseases of the Fat Pads of the Feet and Plantar Vein Thrombosis

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Disorders of the Nerves and Compression Syndrome 402

8.10

Osteoarthritis

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8.11

Arthritis

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8.12

Other Form of Synovitis

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Diabetic Foot Syndrome

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Hemophilic Osteoarthropathy

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Bursitis and Haglund’s Heel

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Pseudobursae

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Typical Foot Tumors

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Disorders of the Toes

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8.19

Pitfalls in Interpreting Images

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Clinical Relevance of Magnetic Resonance Imaging 417 References

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Chapter 8

The Lower Leg, Ankle, and Foot

8 The Lower Leg, Ankle, and Foot 8.1 Introduction

8.2.2 Coil Selection

With their many different bony elements as well as their passive and active stabilizers, the ankle and foot constitute an atomically complex functional unit adapted to the various movements of standing, walking, and running. Together with the knee, the talocrural joint (upper ankle joint) is the joint most at risk for lower extremity injuries. However, patients may present with ankle complaints and no recollection of trauma. In such settings, acute and chronic pain can often only be localized and diagnosed through fine-tuned clinical examination. In recent years, degenerative and posttraumatic disorders of the foot have increasingly become the focus of clinical attention. Reflecting that trend, radiologists, too, must now deal with more specialist cases. Since magnetic resonance imaging (MRI) is adept at visualizing both the osseous and cartilaginous structures of the ankle and foot as well as the soft tissues, it has become an indispensable diagnostic imaging modality.

To achieve an adequately high signal, the hindfoot and the talocrural joint should be examined with an extremity coil. There are combination coils designed to image both the knee and the foot, and since they open upward, they allow examination of the foot in a neutral position. The forefoot is examined with (flexible) surface coils or a multichannel coil, for example, a dedicated foot and talocrural joint coil.

8.2 Examination Technique 8.2.1 Patient Positioning To examine the hindfoot and the talocrural joint, as well as the entire foot, the patient should ideally be placed supine in the feet-first position. The foot should be placed in a neutral position (90 degrees in respect to the lower leg axis and without any mentionable external rotation) and held in this position with positioning aids. This position improves reproducibility of the anatomic structures and reduces the incidence and intensity of movement artefacts. The forefoot (toes and metatarsals) should be examined with the patient in the prone position and the foot in the plantarflexed position, as this position helps minimize movement artefacts. Provision must be made for supporting materials (foam cushion wedges) and stabilization (sandbag).

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8.2.3 Magnetic Resonance Imaging Protocols with Regard to Sequences and Parameters As when imaging other joints, here, too, imaging is conducted in three spatial planes using T1w turbo spin-echo (TSE), turbo short-tau inversion recovery (STIR), and proton density–weighted (PDw) fat-suppressed TSE sequences. Visualization of oblique ligaments (in particular the anterior syndesmosis and fibulocalcaneal ligament) can be improved by using a T2w TSE sequence with high turbo factor (TF) or by applying a magnetization transfer contrast (MTC) pulse along these ligaments. The following order of sequence is recommended: ● Sagittal T1w TSE sequence. ● Sagittal turbo STIR sequence. ● Coronal PDw fatsat TSE sequence. ● Axial PDw fatsat TSE sequence. With the foot in neutral position (discussed earlier), anatomic images of the talocrural joint and hindfoot are obtained to the extent permitted by the foot’s position within the MRI scanner, without special angulation. This also provides for good demonstration of the anterior and posterior fibulotalar ligaments (▶ Fig. 8.1). Some imaging specialists recommend that the coronal and sagittal imaging planes for the talocrural joint and hindfoot be oriented along the bimalleolar line, since this allows for slight external rotation of the slices. The term mortise plane (derived from “mortise and tendon joint”) is also used for conventional

Fig. 8.1 MR imaging planes of the foot. Schematic diagram. (a) Strict sagittal (1) and coronal sections (2), planned on axial localizer. Oblique sagittal and oblique coronal sections (Mortise plane, 3) oriented toward the malleolar fork, optional for exploring specific issues (e.g., osteochondritis dissecans). (b) Axial (1) and coronal (2) sections, planned on sagittal image. Oblique axial and coronal sections (3) for visualization of the fibulocalcaneal ligament. If the anterior and posterior fibulotalar ligaments cannot be clearly identified on the axial sections, an oblique axial section can be added (dashed line). (c) Syndesmotic tilting (oblique axial and sagittal), planned on coronal image.

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M. Vahlensieck, A. Sikorski, and C. Glaser

8.3 Anatomy

Contrast Media Fat-suppressed contrast media (CM)-enhanced sequences yield additional information on tumor and certain inflammatory diseases, as well as on diabetic osteoarthropathy. Some centers also recommend the use of intravenous (IV) CM for other diagnostic issues, in particular, in association with impingement as well as chronic disorders of tendons and capsular ligaments. An excellent image quality is obtained by using robust T1w sequences following

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CM injection. There is broad variability in the proportion of cases that can be successfully diagnosed on native images, depending on the patient collective: some centers report this as being 90%, whereas others routinely use IV CM. The aspects to be borne in mind include essentially the duration of examination, the (low) risk of CM intolerance, possibly the discomfort of the injection, and especially the benefits expected for the individual patient.

Arthrography Arthrography, both indirect and direct, is advantageous for the evaluation of osteochondritis dissecans.

8.3 Anatomy 8.3.1 General Anatomy Talocrural Joint Downloaded by: Collections and Technical Services Department. Copyrighted material.

radiographs. This imaging plane can be advantageous when assessing cartilage diseases of the talocrural joint. However, based on the authors’ experiences, when the foot is properly positioned, sagittal and coronal images generally suffice for routine diagnosis in settings of high patient throughput. If the anterior and posterior lateral ligaments cannot be evaluated across their entire length, a posteroanterior (P/A) oblique axial/ coronal imaging plane angled around 20 degrees in an anteroinferior direction (planned in the sagittal plane) may be useful.70 For evaluation of the fibulocalcaneal ligament and the tarsal tunnel, an oblique axial/sagittal sequence angled inferiorly at around 45 degrees (planned in the coronal plane) is recommended. For assessment of the tibiofibular syndesmoses, an oblique axial 40-degree angled sequence should be used.31,32 The forefoot and toes are examined in special imaging planes adapted to the foot anatomy, that is, in the sagittal plane parallel to the metatarsals or the phalanges. The axial plane of the foot is perpendicular to the sagittal plane (short axis), and the foot coronal plane is oriented through the centers of the first and fifth metatarsals (long axis). Smaller adaptations may be needed in accordance with the clinical questions to be explored (▶ Fig. 8.2 and ▶ Fig. 8.3). The higher the resolution provided for in the protocols, the better the results. A slice thickness of at least 3 mm and an “in-slice resolution” of 0.6 mm × 0.8 mm should be used. The examination protocol is based on the aforementioned native sequences in compliance with the recommendations by the Radiology Musculoskeletal Working Group of the German Society of Radiology.

The fibula, tibia, and talus articulate in the talocrural joint. The fibula and tibia form the malleolar fork (ankle mortise), which is stabilized by the taut anterior (anterior tibiofibular ligament) and posterior (posterior tibiofibular ligament) as well as strong interosseous ligamentous structures, also collectively termed the tibiofibular syndesmosis. The joint capsule inserts into the anterior tibia around 1 cm proximal to the joint space as well as at the middle portion of the talar neck. Elsewhere, it inserts near the bone–cartilage junction. Along its external plantar surface, the talus has a deep sulcus (the sulcus tali), which forms the roof of a fat-containing space, the sinus tarsi. The interosseous talocalcaneal ligament and cervical ligaments course through the sinus tarsi. Laterally, the sinus tarsi is bordered by the inferior extensor retinaculum (▶ Fig. 8.4a).39 The medial collateral ligament (deltoid ligament; ▶ Fig. 8.4b) is composed of four ligament bundles that originate at the tip of the medial malleolus and extend from the navicular tuberosity via the talar neck and the sustentaculum tali to the posterior talar process. The lateral ligament complex (▶ Fig. 8.4c) consists of three ligaments, the anterior fibulotalar ligament, the posterior fibulotalar ligament, and the fibulocalcaneal ligament. The

Fig. 8.2 MR imaging planes of the forefoot in prone position. Schematic diagram (gray lines: sequential image borders). (a) Planning the foot coronal section (long axis) on axial image: planned through the centers on first and fifth metatarsals (dashed line). If there are specific queries about individual metatarsals, angle is toward the respective metatarsal (thin dashed line). (b) Orientation of the long and short axes (dashed lines) on sagittal image. (c) Planning the sagittal section and orientation of the short axis (dashed lines) on the coronal image of the foot. If there are specific queries about individual metatarsals, the long axis is tailored to these bones (thin dashed line).

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The Lower Leg, Ankle, and Foot anterior fibulotalar ligament arises at the anterior circumference of the tip of the fibula and inserts into the lateroanterior aspect of the talar neck. With the foot in dorsal extension, it embarks on an almost transverse course. The ligament is often divided into two portions and prevents anterior translation of the talus as well as, in particular, varus deviation in plantar flexion. The posterior fibulotalar ligament originates on the

posterior inner aspect of the fibular tip and extends in a horizontal direction to the posterior talar process and inserts at the lateral tubercle. The fibulocalcaneal ligament arises near the medial tip of the lateral malleolus and courses obliquely in a dorsoplantar direction to the lateral surface of the calcaneus. It has an extra-articular course and is separated from the joint capsule by a mobile layer of fatty tissue. Its primary function is to impede supination of the fibulocalcaneal ligament and stabilize the subtalar joint. The course embarked upon by these ligaments is determined by how the foot is positioned at the talocrural joint (▶ Fig. 8.5).

The talus, calcaneus, and navicular articulate in the subtalar joint (lower ankle joint) (talocalcaneonavicular articulation), forming a single functional unit. The joint is composed of three joint facets separated by the interosseous talocalcaneal ligament: ● In the posterior facet, the posterior calcaneal articular facet of the talus articulates with the posterior articular surface of the calcaneus. ● The middle facet forms the body of the talus and the sustentaculum tali of the calcaneus. ● In the anterior chamber (the talonavicular joint), the spherical head of the talus articulates with the concave articular surface of the navicular. This joint is often viewed as a single entity and is known as the “coxa pedis.”

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c Fig. 8.3 MR imaging planes of the toes. Schematic diagram (gray lines: sequential image borders). As in the case of tilting of the forefoot, the angle is oriented in the direction of the toe axis. (a) Planning the long and short axes (dashed lines). (b) Alignment of the long axis (dashed line). (c) Sagittal section of toes.

The extensor group of muscles of the lower leg comprises, in mediolateral direction, the tibialis anterior, extensor hallucis longus, and extensor digitorum longus. The tendon of the tibialis anterior inserts into the medioplantar base of the first metatarsal and the medial cuneiform. The tendon of the extensor hallucis longus inserts into the distal phalangeal base of the first toe, whereas the extensor digitorum longus

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Fig. 8.4 Anatomy of the talocrural joint. Schematic diagram. (a) Coronal plane. Ligament in the sinus tarsi. (b) Medial ligament complex. (c) Lateral ligament complex and syndesmotic ligaments. 1, cervical ligament; 2, interosseous talocalcaneal ligament; 3, medial fiber bundle of the inferior extensor retinaculum; 4, intermediate fiber bundle of the inferior extensor retinaculum; 5, lateral fiber bundle of the inferior extensor retinaculum; 6, tibionavicular ligament; 7, anterior tibiotalar ligament; 8, tibiocalcaneal ligament; 9, posterior tibiotalar ligament; 10, anterior tibiofibular ligament; 11, anterior fibulotalar ligament; 12, fibulocalcaneal ligament; 13, posterior fibulotalar ligament; 14, posterior tibiofibular ligament.

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Subtalar Joint

8.3 Anatomy Fig. 8.5 Variable course of the lateral ligaments, depending on the foot position. Schematic diagram of the foot; lateral view in two foot positions. 1, anterior fibulotalar ligament; 2, fibulocalcaneal ligament; 3, fibulotalar ligament.

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Plantar flexion

extends with four tendon bundles to the middle and distal phalanges of the second to fifth toes. The lateral group of muscles of the lower leg consists of the peroneus longus and brevis. The tendons of both muscles course posteriorly to the lateral malleolus in one common tendon sheath and are held in place by the superior peroneal retinaculum. The peroneus longus inserts into the plantar base of the first metatarsal and the intermediate cuneiform. It is not uncommon to find an os peroneum on the plantar aspect of the foot, where the peroneus longus diverts its course. This sesamoid helps protect the tendon. The peroneus brevis inserts into the base of the fifth metatarsal. The superficial flexor compartment on the dorsum of the lower leg contains the triceps surae, which is composed of the gastrocnemius medialis and lateralis, soleus, and variably developed plantaris. This group of muscles inserts via a powerful tendon, the calcaneal tendon, commonly known as the “Achilles tendon,” over a large area into the calcaneal tuberosity. This tendon is protected by two bursae: the calcaneal bursa, which acts as a cushion between the Achilles tendon and the calcaneus, and the subcutaneous calcaneal bursa. The deep flexor compartment contains, from medial to lateral, the flexor digitorum longus, tibialis posterior, and flexor hallucis longus. In the distal third of the lower leg, the tendon of the flexor digitorum longus crosses the tibialis posterior, placing the latter in the most anteromedial position above the talocrural joint. Between the medial malleolus and the calcaneus, obliquely oriented fibers in the crura fascia cover and restrain the tendons in their compartment (flexor retinaculum). The tarsal tunnel is bordered by the sustentaculum tali as its roof, laterally by the calcaneus and medially by the flexor retinaculum. The posterior tibial vessels, the tibial nerve, and the tendon of the flexor hallucis longus course through the tarsal tunnel. The tendons of the tibialis posterior and the flexor digitorum longus extend posteriorly to the inner ankle and insert as stabilizers of the medial longitudinal arch into the plantar surface. The insertion of the tibialis posterior at the navicular tuberosity varies (▶ Fig. 8.6).37 The extensor digitorum brevis and extensor hallucis brevis course on the flexor aspect of the foot as the intrinsic muscles of the foot. In the interosseous spaces between the metatarsals, the dorsal interossei are found dorsally; the plantar interossei and the lumbricals are found in the plantar region. The plantar muscles run in three longitudinal

compartments that are incompletely separated by connective tissue septa: ● The medial compartment contains the abductor hallucis, adductor hallucis, and flexor hallucis brevis. ● The middle compartment contains the flexor digitorum longus, flexor hallucis longus, flexor digitorum brevis, quadratus plantae, and lumbricals. ● The lateral muscle compartment contains the abductor digiti minimi, flexor digiti minimi brevis, and opponens digiti minimi.

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Dorsal flexion

The plantar fascia extends the length of the foot in the superficial plantar layers. It arises at the calcaneal tuberosity with a powerful medial portion and a slim lateral portion and inserts into the plantar plate and the plantar joint capsules of the second to fourth metatarsal bases.

8.3.2 Specific Magnetic Resonance Imaging Anatomy Talocrural and Subtalar Joints Transverse Plane ▶ Fig. 8.7, ▶ Fig. 8.8, and ▶ Fig. 8.9 display the sectional anatomy of the ankle in the transverse plane. The anterior muscle group is demonstrated on axial sections proximal to the talocrural joint, showing, from medial to lateral, the tendons of the tibialis anterior, extensor hallucis longus, extensor digitorum longus, and, possibly, peroneus tertius. In the posterior compartment, the muscle tendons of the tibialis posterior, flexor digitorum longus, and flexor hallucis longus are displayed from medial to lateral. Recollection of the order of the tendons in the posterior compartment for routine activities can be facilitated with the mnemonic “Tom, Dick and Harry” (tibialis posterior, flexor digitorum longus, and flexor hallucis longus). The dorsalmost tendon is the strongest of all tendons, the transverse ovoid Achilles tendon. The posterior border of the Achilles tendon is characteristically convex, whereas its anterior surface is flattened. The muscle and tendon of the peroneus brevis as well as, posterolateral to it, the tendon of the peroneus longus pass as the

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11

1

10

2

Fig. 8.6 Anatomic characteristics of the tarsal tunnel. Schematic diagram of the foot, from medial. Dashed lines: extension of the tarsal tunnel. 1, posterior tibial nerve; 2, flexor hallucis longus tendon; 3, Achilles tendon; 4, medial calcaneal nerve; 5, flexor retinaculum; 6, abductor hallucis; 7, flexor digitorum brevis; 8, lateral plantar nerve; 9, medial plantar nerve; 10, flexor digitorum longus tendon; 11, tibialis posterior tendon.

3 4

5 8

7

6

Tibialis anterior tendon Extensor hallucis longus muscle and tendon

Fig. 8.7 Sectional anatomy of the talocrural joint and subtalar joint. MRI, transverse plane.

Extensor digitorum longus tendon Peroneus tertius

Fibula Peroneus brevis muscle and tendon Peroneus longus tendon

Small saphenous vein

Tibia

Tibialis posterior tendon Flexor digitorum longus tendon Posterior tibial artery/vein Tibial nerve Flexor hallucis longus muscle and tendon Soleus Achilles tendon

lateral muscle group posteriorly to the lateral malleolus. The anterior neurovascular bundle (anterior tibial artery and vein and deep peroneal nerve) courses posteriorly to the extensor tendons, whereas the posterior neurovascular bundle (posterior tibial artery and vein, and tibial nerve) manifests as a hypointense structure on T1w images anteromedially to the flexor hallucis longus. The sural nerve can be identified as a hypointense structure in the hyperintense fatty tissue posterior to the peroneal tendons. In addition to the aforementioned muscles, ligaments, and neurovascular structures, the axial sections at the level of the distal fibular tip show medial segments of the deltoid

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ligament. This medial collateral ligament is composed of the following parts: ● Tibionavicular part. ● Anterior tibiotalar part. ● Posterior tibiotalar part. ● Tibiocalcaneal part. ● Ligament strands from the tibia to the superior part of the spring ligamentous complex. The entire length of the posterior fibulotalar ligament can be identified as a strong hypointense structure; however, only segments of the anterior fibulotalar and fibulocalcaneal ligaments can be visualized. The position of the foot or the imaging plane

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8.3 Anatomy

Extensor digitorum longus tendon Peroneus tertius

Tibialis anterior tendon Extensor hallucis longus tendon Great saphenous vein Medial malleolus Distal tibia

Tibialis posterior tendon Lateral malleolus Flexor digitorum longus tendon

Peroneus brevis

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Peroneus longus and brevis tendons

Flexor hallucis longus muscle and tendon

Soleus Achilles tendon

Fig. 8.8 Sectional anatomy of the talocrural joint and subtalar joint. MRI, transverse plane.

Tibialis anterior tendon Extensor digitorum longus tendon Peroneus tertius tendon

Neck of talus Anterior fibulotalar ligament Lateral talar process Posterior fibulotalar ligament Tip of fibula Peroneus longus tendon Peroneus brevis muscle and tendon

Navicular

Great saphenous vein

Tibiocalcaneal ligament Tibialis posterior tendon Flexor digitorum longus tendon Medial tubercle of posterior talar process Posterior tibial artery Flexor hallucis longus tendon Posterior talar process Lateral tubercle of posterior talar process Achilles tendon

Fig. 8.9 Sectional anatomy of the talocrural joint and subtalar joint. MRI, transverse plane.

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Sagittal Plane The sectional anatomy in the sagittal plane is demonstrated in ▶ Fig. 8.10, ▶ Fig. 8.11, and ▶ Fig. 8.12. The entire longitudinal course of the tendons of the extrinsic muscles of the foot is visualized in the sagittal plane. Besides, the sagittal plane gives a good overview of the osseous structures of the talocrural and subtalar joints and is particularly suitable for evaluation of the articular surfaces and cartilage. The medial sagittal sections demonstrate the tendons of the tibialis posterior and flexor digitorum longus, which course posteriorly to the medial malleolus. The flexor hallucis longus runs along the posterior surface of the talus through the talar trigonal process and deep to the sustentaculum tali in the tarsal tunnel. In the plantar region, it crosses the tendon of the flexor digitorum longus (the knot of Henry). Tendinous bands (vincula) normally run between both tendons. The plantar sagittal sections demonstrate, as the stabilizers of the medial longitudinal arch close to the bone, the plantar talonavicular ligament and then the strong quadratus plantae, which arises from the plantar surface of the calcaneus and inserts distally along the tendons of the flexor digitorum longus. All muscles on the sole of the foot are covered by the plantar aponeurosis (plantar fascia). This is a strong plate of fibers that extends from the calcaneal tuberosity and inserts at the metatarsophalangeal joints. The central sagittal sections are ideal for visualization of the articular surfaces of the talocrural and subtalar joints. The joint cartilage in both joints can be identified as a linear zone of intermediate signal intensity on T1w images. Three compartments, which are separated by the sinus tarsi, can be delineated in the subtalar joint. The sinus tarsi contains fine

neurovascular structures enclosed in hyperintense fatty tissue. Ligamentous structures include the interosseous talocalcaneal ligament on the medial aspect and the stronger cervical ligament on the anterior and lateral aspects. The transected muscle and muscle tendon of the flexor hallucis longus are seen posterior to the Achilles tendon. Directly posterior to that are the Achilles tendon fat pad, the calcaneal bursa, and the Achilles tendon. The tibialis anterior tendon is visualized on the dorsum of foot. Sagittal sections through the distal fibula are used primarily for longitudinal visualization of the peroneal tendons. The peroneus brevis tendon lies posterior to the peroneus longus tendon and extends distally to the base of the fifth metatarsal. Early on, the muscle tendon of the plantar peroneus longus exits the imaging plane at the level of the calcaneocuboid joint, continuing its plantar course medially to the base of the first metatarsal and the intermediate cuneiform.

Coronal Plane The sectional anatomy of the talocrural and subtalar joints in the coronal plane is illustrated in ▶ Fig. 8.13 and ▶ Fig. 8.14. Coronal sections through the distal portion of the tibia and fibula demonstrate, medial to the tibia, segments of the tendons of the tibialis posterior and flexor digitorum longus. The tendon of the flexor hallucis longus is located medial to the partially transected talus. Medial to the calcaneus, parts of the quadratus plantae can be identified, whereas the peroneal tendons manifest as hypointense structures, inferior to the tip of the fibula. Central coronal sections, like sagittal sections, are particularly suitable for evaluation of the talar and tibial articular surfaces and joint cartilage. The powerful posterior tibiotalar ligament can be identified as a hypointense structure between the medial malleolus and the medial surface of the talus. Inside the subtalar joint space, the sinus tarsi with its hyperintense fat pad and

Lateral malleolus Peroneus longus tendon

Calcaneus Lateral cuneiform

Peroneus brevis tendon Small saphenous vein

Fourth metatarsal Cuboid

Fig. 8.10 Sectional anatomy of the talocrural joint and subtalar joint. MRI, sagittal plane.

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Abductor digiti minimi

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has to be changed to allow visualization of the entire course of these ligaments.

8.3 Anatomy

Tibia Flexor hallucis longus

Tibialis anterior tendon

Achilles tendon

Talus

Sinus tarsi Navicular Interosseous talocalcaneal ligament

Intermediate cuneiform

Calcaneus

Lateral cuneiform

Long plantar ligament

Cuboid Quadratus plantae Flexor digitorum brevis

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Abductor digiti minimi Plantar aponeurosis

Fig. 8.11 Sectional anatomy of the talocrural joint and subtalar joint. MRI, sagittal plane.

Medial malleolus Tibialis anterior tendon Talus

Fig. 8.12 Sectional anatomy of the talocrural joint and subtalar joint. MRI, sagittal plane.

Tibialis posterior tendon

Navicular

Medial cuneiform

Quadratus plantae Flexor digitorum brevis

segments of the interosseous talocalcaneal ligament as well as the cervical ligament can be identified (see ▶ Fig. 8.4). A crosssection of the tendon of the flexor hallucis can be seen in the tarsal tunnel beneath the sustentaculum tali. The medialmost plantar muscle is the abductor hallucis. The muscles of the plantar middle foot include the superficial flexor digitorum brevis and the quadratus plantae beneath it. In the lateral sole of the foot, the abductor digiti minimi is situated.

Forefoot The axial imaging plane of the foot (also termed axial foot plane or “short axis”; ▶ Fig. 8.15) shows at the level of the

metatarsals, posterior to the bones, the extensor tendons as hypointense structures in the hyperintense subcutaneous fatty tissue. Between the bones, the interosseous muscles can be identified, whereas lateral to the fifth metatarsal the muscle bellies and tendons of the abductor digiti minimi and flexor digiti minimi brevis are visualized. On the plantar aspect, from medial to lateral, the abductor hallucis, flexor hallucis brevis, tendon of the flexor hallucis longus, adductor hallucis, tendons of the flexor digitorum longus and brevis, and the lumbricals are seen. The coronal section of the foot (also known as the “long axis”) demonstrates the metatarsals, phalanges, metatarsophalangeal joints, sesamoids, interphalangeal joints, ligaments of joints, and the interosseous muscles (▶ Fig. 8.16).

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Tibialis posterior tendon

Tibia Fibula

Talus Posterior fibulotalar ligament Peroneus brevis tendon Peroneus longus tendon

Flexor digitorum longus tendon Flexor hallucis longus tendon

Calcaneus

Abductor digiti minimi

Abductor hallucis

Flexor digitorum brevis

Plantar aponeurosis

Fig. 8.13 Sectional anatomy of the talocrural joint and subtalar joint. MRI, coronal plane.

Fig. 8.14 Sectional anatomy of the talocrural joint and subtalar joint. MRI, coronal plane.

Tibia

Talus

Posterior tibiotalar ligament Tibialis posterior tendon

Sustentaculum tali Calcaneus Peroneus brevis tendon Peroneus longus tendon

Flexor digitorum longus tendon Flexor hallucis longus tendon Quadratus plantae Abductor hallucis

Abductor digiti minimi

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Flexor digitorum brevis

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Quadratus plantae

8.4 Disorders of Bones Extensor hallucis longus tendon

First to fourth metatarsals

Adductor hallucis Abductor hallucis muscle and tendon

Extensor digitorum tendons

Flexor hallucis brevis Flexor digitorum longus tendons

Flexor digiti minimi brevis tendon

Flexor hallucis longus tendon

Head of fifth metatarsal

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Flexor digitorum brevis tendons

Abductor digiti minimi muscle and tendon Interosseous muscles Lumbricals Fig. 8.15 Sectional anatomy of the forefoot. MRI, axial plane (also referred to as the “short axis” of the foot).

8.4 Disorders of Bones 8.4.1 Osteochondral Injuries, Osteochondritis Dissecans, and Osteonecrosis of the Talus Talus The talus is prone to spontaneous (often because of malnutrition) or posttraumatic osteochondral lesions, causing focal damage to the bone–cartilage junction. ● Spontaneous osteochondritis (osteochondritis dissecans): This generally affects the medial portion of the talus, and, as per its definition, it is a disease that is predominantly seen in younger patients (typically: 20–40 years). Its etiology has not been fully determined, but it is hypothesized to be linked to vascular disorders and microtrauma; it causes avascular necrosis, mainly in the medial aspect of the talar trochlea, and can manifest bilaterally. ● Posttraumatic osteochondritis: This often affects the mediodorsal portion and is preceded by lateral avulsion fracture. Traumatic osteochondral injuries are often caused by severe supination injuries. Fractures of the lateral talar margin are associated with concurrent dorsiflexion, and injury to the medial talar margin is related to concurrent plantar flexion. Based on the absence of edema, historic chipped fragments or accessory bones can be differentiated from more recent fractures and osteochondritis dissecans. Fracture and dislocation of the talus that cause damage to the nutrient vessels can result in partial or total talar necrosis (osteonecrosis). This can be easily identified on native radiographs from the absence of demineralization following immobilization, whereas the MRI scan shows extensive segmental or complete bone marrow edema (▶ Fig. 8.17), with necrosis spreading to the marrow spaces within bones. Over time, characteristic bandlike

Metatarsals

Interosseous muscles

Collateral ligaments

Phalanges Interdigital fat

Fig. 8.16 Sectional anatomy of the forefoot. Coronal and plantar T1w images of the foot. This section is also called the “long axis” of the foot.

signal changes can also be occasionally observed, in association with bone marrow necrosis. MRI is an excellent imaging modality for early diagnosis of osteochondral lesions in the talar articular surface of the talocrural joint. Both the sagittal and coronal imaging planes should be selected, as they permit evaluation of bone defects as well as of the integrity of the overlying cartilage layer. Fat-suppressed images have proved useful for assessment of cartilage integrity (▶ Fig. 8.18). On direct MR arthrography (intra-articular CM injection), the spread of contrast agent from the joint space into the mouse bed can be directly observed. On indirect MR arthrography (IV CM injection, exercising of the joint), the mouse bed is also

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Fig. 8.17 Osteochondritis and avascular necrosis. Schematic coronal diagram of the talocrural joint. (a) Normal findings. (b) Osteochondritis dissecans, typically in the medial posterior third of the talar trochlea at a very advanced stage. Fragment in the mouse bed (bone crater). Discrete perifocal edema. (c) Necrotic osteochondral fragment, undisplaced, after relatively acute trauma and fracture (flake fracture), typically at the lateral talar trochlea, with discrete perifocal edema. (d) Bone fragment at the medial talar trochlea, with signal isointense to fatty marrow and without perifocal edema, as status post historic, undisplaced fracture or as an accessory bone element. (e) Extensive signal changes in the talus or in large parts of the talus because of total or partial talar necrosis secondary to injury to the blood vessels in the sinus tarsi or tarsal tunnel, in association with fractures or dislocations. The talar body is affected more often than the talar neck.

completely filled with CM. However, here, it must be borne in mind that the granulation tissue around the fragment will also manifest as hyperintensity and could be mistaken for the spread of contrast agent into the cartilage defect. However, the authors are of the opinion that the signal intensity exhibited by the granulation tissue during CM uptake on MR arthrography (see Chapter 1.8) is less than that seen in association with intra-articular CM after an appropriate interval following IV injection (▶ Fig. 8.18 and ▶ Fig. 8.19).

▶

Fig. 8.18 Osteochondritis dissecans. (a) Fat-suppressed SE image, coronal plane; magnified section. The integrity of the cartilage can be relatively well evaluated. (b) Indirect MR arthrography. No CM spread into the mouse bed. The granulation tissue around the fragment exhibits only a slight increase in signal intensity. (c) Indirect MR arthrography in another patient. Very high signal intensity in the mouse bed, consistent with the intra-articular fluid in the lateral joint space. This finding should be interpreted as CM spread from the joint cavity into the mouse bed, in association with discontinuity of the cartilage.

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8.4 Disorders of Bones

●

by a fluid rim is an indirect sign of cartilage damage and instability of the fragment (see ▶ Fig. 8.18). Grade IV: By stage IV, the joint cartilage is completely disrupted and the subchondral bone defect is often macerated or has been absorbed and filled with joint fluid. Alternatively, the bone fragment may have separated and can now be identified as a loose joint body.

Other Bones of the Foot Skeleton In addition to avascular necrosis of the talar trochlea, there are numerous other less common spontaneous forms of avascular necrosis of the foot skeleton, involving the following: ● Navicular (Köhler I disease). ● Second and third metatarsal heads (Köhler II and Freiberg– Köhler disease; ▶ Fig. 8.20 and ▶ Fig. 8.21). ● Calcaneal apophysis (Sever’s disease). ● Phalangeal base (Thiemann’s disease). ● Base of the fifth metatarsal (Iselin’s disease). ● Medial sesamoid (Renander’s disease).

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Nelson et al54 devised a system for the classification of osteochondral lesions, in order to categorize the changes identified on MRI with those on arthroscopy into four grades of severity: ● Grade I: Subchondral lesions seen during stage I show intact cartilage coverage on MRI. The bone defects exhibit low signal intensity on T1w images. On T2w images, these defects may appear both hypointense (sclerosis) and hyperintense (blood and joint fluid). Often, reactive bone marrow edema can be observed in the vicinity of bones, with the associated hyperintensity best appreciated on STIR sequences. ● Grade II: During this stage, the osteochondral lesions can be delineated as an interface zone versus the surrounding bones. This interface zone may be indicative of reactive sclerosis or fibrovascular connective tissue, thus exhibiting different signal intensities. While sclerosis manifests as hypointense on all sequences, fibrovascular connective tissue exhibits high signal intensity on T2w sequences, making it difficult to differentiate from fluid. Administration of IV contrast agent could help overcome that obstacle, since, in most cases, fibrovascular connective shows strong CM uptake. ● Grade III: In stage III, joint fluid can seep through tears in the joint cartilage into the space between the subchondral defect and the surrounding bones. Hence, a bone defect surrounded

These diseases are seen primarily in children and adolescents. However, some forms such as avascular necrosis of the metatarsal head can also be encountered in adults and may be accompanied by clinical symptoms such as severe pain (metatarsalgia). In

Fig. 8.19 Osteochondritis dissecans stage III. Indirect arthrography. The fragment is surrounded by contrasting joint fluid (arrows). (a) Sagittal MRI section. (b) Coronal MRI section.

a

b

Fig. 8.20 Köhler II disease. Pain in the metatarsophalangeal joint of the second toe. Subcortical, lentiform edema (arrows) in the head of the second metatarsal, with incipient flattening, consistent with avascular necrosis. (a) Sagittal T1w image. (b) Coronal PDw fatsat MR image of the foot.

a

b

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general, in the early stages of avascular necrosis, the subchondral region exhibits reduced signal intensity on T1w images and increased signal intensity on T2w and, in particular, on STIR images. This may be attributable to bone marrow edema. As the disease progresses, reduced signal intensity may be observed on T1w and T2w sequences because of the now-preponderant sclerotic changes. Typical manifestations range from deformation and flattening to central fracture of the metatarsal head, even in the early stages of disease. Identification of hyperintense granulation tissue, especially on T2w and T2*w sequences, is a sign of revascularization.77 MRI is endowed with high sensitivity and is thus able to detect avascular necrosis earlier than any other imaging modality.

8.4.2 Apo- and Epiphysitis Occasionally, a painful reaction occurs in the adolescent apo- or epiphyses (▶ Fig. 8.22), affecting mainly the calcaneal apophysis (calcaneal apophysitis, Sever’s disease). Depending on the classification system applied, this may be classified as juvenile avascular necrosis. The tension exerted on the Achilles tendon, in particular, during growth spurts, causes overloading of the apophysis, with painful irritation and inflammation, often manifesting bilaterally (in around 60% of cases). Physiologically increased radiopacity of the apophysis is frequently observed, in addition to persistence of multiple ossification centers. Hence, radiographic diagnosis based on criteria such as high radiopacity, fragmentation, inhomogeneous density, and osteolysis is relatively unreliable. Some authors consider radiographs to be indispensable when typical clinical symptoms are manifested. The findings generally identified on MRI are edema-isointense increased signal intensity in the apophysis, with or without fragmentation, as well as, depending on severity, inflammatory reactions by the surrounding soft tissues. The areas with inflammatory processes take up CM. The apophyseal structure remains unchanged. A CM-enhanced sequence is indispensable for successful diagnosis. MRI is indicated if no conclusive

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diagnosis can be made on the basis of the clinical symptoms and radiographs (lateral views of the heel) (▶ Fig. 8.23).2,5

8.4.3 Sesamoids and Accessory Bones Accessory Bones Accessory bones are commonly found at different locations in the foot, often bilaterally.57 In general, although they do not give rise to any clinical symptoms, the following mechanisms could cause complaints: ● If the accessory bone is located in proximity to the tendon insertion, this can result in inflammation at that site (enthesopathy, insertional tendinopathy), with concomitant inflammation of the accessory bone (osteitis) with its own specific range of problems. Clinically relevant manifestations include an os tibiale externum and/or secondary navicular bone as a sequela of overloading of the tibialis posterior tendon. ● A contusion mechanism can cause impingement symptoms. ● “Synchondritis” can present following irritation of the oftentenuous articulated connection to the adjacent bones. Complaints are frequently caused by changes in the foot statics, overloading while engaging in athletic activities (ballet, soccer, etc.), status post fractures, etc. Fractures of accessory bones may be caused by direct application of force. A bipartite or multipartite anlage can be encountered and must be differentiated from stress-mediated or traumatic fracture. When confronted with such findings, it is advisable to initially obtain conventional radiographs. Examples: ● Os peroneum: This may become clinically symptomatic following damage from direct or indirect trauma (e.g., talocrural joint sprain). A symptomatic os peroneum (sesamoid in or on the peroneus longus tendon is identified in around 10% of the population) gives rise to discrete symptoms along the cuboid course of the peroneus longus tendon.

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Fig. 8.21 Köhler II disease. Late stage, with cortical disruption at the head of the second metatarsal (arrows). Concomitant bone marrow edema in the region of the metatarsal shaft with slight surrounding soft tissue, while the entire cortex is preserved and can be well delineated. (a) STIR image. (b) Paracoronal T1w image.

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8.4 Disorders of Bones

Fig. 8.22 Epiphysitis. Nine-year-old girl with intermittent pain in big toe. Radiopaque, bipartite metatarsal base epiphysis. On MRI, edemaisointense, homogeneous signal intensity in the bipartite, smoothly outlined, epiphysis as a sign of epiphysitis (b, arrows). (a) T1w plantar plane. (b) STIR sequence.

●

●

Os trigonum: This is an independent or fibrous ossicle found at the lateral tubercle posterior talar process, which can occasionally cause posterior impingement syndrome of the talocrural joint (see Posterior Impingement p. 399) or tendinitis of the flexor hallucis longus tendon (see Flexor hallucis longus p. 392 tendon). Os tibiale externum: Likewise, there are reports of os tibiale externum syndrome (▶ Fig. 8.24).62

Other accessory bones rarely exhibit symptoms.50 On MRI, edema of the accessory bone as well as edematous swelling of adjacent soft tissues and often focal joint effusion are identified. Edematous thickening of the entire tendon insertion is observed in association with insertional tendinopathy (enthesopathy).

Sesamoids Paired sesamoids are an inherent part of the first metatarsophalangeal joint. Aplasia of one or both sesamoids is rare. The manifold morphologic variants of these bony elements were characterized by Keventer already back in 1914. Variants ranging from bi- to multipartite forms are possible and can give rise to suspected fracture or avascular necrosis in settings of metatarsalgia. Besides, it is not uncommon to encounter one or two sesamoids in the other metatarsophalangeal joints, but these are generally not of any clinical consequence.57 A rarely observed sesamoid in the long big toe flexor at the interphalangeal joint of the big toe may be identified as the cause of a plantar lesion (ulcer) in association with neuropathically numb foot. Occasionally, sesamoids may also become completely necrotic and fractured (▶ Fig. 8.25).50 As regards the sesamoids of the first metatarsophalangeal joint, a distinction must be made between idiopathic avascular necrosis (Renander’s disease) and avascular necrosis from overloading (e.g., hollow foot, clipless pedals in cyclists).

The cuneiform can very rarely have two persistent ossification centers (bipartite cuneiform). This congenital variant should not be mistaken for fractures. When imaged, a bipartite cuneiform is seen with a synchondrosis, which may become painful (synchondritis; ▶ Fig. 8.26).

8.4.4 Stress Reactions, Stress Fractures, and Occult Fractures MRI is able to identify radiographically occult bone marrow changes, often implicated as the cause of complaints of unknown origin. It is important to differentiate a number of terms to ensure a uniform and accurate description of the changes identified: ● Stress reactions of bone: These can present as a sequela of repetitive strain injury, for example, in the presence of foot deformities or unusual loading when engaging in athletic activities, and may be viewed as a precursor to a stress fracture. ● Stress fractures: As per its definition, a stress fracture (overloading fracture) is a fracture in healthy bone (as opposed to pathologic or insufficiency fracture) caused by repetitive microtraumas. Stress fractures are characterized by a pattern of insidious bone disruption coincident with repair mechanisms. A characteristic finding on MRI is pronounced bone marrow edema, which can be distinguished from the stress reaction by means of an additional line of hypointensity (▶ Fig. 8.27 and ▶ Fig. 8.28). Similarly, a distinction can be made between a posttraumatic bone bruise (bone contusion) and a manifest (occult) fracture: ● Bone bruise: If, following injury, MRI shows only diffuse bone marrow edema, the term bone bruise or trabecular microfracture is used.

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b

c

Fig. 8.23 Calcaneal apophysitis (Sever’s disease). Ten-year-old boy with weight-bearing heel pain. Inhomogeneous CT density, edema pattern at calcaneal apophysis. (a) Sagittal CT reconstruction. (b) Sagittal T1w image. (c) Sagittal STIR image.

Fig. 8.24 Os tibiale externum syndrome. Painful swelling on inner aspect of the foot, in particular when playing football. Large accessory bone element (os tibiale externum) with hypointensity on T1w contrast images due to edema (a, arrow) and with surrounding edematous soft tissue swelling, best appreciated on fat-suppressed images (b, arrow). (a) Coronal T1w sequence. (b) Axial PDw fat-saturated TSE sequence.

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a

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8.4 Disorders of Bones

Fig. 8.25 Metatarsophalangeal sesamoid necrosis of the big toe. Professional cyclist with pain at rest and on exertion of metatarsophalangeal joint D I. The bipartite medial sesamoid has normal fatty marrow–isointense signal intensity (a, arrow). The lateral sesamoid exhibits hypointensity throughout (b, arrow), with edema-isointense increased signal intensity on STIR images (c, arrow), consistent with necrosis. (a) Sagittal T1w sequence. (b) Sagittal T1w sequence; other imaging plane. (c) Sagittal STIR sequence.

●

Occult fracture: However, if a line of low signal intensity can be delineated, this is indicative of an occult fracture if the radiographic results were negative.53

Small fractures and avulsion fractures of the bony prominences, for example, of the anterior calcaneal process (▶ Fig. 8.29) or the lateral and posterior talar processes, are frequently occult on radiography.59 The posterior talar process has two projections (the lateral and medial tubercles), separated by the tendon of the flexor hallucis longus. Fractures of the lateral tubercle of the posterior process are more common (Shepard’s fracture) than those of the medial tubercle (▶ Fig. 8.30). They are accompanied by soft tissue swelling and a small joint effusion. The shear forces exerted by the flexor hallucis tendon is thought to play a role in the fractures of the medial tubercle. Force is also transmitted via the talotibial ligament. Flexion of the big toe is often painful. Just as in the hip, in the talocrural joint too, and especially in the talus, transient bone marrow edema may be the cause of persistent symptoms. It should be possible to arrive at a diagnosis if the bone marrow changes observed cannot be attributed to trauma, incorrect loading, and overloading or similar causes, for example, inflammation. In most cases, the changes will resolve by offloading and immobilization of the foot.15 STIR sequences are particularly sensitive for detection of bone marrow edema, thanks to suppression of the fatty marrow signal and hyperintense visualization of the edematous zone.

Stress fractures are typically associated with certain predilection sites because of the static conditions of the human musculoskeletal system (▶ Fig. 8.31). In the foot, these include, for example, the anterior and posterior calcaneus as well as the middle foot (▶ Fig. 8.32, ▶ Fig. 8.33, and ▶ Fig. 8.34). In the central region, apart from stress reaction and/or stress fracture, stress-associated absorption processes are also observed, which, over a period of only a few weeks to months, can give rise to cysts measuring several centimeters in size (▶ Fig. 8.35). Over time, this can result in what appears to be a “calcaneal lipoma”—also seen with secondary calcification. Depending on the changing on weight-bearing mechanisms in response to pain, the stress reactions may also spread to other sites within the space of a few weeks (migration; ▶ Fig. 8.36). Predilection sites have also been identified for talar stress fractures (▶ Fig. 8.37). Stress reactions and fractures of the second and third metatarsals are particularly common and clinically relevant (▶ Fig. 8.38), in both the diaphyseal and head regions of these bones (▶ Fig. 8.39).86 These subchondral stress fractures can be distinguished from juvenile avascular necrosis of the metatarsal head corresponding to Köhler II disease (see Other Bones of the Foot Skeleton p. 369) on the basis of the patient’s age as well as the location and morphology of the fractures.

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c

Fig. 8.26 Bipartite cuneiform. Sagittally oriented cleft through the cuneiform (arrows), with reactive changes (symptomatic) due to congenital bipartite structure. No trauma and no increased stress. (a) Radiographs. (b) CT. (c) Sagittal T1w MR image.

8.4.5 Bone Marrow Edema Syndrome of the Foot and Transient Osteoporosis Often, symptomatic, or also asymptomatic, bone marrow edema that cannot be conclusively attributed to any particular disease or cause is observed in the foot skeleton: ● In children, areas of patchy edema of no particular predilection are occasionally seen. These are mainly of a transient nature and resolve over months to years, without exhibiting any symptoms (“growth-associated”).28 Based on the authors’ observations, the predilection site for this type of edema is along the tarsal growth zones. Among the explanations posited for these signal variations in children and adolescents (often up to 18 years) is the changing biomechanics of the growing skeleton. Furthermore, residual hematopoietic bone marrow still persists, in particular, in younger children (high turnover).48 ● In older adults with altered foot statics, the principal finding is symptomatic multiple edema as a stress reaction; this persists for as long as the pathologic statics of the foot continues to be evidenced (▶ Fig. 8.40). ● In the posttraumatic setting—somewhat after the traumatic event—multiple areas of patchy edema that take up CM may be formed in association with chronic regional pain syndrome (CRPS), formerly known as Sudeck’s disease or algodystrophy,

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mainly accompanied by the typical clinical and radiographic signs of this disease. These patchy changes are consistent with mottled osteopenia, as seen on radiographs or CT images, manifesting as inactivity osteoporosis. In adults, multiple areas of mottled, mainly symptomatic, bone marrow edema can present in the tarsal bones without any discernible reason; these are of transient (generally persisting for 3–12 months) and changing (migratory) nature (▶ Fig. 8.41). Such changes have been termed bone marrow edema syndrome or transient osteoporosis of the foot (analogous to transient osteoporosis of the femoral neck or knee) (see ▶ Fig. 8.40).28 In diabetic foot syndrome (see Chapter 8.13), various edema patterns can be observed. These are caused by neuro-osteoarthropathy or ulcer osteitis/osteomyelitis. The patient history is key to diagnosis.

8.4.6 Osteomyelitis Bacterial inflammation of the foot skeleton can present following surgery or because of neuropathic lesions (ulceration). Manifestations of hematogenous osteomyelitis of the foot are rare. However, a local or multifocal edema pattern may be observed as a nonspecific sign of the affected bones as well as, in association with protracted or complicated courses, a periosteal reaction,

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8.4 Disorders of Bones

8.4.7 Shin Splint Syndrome Shin splint syndrome is a condition that involves chronic pain along the edge of the shinbone; it is also termed tibial edge

syndrome. This condition may have different causes, for example, overloading-induced stress reactions, periosteitis, osteitis, and varicose veins. As opposed to horizontal stress fractures of the distal and proximal tibial metaphysis, stress reactions along the edge of the tibia can embark on a longitudinal perpendicular course (longitudinal stress fracture; ▶ Fig. 8.43). The trigger for this is thought to be the insertion of the lower leg fascia at the medial tibial edge and resultant longitudinal transmission of forces to the tibia, as seen, in particular, among runners or those engaging in ball sports. Initially, there is onset of periosteitis, which can be identified especially on STIR and contrast-enhanced MR images. In the ensuing course, against a background of persistent loading, the periosteal reaction continues to increase and can cause tissue proliferation of several centimeters (mainly without calcification and therefore not visible on conventional radiographs). The findings demonstrated at this stage on MR images are often mistaken for bone tumors (▶ Fig. 8.44). In the later course, manifestations ranging from a longitudinal line of tibial fatigue to a full-blown longitudinal stress fracture are seen. Periosteitis along the anterior edge of the shinbone can present secondarily to impact or in association with varicose veins (▶ Fig. 8.45). Osteomyelitis (▶ Fig. 8.46) or skin diseases (▶ Fig. 8.47) can be differentiated on the basis of the patient history, radiographic findings, and inspection.

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sequester, soft tissue abscess, and/or fistula (see Chapter 11.4.4). Well-delineated areas of inflammation (Brodie’s abscess or plasma cell osteomyelitis; ▶ Fig. 8.42) are commonly seen in the distal tibia.

8.4.8 Pediatric Fractures

Fig. 8.27 Calcaneal stress fracture. Sagittal T2w TSE image. Calcaneal stress fracture with low-signal intensity fracture line and surrounding hyperintense edema (arrows).

The clinical significance of pediatric epiphyseal plate injuries and, in some cases, the limited power of conventional radiographs, have led to an increase in the deployment of MRI for diagnostic imaging of pediatric fractures. MRI lends itself particularly for visualization of complex fractures or severe, radiographically occult epiphyseal injuries (Salter–Harris V).65

Fig. 8.28 Stress fracture of the distal tibial metaphysis. (a) Radiographs. Bandlike sclerotic halo and periosteal new bone formation. (b) Coronal T1w SE image. Signal-void fracture line and hypointense edema. (c) Coronal STIR image. Signal-void fracture line and hyperintense edema. Hyperintense edema also in the surrounding soft tissues.

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Fig. 8.29 Pseudarthrosis of the anterior calcaneal process, secondary to nonimmobilized fracture. Persistent pain, over many months, of the lateral midfoot after relatively minor trauma 7 months previously. Radiographs were interpreted as being normal. The arrowheads point to the fracture. (a) Sagittal T1w sequence. (b) Sagittal PDw fatsat sequence.

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Fig. 8.30 Fracture of the medial tubercle. Pain in the talocrural joint following injury 2 weeks previously. The radiographs were interpreted as being normal. Edema in the lateral tubercle of the posterior talar process, as well as small avulsed bone fragment (arrows). (a) Axial PDw fatsat image. (b) CT.

8.4.9 Tarsal Coalitions Incomplete separations of the bones of the foot skeleton are generally congenital but can, in rare cases, be caused by trauma or infection. In principle, they can occur between any tarsal bones.55 Ever since clinicians began to ponder the existence of tarsal coalitions, their incidence is growing, and they are found bilaterally in 50% of cases, with various types presenting in the same foot. These are classified in terms of their bridging tissue type: ● Synfibrosis: Connective tissue (fibrous) coalition.

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Synchondrosis: Cartilaginous coalition. Synostosis: Bony (osseous) coalition.

A coalition can be complete or incomplete. Depending on its extent, a coalition can have a major impact on the biomechanics of the foot but can often also go undetected in the absence of clinical symptoms (asymptomatic coalition). Symptomatic coalitions can present at any age, from early childhood (“stay-at-home children”) up to 30 years and rarely afterward. Hitherto clinically silent coalitions may become symptomatic when subjected to

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Fig. 8.31 Typical stress fracture of the distal fibula. Coronal PDw fatsat image. Pain in the lateral lower leg, in particular during and after jogging. Bone marrow edema, soft tissue edema, and stress fracture line (arrow).

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8.4 Disorders of Bones

Fig. 8.32 Predilection sites of calcaneal stress fractures. Sagittal schematic diagram of the calcaneus. Predilection sites of calcaneal stress fractures (lines) and vulnerable site at the center of the calcaneus (dashed circle), where stress phenomena can present with the formation of absorption cysts.

Fig. 8.33 Central calcaneal stress reaction. Sports-related pain. Edema pattern at the vulnerable site at the center of calcaneus (arrows). (a) Sagittal T1w sequence. (b) Sagittal STIR sequence.

strenuous physical demands, with attendant injuries to the foot and ankle joint and persistent symptoms. The possibility of tarsal coalitions should also be contemplated when investigating the cause of overloading of the extrinsic muscles of the foot.

Coalitions are used to repair malpositions of the foot, for example, symptomatic juvenile flatfoot. This calls for correct clinical differentiation of flexible and rigid malpositions. Radiologists must also make that distinction before exploring the possibility

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Fig. 8.34 Stress fracture at predilection site on posterior calcaneus. Edema and stress fracture line (arrows) on posterior dorsal calcaneus. (a) Sagittal T1w sequence. (b) Sagittal STIR sequence.

of tarsal coalitions. Failure by the radiologist or clinicians to identify a tarsal coalition can result in inappropriate treatment. The most frequent synostoses are those between the calcaneus and navicular (calcaneonavicular coalition) as well as between the talus and calcaneus (talocalcaneal coalition). Coalitions between other bones are less commonly observed, and when seen they are associated with other deformity syndromes (▶ Fig. 8.48). Osseous tarsal coalitions can often be identified already on conventional radiographs. Cartilaginous coalitions are better demonstrated on computed tomography (CT) and, in particular in association with irritation, on MRI. Fibrous coalitions are difficult to detect; diagnosis is based on identification of decreased signal intensity and an irregular zone, different from a smooth joint line, between the affected bones on MR images. In cartilaginous coalitions, the cleft between the bones is narrower than a normal joint space and is irregularly outlined. In the osseous coalition, a bridge of fatty bone marrow is seen to replace the obliterated joint space. It is also very difficult to detect fibrous coalitions on MRI, with the normal joint space replaced by an area of low signal to signal void (▶ Fig. 8.49). Absence of edema is not a proof of absence of a tarsal coalition.

Calcaneonavicular Coalition In the calcaneonavicular coalition, there is a connection between the laterocaudal base of the navicular and the anterior calcaneal process (▶ Fig. 8.50). This form of osseous coalition is best identified on oblique radiographic views. MRI, especially of the sagittal and axial sections, is generally able to produce a conclusive diagnosis when calcaneonavicular coalition is suspected.

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Talocalcaneal Coalition There are different forms of this synostosis, which affects the subtalar joint, restricting its mobility. Depending on location, a distinction must be made between coalitions of the medial and posterior joint facets; combinations are possible (▶ Fig. 8.51). There are three radiographic signs suggestive of a medial facet coalition: ● (C sign) on lateral views due to the absence of a joint space or caudal deviation of the sustentaculum tali. ● Dorsal bone apposition at the talar neck (dorsal “talar beak”). ● Spherical deformity of the talocrural joint on A/P view (ball and socket joint).21 In osseous coalitions, MRI demonstrates a bony connection with mature fatty marrow (▶ Fig. 8.52), and, in connective tissue coalitions, it demonstrates synchondritis exhibiting a serrated tooth pattern and edema (▶ Fig. 8.53, ▶ Fig. 8.54, ▶ Fig. 8.55, and ▶ Fig. 8.56). The coalition between the posterior facets is frequently overlooked. In addition to deformity of the articular surface, coalition of the posterior articular surface often involves cone-shaped bone apposition at the medial posterior joint facet. In general, the talocalcaneal coalition starts to become symptomatic from the age of 20 years.43

Secondary Synostoses Secondary synostoses (ankylosis) may also contain fatty bone marrow following a certain period of time after infection or trauma.

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Fig. 8.35 Formation of stress-associated calcaneal cyst at typical site. Ballet dancer with increasing symptoms. (a) Radiographs at the time of first medical consultation due to foot pain, in particular during and after ballet rehearsal. Unremarkable findings. (b) Radiographs 7 months later, with detection of central calcaneal cyst (arrow). (c) Sagittal T1w sequence. Calcaneal cyst (arrow). (d) Sagittal STIR sequence. Visualization of calcaneal cyst of variable fluid composition and with mirror reflections.

8.4.10 Cartilage Deformity The range of conditions to be borne in mind here includes focal tumorlike cartilage proliferation, dysplasia epiphysealis hemimelica, Trevor’s disease, tarsoepiphyseal aclasis, and tarsomegaly. A rare disease of unknown etiology causes discrete, reorganized, partially tumorlike proliferation at the osteochondral bordering lamella during skeletal growth. This affects mainly the epiphyses of the knee and, in the foot, the talus, navicular, and tarsometatarsal joints. In addition to discrete foci affecting only one epiphyseal region, several areas, even involving the entire extremity, may be observed.4 The areas of cartilage proliferation at the epiphyses of the knee manifest as cartilaginous exostoses (osteochondroma). A discrete area of cushionlike cartilage thickening is seen at the talus (▶ Fig. 8.57). Typically, only either the medial (around two-thirds) or the lateral aspect of the extremity or region is affected. Clinical symptoms mainly include painless swelling, occasionally causing

restricted joint mobility and blockage. This growth is surgically resected if it causes clinical problems.

8.5 Disorders of the Tendons Tendons are mainly composed of dense bundles of collagen fibers embedded in an amorphous ground substance. Because of their extremely short T2 relaxation time, tendons exhibit low signal intensity on all pulse sequences. Degenerative changes, inflammation, and partial or full-thickness tears result in obliteration of the original tendon structure, rendering them visible on MRI. Lipid deposits secondary to tendon degeneration and hemorrhage give rise to increased intratendinous signal on T1w images. Depending on its extension and configuration, high signal intensity on T2w images points to inflammatory changes or tears. Tendon thickening is seen in association with chronic inflammatory

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Fig. 8.36 Migrating stress fracture in calcaneus. Stress-associated pain in midfoot of overweight female patient with occupational overloading of foot. She reported that the pain had changed or “migrated.” Sagittal T1w MR image a few weeks after onset of symptoms, with stress fracture in the calcaneus (a, arrow) and normal visualization of the anterior calcaneal process (b). Follow-up 5 months later because of changes in pain symptoms (c, d). Resolution of stress fracture, with persistent edema in the anterior calcaneus as well as onset of a new stress fracture at the anterior calcaneal process (d, arrow). (a) Sagittal T1w MR image a few weeks after onset of complaints (section 1). (b) Sagittal T1w MR image a few weeks after onset of complaints (section 2). (c) Sagittal T1w MR image 5 months after initial consultation (section 1). (d) Sagittal T1w MR image 5 months after initial consultation (section 2).

Fig. 8.37 Predilection sites of talar stress fractures. Sagittal schematic diagram.

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Fig. 8.38 Stress reaction of the second metatarsal. A 48-year-old female patient with forefoot pain, in particular during occupational overloading, when working as waitress. Typical stress reaction of the second metatarsal with bone marrow edema, adjacent soft tissue edema, and cortical irregularity (a, arrow). No sign of stress fracture line. Radiographs normal (not illustrated). (a) Coronal PDw fatsat sequence. (b) Axial PDw fatsat sequence.

b

Fig. 8.39 Stress fracture of the head of the second metatarsal. A 58-year-old female patient who had worn insoles over previous 5 months. Increasing pain at the level of second toe. Bone marrow edema and signal-void line (arrows) in the weight-bearing subchondral region of the head of the second metatarsal. (a) Sagittal T1w image. (b) Axial PDw fatsat image.

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changes, whereas localized cross-sectional reduction may be suggestive of partial tears. Tendon damage can have various causes: ● Trauma. ● Impingement problems. ● Incorrect loading and/or overloading secondary to changes in foot statics.

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Drug-induced damage, for example, due to fluoroquinolones80 or gyrase inhibitors. Rheumatoid disease. Gout.

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The Lower Leg, Ankle, and Foot Fig. 8.40 Patchy edema of the tarsal bones. Schematic diagram, sagittal plane. (a) Multiple patches of bone marrow edema of the tarsal bone, with changes in size and location after 3 months and resolution after 6 months. This pattern of migrating and, after a few months, transient edema is more suggestive of transient bone marrow edema syndrome (transient osteoporosis). (b) Multiple patches of bone marrow edema with no notable change over months more suggestive of impaired foot statics or angio- and algodystrophic bone marrow edema of the foot.

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6 months

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Fig. 8.41 Migrating bone marrow edema syndrome of the foot (probably due to static dysregulation). Sagittal PDw fatsat images. A 52-year-old female sales assistant with pain in the region of the tarsal bones. For several weeks, she had been wearing “insoles.” (a) Baseline MRI showing widespread bone marrow edema at the anterior talar process (arrow) and a small irritative synovial effusion. (b) Follow-up MRI after 5 months. After 5 months, the talar signal is completely normal; however, now, edema is seen in the intermediate cuneiform and at the basis of the second metatarsal (arrow).

8.5.1 Achilles Tendon Tears of the Achilles tendon occur primarily in men and between the ages of 30 and 50 years. Predisposing factors include the following: ● Rheumatoid arthritis. ● Lupus erythematous. ● Various metabolic disorders such as diabetes mellitus, gout, hyperparathyroidism, and chronic kidney failure. ● Long-term corticosteroid medication. ● Other medication detrimental to connective tissues (e.g., fluoroquinolones; ▶ Fig. 8.58). ● Overloading when engaging in athletic activities.

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Partial and full-thickness tears are found predominantly in the poorly vascularized zone, situated around 2 to 8 cm above the calcaneal insertion.72 Most full-thickness tears can be reliably diagnosed clinically, based on palpable dehiscence of the tendon and the Thompson test. Hemorrhage and edematous changes, as well as the intact plantaris tendon, can also produce a negative palpation result, whose incidence is reported in the literature to be around 25%.33,72 Hence, other imaging modalities are used in addition to clinical examination, especially ultrasonography and MRI. Ultrasonography has the advantage of being a dynamic examination, whereas MRI permits more detailed assessment, even for the detection of discrete structural changes.

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c

Fig. 8.42 Brodie’s abscess in distal tibia. Relatively sharply marginated focal lesion with pronounced CM enhancement at the margins. Inflammation extends to the cartilage–bone junction and can be recognized from concomitant synovitis with effusion and thickened capsule (c, arrow). (a) Coronal PDw fatsat sequence. (b) Coronal T1w sequence. (c) Coronal T1w sequence after CM administration.

Fig. 8.43 Shin splint syndrome. Pain during and after jogging. Longitudinal stress fracture of the anterior edge of the shinbone. Tibial bone marrow edema (longitudinally oriented) with periosteal reaction (a, arrow) and cortical discontinuity due to longitudinal stress fracture (b, arrow). (a) Coronal PDw fat-saturated TSE sequence. (b) Axial STIR sequence.

Tendinitis (Noninsertional Tendinitis) The first finding in settings of tendinitis or tendinopathy is thickening of the Achilles tendon. There may be inflammation and hyperintensity of the surrounding tissue layers (paratenon) (▶ Fig. 8.59). Because of the edematous changes occurring in

association with (noninsertional) tendinitis, focal and/or diffuse hyperintensity of the tendon tissue is identified on T2w, T2*w, and fat-suppressed sequences; areas of focal or linear increased signal intensity in the tendon may also be observed. At the transition to the partial tear, it is very difficult to differentiate inflammatory increased signal intensity from discrete disruption of the

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Fig. 8.44 Tibial stress reaction. Young woman, despite pain, jogs five times a week to lose weight. MRI of the proximal lower leg, right (here, the most severe pain point is present). Severe periosteal reaction around the tibia, with typical strong CM uptake (b, arrow). Only very few cortical irregularities are seen. On scintigram, maximum enrichment is seen in the proximal tibia, right. However, increased enrichment is also seen because of other stress reaction in the distal tibia, right, and the proximal tibial metaphysis, left, corresponding to the predilection sites of stress reactions and fractures of the lower leg (c, arrows). (a) Axial T1w sequence. (b) Axial contrast-enhanced sequence. (c) Bone scintigram.

Fig. 8.45 Periosteitis of the anterior edge of the shinbone in the presence of varicose veins. Pain of unknown origin at the anterior tibial edge. At the level of the pain point (marking ball), opening for nutrient vessels (a, arrow) incoming vein, as well as pain-inducing periosteal reaction (b, arrow) and slight bone marrow edema. (a) CT. (b) Axial STIR sequence.

fibers. Because of tendon thickening, the anterior tendon contour appears convex on axial and sagittal images. Since the Achilles tendon does not have a tendon sheath, concomitant inflammatory reactions are seen in the peritendinous connective tissue. Administration of IV CM can ensure better visualization and delineation versus inflammatory changes.

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Insertional Tendinopathy (Insertional Tendinitis) Mechanical stress (Haglund’s heel, hollow foot, and dorsal heel spurs) or pressure (footwear) can cause inflammation at the tendon insertion (enthesopathy). The pain can affect the

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Fig. 8.46 Chronic osteomyelitis. Circular irregular cortical thickening, circular periosteal reaction, and bone marrow edema. Typical radiographs (not illustrated), signs of infection, negative sports history. (a) Axial T1w sequence. (b) Axial PDw fat-saturated TSE sequence.

Fig. 8.47 Dermatofibrosis in chronic venous insufficiency. Irregular cutis thickening (based on inspection; (a, arrow), mild anterior periosteal reaction and anterior cortical irregularity (b, arrow), consistent with osteitis. No bone marrow edema. (a) Axial STIR sequence. (b) Axial T1w sequence.

entire calcaneal tuberosity. MRI demonstrates edema at the superior margin of the calcaneus, inflammatory fraying, and/ or thickening of the inserting tendon as well as often concomitant bursitis of the superficial and deep bursae (see Chapter 8.15 ).

Partial Tear Partial tears are differentiated from full-thickness tears by detection of residual continuity on axial or sagittal sections. The

tendon structure exhibits focal hyperintensity on T1w images and areas of high signal intensity on T2w sequences, consistent with blood or fluid collections. Similar changes are observed in tendinitis or tendinosis and cannot be reliably distinguished from a partial tear on MRI. A mixed constellation of findings is often identified, including degenerative changes, partial tears, and fibrovascular, inflammatory processes. Avulsion of the gastrocnemius medialis from the soleus is typically seen in tennis players (tennis leg). Here, MRI demonstrates a

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The Lower Leg, Ankle, and Foot fluid-isointense halo around the gastrocnemius and increased distance between the two muscles (▶ Fig. 8.60).

whether conservative or surgical treatment is to be instigated.36 Besides, MRI is suitable for following up patients treated conservatively.47

Tear

Fig. 8.48 Bone fusion of calcaneus and cuboid. Sagittal T1w images. The arrowhead points to the coalition. Absent joint, bridging with mature fatty marrow.

Fig. 8.49 Fibrous tarsal coalition. Axial PDw fatsat MR image. Pain in the midfoot. Signal-void structure between navicular and anterior calcaneal process (arrow) as a sign of fibrous coalition. Edema of the adjacent tarsal bones as a sign of symptomatic incorrect loading (stress reaction).

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Fig. 8.50 Cartilaginous coalition between anterior calcaneal process and navicular. The arrowheads point to the coalition. Undulating border between the bones, extended anterior calcaneal process, and edema as a sign of symptomatic synchondritis. (a) Sagittal T1w image. (b) Sagittal PDw fatsat image.

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A reliable MRI sign of a full-thickness tear of the Achilles tendon is detection of complete discontinuity of the original tendon structure, best viewed in the sagittal imaging plane (▶ Fig. 8.61). Retraction of the tendon stumps results in a corkscrewlike appearance of the proximal segment and increased buckling of the distal portion. Often, interposed fat or fluid (edema and/or blood) is seen at the torn site. Changes to the peritendinous tissue can be demonstrated in the axial plane. In addition to diagnosis, MRI is also able to provide important information on treatment planning, since the distance between the tendon stumps is the chief determinant of

8.5 Disorders of the Tendons

Postoperative Status Surgically treated tendons appear thicker than their nonsurgical counterparts on MRI and often continue to exhibit inhomogeneous signals for up to 2 years after surgery, with these being most pronounced between 3 and 6 months postoperatively. After 2 years, the signal intensity will generally have reverted to normal.97 Typically, focal susceptibility artefacts, with multifocal areas devoid of signal, are seen at the surgical site. Postoperative

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Nodules

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1 Fig. 8.51 Anatomy of the talus. Schematic diagram of the talus surface illustrating the articular surfaces (of variable structure). Coalitions are mainly found in the middle articular surface. 1, posterior articular surface of the subtalar joint; 2, middle articular surface of the subtalar joint; 3, anterior articular surface of the subtalar joint (here, confluent with the middle surface); 4, articular surface to navicular.

Nodular thickening of the Achilles tendon, which can often be very painful and is known as “achillodynia,” can, as described above, be caused by tendinitis or occur in association with tumors and substance deposition. For example, ganglion cysts of the Achilles tendon are not uncommon (▶ Fig. 8.62). Giant cell tumors of the tendon sheath are also encountered. Less common tumors are fibromas or xanthomas; on MRI, xanthomas (see Chapter 8.17.1) lead to an inhomogeneous signal change, often of mottled appearance due to interspersed foci of intense signal. Gouty tophi can also be formed along the Achilles tendon.

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complications include recurrent tear (3–5% of cases) and/or infection, also with abscess and/or fistula formation (10–15% of cases). Alternatively, conservative treatment can be administered if the tendon stumps are situated less than 1 cm apart.6,34,79,93 Grafts can be used to cover larger defects (tendons, other soft tissues, and allografts). Only in around half of such cases is there signal isointensity of the various materials. In the remaining cases, signal differences persist, with certain areas of varying hyperintensity.

8.5.2 Plantaris Tendon The plantaris tendon together with the medial head of the gastrocnemius can be injured at the myotendinous junction, in particular when taking sidesteps in tennis, squash, badminton, etc. (middle lower leg; tennis leg). Injuries to the distal

b

Fig. 8.52 Bone connection between talus and calcaneus. Bone fusion of the medial joint facet (arrows). (a) Coronal T1w image. (b) Sagittal T1w image.

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8.5.3 Peroneal Tendons The clinical relevance of disorders of the peroneal tendons is growing. Chronic symptoms secondary to talocrural joint sprain are often caused by damage to these tendons, too. Fullthickness or partial tears of the peroneal tendons are relatively rare.

Tear Full-thickness tears are generally found in the peroneus longus at the level of the cuboid, where the tendon diverts its course toward the sole of foot.61 At this point, the tendon is often diverted through a bony groove in the cuboid (cuboid tunnel) to the sole of foot. Tendon irritation or constriction may occur at this site (▶ Fig. 8.64). A tear is long preceded by painful tendons and/or tenosynovitis (cuboid tunnel syndrome; ▶ Fig. 8.65). It is not uncommon to encounter an os peroneum sesamoid protecting the tendon at this diversion, deep to the calcaneocuboid joint. That ossicle should be taken into account when investigating

tears of the peroneus longus tendon. Fractures or bipartite bony elements are encountered and are suggestive of tendon damage. Bone marrow edema of the cuboid adjacent to the inflamed tendon sheath is frequently observed in association with tendinitis or cuboid tunnel syndrome.

Partial Tear Partial tears are mainly found in the peroneus brevis tendon (▶ Fig. 8.66), especially in association with peroneal tendon dislocation and in the form of an intratendinous, longitudinal tear (peroneal tendon split, known as split syndrome), mainly at the fibular tip or distal to it.78 Because of overloading or injury, the peroneus longus tendon can prolapse into the peroneus brevis tendon or vice versa, thus causing painful tendinitis. MRI axial sections often demonstrate the characteristic findings, where parts of the longus tendon are pressed apart and enclose the central brevis tendon (tulip sign). Clinicopathologic correlation with the MRI findings is important for interpreting the results. On MRI, the tendon cross-section has a central area of increased signal intensity, with splitting of the normal dark signal exhibited by the tendon (▶ Fig. 8.67).94 Marked tenosynovitis is often seen additionally.

Fig. 8.53 Talocalcaneal coalitions. Schematic diagram. (a) Coronal section. Osseous coalition between medial joint facet (bone bridging, arrow). (b) Sagittal section. Cartilaginous coalition of the medial facet (serrated tooth pattern, arrow). (c) Sagittal section. Cartilaginous coalition of the posterior facet (serrated tooth pattern, arrow).

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Fig. 8.54 Cartilaginous talocalcaneal coalition of the medial facet. Serrated tooth pattern of the articular surface (arrows). (a) Sagittal T1w image. (b) Axial T1w image.

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lower leg are often seen in association with Achilles tendinopathy (▶ Fig. 8.63).8

8.5 Disorders of the Tendons

Tendinitis and Tendovaginitis Tendinitis is mainly accompanied by diffuse thickening of the tendon. Often, the tendon is surrounded by fluid, which is also found within the tendon sheath and manifests on T2w images as a rim of intense signal surrounding the tendon, pointing to inflammatory involvement of the tendon sheath in the form of tendovaginitis. Tendinitis and tendovaginitis can have different causes. Morphologic causes visible on MRI include the following:

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Hyperplastic peroneal trochlea (crista), possibly causing narrowing of the peroneus longus tendon groove (sulcus; ▶ Fig. 8.68 and ▶ Fig. 8.69).84 Very distally situated myotendinous junction. Peroneus quartus (accessory muscle that has split from the peroneus brevis and is found in 6% of cases).18,71,89 Over- and incorrect loading, for example, in hollow foot.

Dislocation

Fig. 8.55 Bone apposition at anterior capsular insertion at the anterior talar process (dorsal talar beak) in association with coalition. Different patient. Sagittal T1w image. The arrowhead points to the bone apposition.

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Peroneal tendon dislocation is often seen in association with traumatic stretching or tearing of the superior peroneal retinaculum. The peroneal tendons are displaced lateroanteriorly over the fibular tip from their normal anatomic position, along the posterior surface of the lateral malleolus. A very distally situated myotendinous junction or an absent or flat bony groove on the posterior surface of the lateral malleolus is a predisposing factor for peroneal tendon dislocation (malleolar sulcus).67 Detection of the tendons lateral to the

Fig. 8.56 Tarsal cartilaginous coalitions on MRI. Schematic diagram. (a) Talocalcaneal coalition on coronal image, illustrating the synchondrosis between the sustentaculum tali and talus (middle form; arrow). (b) Calcaneonavicular coalition on sagittal image, with prominent anterior calcaneal process and synchondrosis to navicular (arrow).

Fig. 8.57 Dysplasia epiphysealis hemimelica (Trevor’s disease). Irregular, osteocartilaginous formations in the medial portion of the talar trochlea, with slight space-occupying aspect (increased growth compared with nonaffected lateral portion of the talar trochlea). Good delineation of both cartilaginous and bone portions, especially on GRE sequences. Reactive joint effusion. (a) Moderate T2w fast spin-echo (FSE) sequence. (b) T2*w double-echo steadystate (DESS) image.

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The Lower Leg, Ankle, and Foot lateral malleolus, instead of at their normal posterior location on MRI, in addition to the clinical findings, will help diagnose this condition. An additional common finding is soft tissue edema.69

Other Lesions Insertional tendinopathy of the peroneus brevis tendon is often accompanied by soft tissue and, frequently, bone marrow edema at the base of the fifth metatarsal. Avulsion fractures tend to have a horizontal course, whereas in children apophyseal fractures are generally perpendicularly oriented. Fatigue fractures (Jones’ fractures), secondary to chronic overloading of the peroneus brevis tendon, may also be identified, as can the very rare os vesalianum.

8.5.4 Deep Flexor Tendons

Fig. 8.58 Full-thickness tear of the Achilles tendon following longterm fluoroquinolone use. Sagittal T1w image. The arrowhead points to the tear.

The tibialis posterior arises from the interosseous membrane and crosses, with its tendon proximal to the inner ankle, beneath the flexor digitorum tendon, before inserting at the navicular tuberosity and, with broad variability, at the bases of the second to fourth metatarsals. Anatomic variants of its insertion at the navicular have been characterized, of which the following can be of clinical relevance: cornuate navicular, secondary navicular, and/or an os tibiale externum. In addition to the main portion of the tendon inserting at the navicular, there is a smaller segment of the tibialis posterior tendon situated above it, which runs farther distal beneath the plantar surface and inserts into the cuneiform bones and the bases of the metatarsals.60 The tibialis posterior tendon is an important stabilizer of the medial longitudinal arch of the foot. Together with the peroneus longus, it stabilizes the tarsal transverse arch of the foot (“stirrup”). It was only with the advent of sport types such as Nordic walking that there has been a sharp rise in the incidence of full-thickness tears. These tears are generally preceded by chronic degenerative changes linked to overloading of the tendon against a background of an unstable subtalar foot plate, leading to skewed flatfoot. Other predisposing factors include the following: ● Rheumatoid arthritis. ● Long-term corticosteroid medication.

Fig. 8.59 Achilles tendinopathy. Painful thickening of the Achilles tendon. Homogeneous hypointense thickening of the Achilles tendon and inflammatory halolike increased signal intensity in paratenon (a, arrow). (a) Axial PDw fatsat image. (b) Sagittal PDw fatsat image.

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Tibialis Posterior

8.5 Disorders of the Tendons

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Fig. 8.60 Tennis leg. A 56-year-old male patient. Calf pain after sidestep while playing tennis. A load sound could be heard. Fluid halo around gastrocnemius medialis (arrows) and increased distance to soleus as a sign of laceration injury (tennis leg). Edema and bloody fluid in subcutis and muscle (pennate structure). (a) Coronal PDw fatsat image. (b) Axial PDw fatsat image.

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Fig. 8.61 Achilles tendon rupture. Status post falling down stairs. Full-thickness tear of the Achilles tendon, with retraction of the tendon stumps and hemorrhagic, fluid-containing defect of more than 3 cm (arrows). (a) Sagittal T1w image. (b) Sagittal PDw fatsat image.

The clinical picture of tendon insufficiency is termed tibialis posterior dysfunction and ranges from painful swelling posterior to the inner ankle to complete symptomatic skewed flatfoot. Tibialis posterior dysfunction has been staged by Johnson and Strom as follows: ● Stage 1: Tenosynovitis (pain along the tendon course). On MRI, a central area of hyperintensity, in addition to tendon

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thickening, is observed. Occasionally, fluid is identifiable in the tendon sheath in all stages. Stage 2: Elongation of the tendon (flexible pes valgus). On MRI, very high signal intensity and, sometimes, signs of a partial tear can be seen. Stage 3: Tear (pes planovalgus). MRI demonstrates discontinuity of the tendon.

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Fig. 8.62 Nodular thickening of the Achilles tendon. Fluid-isointense space-occupying lesion along the course of the Achilles tendon (a, c, arrows), with relatively high signal intensity on T1w contrast images, smooth margins, and septation, consistent with cyst containing high protein content or ganglion cyst. The displaced tendon is normal. (a) Axial PDw fat-saturated TSE sequence. (b) Axial T1w sequence. (c) Sagittal T1w sequence.

Stage 4 has been added by M. Myerson, who described valgus tilting of the talus in the talocrural joint. In the more severe forms, fibial fractures are seen as a sequela of hindfoot tilting; this was characterized as stage 5 by L. Schon. Today, MRI is the primary imaging modality for staging and differential diagnosis of tibialis posterior dysfunction (▶ Fig. 8.70).

Flexor Digitorum Longus Tears of the flexor digitorum longus tendon are extremely rare and can be recognized from the resultant characteristic claw-foot deformity. Tendovaginitis is commonly encountered and recognized on MRI from the increased fluid content and CM uptake by the tendon sheath.

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Flexor Hallucis Longus This muscle arises from the lateralmost part of the lower leg and is the only deep flexor to course deep to the sustentaculum tali and insert at the medialmost part of the base of the distal phalanx of the big toe. The point where it crosses the flexor digitorum tendon is known as the “plantar chiasm” or the “knot of Henry” (▶ Fig. 8.71). Very fine tendinous bands (vincula) connect both tendons. This connection is advantageous in foot surgery if one of the two tendons is used for augmentation, since careful dissection of the tendon at this site reduces the risk of functional failure.

8.5 Disorders of the Tendons

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Fig. 8.65 Cuboid tunnel syndrome. Sagittal PDw fatsat MR image. A 50-year-old male patient with increasing weight-bearing pain on outer margin of foot, radiating into the sole of foot. Thickening of the peroneus longus tendon in the region of the cuboid, in some cases with increased signal intensity and ill-defined margins, as well as with edematous thickening of the surrounding soft tissues, including the tendon sheath (arrow).

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Fig. 8.63 Lesion in plantaris tendon. Axial PDw fatsat image. Status post painful sidestep while playing tennis. Fluid collection above medial aspect of soleus as well as irregularity of tendon contour (arrow), consistent with muscle fiber tear or lesion in plantaris tendon.

Fig. 8.64 Cuboid tunnel and peroneus longus tendon. Schematic diagram. Course of peroneus longus tendon. The tendon courses posterior to the outer ankle along the lateral calcaneal surface and is reinforced by a strand of connective tissue (superior and inferior retinaculum), passing by a more or less well-developed prominence (crista/peroneal trochlea) to the cuboid. Here, it diverts to the sole of foot and inserts finally on the plantar aspect at the intermediate cuneiform and at the base of the first metatarsal. By virtue of its transverse course, this tendon together with the medial tibialis posterior reinforces the transverse arch of the foot (“stirrup tendon”). (a) Lateral view of foot. (b) View of the sole of foot.

Fig. 8.66 Anatomic course of the peroneus brevis tendon. Schematic diagram. View from above of the foot, from lateral, illustrating the course of the peroneus brevis tendon posterior to the outer ankle, along the calcaneus from the bony prominence of calcaneus (peroneal trochlea) to the base of the fifth metatarsal.

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Fig. 8.67 Peritendinitis of the peroneus brevis tendon. Tendinitis, peritendinitis, and longitudinal tear of the peroneus brevis tendon at a typical site due to pressure exerted by the peroneus longus tendon. Increased signal intensity of tendon and tendon sheath (a, b, arrows) as well as longitudinal tear with thinning. (a) Sagittal T1w image. The respective positions on the axial sections are marked for c and d. (b) Sagittal PDw fatsat image. (c) Axial PDw fatsat image. Compression of the peroneus brevis tendon due to the prolapsed peroneus longus tendon (arrow). (d) Axial PDw fatsat image. Partial tear of inflamed peroneus brevis tendon (arrow).

Partial or full-thickness tears are generally caused by injury, especially to the distal tendon segments. Tendinitis and tendovaginitis are mainly found to affect the proximal portions of the tendon in the region of the talar trigonal process as a sign of overloading, also among ballet dancers. Since the tendon sheath frequently (in around 70% of cases) communicates with the joint cavity of the talocrural joint, fluid accumulation in the tendon sheath need not always have pathologic implications.75

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8.5.5 Anterior Muscle Group (Extensor Group) Tendinitis or tendovaginitis of the tibialis anterior is seen primarily in settings of chronic overuse, when running, walking downhill, or dancing. Degenerative processes of the talocrural joint can, for their part, affect the tendon. Tears of the tibialis anterior tendon are often missed, since they are associated with only a brief painful phase, despite their potential to cause severe gait impairment, because of unimpeded

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Cross-section d

8.6 Ligament Injuries and Impingement Problems following Ligament Damage Further distal, insertional tendinopathy of the tibialis anterior tendon at the medial cuneiform is a relatively frequent observation (▶ Fig. 8.73). Here, MRI plays a key role in differential diagnosis by distinguishing between tendinopathy and bone stress reactions. It is also able to identify degenerative changes to the first tarsometatarsal joint to ensure appropriate treatment. MRI also demonstrates edematous swelling on the arch of the foot along and at the insertion of the tibialis anterior tendon. Clinical symptoms are manifested only in the acute phase and include swelling, localized pressure point pain, and pain at rest at characteristic sites. Pathologic changes to the tendons of the extensor hallucis longus and extensor digitorum longus are rare. Demonstration of such changes is important only in the context of their differential diagnosis from ganglion cysts on the arch of the foot. The MRI findings are similar to those described above for other tendons. Downloaded by: Collections and Technical Services Department. Copyrighted material.

plantar flexion. They are mainly found distal to the talocrural joint. There may be marked proximal retraction of the tendon, with formation of an “empty” tendon sheath at a characteristic site (▶ Fig. 8.72) as well as a “pseudotumor” on the arch of the foot.40

8.6 Ligament Injuries and Impingement Problems following Ligament Damage 8.6.1 Talocrural Joint

Fig. 8.68 Peroneal tendinitis and peritendinitis with prominent peroneal trochlea of calcaneus. Axial PDw fatsat image. Pronounced inflammatory changes in peroneal tendons, tendon sheath, and surrounding soft tissues (black arrow) with prominent peroneal trochlea (white arrow). Concomitant bone marrow edema in calcaneus.

In the region of the talocrural joint, there are three ligamentous complexes that play a pivotal role in the stability and integrity of the joint: ● Detection and differentiation of deltoid ligament injuries are gaining more attention, in line with the increasing use of endoprosthetic ankle joint devices, to treat posttraumatic osteoarthritis of the talocrural joint. Persistent medial instability results in valgus displacement of the talocalcaneal complex, ultimately necessitating reinforcement of the talocrural joint (talocrural joint arthrodesis). The medial collateral ligament (deltoid ligament) comprises four segments: ○ Tibionavicular part.

Fig. 8.69 Peroneal peritendinitis (longus and brevis) with prominent peroneal trochlea. Tendon sheath effusion and slight increase in signal intensity of peroneus longus (dorsal) and brevis (ventral) tendon at the level of the prominent trochlea (arrows). (a) Axial PDw fatsat image. (b) Coronal PDw fatsat image.

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Fig. 8.70 Tendinitis of the tibialis posterior tendon. Axial PDw fatsat MR image. Central increased signal intensity in the tendon of the tibialis posterior (arrow).

Fig. 8.71 Courses of the deep flexors of foot. Schematic diagram, view from above of the foot, from medial. Above, the tibialis posterior tendon courses and inserts at the navicular. In the middle, the course of the flexor digitorum longus tendon is illustrated, and below, the flexor hallucis longus tendon is illustrated. The latter tendons intersect at the level of the navicular (plantar chiasm and master knot of Henry, arrow).

Fig. 8.72 Avulsion of the tibialis anterior tendon, with major tendon retraction. (a) Sagittal STIR sequence. The retracted tendon stump manifests as a swollen protrusion (arrow). (b) Axial PDw fat-saturated TSE sequence. Proximal to the swollen protrusion (s.a) altered signal intensity in tendon stump (arrow). (c) Axial PDw fat-saturated TSE sequence, other section. Distal to the retracted tendon stump “empty” tendon sheath (arrow).

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The Lower Leg, Ankle, and Foot

8.6 Ligament Injuries and Impingement Problems following Ligament Damage Fig. 8.73 Painful insertional tendinopathy of the tibialis anterior tendon. Thickening and increased signal intensity of tendon insertion (arrows) on medial cuneiform. (a) Sagittal PDw fatsat sequence. (b) Sagittal T1w sequence. (c) Axial T2w sequence of foot.

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Tibiocalcaneal part. Anterior tibiotalar part. ○ Posterior tibiotalar part. The lateral (collateral) ligaments account for around 85% of all ligament injuries. The injury mechanism usually involves inversion trauma (supination trauma), which, depending on the severity, causes damage first to the anterior fibulotalar ligament, then to the fibulocalcaneal ligament, and finally to the posterior fibulotalar ligament. In clinical terms, it is important to differentiate between a single-, two-, and multiple-ligament injuries. The third ligamentous complex is the tibiofibular syndesmosis (ligamentous structure between the distal fibula and tibia), which stabilizes the malleolar fork (ankle mortise) and comprises the anterior tibiofibular ligament (anterior syndesmotic ligament) and posterior tibiofibular ligaments (posterior syndesmotic ligament, variable segments), as well as a strong interosseous ligamentous connection (interosseous tibiofibular ligament). ○ ○

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In addition to clinical examination, diagnostic exploration of ligament injuries should include radiographs in two projections to rule out bone damage and, if necessary, radiographic stress views. However, without fibularis block (anesthesia of the peroneal nerve), the latter can often produce false-negative results because of the reflex muscle tension of the extrinsic muscles and the frequently widespread posttraumatic edema.82

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MRI is able to demonstrate the ligaments of the talocrural joint and assess the extent of ligament injury.11,73 Depending on the foot position, it may be advisable to acquire angulated sequential slices of the ligaments (see Chapter 8.2.3) (▶ Fig. 8.74). MRI is also endowed with high sensitivity for detection of syndesmosis rupture, especially on angulated axial and nonangulated coronal images at angles of between 30 degrees (posterior syndesmosis) and 45 degrees (anterior syndesmosis).9,12,58 Exclusion of anterior syndesmosis rupture has clinical implications for any surgical indication. It is mainly bony avulsion (detection of Volkmann’s triangle), which is observed at the posterior syndesmosis. Lateral ligament lesions are often accompanied by sinus tarsi injuries, manifesting on MRI as edema or ligament injuries.10 Just like muscle tendons, intact ligaments also have low signal intensity on all sequences (▶ Fig. 8.75 and ▶ Fig. 8.76). Streaky areas of hyperintensity, consistent with intraligamentous fat deposits, have been reported for the posterior tibiofibular and talofibular ligaments and for deep segments of the deltoid ligament.41 Ligament evaluation must include signal pattern, thickness, contour, and continuity.73 Sprains or partial tears will give rise to intraligamentous edema, intraligamentous hemorrhage, and attendant rise in signal intensity on T2w sequences. If there is a full-thickness tear, the ligamentous structure will be disrupted (▶ Fig. 8.77; see also ▶ Fig. 8.75b). Thickening or an undulating ligament contour may be an indicator of a historic injury or may point to chronic ligament injuries, which are often associated with insufficiency of the implicated ligament. For detailed assessment, the entire course of

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the ligaments should be demonstrated,73 using different imaging planes tailored to the orientations of the various ligaments. The slice thickness should not exceed 3 mm because of the relatively narrow width of most ligaments. The course of the lateral ligaments is determined by the foot position.

8.6.2 Lisfranc Injury In clinical terms, the tarsometatarsal joints can be viewed as a single joint. The Lisfranc injury is named after Napoleon’s physician, Jacques Lisfranc (1790–1847), and is also referred to as the “Lisfranc joint” or “Lisfranc joint line.” However, the medial Lisfranc joint (metatarsocuneiform joints) must be functionally differentiated from the lateral Lisfranc joint (metatarsocuboid joints). The retropositioned second metatarsocuneiform joint, an amphiarthrosis joint, ensures highly stable fixation of the second metatarsal, while complex ligament

connections provide for ligamentous stability; the ligamentous structure between the medial cuneiform and second metatarsal is termed the Lisfranc joint ligamentous complex. This ligamentous structure runs obliquely from the lateral edge of the medial cuneiform to the medial edge of the base of the second metatarsal and is composed of three bundles: a strong interosseous, a posterior, and a plantar bundle. This ligament and damage to it can be identified only on MRI scans.16 Regrettably, even today, 40% of injuries to the Lisfranc joint are not initially detected, and only the onset of painful instability, posttraumatic osteoarthritis, and defective foot positions draw attention to previous trauma. Severe injuries are generally diagnosed as dislocation fractures on radiographs and/or CT on the basis of the bone fragment chipping and misalignment of the metatarsals.64 MRI is the imaging modality of choice for detection of purely ligamentous injuries that cause clinically relevant instability and pain. It is occasionally able to directly visualize discontinuity of the Lisfranc ligament, or by demonstrating edematous increased signal intensity, it is able to point to injury to this complex joint line. The above explanation provides the rationale for many trauma surgeons recommending both CT and MRI scans where there is clinical suspicion of Lisfranc injury (e.g., plantar ecchymosis).

8.6.3 Sinus Tarsi Ligament Injuries and Sinus Tarsi Syndrome

Fig. 8.74 Normal visualization of the anterior fibulotalar ligament. T2w TSE sequence with high ETL (echo length train) to increase the MTC effect. Plantar-flexed foot position and corresponding angulation of the oblique axial ligament sequence. The arrowhead points to the ligament.

Together with the calcaneal sulcus, the talar sulcus forms an anatomic groove that opens laterally to form the sinus tarsi and separates the subtalar joint from the talocalcaneonavicular joint, with both joints always viewed as a functional unit. The sinus tarsi contains nerves, blood vessels, and ligamentous structures embedded in a fat pad (see ▶ Fig. 8.4 and ▶ Fig. 8.11). The sinus tarsi is well visualized on axial and coronal sections. Depending on the force applied, injury to the talocrural joint and the subtalar joint can cause tears in the ligaments, close to the sinus tarsi, especially the interosseous talocalcaneal ligament, following rupture of the anterior fibulotalar ligament and fibulocalcaneal ligament. The term sinus tarsi syndrome is used to denote the constellation of symptoms frequently manifesting secondarily to supination

Fig. 8.75 Lesions of the fibulotalar ligament (various patients). Axial PDw fatsat sequences. (a) Intact anterior fibulotalar ligament (black arrow) and sprained posterior fibulotalar ligament (white arrow). (b) Ruptured and lacerated anterior fibulotalar ligament (black arrow) as well as unremarkable posterior fibulotalar ligament (white arrow).

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8.6 Ligament Injuries and Impingement Problems following Ligament Damage

Fig. 8.76 Fibulocalcaneal ligament. Oblique axial T1w MRI section showing longitudinal course of the ligament (arrow).

trauma and presenting as longstanding lateral foot pain, tenderness over the sinus tarsi, instability, and improvement of symptoms after injection of a local anesthetic into the region of the sinus tarsi. This syndrome is often a sign of instability or inadequate healing of ligamentous injuries. With growing knowledge of the disorders of the adjacent structures, the term becomes less apt. MRI is able to demonstrate signal changes in the ligaments or discontinuity on T1w or T2w images. Moreover, nonspecific inflammatory changes with low signal intensity can be seen on T1w and those with increased signal intensity can be seen on T2w images; in addition, scar tissue with low signal intensity can be seen on T1w and T2w images. Synovial cysts and ganglion cysts can also cause sinus tarsi syndrome (▶ Fig. 8.78).

8.6.4 Plantar Calcaneonavicular Ligament This strong ligamentous connection between the sustentaculum tali and the medial and plantar lower margin of the navicular is one of the most important stabilizers of the talonavicular joint and is, at the same time, the most deep seated of the flexors of the medial longitudinal arch. This ligament is also known as the “spring ligament.” In terms of its MRI anatomy, three ligament portions have been characterized (▶ Fig. 8.79).51,87 Its visualization is key to differentiating between posttraumatic flatfoot and degenerative skewed flatfoot.

8.6.5 Impingement Syndrome Impingement syndrome is often thought to be the cause of restricted motion and chronic joint pain. In general, the following forms can be identified in the talocrural joint: ● Anterior impingement. ● Posterior impingement.

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Fig. 8.77 Tear of the fibulocalcaneal ligament. Oblique axial T2w TSE sequence with high ETL (TF = 20) along the ligamentous course (“ligament sequence”). Status post inversion trauma with lateral ligament injury. Discontinuity of the fibulocalcaneal ligament and partial thickening pointing to a tear (arrow).

Anterolateral impingement. Medial impingement.

There are various possible causes for this mechanically induced, inflammatory pain syndrome: in addition to widespread scarring following ligament and capsular tears, arthritic osteophytes or accessory bone elements can result in periarticular masses exhibiting similar symptoms.23

Anterior Impingement Anterior impingement is seen especially in footballers in whom forced dorsiflexion of the talocrural joint has led to bone impingement between the anterior tibial edge and talar neck. Anterior osteophytes in association with osteoarthritis talar beak can also cause impingement.

Posterior Impingement Posterior impingement can involve both bones and soft tissues (▶ Fig. 8.80), and is observed especially in ballet dancers, with repetitive extreme plantar flexion causing impingement of the posterior talar process or of an independent os trigonum on the posterior tibial edge.49 This os trigonum syndrome is often accompanied by inflammation of the periarticular synchondrosis, manifesting as a hyperintense band with strong CM uptake (synchondritis) as well as inflammation of the surrounding joint capsule and soft tissues. Unhealed fractures of the posterior talar process also frequently cause impingement or mechanical inflammation of the pseudarthrosis, accompanied by discrete effusions secondary to focal synovitis, and, occasionally, bone marrow edema of the posterior talar process or os trigonum. The flexor hallucis longus tendon is also often implicated because of its proximity to the aforementioned structures (▶ Fig. 8.81).

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Fig. 8.79 Spring ligament. Sagittal T1w image. The plantar calcaneonavicular ligament (spring ligament) can be identified as a broad, signal-void ligamentous structure between the calcaneus and navicular (arrow). Tears of this ligament complex can be detected on the MR image (discontinuity and nonvisualization).

Fig. 8.78 Sinus tarsi syndrome. Axial T2w image. In this patient, hyperintense cystic changes, consistent with synovial cysts or a ganglion cyst, can be identified as the cause of sinus tarsi syndrome (arrow). C, cuboid; H, flexor hallucis longus; K, calcaneus; St, sustentaculum tali; T, talus.

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Anterolateral Impingement Anterolateral impingement syndrome usually results from injury to the lateral ligament complex, whereby a partial or full-thickness ligament tear leads to synovial hypertrophy and connective tissue proliferation, which infiltrates the lateral talofibular joint space, causing chronic mechanical irritation. On MRI, this hypertrophic (“meniscoid”) tissue mainly exhibits intermediate signal intensity on T1w and T2w sequences. Likewise, a thickened anterior fibulotalar ligament can point to anterolateral impingement.27,35

Medial Impingement An excessive scarring reaction to deltoid ligament ruptures can cause mechanical, motion-dependent pain syndrome (▶ Fig. 8.82).

8.7 Diseases of the Plantar Fascia (Plantar Aponeurosis) The plantar fascia is prone to painful disorders, which are accurately diagnosed on MRI as stress-related changes. In lay terms, these manifestations are known as “heel spurs.”

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Fig. 8.80 Posterior impingement. Schematic diagram of the talocrural joint, axial plane. Potential causes as well as MRI sign of posterior impingement (see text). 1, navicular; 2, talus; 3, medial tubercle of posterior talar process; 4, flexor hallucis longus tendon; 5, lateral tubercle of posterior talar process; 6, edema, effusion in dorsal recess, synovitis, and os trigonum variants; 7, lateral malleolus; 8, lateral talar process; 9, sinus tarsi.

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The Lower Leg, Ankle, and Foot

8.7 Diseases of the Plantar Fascia (Plantar Aponeurosis)

8.7.1 Plantar Fasciitis In plantar fasciitis, chronic stress causes degenerative inflammatory changes in the plantar aponeurosis. The main clinical symptoms are morning pain, generally around the calcaneal tuberosity, radiating distally because of the stress applied during extension of the fascia. This is mainly caused by more or less pronounced instability of the subtalar foot plate occurring in a defective foot position of the fore- and hindfoot. The changes identified on MRI are mainly in the region of the calcaneal insertion of the fascia. In addition to hyperintensity on T1w and T2w sequences, consistent with the edematous-inflammatory changes within the fascia and in the surrounding soft tissue, calcaneal bone marrow edema is often seen.81 An additional characteristic sign is thickening of the fascia (standard value: around 4 mm; ▶ Fig. 8.84).7 A plantar heel spur is seen in around 50% of these patients. Spur formation is now interpreted as a sign of insertional tendinopathy of the plantar aponeurosis rather than as a pain-inducing new growth that calls for surgical resection. Chronic inflammation can result in (partial) tears (▶ Fig. 8.85). There is an initial rise in edematous changes following ultrasonography or shockwave therapy. This initial progression of edema in plantar fasciitis may be observed for up to 30 hours after treatment and should not be interpreted as deterioration.99

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The plantar fascia is the plantarmost component of the stabilizer system of the medial longitudinal arch and, by virtue of its horizontal fibers, also of the transverse arch. The plantar fascia is attached by two of its portions to the plantar calcaneal tuberosity, of which one is a thick medial branch and the other a slimmer lateral branch (▶ Fig. 8.83). Its distal end inserts into the plantar capsule of all metatarsophalangeal joints. This anatomic composition must be taken into account on MRI evaluation. Full-thickness tears are rare and do not always need strong force. There are reports of spontaneous tears without prodromal pain. However, inflammation of the plantar fascia is more common.

8.7.2 Plantar Fibromatosis (Ledderhose’s Disease)

Fig. 8.81 Os trigonum syndrome. Sagittal STIR sequence. Accessory bone element posterior to talus (os trigonum), surrounded by irritative synovial focal effusion (arrow). Pain at rest and on exertion.

While these changes in the plantar fascia are rarely symptomatic, they are a source of concern to the patient if nodular thickening of the tendon increases. However, surgery is indicated only if the nodules reach the weight-bearing zone of the forefoot or on loading cause compression of the underlying medial plantar nerve. MRI should always be conducted prior to surgery. In plantar fibromatosis, excess fibrous connective tissue is deposited mainly in the medial aspect of the plantar aponeurosis (there is an association between this condition and Dupuytren’s disease of the

Fig. 8.82 Medial impingement syndrome of the talocrural joint. Coronal T1w sequences. (a) Immediately after sprain injury, with tear of deltoid ligament (arrow). (b) One year later, weight-bearing pain syndrome of medial malleolus and persistent swelling. Hypointense scar tissue distal to medial malleolus (arrow) pointing to medial impingement.

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8.8 Diseases of the Fat Pads of the Feet and Plantar Vein Thrombosis With their loculated histologic structures, the main function of the plantar fat pads is, like that on an innerspring mattress, to provide for shock absorption and load distribution during the gait cycle. They also minimize the shear forces exerted on the sole of foot. Over- or incorrect loading can result in painful inflammatory irritation of these fat pads (obesity, panniculitis). Atrophy of the fat pads is seen secondarily to impaired perfusion (peripheral arterial occlusive disease, compartment disease), nicotine abuse, and rheumatoid arthritis. Absence of fat pads leads to heel pain and metatarsalgia. MRI is indicated for differential diagnosis of pain of unknown origin. During the inflammatory stage, poorly defined discrete edema that appears dark on T1w images but bright on PDw fatsat images is identified (▶ Fig. 8.89). In chronic stages, there may be thinning of the subcutaneous adipose tissue and a fibrous reaction (with a trend toward reduced signal intensity on T1w and T2w images).83 Plantar vein thrombosis has been identified as a less common cause of swelling and foot pain. Occasionally, a thickened vein with surrounding edema can be identified on MRI but without any flow effects.

8.9 Disorders of the Nerves and Compression Syndrome Fig. 8.83 Normal plantar aponeurosis. Schematic diagram. The plantar aponeurosis comprises two portions of different sizes, which can be clearly identified on coronal slices (right). Fasciitis well visualized on sagittal images (below). Longitudinal slices on sagittal image must be precisely angled because of the anatomic structure of the aponeurosis.

a

In many cases of nerve compression caused by space-occupying lesions, external pressure, or compression at physiologically narrow sites, diagnosis can be made on the basis of the typical range of clinical symptoms, electrophysiology tests, and diagnostic instillation of a local anesthetic. MRI is useful in unclear cases and in the presence of space-occupying lesions, since, based on direct or indirect signs, it can help diagnose nerve compression

b

Fig. 8.84 Painful plantar fasciitis. Marked thickening of the plantar fascia and increased signal intensity at the insertion (arrows) as well as reactive increased signal intensity of the surrounding soft tissues of the posterior fat pad and muscles. (a) Sagittal T1w image. (b) Sagittal PDw fatsat image.

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palm of the hand and Peyronie’s disease of the penis). In the majority of cases, a single large fibroma of around 2 to 3 cm is found. Only in around 10% of cases, multiple nodules are identified.1 MRI demonstrates nodular structures in the subcutaneous soft tissue of the medial sole of foot, which exhibits low signal intensity on both T1w and T2w sequences or manifest as a soft tissue tumor with intermediate signal intensity on T1w and with intense signal on fat-suppressed T2w and PDw images (▶ Fig. 8.86 and ▶ Fig. 8.87).92 Only very rarely do these benign growths turn out to be a fibrosarcoma. In addition to this nodular form of disease, extensive focal thickening of the plantar fascia may be identified without any central areas of hyperintensity (▶ Fig. 8.88).

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8.9 Disorders of the Nerves and Compression Syndrome

Fig. 8.85 Plantar fasciitis. Longstanding heel pain. MRI shows thickened plantar fascia, with edema-isointense signal intensity in the fascia (c, arrows) as well as in the surrounding soft tissues, especially in the medial segment close to the calcaneus. Partial discontinuity due to incipient tear. (a) Sagittal T1w sequence. (b) Sagittal STIR sequence. (c) Axial (plantar) STIR sequence.

a

b

Fig. 8.86 Plantar fibromatosis (Ledderhose’s disease). Nodular thickening along the course of the plantar fascia because of fibromatous growth. (a) Axial PDw fatsat sequence of foot. High signal intensity (arrow). (b) Sagittal T1w sequence. Intermediate signal intensity (arrow), partly interspersed with lines devoid of signal.

damage or completely visualize space-occupying lesions. MRI should be performed prior to surgical treatment.

8.9.1 Tarsal Tunnel Syndrome Posterior Tarsal Tunnel Syndrome The term tarsal tunnel syndrome refers to compression neuropathy of the tibial nerve and its branches in the region of the tarsal tunnel. The tarsal tunnel is formed by the medial calcaneal surface, sustentaculum tali, and the flexor retinaculum. Further distal, the abductor hallucis (see ▶ Fig. 8.6) forms a hiatus for entry of the lateral plantar nerve.37 Together with the nerve, the tibial artery and vein as well as the flexor hallucis longus tendon course through the tarsal tunnel. Branching of the tibial nerve is very variable, but in general, the neve divides into two main branches on entering the tarsal tunnel, comprising the stronger medial

plantar nerve and the more delicate lateral plantar nerve. The origin of the calcaneal branches is often located before the tunnel, but extreme variations are possible, with the origin even situated outside the retinaculum. Today, a diagnosis of tarsal tunnel syndrome is interpreted as a diagnosis of exclusion, that is, all other pathologic conditions in the heel region must be excluded. Diagnostic exploration must include neurology and radiology, with MRI playing a pivotal role. Clinical symptoms include nocturnal nonexertional pain radiating into the sole of foot. Likewise, very nonspecific heel pain may be imputable to tarsal tunnel syndrome. The term distal tarsal tunnel syndrome refers to nerve compression syndrome not involving the main trunk of the tibial nerve but confined to one of its main branches, that is, the medial (jogger’s foot) or lateral plantar nerves with correspondingly different symptoms. On MRI, it may be possible to detect acute or chronic signs of denervation of the medial (medial branch) or

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Fig. 8.87 Recurrence of plantar fibromatosis (Ledderhose’s disease). (a) Sagittal native T1w sequence. Dense soft tissue mass within hypointense plantar fascia (arrow). (b) Sagittal T1w sequence after CM administration. The structure exhibits strong enhancement. (c) STIR sequence. The fibroma exhibits high signal intensity. The defect in the region of the fat pad at the sole of foot is due to previous surgery.

central and/or lateral plantar muscles (lateral branch).25 Oblique axial and coronal sections are best for delineation of the anatomic structures of the tarsal tunnel.98 The causes of tarsal tunnel syndrome are as follows37: ● Tumorous or tumorlike space-occupying lesions. ● Ganglion cysts. ● Varicose veins. ● Arterial aneurysms. ● Tendinitis of the flexor hallucis longus tendon. ● Fibrous nerve cords. ● Bone spurs. ● Historic trauma. ● Tarsal coalitions. With the advent of higher-resolution MRI scans, it is now possible to directly visualize and evaluate the nerves and surrounding areas more precisely (MR neurography). MRI can also provide important information on persistent or recurrent symptoms (thickening, signal abnormality, dislocation, structural defects, and fibrosis) in the postoperative setting.17

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Compression of the First Branch of the Lateral Plantar Nerve (Baxter’s Nerve Entrapment) After the posterior tibial nerve has divided into the medial and lateral main branches, the lateral plantar nerve first gives off the muscular branch, which innervates the abductor digiti minimi and the quadratus plantae. This branch runs between the deep fascia of the abductor hallucis and the calcaneus, situated more distally on the quadratus plantae, laterally to the abductor digiti quinti (minimi). It can become entrapped between the fascia and bones and between the flexor digitorum brevis and quadratus plantae. The eponymous term Baxter’s nerve is used to denote the first side branch of the lateral plantar nerve, ever since in 1992, Baxter identified entrapment of this nerve as one of the many causes of heel pain (▶ Fig. 8.90). The clinical findings associated with treatment-refractory heel pain include possible hypoor paranesthesia of the plantar heel dermis or pressure pain at the superior margin of the abductor hallucis. Absence of abduction of the small toes is not a constant diagnostic criterion. Here,

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The Lower Leg, Ankle, and Foot

8.9 Disorders of the Nerves and Compression Syndrome Fig. 8.88 Plantar fibromatosis. Extensive form, with discrete, signal-void thickening of the anterior medial plantar fascia (arrows). (a) Axial PDw fatsat image of foot. (b) Sagittal T1w image. (c) Sagittal PDw fatsat image. b

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c

Fig. 8.89 Obesity of anterior foot fat pad. Over past months, pain while walking. Edema-isointense signal intensity of the anterior foot fat pad (arrows). (a) T1w image. (b) PDw fatsat image.

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a valuable differential diagnostic aid is a nerve block with a local anesthetic at its entry through the abductor hallucis. Sometimes, a typical finding identified on MRI is an acute (edema) or chronic denervation pattern (fatty atrophy) of the abductor digiti minimi.19,91

function between the first and second toes as well as with pain of the arch of the foot.22

Anterior Tarsal Tunnel Syndrome

The term Morton’s metatarsalgia is used to describe pain symptoms of the forefoot caused by compression of the intermetatarsal nerve, typically manifesting between the third and fourth metatarsals and less commonly also between the second and third

This term coined by Marinacci in 1968 is used to describe compression of the terminal branch of the deep peroneal nerve deep to the inferior extensor retinaculum, with impaired sensory

Morton’s Metatarsalgia (Morton’s Neuroma)

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8.9.2 Other Compression Syndromes of the Foot Sural nerve entrapment is seen either in settings of injury to the foot skeleton or following orthopedic procedures on the lateral hindfoot or at the base of the fifth metatarsal.

8.10 Osteoarthritis In general, MRI plays only a minor role in visualization of osteoarthritis. However, MRI is superior to radiographs for identification of early osteophytes (tiny spurs on the edge of the articular surfaces) and for evaluation of the extent of reactive soft tissue thickening and cartilage damage. For example, time and again, there are patients in whom a diagnosis of “osteoarthritis” is only confirmed on MRI, regardless of what consequences that might have. Osteoarthritis of the foot often affects the talocrural and subtalar joints as well as the peritalar joints. In men, in particular, osteoarthritis of the forefoot often affects the first metatarsophalangeal joint. Posttraumatic osteoarthritis can be found in all joints of the foot. Signs of overuse of the Lisfranc joint (see Chapter 8.6.2 ) may be suggestive of an overlooked injury or chronic overloading secondary to impaired foot statics (also referred to as midfoot arthritis). Loose joint bodies can be identified on MRI, especially on fat-suppressed sequences in the hyperintense joint fluid, as hypointense particles (in the three forms of synovial metaplasia, chondroma, and osteoma).

8.11 Arthritis Large joint effusions are often a characteristic, and the only, sign of arthritis. On MRI, a large fluid-isointense effusion is the only finding. If changes of acute onset are observed in the talocrural joint, borreliosis should always be excluded. Findings identified in rheumatoid arthritis (chronic polyarthritis) include, in addition to the characteristic manifestations, chronic synovial proliferation with pannus tissue (CM enhancement varies in accordance with fibrous tissue content and has lower signal intensity than the effusion) and pannus tissuemediated erosions as well as subcortical signal cysts. Besides, cartilage thinning and subcortical bone marrow edema can be identified. There is frequent involvement of the soft tissues and tendon sheaths. Occasionally, periarticular inflammatory pseudotumors may be observed (rheumatoid nodules). A typical finding for seronegative arthritis is slight pannus formation, involvement of a toe (dactylitis), enthesopathy (Achilles tendon insertion, plantar fascia), bone marrow edema, and/or bursitis.

8.12 Other Form of Synovitis If the foot is affected by diseases such as pigmented villonodular synovitis, chondromatosis, and amyloidosis, the respective characteristic findings will be demonstrated on MRI as for other body regions (see corresponding sections).

2 1 3 1 a

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Fig. 8.90 Baxter’s compression neuropathy. Schematic diagram illustrating the position of the inferior calcaneal nerve (first branch of the lateral tibialis posterior). (a) Plantar view. Baxter’s nerve immediately anterior to the calcaneus. 1, medial plantar nerve; 2, lateral plantar nerve; 3, Baxter’s nerve. (b) Internal view. Branching of the posterior tibial nerve in the tarsal tunnel or somewhat distal to it. (c) Coronal visualization with potential compression points between the muscle (1) and at inferior calcaneal edge (2).

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8.13 Diabetic Foot Syndrome 8.13.1 Diabetic Neuro-Osteoarthropathy Diabetic foot syndrome is one of the complications of diabetes mellitus, now a disease of civilization, which in Germany is associated with an inexorable rise in treatment costs and amputation rates of the lower leg.

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metatarsals. The cause of this metatarsal compression syndrome is not exactly known, but it is thought to be linked to changes in nerve calibers, inflammatory thickening of the deep transverse metatarsal ligament, or relevant differences in length between the medial and lateral arches of the foot. Middle foot fractures can also result in irritation of the intermetatarsal nerves, with formation of a 3- to 9-mm pseudotumor consistent with poststenotic swelling of the perineural tissue. Real neuromas are seen only if the nerve had already been surgically removed and the resection site at the level of the metatarsal head is still within the weight-bearing region. The former belief that a reliable diagnosis could always be made with MRI proved to be unfounded. Changes are best identified in the axial and sagittal planes. The prone position is the most suitable for patient examination, since the mobile nodules then move in a more plantar direction and can be more easily delineated from the metatarsal heads. The lesions are hypointense in relation to the surrounding fatty tissue and are isointense to muscle, in particular, on T1w images (▶ Fig. 8.91).85,96 Often, administration of contrast agent (with fat suppression) is of little benefit, since pseudotumor perfusion varies and is often minimal. Differential diagnosis must also take account of intermetatarsal bursitis and plantar calluses as well as synovitis of the metatarsophalangeal joints. Up to 35% of patients undergoing surgery for Morton’s metatarsalgia experience recurrent symptoms. Therefore, many foot surgeons have decided not to resect a pseudotumor, opting instead for dissection of the deep intermetatarsal ligament, as in the case of other nerve compression syndromes. On MRI examination, such patients are often found to have fluid accumulation at the operation site, pointing to pseudobursitis or a stump neuroma. Postoperative scars should not be mistaken for a recurrent neuroma.97

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8.13 Diabetic Foot Syndrome

Fig. 8.91 Morton’s neuralgia. (a) Native axial T1w sequence. (b) Axial T1w sequence after CM administration. Moderately enhancing spaceoccupying lesion between the third and fourth metatarsal, consistent with perineural fibrosis of the interdigital nerve (arrows). (c) T2w fatsuppressed sequence, different patient. Hyperintense structure inferior to interdigital space Dlll/DIV and soft tissue proliferation, which continues in the posterior direction between the metatarsals (arrow).

The diagnosis “diabetic foot syndrome” is being overly used and unfortunately often applied to all disorders of a diabetic patient’s foot. However, sensory neuropathy must be diagnosed before referring to the disorder as diabetic foot syndrome. This can easily be done by a registered podologist, diabetologist, or general practitioner. Based on the most recent findings, glucose-breakdown products appear to be responsible for the irreversible damage to the sensory peripheral nerves. The resultant absence of control of intrinsic factors that stabilize the foot leads to collapse of the foot skeleton. In addition, release of a bone hormone appears to induce leaching of bones (RANKL System [Receptor Activator of NF–KB Ligand System]), together with osteoclast activation, in turn causing increasing deformation and destruction (diabetic neuro-osteoarthropathy) of the weight-bearing, pain-free foot in the absence of timely diagnosis and immediate offloading of the foot. This disease can present in flares, affecting different regions of the foot. Conduct of surgery on an undiagnosed sensory neuropathic foot can trigger osteoarthropathy. There is no microangiopathy of the foot, as previously thought: the feet are excessively warm and red in the acute stage but free of pain; this can facilitate diagnosis of diabetic foot syndrome. The term Charcot foot is currently used to characterize destruction of the anatomic shape of the foot, bearing in mind that diabetes mellitus is not the sole condition implicated in onset of neuro-osteoarthropathy. Based on the guidelines of the German Diabetes Society, staging of diabetic foot syndrome is based on the Wagner and Armstrong classification scheme. The Armstrong classification system describes the diseased foot in terms of infection and (reduced) arterial blood flow, imputed to concomitant peripheral arterial occlusive disease:

● ● ● ●

A: Well perfused, no infection. B: Well perfused, infection. C: Poorly perfused, no infection. D: Poorly perfused, infection.

The Wagner classification system describes the lesions (ulcers) and their depth: ● 0: Foot distortion and hyperkeratosis. ● 1: Ulcers on only the skin. ● 2: Ulcer extending to tendons and joints. ● 3: Ulcer extending to bones. ● 4: Discrete gangrene. ● 5: Gangrene affecting the entire foot. Predilection sites for ulcers are the weight-bearing regions on the sole of foot, which, because of impaired foot statics, are subjected to painless overloading. Characteristic painless ulcers are seen at the tips of the toes, in association with toe deformities (apex lesions). Apart from the lesions on the sole of foot, there is also a high risk of ulcers at sites subjected to increased pressure from the inside (skeletal destruction) and outside (footwear). These ulcers can manifest on the inner and outer margins of the foreand hindfoot, depending on the location of osteoarthropathy. These classifications, which are essentially aimed at internal medicine practitioners and podologists, should be further characterized in terms of their orientation and the location of (impending) destruction. Diabetic neuro-osteoarthropathy can be classified in terms of the region of the foot affected. The Sanders and Frykberg classification is commonly applied: ● Sanders 1: Forefoot.

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● ● ●

Sanders 2: Midfoot. Sanders 3: Chopart joint. Sanders 4: Ankle joints and talocrural joint. Sanders 5: Calcaneus.

Details of other systems used to classify the location of diabetic neuro-osteoarthropathy of the foot have been published by Brodsky and Schon. Various schemes are used to classify the courses and stages, of which the most common is the Levin classification system: ● Stage I: Acute stage (redness, swelling, and overheating). ● Stage II: Joint changes and fractures. ● Stage III: Foot deformity. ● Stage IV: (Plantar) lesions (ulcers). The aforementioned classification systems highlight the paramount importance of MRI for diagnosis of diabetic neuroosteoarthropathy. This is the primary imaging modality that is able to provide conclusive insights into the myriad unresolved clinical issues. These include the course of disease, with identification of all the processes affecting tissues of the diseased foot. It must be emphasized that MRI is the only imaging modality able to detect the radiographically occult stage I, the earliest stage involving bone and soft tissue edema. The ability to detect diabetic neuro-osteoarthropathy at this stage and immediately instigate offloading of the foot is seen as an important milestone toward reducing amputation rates and treatment costs. MRI of the entire foot, including the talocrural joint, is needed to address the following (▶ Fig. 8.92): ● Location affected. ● Adjunct to follow-up (“hot” or “cold”). ● Assessment of the skeletal elements. ● Assessment of the soft tissues in the presence of lesions. ● Differentiation between inflammatory and noninflammatory bone changes. ● Evaluation of the larger arteries with magnetic resonance angiography.

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Differentiation of (post)traumatic and osteoarthropathic changes.

The Levin staging scheme can also be applied for classification of the severity and course on standard radiographs and MRI: ● Stage 0: Normal imaging results. ● Stage I: Acute synovitis and cellulitis (clinical redness, swelling, and overheating; normal radiographs; on MRI, synovitis and/or multifocal patchy bone marrow edema). ● Stage II: Increasing microfractures (stress reactions and increasing confluent edema pattern, with isolated areas of reduced signal intensity). ● Stage III: Fractures, erosions, and localized bone necrosis. ● Stage IV: Fractures and dislocation; later, also, exostoses, periosteal proliferation, and remodeling (▶ Fig. 8.93 and ▶ Fig. 8.94). Following protracted, chronic courses, bone sclerosis, dislocation, and resolution of hyperemia are observed. High-grade skeletal deformities are the predisposing factors for ulceration. Tendinitis and peritendinitis as well as enthesopathy attesting to incorrect loading against a background of progressive disruption of the foot statics are frequent concomitant manifestations. MRI is indispensable for patient management, especially for the conservative treatment of patients with (diabetic) neuroosteoarthropathy. The indications for MRI (including contrastenhanced sequences) are as follows: ● Grading of severity. ● Follow-up (MRI is able to detect incipient resolution of edema and hyperemia; bone contours are once again better delineated, bone marrow edema starts to recede, and the contrast–time curves are flatter on dynamic MRI; ▶ Fig. 8.95).95 ● Evaluation of infection. Bacterial infection originating from ulcers or excessive surgical incisions can spread to the skin, subcutis, muscles (cellulitis, abscess, and fistula), periosteum (periosteitis), bone surfaces (osteitis), bone marrow space (osteomyelitis), and joints (arthritis). Diagnosis of osteomyelitis has major clinical implications.

b

Fig. 8.92 Diabetic foot with intertarsal changes. Incipient deformation of the navicular and medial cuneiform, subchondral cysts, bone marrow edema, and slight soft tissue edema. Incipient deformation of the longitudinal arch of the foot. (a) Sagittal STIR image. (b) Sagittal T1w image.

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●

8.15 Bursitis and Haglund’s Heel

Periosteal reactions are less intense than those otherwise seen in association with osteomyelitis. MRI is endowed with similar sensitivity (95%) and specificity (80–85%) to that of inflammation scintigraphy for detection of osteomyelitis. Based on these insights, the following diagnostic algorithm can be applied for suspected osteomyelitis: ● Screening is based on radiography. ● Reduced density in the absence of an ulcer makes the possibility of osteomyelitis unlikely. ● If radiographs are normal but there is clinical suspicion of osteomyelitis, carry out MRI. ● If there is a reliable MRI sign of osteomyelitis, instigate treatment; if there is no reliable MRI sign but there are radiographic changes, take a biopsy. If MRI does not identify any bone changes, there is no osteomyelitis.

8.13.2 Nondiabetic Neuropathy Apart from diabetes mellitus, several other diseases cause sensory neuropathy with considerable skeletal changes, for example: ● Syringomyelia. ● Polyneuropathy of diverse etiology, for example, nutritive-toxic or drug-induced causes. ● Meningomyeloceles. ● Genetically mediated neuropathy (hereditary sensorimotor neuropathy [types I–VII; type I is also called Charcot–Marie– Tooth disease]; ▶ Fig. 8.96). ● Syphilis and leprosy (despite the fact that these diseases have now been largely eradicated in Central Europe, they are

mentioned here primarily for historic reasons, since the very first reference made by Charcot to the skeletal destruction of the foot was to syphilitic bone changes). Sensory neuropathy of unknown origin (idiopathic sensory neuropathy) exhibits clinical symptoms similar to those of diabetic neuro-osteoarthropathy. Other genetically mediated forms of sensory neuropathy are subsumed under the collective term hereditary sensorimotor neuropathy or Charcot–Marie–Tooth syndrome. This type of neuropathy is being found increasingly in association with hollow foot and club foot malformation involving muscular atrophy.

8.14 Hemophilic Osteoarthropathy Widespread joint changes are observed, especially in settings of hemophilia A, secondary to recurrent joint hemorrhage with synovitis and bleeding into the subchondral bones. The most commonly implicated joints are the talocrural joint as well as the elbow and knee joints. Clinical symptoms include recurrent painful swelling that progresses to arthropathy, with restricted motion and secondary osteoarthritis. Imaging techniques are able to detect numerous changes of varying severity, depending on the duration and intensity of the disease: ● MRI demonstrates, at an early stage, even small bloody and/or nonbloody effusions as well as synovitis, with or without hemosiderin deposition (best identified on gradient-echo [GRE] sequences as diffuse patches devoid of signal). ● Severe joint hemorrhage already during childhood will result in growth deformities and growth reduction of various bones. At a later age, there is often deformation of the talus and tibia against a background of increasing secondary osteoarthritis. ● Cysts of varying sizes are often found in the subchondral region, consistent with (fluid-isointense) subchondral cysts, more recent hemorrhage (methemoglobin intense), or older hemorrhage with fibrosis components (dark on all sequences) (▶ Fig. 8.97 and ▶ Fig. 8.98). ● Chronic recurrent synovitis secondary to recurrent joint hemorrhage not only results in hemosiderin deposition but also in increasingly thicker pannus tissue with hypertrophic villi. Direct cartilage damage and bone deformities lead to increasing secondary osteoarthritis, with cartilage thinning and osteophytes. ● Hemophilic pseudotumors in bones and soft tissues can grow to a very large size and occasionally exhibit strong signal inhomogeneity because of blood constituents of different ages and/or calcification.

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Although osteomyelitis cannot be reliably delineated based on the edema pattern, there are MRI signs that underpin the possibility of infection24: ● Infected ulcer. ● Bone–soft tissue fistula in direct proximity to bone edema. ● Adjacent abscess (capsule revealing CM uptake). ● Very high signal intensity of the affected bone segment on T2w contrast images. ● Cortical erosion. ● Gas pocket. ● Sequester (signal-void inclusions in bone).

8.15 Bursitis and Haglund’s Heel

Fig. 8.93 Diabetic foot with pronounced tarsal destruction. Sagittal T1w image. Soft tissue and bone marrow edema, flattening of the longitudinal arch of the foot.

Acute or chronic bursitis of the foot can occur in isolation or together with inflammation of the joints or soft tissues (gout) as well as in association with insertional tendinopathy of the Achilles tendon (▶ Fig. 8.99). The diagnosis can already be made on the basis of clinical symptoms such as pressure point pain and/or pain at rest at characteristic sites.

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Fig. 8.94 Chronic osteomyelitis in association with diabetic foot. The images show diffuse soft tissue infection and extensive osteomyelitis of the mid- and forefoot. (a) Sagittal T1w sequence before CM administration. Incipient infiltration of the calcaneus (arrow). (b) Sagittal T1w sequence after CM administration. After CM administration, a fistula duct with marginal CM uptake can be identified close to the plantar aspect (arrow).

Fig. 8.95 Diabetic foot during treatment course. Axial PDw fatsat images. Marked bone marrow edema and reduced contour, as findings improve during course (see, in particular, resolution of edema in cuboid; arrows). (a) Baseline MR image. (b) MR image after 3 months of treatment.

a

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MRI demonstrates a fluid-filled bursa, with low-signal intensity on T1w and high signal intensity on T2w images. Hemorrhagic or chronic effusions with high protein content can exhibit high signal intensity on T1w images, too. In addition, chronic bursitis is also associated with visible hyperintense wall thickening (specific to the effusion fluid), in particular on T1w images. Bursitis in settings of arthritic diseases can give rise to small round areas of reduced signal intensity within the fluid-filled bursa due to synovial hypertrophy with villous fronds.

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There are two bursae in the heel region that protect the Achilles tendon at its insertion and can trigger pain if inflamed. The bursa of the calcaneal tendon is situated at a deep level between the calcaneal tuberosity and the tendon insertion. Inflammation of this bursa is often observed in association with exostosis formation on the calcaneus (posterior heel spur) or with a prominent superior calcaneal tuberosity (Haglund’s exostosis). The hindfoot/hollow foot with a large calcaneal

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The Lower Leg, Ankle, and Foot

8.17 Typical Foot Tumors inclination angle can also cause inflammation of this bursa. The resultant mechanical irritation can, in turn, result in insertional tendinitis of the Achilles tendon and bursitis of the superficial, subcutaneous calcaneal bursa. Chronic pressure exerted by footwear or an impaired gait may also be implicated.

8.16 Pseudobursae

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a

Chronic and/or repetitive pressure secondary to chronic inflammation can cause sterile abscesses at certain predilection sites. These fluid-filled nodules, also known as “pseudobursae,” have walls that strongly take up CM and are found mainly at sites subject to footwear pressure at the toes or weight-bearing zones. Often, they are seen in association with foot deformities, combined with hallux valgus and digitus quintus valgus, or also chronic pressure in occupational settings (footwear, cross-legged position, tailor’s bunion or bunionette), frequently lateral to the head of the fifth metatarsal.

8.17 Typical Foot Tumors 8.17.1 Xanthomas b

Deposition and accumulation of lipid-containing histiocytes in settings of hyperlipidemia can give rise to nodular thickening (xanthomas) in tendons (typically the Achilles tendon) and fasciae (often plantar fascia). These xanthomas are found most commonly in the cutis and subcutis. MRI demonstrates inhomogeneous thickening, with patches of increased signal intensity (fat) in the striated loosening tendon or fascia.

8.17.2 Ganglion Cysts Fluid-isointense ganglion cysts are commonly found in the foot. As in other body regions, these may manifest as simple unicameral, lobulated, polylobulated, or septated cysts of varying sizes and are found at different locations in the foot. The origin of the cyst should be pinpointed as closely as possible on MRI to enable surgeons to remove the entire cyst and thus reduce the recurrence rate of over 20%. A distinction should always be made between tendons, tendon sheaths, and joints as the potential sources of a ganglion cyst; common sites are the sinus tarsi and tarsal tunnel. There are also reports of ganglion cysts within tendons. Periarticular ganglion cysts frequently cause impingement syndrome. MRI plays a key role in differential diagnosis in the presence of tarsal tunnel syndrome (see Chapter 8.9.1) (▶ Fig. 8.100).

8.17.3 Bone Tumors c

Fig. 8.96 Hereditary sensorimotor neuropathy. A 25-year-old female patient with diagnosis of type I genetic hereditary sensorimotor neuropathy. Patient was admitted with painful swelling of the foot of unknown origin; normal sports activities. Bone marrow edema of the tarsals, in particular of navicular; soft tissue edema; horizontal stress fracture in navicular (a, b, arrows); perpendicular navicular fracture with severe fragment dislocation (c, arrow). (a) Sagittal T1w MR image. (b) Sagittal STIR image. (c) Axial PDw fatsat MR image of foot.

The following entities can be observed in descending order: ● Giant cell tumors. ● Chondromyxoid fibroma. ● Lipoma. ● Osteochondroma. ● Osteoid osteoma (▶ Fig. 8.101).76 ● Chondroblastoma. ● Aneurysmal bone cyst. Common malignant bone tumors include the chondrosarcoma, osteosarcoma, and Ewing’s sarcoma.

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Fig. 8.97 Hemophilia A and recurrent swelling, including that of the ankle joints. A 30-year-old male patient. Cartilage destruction, large subcortical cysts and hemorrhagic pseudocysts, subluxation, bone marrow and soft tissue edema, and chronic synovitis. (a) Sagittal T1w image. (b) Sagittal contrast-enhanced fatsat T1w image.

Fig. 8.98 Osteoarthropathy in association with hemophilia. Inhomogeneous, medial narrowing of the joint space in early-onset osteoarthritis. Subchondral cystoid (seemingly necrotic) foci in talus and tibia. (a) Coronal T1w sequence. (b) Coronal STIR sequence.

8.17.4 Calcaneal Tumors Very large cysts are also frequently encountered in the calcaneus (simple bone cysts) and manifest as fluid-isointense on MRI. Typical calcaneal lipomas are fat-isointense and may have dystrophic, calcified, and/or liquefied components at their center (▶ Fig. 8.102).

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8.17.5 Giant Cell Tumors of the Tendon Sheath These benign growths are not uncommon in the region of the joints and tendons of the hand as well as at other body sites and are caused by proliferation of synovial structures and appear reddish brown because of iron pigment deposition. On MRI, they often have low signal intensity on T1w and T2w contrast images.

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Fig. 8.99 Achilles bursitis. Pain at insertion of the Achilles tendon. Deep (arrows) and superficial Achilles bursitis with mild insertional tendinopathy of the Achilles tendon. (a) Sagittal PDw fatsat image. (b) Axial PDw fatsat image.

b

Neurogenic growths are not uncommon in association with tunnel syndrome (see Chapter 8.9.1).

8.17.6 Malignant Soft Tissue Tumors Malignant tumors of the foot are rare and consist mainly of synovial tumors and other sarcomas (malignant fibrous histiocytoma, Kaposi’s sarcoma, and leiomyosarcoma).

8.17.7 Subungual Tumors Tumors can grow beneath the finger and toe nails, often causing nail discoloration and severe pain. The main tumors found at the toes are as follows: ● Glomus tumors are highly vascularized neoplasms of the neuromyoarterial glomus bodies, most frequently found under the finger nails. MRI demonstrates hypointensity on T1w and very high signal on T2w contrast images as well as strong CM uptake. ● Subungual exostoses have mature bone marrow and are diagnosed on the basis of radiographs. ● Soft tissue chondromas exhibit inhomogeneous signal intensity and inhomogeneous CM enhancement. ● Keratoacanthomas manifest as signal inhomogeneity, with no or only marginal CM enhancement. ● Hemangiomas are hypointense on T1w images and hyperintense on T2w images; they actively take up CM. ● Phleboliths are common. ● Epidermal cysts exhibit inhomogeneous signal intensity with bright foci on T1w images and variable hypointense components on T2w images. There is no or only marginal CM enhancement. ● Mucoid cysts are fluid-isointense, with only marginal CM enhancement. ● The malignant tumors found at this site can include squamous epithelial carcinomas and malignant melanomas (T1w signal intensity varies greatly in accordance with melanin content and/or hemorrhage).3

Fig. 8.100 Ganglion cyst on the forefoot. Axial (plantar) PDw fatsat image of foot. Slighty painful nodules on midfoot. Fluid-isointense space-occupying lesion characteristic of ganglion cyst at the base of the first metatarsal (arrow).

8.17.8 Epidermal Inclusion Cysts Dermal cysts can grow to a relatively large size, giving rise to cushionlike tumors. MRI demonstrates iso- to hyperintensity on

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Fig. 8.101 Osteoid osteoma of the foot. A highly calcified marginal (cortical) nidus surrounded by moderate sclerosis of the talus can be seen on radiographs. On MRI, the predominant findings are areas devoid of signal, but there is also a CM-enhancing nidus and edema-isointense signals in bone marrow and soft tissues. (a) Radiographs. (b) Sagittal T1w image. (c) Sagittal STIR image. (d) Sagittal contrast-enhanced MR image.

T1w contrast and hyperintensity on T2w contrast images, possibly with zones of reduced intensity (fatty debris and keratin).63

8.18 Disorders of the Toes 8.18.1 Trauma

Fig. 8.102 Calcaneal lipoma. Sagittal T1w image. Incidental finding on exploring other question. Typical calcaneal lipoma with central dystrophic, necrotic changes (arrow).

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Toe-specific injuries, such as damage to collateral ligaments, tendons, and fasciae, and also capsular injuries, can be better visualized on MRI, thanks to higher resolution. Capsular injuries, especially of the first metatarsophalangeal joint in hyperextension, can cause avulsion of the capsule and plantar plate from the plantar base of the proximal phalanx, also referred to as turf toe injury (▶ Fig. 8.103). This can also result in dislocation or fracture of a sesamoid. This injury can be visualized on MRI, sagittal sections. Fibrous scar thickening of the second metatarsophalangeal joint, for example, in chronic overloading, can be mistaken for Morton’s neuroma, as it results in tissue thickening, with inhomogeneous signal between the second and third metatarsal heads but with no shift in position.42

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8.19 Pitfalls in Interpreting Images

Fig. 8.104 Posttraumatic peritendinitis. Axial PDw fatsat image of the foot. Pain in second toe 5 days after sports accident. Hyperintense thickening of the flexor tendon sheath DII due to posttraumatic peritendinitis.

b

Fig. 8.103 Turf toe. Status post ball sports injury, with pain at the base of the big toe. Avulsion of capsular structures (plantar plate) from the base of the plantar proximal phalanx (a, arrow), with intact flexor tendon. (a) Sagittal PDw fatsat image. (b) Sagittal T1w image.

Posttraumatic tenosynovitis may present sometime after the traumatic event (▶ Fig. 8.104).

8.18.2 Sesamoids Defects in the normally paired sesamoids of the first metatarsophalangeal joint may be the cause of metatarsalgia of the first metatarsal ray. Partial or complete avascular necrosis as well as fractures, presenting as a sequela of injury or chronic overloading (stress fractures), are observed. Congenital avascular necrosis (Renander’s disease) is rare. Partite sesamoids with multiple bone elements can compound differentiation between various pathologies. Imaging of sesamoids (see Chapter 8.4.3 ) should also include high-resolution axial T1w sequences for evaluation of the normally encountered fatty marrow signal. In avascular necrosis, the entire sesamoid exhibits hypointensity. Fracture lines have an irregular margin. Stress fractures give rise to a bandlike change in signal intensity. CM injection is usually indispensable for differentiation.

8.18.3 Gout Hyperuricemia typically results in arthritis of the first metatarsophalangeal joint as well in urate crystal deposition in the surrounding soft tissues, in some cases, giving rise to a space-occupying mass (gouty tophus). These changes may also be found, albeit rarely, at the Achilles tendon insertion. MRI is not essential for management of the first metatarsophalangeal joint but can be valuable for differential diagnosis of heel manifestations (▶ Fig. 8.105). Tophi exhibit relatively low signal intensity on T1w images and, in most cases, relatively heterogeneous hypointensity on T2w images.

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8.18.4 Hallux Valgus and Metatarsalgia MRI examination is needed for hallux valgus deformity only for differential diagnosis versus suspected avascular necrosis of the sesamoids. MRI is often indicated before revisional surgical procedures to exclude metatarsal head necrosis. The following may be of relevance in diagnosing metatarsalgia and are sometimes the reason why clinicians deem MRI necessary: ● Exclusion of stress trauma or microfractures (▶ Fig. 8.106). ● Stress edema. ● Avascular necrosis of the second and third metatarsal heads (Köhler II disease; ▶ Fig. 8.107). ● Exclusion of synovitis at the metatarsophalangeal joints of the toes. ● Intermetatarsal space-occupying lesions of any type. ● Lesions of the plantar plate.

8.19 Pitfalls in Interpreting Images 8.19.1 Signal Patterns of Anatomic Structures To avoid making mistakes when interpreting MRI examination results, a few peculiarities in the signal patterns of various anatomic structures are mentioned here. Like the anterior cruciate ligament, the posterior tibiofibular and fibulotalar ligaments as well as the deep portions of the deltoid ligament may exhibit hyperintensity on T1w and T2w sequences because of fat deposition and should not be mistaken for distortions/sprains or partial tears. Similar hyperintensity may also be identified as a normal variant at the insertion of tibialis posterior tendon on the navicular.56 Intra-articular and peritendinous fluids should not invariably be equated with pathologic changes. In particular, in the region of the posterior tendons, especially of the flexor hallucis longus, large fluid accumulations are also identified even in asymptomatic patients. Besides, the various compartments communicate with each other, something that compounds precise anatomic assignment of the changes.75

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Fig. 8.105 Pellagra. Coronal PDw fatsat image of foot. Acute painful, reddened toe, and hyperuricemia. Sign of arthritis, with narrowing of the joint space, bone marrow edema, and soft tissue edema of the first metatarsophalangeal joint.

On sagittal sections, the posterior tibiofibular and fibulotalar ligaments should not be misinterpreted as loose joint bodies. Likewise, sagittal sections can be used for visualization of talar pseudodefects, which should not be mistaken for osteochondral lesions. Additional coronal sections and the absence of signal changes on T2w sequences provide for reliable differentiation.52,66 Intact tendons are normally hypointense on all sequences. However, depending on the orientation versus the stationary magnetic field, changes in signal intensity can be observed, which could mimic tears or inflammation. This magic angle phenomenon is seen on SE and GRE sequences with short TE, if the tendon forms an angle of around 55 degrees versus the stationary magnetic field. Since these signal changes disappear with longer TE (over 60 ms), they can usually be differentiated from pathologic changes by taking account of the T2w findings. Differentiation can also be facilitated by imaging the patient in different body positions.

8.19.2 Accessory Bones and Sesamoids Accessory bones and sesamoids found at various sites of the foot should not be misinterpreted as loose joint bodies or bone fragments. Congenital, generally asymptomatic bipartite talus can present a diagnostic challenge, in particular if there are no radiographs (▶ Fig. 8.108). Conventional radiographs should, therefore, be carefully reviewed before interpreting the MRI findings.41

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Fig. 8.106 Metatarsalgia with fracture. Sagittal T1w sequence. Pain in the forefoot. Osteochondral lesion with stress fracture (arrow).

8.19.3 Accessory Muscles Congenital normal variants of muscles have been identified in most body regions: ● Variations in the course of muscle bellies and tendons. ● Cleft formation. ● Origin and insertion variants. ● Absence (negative variance) or supernumerary duplicated muscle bellies (positive variance). Familiarity with common variations is important not just for surgeons. The diagnostic radiologist must be able to recognize positive variance of muscles, since supernumerary muscle bellies are often mistaken for tumorous masses. On MRI, supernumerary muscles can be identified from their muscle-isointense signal pattern, pennate structure, and interposition of fatty tissue within the intramuscular connective tissue septa, as well as from the transition to a hypointense tendon. Besides, the more common variants can be identified from their characteristic location. Accessory muscles tend to occur unilaterally. Although the incidence of accessory muscles is unknown, it is generally thought to be low. The following examples of positive variance are important in the lower leg and ankle (▶ Fig. 8.109): ● Accessory soleus. ● Accessory flexor digitorum longus.

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Fig. 8.107 Valgus osteoarthritis. Hallux valgus before elective operation. Severe pressure point pain over medial sesamoid. Exclusion of sesamoid necrosis; the sesamoids are normal. Local osteochondral focus (arrows) on head of the first metatarsal, directly below the medial sesamoid. Active osteoarthritis with effusion. (a) Sagittal PDw fatsat image. (b) Axial PDw fatsat image.

b

Peroneus tertius. Peroneus quartus.

Accessory Soleus An “accessory soleus” refers to the third head of the normally bicapitate soleus. It is situated anteromedially or anterotibially to the myotendinous junction of the soleus, arises from the transversalis fascia or the posterior edge of the tibia, and inserts anteromedially to the Achilles tendon on the superior edge of the calcaneus.26,44 On MRI, the muscle is demonstrated in the otherwise fat-containing space anteromedially to the Achilles tendon (▶ Fig. 8.110). Clinical manifestations include swelling above the heel, which can occasionally cause pain on exertion.88 Besides, another variant of the third soleal head inserts into the Achilles tendon or merges with the Achilles tendon.

Peroneus Quartus This is an accessory muscle in the region of the distal peroneal compartment.14 This variant of the peroneus muscle is thought to occur in 6% of the population (▶ Fig. 8.111).

Accessory Flexor Digitorum Longus The accessory flexor digitorum longus arises with its long head at the transversalis fascia and with short head at the medial and plantar surface of the calcaneus. It inserts into the plantar aspect of the flexor digitorum longus tendon after passing through the medial flexor compartment. The muscle bellies are small. On MRI, a tendon not normally present can be identified in the

medial flexor compartment, medial to the flexor hallucis longus tendon.

8.20 Clinical Relevance of Magnetic Resonance Imaging Clinical Interview

●i

Clinical interview with Dr Alexander Sikorski, Medical Director, Malteser Fußzentrum, Rheinbach: Preliminary Remark by Dr. Sikorski: “At the outset, it must be pointed out: the team composed of the radiologist and foot therapist is in a good position if the clinician has formulated precise questions to be answered by imaging. Referral forms mentioning, for example, “foot,” draw a blank, and the radiologist will be happy to describe a heel spur or plantar fasciitis. The images should ideally be interpreted in a dialog between “clinician” and “radiologist.” Question: “For which disorders do you encounter false-positive MRI results most often?” Answer: “And this takes us straight to plantar fasciitis: plantar heel spurs and insertional tendinopathy and/or plantar fasciitis can be easily identified based on the clinical picture, without resorting to radiologic imaging. Therefore, pointing out such findings is not very beneficial. On the contrary: all it does is burden the patient with an additional diagnosis: “Now I have heel spurs on top of everything else.” Radiologic evaluation of the plantar fascia, when requested by the clinician, can be helpful, for example, to exclude

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Fig. 8.108 Bipartite talus. In the sagittal imaging plane (a) visualization of the two separate bone elements, both of which, unlike the os trigonum and posterior talar process, contribute to the talus-sided articular surface of the talocrural joint. The morphologic structure of the connection between the bone elements is similar to that of pseudarthrosis. Pronounced edema zones in both osseous segments of the talus and the periarticular portions of the calcaneus (b) as well as CM uptake (c) in the region of the “pseudarthrosis,” thought to be suggestive of chronic, mechanical irritation. Some concomitant joint effusion. (a) Sagittal MR image. (b) Coronal STIR image. (c) Axial T1w fatsat image.

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a tear in association with a suspect palpation result, or in Ledderhose’s disease to exclude a malignant growth. Much emphasis is placed on evaluation of the cartilage of the talus to explore longstanding persistent complaints following high upper-ankle sprain. Clinical experience has revealed that this often involves the peroneal tendons and tarsal coalitions that have loosened following injury. Hence, it would be advisable to focus on these structures, too, during radiologic diagnostic imaging, when trying to explain longstanding clinical symptoms following high ankle sprain or fracture.”

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Fig. 8.109 Position of accessory muscles and their tendons in the region of the talocrural joint. Axial schematic visualization illustrating the position of accessory muscles and their tendons in the region of the talocrural joint (peroneus quartus, accessory soleus, and accessory flexor digitorum longus). 1, tibia; 2, tibialis posterior tendon; 3, flexor digitorum longus; 4, tendon of the accessory flexor digitorum longus; 5, flexor hallucis longus; 6, accessory soleus; 7, Achilles tendon; 8, peroneus quartus; 9, peroneus longus and brevis; 10, fibula.

Question: “For which disorders do you encounter false-negative MRI results most often, and why were diagnostic measures continued in such cases?” Answer: “Tarsal coalitions turn out time and again to be the overlooked triggers of foot pain with weightbearing that has persisted over many years. Both clinical examination and the radiology images point exactly to that diagnosis, which even today is relatively unknown to many foot therapists. Here, too, the clinician must formulate the question accordingly if there is any reason to suspect a fixed defective position on examining the patient in a standing position and with the foot hanging. Only then does the radiologist have a real chance of visualizing blockage of the hindfoot joints. MRI is superior to CT examination in that it is also able to visualize fibrous synostoses. Radiologic assessment of metatarsalgia also demonstrates findings that do not always correlate with the clinical reality. For example, a distinction should be made between propulsion metatarsalgia of the second metatarsal and Köhler II disease. Overloading of the first midfoot ray often causes vascular necrosis of the sesamoids. Here, too, we are reliant on fine-tuned MRI diagnostic exploration. Another issue on which there is not always a consensus relates to neuro-osteoarthropathy. It is not uncommon for a Sanders-2 finding to be misinterpreted as a Lisfranc fracture, either because all therapists have failed to detect the sensory neuropathy or because the clinician did not pass on this important information to the radiologist. In such settings, it is also difficult to distinguish between osteitis and osteopathy.” Question: “For which disorders can MRI be omitted and for which is it being overly used?” Answer: “MRI is not needed for diagnosis of Morton’s metatarsalgia, since the clinical parameters are easy enough to work out for reliable diagnosis. The same is true for plantar fasciitis and associated heel pain (see above).”

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Fig. 8.110 Accessory soleus. Examination of a 35-year-old male patient with increasingly painful swelling of right lower leg to exclude tumor. Muscle-isointense structure anterior and medial to the Achilles tendon, characteristic of accessory muscle tissue (accessory soleus). The increasing swelling was found to be attributable to increased athletic activities. (a) Sagittal T1w image. (b) Coronal T2w image. (c) Axial PDw fatsat image.

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Fig. 8.111 Supination trauma. Clear areas of contusion on the (postero)medial and (antero)lateral aspects of the talar trochlea on moderate T2w fatsat sequences (a, b). The sagittal views (e, f) demonstrate a peroneus quartus, whose deep muscle belly is manifested posteromedially to the tendons of the peroneus longus and brevis. (a) Coronal T2w fatsat image. (b) Sagittal T2w fatsat image. (c) Paraxial T2w image. Grade I lesion of the anterior fibulotalar ligament. (d) Paraxial T2w image. Visualization of the three tendon segments on the outer ankle. (e) Sagittal T1w image. (f) Sagittal T1w image, other section.

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diagnosis. Eur Radiol. 2003; 13 Suppl 4:L164:L1–77 [51] Mengiardi B, Zanetti M, Schöttle PB, et al. Spring ligament complex: MR imaging-anatomic correlation and findings in asymptomatic subjects. Radiology. 2005; 237(1):242–249 [52] Miller TT, Bucchieri JS, Joshi A, Staron RB, Feldman F. Pseudodefect of the talar dome: an anatomic pitfall of ankle MR imaging. Radiology. 1997; 203(3):857– 858 [53] Mink JH, Deutsch AL. Occult cartilage and bone injuries of the knee: detection, classification, and assessment with MR imaging. Radiology. 1989; 170(3, Pt 1):823–829 [54] Nelson DW, DiPaola J, Colville M, Schmidgall J. Osteochondritis dissecans of the talus and knee: prospective comparison of MR and arthroscopic classifications. J Comput Assist Tomogr. 1990; 14(5):804–808 [55] Newman JS, Newberg AH. Congenital tarsal coalition: multimodality evaluation with emphasis on CT and MR imaging. Radiographics. 2000; 20(2):321– 332, quiz 526–527, 532 [56] Noto AM, Cheung Y, Rosenberg ZS, Norman A, Leeds NE. MR imaging of the ankle: normal variants. Radiology. 1989; 170(1, Pt 1):121–124 [57] Nwawka OK, Hayashi D, Diaz LE, et al. Sesamoids and accessory ossicles of the foot: anatomical variability and related pathology. Insights Imaging. 2013; 4 (5):581–593 [58] Oae K, Takao M, Naito K, et al. Injury of the tibiofibular syndesmosis: value of MR imaging for diagnosis. Radiology. 2003; 227(1):155–161

[32] Hermans JJ, Beumer A, Hop WCJ, Moonen AF, Ginai AZ. Tibiofibular syndes-

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clinical follow-up. HSS J. 2009; 5(2):161–164 [60] Pastore D, Dirim B, Wangwinyuvirat M, et al. Complex distal insertions of the tibialis posterior tendon: detailed anatomic and MR imaging investigation in cadavers. Skeletal Radiol. 2008; 37(9):849–855

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8.20 Clinical Relevance of Magnetic Resonance Imaging

the peroneus longus tendon. A case report and review of the literature. Clin Orthop Relat Res. 1986(202):223–226 [62] Perdikakis E, Grigoraki E, Karantanas A. Os naviculare: the multi-ossicle configuration of a normal variant. Skeletal Radiol. 2011; 40(1):85–88 [63] Pham H, Fessell DP, Femino JE, Sharp S, Jacobson JA, Hayes CW. Sonography and MR imaging of selected benign masses in the ankle and foot. AJR Am J Roentgenol. 2003; 180(1):99–107 [64] Rankine JJ, Nicholas CM, Wells G, Barron DA. The diagnostic accuracy of radiographs in Lisfranc injury and the potential value of a craniocaudal projection. AJR Am J Roentgenol. 2012; 198(4):W365:9 [65] Rogers LF, Poznanski AK. Imaging of epiphyseal injuries. Radiology. 1994; 191 (2):297–308 [66] Rosenberg ZS, Mellado J. Central pseudodefect of the talus: a potential ankle MR interpretation pitfall. J Comput Assist Tomogr. 1999; 23(5):718–720 [67] Rosenberg ZS, Feldman F, Singson RD. Peroneal tendon injuries: CT analysis. Radiology. 1986; 161(3):743–748 [68] Rosenberg ZS, Jahss MH, Noto AM, et al. Rupture of the posterior tibial tendon: CT and surgical findings. Radiology. 1988; 167(2):489–493 [69] Rosenberg ZS, Cheung Y, Jahss MH. Computed tomography scan and magnetic resonance imaging of ankle tendons: an overview. Foot Ankle. 1988; 8 (6):297–307 [70] Rubin DA, Towers JD, Britton CA. MR imaging of the foot: utility of complex oblique imaging planes. AJR Am J Roentgenol. 1996; 166(5):1079–1084

[81] Steinborn M, Heuck A, Maier M, et al. MR-Tomographie der Plantarfasciitis. Fortschr Röntgenstr. 1999; 170(1):41–46 [82] Hergenroeder AC. Diagnosis and treatment of ankle sprains. A review. Am J Dis Child. 1990; 144(7):809–814 [83] Studler U, Mengiardi B, Bode B, et al. Fibrosis and adventitious bursae in plantar fat pad of forefoot: MR imaging findings in asymptomatic volunteers and MR imaging-histologic comparison. Radiology. 2008; 246(3):863–870 [84] Taneja AK, Simeone FJ, Chang CY, et al. Peroneal tendon abnormalities in subjects with an enlarged peroneal tubercle. Skeletal Radiol. 2013; 42(12):1703– 1709 [85] Terk MR, Kwong PK, Suthar M, Horvath BC, Colletti PM. Morton neuroma: evaluation with MR imaging performed with contrast enhancement and fat suppression. Radiology. 1993; 189(1):239–241 [86] Torriani M, Thomas BJ, Bredella MA, Ouellette H. MRI of metatarsal head subchondral fractures in patients with forefoot pain. AJR Am J Roentgenol. 2008; 190(3):570–575 [87] Toye LR, Helms CA, Hoffman BD, Easley M, Nunley JA. MRI of spring ligament tears. AJR Am J Roentgenol. 2005; 184(5):1475–1480 [88] Urhahn R, Klose KC. [A painful space-occupying lesion in front of the Achilles tendon–MR diagnosis. Accessory muscle of the lower calf]. Radiologe. 1992; 32(2):91–93 [89] Wang XT, Rosenberg ZS, Mechlin MB, Schweitzer ME. Normal variants and diseases of the peroneal tendons and superior peroneal retinaculum: MR imaging features. Radiographics. 2005; 25(3):587–602

[71] Saupe N, Mengiardi B, Pfirrmann CWA, Vienne P, Seifert B, Zanetti M. Ana-

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ings in volunteers with asymptomatic ankles. Radiology. 2007; 242(2):509– 517 [72] Scheller AD, Kasser JR, Quigley TB. Tendon injuries about the ankle. Orthop Clin North Am. 1980; 11(4):801–811 [73] Schneck CD, Mesgarzadeh M, Bonakdarpour A, Ross GJ. MR imaging of the most commonly injured ankle ligaments. Part I. Normal anatomy. Radiology. 1992; 184(2):499–506 [74] Schweitzer ME, Caccese R, Karasick D, Wapner KL, Mitchell DG. Posterior tibial tendon tears: utility of secondary signs for MR imaging diagnosis. Radiology. 1993; 188(3):655–659 [75] Schweitzer ME, van Leersum M, Ehrlich SS, Wapner K. Fluid in normal and abnormal ankle joints: amount and distribution as seen on MR images. AJR Am J Roentgenol. 1994; 162(1):111–114 [76] Shukla S, Clarke AW, Saifuddin A. Imaging features of foot osteoid osteoma. Skeletal Radiol. 2010; 39(7):683–689 [77] Sierra A, Potchen EJ, Moore J, Smith HG. High-field magnetic-resonance imaging of aseptic necrosis of the talus. A case report. J Bone Joint Surg Am. 1986; 68(6):927–928 [78] Sobel M, DiCarlo EF, Bohne WH, Collins L. Longitudinal splitting of the peroneus brevis tendon: an anatomic and histologic study of cadaveric material. Foot Ankle. 1991; 12(3):165–170 [79] Soroceanu A, Sidhwa F, Aarabi S, et al. Surgical versus nonsurgical treatment of acute Achilles tendon rupture. J Bone Joint Surg Am. 2012; 94:2136–2143 [80] Stahlmann R, Shakibaei M. Fluorchinolon-induzierte Tendopathien - klinische und experimentelle Aspekte. Chemother J. 2000; 4:140–147

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infections. Foot Ankle. 1993; 14(1):18–22 [91] Weishaupt D, Andreisek G. [Diagnostic imaging of nerve compression syndrome]. Radiologe. 2007; 47(3):231–239 [92] Wetzel LH, Levine E. Soft-tissue tumors of the foot: value of MR imaging for specific diagnosis. AJR Am J Roentgenol. 1990; 155(5):1025–1030 [93] Willits K, Amendola A, Bryant D, et al. Operative versus nonoperative treatment of acute Achilles tendon ruptures: a multicenter randomized trial using accelerated functional rehabilitation. J Bone Joint Surg Am. 2010; 92 (17):2767–2775 [94] Yao L, Tong DJF, Cracchiolo A, Seeger LL. MR findings in peroneal tendonopathy. J Comput Assist Tomogr. 1995; 19(3):460–464 [95] Zampa V, Bargellini I, Rizzo L, et al. Role of dynamic MRI in the follow-up of acute Charcot foot in patients with diabetes mellitus. Skeletal Radiol. 2011; 40 (8):991–999 [96] Zanetti M, Ledermann T, Zollinger H, Hodler J. Efficacy of MR imaging in patients suspected of having Morton’s neuroma. AJR Am J Roentgenol. 1997; 168(2):529–532 [97] Zanetti M, Saupe N, Espinosa N. Postoperative MR imaging of the foot and ankle: tendon repair, ligament repair, and Morton’s neuroma resection. Semin Musculoskelet Radiol. 2010; 14(3):357–364 [98] Zeiss J, Fenton P, Ebraheim N, Coombs RJ. Normal magnetic resonance anatomy of the tarsal tunnel. Foot Ankle. 1990; 10(4):214–218 [99] Zhu G, Fang B, Johnson J, et al. Chronic plantar fasciitis: acute changes in the heel after extracorporal high-energy Shockwave therapy in diabetic foot. Radiology. 2005; 234:206

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9.1

Introduction

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9.2

Examination Technique

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The Temporomandibular Joint

9.3

Anatomy

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9.4

Disorders of the Articular Disk

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9.5

Arthritis and Other Synovial Disorders

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9.6

Bone Disorder

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9.7

Treatment Outcomes

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9.8

Clinical Relevance of Magnetic Resonance Imaging 439 References

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Chapter 9

The Temporomandibular Joint

9 The Temporomandibular Joint S. Robinson and R. Fischbach

9.1 Introduction

referred for MRI examination to evaluate the success of treatment.

Internet Link

●i

Information on the topic “Temporomandibular Joint Disorder” can be found on the homepages of the following providers: ● MedlinePlus ● Prof. Dr. Gerhard Undt ● The Journal of Craniomandibular & Sleep Practice ● TMJAnatomy.com ● German Society of Dental, Oral and Craniomandibular Sciences (DGZMK)

9.2.2 Coil Selection Imaging of the TMJ calls for a high-resolution technique in view of its small size. For magnetic field strengths up to 1.5 T, a small field of view (FOV) is needed; hence, bilateral surface coils with a small diameter (6–12 cm) are used to achieve adequate spatial resolution with good signal-to-noise ratio (SNR). The coil is positioned above the TMJ, with its center 1 to 2 cm anterior to the external auditory canal. There are special commercially available retainer devices to prevent coil movement (▶ Fig. 9.1). With a magnetic field strength of 3 T, the head coil in itself provides excellent image quality as well as a good overview of any concomitant pathologic processes.50,57 As both TMJs constitute a single masticatory unit, a TMJ disorder affecting one joint is also seen in the contralateral joint in up to 80% of cases, thus necessitating bilateral imaging.52 It is not uncommon for a previously healthy joint to relieve the pressure on its diseased counterpart until it, too, becomes symptomatic. Hence, treatment of the first implicated joint alone would not prove very successful.

9.2.3 Sequences and Parameters Routine examination of the TMJ in patients exhibiting symptoms of disk displacement comprises the following sequences: The examination begins with a fast axial overview sequence through the TMJ region with a spin-echo (SE) or GRE sequence to locate the TMJ and determine the transverse condylar axis. This transcondylar image is then used to plan further high-resolution sequences for imaging the joint with the mouth open and closed. In the presence of osteoarthritis or asymmetrical masticatory

Information for patients can be found on the website of the TMJ Association, Ltd.

9.2 Examination Technique 9.2.1 Patient Positioning The patient is examined in the supine position with the mouth closed in normal intercuspation. The examination continues with the mouth open about 30 mm to achieve adequate movement of the disk and mandibular condyle. Dental wedges made of plastic or wood or, alternatively, adjustable jaw openers can be used to keep the mouth open.5 Incremental jaw openers are useful, in particular, for dynamic motion studies.3 However, very fast gradient-echo (GRE) sequences with reduced resolution are able to demonstrate real-time mouth opening without any aids. Occasionally, patients fitted with a repositioning appliance may be

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Fig. 9.1 Placing the patient in a supine position for examination of the temporomandibular joint. The use of a retainer device makes it easier to secure both surface coils above the region of the external auditory canal.

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The temporomandibular joint (TMJ) is imaged to detect any clinically suspected anomalies and functional disorders. Conventional radiology has but a limited diagnostic role in exploring this complex joint, as it is able to detect only osseous changes with any degree of certainty due to the fact that the adjacent structures of the skull are obscured by the overlying bones. In particular, native radiographs are unable to permit assessment of the position, shape, and mobility of the articular disk, which is of crucial importance in settings of impaired TMJ function. Although computed tomography (CT) or digital volume tomography (DVT) provide good visualization of bone abnormalities, they have not become established as diagnostic imaging modalities for disk disorders because of their inadequate sensitivity.1 Within a short time of its clinical debut, magnetic resonance imaging (MRI) proved to be the primary imaging modality for diagnosis of TMJ disorders, thanks to its superior ability to demonstrate the internal joint structures. The high accuracy of MRI in evaluating the shape and position of the articular disk as well as osseous changes of the condyle and temporal articular surface has been documented in numerous studies.18,51,58 MRI is also superior to other modalities in diagnosing synovial diseases.27,55,64

9.2 Examination Technique

muscle activity, the longitudinal condylar axis may be asymmetrical and must be precisely determined for optimum assessment of the joints on each side (▶ Fig. 9.2). The FOV used for the following acquisitions with the surface coils is 8 to 12 cm and should not exceed 13 to 15 cm for head coils. A majority of authors prefer PDw or T1-weighted (T1w) SE sequences. Since the area of hyperintensity around the bilaminar zone on T2-weighted (T2w) images as well as bone marrow edema are often linked to acute complaints, a second T2w sequence is also recommended7 to identify any pathologic fluid collections or edematous changes associated with arthritic/infectious processes or joint injury.61 Turbo spin-echo (TSE) or fast spin-echo (FSE) sequences together with fat suppression can also be used in such settings.44 The slice thickness should ideally be 2 to 3 mm, and in general, 15 sections suffice to image the entire joint region. Reducing the slice thickness from 3 to 1.5 mm improves, in particular, demarcation of the discoligamentous joint structures on coronal images.68 A reduced slice thickness is important for demonstration of complex deformities, which can be achieved with 3D GRE sequences with good image quality and acceptable measurement times. The parasagittal plane is selected perpendicular to the transverse axis of the condylar head identified in the planning scan (see ▶ Fig. 9.2). This section includes the external auditory canal, floor of the temporal fossa, and, at the bottom, the ascending mandibular ramus. The articular disk and other joint structures are best evaluated in the parasagittal plane. Maintaining the closed mouth (intercuspation) is crucial for assessment of the disk position, as even partial opening of the mouth can cause reduction of a displaced disk.12 As the low signal disk is situated directly between the likewise hypointense condylar cortex and the mandibular fossa, some authors recommend that the morphology and signal intensity of the disk be evaluated on T2w sequences, because any intra-articular fluid lamella will improve disk delineation.7 Next, images will have to be obtained with the mouth open. As imaging with the mouth open is performed primarily to assess the disk position and condylar mobility, the number of signal averages can be reduced without appreciable loss of image quality in order to shorten the acquisition time. Besides, maintaining the open-mouth position for a long time is uncomfortable for the

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Fig. 9.2 Transverse condylar axis. Axial viewfinder at the level of the condyles with marked plane: on the right, paracoronal plane, and, left, parasagittal plane with asymmetrical condylar axis.

patient and induces involuntary swallowing due to pharyngeal pooling of saliva. Therefore, the acquisition time should be kept to a minimum to avoid motion artefacts, but the basic scanning method or the contrast characteristics should not be altered so as to improve comparability of the two series of images. If the patient uses a repositioning appliance (protrusive splint), an additional parasagittal overview image should be obtained, with the repositioning appliance in place to document disk reduction or the adopted disk position. A paracoronal section parallel to the transverse condylar axis should be added for examination of both joints (see ▶ Fig. 9.2). This plane is best for assessing the extent of medial or lateral disk displacement.25 If MRI is indicated because of a space-occupying tumor, the entire TMJ region should be imaged in the transverse plane using T2w sequences and an unenhanced T1w SE sequence. For more extensive processes, a head or head and neck coil is recommended, as the penetration depth afforded by a small-diameter surface coil may not be sufficient. After administration of gadolinium diethylenetriamine pentaacetic acid (Gd-DTPA) in a concentration of 0.1 mmol/kg body weight, T1w SE images are added in the transverse and coronal plane. Administration of contrast media (CM) has also proved useful for diagnosing involvement of the TMJs in rheumatoid diseases.

9.2.4 Special Examination Techniques Scanning time can be greatly reduced by using fast 2D GRE sequences. Although the disk can generally be well delineated on GRE images, the anatomic resolution of the surrounding structures and of the disk itself is markedly inferior to that of SE images.10,19 Hence, these sequences are used primarily in dynamic motion studies.

9.2.5 Dynamic Studies One disadvantage of static MR images confined to two mandibular positions is their inability to follow disk reduction when opening the mouth, especially where there is marked disk displacement. Besides, the dynamics and time of disk reduction may be of clinical interest, and as such, some authors have emphasized the role of cinematic studies in evaluating TMJ function.5,63 Sequential images of several static mandibular positions controlled by a mechanical mouth-opening device can provide for pseudodynamic demonstration of the movements involved in opening the mouth by combining the individual images in a cine loop. In general, 8 to 12 individual images will ensure continuous visualization of movements. Fast GRE sequences are particularly suitable for generation of such dynamic motion studies (cine technique) within an acceptable period of time. However, a T1w SE sequence with very short repetition time (TR) and reduced image matrix permits an adequate acquisition time. Simultaneous demonstration of both joints is especially important in motion studies to identify any functional differences of relevance between the two sides. Translation, rotation, and time of disk reduction as well as condylar hypermobility can be assessed. With acquisition times of only seconds, even the end points of mandibular positions can be documented, depending on the scanning equipment used. On static MR images using a conventional SE sequence, it is virtually impossible to display, in

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particular, joint hypermobility with condylar subluxation anterior to the apex of the articular tubercle (articular eminence).27 Although a cine loop displaying the motions of the TMJs is impressive for clinicians and patients, the therapeutic implications of dynamic MRI have not been conclusively elucidated so far.3,4 One drawback of this method is the extreme passive mouth opening when using a mechanical mouth-opening device, as only a distorted view of the intrinsic functions is obtained.

9.3 Anatomy 9.3.1 General Anatomy The TMJ is a diarthrosis constituting the articulation between the mandible and the temporal bone. The lentiform to ellipsoid condylar head is situated on the ascending mandibular ramus. Its transverse diameter is greater than its sagittal diameter. The transverse axis of the condylar head is oriented perpendicular to the ascending mandibular ramus, resulting in anterolateral to posteromedial tilting by 15 to 25 degrees of the transverse condylar axis as well as of the articular fossa relative to the frontal plane. The concave articular fossa is limited anteriorly by the articular tubercle and posteriorly by the bony wall of the external auditory canal (▶ Fig. 9.3a). The depth of the articular fossa and the inclination angle of the dorsal slope of the articular tubercle are variable. The osseous articulating surfaces of the articular fossa, articular tubercle, and mandibular condyle are covered by thin fibrocartilage. The joint is divided by a fibrocartilaginous, mobile meniscus,

Fig. 9.3 Anatomy of the temporomandibular joint. Schematic diagram of the oblique sagittal plane. (a) With mouth closed. (b) With mouth open and physiologic disk position. With the mouth open, the condyle reaches the apex of the articular tubercle. 1, disk; 2, bilaminar zone; 3, external auditory meatus; 4, joint capsule; 5, condyle; 6, lower joint compartment; 7, inferior head of lateral pterygoid; 8, superior head of lateral pterygoid; 9, upper joint compartment; 10, articular tubercle.

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the articular disk, into two completely separate compartments. The upper meniscotemporal compartment is bigger than its lower meniscocondylar counterpart. Anterior and posterior thickened portions of the disk, also known as the “anterior and posterior bands,” are interconnected by a narrow intermediate zone, giving the disk a biconcave appearance. Anteriorly, the disk is attached to the joint capsule and the superior head of the lateral pterygoid. The bilaminar zone is the continuation of the posterior band of the disk. It consists of two connective tissue leaflets, with the superior leaflet inserting into the posterior aspect of the articular fossa at the Glaser fissure in front of the external auditory canal, and the lower leaflet attached to the posterior aspect of the mandibular neck together with the joint capsule. The joint capsule is a thin, loose structure, whose attachment at the margin of the mandibular fossa of the temporal bone extends to the anterior slope of the articular tubercle. The capsule encompasses the condyle and inserts at the mandibular neck. It is reinforced laterally and medially by connective tissue fibers, whereas its anterior and posterior aspects are more flaccid. Medial to, but separated from, the capsule is the thin, flat sphenomandibular ligament, which is attached superiorly to the sphenoid spine of the temporal bone and inferiorly to the mandibular foramen. The stylomandibular ligament acts as a further stabilizing structure. The group of masticatory muscles, in a narrower sense, consists of four muscles: ● The temporalis arises like a fan from the temporal fossa and inserts at the coronoid process. It is the strongest elevator of the mandible. ● The masseter has its origin at the zygomatic arch and inserts at the mandibular angle. ● The medial pterygoid extending from the pterygoid fossa of the medial sphenoid to the mandibular angle serves as the medial pedant to the masseter. Acting in concert with the temporalis and masseter, the main function of this muscle is to close the mouth. ● The digastric lateral pterygoid participates in all joint movements and is seen as the most important of the muscles acting on the TMJs: ○ Its superior head plays an important role in opening the mouth. It arises medially from the greater wing of the sphenoid and courses posterolaterally with a number of fibers to the articular disk. There is a tendency toward anteromedial disk displacement in settings of anterior disk subluxation because of the anteromedial pull of this muscle. ○ The inferior head of the lateral pterygoid arises from the outer aspect of the lateral lamina of the pterygoid process and inserts at the mandibular condyle.

9.3.2 Special Magnetic Resonance Imaging and Variants Oblique Sagittal Plane The oblique sagittal plane running parallel to the ascending mandibular ramus generally shows the condyle as a hook-shaped structure. On T1w SE images, the low-signal cortex and equally low-signal fibrocartilage layer covering the condyle and articular

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The Temporomandibular Joint

9.3 Anatomy

a

b

c

12 o’clock position

Fig. 9.5 Physiologic disk position. Schematic diagram. The disk is within ±10 degrees of the 12 o’clock position in 95% of normal cases.

fossa are easily distinguished from the hyperintense, fat-containing trabecular bone. The condyle and temporal (articular) fossa are smoothly outlined and rounded. With the mouth closed, the condyle is centered in the articular fossa (see ▶ Fig. 9.3a). The biconcave, elongated disk can be identified on PDw or T1w SE sequences as a low-signal, homogeneous structure, as it is composed of densely packed, intertwined fibrocartilage bundles interspersed with isolated chondrocytes. A slight increase in signal intensity can be identified in the posterior band in more than 50% of normal disks20 and should not be considered pathologic in the absence of changes in the disk shape or position. With the mouth closed, the disk is normally located between the mandibular condyle and the temporal articular surface. The small anterior band is adjacent to the posterior slope of the articular tubercle. The thin intermediate zone is located between the anterior circumference of the condyle and the temporal articular surface (▶ Fig. 9.4). In 95% of asymptomatic joints, the transition between the posterior band, posterior ligament, and high-signal bilaminar zone does not deviate by more than 10 degrees from its vertical 12 o’clock position above the upper condylar pole (▶ Fig. 9.5).12 A slightly anterior, rather than posterior, position is observed more often. The physiologic disk position is slightly

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Fig. 9.4 Normal temporomandibular joint. (a) Oblique sagittal T2w sequence with mouth closed. Centric position of the condyle and posterior band (arrowhead) of disk in 12 o’clock position. Bilaminar zone (arrow). Good delineation of superior versus inferior head of lateral pterygoid. (b) Oblique sagittal PDw sequence with 30-mm mouth opening. Normal translation: the mandibular condyle slides beneath the articular tubercle (arrow). (c) Coronal T1w sequence with mouth closed. In the oblique coronal plane, the disk sits like a cap on top of the condyle (arrow).

more anterior in association with very steep sockets (posterior slope of articular eminence close to perpendicular line).24 The bilaminar zone composed of fibrovascular connective tissue is attached to the posterior band and connects the disk with the posterior joint capsule. The transition between the hypointense disk and the hyperintense bilaminar zone is clearly visualized on T1w SE images, making it easy to identify the disk. If the location of the disk is unclear on SE images, delineation of the posterior band can be improved following administration of GdDTPA due to increased signal intensity of the retroarticular vascular plexus.19,49 However, the authors believe that only rarely is it necessary to administer CM to determine disk displacement. The upper layer of the bilaminar zone, composed of fibroelastic tissue, is attached to the articular fossa. The hypointense structures occasionally detected in the bilaminar zone are attributed to elastic fibers (see ▶ Fig. 9.4). In rare cases, a coalesced bifid mandibular condyle is also seen (▶ Fig. 9.6), and there are even reports of a tetrafid mandibular condyle in the literature.46 With its two compartments, the TMJ functions as a combination of two joints. As the mouth opens, the mandibular condyle rotates in the lower jaw around the horizontal condylar axis, creating a sliding surface of changing shape for the mandibular condyle, which offsets any incongruence and acts as an elastic cushion in the articular surfaces exposed to pressure.16 Rotation may be impaired on one side. Once the condylar apex has reached the intermediate zone of the disk, mouth opening is facilitated by a forward horizontal sliding movement, translation, of the upper temporomeniscal joint. This horizontal sliding movement is largely facilitated by the lateral pterygoid. When the mouth is fully open, the condyle has reached the apex of the articular tubercle. In this position, the disk covers the condyle such that the intermediate zone of the disk lies between the articular tubercle and the condyle. The posterior band is now in the 2 o’clock to 3 o’clock position (▶ Fig. 9.3b).

Oblique Coronal Plane The oblique coronal plane permits assessment of sideways, in a medial or lateral direction, disk displacement. The disk sits, centrically, as a hypointense caplike structure on the condyle

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The Temporomandibular Joint

a

b

c

on oblique coronal images (see ▶ Fig. 9.4c). Its lateral attachment to the condyle is generally not well delineated. Oblique coronal images are particularly suitable for demonstration of the position of the condyle in the articular fossa and for detection of lateral abrasive denudations or osteophytic spurs on the condylar head.

ments to harmonious movement of the mandible when opening and closing the mouth. Internal derangement is a dynamic progressive condition that must be evaluated on the basis of its degree of severity. The most commonly applied clinical and radiologic staging system has been proposed by Wilkes69 and is summarized in ▶ Table 9.1.

9.4 Disorders of the Articular Disk 9.4.1 Abnormal Changes in the Degenerative changes and various stages of disk displacement, also known as “internal derangement,” are the most common causes of clinical TMJ complaints. TMJ dysfunction manifests as clicking sounds, pain, and impaired mouth opening. Internal derangement typically refers to anterior disk displacement. It is thought that up to 28% of all adults exhibit disk displacement,54 of whom, however, only a small proportion seek treatment or undergo diagnosis because of clinical complaints. Likewise, MRI examination has also identified a high prevalence of disk displacement in up to 33% of asymptomatic volunteers.26,59 Therefore, caution is needed when evaluating the disk position as identified on MRI since, against the background of such a large proportion of positional anomalies, it can be assumed that there is broad variability in what constitutes a normal disk position and that disk displacement may not always be the cause of the TMJ complaints.9,61 The proportion of cases of disk displacement among symptomatic patients is estimated to be 54 to 80%39,42; the extent of displacement is more pronounced in symptomatic patients.33 The factors implicated in triggering disk displacement include12,39: ● Joint injuries. ● Iatrogenic hyperextension of the joint during dental or orthodontic/oral surgical treatment. ● Muscular discoordination, also in association with kyphosis/ scoliosis and pelvic obliquity. ● Stress, including psychologic stress. Dysfunctions may also be caused by changes in the shape and position of the articular disk secondary to mechanical impedi-

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Structure and Shape of the Disk Pathologic changes in the disk can be detected on MR images as abnormal morphology and signal patterns. Degenerative processes generally originate in the posterior band at the transition to the bilaminar zone, as this is the region exposed to the highest mechanical stress and also has the highest incidence of perforations or disk avulsion.37 The normally homogeneously low signal disk may exhibit areas of hyperintensity due to mucoid degeneration (▶ Fig. 9.7).47 Areas of reduced signal intensity are interpreted as microcalcifications. Often, signal changes are associated with a loss of the harmonious, biconcave disk configuration. Early morphologic changes present as thickening of the posterior band. The condition progresses with further loss of the normal disk shape, rendering the posterior band indistinguishable from the intermediate zone. Clinically, the structural changes are accompanied by a loss of elasticity, which can also be assessed early on during MRI examination.66,70 Severe biconvex or sickle-shaped deformities are observed in association with chronic, irreducible disk displacement. Insights into the chronicity of the disorder can be gained from the severity of the deformities and may be useful for treatment decision-making. It must, however, be borne in mind that changes in disk morphology are also seen in a large proportion of asymptomatic persons, and hence they must be interpreted in the light of the clinical symptoms. In one study, the normal and characteristic biconcave disk shape was identified in only just under half of TMJ joints of symptom-free volunteers.23

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Fig. 9.6 Rudimentary bifid condyle. (a) Oblique sagittal T2w image with mouth closed. Distraction of the saddle-shaped, cranially retracted condyle. (b) Oblique sagittal PDw image with 30-mm mouth opening. Thickened posterior ligament as a sign of disk degeneration (arrowhead). (c) Paracoronal T1w image with mouth closed. Condylar retraction (arrow).

9.4 Disorders of the Articular Disk Table 9.1 Staging criteria for internal derangement of the temporomandibular joint (according to Wilkes69) Parameters

Stage I (early stage)

Stage II (early/intermediate stage)

Stage III (intermediate stage)

Stage IV (intermediate late stage)

Clinical findings

No significant mechanical symptoms, apart from reciprocal clicking

1–2 episodes of pain, loud clicking, incipient mechanical restriction on opening the mouth

Multiple episodes of pain; functional impairment, even including jaw locking

Increase in symptoms Grinding symptoms; compared with stage different episodes of III pain; functional impairment, with chronic restricted movement

Radiologic findings

Slight anterior disk displacement, preserved disk shape

Slight anterior displacement, Anterior displaceincipient disk deformity with ment, with significant thickening of the posterior deformity band

Increase in disk changes, incipient degenerative remodeling of condyle and articular fossa

Anatomic findings

As seen on radiology images

Anterior displacement and As seen on radiology slight disk deformity, as seen images on radiology images

Increased disk deAs seen on radiology formity; bone remod- images, multiple adeling with osteophyte hesions detected formation; multiple adhesions in anterior and posterior recess of joint compartment

a

Stage V (late stage)

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Severe disk deformity; perforation of disk or disk attachment; marked degenerative deformity of segments of bone joint, with flattening of condyle and articular tubercle; subcortical cysts

b

Fig. 9.7 Changes in the disk. (a) Slight increase in signal intensity and slight swelling of the intermediate zone (arrow) with mouth open. Somewhat restricted translation. (b) Somewhat restricted translation with mouth open and increased signal intensity of posterior band (arrowhead).

9.4.2 Disk Displacement Anterior Disk Displacement Anterior disk displacement is the most common type of displacement. The term partial disk displacement is used to denote a situation where the posterior band is before the

11 o’clock position but is still in contact with the condyle (▶ Fig. 9.8). Complete disk displacement means that the disk is no longer in contact with the anterior condylar pole (▶ Fig. 9.9). Although further subclassification of partial disk displacement into grades 1 and 2, based on the extent of partial displacement62 or on the presence of deformities and

431

a

b

c

d

e

f

Fig. 9.8 Anterior disk displacement. (a) Partial anterior disk displacement with retropositioning of the condyle. The biconcave disk configuration is preserved; the posterior band is somewhat distended. (b) Reduction takes place on opening the mouth. (c) Complete anterior disk displacement. The disk is positioned markedly anterior to the condyle. Degenerative deformity of the condyle and socket; minor effusion. (d) On opening the mouth, the deformed disk stays anterior to the condyle, without reduction. (e) Severe disk deformity, degenerative flattening, and subchondral cyst (arrow); flattening of the articular tubercle. (f) Reduction does not take place on opening the mouth. No discernible continuity between disk structures and the posterior disk attachment. Anterior osteophyte. Increasing sclerosis of socket and the condyle.

Fig. 9.9 Partial and complete anterior disk displacement. Schematic diagram. (a) The deformed disk is anteriorly displaced but is still in contact with the condyle. Reduction takes place as the mouth opens. (b) Complete disk displacement without reduction on opening the mouth. Restricted condylar translation.

changes in signal intensity,20 has been proposed, it has no implications where treatment is concerned. The ability to distinguish between partial and complete disk displacement with the mouth closed is enough.

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However, what is of major clinical relevance is documentation of reduction of the displaced disk into its normal anatomic position between the condyle and the articular tubercle during mouth opening. Although in partial disk displacement, disk reduction is often possible, in complete disk displacement, reduction is observed only in the early phase. Disk reduction over the condyle during anterior mandibular translation or mouth opening is usually accompanied by an audible click. A reciprocal click may be heard or felt just before mouth closure with recurrence of disk displacement. This reciprocal click is typically heard in cases of disk displacement with reduction (initial to terminal excursive click and initial to terminal click on incursive movement). Maximal mouth opening is needed to detect disk reduction during MRI examination, but this is something that some patients are unable to maintain because of muscle spasms or pain. For example, in almost one-third of symptomatic patients with MRI diagnosis of disk displacement without reduction, functional arthrography documented disk reduction when mouth opening reached its limiting range.14 In anterior disk displacement without reduction, the disk retains its position anterior to the condyle during mouth opening, where it undergoes increasing deformity. Clicks are rarely audible in such patients. The absence of disk reduction may

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The Temporomandibular Joint

9.4 Disorders of the Articular Disk derive from a lack of restorative forces because of flaccidity of the ligamentous structures, mechanical impediments, or, very rarely, disk avulsion. As anterior disk displacement interferes with mouth opening, the extent of condylar translation should also be further investigated. In long-standing disk displacement without reduction, impaired mouth opening is shown to improve over time, thanks to increased extension of the posterior disk attachment.

Sideways Disk Displacement In addition to visualizing strictly anterior disk displacement, MRI is also able to demonstrate anterolateral and anteromedial disk displacements as well as sideways displacement or sideways rotation (▶ Fig. 9.10). The incidence of anteromedial displacement is estimated to be 26 to 68%,16,27 with medial displacement without concurrent anterior displacement observed in up to 11% of cases. Detection of different disk segments in parallel sections in the parasagittal plane is enough to facilitate diagnosis of sideways disk displacement on sagittal scans (▶ Fig. 9.11). Paracoronal images demonstrating the disk in relation to the temporal articular surface and condyle enable precise classification of these findings (▶ Fig. 9.12).

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Displacement of the articular disk behind the 1 o’clock position is rare. While minor disk displacement is generally asymptomatic, severe displacement may be accompanied by jaw locking and pain. Eccentric posterior disk displacement is more common than previously thought (▶ Fig. 9.13)15 and can often be diagnosed on cine MRI or functional arthrography.

Disk Displacement Nomenclature

Fig. 9.10 Transverse disk displacement. Schematic diagram. Oblique coronal plane with mouth closed. (a) Normal disk position. (b) Lateral disk displacement. 1, disk; 2, joint capsule; 3, condyle; 4, lower joint compartment; 5, upper joint compartment; 6, articular fossa.

a

b

Apart from the functional distinction between disk displacement with or without reduction, disk displacement can also be characterized in terms of the direction of displacement relative to the mandibular condyle (anterior, posterior, medial, lateral) and the position of the mandibular condyle (centric, eccentric) (see ▶ Table 9.2). When the mouth is closed, that is, centric position of the condyle in the articular fossa and anterior displacement of the disk, the term centric–anterior disk displacement is used to describe this condition. If disk dislocation occurs during mouth opening, for example, posterior to the condyle, the term eccentric–posterior displacement is used. Combinations of centric and eccentric displacements are possible.

c

Fig. 9.11 Medial disk displacement. (a) With the mouth closed, the disk can be identified as a convex, curved structure facing anteriorly at the level of medial segment of the temporal bone pyramid. Minor effusion. (b) With the mouth open, the disk lies superiorly to the medial condylar segment and inferiorly to the articular tubercle. (c) In the paracoronal section, the disk (arrow) lies medial to the laterally displaced condyle.

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The Temporomandibular Joint

*

a

b

c

Table 9.2 Description of disk displacement Parameters

Description

Condylar position

●

Centric

●

Eccentric

●

Partial

●

Complete

●

Anterior

●

Anteromedial

●

Anterolateral

●

Medial

●

Lateral

●

Posterior

●

Without reduction

●

With reduction

Extent of displacement

Direction of displacement

Reduction on opening the mouth

Fig. 9.13 Posterior disk displacement. Parasagittal PDw sequence. Restricted translation. The disk lies posterior to the condyle. Marked anterior pneumatization of the temporal bone; the cells (arrows) exhibit mucosal swelling or secretory retention.

9.4.3 Disk Adhesion Fine fibrous adhesions go undetected on MRI and can be identified only on double-contrast arthrography or arthroscopy.43 However, even minor adhesions can result in painful restriction of joint functions, despite a normal disk position. In such settings, MRI is able to detect only reduced disk mobility relative to the articular tubercle or increasing disk deformity, but does not show any relevant change in the position of a displaced disk. In such cases, complaints were alleviated following lavage or arthroscopic adhesiolysis, without affecting the disk position.35

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9.4.4 Disk Perforation MRI is able to detect disk perforation only with widespread discontinuity, necessitating several scans to paint a true picture of the condition.21 Perforation and friction sounds are suggestive of advanced osteoarthritic chances, often seen in association with disk perforation. Disk perforation should be suspected in settings of severe anterior disk displacement, marked signal heterogeneity of the disk, and degenerative condylar bone changes (▶ Fig. 9.14). However, only arthrography or arthroscopy is able to reliably diagnose disk perforation.43,65

9.4.5 Malpositions of the Condyle In the normal closed mouth position, the condyle is centered in the articular fossa. Deviations from this normal position are possible and easily recognized on MRI. A summary of common malpositions is given in ▶ Fig. 9.15 and ▶ Table 9.2.

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Fig. 9.12 Lateral disk displacement with reduction on opening the mouth. (a) With the mouth closed, the disk can be identified (arrowheads) as an S-shaped structure lateral to the condyle at the level of the outer ear. (b) With the mouth open, the disk lies superiorly to the lateral segment of the mandibular condyle at the level of the external auditory canal (asterisk). (c) In the paracoronal section, the disk (arrow) lies lateral to the medially displaced condyle.

9.5 Arthritis and Other Synovial Disorders Fig. 9.14 Disk perforation with mouth closed and open. (a) Image with mouth closed. Marked anterior disk displacement and deformity (arrow). The condyle exhibits marginal osteophytes and irregular cortical outline superior to anterior convexity. (b) Image with mouth open. Discontinuity between anterior and posterior bands (arrowhead).

a

b

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9.5 Arthritis and Other Synovial Disorders 9.5.1 Arthritis

Fig. 9.15 Malpositions of the condyle. Schematic diagram. (a) Normal position. (b) Retropositioning. (c) Anterior malposition. (d) Compression. (e) Distraction.

a

Acute pyogenic infection of the TMJ may be hematogenous, occur secondarily to local trauma, or be transmitted from adjacent structures. In addition to the characteristic clinical signs of inflammation, there may be jaw locking or adoption of a pain-avoiding position, with the mouth slightly open. Typical findings on T2w images include effusion in one or both joint compartments. Prolonged courses of disease or local progressive disease can cause severe destruction of bone and discoligamentous structures, in turn possibly resulting in fibrous or bony ankylosis (▶ Fig. 9.16). Apart from septic arthritis, the TMJs are also susceptible to rheumatoid arthritis. In the latter condition, there is involvement of several joints, and unlike degenerative joint diseases, there are no osteophytic spurs or subchondral sclerosis. In view of the uniform morphologic reaction seen in the TMJ, it is not possible to distinguish between rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis, and systemic lupus erythematosus. However,

b

Fig. 9.16 Fibrous ankylosis. (a) Coronal T2w image. Bilateral high-grade deformed condyle and socket and no joint space. Left, temporal susceptibility artefact secondary to aneurysmal clipping. (b) Coronal section almost anterior to that.

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The Temporomandibular Joint

b

c

Fig. 9.17 Rheumatoid arthritis. (a) Parasagittal T2w image. Subchondral hyperintensity (arrowhead) without any appreciable sclerosis, osteophytes, or deformity. The disk (arrow) is displaced anteriorly. (b) Paracoronal T1w image. Subchondral isointense lesion (arrow). (c) Paracoronal T1w image following CM administration. Synovial and subchondral staining.

a

b

Fig. 9.18 Synovial chondromatosis. (a) Axial T1w image. CM enhancement of capsule (arrowheads); the joint space is filled with rounded hypointense structures and is distended. (b) Parasagittal PDw image with mouth open. Condyle and disk in normal position, with expanded capsule filled with chondromas.

rheumatoid arthritis is the most common of these conditions. Although it is thought that up to 50% of all patients have demonstrable changes in the TMJ, the number of symptomatic cases is much smaller.28,53 The findings observed on MRI include small effusions, mainly in the anterior recess; disk deformity (flattening, fragmentation, inhomogeneous hyperintensity, and indistinct outline); and condylar erosions or deformities.28 The prevalence of anterior disk displacement appears to be higher in those with arthritic joints compared with the normal population. Early changes that, in the past, could only be identified on arthrography or arthroscopy can now be easily visualized on MRI T1w SE sequences following Gd administration.53 If TMJ involvement is suspected in patients with rheumatoid arthritis, native T1w and T2w images should be obtained with the mouth closed, in addition to a series of T1w images following Gd administration (▶ Fig. 9.17).

intra-articular, cartilaginous, partially calcified nodules, which are loose or attached to the synovial membrane, obliterate one or both joint compartments, causing impaired joint function. Cortical erosions and intra-articular calcifications are best identified on CT. MRI shows widening of the joint capsule and expansion of the joint compartments due to a hyperintense effusion as well as intra-articular hypointense nodules (▶ Fig. 9.18).11,22 There are rare reports of intracranial extension.36 Other disorders originating in the internal joint space include, as in other regions of the skeleton, pigmented villonodular synovitis and calcium pyrophosphate crystal arthropathy (▶ Fig. 9.19).55

9.6 Bone Disorder 9.6.1 Osteoarthritis

9.5.2 Other Synovial Disorders Synovial chondromatosis is a rare disease that affects patients older than 40 years and is usually monoarticular. It involves benign proliferation of the synovial membrane, where multiple

436

Internal derangement is seen as an important predisposing factor in the development of degenerative changes of the TMJ. Followup examination of TMJ disorders involving disk displacement has revealed ongoing progression of discoligamentous changes as

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a

9.6 Bone Disorder Fig. 9.19 Calcium pyrophosphate crystal arthropathy. (a) Parasagittal T2w image. Anterior disk displacement and rapidly progressive osteoarthritis. (b) Paracoronal T1w image. Calcification medial to condyle (arrowhead).

a

b

a

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Fig. 9.20 Proliferative degeneration with irreducible disk displacement. (a) Parasagittal T2w sequence. Flattened condyle. Abrasive denudations, with corresponding flattening of the dorsal slope of the articular tubercle (arrowhead). Anterior osteophyte and joint effusion. (b) Parasagittal PDw sequence with mouth open. Severe sclerosis of the entire condyle and socket.

b

well as identification of other bone abnormalities in the later course.69 In a study by Rao et al,42 only half of all patients with disk displacement diagnosed on MRI showed an abnormal condylar configuration. In that study, the proportion of patients with degenerative changes in the mandibular condyle associated with irreducible disk displacement was greater than the proportion of those with reducible disk displacement. Only 4% of patients with identifiable condylar bone changes had a normal disk position. Morphologic changes included the following: ● Proliferative degenerative transformation with flattening, osteophytic spurs; sclerosis; and subchondral cysts (▶ Fig. 9.20 and ▶ Fig. 9.21). ● Regressive remodeling with a resultant hypoplastic condyle or small pointed condylar head, without any major osteophytic spur formation (see ▶ Fig. 9.21c). On the whole, regressive remodeling is more common. Incipient signs of condylar remodeling detected on MRI are as follows: ● Reduced signal intensity on T1w images. ● Increased signal intensity on T2w images due to fluid accumulation in the bone marrow, attesting to increased metabolic activity.21 The extent of bone changes can have important implications for treatment, as a successful outcome of conservative splint therapy or discoligamentous surgery is negatively correlated with the degree of degenerative changes to the condyle, especially the extent of osteophytic deformities.20

There are reports of other less common deformities of the TMJs, such as osteochondritis dissecans, avascular necrosis, and hyperuremic arthropathy,6,29,47 with findings on MRI similar to those of other large joints of the body.

9.6.2 Trauma Fractures of the mandibular neck account for around 30% of all mandibular fractures. Fractures are diagnosed by means of conventional radiographs, orthopantomography (OPG), or CT. In most cases, the extent of damage to the soft tissues associated with fractures is disregarded when assessing the fracture and planning treatment, despite the fact that injury to discoligamentous structures can have a major impact on posttraumatic functions and symptoms. Depending on the patient’s age and fracture location, the typical sequelae of mandibular neck fracture include impaired growth and functional impairments such as malocclusion and restricted movement due to disk adhesions. Disk dislocation or perforation as well as direct injury to the mandibular condyle or joint cartilage constitute a preosteoarthritic deformity. Fractures of the mandibular neck have been classified by Spiessl and Schroll into six types (▶ Table 9.3).56 Types I to III fractures, where there is no dislocation, tend to involve less damage to the soft tissues compared with types IV and V, in which dislocation or fracture of the mandibular condyle occurs. MRI is the only noninvasive imaging modality for assessment of TMJ soft tissue injuries (▶ Fig. 9.22 and ▶ Fig. 9.23). To date, there is a paucity of studies on acute posttraumatic soft tissue changes and on the

437

The Temporomandibular Joint Fig. 9.21 Other types of osteoarthritis of the temporomandibular joint. (a) Parasagittal T2w sequence. Anterior disk displacement, with socket sclerosis and subchondral cysts in condyle. (b) Paracoronal T1w sequence. Somewhat flattened condyle with subchondral cysts and laterally oriented osteophyte. (c) Parasagittal T2w sequence. Anterior disk displacement. Tapered condyle and effusions more in the superior than in the inferior compartment.

b

c

Table 9.3 Classification of mandibular neck fracture according to Spiessl and Schroll56 Types

Description

I

Mandibular neck fracture without displacement

II

Deep mandibular neck fracture with displacement

III

High mandibular neck fracture with displacement

IV

Deep mandibular neck fracture with dislocation

V

High mandibular neck fracture with dislocation

VI

Capitulum fracture

impact of MRI on treatment decision-making and functional treatment outcomes.13,17,38 The findings in the literature are inconsistent and based on a limited number of cases and small series, but they suggest that around 20 to 30% of neck fractures involve traumatic disk displacement. Disk injuries are imputed to direct compression or dislocation, with damage to the disk attachment or even disk perforation. As the disk itself is a very stable structure, injuries tend to be encountered in the retrodiscal bilaminar zone. T2w SE or GRE sequences are suitable for demonstration of soft tissue injuries and posttraumatic joint effusions. The extent of capsule and

438

disk injuries correlates with the fracture type, so that types IV and V, with dislocation of the neck fragment, are often associated with joint effusion and disk displacement, whereas the high dislocated fractures cause the most severe soft tissue damage.

9.7 Treatment Outcomes Internal derangement is typically treated conservatively with a protrusive repositioning splint. The fitted repositioning appliance results in joint protrusion and distraction. The joint is offloaded, and this alone often alleviates pain. Anterior displacement of the mandible has an effect on occlusion and on masticatory muscle tension, in turn restoring the normal relationship of the condyle with the disk. MRI can monitor treatment with the repositioning appliance and identify whether the desired disk reduction effect has been achieved (▶ Fig. 9.24). There are also isolated reports of patients being pain free after conservative treatment, despite the disk continuing to be positioned anteriorly to the condyle, but now, scar tissue is transformed into a pseudodisk at its normal position.41 However, reduction can be expected only in the case of partial displacement, without high-grade disk deformity. In addition to monitoring treatment with the repositioning appliance, MRI can therefore also be used to evaluate the treatment outcome.32 Absence of marked degenerative bone changes is also promising.

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a

9.8 Clinical Relevance of Magnetic Resonance Imaging

Fig. 9.22 Deep mandibular neck fracture. (a) Parasagittal T2w GRE sequence. Deep mandibular neck fracture with slight fragment displacement but without dislocation of the mandibular condyle. The disk can be identified at its normal position. A small effusion seen in both joint compartments. (b) Paracoronal section. Fissure identifiable in lateral capsule.

a

b

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clinical outcome of surgical interventions. Therefore, when interpreting the MRI results in a postoperative setting, it is important to be aware of the surgical technique used, of any intraoperative details, and of the clinical findings.71 Residual or recurrent disk displacement can be reliably identified on MRI. Although a successful clinical outcome may be documented postoperatively, disk adhesions are commonly encountered, and therefore, the mandible should be imaged in at least two different positions. Fibrous tissue is often seen in the joint capsule and joint space following surgery, with the fibrotic changes usually confined to the lateral joint capsule in asymptomatic joints. Extensive fibrosis extending into the joint space and medial capsule was detected in 60% of patients with persistent postoperative joint symptoms.67 In such cases, MRI must document the extent of lesions before any decisions on reoperation are taken. Occasionally, metallic abrasion may make it harder to evaluate the results.60 The indication for surgical intervention is viewed in an increasingly more critical light because of the high incidence of foreign body reactions, attendant erosions of the articular surfaces, and the low clinical success rate of disk replacement surgery.34 In one study of 21 joints with autologous dermal implants, MRI was not able to identify the implants in any of the joints.30

9.8 Clinical Relevance of Magnetic Resonance Imaging Fig. 9.23 High mandibular neck fracture with dislocation. Anterior disk displacement; increased signal intensity of bilaminar zone. The lower disk attachment is torn; lipohemarthrosis of superior joint compartment.

Surgical treatment of internal derangement comprises the following techniques: ● Arthroscopy or open disk reduction. ● Lavage. ● Meniscoplasty. ● Diskectomy. ● Diskectomy with implantation of synthetic autologous tissue.8,30,67 The findings of the investigations reported to date have not found any definite correlation between the disk position and successful

A detailed clinical examination is of first and foremost importance for assessment of a patient with TMJ disorder. The imaging modalities chosen will depend on the clinical findings and clinical need for further diagnostic exploration. The goal here must be to pinpoint and document any specific anatomic abnormalities causing the patient’s complaints. Conventional radiographs, including panorama overviews, are endowed with only low sensitivity for the detection of bone and soft tissue disorders but have a role in the examination of trauma patients prior to orthodontic treatment as well as in postoperative settings. While conventional CT of the TMJ permits relatively good insights into bone changes, such abnormalities generally represent the terminal stages of a chronic soft tissue disease. A negative CT result does not, by any means, rule out soft tissue

439

The Temporomandibular Joint

a

b

c

Table 9.4 Diagnostic steps for evaluation of the temporomandibular joint (step 1: most suitable method; steps 2–4: declining suitability) Findings

Conventional radiography

Arthrography

CT

MRI

Disk displacement 4

2

3

1

Disk perforation

1

2

Adhesions

1

2

Arthrosis

1

Arthritis

3

Tumors

3

Synovial chondromatosis Fracture

2 2

3 1

2

1

1

2

1

2

2

pathology. High-resolution CT and volume CT are comparable with conventional CT. Arthrography, which was introduced in the 1940s, came to play a pivotal role in evaluation of internal derangement only in the 1980s. Arthrography permits good delineation of the articular disk and assessment of the functional implications of disk displacement. Besides, arthrography is the method of choice for detection of disk perforation. Arthrography began to be gradually supplanted by the increasing availability of MRI and arthroscopy. CT and DVT are definitely inferior to MRI for detection of soft tissue pathology. MRI is noninvasive and less technically demanding for the radiologist than arthrography. MRI has the advantage of being able to visualize the TMJ in several planes, in particular, in settings of medial and lateral disk displacement. Thanks to its ability to clearly demonstrate the soft tissues, MRI is superior to all other imaging modalities for the examination of patients following surgical disk reduction or meniscectomy. Arthrography, which is the only other method able to demonstrate the articular disk, is often more demanding in such cases.45 As such, in most clinical situations, MRI is the imaging modality of choice for diagnosis of TMJ disorders (▶ Table 9.4). The significance of MRI derives especially from the fact that clinical examination has limitations when it comes to assessment of the disk

440

position and disk mobility.40,45 Although it is relatively easy to diagnose “disk displacement,” only in two-thirds of cases can the question of reduction be correctly evaluated. Asymptomatic disk displacement is often missed on clinical examination.2 Furthermore, as pain in the TMJ region can stem from an extra-articular source, MRI helps refine differential diagnosis.

Clinical Interview

●i

Clinical interview with Prof. Eva Piehslinger, Head of Department of Prosthetics at the Bernhard Gottlieb University Dental Clinic, Sensengasse 2a, 1090 Vienna, Austria: Question: “What role does radiography play for you?” Answer: “Radiographs are no longer indicated for the TMJs, as CT and MRI are more suitable. Orthopantomography is good for getting an initial orientational overview to detect any major asymmetry of the condyles, condylar distortion/rounding, narrowing of the joint space, extension of the styloid process or calcification of the styloid ligament with formation of pseudojoints (Eagle’s syndrome), as well as loose joint bodies (‘joint mice’).” Question: “Which patients do you refer for arthroscopy?" Answer: “Before arthroscopy is indicated, an MRI must always have been carried out first, with a diagnosis of ‘structural changes.’ Arthroscopy should only be conducted for patients experiencing pain and severely restricted movement that had failed to respond to conservative treatment (repositioning appliance and physiotherapy). Besides, if there are inflammatory changes, with loose joint bodies or major adhesions, joint lavage can be performed for removal of loose joint bodies or fragmented disk components.” Question: “For which disorders do you encounter false-positive MRI results most often?” Answer: “When investigating disk displacement, anterior displacement is often diagnosed when the mouth is closed, the articular

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Fig. 9.24 Anterior disk displacement undergoing treatment with repositioning appliance. (a) With mouth closed, the disk is displayed at the level of the external auditory meatus at the lateral circumference of the condyle, with partial anterior displacement. Minor effusion in superior and inferior compartments. (b) Section slightly medial to (a). (c) The condyle is now positioned above, after fitting the repositioning appliance. This represents the physiologic position of the disk above the condyle.

9.8 Clinical Relevance of Magnetic Resonance Imaging [3] Behr M, Held P, Leibrock A, Fellner C, Handel G. Diagnostic potential of pseudo-dynamic MRI (CINE mode) for evaluation of internal derangement of the TMJ. Eur J Radiol. 1996; 23(3):212–215 [4] Bell KA, Miller KD, Jones JP. Cine magnetic resonance imaging of the temporomandibular joint. Cranio. 1992; 10(4):313–317 [5] Burnett KR, Davis CL, Read J. Dynamic display of the temporomandibular joint meniscus by using “fast-scan” MR imaging. AJR Am J Roentgenol. 1987; 149 (5):959–962 [6] Campos PSF, Freitas CE, Pena N, et al. Osteochondritis dissecans of the temporomandibular joint. Dentomaxillofac Radiol. 2005; 34(3):193–197 [7] Chiba M, Kumagai M, Echigo S. Association between high signal intensity in the posterior disc attachment seen on T2 weighted fat-suppressed images and temporomandibular joint pain. Dentomaxillofac Radiol. 2007; 36(4):187–191 [8] Conway WF, Hayes CW, Campbell RL, Laskin DM, Swanson KS. Temporomandibular joint after meniscoplasty: appearance at MR imaging. Radiology. 1991; 180(3):749–753 [9] de Bont LG, Dijkgraaf LC, Stegenga B. Epidemiology and natural progression of articular temporomandibular disorders. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 1997; 83(1):72–76 [10] Dewes W, Krahe T, Luckerath W, et al. MR-Tomographie des Kiefergelenkes

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tubercle is very steep, and the disk is physiologically positioned somewhat before the 12 o’clock position. Besides, irreducible disk displacement can be diagnosed if the selected reduction block is too low, preventing the disk from making contact with the condyle.” Question: “For which disorders do you encounter false-negative MRI results most often, and why were diagnostic measures continued in such cases?” Answer: “False-negative results may be obtained for patients who experience clicking phenomena only on certain days and none on the examination day. Hence, dislocation will not, of course, be revealed on the (MRI) images.” Question: “For which disorders can MRI be omitted and for which is it being overly used?" Answer: “MRI can be omitted when only muscular discoordination is causing pain in the region of the masticatory muscles and there are no clicking sounds. If osteoarthritic changes are suspected, the MR images obtained have no implications for their treatment.” Question: “From which patients to you expect to obtain information of relevance for treatment from an MR movie made during mouth opening?” Answer: “Demonstration of reciprocal clicking phenomena in a movie can be interesting if there is a possibility of using repositioning therapy for a preserved disk shape to obtain lasting (disk) reduction. In such cases, it is important to diagnose in which phase of mouth opening the disk makes contact with the condyle and whether the disk has undergone any structural changes.” Question: “What is the clinical significance of MRI-suspected disk perforation?” Answer: “Disk perforation has important clinical implications, as it expedites progression of osteoarthritic changes, making it easier for inflammatory processes to spread to both compartments.” Question: “What do you think is the impact of adhesions?” Answer: “Adhesions have a major impact on joint mobility and the physiologic production of synovial fluid during movement. They can trigger a vicious circle with lack of mobility, drying of the joint, and even more severe restricted movements and pain.”

unter Anwendung T1 -gewichteter Multislice-Gradientenecho-Sequenzen. Fortschr Röntgenstr. 1988; 148:541–544 [11] Dolan EA, Vogler JB, Angelillo JC. Synovial chondromatosis of the temporomandibular joint diagnosed by magnetic resonance imaging: report of a case. J Oral Maxillofac Surg. 1989; 47(4):411–413 [12] Drace JE, Enzmann DR. Defining the normal temporomandibular joint: closed-, partially open-, and open-mouth MR imaging of asymptomatic subjects. Radiology. 1990; 177(1):67–71 [13] Dwivedi AN, Tripathi R, Gupta PK, Tripathi S, Garg S. Magnetic resonance imaging evaluation of temporomandibular joint and associated soft tissue changes following acute condylar injury. J Oral Maxillofac Surg. 2012; 70 (12):2829–2834 [14] Fischbach R, Heindel W, Lin Y, et al. Vergleich von Kernspintomographie und Arthrographie bei Funktionsstörungen des Kiefergelenkes. Fortschr Röntgenstr. 1995; 162(3):216–223 [15] Foucart JM, Carpentier P, Pajoni D, Marguelles-Bonnet R, Pharaboz C. MR of 732 TMJs: anterior, rotational, partial and sideways disc displacements. Eur J Radiol. 1998; 28(1):86–94 [16] Gerber A. Das normale Kiefergelenk. In: Gerber A, Steinhardt G, Hrsg. Kiefergelenkstörungen – Diagnostik und Therapie. Berlin, Germany: Quintessenz; 1989:21–26 [17] Gerhard S, Ennemoser T, Rudisch A, Emshoff R. Condylar injury: magnetic resonance imaging findings of temporomandibular joint soft-tissue changes. Int J Oral Maxillofac Surg. 2007; 36(3):214–218 [18] Hansson LG, Westesson PL, Katzberg RW, et al. MR imaging of the temporomandibular joint: comparison of images of autopsy specimens made at 0.3 T and 1.5 T with anatomic cryosections. AJR Am J Roentgenol. 1989; 152(6):1241–1244 [19] Held P, Moritz M, Fellner C, Behr M, Gmeinwieser J. Magnetic resonance of the disk of the temporomandibular joint. MR imaging protocol. Clin Imaging. 1996; 20(3):204–211 [20] Helms CA, Kaban LB, McNeill C, Dodson T. Temporomandibular joint: morphology and signal intensity characteristics of the disk at MR imaging. Radiology. 1989; 172(3):817–820 [21] Hermans R, Termote JL, Marchal G, Baert AL. Temporomandibular joint imaging. Curr Opin Radiol. 1992; 4(1):141–147 [22] Herzog S, Mafee M. Synovial chondromatosis of the TMJ: MR and CT findings. AJNR Am J Neuroradiol. 1990; 11(4):742–745 [23] Hugger A, Kordaß B, Assheuer J, et al. Einblicke in die funktionelle Anatomie

References [1] Alkhader M, Ohbayashi N, Tetsumura A, et al. Diagnostic performance of magnetic resonance imaging for detecting osseous abnormalities of the temporomandibular joint and its correlation with cone beam computed tomography. Dentomaxillofac Radiol. 2010; 39(5):270–276 [2] Barclay P, Hollender LG, Maravilla KR, Truelove EL. Comparison of clinical and magnetic resonance imaging diagnosis in patients with disk displacement in the temporomandibular joint. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 1999; 88(1):37–43

des Kiefergelenkes mit Hilfe der Kernspintomographie. Z Stomatol. 1993; 90:527–562 [24] Isberg A, Westesson PL. Steepness of articular eminence and movement of the condyle and disk in asymptomatic temporomandibular joints. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 1998; 86(2):152–157 [25] Katzberg RW, Westesson PL, Tallents RH, et al. Temporomandibular joint: MR assessment of rotational and sideways disk displacements. Radiology. 1988; 169(3):741–748 [26] Katzberg RW, Westesson PL, Tallents RH, Drake CM. Anatomic disorders of the temporomandibular joint disc in asymptomatic subjects. J Oral Maxillofac Surg. 1996; 54(2):147–153, discussion 153–155

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[28] Larheim TA, Bjørnland T, Smith HJ, Aspestrand F, Kolbenstvedt A. Imaging

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Comparison with surgical observations. Oral Surg Oral Med Oral Pathol. 1992;

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73(4):494–501 [29] Laskin DM. Diagnosis of pathology of the temporomandibular joint. Clinical and imaging perspectives. Radiol Clin North Am. 1993; 31(1):135–147 [30] Lieberman JM, Bradrick JP, Indresano AT, Smith AS, Bellon EM. Dermal grafts of the temporomandibular joint: postoperative appearance on MR images. Radiology. 1990; 176(1):199–203 [31] Lin Y, Friedrich R, Fischbach R. Vergleichende Untersuchung von MRT und Kontrastmittelarthrographie bei Patienten mit Kiefergelenkgeräuschen. Dtsch Zahnarztl Z. 1993; 48:339–342 [32] Maeda M, Itou S, Ishii Y, et al. Temporomandibular joint movement. Evaluation of protrusive splint therapy with GRASS MR imaging. Acta Radiol. 1992; 33(5):410–413

(5):1239–1245 [51] Schwaighofer BW, Tanaka TT, Klein MV, Sartoris DJ, Resnick D. MR imaging of the temporomandibular joint: a cadaver study of the value of coronal images. AJR Am J Roentgenol. 1990; 154(6):1245–1249 [52] Shellock FG, Pressman BD. Dual-surface-coil MR imaging of bilateral temporomandibular joints: improvements in the imaging protocol. AJNR Am J Neuroradiol. 1989; 10(3):595–598 [53] Smith HJ, Larheim TA, Aspestrand F. Rheumatic and nonrheumatic disease in the temporomandibular joint: gadolinium-enhanced MR imaging. Radiology. 1992; 185(1):229–234 [54] Solberg WK, Woo MW, Houston JB. Prevalence of mandibular dysfunction in young adults. J Am Dent Assoc. 1979; 98(1):25–34

[33] Maizlin ZV, Nutiu N, Dent PB, et al. Displacement of the temporomandibular

[55] Song MY, Heo MS, Lee SS, et al. Diagnostic imaging of pigmented villonodular

joint disk: correlation between clinical findings and MRI characteristics. J Can

synovitis of the temporomandibular joint associated with condylar expansion.

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[35] Moses JJ, Sartoris D, Glass R, Tanaka T, Poker I. The effect of arthroscopic sur-

[57] Stehling C, Vieth V, Bachmann R, et al. High-resolution magnetic resonance

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mobility. J Oral Maxillofac Surg. 1989; 47(7):674–678 [36] Nokes SR, King PS, Garcia R, Jr, Silbiger ML, Jones JD, III, Castellano ND. Temporomandibular joint chondromatosis with intracranial extension: MR and CT contributions. AJR Am J Roentgenol. 1987; 148(6):1173–1174 [37] Norer B, Pomaroli A, Dietze O. Articular disk degeneration in the TMJ]. Dtsch Z Mund Kiefer Gesichtschir. 1989; 13(4):278–282 [38] Özmen Y, Fischbach R, Lenzen J. Kernspintomographische Untersuchung der Diskusposition nach konservativer und operativer Versorgung der Gelenkfortsatzfrakturen. Dtsch Z Mund Kiefer Gesichtschir. 1995; 19:277–280 [39] Paesani D, Westesson PL, Hatala M, Tallents RH, Kurita K. Prevalence of temporomandibular joint internal derangement in patients with craniomandibular disorders. Am J Orthod Dentofacial Orthop. 1992; 101(1):41–47 [40] Park JW, Song HH, Roh HS, Kim YK, Lee JY. Correlation between clinical diagnosis based on RDC/TMD and MRI findings of TMJ internal derangement. Int J Oral Maxillofac Surg. 2012; 41(1):103–108 [41] Petersson A, Eriksson L, Westesson PL. MR images mimic disc after discectomy. Dentomaxillofac Radiol. 2005; 34(4):237–239 [42] Rao VM, Babaria A, Manoharan A, et al. Altered condylar morphology associated with disc displacement in TMJ dysfunction: observations by MRI. Magn Reson Imaging. 1990; 8(3):231–235 [43] Rao VM, Farole A, Karasick D. Temporomandibular joint dysfunction: correlation of MR imaging, arthrography, and arthroscopy. Radiology. 1990; 174(3, Pt 1):663–667 [44] Rao VM, Vinitski S, Liem M, Rapoport R. Fast spin-echo imaging of the temporomandibular joint. J Magn Reson Imaging. 1995; 5(3):293–296

volunteers. Invest Radiol. 2007; 42(6):428–434 [58] Tasaki MM, Westesson PL. Temporomandibular joint: diagnostic accuracy with sagittal and coronal MR imaging. Radiology. 1993; 186(3):723–729 [59] Tasaki MM, Westesson PL, Isberg AM, Ren YF, Tallents RH. Classification and prevalence of temporomandibular joint disk displacement in patients and symptom-free volunteers. Am J Orthod Dentofacial Orthop. 1996; 109 (3):249–262 [60] Tetsumura A, Honda E, Sasaki T, Kino K. Metallic residues as a source of artifacts in magnetic resonance imaging of the temporomandibular joint. Dentomaxillofac Radiol. 1999; 28(3):186–190 [61] Tomas X, Pomes J, Berenguer J, et al. MR imaging of temporomandibular joint dysfunction: a pictorial review. Radiographics. 2006; 26(3):765–781 [62] Vogl TJ, Eberhard D. MR-Tomographie Temporomandibulargelenk. Stuttgart, Germany: Thieme; 1993 [63] Vogl TJ, Eberhard D, Weigl P, et al. Die Anwendung der “Cine-Technik” in der MRT-Diagnostik des Kiefergelenkes. Fortschr Röntgenstr. 1992; 156(3):232–237 [64] Wang P, Tian Z, Yang J, Yu Q. Synovial chondromatosis of the temporomandibular joint: MRI findings with pathological comparison. Dentomaxillofac Radiol. 2012; 41(2):110–116 [65] Watt-Smith S, Sadler A, Baddeley H, Renton P. Comparison of arthrotomographic and magnetic resonance images of 50 temporomandibular joints with operative findings. Br J Oral Maxillofac Surg. 1993; 31(3):139–143 [66] Westesson PL, Bronstein SL, Liedberg J. Internal derangement of the temporomandibular joint: morphologic description with correlation to joint function. Oral Surg Oral Med Oral Pathol. 1985; 59(4):323–331

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ogy. 1992; 182(1):280–282 [69] Wilkes CH. Internal derangement of the temporomandibular joint. Pathological variations. Arch Otolaryngol Head Neck Surg. . 1989; 115:469–477 [70] Yildirim D, Dergin G, Tamam C, Moroglu S, Gurses B. Indirect measurement of the temporomandibular joint disc elasticity with magnetic resonance imaging. Dentomaxillofac Radiol. 2011; 40(7):422–428 [71] Youssefzadeh S. Postoperative imaging of the temporomandibular joint. Top Magn Reson Imaging. 1999; 10(4):193–202

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10.1

Introduction

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10.2

Examination Technique

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10.3

Anatomy

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10.4

Neuropathy

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10.5

Myotonic Disorders

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10.6

Muscular Dystrophy

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10.7

Inflammatory Myopathy

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10.8

Muscle Changes after Radiotherapy and Local Chemotherapy

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10.9

Traumatic Myopathy

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10.10 Muscle Fibrosis

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10.11 Compartment Syndrome

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10.12 Rhabdomyolysis

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10.13 Secondary Myopathy

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10.14 Muscle Tumors

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10.15 Pitfalls in Interpreting the Images

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10.16 Clinical Relevance of Magnetic Resonance Imaging

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References

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Chapter 10

The Muscles

10 The Muscles A.J. Hoeink, T.-U. Niederstadt, and M. Vahlensieck

In recent years, magnetic resonance imaging (MRI) demonstration of the skeletal muscles, together with their anatomy, physiologic changes, and pathologic abnormalities, has been the focus of intensive research. MRI provides for noninvasive visualization of interesting aspects of muscle physiology and anatomy, which will now be addressed in this chapter.

10.2 Examination Technique 10.2.1 Magnetic Resonance Imaging The muscles of the extremities are preferably imaged in the axial plane. A field of view encompassing both legs should be selected for demonstration of the lower extremities, since important diagnostic information can be obtained by comparing the two legs, for example, symmetrical distribution of pathologic abnormalities. For localized findings confined to one leg, smaller coils adapted to the joint, such as flexible phased-array coils, can be used to achieve high resolution. The pathologic abnormalities detected on MRI include changes in the size or shape of a muscle (atrophy, hypertrophy, or pseudohypertrophy) and changes in signal intensity. The changes observed in the signal intensity reflect essentially the following three pathologies62: ● Fatty infiltration. ● Muscle atrophy. ● Muscle edema. Therefore, the MRI examination protocol should always include the following sequences: ● T1-weighted (T1w) spin-echo (SE) sequences to assess fat distribution and identify fatty muscle atrophy in chronic myopathy. ● T2-weighted (T2w) and/or fat-suppressed sequences, such as short-tau inversion recovery (STIR) sequence, for detection of muscle edema as seen in, for example, myositis, following exercise or in association with tumorous and liquefying processes, manifesting as areas of hyperintensity. STIR sequences (see Chapter 1.6.4) are superior to all other techniques for demonstration of edematous changes in that they visualize the tissues with a long T1 and long T2 time and with high signal intensity. Fat suppression also helps distinguish fat from blood. Since both fat and blood exhibit high signal intensity on T1w and/or T2w images, it might otherwise not be possible to make such a distinction. Therefore, routine imaging of the muscles should include STIR as well as T1w sequences. Novel MRI modalities used, in particular, for diagnosis of various forms of myositis, include T2 mapping, diffusion-weighted imaging (DWI) sequences, and blood oxygenation level–dependent (BOLD) imaging.5 Coronal and sagittal sections are occasionally added to the diagnostic spectrum of muscle imaging to obtain a clearer picture of the extent of a disease process.

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10.2.2 Special Magnetic Resonance Spectroscopy of the Muscles Magnetic resonance spectroscopy (MRS) is a noninvasive method that is able to demonstrate the in vivo concentrations of metabolites in muscle cells. 31P-MRS, which detects the resonance signals of the 31P nucleus rather than the hydrogen nucleus, is able to display the phosphate-containing metabolites involved in muscle energy metabolism. Although exercise MRS is able to measure the metabolic changes occurring during exercise, it is not used routinely in the clinical setting because of its complexity in terms of implementation and the range of equipment needed but not universally available (broadband transmission and receiver channels). Another drawback is the widespread variability in the pattern of physiologic reactions exhibited by muscles, which are determined by the muscle fiber type and energy pathway. Data interpretation is also a problem because, although many of the studies conducted hitherto purport to attest to the sensitivity of the method, they cast doubt on the ability to assign the data to specific metabolic disorders.

Basic Principles of Muscle Energy Metabolism The principal metabolites identified in the phosphorus spectrum are phosphocreatine; inorganic phosphate; the γ, α, and β phosphate groups of nucleoside triphosphates; phosphodiester (glyceryl phosphoryl choline and glyceryl phosphoryl ethanolamine); and phosphomonoester of phospholipid metabolism. Phosphocreatine is used as a reference substance for demonstration of the changes occurring in the chemical shift of the other phosphorus metabolites. The changes in the chemical shift of inorganic phosphates relative to phosphocreatine can be used to measure the intracellular pH value noninvasively. The myocyte (muscle cell) uses adenosine triphosphate (ATP) as energy source for its contractile force. Muscles obtain ATP via different, aerobic or anaerobic, metabolic pathways. In this setting, phosphocreatine is an energy-rich phosphate reservoir that serves as a rapid energy source for short-term bursts of increased energy demands or until onset of glycolysis. However, the energy-rich phosphate content of phosphocreatine cannot be used directly to supply energy for cellular reactions. Instead, the phosphate group must be transferred to adenosine diphosphate (ADP) through the creatine kinase reaction to form ATP. ATP formation from phosphocreatine and energy release from ATP can be summarized in the following reaction formula: 2 Phosphocreatine ! creatine þ P2i þ energy

where Pi = inorganic phosphate To maintain ATP levels during muscle exercise, phosphocreatine dephosphorylation takes place with attendant loss in signal intensity, since without a phosphate group, the creatine molecule cannot be visualized in the 31P spectrum. The phosphate group is then released from ATP for energy supply, increasing the concentration of inorganic phosphate.

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10.1 Introduction

10.2 Examination Technique

Glycolysis refers to the oxidation of glucose to pyruvate. For each mole of glucose, two moles of NADH2 (reduced form of nicotinamide adenine dinucleotide [NAD]) and four moles of ATP are formed. Since two moles of ATP are needed initially for phosphorylation of glucose or glucose 1-phosphate, the conversion of glucose to pyruvate generates a net gain of two moles of ATP. This gain can be increased further by 50% on using the carbohydrate stored as glycogen in the muscles, where each mole of glucose residue produces a total of three moles of ATP, since the first phosphorylation step is omitted, as the glucose residue is already phosphorylated. The ensuing pyruvate conversation pathway is determined by the availability of oxygen in the muscle cell: ● Anaerobic glycolysis: Under anaerobic conditions, pyruvate is converted to lactate by the lactate dehydrogenase reaction. Lactate is formed in anaerobic glycolysis to regenerate the hydrogen acceptor NAD+, which is essential for maintenance of glycolysis. ● Aerobic glycolysis: Under aerobic conditions, pyruvate is broken down further for energy release and is oxidized to carbon dioxide and water in the electron transport chain, yielding a total of 36 moles of ATP.

Oxidation of Fatty Acids Following hydrolysis of triacylglycerides in the cytoplasm, free fatty acids are broken down to their acetyl-CoA moieties by βoxidation in the mitochondria, followed by aerobic degradation via the citric acid cycle and the electron transport chain. The citric acid cycle and the electron transport chain constitute the common final pathway for metabolism of acetyl-CoA, the metabolic intermediate of aerobic glycolysis, β-oxidation, and glucogenic amino acids. Oxidation of fatty acids represents the most economical means of energy release. The activity of the electron transport chain is regulated by the ATP concentration in mitochondria, ensuring that oxidative phosphorylation is sensitively tailored to the cell’s energy demands at any particular time. Oxygen is a limiting factor in ATP availability.

Muscle Energy Demands Which substrate will be preferentially metabolized by a muscle cell is determined, on the one hand, by the level of muscle activity and, on the other hand, by the respective muscle fiber type. At rest, the energy is produced in the vast majority of cases through aerobic metabolic pathways. Since ATP demands are relatively low, even low perfusion is able to assure an adequate supply of oxygen and substrates; hence, oxidative degradation of blood glucose and fatty acids predominates. Matters are different in exercise settings: in the initial phase of muscle loading, the ATP demand immediately rises by a factor of several hundreds compared with that of the resting value. By contrast, it takes several minutes until the oxygen supply can be met through enhancement of the relevant processes such as vasodilation, increased cardiac output, and faster respiratory rate. In the initial phase of muscle exercise, the muscle must therefore meet its increased energy demands through metabolization of endogenous substrates, such as phosphocreatine and glycogen, which can be metabolized under anaerobic conditions regardless

of oxygen availability. ▶ Fig. 10.1 illustrates the temporal course of energy provision in the muscle during exercise. During the very first seconds, energy demands are thus met by a creatine kinase reaction, whereas the oxidative energy generation slowly gets underway to be replaced by glycolysis only after 30 seconds. If exercise is continued, oxidative metabolic processes play an increasingly greater role in energy supply. After around 100 seconds, anaerobic and oxidative metabolic processes each account for around 50% of the metabolic processes at play.

Metabolism Based on Muscle Fiber Types As mentioned, classification of muscle fibers into type I fibers (slow-twitch fibers) and various type II fibers (fast-twitch fibers) is also directly correlated with the preferred metabolic pathway of the specific muscle type. Whereas type I fibers predominantly use aerobic metabolism and are thus less susceptible to fatigue, type II fibers are endowed with high anaerobic glycolytic potential and, as such, permit high maximum contractile velocity, but at the same time they are prone to faster fatigue. Exercise MRS of phosphorus metabolism is the ideal modality for exploring these key aspects of muscle physiology at rest and during exercise. While muscle biopsy continues to be the gold standard, MRS has the advantage of being noninvasive and can be repeated at will. Currently, numerous studies are trying to establish whether the distribution of the fiber types is genetically determined or is the result of various adaptation processes. The debate is ongoing, since there are currently several arguments to support each of the two viewpoints. A study by the present authors found clear evidence of utilization of the various metabolic patterns and their correlation with the different muscle fiber types.8 For example, a sharp drop in the pH value was correlated with a higher concentration of type IIb fibers, and an unchanged pH value during exercise was associated with a predominance of type I muscle fibers. The findings to date would seem to suggest that genetic factors are primarily responsible for the pattern of chemical reactions but that muscle training can achieve redistribution of muscle fiber types, albeit on a lesser scale.

%

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Glycolysis

ATP hydrolysis Creatine phosphate hydrolysis

100 Oxidation 50 Glycolysis 0 0 10

30

50

70 90 110 Exercise time (s)

130

150

Fig. 10.1 Temporal course of energy supply during exercise. Schematic drawing.

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The Muscles

To date, MRS has been deployed to investigate various forms of impaired muscle energy metabolism, with exercise MRS yielding the most interesting and clinically relevant insights.

Glycogenosis McArdle’s syndrome is also known as type V glycogen storage disease. This is an autosomal-recessive hereditary genetic defect, where, because of a defect in myophosphorylase, an isoform of the enzyme glycogen phosphorylase, glycogen can no longer be converted to glucose 1-phosphate in the muscle. 31P exercise spectroscopy was able to provide compelling evidence of the theoretically expected manifestations. A massive decline in phosphocreatine concentration with failure of normal acidosis was observed during exercise. Glucose infusion corrects this imbalance and increases muscle energy metabolism, despite the low pH value.4,43,54 In the presence of phosphofructose kinase deficiency (type VII glycogenosis, or Tarui’s disease), it is not possible to convert fructose 6-phosphate to fructose 1, 6-bisphosphate, disrupting the degradation steps determining glycolysis velocity. MRS was able to detect an increased phosphomonoester peak, corresponding to the accumulation of fructose 6-phosphate in the glycolytic pathway. Concomitant manifestations include only slight intracellular acidosis, attributable to impaired glycolysis and reduced lactate production. Similar findings are observed in patients with phosphoglyceratmutase deficiency (type X glycogenosis). Phosphoglyceratmutase is another glycolytic enzyme that catalyzes conversion of 2-phosphoglycerate to 3-phosphoglycerate (and vice versa).14,55

Mitochondrial Disease Extensive experiences have been gained from spectroscopic studies of patients with respiratory chain defects. Such defects include, for example, NADH-CoQ reductase deficiency, as repeatedly implicated in the slow recovery of phosphocreatine after exercise. MRS documents how a deficiency in the respiratory chain enzyme complex III reduces the ratio of phosphocreatine to inorganic phosphate and delays recovery of metabolite concentrations following exercise. Likewise, MRS was able to demonstrate an improvement in symptoms after administration of vitamin K3 and vitamin C, which replace the missing reductase complex.3 Other types of mitochondrial myopathy include abnormalities caused by a reduced ratio of phosphocreatine to inorganic phosphate and/or an increased concentration of inorganic phosphate at rest as well as prolonged acidosis following exercise. More in-depth studies of mitochondrial encephalopathy conducted by the present authors produced variable MRS results. Exercise MRS proved to be far superior to the spectroscopic findings documented in the resting state, which showed only a slight decrease in the signal intensity of the phosphocreatine peak. By contrast, exercise spectroscopy was able to demonstrate myopathic abnormalities with high sensitivity. Characteristic findings included delayed and incomplete decline in the phosphocreatine concentration during exercise, slow recovery rate, and absence of an exercise-induced decline

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in the pH value, with a tendency toward alkalosis. These changes correlated with the clinical severity of disease and are more sensitive than clinical tests.38

Muscular Dystrophy and Spinal Muscular Atrophy To date, MRS has also been used to investigate muscular dystrophy (e.g., Duchenne’s muscular dystrophy) as well as various types of spinal muscular atrophy (Werdnig–Hoffmann’s disease and Kugelberg–Welander’s disease). Analysis of the metabolite concentrations measured on MRS in the resting spectrum revealed a reduced ratio of phosphocreatine to nucleoside triphosphate as well as reduced ratio of phosphocreatine to inorganic phosphate, abnormally high pH value, and pathologically elevated phosphodiester peak, which continued to rise sharply during muscle exercise.

Myositis Myositis has been investigated by means of both 1H and 31P spectroscopy.63 1H spectroscopy proved to be particularly good at demonstrating the distribution between fat and water in the muscles. Normal leg muscle contains 5 to 7% fat; detection of fatty acid resonances on 1H spectroscopy is challenging without water suppression. No major changes are observed in the fat and water resonances in acute myositis. However, a moderate increase is seen in the T1 time, reflecting inflammatory and edematous tissue changes. The findings identified in chronic myositis include fatty muscular degeneration as well as, on 1H spectroscopy, mono- and polyunsaturated fatty acids (5.4 ppm), carbonyl groups (2.3 ppm), and terminal methyl groups (1.1 ppm). In the phosphorus spectrum, patients with acute myositis exhibit a sharp decline in phosphocreatine levels relative to nucleoside triphosphate, whereas the concentration of inorganic phosphate continues to be within the normal range; additional peaks of phosphomonoester and phosphodiester are also seen. These lines are thought to reflect sugar phosphates metabolized in the anaerobic phase of the glycolytic pathway. The reduction in phosphocreatine levels attests to the increased consumption of the phosphocreatine pool during ATP synthesis. In chronic myositis, the concentration of all phosphorus metabolites is greatly reduced; therefore, the spectrum appears normal at first sight. Since only the inorganic phosphates have a normal concentration, the ratio of inorganic phosphate to the unchanged β-nucleoside triphosphate concentration is increased. The decrease in signal intensity of the phosphorus components is proportional to the extent of muscular degeneration but is independent of the underlying disorder.

10.3 Anatomy 10.3.1 General Anatomy ▶ Fig. 10.2 provides a schematic illustration of the cross-sectional anatomy of the extremities. The fasciae are outlined to facilitate identification of the muscle compartments. The muscle compartments are the spaces along which inflammatory and necrotic muscle diseases spread:

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Magnetic Resonance Spectroscopy for Impaired Muscle Energy Metabolism

10.3 Anatomy Anterior Brachial fascia

Lateral

Medial

Posterior Musculocutaneous nerve Cephalic vein Biceps brachii

Coracobrachialisc

Medial brachial intermuscular septum

Median nerve Ulnar nerve Brachial artery and vein

Humerus

Triceps brachii (medial head)

Lateral brachial intermuscular septum

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Radial nerve Deltoid

Triceps brachii (lateral head) Musculocutaneous nerve

Axillary nerve

Radial nerve

a

Anterior Lateral

Medial

Posterior

Medial brachial intermuscular septum Cephalic vein Musculocutaneous nerve Triceps brachii (long head)

Biceps brachii (short head) Brachial fascia Median nerve Basilic vein Ulnar nerve Brachial artery and vein

Brachialis

Humerus Lateral brachial intermuscular septum Deep brachial artery and vein Radial nerve Triceps brachii (lateral head)

Musculocutaneous nerve

Triceps brachii (long head) Triceps brachii (medial head)

Radial nerve

b

Fig. 10.2 Muscle anatomy on MRI. Cross-sections of arms and legs. The fascial compartments, as the potential sites implicated in the spread of inflammatory processes, are outlined. Color coding of muscles innervated by the same nerve to facilitate recognition of changes in signal intensity due to impaired muscle innervation. (a) Upper arm, proximal. (b) Upper arm, medial.

447

The Muscles

Medial brachial intermuscular septum

Anterior Lateral

Medial

Posterior Cephalic vein

Biceps brachii Brachial artery and veins

Brachioradialis

Basilic vein Brachial fascia

Brachialis Radial nerve Deep brachial artery and vein

Median nerve Medial antebrachial cutaneous nerve Superior collateral ulnar artery and vein

Humerus

Lateral brachial intermuscular septum

Triceps brachii (tendon) Musculocutaneous nerve

Radial nerve

c

Pronator teres

Flexor digitorum superficialis (+ tendon)

Anterior Antebrachial fascia

Cephalic vein Brachioradialis

Lateral

Medial

Posterior Flexor carpi radialis Palmaris longus

Extensor carpi radialis longus (+ tendon)

Septa of the antebrachial fascia Medialantebrachial cutaneous nerve

Supinator Radius

Ulnar artery and vein Ulnar nerve

Extensor carpi radialis brevis

Flexor carpi ulnaris (+ tendon) Basilic vein Medial antebrachial cutaneous nerve Flexor digitorum profundus Median nerve Anterior interosseous artery and vein

Abductor pollicis longus Extensor pollicis longus Extensor digitorum Extensor digiti minimi Extensor carpi ulnaris Ulna Radial nerve

Radial nerve, deep branch

Ulnar nerve

Palmar interosseous nerve (of the median and ulnar nerves)

Median nerve

Interosseous membrane

d

Fig. 10.2 Continued. Muscle anatomy on MRI. Cross-sections of arms and legs. The fascial compartments, as the potential sites implicated in the spread of inflammatory processes, are outlined. Color coding of muscles innervated by the same nerve to facilitate recognition of changes in signal intensity due to impaired muscle innervation. (c) Upper arm, distal. (d) Forearm, proximal.

448

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Ulnar nerve Triceps brachii (long head) Triceps brachii (medial head)

10.3 Anatomy

Flexor carpi radialis (+ tendon) Radial artery and veins

Anterior Ulnar Radial

Antebrachial fascia Palmaris longus (+ tendon)

Brachioradialis (tendon) Radial nerve, superficial branch

Posterior

Flexor digitorum superficialis (+ tendon)

Pronator teres Cephalic vein

Septa of the antebrachial fascia

Extensor carpi radialis longus (tendon)

Flexor carpi ulnaris (+ tendon)

Extensor carpi radialis longus (tendon) Radius

Flexor digitorum profundus (+ tendon)

Flexor pollicis longus

Interosseous membrane

Abductor pollicis longus Extensor pollicis brevis

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Basilic vein Ulna Extensor indicis

Extensor pollicis longus Extensor digitorum (+ tendon)

Extensor carpi ulnaris (+ tendon)

Extensor digiti minimi (+ tendon)

Radial nerve, deep branch

Median nerve

Median nerve, palmar interosseous branch

Ulnar nerve

Palmar interosseous nerve (of the median and ulnar nerves)

e

Flexor carpi radialis (tendon) Radial artery and veins

Anterior Ulnar Radial

Antebrachial fascia Palmaris longus (+ tendon)

Flexor pollicis longus Brachioradialis (tendon) Radial nerve, superficial branch

Posterior Flexor digitorum superficialis (+ tendon) Septa of the antebrachial fascia

Abductor pollicis longus (+ tendon)

Flexor digitorum profundus (+ tendon)

Extensor pollicis brevis (+ tendon)

Flexor carpi ulnaris

Cephalic vein Extensor carpi radialis longus (tendon) Extensor carpi radialis brevis (tendon) Extensor digitorum Extensor pollicis longus (+ tendon) Radial nerve, deep branch

Median nerve

Median nerve, palmar interosseous branch

Ulnar nerve

Pronator quadratus Interosseous membrane Extensor indicis (+ tendon) Extensor digiti minimi (+ tendon)

Extensor carpi ulnaris (+ tendon)

Palmar interosseous nerve (of the median and ulnar nerves)

f

Fig. 10.2 Continued. Muscle anatomy on MRI. Cross-sections of arms and legs. The fascial compartments, as the potential sites implicated in the spread of inflammatory processes, are outlined. Color coding of muscles innervated by the same nerve to facilitate recognition of changes in signal intensity due to impaired muscle innervation. (e) Forearm, medial. (f) Forearm, distal.

449

The Muscles Anterior

Iliotibial tract

Vastoadductor membrane

Lateral Medial Posterior Great saphenous vein

Sartorius

Rectus femoris Deep femoral artery and vein

Femoral artery, vein and nerve

Tensor fasciae latae Vastus lateralis

Medial intermuscular septum

Vastus intermedius Vastus medialis

Obturator nerve (anterior branch)

Femur

Adductor brevis Gracilis Obturator nerve (posterior branch)

Lateral intermuscular septum Iliotibial tract

Adductor magnus

Sciatic nerve

Fascia lata

Biceps femoris (long head, tendon)

Semitendinosus Semimembranosus (tendon)

Obturator nerve, anterior branch

Inferior gluteal nerve

Superficial gluteal nerve

Tibial nerve

Obturator nerve

Femoral nerve

g

Medial intermuscular septum

Iliotibial tract

Anterior Fascia lata

Rectus femoris Vastus lateralis Vastus intermedius Femur

Lateral Medial Posterior Femoral nerve, anterior cutaneous branch Vastus medialis Sartorius Vastoadductor membrane

Linea aspera Biceps femoris (short head)

Great saphenous vein Saphenous nerve

Adductor magnus

Gracilis

Lateral intermuscular septum

Femoral artery and vein Adductor longus Posterior intermuscular septum

Sciatic nerve Biceps femoris (long head) Semitendinosus

Semimembranosus

Femoral nerve

Obturator nerve, anterior branch

Obturator nerve

Common peroneal nerve

Tibial nerve

h

Fig. 10.2 Continued. Muscle anatomy on MRI. Cross-sections of arms and legs. The fascial compartments, as the potential sites implicated in the spread of inflammatory processes, are outlined. Color coding of muscles innervated by the same nerve to facilitate recognition of changes in signal intensity due to impaired muscle innervation. (g) Thigh, proximal. (h) Thigh, medial.

450

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Posterior intermuscular septum

Gluteus maximus

10.3 Anatomy

Quadriceps tendon Suprapatellar fat pad

Anterior Lateral

Medial

Posterior Vastus intermedius

Vastus lateralis

Femur Iliotibial tract

Vastus medialis Femoral artery and vein Adductor magnus (tendon)

Lateral intermuscular septum

Fascia lata

Biceps femoris (short head)

Sartorius

Common peroneal nerve

Great saphenous vein

Biceps femoris (long head) Vastoadductor membrane Gracilis (+ tendon)

Medial intermuscular septum

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Posterior intermuscular septum

Semitendinosus (+ tendon)

Semimembranosus (+ tendon) Obturator nerve, anterior branch

Common peroneal nerve

Tibial nerve

Femoral nerve

i

Anterior Interosseous membrane

Patellar ligament Tibialis anterior Extensor digitorum longus

Lateral

Medial

Posterior Tibia Gracilis (tendon)

Anterior crural intermuscular septum

Crural fascia Popliteus

Tibialis posterior

Semitendinosus (tendon)

Peroneus longus Great saphenous vein

Fibula Common peroneal nerve

Deep crural fascia

Posterior crural intermuscular septum

Popliteal artery and vein Tibial nerve

Soleus

Plantaris (tendon)

Gastrocnemius (lateral head)

Gastrocnemius (medial head) Small saphenous vein Medial cutaneous sural nerve

Deep peroneal nerve Superficial peroneal nerve

Tibial nerve

j

Fig. 10.2 Continued. Muscle anatomy on MRI. Cross-sections of arms and legs. The fascial compartments, as the potential sites implicated in the spread of inflammatory processes, are outlined. Color coding of muscles innervated by the same nerve to facilitate recognition of changes in signal intensity due to impaired muscle innervation. (i) Thigh, distal. (j) Lower leg, proximal.

451

The Muscles

Anterior

Interosseous membrane

Lateral

Tibialis anterior

Medial

Posterior

Extensor digitorum longus

Crural fascia

Anterior crural intermuscular septum

Tibia Deep crural fascia

Peroneus brevis Deep peroneal nerve

Great saphenous vein Flexor digitorum longus

Superficial peroneal nerve Posterior tibial artery and vein

Peroneus longus

Plantar nerve (tendon) Tibial nerve

Anterior tibial artery and vein Posterior crural intermuscular septum

Tibialis posterior

Fibula Peroneal artery and vein Soleus

Medial cutaneous sural nerve Small saphenous

Gastrocnemius (lateral head)

Tibial nerve

Deep peroneal nerve

Superficial peroneal nerve

k Anterior

Interosseous membrane

Lateral

Tibialis anterior Extensor hallucis longus Extensor digitorum longus

Tibia Great saphenous vein

Anterior crural intermuscular septum

Crural fascia

Superficial peroneal nerve Peroneus brevis

Flexor digitorum longus Tibialis posterior

Deep peroneal nerve Fibula Peroneus longus (+ tendon)

Posterior tibial artery and vein Deep crural fascia Tibial nerve

Posterior crural intermuscular septum

Peroneal artery and veins Soleus

Flexor hallucis longus

Gastrocnemius (tendon)

Sural nerve

Tibial nerve

Deep peroneal nerve

Medial

Posterior

Small saphenous vein

Superficial peroneal nerve

l Fig. 10.2 Continued. Muscle anatomy on MRI. Cross-sections of arms and legs. The fascial compartments, as the potential sites implicated in the spread of inflammatory processes, are outlined. Color coding of muscles innervated by the same nerve to facilitate recognition of changes in signal intensity due to impaired muscle innervation. (k) Lower leg, medial. (l) Lower leg, distal.

452

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Gastrocnemius (medial head)

10.3 Anatomy

●

●

●

●

In the upper arm, a distinction is made between the anterior flexor and posterior extensor compartments. These compartments are separated by the lateral and medial brachial intermuscular septa. In the forearm, the septa of the antebrachial fascia and interosseous membrane create four main compartments (posterior and radial extensor compartments and deep and superficial flexor compartments) as well as the compartments for the flexor carpi ulnaris and the flexor carpi radialis. The thigh is divided by the intermuscular septa of the fascia lata into three main compartments (flexor, extensor, and adductor compartments). In addition, the sartorius muscle compartment is demarcated by the vastoadductor membrane. The lower leg is divided by the crural fascia (superficial and deep layers as well as the anterior and posterior intermuscular septa of the leg) and interosseous membrane into four compartments (superficial and deep flexor compartments and extensor and peroneal compartments).

The ability to assign muscle abnormalities precisely to a specific innervation area helps diagnose diseases.

10.3.2 Specific Magnetic Resonance Imaging and Functional Anatomy Fiber Types The striated skeletal muscles have two different fiber types: ● Type I fibers are rich in mitochondria. ● Type II fibers have relatively few mitochondria.

Type I Fibers Type I fibers are designed for slow contractions over an extended period of time. They obtain most of their energy from oxidation of fatty acids and have a red macroscopic appearance because of their high mitochondrial content (▶ Fig. 10.3a). They are also thought to have relatively high water content due to this large number of organelles. Therefore, on MRI, muscles with a majority of type I fibers exhibit relatively high signal intensity on T2w images.20

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Fig. 10.3 Muscle fiber types. Electron microscopy. (a) Type I: Red or dark muscle fibers, rich in large mitochondria. (b) Type II: Light or white, mitochondria-deficient muscle fibers.

Type II Fibers Type II fibers are designed for rapid, short, and strong contractions. They obtain their energy mainly from anaerobic glycolysis and have a whitish macroscopic appearance due to their small number of organelles (▶ Fig. 10.3b). On MRI, type II fibers have a lower signal intensity on T2w sequences compared with type I fibers.

Diagnostic Magnetic Resonance Imaging The differences identified on MRI between the various muscle fiber types are very pronounced in animals. In humans, the differences in signal intensity between the various muscles of different fiber composition are less pronounced, since the fiber types are intermingled. However, distinct differences are observed from one individual to another. Certain muscles of high-endurance athletes (e.g., marathon runners) have a high proportion of type I fibers, whereas peak-performance athletes (sprinters, etc.) have a preponderance of type II fibers. Using relaxometry, a significant correlation was found between the MRI relaxation times and the proportion of type II fibers in humans.40 Normal muscle exhibits relatively low signal intensity on T1w and T2w images, regardless of the dominant muscle fiber type. Connective tissue septa are devoid of signal. Healthy muscles have higher signal intensity on fat-suppressed images. In healthy individuals, physiologic muscle activity increases perfusion of the muscles and the extracellular unbound water content, in turn increasing the signal intensity on T2w images. The rise in signal intensity is determined by the duration and nature of muscle activity and ranges between 20 and 40% of the baseline value. The signal intensity reverts to normal within 45 to 60 minutes of exercise termination. This manifests as an initial rapid decline in signal intensity, probably due to the quick normalization of perfusion, followed by a slower decline linked to the reduction in the extracellular water content (▶ Fig. 10.4).35 When evaluating the increases in signal intensity induced by physiologic muscle activity, allowances must be made for the variations in the functional anatomy of the different groups of muscles. For example, it has been demonstrated that, in around 25% of individuals imaged, parts of the flexor digitorum

453

The Muscles

T2 (ms)

T1w

T2w

Normal

Hypertrophy

Hypotrophy Time (minutes) Atrophy Fig. 10.4 T2 relaxation times of finger flexors (flexor digitorum profundus and superficialis muscles) after 5-minute hand grip exercises. Rapid increase in T2 time within first minutes of exercise termination (over 40%). Biphasic decline in the recovery phase: rapid initial normalization (decline in hyperemia) and slow normalization in late phase (reabsorption of extracellular water) up to 50 minutes after exercise termination (see study by de Kerviler et al35).

Edema

Necrosis

Fibrosis Fig. 10.5 MRI visualization of basic patterns of healthy and pathologic muscles. Schematic drawing.

●

Variants (Developmental Anomalies) Among the muscular variants observed are different abnormalities linked to developmental anomalies. Radiologists should be familiar with these variants in order to interpret the computed tomography (CT) and MR images correctly and avoid mistakes: ● Aplasia: “Aplasia” means the congenital absence of a muscle, despite the anlage being present. This leads to asymmetry that becomes clinically manifest, in particular, during periods of growth or when engaging in athletic activities, and is generally initially misinterpreted as muscle wasting. However, MRI is adept at distinguishing between fatty atrophy (hyperintense muscular remnant) and congenital aplasia (no musculature). Typical examples are as follows: ○ Palmaris longus aplasia. ○ Pectoralis major and/or minor aplasia (special type: aplasia of the sternal head of the pectoralis major combined with other anomalies = Poland’s syndrome). ○ Trapezius aplasia. ● Hypoplasia: Hypoplasia is suspected following bilateral comparison of reduced muscle diameter on MRI, with normal signal intensity and normal fat content in the intramuscular spaces. This can only be confirmed on histology. ● Hyperplasia: In hyperplasia, the muscle diameter is increased but the intramuscular fat content is normal, unlike in hypertrophy (see Hypertrophy p. 455). Hyperplasia must not be

454

●

●

mistaken for space-occupying tumors. One example is hypertrophied palmaris longus, which can manifest as a tumor in the forearm. Supernumerary muscles: Supernumerary muscles may result from double anlage of a muscle belly (e.g., extensor carpi radialis accessorius) or a completely independent muscle anlage with separate origin and insertion (e.g., extensor carpi radialis intermedius). Accessory muscles may manifest clinically as soft tissue tumors. Other examples are the peroneal tertius and quartus muscles and tensor fasciae suralis (popliteal mass) (see respective chapter). These structures can be identified as muscles on MR images from their signal intensity, course, and shape. Fusion: Variable forms of fusion of individual muscle bellies, in particular of the quadriceps, may be seen. Variant insertions: No further details of variant insertions are given here.

Muscle Patterns as Seen on Magnetic Resonance Imaging Muscle abnormalities and disorders may exhibit certain basic patterns on MRI (▶ Fig. 10.5), which can be important, especially for planning muscle biopsy and monitoring the course of treatment. However, often, it is not possible to arrive at a specific diagnosis based on MRI alone. Once the basic pattern of muscle changes has been identified on MRI, it is necessary to determine whether the process is: ● Focal, multifocal, or diffuse. ● Proximal and/or distal. ● Symmetrical or asymmetrical. ● Has a centrifugal or centripetal course.

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superficialis were not used for finger flexion; instead, they were being used for carpal flexion. Therefore, the increases in signal intensity resulting from exercise can have very different distribution patterns. Another example revealed that after handgrip exercises, the flexor digitorum superficialis and profundus muscles as well as the flexor carpi ulnaris of all individuals exhibited increased signal intensity, but only 50% of these persons showed increased signal of the extensor carpi ulnaris and supinator muscles.17 Therefore, in view of the physiologic phenomena outlined, diagnostic MRI of myopathy should not be performed after engaging in athletic activities, since, otherwise, physiologic changes in signal intensity could be mistaken for pathologic muscle edema.

Pseudohypertrophy

10.4 Neuropathy

Hypertrophy

Edema

The increase in muscle size, for example, due to increased exercise, leads to hypertrophy. The muscle diameter is larger, but no changes in signal intensity are seen on MRI. The intermuscular layers of connective tissue are reduced, with virtually no intermuscular fat lines seen on MR images. Unilateral cases of hypertrophied paired muscles may be mistaken clinically for soft tissue tumors, resulting often in unnecessary biopsies. MRI can easily produce a correct diagnosis. Potential causes of unilateral hypertrophy include incorrect loading and overloading with static implications (e.g., following corrective osteotomy), fractures with impaired healing, scoliosis, static disbalance in association with sensorimotor neuropathy (e.g., diabetes mellitus), and also teeth grinding (asymmetrical hypertrophy of the masticatory muscles).56 Ilaslan et al31 reported on seven cases of unilateral hypertrophy of the tensor fasciae latae, where a biopsy was taken in three cases because of suspected soft tissue tumor of the anterior thigh. Hypertrophy is also observed in the presence of endocrine diseases, for example, endocrine orbitopathy,10 hypothyroidism, and Cushing’s disease.20

There are several diseases that cause muscle edema, with increased fluid accumulation in the extracellular space: ● Trauma. ● Rhabdomyolysis. ● Intramuscular bleeding. ● Tumors. ● Polymyositis. ● Other types of myositis. ● Denervation (early stage). ● Radiation and overloading.

A decrease in the size of muscle cells due to reduced muscular activity results in hypotrophy. The muscle diameter is reduced, but the muscle continues to exhibit normal signal intensity on MRI. The intermuscular connective tissue spaces are enlarged and increasingly filled with fat, with identification of more areas of hyperintense muscle striation, especially on T1w images.

Atrophy Several diseases as well as lack of muscular activity cause atrophy. The muscle diameter of atrophied muscles is greatly reduced but with increased inter- and intramuscular fat deposition. This gives rise to areas of diffuse to multifocal patchy hyperintensity on T1w and T2w images. Since muscle tissue exhibits a relatively uniform response to different harmful substances, myriad diseases can result in atrophy, for example: ● Denervation (late stage). ● Inflammation. ● Dystrophy. ● Necrosis. ● Trauma. Irreversible muscle damage can occur depending on the duration and severity of damage and the treatment prescribed.

Pseudohypertrophy Pseudohypertrophy may be observed in association with various types of muscular dystrophy. In this setting, inter- and intramuscular fat deposition secondary to destruction of the muscle cells is so widespread that the muscle cross-section measurements increase despite muscle wasting. MRI demonstrates the enlarged muscle diameter as well as areas of homogeneous to multifocal patchy hyperintensity corresponding to intramuscular fat deposition. Pseudohypertrophy can also result from connective tissue remodeling in muscle.

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Hypotrophy

Edema gives rise to hyperintensity on T2w and, in particular, on fat-suppressed sequences. Often, no changes in signal intensity or only discrete areas of reduced signal are seen on T1w images. The muscle volume is normal or slightly increased, depending on the extent of edema.

Necrosis Extensive muscle damage, for example, secondary to infection, injury, ischemia, and rhabdomyolysis, with irreversible destruction of muscle tissue, can eventually result in necrosis. Muscle necrosis generally manifests as areas of focal reduced signal intensity (or no change in signal intensity) on T1w images and areas of increased signal intensity on T2w images. Whether infective necrosis (abscess) is involved cannot often be concluded from the signal pattern or morphology. Intravenous administration of paramagnetic contrast medium (CM) helps resolve this issue, since intense peripheral CM enhancement is more suggestive of an abscess. A large area of edema with corresponding signal pattern (see above) is generally observed in the surrounding muscle adjacent to the necrotic zone. Ischemic muscle necrosis is observed, for example, among diabetics, in particular in those suffering from type 1 diabetes mellitus or inadequately controlled type 2 diabetes mellitus (diabetic muscle infarction). Muscle infarctions mainly affect the muscles of the thigh.1,48 Ischemic necrosis can be mistaken for an abscess, a tumor, or myositis. Defective healing is followed by hypointense intramuscular scarring and/or replacement of the destroyed muscle segments with fatty tissue.

Fibrosis In addition to atrophy and necrosis, chronic or severe muscle damage can result in a third type of muscle reaction: fibrosis. This is associated with reduced muscle mass and increased fibrous connective tissue. This relatively rare type of scar fibrosis is encountered, for example, in congenital torticollis. The diameter of the affected muscle is reduced, manifesting as reduced signal intensity on T1w and T2w images.

10.4 Neuropathy Damage to peripheral nerves secondary to trauma or chronic or acute compression, etc., has been classified by Seddon on the basis of three degrees of severity59: ● Neuropraxia (type I): Nerve commotion without discontinuity; clinical signs of impaired neural function; no evidence of

455

The Muscles Lesion

Regeneration

Time (days)

Fig. 10.6 Muscle denervation. PDw fatsat image. Increase in signal intensity of forearm muscles innervated by the median nerve (arrow) pointing to acute or subacute denervation.

●

●

muscle atrophy or denervation potentials in the affected muscle on electromyogram (EMG). Axonotmesis (type II) (partial): Discontinuity of the axons, but neural sheaths preserved; clinical signs include impaired nerve conduction of several months’ duration; EMG shows evidence of denervation potentials in affected muscle. Neurotmesis (type III): Nerve contusion with complete severance of neural fibers and neural sheaths; clinical signs of persistent neurologic deficits; EMG shows evidence of denervation potentials in affected muscle; this type has been further classified by Sunderland into grades 3 to 5.61

In types II and III neural lesions, MRI is able to detect changes in the affected muscles. Denervation is thought to result in relative shrinkage of the myofibrils of the affected muscle, with compensatory hypertrophy of the extracellular space. This manifests as a prolonged T2 relaxation time of the muscle.7,49 Irreversible denervation eventually leads to compensatory fat deposition and, in turn, to a shorter T1 relaxation time. These alterations in the relaxation time are reflected in changes in signal intensity on MRI: ● Acute to subacute denervation: Acute to subacute denervation manifests as homogeneous hyperintensity on T2w images but with no major changes in signal intensity observed on T1w images.34 STIR sequences, showing marked hyperintensity, are particularly sensitive in detecting these changes. The affected muscles exhibit a specific signal pattern, reflecting their innervation pathways (▶ Fig. 10.6). Familiarity with these muscle innervation pathways is, therefore, important for correct interpretation of the images. A distinction can be made between root, plexus, and peripheral lesions on the basis of the innervation pattern. In animal experimental studies, it was possible to detect changes in signal intensity already after 24 hours, whereas in clinical human studies these were observed after 4 days.7,68 Persistent lesions manifest as progressive hyperintensity. Reinnervation leads to restoration of normal signal intensity within a period of around 10 weeks (▶ Fig. 10.7).67 As such, MRI may be valuable in monitoring treatment of neural lesions. Persistent denervation is relatively soon evidenced as hypotrophy of the affected muscle. Detection of a combination of hypotrophy, edema, and a peripheral innervation pattern of muscle

456

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damage on MRI should, therefore, be interpreted more as neural rather than primary muscle damage. Chronic denervation: Chronic denervation results in muscle atrophy, with compensatory increase in fatty tissue, manifesting as hyperintensity, in particular on T1w images, and as moderate hyperintensity on T2w images. By contrast, on STIR images, the areas with fat deposition appear hypointense. Chronic progressive nerve damage may be caused by compression, tumors, etc. The implicated nerve compression site(s) can be identified on the basis of the denervation pattern.36,56

10.5 Myotonic Disorders Myotonic disorders result from increased muscle tone and lead to delayed muscle relaxation following voluntary movements. The underlying cause is dysfunctional muscle ion channels.27 No specific changes are seen on MRI.

10.6 Muscular Dystrophy Progressive muscular dystrophy comprises a group of hereditary muscle diseases associated with progressive degeneration of muscle fibers and compensatory proliferation of fatty and connective tissue. Several types have been characterized. In terms of etiology, these diseases are thought to derive from genetic mutations that cause defects in, or absence of, muscle proteins. The abnormalities associated with muscular dystrophy can be identified on MRI, especially on T1w sequences, where they manifest as areas of multifocal to extensive hyperintensity of the affected muscle due to fatty tissue proliferation. Initially, there is an increase in the volume of the implicated muscle, identifiable as pseudohypertrophy. As the disease progresses, the muscle volume declines, now manifesting as muscle atrophy. Fat deposition in muscle (and initially also muscle edema) is seen as areas of increased signal intensity on T2w images. The extent of intramuscular fat deposition, and accordingly the degree of hyperintensity on MRI, is well correlated with the clinical stage of disease.57 In muscular dystrophy, the affected muscles exhibit a varied, generally symmetrical signal pattern, depending on the implicated type of dystrophy and the duration of disease. In

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Fig. 10.7 Reversible muscle denervation. Relative signal intensity (SI) of musculature following reversible denervation (T2w MRI sequences). Marked increase in signal 15 days after denervation. Slow normalization of signal over more than 100 days following injury.

10.7 Inflammatory Myopathy

● ● ● ●

Fig. 10.9 Duchenne’s muscular dystrophy. Schematic drawing, crosssection of the thigh. Increased muscle volume and signal intensity (T1w and T2w contrast) due to fatty infiltration (pseudohypertrophy). The rectus femoris, sartorius, gracilis, and semitendinosus are unaffected. 1, rectus femoris; 2, sartorius; 3, gracilis; 4, semitendinosus.

Duchenne’s muscular dystrophy, changes in the gastrocnemius muscles are often seen early on. Besides, the gluteus maximus, adductor magnus, quadriceps, and biceps femoris show signs of pathologic remodeling processes. In the upper leg, only minor changes are seen in the gracilis, sartorius, rectus femoris, and semitendinosus muscles (▶ Fig. 10.8 and ▶ Fig. 10.9).41,57 These muscles may initially undergo compensatory hypertrophy with increased volume but normal signal intensity. In the lower leg, the tibialis anterior and posterior as well as the peroneal muscles may continue to be largely unaffected. Of the trunk muscles, the psoas often continues to appear normal, but, conversely, abnormalities of the longissimus and iliocostalis muscles are detected early on.26 The extent of fat deposition in muscular dystrophy is not well correlated with the duration of disease but is a good correlate of the clinical severity of muscle weakness.45

10.7 Inflammatory Myopathy Inflammatory myopathy may be caused by different disorders: ● Idiopathic myositis (dermatomyositis, polymyositis, and inclusion body myositis). ● Autoimmune myositis. ● Infectious myositis (bacterial, viral, parasitic, and mycotic).

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Fig. 10.8 Duchenne’s muscular dystrophy. Cross-section of the thigh. (a) PDw SE sequence. Symmetrical increase in signal intensity and decrease in volume of thigh muscles due to fat deposition and atrophy. The rectus femoris, sartorius, and gracilis as well as the knee flexors are relatively unaffected. g, gracilis; r, rectus femoris; s, sartorius. (b) T2w SE sequence. Increase in signal intensity of the thigh muscles due to fat deposition and, to some extent, also muscle edema. b, biceps femoris; m, semimembranosus; t, semitendinosus.

Granulomatous myositis. Paraneoplastic myositis. Focal myositis. Myositis in association with vasculitis.

Polymyositis, dermatomyositis, and inclusion body myositis are the most common diseases belonging to the heterogeneous group of idiopathic inflammatory myopathy disorders.12 The inflammatory processes taking place within the muscles lead to accumulation of extracellular water, manifesting as muscle edema. On MRI, this edema produces nonspecific changes in signal intensity: ● No changes in signal intensity or slightly reduced signal intensity on T1w images. ● Hyperintensity on T2w and, in particular, on fat-suppressed sequences.30 The damage resulting from chronic myositis causes atrophy of the affected muscle, with compensatory proliferation of fatty tissue. Such lipomatous transformation processes can be detected within 1 year by the latest,6 manifesting on MRI as areas of multifocal, linear, or extensive hyperintensity on T1w and T2w images. In general, it is not possible to arrive at a specific diagnosis from the signal pattern exhibited by the affected muscles. However, the signal distribution pattern detected on MRI can be useful when planning a biopsy, since, on that basis, an active inflammatory process can be easily distinguished from fatty atrophy. The following special features, as seen on MRI, for idiopathic and infectious myositis have been described.

10.7.1 Polymyositis, Dermatomyositis, and Inclusion Body Myositis Studies conducted to date on patients with polymyositis or dermatomyositis have demonstrated that the affected muscles exhibit diffuse changes in signal intensity. A typical finding is symmetrical inflammation of the proximal muscles of the lower extremities. The increase in signal intensity varies among the different groups of muscles, with the greatest increase seen in the quadriceps and adductor muscles (▶ Fig. 10.10).6,29 In most cases, no change in signal intensity is identifiable on T1w images.28 By

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The Muscles

10.7.2 Viral and Bacterial Myositis In viral myositis, the affected groups of muscles exhibit diffuse hyperintensity on T2w images.30 In most cases, only one muscle group is involved (see ▶ Fig. 10.10). Myositis may be a concomitant symptom of systemic viral infection (e.g., influenza). Bacterial myositis is also associated with inflammatory-edematous changes in signal intensity as well as intense CM enhancement (▶ Fig. 10.12).

10.7.3 Pyomyositis Purulent myositis is accompanied by isolated or multiple confluent intramuscular abscesses (▶ Fig. 10.13). This type of infection is seen mainly in immunosuppressed patients, often caused by Staphylococcus aureus.5 Muscle enzyme levels may be normal. Areas of partially confluent, polycyclic hypointensity are seen on T1w images,2 and in rare cases, they are surrounded by a hyperintense halo or have overall higher signal intensity than that of normal muscle (▶ Fig. 10.14 and ▶ Fig. 10.15). It is unclear what causes this hyperintense halo, but it may be due to accumulation of paramagnetic substances along the abscess margins.19 The surrounding muscles exhibit normal signal intensity. On T2w images, the abscesses are seen as hyperintense foci, whereas the surrounding muscles may exhibit a homogeneous, slightly hyperintense or isointense pattern (see ▶ Fig. 10.14). Peripheral enhancement may be seen following CM injection (see ▶ Fig. 10.14).

10.7.4 Sarcoidosis

Fig. 10.10 Polymyositis and viral myositis. Schematic drawing, crosssection of the thigh (T2w sequences). (a) Level of the cross-section. (b) Normal findings. (c) Polymyositis, with hyperintensity of quadriceps, adductors, knee flexors, as well as the gluteal muscles. Hyperintensity is homogeneous and varies across the different muscle groups. (d) Viral myositis. Homogeneous hyperintensity confined to quadriceps.

a

Muscular sarcoidosis is relatively rare and generally asymptomatic. In those cases where symptoms are observed, a distinction is made between a nodular and a myopathic type of sarcoidosis. The nodular-type produces characteristic changes on MRI, with central fibrosis, which, however, has only slight signal intensity on all sequences, but in STIR sequences, it is surrounded by an area of hyperintense signal (“dark-star” sign). By contrast, the myopathic form causes only diffuse, nonspecific changes in signal intensity.58

b

Fig. 10.11 Polymyositis. (a) Axial T1w sequence at the level of the thigh. Advanced bilateral fatty atrophy of the posterior thigh muscles. (b) Axial STIR sequence at the level of the thigh. Extensive edematous changes, in particular, of the muscles not affected by fatty atrophy.

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contrast, in association with inclusion body myositis, an asymmetrical, distal pattern of involvement extending to the anterior thigh muscles is seen.12 In some severe cases of dermatomyositis, extramuscular changes in signal intensity can be observed on T2w images because of concomitant edema (▶ Fig. 10.11). The changes in signal intensity may be perimuscular (halo sign) and/ or have a linear subcutaneous distribution. The changes in signal intensity observed on MRI correlate with the clinical (muscle weakness) and laboratory parameters of disease activity (elevated enzyme levels). However, these changes identified on MRI can occasionally persist long after enzyme levels have reverted to normal.29

a

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10.7 Inflammatory Myopathy

b

Fig. 10.12 Bacterial myositis. Young woman with painful red swelling of the upper arm. Strong CM enhancement of inflamed muscles and of surrounding thoracic fascia (arrows) in association with bacterial myositis and fasciitis (streptococci) with fulminant course. (a) Axial contrastenhanced fatsat sequence. (b) Coronal contrast-enhanced fatsat sequence.

Fig. 10.13 Pyogenic myositis of peroneal muscles. (a) T1w SE sequence. Inhomogeneous signal intensity of affected muscles with areas of reduced and increased signal intensity. (b) T2w SE sequence. Increase in signal intensity of affected muscles. Hyperintense foci consistent with abscesses (arrow).

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Fig. 10.14 Pyogenic myositis of the thigh 4 weeks after surgical stripping of the great saphenous vein. Myositis was confirmed by biopsy. (a) Contrast-medium CT. Central ringlike enhancement (arrow) along the course of the vastus intermedius as well as inhomogeneity of the vastus intermedius and medialis muscles. It is not possible to determine the exact extent of the myositic process. Linear thickening of the subcutaneous fatty tissue is consistent with edema. (b) Sagittal T1w image. The central focus exhibits higher signal intensity than that of the surrounding muscles, suggestive of an abscess (arrow). (c) Sagittal T1w image after CM injection. Marked increase in signal intensity of the inflamed muscles as well as central zone with no enhancement, likewise consistent with an abscess (arrow). (d) Transverse T2w image showing the extent of inflammation. There is also involvement of the rectus femoris and vastus lateralis (discrete marginal hyperintensity) as well as central abscess (arrow).

10.8 Muscle Changes after Radiotherapy and Local Chemotherapy 10.8.1 Radiotherapy The changes induced by radiotherapy in the muscles and skin can be detected on MR images. In one study, changes in signal intensity of the muscles, skin, and subcutaneous tissues were observed in patients who had undergone radiotherapy 6 weeks previously for primary bone and soft tissue tumors, with radiation doses of between 59 and 65 Gy.23 These changes consisted of hyperintensity on T2w and STIR sequences as well as CM enhancement. The radiation-induced changes in signal intensity were sharply demarcated, following the outline of the radiation fields. All patients in that study also experienced acute or subacute skin reactions.

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Radiation-induced changes in signal intensity of muscles and other soft tissues should not be mistaken for a neoplastic process. The changes visualized on MRI can be attributed to an inflammatory reaction and increased concentration of extracellular water and can persist for up to 1 year after radiotherapy.23

10.8.2 Local Chemotherapy Similar changes are seen after local intra-arterial chemotherapy, for example, for advanced breast cancer or recurrent rectal carcinoma. It is virtually impossible to target treatment specifically to the tumor, so smaller vessels supplying the muscles and skin are generally also affected, giving rise to the changes described above. It can be very difficult to distinguish such myositic changes from tumor infiltration, and this limits the use of MRI in such settings. The changes in signal induced by local chemotherapy can persist for up to 14 months following completion of chemotherapy.39

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The Muscles

10.9 Traumatic Myopathy

10.9.1 Acute Muscle Overload Muscle damage caused by acute overload is often observed in physically unconditioned individuals. Injuries are caused primarily by athletic activities involving eccentric overload, that is, muscle overloading and elongation. Conversely, concentric muscle action involving muscle shortening rarely causes injury.60 A distinction is made between injuries with onset of symptoms already during exercise (strain, contusion) and those with delayed onset (after 1–2 days) (delayed-onset muscle soreness [DOMS]). Both types of injury can be identified on MRI.

Muscle Strain Muscle strain can first be identified as areas of increased signal intensity at the myotendinous junction on T2w and fat-suppressed images, with no changes generally seen on T1w sequences. The changes in signal intensity observed on T2w sequences completely regress during the healing process, with normalization of changes generally preceded by resolution of the clinical symptoms.11

Delayed-Onset Muscle Soreness DOMS manifests on T2w images as hyperintensity of the affected muscles and is thought to be imputable to edematous changes (▶ Fig. 10.16): ● Initially, a diffuse, predominantly homogeneous increase in signal intensity is seen after 1 to 3 days. ● Signal intensity continues to rise, peaking after 3 to 6 days. Hence, the increased signal intensity is poorly correlated with the clinical manifestations, with maximum hyperintensity seen at a time when pain is already resolving. ● The increased signal intensity still persists in muscles long (for up to several weeks) after resolution of symptoms and of any previously elevated enzyme concentrations. The changes in signal intensity do not necessarily apply to the entire muscle group involved in a muscle action; only one muscle or muscle belly may be affected.18 This may be due to the variations in muscle loading throughout a muscle group. Besides, the signal intensity is highest in proximity to the tendon insertions of the respective muscle.60 Extramuscular changes in signal intensity thought to derive from microbleeding or edema can also be detected in severe cases (see ▶ Fig. 10.16). These extramuscular changes in signal intensity are often seen to encircle the affected muscle like a ring and are similar to the extramuscular changes observed in association with strains and ruptured fibers. There is also widespread interindividual variability in the high-signal distribution patterns during similar muscle actions due to the variations in functional anatomy and innervation pathways. Specific athletic activities predispose to injury of certain muscles. For example, the rectus femoris (sprinter muscle) was found to be implicated in up to 40% of injuries suffered by athletes engaging in activities involving the legs.24 In addition to its role in evaluating pain linked to muscle damage from overloading, MRI is adept at differential diagnosis in ruling out hematomas or fascial herniations.

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10.9 Traumatic Myopathy

Contusion and Strain-Related Injury Fig. 10.15 Pyomyositis of the psoas, bilateral. Axial T2w TSE image. Diffuse increase in signal intensity of the psoas muscles. Hyperintense abscesses surrounding a hypointense capsule, bilateral.

Muscle injuries can be caused by direct contusion or indirectly as a result of strains. The resultant changes in signal intensity on T2w sequences are typically seen at, often peripheral, sites exposed to external force.11

Fig. 10.16 Delayed-onset muscle soreness. Pain in lower leg 3 days after intense exercise. (a) PDw SE sequence. Bilateral increase in signal intensity of gastrocnemius. (b) T2w SE sequence. Marked increase in signal intensity of both heads of gastrocnemius. Besides, perimuscular increase in signal intensity (arrows).

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Muscle Fiber Tears

Full-Thickness Tear

A distinction is made between muscle fiber tears and partial tears. Patients with a muscle fiber tear report pain but without any functional loss of the affected muscle. Discrete changes are seen on imaging; on MRI, there is local edema, methemoglobin (depending on lesion age), and, possibly, fluid accumulations within the muscle and around the fascia (▶ Fig. 10.17), as well as scarred granulation tissue in the later stages (▶ Fig. 10.18).

Full-thickness tears, mainly seen at the transition between tendon and muscle, result in a loss of muscle strength. In the event of retraction of the torn muscle, a muscle-isointense mass may be seen (comparison with contralateral side) and diagnosed further on the basis of the patient history.15 A fluid-filled defect is also

Partial tears entail more extensive injuries seen in association with a loss of strength of the affected muscles (▶ Fig. 10.19). Accordingly, the changes demonstrated on MRI are more extensive; copious amounts of perifascial fluid and, possibly, a defect may be identified, depending on whether there is also fascial damage.13 A more recent system for classification of acute muscle injuries is used to distinguish between direct and indirect injuries and categorize these further (▶ Table 10.1).44

Hemorrhage/Hematomas In addition to a discrete space-occupying hematoma, occasionally diffuse hemorrhage causing swelling of the affected muscle is also seen. Intramuscular hematomas with intact fascia increase pressure within the muscle compartment and present a risk of rhabdomyolysis; a distinction is made between these and intermuscular hematomas associated with fascial avulsion, which can also spread within intermuscular spaces that are not exposed to increased pressure (▶ Fig. 10.20 and ▶ Fig. 10.21). Unabsorbed hematomas may persist as seroma exhibiting fluid-isointense signal.

Fig. 10.17 Muscle fiber tear. Axial STIR image. Status post acute painful sports injury; no functional impairment. Fluid-isointense signal intensity along the fascia and in the vastus intermedius pointing to a muscle fiber tear (arrow).

Fig. 10.18 Muscle fiber tear. The changes are consistent with a healing muscle fiber tear (confirmed on biopsy). (a) Ultrasonography image. Elongated hyperechoic changes in quadriceps muscle (arrow). (b) T2w image. Corresponding hyperintense area (arrow). (c) Subtraction image. CMenhanced image (arrow).

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Partial Tears (Fiber Bundle Tears)

10.9 Traumatic Myopathy Fig. 10.19 Fiber bundle tear. Painful functional impairment of thigh following sports injury. Partial discontinuity of the rectus femoris, with fluidfilled defect and minor retraction (c, arrow) due to fiber bundle tear (partial tear). (a) Axial T1w sequence. (b) Sagittal PDw fatsat sequence. (c) Axial PDw fatsat sequence.

c

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a

b

Table 10.1 Classification of muscle injuries after Mueller-Wohlfahrt et al44 Type of muscle disorder/injury subclassification Indirect muscle disorders/injuries Functional muscle disorder

Type 1: linked to overloading

Type 1A: due to fatigue Type 1B: delayed-onset muscle soreness

Type 2: neuromuscular muscle disorder

Type 2A: linked to spinal column Type 2B: linked to the muscles

Structural muscle injury

Type 3: muscle fiber tear (partial tear)

Type 3A: minor Type 3B: moderate, fiber bundle tear

Type 4: (sub)total tear

Subtotal or full-thickness muscle tear Tendon avulsion

Direct muscle injuries Contusion Laceration

observed. Full-thickness tears that are not repaired eventually cause fatty atrophy of the torn muscle.

the muscle (thickening, duplication) (▶ Fig. 10.22). Clinical manifestations include reduced strength and functional loss.

Avulsion

Muscle Hernias

The term avulsion is used in settings where a muscle tendon is torn from its bony insertion. Avulsion injuries involving a torn bone fragment can be easily detected on projection radiography and are categorized in terms of the implicated trauma. A conclusive diagnosis can be made on MRI if there is only tendon avulsion, without bone involvement. A defect and soft tissue edema are identified at the normal anatomic position of the tendon, and retracted tendon remnants can be observed along the course of

Traumatic avulsion of the fascia enclosing muscles can occasionally result in a defect causing herniation of the underlying muscle through the defect. This phenomenon is typically seen in the region of the peroneal muscles. Clinically, it manifests as a space-occupying mass, whose size is determined by the applied stress. A muscle-isointense protrusion may also be observed on MRI (▶ Fig. 10.23). Hernias rarely give rise to symptoms.

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10.9.2 Chronic Overload

Traumatic Myositis Ossificans

Myotendinitis

Traumatic myositis ossificans may be a sequela of soft tissue injuries, which in the World Health Organization (WHO) classification system are categorized as tumorlike lesions. In total, four

Chronic muscle overloading can cause an inflammatory reaction generally affecting the myotendinous junction. Myotendinitis is visualized on T2w images as areas of discrete hyperintensity within the affected muscle and/or the respective tendon (▶ Fig. 10.24). Typical examples include tennis elbow and typewriter wrist.

Fig. 10.20 Hematoma. Axial schematic diagram. (a) Intramuscular hematoma (1) with intact fascia and increased pressure. (b) Intermuscular hematoma (1) with torn fascia but no increase in pressure.

Fig. 10.21 Hematoma. Axial STIR sequence of lower leg after sports accident. Intermuscular hematoma or seroma in the region of the gastrocnemius.

Fig. 10.22 Avulsion injury. Patient with reduced knee flexion strength after football injury. (a) Axial STIR sequence at the level of the ischial tuberosity. Fluid-filled defect in the biceps femoris and semitendinosus and semimembranosus insertions on the ischial tuberosity following avulsion injury (arrow). (b) Axial slice further distal, with evidence of thickened, seemingly duplicated tendon due to retraction (arrow).

a

b

Fig. 10.23 Muscle hernia. Young patient with pain-free mass on thigh (arrows), whose size is determined by the applied stress. The “mass” is consistent with a herniated portion of a muscle, showing low-grade edematous irritation. (a) Axial T1w sequence. (b) Axial STIR sequence.

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The Muscles

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10.10 Muscle Fibrosis

Fig. 10.24 Myotendinitis of the right gluteus maximus at the origin of its superficial segment at the iliac crest. This female patient complained of exercise-induced pain that responded to anti-inflammatory treatment. (a) Transverse T1w image. No appreciable changes in signal intensity. (b) Transverse T1w image after CM injection. Linear hyperintensity along the course of the gluteus maximus (arrow). (c) Transverse T2*w image (Fast Field Echo [FFE]; see ▶ Table 1.2). Marked hyperintensity at muscle origin (arrow). (d) Coronal fat-suppressed STIR image. Similar findings as in (c).

types of myositis ossificans have been distinguished, with the traumatic type accounting for up to 75% of cases25: ● Traumatic myositis ossificans. ● Local (circumscribed) myositis ossificans. ● Myositis ossificans with paraplegia. ● Fibrodysplasia ossificans progressiva. Two theories have been posited for development of this condition. The first theory implicates traumatic displacement of minute periosteal fragments, whereas the other ascribes this to traumatic differentiation of pluripotent mesenchymal cells to chondroblasts.25 Clinical signs with painful swelling are manifested within the first 2 weeks of injury. MRI demonstrates a nodular intramuscular structure that exhibits homogeneous signal on T1w sequences and heterogeneous signal on T2w images. CM administration is followed by intense enhancement of the variable and concentrically configured signal patterns. The surrounding muscles appear hyperintense on T2w sequences.37 During the subsequent weeks (around 3–8 weeks following trauma), pronounced calcification can be seen, starting at the periphery and progressing toward the center.37 Central calcification gives rise to areas of inhomogeneous hypointensity, whereas

ossified regions are seen as signal void. Since the ossification process begins at the periphery, lesions are characterized by a signal-void halo and an inhomogeneous hyperintense center. As the ossification process becomes further established, there may be fatty transformation of large areas of the lesions secondary to degeneration and necrosis.52 The ossification process is completed after 5 to 6 months, now showing bizarre bone formation (▶ Fig. 10.25). The lesions may shrink or even, in rare cases, be absorbed. With cystic transformation of the center, eggshelllike calcification of the soft tissues may be observed. Areas of hyperintensity reflecting the fat content of the focal myositic lesions are seen, in particular, on T1w images (▶ Fig. 10.26). Detection of fat and concentric layering is an important diagnostic pointer in distinguishing myositis ossificans from parosteal, periosteal, and extraosseous osteosarcomas, chondrosarcomas, osteomas, or chondromas.

10.10 Muscle Fibrosis Repetitive or very severe muscle trauma can result in fibroblastic proliferation and, in turn, in intramuscular fibrous connective tissue hypertrophy. Such changes are seen, for example, in the

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T1w

T2w

2 to 6 weeks

6 to 8 weeks

5 to 6 months

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7 to 10 days

Fig. 10.25 Traumatic myositis ossificans. Schematic drawing of MRI changes (T1w and T2w contrast) observed during the “maturation process.” Initially (7–10 days after traumatic event), a hypointense lesion is seen within the periosseous soft tissues on T1w images and a hyperintense lesion is seen on T2w images. In the course of disease, inhomogeneous areas of signal-void calcifications and/or fat deposits are detected as diffuse or discrete hyperintensity on T1w images as well as a slight change in signal intensity on T2w images. After 6 to 8 weeks, peripheral ossification may result in a signal-void halo, and after 5 to 6 months, extensive ossification often manifests as areas devoid of signal.

Fig. 10.26 Traumatic myositis ossificans. (a) Conventional radiograph. Four weeks after an accident, there is swelling, with extensive calcification as well as areas of fat density around the left hip (arrow). (b) CT shows mass containing calcium-equivalent (curved arrow) and fat-equivalent (arrow) densities. (c) MRI T1w SE sequence demonstrates a mass with very low calcium-equivalent (curved arrow) and hyperintense fat-equivalent (arrow) signals. The fat content is suggestive of mature, relatively advanced myositis ossificans.

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10.13 Secondary Myopathy

10.11 Compartment Syndrome An increase in pressure within a muscle compartment, for example, secondary to trauma or surgery, may result in muscle ischemia. This causes edema and, unless decompression measures are taken, may eventually lead to rhabdomyolysis. On T2w and especially on fat-suppressed images, MRI demonstrates hyperintensity and an increase in the volume of the affected muscle compartment (e.g., tibialis anterior syndrome; ▶ Fig. 10.27). On T1w sequences, at most, a slight decrease in signal intensity is seen. The muscles of the affected compartment exhibit intense, extensive, or partially patchy CM uptake.53 If necrosis is already well established, corresponding CM enhancement defects can be observed.

10.12 Rhabdomyolysis The term rhabdomyolysis denotes the destruction of skeletal muscle cells as a result of various damaging effects (▶ Table 10.2). Muscle damage occurs in phases, starting with pain of rapid onset and, depending on severity, a sharp increase in creatine kinase activity and myoglobinuria. In the subacute regeneration phase, around 1 week after onset of complaints, the symptoms slowly resolve and the laboratory values revert to normal.

Possible complications seen in association with extensive findings are as follows: ● Compartment syndrome due to severe swelling. ● Irreversible muscle necrosis. ● Recurrent rhabdomyolysis. ● Acute kidney failure due to myoglobinemia. ● Hyperkalemia. ● Hypokalemia.42,71 Depending on the extent of damage, a distinction is made between full-blown rhabdomyolysis and subclinical fiber myolysis. MRI demonstrates edematous changes that appear muscle-isointense to hypointense on T1w sequences and hyperintense on T2w images and fat-suppressed sequences. CM enhancement is observed in the acute stages. Depending on the nature of the damage, a focal, multifocal, or diffuse asymmetrical distribution pattern with or without muscle swelling is detected, often affecting the lower extremities. Edematous changes persist on MRI longer than the elevated creatine kinase activity and the clinical symptoms. The transient calcification detected on projection radiographs during the subacute phase generally has no tangible correlate on MRI findings.

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sternocleidomastoid in association with congenital torticollis, and are thought to be caused by obstetric or in utero complications.69 On MRI, the affected muscles exhibit diffuse, homogeneously reduced signal intensity on all sequences and often a decrease in muscle diameter.

10.13 Secondary Myopathy “Secondary myopathy” is a collective term denoting muscle abnormalities presenting in association with endocrine and metabolic diseases, intoxication, or the use of particular types of medication and drugs. MRI is used to demonstrate the extent of damage and for differential diagnostic purposes.

Fig. 10.27 Tibialis anterior compartment syndrome. (a) Coronal T1w SE sequence. Slight bulging of the anterior muscles of the lower right lower leg (arrow); no appreciable changes in signal intensity. (b) Coronal STIR sequence. Marked increase in signal intensity of the tibialis anterior, extensor hallucis longus, and extensor digitorum longus muscles (arrow).

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The Muscles Table 10.2 Various causes and diseases predisposing to rhabdomyolysis6,22

10.14 Muscle Tumors

Type of injury/disorder

Examples

Direct injury

●

Trauma

Muscle infarction

●

Burns

●

Electric shock

On the whole, muscle tumors are relatively rare. One limitation of the use of MRI in this setting is its potential inability to differentiate between the often-extensive tumor-associated edema and tumor infiltration. Tumors are discussed in Chapter 12.

●

Arterial occlusion

●

External compression

●

Diabetic muscle infarction (poorly controlled diabetes)9,47,63

●

Vasculitis

●

Embolisms

●

Muscle training

●

Epilepsy

●

Asthma

●

Tetanus

●

Alcohol

●

Heroin

●

Cocaine

●

Strychnine

●

Hornet/wasp venom

●

Snake venom

●

Amphetamines

●

Barbiturates

●

Amphotericin B

●

Laxatives

●

Diuretics

●

Sedatives

●

Salicylates

●

Lipid reducers (e.g., lovastatin)

●

Azathioprine

●

Carbon monoxide

●

Hypokalemia

●

Hypophosphatemia

●

Diabetic ketoacidosis

Medication, toxins, drugs

Metabolic diseases

Metabolic myopathy Myositis Idiopathic

The principal symptoms associated with endocrine myopathy are proximally pronounced paresis and, possibly, myalgia. The changes visualized on MRI are symmetrical and proximally pronounced, and they generally resolve after treatment (▶ Fig. 10.28).6,20,22

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10.15.1 Signal Variations in Superficial Muscles The use of surface coils, or also arrays of surface coils (phasedarray coils), can give rise to an artificial increase in signal intensity of the superficial muscles in close proximity to the coil, which cannot be corrected by means of the signal equalization algorithms normally used. The coils should not come into direct contact with the skin. Precise positioning of the coils is particularly important for spectroscopy.17

10.15.2 Inversion Recovery Sequences With inversion recovery sequences, in particular, STIR sequences, the distance between the sections should be 20% of the slice thickness, since otherwise artificial section-related signal variations might occur. These should not be misinterpreted as a true increase in muscle signal intensity. Since blood vessels appear particularly hyperintense on STIR sequences, partial volume effects can give rise to discrete areas of hyperintensity, especially in coronal and sagittal sections, and should not be mistaken for pathologic changes.

10.15.3 Misinterpretation of Findings in Association with Denervation To avoid misinterpreting findings in association with denervation, it should be borne in mind that identification of muscle hyperintensity on T2w images is in principle a nonspecific sign that can be caused by numerous disorders. In posttraumatic settings, muscle contusion and rhabdomyolysis must, in particular, be distinguished from acute denervation. Unlike denervation, posttraumatic changes are often accompanied by subcutaneous edema, and the changes in signal intensity do not correspond to the innervation pattern of any particular nerve. Subcutaneous edema resulting from direct trauma resolves after a few weeks, whereas, conversely, the increase in signal intensity secondary to denervation continues to rise in line with persistent neural lesions. Besides, interpretation of acute denervation may be hampered by the presence of innervation anatomic variants.32 Another difficulty is that the signal changes occurring during the course of neural damage are not exhibited at the same time by all muscles within a particular innervation territory, with changes observed in some muscle groups only at a later time. This has been reported especially for the muscles in the ulnar territory of the

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Excessive muscle activity

10.15 Pitfalls in Interpreting the Images

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10.16 Clinical Relevance of Magnetic Resonance Imaging

Fig. 10.28 Myopathy. Myopathy of unknown origin in a female patient with autonomous thyroid adenoma. Over a period of 1 year, this 48-year-old patient had experienced initially progressive, then changing, swelling of both legs (in particular the thigh), more pronounced in the left leg than in the right leg. Muscle biopsy did not show evidence of pathology. Levels of muscle enzyme were within the normal range. On scintigraphy, the thyroid-stimulating hormone (TSH) test revealed an autonomous adenoma. MRI was performed to detect or exclude edematous and/or lipomatous changes and plan a second biopsy, if necessary. (a) Axial T1w overview image for comparison of both legs. Strongly developed thigh muscles (in particular on the left) with rarefication of the intramuscular, normally fatty septa, as seen, for example, in well-exercised patients. However, this patient did not engage in any sporting activity and another discrepant finding is the disproportionately thick subcutaneous fatty tissue. (b) Axial, high-resolution T1w SE sequence. The rarefied intramuscular septa are well delineated. No evidence of fatty muscular atrophy. (c) Axial fast STIR sequence. No evidence of edema. In some cases, superimposition of pulsation artefacts is seen. These findings are interpreted as muscle hypertrophy, are more pronounced on the left, and are possibly in association with endocrine myopathy.

hand, where nerve damage first led to hyperintensity of the ulnar lumbricals and later led to hyperintensity of the first dorsal interosseous and abductor digiti minimi muscles.21 This phenomenon may be due to collateral innervation.

10.16 Clinical Relevance of Magnetic Resonance Imaging MRI of the musculature is endowed with high sensitivity but has only low specificity. Therefore, muscle biopsy is often unavoidable to arrive at a conclusive diagnosis. MRI can be used when planning a biopsy to identify a region with clear evidence of pathologic changes in signal intensity. Efforts should be made to obtain the biopsy from a pathologically altered muscle area that is largely free of necrosis and fatty

deposits. The incidence of false-negative biopsies can be greatly reduced by taking these precautions. With modern MRI scanners granting better access (open scanners and widebore scanners) and nonferromagnetic biopsy systems, it is now possible, thanks to the progress in interventional radiology, to take biopsies in the MRI scanner. This improves diagnostic accuracy. In recent years, different working groups have reported on MRI-guided biopsy of musculoskeletal lesions.51 There is, therefore, reason to believe that this biopsy technique will be used increasingly in the routine clinical setting. MRI can also be used to monitor the treatment course. In numerous muscle diseases, the changes in signal intensity are well correlated with the treatment response and may even be more sensitive than other tests and laboratory values. This can help reduce the need for EMG and laboratory tests.

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The Muscles MRI has a number of decisive advantages over competing radiologic imaging modalities, owing to which, in recent years, it soon became the modality of choice for diagnosis of muscle diseases: ● Thanks to its high soft tissue contrast, MRI is superior to other cross-sectional imaging modalities (ultrasonography and CT) for detailed diagnostic imaging of muscles. ● Compared with ultrasonography, MRI provides greater objectivity (hence with lower investigator dependency and better comparability) and can also image body regions that are not readily assessable to ultrasonography. ● Although CT does not have the aforementioned drawbacks associated with ultrasonography, it has lower soft tissue resolution, is hampered by bone-hardening effects in the case of diagnostic imaging of the extremities, and comes with the inherent risks of ionizing radiation.

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▶ Acknowledgements: We thank Dr. Bianca Stubbe-Dräger (University Hospital Münster, Clinic for Sleep Medicine and Neuromuscular Diseases) and Dr. rer. nat. Harald Kugel (University Hospital Münster, Institute for Clinical Radiology) for their support in researching and assembling the material for this chapter.

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11.1

Examination Technique

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Anatomy

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Generalized Disorders

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Focal Diseases

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Chapter 11

Bone Marrow

11 Bone Marrow 11.1 Examination Technique The imaging characteristics of the bone marrow spaces in special magnetic resonance imaging (MRI) sequences depend on the following factors: ● Distribution of red, hematopoietically active marrow and yellow fatty marrow. ● Density of the trabeculae. ● Age. ● Gender. ● Anatomic region. T1-weighted (T1w) turbo spin-echo (TSE) sequences have proved valuable in bone marrow imaging, since they show high contrast between the hyperintense fatty marrow and the more hypointense hematopoietic marrow and pathologic lesions. However, pathologic lesions within hematopoietic marrow show lower contrast on T1w images, since both exhibit low signal intensity. In principle, only in rare cases are T2w TSE sequences more sensitive than T1w sequences for diagnostic imaging of bone marrow, unlike in virtually all other body regions. That is due, first, to the lower contrast between fatty and hematopoietic marrow and, second, to the fact that both pathologic processes and fatty marrow exhibit similar, and higher, signal intensity. Bone containing both red and yellow marrow often appears more homogeneous on T2w images than on T1w images. While pathologic lesions exhibit increased signal intensity on T2w images, they have lower contrast versus the surrounding bone marrow than on T1w images. Fat-saturated or short-tau inversion recovery (STIR) sequences are very effective for evaluation of bone marrow lesions.75 Fat suppression enhances contrast between lesions and bone marrow. Fat-saturated TSE sequences with long repetition time (TR; ~3,000 ms) and intermediate echo time (TE; ~45 ms) have proved useful. On fat-saturated T2-weighted (T2w) sequences, hematopoietic bone marrow has intermediate signal intensity, similar to that of muscles, whereas yellow bone marrow has lower signal intensity than muscles. Conversely, pathologic changes in bone marrow often exhibit higher signal intensity than those of yellow and red bone marrow on fat-saturated sequences.108 Contrast medium (CM) is generally not needed for detection of pathologic bone marrow changes, but should, on occasion, be used for better identification of a pathologic abnormality. The increase in signal intensity in pathologic processes following CM injection means that now the signal intensity exhibited by the originally more hyperintense marrow space equalizes that of the previously more hypointense lesion, thus decreasing the imaging sensitivity. In this setting, fat-suppressed T1w sequences are important for delineation of CM-enhanced lesions. Although marked enhancement is suggestive of an acute inflammatory, posttraumatic, or tumorous process, it generally cannot differentiate between these processes. CM administration is useful for assessment of extraosseous extension of lesions (e.g., in the spinal canal). The intensity and speed of CM enhancement in bone marrow are determined by the distribution ratio of yellow to red bone

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marrow. When both parameters are higher, the proportion of red bone marrow is greater, which explains why younger patients generally show more intense and faster CM uptake than their older counterparts.77 To demonstrate the dynamic parameters underlying CM enhancement, several high-contrast fast T1w sequences are acquisitioned in succession (dynamic contrastenhanced MRI) and then evaluated. Bone marrow–infiltrating diseases, such as diffuse multiple myeloma or lymphoma, induce faster and more intense CM enhancement (by more than 700%) compared with healthy bone marrow. These parameters revert to normal after successful treatment.95 However, dynamic contrastenhanced MRI has not, to date, become an established modality in routine diagnosis of bone marrow disorders. Opposed-phase gradient-echo (GRE) sequences are endowed with high sensitivity60 for detection of hematopoietic marrow, with hematopoietic marrow exhibiting low signal intensity to signal void. That is due, first, to the opposing phases of the fat and water protons and, second, possibly to the susceptibility effects of iron-containing compounds in hematopoietic cells. However, when interpreting GRE images, it should be borne in mind that bone regions with high trabecular density, such as the apo- and epiphyses, will appear more hypointense than those regions with low trabecular density because of susceptibility effects.107 The intensity of these effects increases with longer TE. The SE phase-contrast technique (chemical shift sequences) can be used to identify the ratio of the fat to the water signal within the bone marrow.101,133 Like the opposed-phase GRE technique, this is based on the chemical shift between the protons of fat and water. Although phase-contrast imaging cannot increase the specificity of bone marrow MRI,34 it does improve sensitivity for detection of bone marrow-infiltrating systemic diseases such as Hodgkin’s disease, non-Hodgkin’s lymphoma, and leukemia. It can also be used to monitor treatment, since it is able to detect early on an increase in the relative fat signal, for example, in association with leukemia. The use of this technique for routine diagnosis of bone marrow disorders is restricted to specialist centers because it is technically demanding and the software needed is not universally available. The introduction of 1.5 T multichannel whole-body MRI scanners in combination with automated table movement now permits high-resolution whole-body MRI scanning from head to toe for the first time. Whole-body scanners with multichannel technology for imaging at 3 T field strengths were also introduced in recent years. Various technical prerequisites must be met for whole-body scanning. These differ from one manufacturer to another; for example, there is the rolling table platform or continuous table movement technique, as used for computed tomography (CT) to generate sequential axial images. With the total-imaging matrix technique, four surface coils are placed on the patient: head–neck coil, two body coils, and the angio coil for the legs. The spine array coil is placed at the patient’s back as transmitter and receiver coil. In total, the system has 32 receiver channels and 76 coil elements. Shorter acquisition times are possible on using techniques that accelerate image acquisition, such as parallel imaging. Whole-body MRI has been used successfully

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M. D’Anastasi, M. Vahlensieck, and A. Baur-Melnyk

11.2 Anatomy secondary ossification centers, the apo- and epiphyses contain inactive fatty marrow and appear to be hematopoietically active only for a short time.45 In adults, hematopoietic marrow is still found in the following regions (▶ Fig. 11.2): ● Proximal metaphysis of the humerus and femur. ● Pelvis. ● Vertebral bodies. ● Ribs. ● Sternum. ● Scapula. ● Calvaria (skullcap). This distribution pattern is established by around the age of 20 years, but widespread variability is seen. With advancing age, conversion of active red marrow to inactive marrow continues at a slower pace or at least an increase is observed in the percentage of the fat content of the hematopoietic marrow. The percentage of fat content of hematopoietically active marrow can even be over 70% in octogenarians. There is broad interindividual variability, and this is probably determined by factors such as disease, athletic activities, and various treatments.

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for screening for bone metastases and hematologic diseases such as plasmacytoma, lymphoma, and histiocytosis X. It is also used for assessment of benign bone diseases predisposing to malignity, for example, multiple cartilaginous exostosis.106 Diffusion-weighted imaging (DWI) is an MRI modality that is able to visualize the brownian molecular motion of water molecules19 and can be used to differentiate various bone marrow diseases. For example, tissues with high cellular density (e.g., tumor tissue) have a lower apparent diffusion coefficient (ADC) value because of narrowing of the extracellular space and the greater density of hydrophobic cell membranes as well as the resultant restricted diffusion. The ADC values of normal bone marrow are relatively low (between 0.2 and 0.5 × 10–3 mm2/s).20,67 Pathologic bone marrow has much higher ADC values of normally between 0.7 and 1.0 × 10–3 mm2/s for metastases and pathologic fractures and between 1.0 and 2.0 × 10-3 mm2/s for osteoporotic and traumatic fractures. However, widespread overlap of these values has been identified in various studies. DWI is also valuable for demonstration of changes in bone marrow in response to treatment of tumor infiltration and is able to differentiate between vital and necrotic tumor tissues.55 Different studies have demonstrated that whole-body DWI is comparable with scintigraphy for detection of bone metastases.36,112

11.2 Anatomy 11.2.1 General Anatomy The bone marrow is one of the largest organ systems in the human body. From the fourth month of embryonic development, bone marrow increasingly assumes the function of hematopoiesis,57 with active hematopoiesis taking place in all bones by the time the fetus is born. During childhood, the need for hematopoiesis declines and increasingly more parts of the bone marrow become hematopoietically inactive. The declining hematopoietic cells are replaced with fatty cells, which continue to increase in numbers and size. Hematopoietically active bone marrow has a red macroscopic appearance, whereas inactive marrow appears yellow because of its high fat content. Conversion of hematopoietically active to inactive marrow begins in the distal phalanges of the hands and feet and slowly progresses proximally to the extremities (▶ Fig. 11.1). In tubular bones, conversion to fatty marrow starts in the diaphysis, continuing to the distal metaphysis and then the proximal metaphysis. Already within a few months of development of the

Vertebrae Sternum Tibia

Femur

Ribs

Age Fig. 11.1 Age-related percentage of hematopoietic marrow in different bones.

Fig. 11.2 Hematopoietic bone marrow (black) in young adult. Often, there is already a preponderance of fatty marrow in the distal femoral metaphysis.

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Bone Marrow

The signal intensities exhibited by bone marrow on MRI are determined by the distribution ratio of its constituents, that is, water, fat, and protein.35 The exact mechanisms involved are still not fully understood. For example, water is found in different aggregate states and, accordingly, displays a range of signal intensity patterns depending on its state: ● Complex-bound water. ● Bound water. ● Unbound (free) water. ● Structured water. Which aggregate state predominates in which tissue is still not exactly clear. Likewise, different fat constituents have different resonance frequencies, for example, the protons in the methyl groups and in proximity to double bonds of unsaturated fatty acids. Besides, the relaxation times of proteins are determined by the state of the protein molecules in different solutions.120 In view of the complexities involved, it remains unclear which of these different components is the chief determinant of signal intensity. Hematopoietically active (red) bone marrow has low signal intensity, which is slightly higher than that of muscle, on T1w images. It exhibits slight hyperintensity on T2w images (▶ Fig. 11.3). With advancing age, the signal intensity of hematopoietic marrow increases on T1w images and is then markedly higher than that of muscle. These age-related changes reflect the greater fat content of hematopoietic bone marrow (see above), leading to a shorter T1 relaxation time with correspondingly higher bone marrow signal intensity.1,23 Hematopoietically inactive (yellow) bone marrow has high signal intensity on T1w images because of its high fat content. On T2w images, it has slightly reduced signal intensity, now similar

to that of the subcutaneous fat. MRI is more sensitive than the human eye in detecting fat in bone marrow. On MR images, bone marrow is classified as inactive if it contains less than 60% fat and, in contrast to adolescent hematopoietic marrow, presumably once it has 20 % fat content.78 Bone marrow appears macroscopically “yellow” only if it has a fat content of around 80%. These differences help explain the discrepancies in the stage of bone marrow development based on the pathologic specimen and the MRI findings. The relative distribution of the principal constituents of bone marrow, that is, water, fat, and protein, in red and yellow marrow is as follows100,127: ● Hematopoietic bone marrow: Around 40% water, 40% fat, and 20% protein. ● Inactive marrow: Around 15% water, 80% fat, and 5% protein. These figures apply to macroscopically distinguishable bone marrow types. They are not absolute figures, as intrarange variations are also seen. For interpretation of the MR images, it is important to be familiar with the distribution patterns of fatty and hematopoietic bone marrow to avoid mistaking, for example, residual hematopoietic marrow for infiltrative processes. Age-related distribution patterns for a number of important bone regions are illustrated in ▶ Fig. 11.4, ▶ Fig. 11.5, ▶ Fig. 11.6, ▶ Fig. 11.7, ▶ Fig. 11.8, ▶ Fig. 11.9, and ▶ Fig. 11.10. A salient feature here is that, regardless of gender, there is a preponderance of certain distribution patterns of fatty to hematopoietic marrow with advancing age (▶ Fig. 11.11): ● Pelvic bones: At a young age, areas of inactive marrow are already seen in the acetabulum and anterior ischium.17 With advancing age, fatty marrow is also observed along both sides of the sacroiliac joints. ● Vertebral bodies: Islands or bandlike collections of fatty marrow, which increase with age, can be observed in proximity to the end plates, in particular in the lower lumber spine.40 This is

Fig. 11.3 Hematopoietic bone marrow. A 41year-old female patient. (a) T1w image of the right knee. Homogeneous reduction in signal intensity in the distal femoral (black arrow) and the proximal tibial marrow space (white arrow). (b) STIR image. Corresponding increased signal intensity consistent with hematopoietic bone marrow (arrow).

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11.2.2 Specific Magnetic Resonance Imaging Anatomy

11.2 Anatomy

Fig. 11.5 Normal, age-related distribution of active and inactive bone marrow in the vertebral bodies. Schematic diagram. (a) Predominantly hematopoietic marrow, with fatty marrow around the basivertebral vessels in childhood. (b) Focal deposits of fatty marrow in the hematopoietic marrow in adulthood. (c) Fatty marrow beneath the superior and inferior end plates in old age.

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thought to be due to the mechanical stress to which the lower spine is exposed. Another distribution pattern seen in the vertebral bodies consists of multiple foci of fatty marrow.99 Overall, the signal intensity of vertebral bodies in elderly people continues to rise because of diffuse fat deposition and may be much higher than that of the muscles. Hence, the intervertebral disks appear increasingly more hypointense on T1w images compared with the vertebral bodies. Calvaria: Likewise, the calvaria (skullcap) has a characteristic distribution pattern of fat and hematopoietic marrow, with fatty marrow observed early on in the occipital, temporal, and frontal bones. Hematopoietic marrow can still be identified in the parietal bone in elderly persons.99 Skull base: After birth, the bones of the skull base also contain hematopoietic marrow, which will have been converted to fatty marrow by adulthood.89 This is thought to be the case for the sphenoid by the age of 2 years.131 Conversion to fatty marrow occurs much later in the clivus. In the base of skull, in addition to bone marrow changes, pneumatization processes have a major impact on the MRI findings. Pneumatization occurs after fatty marrow conversion, with growth of respiratory mucosa and subsequent aeration. Pneumatization progresses rapidly in the sphenoid already between the ages of 1 and 5 years and is generally completed between 12 and 14 years once the sphenoid has stopped growing. The signal intensities identified on MRI during the pneumatization process vary greatly in accordance with the stage and extent of pneumatization, ranging from signal void (pneumatized) through intermediate signal (developed mucosa but no aeration) to fat-equivalent signal (no mucosal development). This situation can be further compounded by the broad variations seen in the presence of hyperand hypopneumatization. The term “arrested pneumatization” or “arrested hyperpneumatization” is used to denote the state where the pneumatization process is brought to a standstill during the mucosal growth phase (▶ Fig. 11.12). Such changes in the skull base should not be mistaken for diseases such as fibrous dysplasia, ossifying fibroma, and chordoma.131

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Fig. 11.4 Normal, age-related distribution of active and inactive bone marrow in the pelvis. Schematic diagram. (a) Hematopoietic marrow throughout the pelvis in childhood. (b) Fatty marrow islands in the acetabular region in adolescence. (c) Fatty marrow islands in the acetabular region and ilium in adulthood. (d) Fatty marrow islands in the acetabulum, ilium, and along the sacral plates in old age.

Fig. 11.6 Normal, age-related distribution of active and inactive bone marrow in the calvaria and clivus. Schematic diagram. (a) Only hematopoietic marrow at birth. (b) Increasingly more fatty marrow islands in the frontal, occipital, and temporal bones and clivus in childhood and adolescence. (c) Adult pattern, with residual hematopoietic marrow in the parietal bone and clivus. (d) Old-age pattern, with no hematopoietic marrow.

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Sternum and clavicle: Hematopoietic marrow is largely uniformly distributed in these structures,74,136 with generally no fatty marrow seen. Humerus: The proximal humeral metaphysis of young adults contains predominantly uniformly distributed hematopoietic marrow. With increasing age, the red marrow content declines but continues to be visible longest along the medial shaft.123 Women often have more humeral red marrow than men; this also appears to be the case in heavy smokers. Scapula: The scapula is seen to contain virtually only red marrow. However, discrete yellow marrow can be found in over 95% of cases in the upper region of the glenoid cavity, regardless of age or gender. This is possibly due to mechanical factors linked to the insertion of the long biceps tendon.123 With advancing age, fatty marrow is also encountered in the periarticular medial and superior glenoid portions of the scapula. Femur: A pattern of alternating linear distribution of both marrow types is occasionally seen in the distal femoral metaphysis of adolescents. This is followed by complete regression of hematopoietic marrow with increasing age. A homogeneous hematopoietic marrow distribution pattern is seen in the proximal femoral metaphysis; this decreases in size with advancing age.78,99 In the femur, fatty marrow progresses from the apophyses of the greater and lesser trochanter.

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Fig. 11.8 Normal, age-related distribution of active and inactive bone marrow in the scapula. Schematic diagram. (a) Only hematopoietic marrow in infancy. (b) Adolescent. Fatty marrow deposition in the superior portion of the glenoid cavity in over 95% of cases, regardless of age. (c) Adult. (d) Fatty marrow also in the inferior portion of the glenoid cavity in old age.

Unlike the normal patterns described above, in up to 60% of children, focal, multifocal, and/or extensive signal changes are detected in the tarsals and tibia in particular, and these should not be misinterpreted as pathologic findings. To date, no tangible correlate has been identified to explain these findings. These changes manifest as high-contrast, hyperintense signal, especially on STIR sequences. They may be due to growth-associated, asymptomatic edematous changes in the bone marrow.

11.3 Generalized Disorders Fig. 11.9 Normal, age-related distribution of active and inactive bone marrow in the tibia. GRE sequence of healthy knee of a 12-yearold boy. Linear residual hematopoietic marrow in the proximal tibial metaphysis.

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Certain basic bone marrow patterns that can be ascribed to various disorders may be observed on MRI,127 such as: ● Conversion of fatty marrow to hematopoietic marrow, with hyperplasia of the remaining hematopoietic marrow (reconversion). ● Infiltration of the marrow space with normal or malignant cells or pathologic bone matrix in sclerotic skeletal dysplasia. ● Depletion of hematopoietic marrow with subsequent fatty replacement.

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Fig. 11.7 Normal, age-related distribution of active and inactive bone marrow in the humerus. (a) Normal, age-related distribution of active and inactive bone marrow in the humerus. Schematic diagram. I, hematopoietic marrow throughout the humerus; II, hematopoietic marrow in the proximal and distal humeral metaphysis and diaphysis in childhood; III, hematopoietic marrow in the proximal humeral metaphysis in adulthood; IV, residual hematopoietic marrow in the proximal humeral metaphysis in old age. (b) Normal, age-related distribution of active and inactive bone marrow in the proximal humeral metaphysis. Schematic diagram. I, predominantly hematopoietic marrow in adolescence; II, III, lateral regression of hematopoietic marrow in adulthood; IV, hardly any hematopoietic marrow in old age. (c) T1w TSE sequence. Medial residual hematopoietic marrow manifesting as areas of confluent low signal intensity. (d) GRE sequence. Hematopoietic marrow seen as area devoid of signal.

11.3 Generalized Disorders Fig. 11.10 Normal, age-related distribution of active and inactive bone marrow in the femur. Schematic diagram. (a) Hematopoietic marrow throughout the femur in childhood. The epiphyses are not yet ossified. (b) Incipient fatty marrow deposition in the femoral diaphysis in children below age 10 years. (c) Residual hematopoietic marrow in the proximal and distal femoral diaphysis in adolescents up to age 20 years. A striated pattern is seen in the distal metaphysis. (d) Further regression of hematopoietic marrow with increasing age in adulthood. (e) Adult of older age. (f) Complete regression of hematopoietic marrow surrounding hypointense trabeculae of the proximal metaphysis in older age.

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Depletion with subsequent fibrosis. Depletion with subsequent hyaluronic acid deposition (serous atrophy). Deposition of metabolites. Sequelae of bone marrow transplant.

11.3.1 Reconversion and Hyperplasia If the available hematopoietic bone marrow is no longer able to meet the demands imposed on the body by certain disorders, areas of inactive bone marrow are reconverted from fatty marrow to hematopoietic marrow. This physiologic process is termed reconversion, since it reverses the normal conversion from hematopoietic to fatty marrow seen in childhood. In severe or rapidly progressing forms, hematopoietic marrow also reappears in the epiphysis and apophysis. Furthermore, hematopoiesis is stepped up in the active regions, giving rise to hyperplasia of the existing hematopoietic marrow. Hyperplastic bone marrow exhibits signal intensity similar to that of neonatal hematopoietic bone marrow and is iso- to hypointense to muscle on T1w images. In the axial skeletal region, the intervertebral disks may, therefore, appear relatively iso- to hyperintense to the vertebral bodies on T1w images. The causes of reconversion and hyperplasia include the following: ● Disorders whose needs cannot be met by the existing red marrow, for example: ○ Chronic anemia. ○ Chronic infections. ○ Chronic heart failure. ○ Hyperparathyroidism. ○ Pickwick’s syndrome. ○ Chronic lung disease. ○ Hemoglobinopathy. ○ Renal arterial stenosis. ○ Renal diseases. ○ Right–left shunt. ○ Paraneoplastic disorders. ● Endurance athletic activities (also thought to lead to reconversion).109 ● Heavy smoking (associated with more extensive reconversion).93 ● Diseases where large parts of the red marrow are replaced with cellular infiltration, for example:

Spinal infiltration by lymphoma or plasmacytoma. Diffuse spinal metastases. ○ Leukemia. Therapeutic measures resulting in large parts of the red marrow being replaced by fat, for example: ○ Chemotherapy. ○ Large-field spinal radiotherapy. Diseases where large parts of the red marrow are replaced by fat, for example, osteomyelosclerosis. ○ ○

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Reconversion from yellow bone marrow is also observed during treatment with hematopoietic growth factors, for example, granulocyte colony-stimulating factors (G-CSF).27,35,39,63 The resultant changes in signal intensity may occasionally make it difficult to distinguish between bone tumors and the medullary (marrow) cavity. However, what causes reconversion often remains unclear. It is now thought that following reconversion hematopoietic marrow can persist at atypical sites, although the implicated stress factor can no longer be identified.18,60 To quantify the extent of reconversion, four grades of hematopoietic marrow have been proposed for the distal femoral metaphysis (▶ Fig. 11.13)60: ● Grades I and II: Grades I and II entail a low level of hematopoietic marrow. These manifestations are often encountered without any apparent cause. In one study, it was a frequent finding in young overweight women. ● Grades III and IV: Grades III and IV can generally be attributed to an underlying disease. It may be difficult to distinguish between foci of reconverted bone marrow, in particular those found at atypical locations, for example, in the diaphysis of long tubular bones, and infiltration by a malignant underlying disease.33 Likewise, metastases within reconverted marrow can often present a diagnostic challenge (▶ Fig. 11.14).

Sickle-Cell Anemia Sickle-cell anemia as the potential cause of bone marrow reconversion has been relatively well explored on MRI. The reconversion phenomena triggered by chronic hemolytic anemia are often very pronounced, with hematopoietic marrow frequently observed in the entire femoral shaft. Hyperplasia of the remaining hematopoietic marrow, in particular, of the axial skeleton,

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Fig. 11.11 Age-related signal intensity of the bone marrow. (a) A 5-month-old girl. T1w image of the spinal column. The signal intensity of the vertebral bone marrow is lower than that of the intervertebral disks. (b) A 6-year-old boy. T1w image of the spinal column. Increase in the signal intensity of the vertebral bone marrow— the signal intensity of the bone marrow is now higher than that of the intervertebral disks. (c) A 12-year-old girl. Sagittal T1w image of the lower thoracic and lumbar spine. The signal intensity of the vertebral bone marrow is higher than that of the intervertebral disks. (d) The 12year-old girl from (c); increase in size of marked area. Increasing fatty replacement of the bone marrow, with bandlike collection of fatty marrow around the basivertebral vessels (arrows). (e) A 35-year-old man. T1w image of the lumbar spine. Further increase in fatty replacement of the vertebral bone marrow. (f) A 60year-old man. T1w image of the lumbar spine. Fatty replacement of the bone marrow, with markedly higher signal intensity of the vertebral bone marrow compared with that of the intervertebral disks.

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results in a marked decrease in signal intensity on T1w images (▶ Fig. 11.15).35,38,71,96 Complications of sickle-cell anemia25: ● Metadiaphyseal bone infarcts (in up 20% of cases). ● Bone necrosis, especially humeral head and femoral head necrosis, with bilateral involvement more common than in other diseases. ● Osteomyelitis and septic arthritis. ● In the late stages, areas devoid of signal are identified on all sequences in the red marrow because of susceptibility caused by hemosiderin deposits.

Thalassemia Thalassemia is characterized by abnormal hemoglobin formation due to mutagenic damage to α or β globin production, resulting in chronic microcytic anemia of different severity. A higher incidence is observed in the Mediterranean region. The following courses of disease are distinguished based on the clinical symptoms: ● Severe course (Cooley’s anemia). ● Intermediate course. ● Mild course. Chronic anemia induces bone marrow hyperplasia, occasionally causing marked expansion of the marrow space, thinning of the trabecular bones, and extramedullary hematopoiesis. Radiologic imaging demonstrates the resultant severe osteoporosis, possibly with associated fractures; burst skull fracture (widening of the diploë secondary to radial expansion of the

marrow space); distended ribs with a permeative pattern of destruction; rib-in-rib phenomenon; reduced pneumatization of the paranasal sinuses; and deformed, distended maxilla. MRI demonstrates the morphologic changes and signal intensity associated with hyperplastic marrow. Iron deposition secondary to repeated blood transfusions gives rise to areas devoid of signal or marked reduction in signal intensity. Space-occupying masses isointense to bone marrow are observed secondary to extramedullary hematopoiesis at paravertebral, mediastinal, epidural, and/or presacral locations.71

Drug-Based Stem Cell Stimulation Iatrogenic hyperplasia resulting from granulopoiesis-stimulating factors (e.g., Neupogen) is a special entity. These substances (e.g., sargramostim, granulocyte macrophage colony-stimulating factor [GM-CSF], and filgrastim [G-CSF]) are administered to patients receiving high-dose radiotherapy, patients with aplastic anemia, etc. MRI demonstrates the characteristic findings associated with hyperplastic marrow. The changes in signal intensity identified on MRI in the wake of G-CSF therapy generally revert to normal within around 6 weeks of treatment termination.2

11.3.2 Cell Infiltration, Displacement, Uncontrolled Hyperplasia, and Skeletal Dysplasia An increase in the cellular content of the marrow space generally results in reduced signal intensity on T1w images, with

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Fig. 11.12 Arrested hyperpneumatization. A 40-year-old male patient. First diagnostic workup to investigate transient headache, unchanging findings over 6 years. The left clivus and part of the right clivus (white arrows) exhibit unusual signal intensity, hypointense with isolated fatequivalent foci on T1w and T2w images. Loculation and trabeculation on CT, consistent with arrested hyperpneumatization (see text) of large parts of the clivus. Normal conversion with fatty marrow only in parts of the right clivus (black arrows). (a) Axial T1w image. (b) Axial T2w image. (c) Axial CT image.

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unchanging increased signal intensity on T2w images. Relatively high signal intensity is identified on GRE and STIR sequences, which have higher sensitivity for detection of these changes, with usually prolonged T2 relaxation time. This section now describes neoplastic disorders, which, unlike reactive bone marrow hyperplasia involving an increase in the normal cellular content and preserved regulatory mechanisms, relate to impaired autoregulation, leading to a vast array of cells, with precursor cells seen concomitantly with mature cells. Two groups are distinguished: ● Disorders usually deemed benign myeloproliferative diseases based on their course and prognosis. ● Disorders designated as malignant myeloproliferative diseases.

Benign or Semimalignant Myeloproliferative Diseases and Preleukosis Back in 1951, the following diseases were subsumed under the collective term “myeloproliferative syndrome” by Dameshek in view of their similarities in terms of patient medical history, blood count, and disease course: ● Polycythemia vera. ● Essential thrombocythemia. ● Osteomyelofibrosis. ● Chronic myeloid leukemia. With regard to the MRI findings, osteomyelofibrosis must be discussed separately. Chronic myeloid leukemia is described in the section on malignant myeloproliferative diseases.

Polycythemia Vera Polycythemia vera is now classified as an acquired clonal disease of the pluripotent stem cells, characterized by an elevated concentration of all blood cells and high cell turnover. Its main impact is on erythropoiesis, leading to erythrocytosis. The principal clinical manifestations include, in addition to changes in blood count, splenomegaly and elevated lactate dehydrogenase levels. There is also an increased bleeding tendency. Onset of disease is generally between the ages of 40 and 70 years. The rise in blood viscosity may cause thrombosis, bone infarcts, and avascular necrosis as well as headache, vertigo, tinnitus, insomnia, fatigue, cardiac infarction, and pulmonary embolism. Radiography shows patchy osteopenia as well as signs of marrow expansion (in particular, in the calvaria) and bone infarction.

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Fig. 11.13 Different patterns of bone marrow reconversion in the distal femur. Schematic diagram. (a) No hematopoietic marrow. (b) Focal. (c) Multifocal. (d) Confluent. (e) Complete reconversion of distal femoral metaphysis.

Reflecting the increased cellular content, MRI demonstrates homogeneously reduced signal intensity of the hematopoietic marrow on T1w images, with no, or slightly increased, change in signal intensity on T2w images.35,46 Homogeneous hyperintensity reflecting hypercellularity is seen on fat-suppressed images (e.g., STIR) (▶ Fig. 11.16), with corresponding strong CM enhancement of the bone marrow. Reconversion is observed in the peripheral skeleton because of the high cell turnover. MRI examination of the pelvic region is particularly valuable, since it permits assessment of both the spinal column and the peripheral marrow of the femur. The changes identifiable on MRI regress once treatment becomes effective; this starts with bloodletting and, if ineffective, is followed by chemotherapy. The signal intensity exhibited by the femoral epiphysis appears to be well correlated with the clinical course and laboratory results.52 Bone marrow fibrosis with pancytopenia may be seen in chronic courses of disease, with extramedullary hematopoietic foci also detected in the pleura, retroperitoneum, and perirenal space. Blood transfusions are also needed occasionally in the later stages and may result subsequently in a pattern of bone marrow siderosis (▶ Fig. 11.17).

Essential Thrombocythemia The most salient finding in association with essential thrombocythemia (synonyms: megakaryocytic myelosis, hemorrhagic thrombocythemia) is hyperplasia of thrombocytopoiesis, with continuous platelet counts of over 1 million/L. The leukocyte count is between 10,000 and 40,000/L. In most cases, erythropenia is seen. Platelet functions are impaired, leading to increased bleeding tendency; splenomegaly is also observed. Hyperplastic bone marrow is identified on MRI.

Systemic Mastocytosis This is a disorder in which mast cells are abnormally increased in several organs, especially in the skin. Release of chemical mediators by the mast cells causes typical complaints: ● Urticaria. ● Tachycardia. ● Hypertension. ● Enteritis. ● Edema. ● Bronchoconstriction. ● Anaphylaxis. Systemic involvement is rare and, unlike the purely cutaneous type, is more common in adults. Mast cell proliferation in the bone marrow displaces normal myelopoiesis, leading to peripheral anemia, leukopenia, and thrombocytopenia. For reasons not fully understood, there is onset of diffuse osteopenia, especially of the axial skeleton, and also of patchy bone destruction following osteoclast activation, occasionally exhibiting a permeative destruction pattern, too. In the ensuing course, there is also focal or diffuse reactive sclerosis. In such settings, differential diagnosis must include osteomyelofibrosis, fluorosis, sickle-cell anemia, Paget’s disease, and osteoblastic metastases.28 The MRI findings reflect the respective course of disease: ● The early stage is associated with hyperplasia of the axial skeleton (decrease in signal intensity on T1w contrast, intermediate

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Fig. 11.14 Extensive reconversion of the bone marrow in association with diffuse medulloblastoma metastases. (a) T1w SE sequence, coronal section through pelvis and thigh. Diffuse reduced signal intensity of the femurs and pelvis due to reconverted hematopoietic bone marrow. Isolated areas of homogenous signal intensity, consistent with metastases (arrows). (b) Fat-suppressed STIR sequence of same region. Bone marrow exhibits high signal intensity, with isolated areas of inhomogeneous signal intensity. (c) Sagittal T1w SE sequence of the spinal column following CM administration. Diffuse metastases throughout the entire axial skeleton.

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or increased signal intensity on T2w, and, in particular, diffuse or multifocal signal on STIR contrast sequences) and reconversion on the periphery. The late stage is characterized by myelofibrosis and sclerosis (decrease in signal intensity on all sequences).

Depending on the severity of bone marrow disease, patchier or more diffuse signal changes are observed. If CM is administered,

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areas with increased mast cell infiltration will show stronger CM uptake. However, in systemic mastocytosis, CM administration does not confer any additional benefits over native MRI sequences. Where there is only low-grade mast cell infiltration, it may be difficult to differentiate between pathologic and normal bone marrow, in particular, in younger patients. Familiarity with the distribution pattern of normal red bone marrow is useful for evaluation of such cases. DWI can also be helpful for

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distinguishing normal marrow from pathologic marrow. Besides, it is a promising method for follow-up of pathologic bone marrow changes. Restricted diffusion is often observed in bone marrow regions with mast cell infiltration—but the advantages of DWI over conventional MRI sequences have not been investigated to date.28 Whole-body MRI (▶ Fig. 11.18) permits assessment of the entire skeleton and is the modality of choice in younger patients, since it does not entail the use of radiation. It is also able to give insights into important prognostic factors, for example, hepatosplenomegaly, ascites, and mast cell infiltration of the liver, the spleen, or the gastrointestinal tract.28

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Fig. 11.15 Sickle-cell anemia. A 21-year-old man. (a) T1w image. Hypointense signal throughout the femoral shaft, reflecting extensive bone marrow reconversion. Lesions seen in the femoral heads, bilateral, on T1w image. These are hyperintense at the center and hypointense at the periphery (white arrows), consistent with bilateral avascular necrosis of the femoral head. In the mid-femoral shaft, there is an area with higher signal intensity than that of the surrounding hematopoietic bone marrow (black arrow). (b) STIR image. Overall, increased signal intensity of the femoral shaft, with bone marrow reconversion. Bilateral avascular necrosis of the femoral head (white arrows). Hyperintense area in the middle third of the left femoral shaft, consistent with a recent bone infarct (black arrow). (c) T1w image. Reduced signal intensity in the metaphyses and diaphyses of both femurs (arrows). (d) STIR image. Corresponding increase in signal intensity (arrows), reflecting bone marrow reconversion.

Malignant Myeloproliferative Diseases and Diffuse Infiltrates Leukemia Leukemia is a disorder in which infiltration of the marrow (mainly the red marrow) by leukocytes (white cells) increases the cell count and decreases the fat content. This leads to prolongation of the T1 time, with generally diffuse, partially patchy reduced signal intensity seen on T1w SE images.125 MRI has very high sensitivity for detection of diffuse bone

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Fig. 11.16 Polycythemia vera. MR images of the cervical spine and upper thoracic spine of a 75-year-old patient with polycythemia vera. (a) T1w image. Sharp homogeneous reduction in bone marrow signal intensity. (b) T2w image. Likewise, sharp homogeneous reduction in bone marrow signal intensity. (c) STIR image. Homogeneous increase in bone marrow signal intensity in association with hypercellularity.

Fig. 11.17 Disease course of polycythemia vera (and of general myeloproliferative diseases). Schematic diagram. Coronal plane, axial, and peripheral skeleton. (a) Normal state, with hematopoietic marrow in the vertebral bodies and proximal femoral metaphysis. (b) Early stage. Reduction in signal intensity of the vertebral bodies due to cell infiltration (isointense or hypointense to muscle). (c) Reconversion of the peripheral skeleton during the course of disease. (d) Late stage. Marked reduction in signal intensity of the vertebral bodies due to fibrosis or siderosis.

marrow changes in acute leukemia. However, the diffuse pattern of bone marrow changes is not specific to this disease.82 Occasionally, it may be difficult to delineate leukemic infiltrates within hematopoietic bone marrow. However, if these foci are surrounded by fatty bone marrow, they can be well identified on high-contrast T1w images.5 For example, in

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acute lymphatic leukemia, the T1 time is correlated with the lymphoblast count.33 Depending on the cellular composition, the T2 time remains unchanged or slightly increases, with a small increase in signal intensity on T2w images. These changes are particularly pronounced in chronic myeloid leukemia (chronic myelosis) and acute lymphocytic leukemia.127 The changes are generally diffuse, but occasionally, a multifocal, inhomogeneous pattern is seen. If malignant displacement of the hematopoietic marrow has resulted in hematopoietic insufficiency, reconversion phenomena can be observed in the fatty marrow. In most cases, it is not possible to distinguish between reconverted and leukemic marrow. Often, the leukemia-induced marrow changes may be very acute (▶ Fig. 11.19). On radiographs, chronic leukemia, in particular, chronic myeloid leukemia, is seen to induce low-grade aggressive bone changes, especially osteopenia and increased density secondary to marrow fibrosis. Leukemic extramedullary cell aggregates known as chloromas (synonym: granulocytic sarcoma) can cause bone erosion and bone destruction. On MRI, chloromas appear as an uncharacteristic mass that exhibits low signal on T1w and high signal intensity on T2w contrast images.

Diffuse Lymphoma Infiltration Unlike the various types of leukemia, whose diagnosis is based on the blood count rather than the bone marrow results,

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Fig. 11.18 Systemic mastocytosis. Whole-body MRI of a 63-year-old male patient with systemic mastocytosis to investigate potential organ involvement. Diffuse infiltration in association with underlying disease. (a) T1w image of entire spinal column. Diffuse and inhomogeneous signal reduction of the vertebral bone marrow. (b) STIR image. Increased signal intensity of the vertebral bone marrow. (c) Composed T1w image. Marked signal reduction of the displayed section of lower lumbar spine, pelvis, and both femurs as far as the distal shaft. (d) Fat-saturated T1w image following CM administration. Splenomegaly with axial size of 16 cm × 7.8 cm (arrows).

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detection of bone marrow infiltration by lymphoma (see Primary Bone Lymphoma, p. 535) is of paramount importance for the choice of treatment and disease prognosis. Bone marrow biopsy is currently the standard method of diagnosis; this is an invasive method that is highly selective, since, in cases of focal disease, the biopsy often yields a false-negative result if the specimen is not actually taken from a section of the lymphoma-infiltrated marrow. The incidence of Hodgkin’s disease, which is primarily associated with focal bone marrow infiltration, continues to elicit vigorous debate and is estimated to be between 2 and 34%. MRI demonstrates, with high sensitivity, areas of focal decreased signal intensity on T1w images and increased signal intensity on GRE or STIR images but has a high rate of false-positive results. These stem, in particular, from inflammatory infiltrates and impaired erythropoiesis, both of which result in a higher cell count. The diagnostic results can be improved for Hodgkin’s disease when only focal changes are evaluated as a sign of disease infiltration and extensive or diffuse infiltrates classified as nonspecific concomitant reactions. In any case, MRI can be used to underpin selective biopsy. For non-Hodgkin lymphoma, the possibility of partly focal and partly diffuse bone marrow infiltration must be contemplated. As mentioned, it is advisable to use MRI as the primary diagnostic modality in cases of focal involvement.

Multiple Myeloma Multiple myeloma (plasmacytoma, Kahler’s disease) is a malignant bone marrow disease involving proliferation of a clone of malignant plasma cells or plasma cell precursors in the bone marrow or rarely also in extramedullary regions. A characteristic feature of these cells is that they secrete paraproteins, which can be identified as a narrow-based peak on serum electrophoresis. Diffuse interstitial or focal plasma cell growth is seen in the bone marrow, leading to osteolytic bone destruction or diffuse osteoporosis. Bone marrow biopsy is essential for diagnosis. Patients are staged through a combination of laboratory values (hemoglobin, paraprotein, calcium, creatine, etc.) and imaging techniques. Formerly, the main diagnostic imaging modality was conventional radiographs (skeletal survey) (▶ Fig. 11.20). Now, whole-body CT

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is often used instead of whole-body skeletal survey for multiple myeloma. It is more sensitive than radiographs in detection of myeloma foci and is able to successfully stage significant numbers of patients.31 MRI is able to directly visualize the tumor foci in the bone marrow and is endowed with much higher sensitivity and specificity for detection of plasmacytoma lesions than radiographs.22,29 On projection radiography summation images, bone destruction can be identified only after at least 50% of the trabeculae of spongy bones have been depleted. Thanks to its superior soft tissue contrast, MRI is able to directly and sensitively demonstrate bone marrow infiltration. Several studies have shown that conventional radiographs yield false-negative results in 34 to 80% of cases.4,64,116 MRI was even able to identify characteristic myeloma infiltrates in 29 to 50% of asymptomatic stage I patients.21, 70,83,86,124 These patients experienced early disease progression and benefited from treatment. Five different signal patterns are identified on MRI in multiple myeloma4: ● Normal bone marrow signal intensity: In 28% of cases, bone marrow signal intensity is similar to that of a healthy patient, with high signal intensity on T1w sequences and low signal intensity on fat-saturated sequences. ● Discrete focal infiltration: A discrete focal infiltration form is seen in around 30% of cases. These foci manifest as metastases, with low signal intensity on T1w SE sequences and high signal intensity on fat-saturated sequences (e.g., STIR). ● Diffuse infiltration: A diffuse infiltration form can be detected on MRI if the extent of diffuse interstitial distribution of plasma cells in bone marrow has reached a certain level (over 20 vol.%) (▶ Fig. 11.21). This is reflected in a more or less pronounced homogeneous, diffuse decrease in signal intensity on T1w SE sequences and increased signal intensity on fat-saturated sequences. A relative increase of over 40% in signal intensity following CM administration on T1w SE images is suggestive of SE infiltration.5 ● Combined diffuse and focal infiltration: This infiltration form is observed in around 11% of cases. ● “Salt-and-pepper” pattern: A “salt-and-pepper” pattern is seen in around 3% of patients. This is characterized by inhomogeneous signal on T1w SE sequences, with multiple, tiny hypo- and hyperintense foci. However, on fat-saturated sequences, no focal hyperintense foci are identified, thus ruling out focal

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Fig. 11.19 Acute leukemia. (a) Coronal T1w image. Homogeneous reduction in signal intensity of the metaphysis and parts of the epiphysis, reflecting marrow displacement by leukemic infiltrates and/or reconversion. In leukemia, signal changes are often seen in the epiphysis. (b) Sagittal STIR image. Increase in signal intensity in the metaphysis and in parts of the epiphysis. Hypointense residual fatty marrow in the epiphysis and patella. The patient sustained an injury, with basal avulsion of the posterior cruciate ligament and fracture of Hoffa’s fat pad.

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Fig. 11.20 Multiple myeloma, diffuse pattern of disease. (a) Lateral radiograph of the lumbar spine. Moderate demineralization. (b) Lateral radiograph of the lumbar spine 4 months later. Marked progression of demineralization and evidence of multiple pathologic fractures. (c) Sagittal T1w SE sequence. Homogeneous reduction in signal intensity of the vertebral bodies, now largely equalizing that of the intervertebral disks. Compression fractures. (d) Sagittal contrast-enhanced T1w sequence. Diffuse CM enhancement of the vertebral bodies. Circular enhancement around a fracture in the superior end plate of the T12 vertebral body (arrow). (e) Sagittal T2w sequence.

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Fig. 11.21 Multiple myeloma, diffuse pattern of disease. Three patients; T1w SE sequences. (a) Normal visualization of bone marrow, with slight interstitial infiltration (less than 20 vol. %). (b) Moderate SE infiltration (20–50 vol. %), with identifiable homogeneous decrease in signal intensity on T1w SE image. (c) Extensive diffuse infiltration, with sharp homogeneous decrease in signal intensity on T1w SE images. The signal is similar to that of the intervertebral disk and of muscle tissue.

infiltration. This inhomogeneous signal pattern exhibited by the bone marrow stems from the interposition of focal discrete fatty islands. Alongside these is normal bone marrow with only low-grade interstitial infiltration of plasma cells. The majority of such patients are in stage I and do not require therapy. Multiple myeloma has a very variable clinical course. The average life expectancy is 3 to 5 years, but this can vary greatly and may even be 10 years, depending on how aggressive the tumor cells are, and the extent of disease at the time of initial diagnosis. The extent of infiltration can be verified directly with MRI. Various studies have demonstrated that the magnitude of infiltration, as identified on MRI, is a highly significant prognostic parameter for patient survival.6,59 Hence, clinical staging of patients with multiple myeloma now includes whole-body MRI (▶ Table 11.1).24 If MRI results are available only for the spinal column, these can also be taken into

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account for clinical staging. A study conducted by the present authors demonstrated that integration of MRI into the Durie and Salmon staging system made it much easier to assign patients to one of the three stages. If conduct of MRI is not feasible, whole-body multislice CT can be used alternatively, with high-resolution visualization of bones by using a low current strength (100 mA, 120 kV). The results can be enhanced on using multiplanar reconstruction. Bone destruction can be identified earlier with this method than with conventional radiographs. However, in terms of sensitivity, multislice CT is inferior to MRI (▶ Fig. 11.22).8 Whole-body MRI is superior to MRI of the spinal column (including the sacrum) for initial diagnosis of myeloma, since it is able to demonstrate any extra-axial lesions. In a study by Bäuerle et al, 37% of patients imaged were found to have extra-axial lesions; 9% of patients with extra-axial lesions had no lesions in the axial skeleton. Only whole-body MRI was able to detect

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Classification

Whole-body MRI and/or FDC-PET

Stage I A

0–1 lesion

Stage I B

2–4 lesions or slight diffuse infiltration

Stage II A/B

5–20 focal lesions or moderate diffuse infiltration

Stage III A/B

> 20 lesions or severe diffuse infiltration

Abbreviations: FDC-PET, fluorodeoxyglucose positron emission tomography; MRI, magnetic resonance imaging.

the extra-axial lesions. Such lesions cannot be ruled out on the basis of the clinical parameters.3 As for other diseases associated with high cell counts, MRI is adept at demonstrating early on response to treatment or deterioration of the results with changes in the cell count.85 Demonstration of an increase in the fat content, as reflected by a diffuse or multifocal rise in signal intensity on T1w images as well as reduced CM uptake, is suggestive of a positive response to treatment.85 The initial findings on whole-body DWI show a significant negative correlation between changes in the ADC values and changes in the clinical laboratory parameters,30 thus attesting to the potential role of whole-body DWI in monitoring the response to treatment. The MRI changes unfolding in multiple myeloma show a certain correlation with the clinical parameters. For example, patients with diffuse involvement have a higher bone marrow plasma cell content, higher serum calcium levels, higher β2 microglobulin levels, and lower hemoglobin values than patients

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Table 11.1 Durie and Salmon PLUS staging system. Note: Staging of multiple myeloma after Durie and Salmon, based on the number of myeloma foci or diffuse infiltrates. Moderate diffuse infiltration is demonstrated as a decline in the signal intensity of the bone marrow on native T1w SE images, but there is no contrast versus the adjacent intervertebral disk. In severe diffuse infiltration, the bone marrow exhibits low signal intensity, similar to that of intervertebral disks or muscles.

Fig. 11.22 Multiple myeloma. A 68-year-old female patient. (a) Multislice CT. No evidence of characteristic osteolytic myeloma lesions. (b) MRI STIR image. Small multifocal infiltrates throughout the entire spinal column, consistent with stage III disease.

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Bone Marrow

By now, the hematopoietic marrow exhibits muscle-isointense or hypointense signal and the intervertebral disk hyperintense signal. Increased cellularity appears to be accompanied by increased perfusion and, accordingly, by intense CM uptake. The extent of CM enhancement is correlated with the plasma cell count.84 Hence, MRI appears to be suitable for disease staging. Occasionally, increased signal intensity is observed on T2w images. However, often, no changes are identifiable. Bone marrow signal intensity rises again following successful therapy and may revert to normal. As such, MRI can serve as a noninvasive method for monitoring the response to treatment. Focal involvement is only thought to be implicated in less than 10% of cases of Waldenström’s disease.

11.3.3 Sclerotic Skeletal Dysplasia Sclerotic skeletal dysplasia is a group of diseases involving disrupted bone metabolism leading to generation of immature

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and excessively mature bone because of impaired osteoblastic or osteoclastic activity. In general, radiographs suffice for management of these disorders. Depending on the underlying disease, MRI demonstrates different signal patterns, ranging from a signal-void exuberant bone matrix to diffuse signal changes with immature bone matrix, for example, osteopetrosis (▶ Fig. 11.23).

11.3.4 Hypoplasia and Fatty Replacement Disease processes involving fatty replacement of hematopoietic bone marrow must be distinguished from the normal physiologic narrow conversion to fatty marrow. Serial MRI examination and knowledge of the physiologic age-related changes are important in this setting. It should be borne in mind that several conditions involving degenerative pathologic changes (see Chapter 2.3), for example, spondylolysis, kyphoscoliosis, and osteochondrosis, are accompanied by focal fatty deposition.37,76

Panmyelopathy (Aplastic Anemia) This disease is characterized by a decline in the number of red blood cells, white blood cells, and platelets produced in the hematopoietic bone marrow, leading to cytopenia; there is also reduced stem cell generation. This decline in hematopoietic marrow cellularity is compensated for by an increase in the fat content. These changes are reflected on MRI, with homogeneous hyperintensity of hematopoietic marrow on T1w and T2w images, now almost equalizing the signal intensity of subcutaneous fat.82 The proximal humeral and femoral metaphyses, pelvis, and vertebral bodies may exhibit homogeneous high signal intensity.51

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Fig. 11.23 Osteopetrosis. A 20-year-old male patient. (a) Radiograph. (b) MRI T1w image. (c) MRI PDw fatsat image.

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with no visible marrow changes or patients with focal involvement patterns. Besides, patients with diffuse disease patterns have a poorer prognosis.87 In a study with 149 patients with asymptomatic myeloma, identification of focal lesions and more than one lesion on multivariable analysis was the chief determinant of a poorer prognosis with regard to progression to symptomatic myeloma.42 Diffuse infiltration of the hematopoietic marrow by plasma cells in Waldenström’s disease leads to higher cell count and reduced fat content. Spinal column involvement is detected on MRI in over 90% of cases with laboratory diagnosis. Depending on the cell count, the following changes are observed on T1w images: ● Initially, patchy reduced signal intensity. ● In later stages, diffuse reduced signal intensity.

11.3 Generalized Disorders

Panmyelopathy Fig. 11.24 Distribution of hematopoietic and fatty marrow in a patient with panmyelopathy (aplastic anemia). (a) Before treatment, only fatty marrow identified. (b) After treatment, multifocal replacement by hematopoietic marrow.

The etiology of this condition is often unclear but is thought to be linked to drug abuse, viral infections, toxic substances, or hepatitis. Successful treatment (e.g., cyclosporin A and steroids) results in restoration of hematopoietically active cell nests, especially in the vertebral body marrow spaces. In this stage, the vertebral bodies exhibit an inhomogeneous pattern, with multiple foci of hypointensity observed within the hyperintense vertebral bodies on T1w and T2w images (▶ Fig. 11.24).51 On resolution, the MRI findings revert to normal, with regular adult pattern of bone marrow distribution.

Chemotherapy-induced Changes Chemotherapy leads to a decrease in the hematopoietic bone marrow cell count, with compensatory fatty replacement. MRI shows homogeneous diffuse or also patchy increase in signal intensity on T1w and T2w SE sequences.16 The extensive bone marrow damage observed in the late stages may be accompanied by fibrosis, with reduced signal intensity once again on all sequences.

11.3.5 Bone Marrow Fibrosis The bone marrow can react to a number of toxic substances, with proliferation of fibrous connective tissue in the following settings: ● Myeloproliferative diseases: ○ Polycythemia vera. ○ Idiopathic osteomyelofibrosis. ○ Essential thrombocythemia. ○ Chronic myeloid leukemia. ● Metastases. ● Leukemia. ● Lymphomas. ● Ionizing radiation. ● Chronic infections, for example, tuberculosis. ● Toxins (e.g., hydrocarbons, fluorine, phosphorous, aniline dyes). Progressive bone density is seen on radiographs. MRI demonstrates bone marrow fibrosis, with reduced signal intensity on T1w and T2w sequences (▶ Fig. 11.25 and

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Treatment

▶ Fig. 11.26).61 This reduced signal intensity may be diffuse or also patchy. Nonfibrotic areas of the bone marrow appear differently, depending on the underlying disease. Idiopathic osteomyelofibrosis (synonyms: osteomyelosclerosis, aleukemic myelosis, leukoerythroblastic anemia, agnogenic myeloid metaplasia) is a myeloproliferative disorder that, for unknown reasons, results in early onset of bone marrow fibrosis, later followed by sclerosis. Onset is generally in patients aged 60 to 70 years. Prepolycythemic stages are rarely identified, but patients complain of increasing weakness and bleeding tendency, possibly with hemarthrosis. Disease manifestations include enlarged spleen and leukocytosis, with leukocytes of different maturity stages, initially thromboand erythrocytosis, later followed by thrombo- and erythropenia. The later stages are characterized by anemia, with increasing extramedullary hematopoietic foci and paravertebral space-occupying masses (also spinal cord compression); a terminal blastic flare is seen in 20% of cases. Mean survival is 5 years. Increasing amounts of fibrous connective tissue and, in the ensuing course, fibrous bone are observed in the bone marrow and later also in the extramedullary hematopoietic foci, accompanied by areas of hypercellularity. Initially, radiographs demonstrate discrete osteopenia, in some cases with bandlike, small osteolytic foci; this is later followed by more extensive multifocal or diffuse sclerosis of the vertebral bodies.7 Cortical thickening or a periosteal reaction may be rarely identified. The calvaria has a typically blurred threelayered appearance. On MRI, multifocal or diffuse reduction in signal intensity of the axial skeleton is identified on T1w and T2w sequences due to the initial increase in cellularity and decrease in the fat content in the early stage as well as fibrosis in the later stages.7 A slight increase in signal intensity and patchy or diffuse CM uptake are seen on STIR images. The signal intensity of the axial skeleton declines as the disease progresses; bone marrow reconversion is seen in the peripheral skeleton, possibly with formation of extramedullary hematopoietic foci. In the late stages, sclerosis or, following frequent blood transfusions, bone marrow siderosis gives rise to areas that are virtually devoid of signal, with increased signal extinction on GRE images due to susceptibility effects.

11.3.6 Serous Atrophy A number of different wasting diseases result in a decline in fatty marrow, with replacement by a watery ground substance (hyaluronic acid accumulation). This, in turn, leads to a reduction in the cell count. The implicated diseases include, for example: ● Anorexia nervosa. ● Kidney failure. ● Tuberculosis. ● Cachexia. ● HIV infection (late stages).

In the affected regions of the peripheral skeleton, typically in the femur, MRI displays mainly diffuse, rarely patchy, hypointensity on T1w and often pronounced hyperintensity on T2w images. As the disease progresses, similar multifocal changes in signal intensity may be identified in the axial skeleton.

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Bone Marrow

Fig. 11.25 Osteomyelosclerosis. (a) Lateral radiograph of the lumbar spine. Increased density of the vertebral bodies. (b) Overview radiograph of the pelvis. Increased density of the visualized bones. (c) MRI T1w SE image of the pelvis. Marked reduction in signal intensity of the vertebral bodies (arrow), with relative increase in signal intensity of the intervertebral disk. Reduced signal intensity of the pelvic bones and both femurs.

11.3.7 Storage Diseases Gaucher’s Disease Gaucher’s disease is caused by a metabolic defect, with deficiency in the enzyme glucocerebrosidase leading to accumulation of glucocerebrosides in, for example, the brain, spleen, and reticuloendothelial bone marrow cells, and particularly in the hematopoietic marrow. Displacement of the functional marrow is soon followed by early onset of reconversion phenomena, also affecting the peripheral bone marrow. Prolongation of the TI time and shortening of the T2 time are seen on MRI, giving rise to hypointensity of the implicated areas on T1w and T2w images (▶ Fig. 11.27). Depending on the extent of glucocerebroside deposition, an inhomogeneous, patchy, or

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homogeneous signal pattern is identified.41 The entire marrow space appears altered in advanced cases of disease. Disease manifestations have been assigned to 10 stages based on the extent of peripheral disease detected on the MR images.102 Bone infarcts are a common complication of this disease. Occasionally, it may be difficult to identify old infarcts in the affected skeletal regions because of the reduced signal intensity of the bone marrow space. Since 1991, enzyme replacement therapy has been available for Gaucher’s disease. MRI is a noninvasive radiation-free modality for monitoring the response to treatment. Various methods have been proposed to that effect: ● A quantitative chemical shift method that measures the fatty fraction of the lumbar spine bone marrow. The fat content is

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11.3 Generalized Disorders

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Fig. 11.26 Myelofibrosis. MR images of the spinal column of a 66-year-old female patient with myelofibrosis. Marked diffuse reduction in bone marrow signal intensity on all sequences. (a) T1w image. (b) T2w image. (c) STIR image.

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markedly reduced in the setting of Gaucher’s cell infiltration and rises again following successful enzyme replacement therapy.103 Semiquantitative scoring systems are now easier to implement and are based on classification of the signal changes on T1w and T2w SE images or on the extent of the signal changes observed in the various skeletal regions.68,69 Whole-body MRI is a valuable method for assessment of the entire skeleton and can play an important role in monitoring and treatment of type 1 Gaucher’s disease.92

Hemosiderosis A distinction is made between primary and secondary hemosiderosis, as seen, for example, secondarily to frequent blood transfusions and hemolytic anemia.120 The resultant bone marrow iron stores lead to a marked decline in signal intensity on T1w and T2w images. The changes identified are mainly multifocal and patchy but may also be diffuse. Excessive iron deposition can be seen on MRI as areas of “black marrow” virtually devoid of signal. In advanced-stage HIV-infected patients (acute immunodeficiency syndrome [AIDS]), increased extracellular hemosiderin deposition is also detected. This produces multifocal, patchy to

diffuse signal reduction on T1w and T2w images. Such changes have been identified, in particular, in the calvaria and clivus, and in over 50% of patients, these changes were accompanied by a sharp decline in the CD4 helper cell count and severe AIDS symptoms.26

Amyloidosis Amyloidosis, both primary and secondary, is a condition involving diffuse or focal amyloid deposition in the bone marrow. On MRI, diffuse or focal moderately reduced signal intensity can be detected on T1w images. Reduced, or unchanged, signal intensity is also seen on T2w images.

11.3.8 Posttransplant Bone Marrow Changes Bone marrow transplant is occasionally used as early treatment for malignant blood diseases. This provides for myeloablative high-dose chemotherapy. First of all, in phase 1, immunosuppression is induced through combined chemo- and radiotherapy (fractionated whole-body radiation) so as to destroy malignant cells and minimize any incompatibility reactions. On completion

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11.4 Focal Diseases 11.4.1 Edema

Fig. 11.27 Gaucher’s disease. Coronal T1w image. Marked homogeneous reduction in signal intensity of the axial skeleton (relative to muscle) and proximal femoral metaphyses. Residual fatty marrow in the femoral epiphyses.

of this phase, the bone marrow cells to be transplanted are administered to the patient as an infusion so as to regenerate the marrow in the medullary space. For autologous peripheral bone marrow transplant, the cells to be transplanted are harvested from the patient before chemotherapy (mobilized stem cells from peripheral blood). MRI demonstrates characteristic changes in the vertebral bodies following bone marrow transplant.113,114 Initially, radiotherapy- and chemotherapy-induced changes are identified, followed first by edema-equivalent signal intensity. Around 2 to 3 months after bone marrow transplant, bandlike reduced signal intensity is detected in the superior and inferior end plates of the vertebral bodies on T1w images, showing a hyperintense central band (▶ Fig. 11.28). This bandlike pattern can be explained by repopulation of the marrow space, with hematopoietic cells at the periphery and persistence of fatty transformation at the center (▶ Fig. 11.29). The pattern is thought to reflect the distribution of the vascular sinusoids in the vertebral bodies. On fat-suppressed sequences, in particular, STIR images, a bandlike pattern with reverse signal intensities is seen: low-signal central band surrounded by two peripheral hyperintense bands. This posttransplant bandlike pattern is thought to persist for at least 8 to 14 months before restoration of normal signal intensity. However, this bandlike pattern is not always identified, with only diffuse changes observed. MRI is able to estimate repopulation of the marrow space and is thus a valuable diagnostic tool for follow-up, also reducing the need for bone marrow biopsy.

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Fig. 11.28 Status post bone marrow transplant. Schematic diagram. Bandlike distribution of hematopoietic (dark) and fatty marrow (bright) in the vertebral body following bone marrow transplant.

Fig. 11.29 Repopulation of the marrow space. Sagittal STIR image of the spinal column. Patient with Hodgkin’s stage IV disease following radiochemotherapy. Three-layered signal intensity pattern of the vertebral bodies with low-signal, fat-equivalent center and hyperintense peripheral halo, reflecting repopulation.

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Bone reacts to various toxic substances, with edema formation as a sign of impaired vascular permeability or hyperperfusion. Edema consists of increased fluid accumulation in the interstitial spaces. Underlying bone diseases causing edema, such as trauma, tumors, infection, or ischemia, generally give rise to radiologically identifiable changes, for example, demineralization, bone destruction, or bone remodeling. MRI is able to diagnose bone marrow edema as the only sign of bone disease or as an early sign of a disorder identifiable only later with other imaging modalities.122 No other diagnostic technique rivals the high sensitivity of MRI. Owing to increased

11.4 Focal Diseases

11.4.2 Ischemia Whether bone marrow ischemia gives rise to a bone infarct or to osteonecrosis (avascular necrosis) is determined by its severity, extent, and location. Although both these bone disorders exhibit characteristic signs on radiographs in the late stages, they may be radiographically occult in the early stages. However, MRI is able to detect reactive perifocal edema already at an early stage. This edema is thought to be caused by reactive hyperemia. It is hypointense on T1w images and hyper- or isointense on T2w images.

Osteonecrosis (Avascular Necrosis) Osteonecrosis is observed primarily in subchondral regions with yellow bone marrow. This is probably linked to the sparse vascularity in these areas. The characteristic signs and course of this disorder are discussed in other chapters that deal with the joints. Osteonecrosis of the femoral head has been most extensively investigated (see Chapter 6.4).

Bone Infarction Bone infarcts are a form of osteonecrosis presenting in the metadiaphyseal regions of tubular bones,104 regardless of the predominant bone marrow type. This is due to the blood supply and vascular anatomy of tubular bones. Several predisposing factors have been identified, for example: ● Hyperglobulinemia. ● Sickle-cell anemia and other hemoglobinopathies. ● Gaucher’s disease. ● Systemic cortisone therapy and Cushing’s disease. ● Caisson’s disease. ● Radiation. ● Alcohol abuse. ● Protein S deficiency, etc. Often, multiple infarcts are observed. For example, characteristic multifocal bone infarcts are seen in 20% of cases of sickle-cell disease.97 Reflecting necrotic liquefaction and edema, early-stage infarcts have reduced signal intensity on T1w images and high signal intensity on T2w images. The signal changes are generally linear or, in some cases, extensive and have a garlandlike appearance. This acute stage is mostly painful. Identification of bone marrow edema on the initial MRI to investigate hip pain is an important prognostic marker, as it is well correlated with the necrotic volume and is an important risk factor for deterioration of hip pain in the later course.44 Acute bone infarcts in hyperplastic or

infiltrated marrow may be occult on T1w images, since by then, the infarct and the surrounding hypercellular marrow are isointense. Often, a double-line sign is seen on T2w fast spin-echo (FSE) sequences at the boundary between vital tissue and nonvital tissue. This is composed of a hyperintense line on the necrotic side (reflecting granulation tissue) and a hypointense line (corresponding to the sclerotic bone) (▶ Fig. 11.30 and ▶ Fig. 11.31).104 Calcifications are observed in the late stage, with reduced signal intensity on all sequences. This low to signal-void area may also be surrounded by a rim that is devoid of signal, consistent with a sclerotic margin. Bone infarcts can become infected and cause osteomyelitis.

Transient Osteoporosis Transient osteoporosis (bone marrow edema syndrome) is occasionally seen in the hip. This disorder can also give rise to an “edematous pattern” in the femoral and, possibly, acetabular bone marrow (▶ Fig. 11.32 and ▶ Fig. 11.33). The etiology of this condition is still unclear. Among the causes posited are ischemia, localized hyperemia, neural changes, stress fractures, and complex regional pain syndrome (CRPS) type I. Several authors have implicated microdamage to bones with ensuing subchondral trabecular microfractures as a possible cause.117,118 These microfractures are then thought to result in increased bone metabolism, modeling, and remodeling.117 This phenomenon could explain the following changes: ● Positive bone scintigram. ● Moderate osteoporosis on radiographs. ● Edematous bone marrow pattern on MRI.

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interstitial fluid accumulation, bone marrow edema results in prolongation of the T1 and T2 relaxation times. These changes can be delineated with adequate clarity on conventional SE sequences. T1w SE sequences have excellent negative contrast (dark edema and bright marrow). T2w SE sequences assure positive contrast (bright lesion, surrounded by dark marrow). STIR sequences showing fatty tissue as low signal intensity and edema as high signal intensity are endowed with the highest sensitivity for detection of bone marrow edema.

A concomitant joint effusion is frequently observed. This condition presents unilaterally in most patients, but bilateral involvement is also seen in pregnant women who have no history of trauma. Transient osteoporosis is painful and resolves spontaneously within 6 to 12 months.10,132 Often, a clinical diagnosis can only be issued retrospectively after evaluating the course of disease and excluding other hip disorders.

11.4.3 Postradiation Changes Depending on the dose administered, ionizing radiation can damage cells as well as the sinusoids and vessels, in particular, in the hematopoietic bone marrow. Initially, edema and necrosis are seen, followed in the later stages by compensatory proliferation and hypertrophy of fat cells. Fatty replacement may be irreversible, depending on the extent of sinusoidal and connective tissue damage (reticulohistiocytic system). These changes are complex. The temporal course and severity of changes are determined by the following factors: ● The composition of the bone marrow prior to radiation therapy. The radiosensitivity of mature and immature cellular constituents differs. ● Fat content. ● Patient age. ● Radiation duration. ● Radiation dose. ● Radiation technique.

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Fig. 11.30 Bone infarct. A 51-year-old female patient. (a) T1w image. Predominantly, metaphyseal lesion with fat-equivalent signal and hypointense margin (arrow). (b) STIR image. Hyperintense halo surrounding the lesion (granulation tissue; arrow).

Fig. 11.31 Multiple bone (marrow) infarcts following long-term cortisone therapy. (a) Sagittal T1w TSE image of the knee. Multiple hypointense, geographic bone marrow lesions (arrows) with, in some cases, garlandlike appearance (dotted arrow). (b) Sagittal STIR image of the knee. The characteristic infarction sites have high signal intensity.

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Fig. 11.32 Transient osteoporosis of the hip. (a) T1w SE image. Diffuse decrease in signal intensity in the femoral metaphysis and epiphysis. The greater trochanter apophysis is not affected and exhibits normal fat-equivalent signal. (b) T2w SE sequence. Corresponding hyperintensity. Small joint effusion (arrow).

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Fig. 11.33 Transient osteoporosis of the knee. A 51-year-old male patient with 6-month history of pain in the right knee but no trauma. (a) T1w image. Hypointense signal in the region of the lateral femoral condyle (arrow). (b) PDw image. Corresponding increase in signal intensity (arrow).

Doses of less than 2 Gy do not appear to induce any visible changes on T1w images.13 Doses between 8 and 15 Gy seem to result in characteristic changes in vertebral bodies, which are identifiable on MRI98,113,114: ● During week 1 of fractionated radiation or after radiation termination, bone marrow edema develops, exhibiting moderate reduced signal intensity on T1w images, slight hyperintensity on T2w images, and a sharp increase in signal intensity on STIR images. ● From week 2 to 3 after completion of radiotherapy, resolution of edema and an increase in the fat content are seen, especially

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around the central basivertebral vessels. This results in a central line of increased signal intensity and/or increased diffuse inhomogeneity on T1w images.134 After a few weeks, extensive fatty replacement with homogeneous increase in signal intensity is seen on T1w images. In this late stage, there may also be an area of central hyperintensity surrounded by reduced signal intensity.113,114 After several years, the vertebral bodies revert to normal in patients who had received doses of 30 to 40 Gy.13 It is thought that doses in the range 30 to 50 Gy result in persistent hyperintensity because of fatty replacement.53,54

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Bone Marrow The visible changes are confined to areas within the radiation field (▶ Fig. 11.34). Occasionally, distinct horizontal demarcations can be identified between normal and damaged marrow. However, quantitative analysis has revealed a slight increase in the fat content in areas adjacent to irradiated bone marrow sections because of scatter radiation; these were not visible on T1w images.54 The temporal course of the signal changes on T1w images is determined by the magnetic field strength. Signal changes are seen earlier with low field strengths than with high field strengths. The findings of the investigations conducted to date are comparable only to an extent, since they are based on different field strengths and different radiation protocols. Hence, the values given are merely a guide.

MRI has the same sensitivity as scintigraphy (up to 100%) for detection of inflammatory bone changes. However, thanks to its superior spatial resolution and high soft tissue contrast, MRI has higher specificity (over 90%) than scintigraphy (65%).121,137 MRI visualization of osteomyelitis can be further enhanced by using fat-suppressed, CM-enhanced sequences.81

Acute Osteomyelitis

Fig. 11.34 Postradiation changes. Sagittal T1w SE image of the pelvic region of a female patient following radiotherapy and 12 months before MRI. Fat-equivalent signal intensity of L5 vertebral body and of the sacrum. Normal signal intensity of the more cranial vertebral bodies.

Acute osteomyelitis manifests on MRI as reduced signal intensity on T1w images and hyperintensity on STIR or T2w images (▶ Fig. 11.35). Besides, there is intense CM enhancement, in particular, at the periphery of inflammatory foci.81 The inflammatory foci are poorly delineated against the normal bone marrow.14,15 Complications, such as soft tissue abscesses, soft tissue inflammatory processes, necrosis, and fistulas, can be detected with high sensitivity on MRI: ● Skin fistulas (sinus tracts): These exhibit high signal intensity on T2w images, take up CM, and extend from the bone to the surface of the skin.

Fig. 11.35 Bone marrow edema in osteomyelitis. (a) Sagittal T1w SE sequence. Homogeneous reduction in signal intensity of the tibia. (b) Sagittal T2*w GRE sequence. Homogeneous hyperintensity of the tibia.

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11.4.4 Inflammation

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Necrotic bone: This manifests as areas of homogeneous hyperintensity. Concomitant soft tissue inflammatory processes: These appear as high signal intensity, especially on T2w images (▶ Fig. 11.36).

The bone marrow changes identified on native MRI in association with acute osteomyelitis may, in terms of morphology and signal pattern, resemble those exhibited by contused bone and occult fractures. In the absence of explicit clinical symptoms, differential diagnosis may only be possible on the basis of the clinical course. An osteomyelitic focus is invariably surrounded by bone marrow edema. The absence of perifocal bone marrow edema makes a diagnosis of acute osteomyelitis less likely. Gd administration is a very sensitive method for detection of infection-related bone marrow changes and can also reliably differentiate between abscesses, necrosis, and inflammatory edema.43,50 The underlying pathophysiology with increased fluid accumulation in the bone marrow is thought to be similar. Healed osteomyelitis appears as localized fatty replacement within displaced hematopoietic marrow. Such changes can be seen, in particular, in the spinal column.

Chronic Osteomyelitis Active foci of chronic osteomyelitis exhibit the same signal pattern as acute osteomyelitis but are generally surrounded by a sclerotic halo devoid of signal and are more clearly delineated against the normal bone marrow. The distribution pattern of inflammatory foci is variable and may be multifocal or confluent (▶ Fig. 11.37, ▶ Fig. 11.38, and ▶ Fig. 11.39). Sequestered bone is devoid of signal on all sequences. Sinus tracts and reactive soft

tissue lesions have a similar signal pattern to that of acute osteomyelitis.72,94 The lesions seen in atypical forms of chronic osteomyelitis, such as Brodie’s abscess and plasma cell osteomyelitis (see ▶ Fig. 11.38 and ▶ Fig. 11.39), are more distinct. In plasma cell osteomyelitis, these are often found in proximity to epiphyseal regions and have intermediate signal intensity on T1w images and inhomogeneous high signal intensity on T2w images. Chronic Garré’s sclerosing osteomyelitis has diffuse reduction in signal intensity on all sequences. Chronic recurrent multifocal osteomyelitis (CRMO) is a relatively rare disease that mostly affects children. Because of the commonly observed characteristic palmoplantar pustular skin lesions, CRMO, like sternoclavicular hyperostosis, pustular arthro-osteitis, and SAPHO syndrome (synovitis, acne, pustulosis, hyperostosis, and osteitis), is assigned to the group of cutaneous osteoarthritic disorders, which are a subgroup of seronegative arthropathies. The disease is generally self-limiting, with spontaneous resolution within 2 to 7 years. Nonsteroidal anti-inflammatories can be effective for treating symptoms, but antibiotics are not effective. The diagnostic criteria are as follows: ● No pathogen detected. ● Multifocal skeletal lesions. ● Nonspecific, often normal laboratory results. ● No abscesses or fistulas.

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The clinical course is mainly punctuated by flares interspersed with symptom-free periods. The affected regions are painful during active flares.61,115 Bone lesions are encountered primarily in the metaphysis, epiphyseal plate, and, occasionally, extending into the epiphysis of tubular bones, as well as the sternum, clavicle,

Fig. 11.36 Chronic osteomyelitis of the midfoot and the hindfoot. (a) Lateral CT scan. Diffuse osteopenia with partially osteosclerotic and partially osteolytic changes, mainly in the calcaneus. (b) Fat-suppressed STIR sequence. Increase in signal intensity in infected bone areas. Concomitant soft tissue infection, with marked increase in signal intensity.

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Fig. 11.37 Chronic osteomyelitis. A 25-year-old male patient with chronic osteomyelitis of the left humerus. (a) Radiograph. (b) Coronal T1w image. (c) Coronal STIR image. (d) Axial CM-enhanced image.

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11.4 Focal Diseases

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Fig. 11.38 Plasma cell osteomyelitis of the distal tibia. (a) Axial T1w SE sequence following CM administration. Hyperintense tibial defect surrounded by signal-void halo (sclerotic margin). Slight signal inhomogeneity of the surrounding soft tissues. (b) Coronal T2w TSE sequences. Hyperintense defect in the distal tibial metaphysis, extending into the epiphysis and surrounded by a thin halo devoid of signal.

Fig. 11.39 Plasma cell osteomyelitis. The patient had experienced localized sternal pain for several weeks. Histology: plasma cell osteomyelitis (arrows). (a) Axial CT. Increased sclerosis of the body of sternum (arrow). (b) Coronal T1w image. Focal lesion, with central nidus (arrow) in the body of sternum, at the manubriosternal synchondrosis, surrounded by sclerotic halo and bone marrow edema. (c) Coronal T2w image. Here, too, the arrow points to the focal lesion.

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Sarcoidosis This autoimmune, inflammatory, systemic disorder of unclear etiology affects mainly the lymph nodes (90–100% of cases), lungs (70% of cases), and skin but many other organs can also be involved, for example, the eyes, liver (up to 60% of cases), spleen (up to 60% of cases), heart, central nervous system (CNS), muscles, bones (up to 10% of cases), and joints. Joint manifestations may present as sarcoidosis osteoarthritis and sarcoidosis synovitis. Inflammatory granulomas are identified within the affected muscles, whereas within bones, multiple small, often osteolytic foci of epithelioid cell granulomas are detected on radiographs (Jüngling’s osteitis multiplex cystoides), often in the intermediate and distal phalanges of the hands and feet. However, other parts of the skeletal system may also be implicated. A permeative pattern or osteopenia of the affected bone may also be identified, depending on the extent of osteolysis. Reactive osteosclerosis may be observed in later stages, too. On MRI, the epithelioid cell granulomas appear as small focal bone lesions, found mainly in the epiphyses and metaphyses of the affected tubular bones. These do not have characteristic signal intensity (low signal intensity on T1w and high signal intensity on T2w contrast images; ▶ Fig. 11.40). Multiple foci are encountered in various regions. It is not possible to clearly distinguish the multifocal sarcoidosis lesions from metastases on the basis of their morphology alone.80

Noninfectious Inflammatory Diseases Noninfectious inflammatory bone marrow edema may present in the adjacent bones, for example, following arthroscopy and, in particular, cartilage smoothing (▶ Fig. 11.41). In such settings, even progressive bone necrosis may be observed.58 The signal pattern is similar to that of bone marrow edema, with reduced signal intensity on T1w images and hyperintensity on T2w images. Sudbeck’s disease is thought to be caused by impairments in the autonomic nervous system, leading to abnormal perfusion in association with fractures, blunt trauma, or inflammation.105 The clinical, radiographic findings are classified into four stages: ● Stage I: No changes are identified on MRI. ● Stage II: Mainly patchy areas of partially confluent reduced signal intensity of the bone marrow are seen on T1w images as well as hyperintensity on T2w images, consistent with hyperperfusion and bone marrow edema.105 ● Stage III: The stage II changes in signal intensity now become more intense and widespread in stage III. ● Stage IV: Changes in signal intensity are only very rarely observed in stage IV. Stage IV “hypertrophic atrophy” exhibits no changes on MRI.

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Bone marrow enhancement after administration of paramagnetic CM is seen in stage II and, less pronounced, also in stage III. The most important radiographic signs are linked to osteoporosis, which, by definition, is visible on radiographs from stage II and becomes less severe in stages III and IV.

Arthritis More than 90% of cases of septic arthritis are found to contain multifocal, periarticular, edema-isointense, noninfectious foci in the marrow of adjacent bones. These areas take up CM. Conversely, osteomyelitis, as seen in septic arthritis, is more extensive, accompanied by periosteal reactions,66 and must be distinguished from such noninfectious bone marrow changes. The characteristic CM-enhanced erosions seen on radiographs can be observed in the later stages of septic arthritis. No changes are seen in the marrow of adjacent bones in noninfectious synovitis.

11.4.5 Trauma Bone Bruise Direct or indirect traumatic impact to the bone will eventually have different implications for the bone marrow, depending on the severity of impact. As in the case of parenchymatous organs, the term “bone bruise” (“bone contusion”) is used to denote the sequelae of mild trauma. These are characterized by bone marrow edema and hemorrhage but no trabecular fractures. On MRI, bone bruises appear as hypointense (T1w images) or hyperintense (T2w image) geographic (nonlinear) areas. Whereas radiographs do not show any abnormality, bone scans demonstrate tracer accumulation. Bone bruises resolve within 6 to 9 weeks and are no longer identifiable on MRI either.73 Bone bruises are often seen in the metaphyseal and epiphyseal segments of the femur and tibia, close to the knee joint, as well as in subchondral regions. They are frequently associated with ligament and meniscal injuries. Collateral ligament tears are generally accompanied by a bone bruise in the contralateral femoral condyle,73 whereas medial collateral ligament tears often involve a subchondral bone bruise in the lateral femoral condyle. Characteristic bone bruises are seen in the posterolateral tibial plateau as well as in the lateral femoral condyle following an external rotation injury that results in a torn anterior collateral ligament (▶ Fig. 11.42).88 Surgery is not indicated, as bone bruises resolve after offloading the affected joint.

Occult Fractures More severe trauma can also cause trabecular breakage or impaction. Microfractures with dimensions in the microscopic range are not visible on conventional radiographs and are thus termed “occult fractures.” Skeletal scintigraphy is generally positive in such cases. MRI demonstrates on all sequences a central band devoid of signal and surrounded by an irregularly outlined area that has low signal intensity on T1w images and high signal intensity on T2w images (▶ Fig. 11.43). Occult fractures are often found in periarticular regions. They can extend into the joint space and involve the articular cartilage (cartilage fracture). These are also visible

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spinal column, and pelvis. These resemble chronic osteomyelitic foci, initially of a more osteolytic nature with sclerotic halo and with more pronounced sclerosis during the symptom-free periods, and swelling. On MRI, the active foci are hypointense on T1w images and hyperintense on T2w images and, in particular, on STIR images. The sclerotic foci tend to have inhomogeneous low signal intensity. Signs of mild spondylodiscitis are seen in the spinal column. In view of the multifocal distribution of CRMO, whole-body MRI is an excellent technique for evaluating the extent of disease.128,130

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11.4 Focal Diseases

Fig. 11.40 Sarcoidosis of the skeletal system. (a) T2w FSE image, coronal section through the knee. Multiple hyperintense small focal lesions in the femoral and tibial metaphyses and epiphyses (arrows). (b) Sagittal STIR image of the knee. Multiple small focal lesions in the fibular epiphysis and metaphysis (arrows). (c) Sagittal T1w image of the foot. Multiple, slightly hypointense focal lesions in tibial metaphysis and epiphysis (arrows).

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Fig. 11.41 Bone marrow edema of the lateral femoral condyle after arthroscopy. (a) Coronal T1w SE sequence. Diffuse reduced signal intensity of the femoral condyle (arrows). (b) Coronal T2*w GRE sequence. Corresponding hyperintensity (arrows).

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Fig. 11.42 Bone marrow edema in association with anterior cruciate ligament (ACL) tear. A 27-year-old man following rotational trauma to the left knee while skiing. (a) Sagittal PDw image. Full-thickness ACL tear (arrow). (b) Bone marrow edema of the lateral femoral condyle (black arrow) as well as the posterior tibial plateau (white arrow) following traumatic ACL tear with pivot-shift injury mechanism. Joint effusion.

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Fig. 11.43 Occult fracture of the fibula. A 32-year-old female patient after rotational injury sustained while skiing. No fracture identifiable on radiographs. (a) A/P radiograph of the knee. (b) Lateral radiograph of the knee. (c) Coronal T1w image. Transverse hypointense line in the fibular head and longitudinal hypointense vertical line in the metadiaphyseal region (arrow). (d) Coronal PDw image. Corresponding linear increase in signal intensity (arrow).

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Bone Marrow with the MRI findings. The latter must also be interpreted in the light of other diagnosed bone fractures and follow-up observations.

Fractures When fractures causing cortical disruption are detected on MRI, it is also possible to identify concomitant changes in the surrounding soft tissues (fracture hematoma) as well as bone marrow involvement with an “edematous pattern.” Fractures that cannot, or can only indirectly, be identified on radiographs have been clearly visualized on MRI, in the femoral shaft (▶ Fig. 11.44).

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on MRI (osteochondral or subchondral occult fracture).73,126,135 The central signal-void band is caused by dephasing artefacts at the irregular, newly created boundaries between the trabeculae and bone marrow with their different susceptibility profiles. It has also been postulated that this is due to trabecular compression.135 The hypointensity on T1w sequences and hyperintensity on T2w sequences reflect bone marrow edema and hemorrhage in the vicinity of the trabecular fractures. Occult fractures have a favorable prognosis, although osteochondral lesions are known to cause progressive cartilage damage. Since operative interventions are not recommended in such cases, no biopsy material is available for histologic comparison

Fig. 11.44 Fracture of the femur. (a) Radiograph. Discontinuity of the greater trochanter (arrow) as well as short radiolucent line. Conventional tomography did not provide any additional insights. (b) T1w SE sequence. Reduced signal intensity of the right greater trochanter as well as lines of reduced signal intensity in the right femur, extending into the metadiaphyseal region (arrow). Normal linear decrease in signal intensity in the left femur due to compression and tensile trajectories as well as residual hematopoietic bone marrow (open arrow). (c) T2*w GRE sequence. Discontinuity of the greater trochanter (curved arrow) and linear hyperintensity in the right femur (arrow). The extent of fracture was better evaluated on MRI.

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MRI can also play a role in differentiating between malignant and osteoporotic fractures (see Chapter 12.4.4).

Avulsion Fracture Avulsion fractures in the periarticular region constitute a special type of fracture. The radiographic results may be negative if the avulsed cortical fragment is not, or only minimally, displaced. However, in such settings, MRI will show subcortical edema, with low signal intensity on T1w images and high signal intensity on T2w images. The fracture line and avulsed cortical fragment are devoid of signal and, as such, only indirectly identifiable. A typical example here is the avulsion fracture of the lateral proximal tibial plateau following internal rotation and varus stress injury (Segond’s fracture).129

Overloading (Stress Fractures) Fig. 11.45 Predilection sites of tibial and fibular horizontal stress fractures. Schematic diagram (n = 111). Downloaded by: The University of Edinburgh. Copyrighted material.

Stress fractures (fatigue fractures) are caused by an imbalance between the strength of a bone and the mechanical stress applied to the bone. Bones weakened by underlying bone diseases (osteomalacia, osteoporosis, and Paget’s disease) can fracture as a result of normal everyday activity (insufficiency fracture), or normal bone can fracture following chronic microtrauma (march fractures, jogging, and chronic cough) (stress fracture). The characteristic radiographic sign of a stress fracture is a transverse or oblique sclerotic band extending into the cortex and possibly containing a central radiolucent line. This fracture line reflects the typical orientation seen in this region. In tubular bones, the fracture line is generally horizontal, but in a number of cases (around 10%), the stress reaction in tubular bones also runs longitudinally (longitudinal stress fractures).119 Certain predilection sites reflecting the skeletal load have been identified for stress fractures (▶ Fig. 11.45, ▶ Fig. 11.46, and ▶ Fig. 11.47). MRI has been shown to have higher sensitivity for detection of stress fractures than conventional radiographs or computed tomography.56,65 This is particularly true for the early stages, when MRI is already able to clearly demonstrate changes, whereas radiographs have a sensitivity of only around 30%.32 On MRI, these changes are visualized as a bandlike area devoid of signal, which is generally surrounded by a pattern of reactive edema in the bone marrow.65,111 This signal-void band is indicative of trabecular microfractures and intratrabecular callus formation. Stress fractures may also be accompanied by subperiosteal hematoma and/or edema, and this should not be mistaken for soft tissue infiltration by a bone tumor. The signal-void band is a useful differential diagnostic pointer in such settings. It may be difficult to distinguish stress fractures from occult fractures, especially in patients with atypical histories. The stress fractures seen in tubular bones are usually metadiaphyseal fractures, whereas occult fractures are located in epiphyseal and subchondral regions.65

11.5 Clinical Relevance of Magnetic Resonance Imaging MRI is a highly sensitive modality for detection of bone marrow disease. Unlike conventional radiography, it is able to visualize changes even at the cellular level. MRI is also more sensitive than scintigraphy in diagnosing numerous diseases. When taking account of the available clinical data and of quantitative analyses, MRI is the most precise imaging modality for identification of pathologic bone marrow changes. However, its specificity for detection of diffuse or focal infiltration diseases is often not very high. Bone marrow MRI can also be used in principle as a screening method, but because of the high costs and limited availability, it is generally reserved for unclear cases where other diagnostic modalities were negative but a particular disease with clinical implications is suspected, for example, avascular necrosis, occult fractures, and metastases. The authors recommend MRI for diagnosis of bone marrow disorders subject to the following indications: ● Differential diagnosis between osteoporosis and diffuse plasmacytoma. ● Lymphoma staging. ● Pediatric tumor staging. ● Investigation of metastatic disease in unclear cases and prior to radiotherapy. ● Diagnosis of avascular necrosis. ● Acute osteomyelitis and CRMO. ● Radiographically “occult” fractures.

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Fig. 11.46 Stress fracture of the fourth metatarsal. A 25-year-old female jogger with pain along the fourth digital ray of the left foot. (a) Lateral radiograph. Slight radiolucency in the distal shaft of the fourth metatarsal, left (arrow), but no evidence of cortical disruption or step deformity. (b) A/P radiograph. No correlation. (c) T1w image. Cortical discontinuity in the distal shaft of the fourth metatarsal (arrow). (d) PDw image. Marked bone marrow edema of the fourth metatarsal and edema of the surrounding soft tissues (arrow). (e) CT image. Fracture in the distal shaft of the fourth metatarsal, with cortical disruption and step deformity (arrow).

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Fig. 11.47 Insufficiency fractures of the sacrum. A 73-year-old female patient. Bilateral insufficiency fractures of the sacrum (a, b, arrows). (a) Axial CT image of the pelvis. (b) Coronal CT image of the pelvis. (c) STIR image of the sacrum, showing bilateral insufficiency fractures surrounded by bone marrow edema (arrows). (d) Status post CT-guided bilateral sacroiliac screw fixation of S1 and S2 with augmentation. (e) Radiograph after screw fixation.

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12.1

Introduction

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12.2

Examination Technique

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Bone and Soft Tissue Tumors

12.3

Tumors: General Information

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12.4

Tumors: Specific Section

529

References

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Chapter 12

Bone and Soft Tissue Tumors

12 Bone and Soft Tissue Tumors M. Vahlensieck and A. Baur-Melnyk

Before the introduction of cross-sectional imaging, primary bone tumors were diagnosed and classified by conventional radiography and conventional tomography. Even today, with the widespread use of computed tomography (CT) and magnetic resonance imaging (MRI) in the routine clinical setting, conventional radiography continues to be the imaging modality of choice for initial diagnostic assessment of the biological activity of bone tumors. Conventional radiographs play a key role when evaluating bone tumors on MRI, and often provide for histopathologic classification of tumors of the skeletal system. However, it can at times be difficult to visualize tumors of the scapula, ribs, vertebrae, and pelvis on conventional radiography.134 Today, MRI is one of the diagnostic mainstays for detection of tumors of the skeletal system. MRI is superior to CT for the following reasons: ● MRI has better soft tissue contrast. ● MRI offers direct multiplanar imaging. ● MRI permits better tissue differentiation because of the different signal patterns of the various tissues in specific sequences.10 MRI is more accurate than other imaging techniques for staging bone and, in particular, soft tissue tumors.13,46,157 Besides, MRI is better than CT at detecting tumor infiltration of neurovascular bundles.13,157 In this chapter, we present the methods currently employed for demonstration of bone and soft tissue tumors on MRI. We will also discuss staging, tissue-specific imaging findings, chemotherapy- and radiotherapy-induced changes, detection of tumor recurrence, and the characteristic findings of specific tumors.

12.2 Examination Technique The first sequence should be acquired with a body coil to allow adequate assessment of the proximal and distal extent of the lesion and assure visualization of the tumor in its entirety. Body coil imaging is also useful for ruling out any proximal or distal metastases (skip lesions) (▶ Fig. 12.1). Depending on the size of the lesion, the examination can then be continued with a surface coil, torso phased-array coil, or a circumferential extremity coil. In general, a small field of view (FOV) should be selected to achieve high spatial resolution but it should be big enough to include the entire tumor and, in particular, any tumor infiltration of blood vessels, nerves, or muscles. A spinal phased-array coil should be used if the entire spinal column is to be imaged for the presence of metastases. If the pelvis or both upper and lower extremities are to be examined for metastatic disease, a torso phased-array coil or body coil can be used. A standard protocol for tumor assessment includes coronal or sagittal T1-weighted (T1w) and/or short-tau inversion recovery (STIR) images with a large FOV to evaluate the extent of the tumor, as well as high-resolution axial T1w, T2-weighted (T2w), or STIR and contrast-enhanced T1w images with subtraction

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images. Fat-suppressed proton density–weighted (PDw) turbo spin-echo (TSE) sequences and fat-suppressed contrast medium (CM)-enhanced sequences, as normally used in diagnostic imaging of the joints, can yield incorrect results with regard to tumor extension and tissue assignment. The authors suggest the following protocol in such settings: ● Coronal or sagittal (depending on tumor extension and location) T1w and STIR images. ● Axial T2w image (for assessment of neurovascular invasion or encasement). ● Coronal or sagittal and axial T1w fatsat images following CM administration.

12.3 Tumors: General Information 12.3.1 Comparison of Benign and Malignant Tumors Magnetic Resonance Imaging Many of the criteria used in conventional radiography and CT for classification of potentially malignant bone tumors can also be applied to MRI. Benign lesions are generally sharply delineated against the adjacent healthy, noninfiltrated bone marrow and surrounding soft tissues.111,157 Conversely, malignant tumors are less sharply marginated and tend to infiltrate the surrounding tissues.111 If the tumor has a well-defined, hypointense capsule, it is likely to be benign.157 However, this is not definite since such a tumor capsule can also be identified in malignant tumors.157 Petasnick et al111 reported that the majority of benign tumors had homogeneous signal intensity on T1w as well as T2w sequences; however, neurofibromas and hemangiomas often exhibited inhomogeneous signal intensity on T2w images. Most malignant tumors had homogeneous low signal intensity on T1w sequences but with a distinct inhomogeneous signal pattern on T2w images.111 Based on these findings, detection of homogeneous signal intensity on T2w sequences would therefore be suggestive of a benign lesion. In general, it can be said that the signal pattern exhibited by a tumor can give insights into its dignity. However, the specificity is inadequate; therefore, the diagnosis is mainly based on histologic examination. Since there is widespread overlap between the T1 and T2 relaxation times of benign and malignant lesions, these are not suitable for clinical assessment of tumor dignity.111,157

Dynamic Magnetic Resonance Imaging Erlemann et al35 reported that dynamic MRI with rapid sequential image acquisition after intravenous bolus injection of GdDTPA could possibly be useful in distinguishing between benign and malignant skeletal tumors (▶ Fig. 12.2). In their study, the slope of the enhancement time curve (signal intensity per unit of time) after bolus injection was greater than 30% and more per minute in 84.1% of malignant tumors; that slope was less than 30% in 72% of benign tumors.35 While these results are an

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12.1 Introduction

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12.3 Tumors: General Information

Fig. 12.1 Osteogenic sarcoma with bone daughter metastases (skip lesion). (a) T1w MRI. Hypointense primary tumor in distal femur. (b) T1w MRI. The metastatic lesion (arrow) in the proximal femur can be identified as an area of low signal intensity. (c) Coronal PDw GRE MR image. Hyperintense metastatic lesion (arrow) in proximal femur.

improvement on those obtained with native MRI, there continues to be widespread overlap between the values of benign and malignant tumors.35 Therefore, biopsy is still needed for a conclusive diagnosis.

Verstraete et al149 also investigated the slope of the enhancement time curve after CM administration and, using a linear curve fitting algorithm, calculated a maximum CM enhancement rate during the first minute after injection. The slope steepness was

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Fig. 12.2 Osteosarcoma. Representative example of dynamic MRI. The images were generated at intervals of 3.5 s. Viable tumor rapidly takes up CM; this is typical of most malignant lesions. (a) Time point 0: before bolus injection (0 s). (b) Time point 1: 35 s after bolus injection. (c) Time point 2: 4 min after bolus injection.

calculated pixel by pixel and displayed as a grayscale in a computer-generated first pass image. In that computer-generated image, high-signal pixels corresponded to the tumor regions, with fastest CM enhancement, whereas areas with lower signal intensity exhibited correspondingly slow increase in signal intensity after Gd-DTPA administration. These computer-generated images were well correlated with tissue vascularization and perfusion. However, here, too, there was considerable overlap between malignant and highly vascularized benign tumors, such as an eosinophilic granuloma, giant cell tumor, or an osteoid osteoma. Nonetheless, the computer-generated images were useful in identifying vital tumor tissue, in particular, after chemotherapy and differentiating this from necrotic tumor and from surrounding inflammatory changes.

Diffusion Weighting Like dynamic MRI, perfusion-corrected diffusion-weighted imaging (DWI) is potentially able to assess the dignity of tumors,148 with malignant soft tissue tumors having a significantly lower apparent diffusion coefficient (ADC). However, as mentioned, a clear distinction is not possible because of widespread overlap of values.31

Fig. 12.3 Lipoma. The lesion on the thigh (arrows) has high signal intensity on T1w sequences, reflecting the fat signal.

12.3.2 Characteristic Signal Intensity Patterns Certain tissues identified on histologic examination in tumors of the musculoskeletal system can be identified on the basis of their signal intensity pattern: ● Fat within a tumor, such as in a lipoma (▶ Fig. 12.3), liposarcoma, or vertebral hemangioma, exhibits high signal intensity

518

●

●

on T1w images and intermediate to high signal intensity on T2w images (▶ Table 12.1). Fibrotic tissue is characterized by low signal intensity on all sequences or by the presence of cordlike areas of reduced signal intensity (see ▶ Table 12.1).113 Likewise, sclerotic bone, as often seen, for example, in osteosarcomas, has low signal intensity on all sequences.

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Bone and Soft Tissue Tumors

12.3 Tumors: General Information Table 12.1 Signal intensity of normal and neoplastic tissues on various sequences T2w SE

T2w FSE

“T1w” GRE

T2*w GRE

STIR

“T1w” SE postcontrast

“T1w” GRE postcontrast

Yellow bone marrow High

Intermediate to high

High

High

Low to intermediatea

Low

High

High

Cortical bone

Low

Low

Low

Low

Low

Low

Low

Low

Muscle

Low

Low to intermediate

Low to intermediate

Low

Intermediate

Low to intermediate

Low to intermediate

Low to intermediate

Ligaments

Low

Low

Low

Low

Low

Low

Low

Low

Tendons

Low

Low

Low

Low

Low

Low

Low

Low

Vessels

Low

Low

Low or highb

Low, intermediate, highb

Low, intermediate, highb

Low or high

Low

Low

Nerves

Low

Low to intermediate

Low to intermediate

Low

Intermediate

Low

Low

Low

Subcutaneous fat

High

Intermediate to high

Intermediate to high

High

Intermediate

Low

High

High

Intraosseous tumor

Low, intermediate

High, intermediate

High, intermediate

Low, intermediate

Highc

Highc

High

High

Extraosseous tumor

Low, intermediate

High, intermediate

High, intermediate

Low, intermediate

Highc

Highc

High

High

Fatty tumor

High

Intermediate to high

Intermediate to high

High

Intermediate

Low

High

High

Sclerotic tumor

Low

Low

Low

Low

lowd

Low

Low

Low Lowe

Tissue

T1w SE

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Normal tissue

Pathologic tissue

Tumor cyst

Low

High

High

Low

High

High

Lowe

Hemorrhage—fresh (deoxyhemoglobin)

Low

High

High

Low

High

High

Low

Low

Hemorrhage—4 weeks old (methemoglobin)

High

High

High

High

High

High

High

High

Hemorrhage—old (hemosiderin)

Low

Low

Low

Lowd

Lowd

Low

Low

Lowd

Peritumoral edema

Low

High

High

Low

High

High

High

High

aCaused

by inhomogeneous magnetic susceptibility at the interface between trabecular bone and bone marrow (see text). on flow direction and velocity, direction of phase encoding, and distance from the entry section. cExcept for tumors that are primarily fibrous or sclerotic. dIn many cases with irregular, partially cauliflowerlike appearance due to inhomogeneous magnetic susceptibility with corresponding artefacts. eIn some cases, with peripheral enhancement reflecting viable tumor or blood vessels in cyst wall. bDepends

●

●

Cystic, fluid-filled tumor regions, in general, exhibit low signal intensity on T1w images and high signal intensity on T2w images, without any appreciable CM enhancement after administration of paramagnetic CM.113 A cyst can, however, have high signal intensity on T1w image if it contains protein-rich materials or methemoglobin following hemorrhage.

Tumors that typically have a short T1 relaxation time, that is, high signal intensity on T1w sequences, include (see ▶ Fig. 12.3): ● Fatty tumors: ○ Lipoma.

Liposarcoma. Hemangioma. Tumors with methemoglobin: ○ Telangiectatic osteosarcoma. ○ Hemorrhagic metastases. ○ Malignant tumors following chemo- or radiotherapy. ○ Pseudotumor in hemophilia. ○ Lymphangioma. ○ Arteriovenous malformation. ○ Melanotic metastasis in association with malignant melanoma. ○ ○

●

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Bone and Soft Tissue Tumors Table 12.2 Tumors with fluid–fluid levels (in 624 bone tumors, total incidence of fluid–fluid levels: 11%)105 Tumors

Proportion with fluid–fluid levels (%)

Benign tumors (incidence: 20%) Aneurysmatic bone cyst

87

Simple bone cyst

36

Benign fibrous histiocytoma

33

Chondroblastoma

25

Intraosseous lipoma

20

Fibrous dysplasia

19

Giant cell tumor

16

Enchondroma

9

Fig. 12.4 Aneurysmatic bone cyst of the tibial metaphysis. T2w TSE image. Fluid–fluid levels following sedimentation of corpuscular blood components (arrow).

Glycosaminoglycans with sulfur-containing (chondroitin sulfate) and non-sulfur-containing components (hyaluronic acid) are typical constituents of a myxoid matrix, as found in certain tumors85: ● Ganglion cysts. ● Myxoma. ● Nerve sheath tumor (schwannoma, nerve sheath fibroma, malignant peripheral nerve sheath tumor). ● Myxoid liposarcoma. ● Myxofibrosarcoma. ● Myxoid chondrosarcoma of the soft tissues. ● Low-grade fibromyxosarcoma (Evans’ tumor). ● Myxoinflammatory fibroblastic sarcoma. A myxoid matrix is characterized by fluid-isointense signal on T2w and T1w images (somewhat brighter on T1w and somewhat darker on T2w contrast images) as well as by more or less strong CM enhancement (apart from ganglion cysts). These characteristic signal intensity patterns often serve as differential diagnostic pointers. Furthermore, the presence of fluid– fluid levels on T2w images also facilitates differential diagnosis. Fluid–fluid levels represent a nonspecific change secondary to hemorrhage and help differentiate between an aneurysmatic and a simple bone cyst (▶ Fig. 12.4), necrosis, etc., and are encountered in malignant and benign tumors (▶ Table 12.2).

12.3.3 Staging Staging Systems Enneking’s Staging The choice between limb salvage surgery and amputation is determined by the aggressiveness and local spread of the tumor.5, 43,101,121 This staging system has proved useful for assessment of primary bone or soft tissue tumors, in particular, with regard to prognosis, treatment, and recurrence rate.32 This system classifies

520

Spindle cell sarcoma

33

Osteosarcoma

23

Malignant fibrous histiocytoma

15

Paget’s sarcoma

14

Metastases

5

the tumors into different stages (▶ Fig. 12.5), based on the following parameters: ● Histologic grade of malignancy G: ○ G0 = benign. ○ G1 = low-grade malignant. ○ G2 = high-grade malignant. ● Local spread and infiltration T: ○ T0 = intracapsular. ○ T1 = extracapsular but compartment confined. ○ T2 = extracapsular, spread beyond compartment of origin. ● Metastases M: ○ M0 = no metastases. ○ M1 = regional or distant metastases. The Enneking’s staging system does not apply to staging of leukemia, lymphomas, myelomas, Ewing’s sarcoma, or metastases. A distinction must be made between this method of staging bone and soft tissue tumors and the system proposed by Lodwick et al for assessment of the growth rate of bone tumors based on the radiographic destruction pattern.88 MRI provides for accurate staging, thanks to its ability to delineate the tumor in relation to compartment boundaries (see Transcompartmental Tumor Extension, p. 524) and its spatial relationship to neurovascular bundles (see Neurovascular Bundle Infiltration, p. 524). The potential surgical procedures available include limb salvage surgery (resection and reconstruction) and amputations with four different curative surgical margins (▶ Table 12.3). Surgical planning is guided by the tumor stage and the different recurrence rates in relation to the surgical margin (▶ Table 12.4). Accurate assessment of local tumor spread on MRI is vital for planning and conduct of, in some cases, very intensive reconstructive surgical procedures.43

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Malignant tumors (incidence: 9%)

12.3 Tumors: General Information

Stages 1–3: Histologically benign (G0) with variable clinical course and biological behavioral patterns

Benign

Stage 1: Remains stationary or heals spontaneously with indolent clinical course. Well encapsulated (T0)

Soft tissue tumor Bone tumor

Stage 2: Active disease. Progressive symptomatic tumor growth. The tumor continues to be intracapsular. Limited by natural boundaries which, however, are often deformed (T0)

Stage 3: Aggressive disease. Aggressive growth not limited by capsule or natural boundaries. The tumor can penetrate cortex or compartment boundary. Higher recurrence rate (T1–T2)

IA

Malignant

IB

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Stage I: Histologically low-grade malignancy (G1), well differentiated, few mitoses, moderate nuclear atypia. Tends to recur locally. Moderate radioisotope uptake

Intraosseous or intracompartmental (T1)

Extraosseous or extracompartmental, penetrates cortex or compartment boundaries (T2)

Stage II: Histologically high-grade malignancy (G2), undifferentiated, high cell-to-matrix ratio, many mitoses, severe nuclear atypia, necrosis, neovascularity, patchy osteolytic destruction. Intense radioisotope uptake. Higher tendency toward metastases

IA

IB

Intraosseous or intracompartmental (T1)

Extraosseous or extracompartmental, penetrates cortex or compartment boundaries (T2)

Stage III: Metastatic stage: regional or remote metastases (viscera, lymph nodes, or bones)

Fig. 12.5 Staging tumors of the musculoskeletal system after Enneking.

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Bone and Soft Tissue Tumors Table 12.3 Curative surgical strategies for tumors of the musculoskeletal system depending on stage Enneking’s stage

Resection

Amputation

1 (inactive)

Intracapsular resection

Subtotal amputation

2 (active)

Extracapsular resection (en-bloc resection within the reactive zone) Marginal amputation

3 (aggressive)

Further resection (including resection of 2–3 cm healthy tissue safety margin)

Extensive amputation

I (low-grade malignant)

Extensive resection

Extensive amputation

II (high-grade malignant)

Radical resection (complete resection of affected compartments, thus often including the joint)

Radical amputation

Benign

Malignant

Table 12.4 Recurrence rates in percentage of bone and soft tissue tumors based on Enneking’s stage curative surgical margins (not further categorized)103 Stage Benign

Malignant

1

2

3

IA

IB

IIA

IIB

Intracapsular enucleation

0

30

70

90

90

100

100

Excision along the tumor margins

0

0

50

70

70

90

90

Excision in healthy tissue

0

0

10

10

30

30

50

Radical resection

0

0

0

0

0

10

20

Table 12.5 Staging bone tumors based on TNM classification Stage

Grading

Primary tumor

Local lymph nodes

Distant metastases

IA

G1, G2

T1

N0

M0

IB

G1, G2

T2

N0

M0

IIA

G3, G4

T1

N0

M0

IIB

G3, G4

T2

N0

M0

III

Not defined

IVA

Each G

Each T

N1

M0

IVB

Each G

Each T

Each N

M1

TNM Classification TNM classification of bone tumors is based on cortical infiltration: ● T1 = no transcortical infiltration. ● T2 = transcortical infiltration. The TNM classification system does not apply to malignant lymphomas, multiple myelomas, superficial and juxtacortical osteosarcomas, or chondrosarcomas. The histology grading system recognizes four different grades: ● G1 = good. ● G2 = moderate. ● G3 = poor. ● G4 = undifferentiated. This system also takes account of locoregional lymph node metastases (N1) and of distant metastases (M1), which are then

522

classified into four stages (▶ Table 12.5). TNM classification of soft tissue sarcomas takes the size into consideration: tumors whose maximum extension is less than 5 cm are designated as “T1” and tumors greater than 5 cm as “T2.” Furthermore, a distinction is made between superficial (a) and deep tumors (b) with regard to the fascia. As for bone tumors, there are four histopathology differentiation grades. These also provide for classification into four main stages (▶ Table 12.6).

Tumor Extension Intramedullary Extension MRI is vastly superior to CT in determining intramedullary extension of a tumor.1,13,14,15,46,57,82,84,106,111,134,135,136,137,157 Gillespy et al46 compared CT and MRI for assessment of intramedullary extension of bone tumors by comparing the sectional images with the macrohistology specimens. While the mean difference

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Curative surgical margin

12.3 Tumors: General Information Table 12.6 Staging soft tissue sarcomas based on TNM classification Stage

Grading

Primary tumor

Local lymph nodes

Distant metastases

IA

G1, G2

T1a and T1b

N0

M0

IB

G1, G2

T2a

N0

M0

IIA

G1, G2

T2b

N0

M0

IIB

G3, G4

T1a and T1b

N0

M0

IIC

G3, G4

T2a

N0

M0

III

G3, G4

T2b

N0

M0

IV

Each G

Each T

N1 (or N0)

M1 (or N0)

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between CT images and the macrospecimens was 16.5 ± 10.7 mm, the mean deviation between MRI and the macrospecimens was only 4.9 ± 4.3 mm. Most of the differences between MRI and the histology specimens appear to derive from the fact that the MR images were not in the same sectional plane as the histology specimens. The mean difference was only 1.8 ± 1.6 mm for a subgroup of patients whose MRI and histology findings were in the same plane.46 Bloem et al13 also compared intraosseous tumor extension with CT and MRI measurements. There was virtually complete correlation between MRI and the histopathology specimen (correlation coefficient, r = 0.99), whereas this correlation was less good for CT (r = 0.86). The poorest correlation was identified for bone scintigraphy with technetium-99m-methylene diphosphonate (r = 0.56). These data show that MRI is far superior to CT in assessing intraosseous tumor extension.

Epiphyseal Extension MRI is better at identifying epiphyseal tumor extension than conventional radiography.104 Norton et al104 detected epiphyseal infiltration in 12 of the histology specimens belonging to a group of 15 patients with osteogenic sarcoma. While conventional radiography detected this only in 9 cases, MRI correctly identified all 12 cases.

Intra-articular Extension It is unclear whether MRI is more accurate than CT at identifying intra-articular tumor extension. Bloem et al13 reported similar results for both modalities, with sensitivity and specificity in the 90% range. However, Aisen et al1 as well as Zimmer et al157 found that MRI was more accurate than CT for a small proportion of patients, but the two methods produced comparable results for the majority of patients (▶ Fig. 12.6).

Periosteal Reaction and Cortical Destruction Several studies have reported the superiority of conventional radiography and CT over MRI at detecting cortical destruction, tumor calcification, and ossification as well as periosteal or endosteal reaction.7,113,132,133,134,157 The high bone density in regions with periosteal reactions or osteoblastic activity reduces the concentration of resonating protons, in turn producing low signal intensity on MRI. This low signal intensity explains the difficulty

Fig. 12.6 Acetabular tumor. Oblique sagittal, high-resolution, contrast-enhanced SE image. Acetabular tumor of the pelvis extending into the joint. The cartilage of the acetabular roof has been infiltrated but, so far, not the joint space or the femoral cartilage. Joint infiltration can be clearly identified here on the high-resolution, multiplanar section. The tumor exhibits inhomogeneously high signal intensity following CM uptake. Reconverted bone marrow is seen in the entire acetabulum (see Chapter 11.3.1), a normal finding for a 65-year-old patient.

of visualizing these changes on MRI. However, the majority of studies reporting the superiority of CT over MRI in this regard are several years old and were carried out with low field strengths and outdated coil technology. Zimmer et al157 attested to the ability of MRI to demonstrate cortical destruction as well as peri- and endosteal new bone formation. MRI sensitivity at detecting discrete sclerotic changes can be improved with gradient-echo (GRE) sequences (▶ Fig. 12.7). Focal sclerotic areas show local inhomogeneous magnetic susceptibility with ensuing signal loss as, unlike SE images, spin rephasing was not carried out. That signal loss can be exploited to demonstrate focal sclerosis or periosteal reaction.

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Bone and Soft Tissue Tumors

Both CT and MRI are able to demonstrate soft tissue extension of primary soft tissue and bone tumors. To that effect, CT relies, in particular, on indirect signs when determining soft tissue extension. For example, there is obliteration of the fat layers between the individual muscle groups and the tumor as well as displacement of the structures adjacent to the lesion. Often, however, the healthy soft tissues and the soft tissue tumor components have similar density on native CT, thus precluding accurate differentiation. That distinction can only be made after administration of intravenous CM.89, 124,140 However, even when intravenous CM is used, CT is much less accurate than MRI in identifying soft tissue lesions.111 Overall, MRI is far superior to native and CM-enhanced CT at detecting soft tissue extension of primary bone and soft tissue tumors. That is mainly due to the essentially higher contrast between the tumor and surrounding healthy tissues.1,157

Transcompartmental Tumor Extension Tumor extension is an important criterion for staging. The extremities (limbs) are divided into different compartments by fascia, bone, and membranes, and one of the aims of diagnostic imaging is to determine whether the tumor is confined to the compartment of origin or has also infiltrated adjacent compartments (extracompartmental stage). The following compartments are distinguished: ● Bone. ● Parosteal or periosteal bone. ● Joint. ● Superficial space (above the superficial fascia). ● Muscle compartments (within the superficial fascia [intrafascial]).

The muscle compartments are classified as follows depending on the extremity portion involved (▶ Fig. 12.8)138,139: ● Upper arm: anterior, posterior, and deltoid compartment. ● Forearm: volar or flexor compartment, dorsal or extensor compartment (there is also a four-compartment classification system based on other muscle subgroups divided into deep and superficial groups). ● Thigh: anterior, posterior, and medial compartment. ● Lower leg: anterior, lateral, superficial posterior, and deep posterior compartment. ▶ Table 12.7 gives an overview of the tumor compartment classification.

Neurovascular Bundle Infiltration MRI is also superior to CT at detecting neurovascular bundle infiltration.1,13,111,113,157 Bloem et al13 identified a sensitivity, specificity, and accuracy of 33, 93, and 82%, respectively, for CT, whereas MRI had a sensitivity of 100%, specificity of 98%, and accuracy of 98%. It is often difficult to differentiate between tumor and surrounding fat after administration of Gd-DTPA.124 On precontrast images, the tumor typically exhibits low signal intensity and can be clearly delineated from the adjacent hyperintense fat. On postcontrast images, however, the tumor often has high signal intensity, thus obscuring its identification.35,124 Visualization can be enhanced using image subtraction for contrast-enhanced and native images. Whether there is tumor infiltration of a vessel or nerve is determined on axial T2w SE images. There is a probability of neurovascular invasion if the circumferential encasement of the vessel by the tumor is more than 180 degrees. If encasement is more than 270 degrees, vascular invasion can be assumed.153 MR angiography (MRA) is particularly adept at demonstrating displacement, compression, and encasement of blood vessels by tumors.78

Fig. 12.7 Periostitis in association with malignant bone tumors. Axial GRE images. (a) Osteosarcoma of the femur with “sunburst” calcifications in the periosteal reaction (arrow). (b) Ewing’s sarcoma of the femur. More lamellar calcification of the periosteal reaction in the region of the extraosseous tumor component (arrow). Thanks to the short TE (9 ms), calcifications can be clearly identified despite this measurement sequence having a high sensitivity to susceptibility artefacts.

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Soft Tissue Extension

12.3 Tumors: General Information

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Fig. 12.8 Muscle compartments. Schematic diagram of the various muscle compartments. For a precise designation of the muscles and fascia, please see ▶ Fig. 10.2. (a) Section through the proximal upper arm. (b) Section through the proximal forearm. (c) Section through the medial forearm. (d) Section through the proximal thigh. (e) Section through the medial thigh. (f) Section through the distal thigh. (g) Section through the medial lower leg. 1, anterior compartment (upper arm): biceps brachii, brachialis, and coracobrachialis muscles; 2, posterior compartment (upper arm): triceps brachii (lateral, long, and medial heads). 3, deltoid compartment (upper arm): deltoid; 4, volar or flexor compartment (forearm): pronator teres, flexor carpi radialis, palmaris longus, flexor digitorum superficialis and profundus, flexor pollicis longus, and carpi ulnaris muscles; 5, dorsal or extensor compartment (forearm): brachioradialis, extensor carpi radialis brevis and longus, supinator, extensor digitorum, extensor pollicis brevis and longus, extensor digiti minimi, extensor carpi ulnaris, and abductor pollicis longus muscles; 6, medial compartment (thigh): gracilis and adductor magnus, longus and brevis muscles; 7, posterior compartment (thigh): semitendinosus, semimembranosus, and biceps femoris muscles (long and short heads); 8, gluteus maximus; 9, anterior compartment (thigh): sartorius, rectus femoris and vastus medialis, intermedius and lateralis muscles, quadriceps tendon; 10, anterior compartment (lower leg): tibialis anterior, extensor hallucis longus, and extensor digitorum longus muscles; 11, deep posterior compartment (lower leg): tibialis posterior, flexor hallucis longus, and flexor digitorum longus muscles; 12, superficial posterior compartment (lower leg): soleus and gastrocnemius (medial and lateral heads); 13, lateral compartment (lower leg): peroneus longus and brevis muscles.

Differentiation between Perineoplastic Edema and Extraosseous Tumor Both viable tumor and perineoplastic edema have high signal intensity on postcontrast T1w images. Pettersson et al114 studied the conventional T1w postcontrast images belonging to five patients with soft tissue tumors after administration of Gd-DTPA.

They found that the tumor tissue as well as the surrounding perineoplastic edema showed intense CM uptake. Hanna et al54 similarly identified high signal intensity in viable tumor, granulation tissue, and peritumoral edema. Dynamic MRI after Gd-DTPA bolus injection appears to be the most promising method for differentiating between tumor and extraosseous edema. Lang et al79 carried out dynamic imaging

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Bone and Soft Tissue Tumors Table 12.7 Compartmental classification after Enneking Infiltration (if there is involvement of these structures → designated as “extracompartmental”)

In bone

Soft tissue infiltration

In joint

Soft tissue infiltration

Superficial (above the fascia)

Facial infiltration or deeper

Parosteal

Bone infiltration or extending beyond the superficial fascia

Intrafascial compartments

Extending beyond the superficial fascia or into the adjacent compartment

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Site of origin (if tumor identifiable only there → designated as “intracompartmental”)

Fig. 12.9 Osteogenic sarcoma with viable and necrotic components. (a) T1w precontrast MR image. The tumor in the distal femur has, to a large extent, homogeneously low signal intensity. (b) T1w postcontrast MR image. Most of the tumor exhibits intense CM enhancement reflecting viable tissue. Necrotic areas do not take up CM and continue to have low signal intensity (arrows).

with a temporal resolution of 3.5 s per image. These images were generated sequentially after CM bolus injection. An algorithm with an exponential function was used to measure the slope of the contrast-enhancement curve from the outset. The slope was calculated pixel by pixel and displayed as a rescaled gray value; in this way, a computer-generated image of the slope was produced for each individual element of an image. Thanks to the high temporal resolution of the sequence and the exponential algorithm, it was possible to distinguish between viable tumor and extraosseous edema on reviewing the curve slope images: the curve slope values of viable tumor and tumor-infiltrated muscle tissue were 20% and higher than those of perineoplastic edema.79 Computer-generated curve slope images appear to be particularly useful for preoperative planning of joint salvage surgery since they permit better

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assessment of the tumor margins. This method might also lend itself for monitoring chemotherapy response.

Differentiation between Viable and Necrotic Tumor MRI is able to distinguish viable from necrotic tumor after intravenous administration of Gd-DTPA. Except for hypovascular lesions, viable tumor shows strong CM enhancement. Conversely, necrotic tumor does not generally take up CM and continues to exhibit low to intermediate signal intensity on postcontrast images (▶ Fig. 12.9).35,77 However, one drawback is that the Gd complexes used in the clinical setting have a low molecular weight and, because of their small size and distribution within the intracellular space, could diffuse into the necrotic tumor.

12.3 Tumors: General Information

Currently, biopsy sites are selected on the basis of the clinical findings, such as local soft tissue swelling. However, if the biopsy is taken from a necrotic area, it will often have no diagnostic value. Hence, MR postcontrast images may be useful in identifying viable tumor regions and, as such, in selecting a suitable biopsy site.35,77 A biopsy should be planned such that the biopsy canal is also resected in accordance with the intended curative surgical margins of the planned surgical procedure. This helps to avoid development of inoculation metastases at a later date. Contact with any adjacent compartments not scheduled for resection should be avoided when taking a biopsy.

12.3.5 Monitoring the Response to Chemotherapy It is difficult to determine the response to chemotherapy through clinical examination alone. However, it is important to already know at an early stage whether the tumor has responded to treatment or whether the chemotherapy regimen should be changed. The decisive criterion for assessment of the response rate to treatment is currently the extent of cell necrosis in the histology specimens. Patients with tumor cell necrosis of more than 90% are deemed to have a good response rate, while those with less than 90% have a poor response rate. Clinical parameters such as local soft tissue swelling or local hyperthermia are poorly correlated with the histology results.67,152 Conventional radiography, angiography, CT, and bone scintigraphy were used in the past for assessment of treatment effectiveness. However, the specificity of these modalities in distinguishing effective from ineffective

therapy is low, and was even found to be less than 50% in various studies.19,126 By contrast, MRI is able to provide both morphologic and quantitative information on the treatment response. The morphologic signs of treatment effectiveness are as follows: ● Decrease in tumor volume. ● Enhanced visualization of muscle and fat layers. ● Appearance of cystic areas in the tumor tissue.60,109 An increase in tumor volume is a marker of chemotherapy failure (▶ Fig. 12.10). Progressive calcification along the tumor periphery, as well as at the center of the tumor, is a sign of a good response to treatment in osteosarcomas.21,95 In most cases, perineoplastic edema regresses in line with effective treatment.60,109 Malignant tumors are often surrounded by a hypointense rim which is composed of collagen fibers and which extends into the periosteum. This peripheral zone may become thicker as the tumor responds to treatment and the perineoplastic edema resolves.109 Pan et al109 described four different postchemotherapy patterns: ● A “low signal” pattern largely surrounded by dark areas on T1w and T2w sequences. This pattern reflected the good response to treatment with least amount of residual viable tumor. ● A mottled or speckled pattern with areas of intermediate signal intensity on T1w sequences and high signal intensity on T2w images interspersed with areas of low signal intensity on T2w images. That pattern was also well correlated with the histology specimen showing largely nonviable tumor with only a small proportion of viable tumor cells.109 ● Identification of areas of predominantly intermediate signal intensity on T1w images and homogeneously high signal intensity on T2w sequences was associated with more viable tissue.

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12.3.4 Biopsy Planning

Fig. 12.10 Osteogenic sarcoma before and after chemotherapy. (a) T2*w GRE MR image. The tumor has high signal intensity. There was only a small extraosseous component before chemotherapy (arrow). (b) T2*w GRE MR image. The extraosseous component has increased in size (arrows). The intramedullary tumor component, too, is larger. These findings point to chemotherapy failure.

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Bone and Soft Tissue Tumors A cystic pattern that was characterized by areas of low signal intensity on T1w images and high signal intensity on T2w images, with multiple, rounded cysts, often with a bullous appearance. This pattern was likewise associated with a high proportion of viable tumor as the cyst periphery was generally surrounded by viable tumor cells.

Holscher et al60 demonstrated a significant correlation between treatment failure and increase in signal intensity of the extraosseous tumor components on T2w follow-up images (r = 0.57, statistical significance, p = 0.02). However, an increase in signal intensity may also be observed in association with tumor necrosis and tissue liquefaction.91 A decrease in signal intensity of extraosseous tumor components on T2w follow-up images is well correlated with effective treatment.60 However, MacVicar et al91 reported that areas of low signal intensity on T2w sequences could also contain viable tumor cells. Therefore, since such findings had only low specificity, they should at most be interpreted as a general guide to effective treatment. Erlemann et al36 demonstrated that dynamic MRI with rapid GRE sequences after Gd-DTPA bolus administration could be used for quantification of chemotherapy response. A decline in the slope of the CM enhancement curve of 60% or more compared with the baseline value was a marker of effective treatment. Conversely, the decline was in general less than 60% in nonresponders.36 Similar results were reported by Fletcher et al and Hanna et al.38,39,55,56,116 Reddick et al116,117 demonstrated that the changes observed on dynamic MRI in combination with the tumor size in children receiving preoperative chemotherapy for osteosarcomas were an important additional prognostic factor for absence of recurrence. Van der Woude et al144 reported that residual, viable tumor was often found along the tumor periphery or in the subperiosteal region, and was characterized by early and rapid CM enhancement. MRA can in certain situations provide additional insights into the chemotherapy response. A characteristic decline in neovascularity is observed in response to chemotherapy, whereas this persists or may even increase when treatment is ineffective.78,80 Chemotherapy often induces changes in the diffusion movements of water molecules in the tumor and, in turn, a decline in signal intensity on DWI images. In one study, significant differences were identified in the ADC values between patients with good and poor response rates. Good response was accompanied by a sharper rise in the minimum ADC rate.107 That applied to areas with the lowest values and not to the mean value. The authors attributed that to tumor heterogeneity. Positron emission tomography (PET) holds out prospects for monitoring metabolic activities within the tumor tissue. That modality is being used increasingly to monitor treatment response and tumor recurrence.

12.3.6 Tumor Recurrence and Postoperative Fibrosis and Edema It is difficult to differentiate between tumor recurrence and postoperative or chemotherapy- and radiotherapy-induced changes. There is reason to suspect tumor recurrence on detection of a nodular lesion with low signal intensity on T1w and high signal

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intensity on T2w sequences.20,48,119,146 Likewise, a displacement effect on the surrounding tissues is also suggestive of tumor recurrence, as is infiltration of soft tissues or bone destruction. Identification of lesions with high signal intensity on T2w sequences in patients who had received radiotherapy can be a sign of both tumor recurrence and radiotherapy-induced changes.146 Other causes of T2 prolongation (based on follow-up examination of patients with tumors of the musculoskeletal system as conducted by Panicek et al110) include the following: ● Tumor recurrence. ● Residual perineoplastic edema. ● Postoperative changes: edema, granulation tissue persisting up to 6 months after surgery. ● Radiotherapy-induced edema. ● Postoperative seroma. ● Hematoma. ● Fat necrosis. ● Muscle denervation (e.g., due to intraoperative injury). ● Intercalary bone graft. Areas of homogeneously low signal intensity on T1w sequences that show no appreciable increase in signal intensity on T2w images and have no focal or nodular components generally reflect chronic postoperative, chemotherapy- or radiotherapy-induced changes. However, in rare cases, malignant fibrous histiocytomas with predominantly fibroblastic components may produce similar findings, thus precluding definitive differentiation.119 Reuther and Mutschier119 compared CT and MRI for diagnosis of tumor recurrence: CT was found to have a sensitivity of 57.5% and specificity of 96.3%, whereas for MRI the sensitivity was 82.5% and specificity 96.3%.119 As such, MRI is essentially more sensitive than CT in detecting tumor recurrence.119 Postoperative scars generally continue to exhibit edema-equivalent signal intensity for up to 6 months after surgery. In some cases, edema with correspondingly high signal intensity can still be identified on T2w images of the surgical area for much longer or following radiotherapy. In such cases, it is not possible to conclusively detect early tumor recurrence if it is not associated with a spaceoccupying effect. The time course is an important criterion in such settings: seromas and edema always decline over time. Hence, if these findings become more widespread, the possibility of tumor recurrence should always be contemplated. Based on the present authors’ own experience, the use of magnetization transfer contrast (MTC) (see Chapter 1.10) may permit differentiation in such cases since, compared with malignant tissue and the majority of benign tumors (MTC effect less than 25%), scar tissue has a very high MTC effect of over 50% (▶ Fig. 12.11 and ▶ Fig. 12.12).143

12.3.7 Effects of Radiochemotherapy on Healthy Bone The healthy bone marrow of tubular bones often reacts to administration of radiochemotherapy for soft tissue sarcomas with changes in signal patterns, with onset up to several months after treatment. These changes are mainly confined to areas that were within the radiation field, but changes are also observed in extremity portions that had been outside the field, or these can

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12.4 Tumors: Specific Section

present after chemotherapy alone. These areas may have a mottled, more linear, or extensive appearance and exhibit signal intensity similar to that of hematopoietic marrow. However, on histology examination no reconverted bone marrow is detected here; instead, gelatinous transformation is seen,63 as in cachexia, AIDS, anorexia nervosa, or alcoholism.

12.4 Tumors: Specific Section Myriad benign and malignant bone and soft tissue tumors are distinguished depending on their tissue of origin (▶ Table 12.8). Imaging technologies alone often do not permit conclusive differentiation and histologic classification of these tumor entities. The pivotal role of conventional radiography in this setting derives from the vast experience already available of using that modality. However, MRI can contribute not only to staging but also to preoperative diagnostic work-ups. In the following sections of this chapter, we give an overview of the current state of the art regarding MRI visualization of different tumor entities and their specific characteristics. Today, genetic and immunohistochemical criteria are increasingly used for histopathology differentiation and classification of tumors.

12.4.1 Bone Tumors Malignant Bone Tumors Osteosarcoma Around 20% of all primary malignant bone tumors are osteosarcomas. Onset of osteosarcoma is generally between the ages of 10 and 15 years. Osteosarcomas are mainly encountered in the

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Fig. 12.11 Follow-up of surgical resection of malignant fibrous histiocytoma of the lower leg. Axial plane. Scarring at skin level with marked signal reduction following application of MTC pulse. Hypointense visualization on T1w image, hyperintense visualization on fat-suppressed STIR image. Hence, the scar exhibits a signal pattern similar on T1w and fat-suppressed images to that of a tumor. But the strong MTC effect is suggestive of a scar. (a) GRE sequence. (b) MTC image. (c) T1w SE sequence. (d) Fatsuppressed STIR sequence.

metaphyses of long tubular bones, in particular of the following tubular bones: ● Distal femur. ● Proximal tibia. ● Humerus. The main clinical contribution of MRI lies in its ability to detect intramedullary daughter metastases (i.e., skip lesions) in up to 25% of cases (see ▶ Fig. 12.1) as well as to determine the extent of intramedullary and soft tissue infiltration.15,136,157 Dense, sclerotic tumor regions have low signal intensity on T1w and T2w sequences. Cortical destruction and extensive perineoplastic edema are common findings.127 The tumor is frequently surrounded by a hypointense halo on T1w and T2w images, reflecting the periosteal reaction. Cystic and necrotic changes as well as fluid–fluid levels are commonly observed following chemotherapy.60 Preoperative adjuvant chemotherapy is administered to control micrometastases and often reduce the tumor size and extent of perineoplastic edema. At present, the main focus of surgery is on joint salvage procedures even though amputations may still be necessary. MRI is particularly adept at monitoring postoperative response to treatment. The chemotherapy regimen can be changed for nonresponders to improve prognosis and reduce the risk of micrometastases. Besides, MRI is able to detect tumor recurrence. Osteosarcomas are typically found in the intramedullary cavity (▶ Fig. 12.13). The following forms are distinguished on histology, radiography, and in terms of their prognosis: ● Parosteal (juxtacortical) osteosarcoma: with lower grade malignancy, growing primarily between the cortex and muscle, with medullary cavity infiltration seen only in the late stage.

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Table 12.8 Primary tumors of the musculoskeletal system (usual Enneking presenting stage in brackets)103 Tissue type

Benign tumors

Malignant tumors

Bone tumors Bone tissue

Cartilaginous tissue

Connective tissue

Reticuloendothelial tissue

Vessels

Unknown

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●

Osteoid osteoma (2)

●

Classic osteosarcoma (IIB)

●

Osteoblastoma (2–3)

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Parosteal osteosarcoma (IA)

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Osteoma (1)

●

Periosteal osteosarcoma (IIA)

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Enchondroma (2)

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Primary chondrosarcoma (IIB)

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Exostosis (2) (ecchondroma)

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Secondary chondrosarcoma (IA)

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Periosteal chondroma (2)

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Chondroblastoma (2–3)

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Chondromyxoid fibroma (2–3)

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Nonossifying bone fibroma (1–2)

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Bone fibrosarcoma (IIB)

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Desmoplastic bone fibroma (2–3)

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Malignant fibrous histiocytoma (IIB)

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Fibrous dysplasia (NA)

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Ossifying bone fibroma (2–3)

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Eosinophilic granuloma (NA)

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Ewing’s sarcoma (IIB)

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Hand–Schüller–Christian disease (NA)

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Reticulum cell sarcoma (IIB)

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Abt–Letterer–Siwe disease (NA)

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Myeloma (III)

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Aneurysmatic bone cyst (2)

Angiosarcoma (IIB):

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Bone hemangioma (2)

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Hemangioendothelioma (IA)

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Hemangiopericytoma (IA)

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Solitary bone cyst (NA)

●

Giant cell sarcoma (IIB)

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Giant cell tumors of bone (2–3)

●

Chordoma (IB)

●

Adamantinoma (IA)

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Fig. 12.12 Follow-up of surgical resection of a leiomyosarcoma of the lower leg. Axial plane. Scarring at skin level with marked signal reduction on the MTC image. The signal reduction is almost as pronounced as in muscle. The MTC subtraction image highlights that effect with depiction of the scar and muscle as bright structures. The scar tissue can be identified on the fat-suppressed STIR image as high signal intensity. This thus constitutes an atypical signal pattern, as also seen for tumor tissue on using this sequence. (a) GRE sequence. (b) MTC image. (c) MTC subtraction image. (d) Fat-suppressed STIR sequence.

12.4 Tumors: Specific Section Table 12.8 continued Tissue type

Benign tumors

Malignant tumors

Soft tissue tumors Bone tissue

●

Myositis ossificans (NA)

●

Extraosseous osteosarcoma (IIB)

Cartilaginous tissue

●

Chondroma (2)

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Extraosseous chondrosarcoma (IB)

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Synovial chondromatosis

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Fibroma (1–2)

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Fibrosarcoma (l-IIB)

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Fibromatosis (3)

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Malignant fibrous histiocytoma (IIB)

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Pigmented villonodular synovitis (2)

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Synovial sarcoma (IIB)

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Synovial bone cyst (intraosseous ganglion1)

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Hemangioma (2–3)

Synovial tissue

Vessels

Fatty tissue

Neural tissue

Muscle tissue

Unknown

Angiosarcoma (IIB): ●

Hemangioendothelioma (IB)

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Hemangiopericytoma (IB)

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Liposarcoma (IA)

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Lipoma (1)

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Angiolipoma (3)

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Neurinoma (2)

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Neurosarcoma (IIB)

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Neurofibroma (2–3)

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Neurofibrosarcoma (IIB)

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Leiomyoma (2)

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Leiomyosarcoma (IIB)

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Rhabdomyoma (2–3)

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Rhabdomyosarcoma (IIB)

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Giant cell tumor of tendon sheath (2)

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Epithelioid sarcoma (IB)

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Clear-cell sarcoma (IB)

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Mesenchymoma (IIB)

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Undifferentiated sarcoma (IIB)

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Connective tissue

Note: NA, Enneking's staging not applicable.

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Periosteal osteosarcoma: with craterlike cortical erosions, growing along the outer surface of the cortex, with predominantly nodular macroscopic appearance; likewise with concomitant periosteal reaction (▶ Fig. 12.14). Telangiectatic osteosarcoma: manifesting mainly as an osteolytic, hyperemic, pseudocystic tumor, resembling an aneurysmatic bone cyst; a characteristic finding is multiple fluid–fluid levels secondary to hemorrhage into cystoid necrotic cavities (▶ Fig. 12.15).26

On rare occasions, extraosseous osteosarcomas are also found in the soft tissues. The following types are distinguished on the basis of the most dominant type of histologic differentiation: ● Osteoblastic type (around 50% of cases). ● Chondroblastic type (around 25% of cases). ● Fibroblastic type (around 25% of cases). These can be further distinguished on radiographs: Mixed type. ● Osteolytic type. ● Osteosclerotic type.40 ●

Osteosarcomas presenting in association with Paget’s disease are a special entity.

Ewing’s Sarcoma Ewing’s sarcoma is a highly malignant tumor found mainly in children and arising in the reticuloendothelial system of the bone marrow. Ewing’s sarcoma accounts for 10% of all primary bone tumors. Around 90% of patients are aged between 5 and 30 years, with peak incidence between the ages of 5 and 15 years. Ewing’s sarcoma is found mainly in the lower skeleton, with around twothirds of cases affecting the pelvis, sacrum, and the lower extremities. The clinical symptoms may resemble those of osteomyelitis, with fever and hyperthermia. Ewing’s sarcoma is encountered more often in the metadiaphyseal than the diaphyseal region. Unlike neuroblastoma, it is almost always accompanied by soft tissue swelling. Sclerotic components may be seen in the intramedullary cavity but rarely in the soft tissues. In Germany, neoadjuvant chemotherapy is administered to treat the primary tumor, which is then resected as soon as technically feasible. Based on the Ewing’s sarcoma protocol, chemotherapy and, as applicable, radiotherapy are continued. The main role of MRI is in staging, preoperative tumor visualization, and monitoring the response to chemotherapy.42 In certain cases, MRI is able to demonstrate hypointense thickening and periosteal lamellation corresponding to the onion-skin phenomenon identified on conventional radiographs (▶ Fig. 12.16).

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Chondrosarcoma Chondrosarcoma is the third most common primary malignant bone tumor,28 accounting for around 20% of all malignant bone

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tumors. Onset is generally after age 45 years. Secondary chondrosarcomas develop from existing benign cartilage tumors, such as an osteochondroma or enchondroma. Forty-five percent of tumors are located in the long tubular bones; the pelvis is also often affected (▶ Fig. 12.17). Low-signal calcifications are frequently encountered in the cartilage matrix. The tumors often have a delicate microlobulated appearance on T2w images, while on postcontrast T1w images they may exhibit a fine ring-and-arc pattern of CM

c

Fig. 12.13 Poorly differentiated chondroblastic osteosarcoma. A 19-year-old male patient. Radiopaque tumor of proximal humerus with large periosteal component. (a) Radiograph. (b) Coronal T1w image. (c) Coronal STIR image. (d) Coronal contrast-enhanced fatsat image. (e) Axial STIR image.

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On rare occasions, Ewing’s sarcoma is found in the soft tissues or chest (Askin’s tumor). The primitive neuroectodermal tumor is also assigned to the small round cells tumor group.102 The term “Ewing’s sarcoma tumor family” is also used because of the common cytogenetic features shared by these tumors.

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12.4 Tumors: Specific Section

b

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Fig. 12.14 Periosteal osteosarcoma of the distal thigh. A 37-year-old male patient. (a) Sagittal T1w image. (b) Sagittal fatsat image following CM administration. Inhomogeneous, enhancing tumor posterior to the femur with slight infiltration of the intramedullary cavity. (c) Axial T2w image. Relatively low signal intensity on T2w contrast (arrow) with osteogenic matrix.

enhancement.44 Identification of a tumor with microlobulation on T2w sequences in addition to a septal ring-and-arc pattern of CM enhancement is highly suggestive of a virtually undifferentiated chondrosarcoma (▶ Fig. 12.18).23 Apart from the classic, central, and eccentric chondrosarcomas, the following variants are distinguished on the basis of their cell type and location:

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Undifferentiated high-grade chondrosarcoma: Since this tumor continues to be virtually undifferentiated, the chondroid structure is scarcely recognizable anymore; this tumor is particularly aggressive, with few calcifications. Clear cell chondrosarcoma: This low-grade malignant tumor has interspersed clear cells, with few calcifications; it resembles a chondroblastoma.

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Fig. 12.15 Telangiectatic osteosarcoma of the humerus. A 25-year-old woman. Loculated tumor, fluid–fluid levels, and peripheral CM enhancement. (a) Radiograph and histology of a biopsy specimen were first misinterpreted as aggressive aneurysmatic bone cyst. (b) The radiograph taken 2 months later, following progressive swelling and pain, demonstrates increasing bone destruction. (c) T1w MRI sequence. Widespread, distal, medullary infiltration (arrow). (d) PDw fatsat MRI sequence.

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Fig. 12.15 (continued) Telangiectatic osteosarcoma of the humerus. A 25-year-old woman. (e) T2w MRI sequence. (f) Contrast-enhanced fat-suppressed MRI sequence.

any intraosseous components, and can be used to monitor response to chemotherapy.134 Adamantinoma is a very rare tumor which also belongs to the group of malignant bone tumors seen in association with fibrous connective tissue and has similar appearance on histology and imaging.70

Angiosarcoma and Hemangioendothelioma

Fig. 12.16 Ewing’s sarcoma. T2w MRI. Intramedullary portions of the tumor exhibit intermediate signal intensity. The cortex and periosteum appear thickened and partially lamellated (arrows), consistent with the onion-skin–like periosteal reaction seen on conventional radiographs.

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Juxtacortical low-grade chondrosarcoma: This tumor arises from the external bone surface, has well-differentiated cartilage, and may occasionally be difficult to classify as a malignant tumor; it is generally associated with late metastatic spread and has exuberant calcifications.

Fibrosarcoma, Malignant Fibrous Histiocytoma, and Adamantinoma These malignant tumors have an even age distribution between 20 and 70 years and tend to develop in the ends of the long tubular bones. These tumors are not associated with any specific characteristics that can be identified on MRI. However, MRI provides important clinical insights into tumor soft tissue extension as well as

There are several aggressive vascular tumors, such as angiosarcoma, hemangioendothelioma, and hemangiopericytoma, with a similar, though often nonspecific, appearance on MRI.101 However, the presence of vascular structures can be helpful for diagnosis. MRI plays a contributory role in diagnosis, staging, and treatment monitoring. Intraosseous hemangioendothelioma is a bone tumor with low-grade malignancy which arises from blood vessels. In most cases, an osteolytic lesion, in 25% of cases multifocal lesions, is seen also in adjacent bones.37

Primary Bone Lymphoma Primary bone lymphoma is a rare tumor mainly found in the metaphysis and epiphysis of the long bones of the extremities. In general, it exhibits inhomogeneous signal intensity on T2w sequences. Areas of low signal intensity on T2w images may be due to intratumoral fibrosis.130 Soft tissue infiltration is observed in more than 70% of cases.59

Benign Bone Tumors Osteogenic Bone Tumors Osteoid Osteoma The osteoid osteoma is an osteoid-producing neoplasm that is generally no more than 1.5 cm in size (therefore also called a “confined” or “small osteoblastoma”). The predilection sites include the long tubular bones, in particular of the lower extremities. While the bones of the hands and feet as well as the posterior vertebral regions are less often affected, any

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Fig. 12.17 Chondrosarcoma of the right ilium. Exostotic component on ilium. Peripheral, crescent-shaped CM enhancement of the large soft tissue component. (a) CT. (b) Coronal T1w MR image. (c) Coronal contrast-enhanced T1w MR image. (d) Axial T2w MR image. (e) Coronal STIR-MR image. (f) Axial contrast-enhanced MR image.

skeletal region may be involved. The predilection age is between 10 and 35 years. Around 75% of patients complain of localized pain, especially at night, which rapidly responds to aspirin or other salicylates. If the tumor is located within a vertebral body, it may give rise to painful secondary scoliosis. The tumor develops over a number of phases characterized by

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different degrees of activity. The following phases have been distinguished: ● Early phase (cavitation). ● Intermediate phase (filling phase). ● Late phase with growth arrest and possible spontaneous resolution.

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12.4 Tumors: Specific Section Fig. 12.18 Chondrosarcoma of the proximal tibia. A 76-year-old male patient (T2 high grade). Strong peripheral, partially crescentshaped CM enhancement. Large soft tissue component. (a) Radiograph. (b) T1w image. (c) STIR image. (d) Contrast-enhanced fatsat image.

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The imaging findings will depend on the activity phase as well as the location of the osteoid osteoma. Four different types can be distinguished based on their skeletal location: ● Cortical type: The cortical type, accounting for around 80 to 90% of all types, is the most common. The center of the tumor (nidus) is situated in the cortex and can be identified on radiography as a discrete area of radiolucency of less than 1.5 cm. It may contain linear, punctate, or coarse calcifications. Often, the nidus can be demonstrated only on CT, but this is crucial for curative treatment since only removal of the entire nidus (resection or minimally invasive radiofrequency ablation) counters the likelihood of tumor recurrence. CT is superior to native MRI in demonstrating the nidus. Two separate nidi are encountered on rare occasions. A noncalcified nidus has low signal intensity on MRI T1w and high signal intensity on T2w images. Calcifications are devoid of signal. Since the nidus is

hypervascularized, strong, early CM enhancement is observed in over 80% of cases and can be demonstrated on dynamic MRI during the high-contrast, arterial phase (▶ Fig. 12.19).86 Dynamic MRI has advantages over dynamic CT for preinterventional visualization of the nidus in patients who had already been operated on, since on MRI a volume can be investigated and imaging is not confined to a single plane as on CT. Besides, MRI obviates the need for radiotherapy for the, mainly young, patients affected. The nidus is typically surrounded by an extensive reactive zone that develops into a dense sclerotic area as it matures. This area of sclerosis is the most salient finding on radiographs. It may affect a more eccentric part of the circumference of a tubular bone or the entire circumference with marked thickening throughout the bone (▶ Fig. 12.20). This may be difficult to delineate from the sclerotic zone if there is complete calcification of the nidus. Reactive sclerosis is devoid

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Fig. 12.19 Osteoid osteoma in the femoral diaphysis. (a) T1w fat-saturated TSE sequence following CM administration. A typical finding is the inflammatory reaction surrounding the bone, with CM enhancement (arrows). (b) Dynamic MRI. Enhancement pattern similar to arterial enhancement (R1 in the superior femoral artery, R2 in the nidus); these findings underpin the diagnosis.

Fig. 12.20 Cortical osteoid osteoma. Status post nidus resection. (a) Radiograph. Extensive residual sclerosis of the entire tibial circumference. Central surgical defect. (b) Axial T2*w GRE image. The sclerotic area is devoid of signal. No evidence of soft tissue or bone marrow edema of this postoperative inactive process. (c) Coronal STIR image. Signal-void sclerotic zone. Hyperintense, smoothly marginated surficial defect. No edematous changes. Overall, no sign of recurrence.

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of signal on MRI. In the more active stages, concomitant bone marrow and, slight, soft tissue edema (▶ Fig. 12.21), which also takes up CM,4,49,51,154 is frequently seen. Due to the presence of an incompletely mineralized osteoid during the early stages, reactive sclerosis may be markedly more hyperintense than fully mineralized osteoids. Medullary (trabecular) type: The medullary type is much less common. The nidus is situated in the trabecular bone (frequently the femoral neck, carpal and tarsal bones) and is surrounded by a moderate, asymmetrical sclerotic zone. Often, it is highly calcified at its center, which explains its target-shaped appearance. Radiographs show a large area of calcification

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surrounded by a narrow radiolucent halo of up to 2 cm in width. On MRI, the area of central calcification is devoid of signal, surrounded by a thin halo, and exhibits low signal intensity on T1w and high signal intensity on T2w images. There is extensive adjacent bone marrow edema. Periarticular lesions exhibit signs of reactive synovitis with effusion and synovial proliferation. Subperiosteal type: The subperiosteal type is extremely rare. The nidus is situated at subperiosteal level where it induces virtually no reactive sclerosis. The soft tissue side of the nidus is bounded by periosteal ossification and may give rise to reactive

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12.4 Tumors: Specific Section

Osteoblastoma Osteoblastoma, like the osteoid osteoma, is an osteoid-producing neoplasm and is generally more than 1.5 cm in size (hence the term “giant osteoid osteoma”). Its predilection site is the vertebral bodies, less commonly the long tubular bones, and it can in principle affect any skeletal region. Like the osteoid osteoma, the typical age of onset is between 10 and 30 years. This tumor has similar findings on radiography and MRI to the osteoid osteoma, although the osteoblastoma has a somewhat more aggressive appearance. Stage 3 osteoblastoma is also termed a “pseudomalignant osteoblastoma.” Osteoblastoma induces less severe reactive sclerosis and is mainly asymptomatic. Any associated pain responds poorly to salicylates. The tumor may also be completely calcified and/or accompanied by extensive soft tissue and bone marrow edema with corresponding MRI signs.

Osteoma This tumor entity is caused by formation of compact bone tissue in the region of the skull (in particular, paranasal sinuses), trabecular bone (compact bone island, enostoma), or in the juxtacortical parosteal region, extending into the soft tissues. This tumor process is characterized by its high radiodensity (radiopacity) and is devoid of signal on all MRI sequences.

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edematous soft tissue swelling with a corresponding signal pattern on MRI. Intra-articular type: If an osteoid osteoma is located within an intra-articular bone segment (or in a periarticular segment), it can induce severe synovitis (▶ Fig. 12.22) manifesting as a joint infection on radiography and MRI. Osteoid osteoma in the vicinity of the epiphyseal plate can interfere with bone growth. Nidus resection or spontaneous resolution is followed by slow regression of reactive sclerosis. MRI is adept at identifying any recurrent edematous reactions of the bone and soft tissue (see ▶ Fig. 12.20). Differential diagnosis of osteoid osteoma should include Brodie’s abscess, eosinophilic granuloma, plasma cell osteomyelitis, and small chondroblastomas.

Cartilaginous Bone Tumors For more details, please consult the publication by Douis and Saifuddin.27

Fig. 12.21 Osteoid osteoma. T2w MRI. The intracortical nidus has high signal intensity (arrow). Discrete, hyperintense edema seen in the adjacent soft tissues (curved arrows).

Chondroma (Enchondroma) Enchondroma is a very common, and generally asymptomatic, benign bone tumor found in all age groups. It is generally located

Fig. 12.22 Intra-articular osteoid osteoma of the hip. Nocturnal pain that responds to salicylates. (a) Oblique coronal STIR sequence. Extensive bone marrow edema of the femoral neck (arrow), joint effusion. (b) Axial T2w TSE sequence. Signal-void focal lesion (arrow), consistent with a focal sclerotic reaction and/or calcified nidus.

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In the active early stage, the tumor is seen on radiographs as a smoothly marginated, osteolytic lesion, possibly with cortical scalloping. The bone contour may be greatly expanded (enchondroma protuberans). The later stages (latent or inactive stage) are characterized by nodular or stippled calcification of the chondroid matrix. On differential diagnosis, this entity can be distinguished from a bone infarct in that it lacks the denser, garlandlike calcified rim. On MRI, enchondromas have characteristic high signal intensity on T2w SE images, whereas a bone infarct exhibits a hypointense signal pattern due to fibrosis or sclerosis. Tracer uptake on scintigraphy is much higher in the latent compared with the active stage.

On MRI, enchondromas produce characteristic findings resulting from the scalloped contour cartilage matrix (▶ Fig. 12.23): ● T1w images demonstrate a predominantly low signal, inhomogeneous lobulated tumor with a ring-and-arc, and partially linear, pattern of increased signal intensity due to residual fatty marrow. This creates a fine, lacunar pattern. ● T2w images show a predominantly inhomogeneous, hyperintense tumor with a lobulated contour. ● Postcontrast images show rings and arcs of enhancement of the fibrovascular connective tissue between lobulated, nonenhancing cartilage matrix.3 ● All sequences demonstrate punctate or circular areas of signal void caused by calcification of the cartilage matrix. The periosteal or juxtacortical chondroma is a special type of chondroma. This cartilaginous tumor has its origin in the perichondrium of long tubular bones of adolescent and young adults and gives rise to a painful saucerlike erosion and sclerosis of the underlying outer cortex. Calcification is rarely seen. This tumor is typically encountered at the deltoid insertion on the humerus (▶ Fig. 12.24). On MRI, the characteristic findings of a chondroid matrix with displacement of the surrounding soft tissues are identified.

Chondroblastoma Around 90% of chondroblastomas present between the ages of 5 and 25 years. This rare epiphyseal tumor mainly affects the femur, humerus, and tibia and is generally painful. Some 10% of tumors are found in the region of the foot, especially in the talus or calcaneus. In terms of its morphology, the chondroblastoma manifests as a sharply marginated, rounded, and lobulated lesion no bigger than 5 to 6 cm. The tumor may extend into the metaphysis but rarely into the adjacent joint. It has low signal

Fig. 12.23 Enchondroma of the femur. Enchondroma of the femur, latent phase in an asymptomatic 50-year-old male patient. (a) Radiograph. Discrete radiolucency, cortical scalloping, and extensive punctate and coarse matrix calcification. (b) Axial T1w SE image. The tumor has predominantly low signal intensity with signal-void calcifications, hyperintense residual fatty marrow with a partially circular and partially linear configuration. Slight cortical scalloping. (c) T2*w GRE image. Inhomogeneous tumor with high signal matrix and punctate areas of signal-void calcifications.

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in the metaphysis of the long bones and is thought to originate from the proliferation of epiphyseal cartilage cells. The tumor matrix is composed of mature hyaline cartilage with characteristic, partially rounded, lacunae. The predilection sites are the tubular bones, in particular the short tubular bones of the hands and feet. Less commonly affected are the scapula and the pelvis, but pelvic enchondromas are thought to have a greater susceptibility to malignant transformation. The majority of these tumors are solitary but may be multiple when occurring in association with hereditary syndromes (enchondromatosis, Ollier’s disease), and likewise present a higher risk of malignant transformation. The following findings are suggestive of malignant transformation: ● New onset of pain. ● Sudden increase in tracer uptake on scintigraphy. ● Increased blurring and inhomogeneity of the tumor on radiographs. ● Cortical erosions. ● Periosteal reaction. ● Intracortical crest formation due to atypical ossification.

12.4 Tumors: Specific Section

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Fig. 12.25 Highly aggressive chondroblastoma (Enneking’s stage 3) in the tibial epiphysis. Coronal schematic diagram. Metaphyseal infiltration, bone marrow edema, periosteal reaction, soft tissue edema.

Fig. 12.24 Periosteal chondroma. Coronal schematic diagram. Periosteal chondroma in the region of the deltoid insertion on the humerus. Tumor on humeral surface with cortical compression and erosion as well as cartilage matrix.

intensity on T1w and inhomogeneous intensity on T2w sequences. This combination of areas of inhomogeneity and hypointensity on T2w images is characteristic of the cartilage matrix with fibrous stroma and calcifications. The following findings are suggestive of a more aggressive tumor (Enneking’s stage 3) (▶ Fig. 12.25): ● Perineoplastic bone marrow edema. ● Concomitant periosteal thickening. ● Concomitant soft tissue edema.

Chondromyxoid Fibroma This rare, asymptomatic tumor is typically seen in adolescents and presents as an eccentric lesion in the metaphysis of long tubular bones. The matrix has various constituents, but since it is generally free of calcification, MRI does not demonstrate the characteristic findings of a chondroid matrix; instead, a nonspecific pattern of low signal intensity on T1w and high signal intensity T2w images is observed (▶ Fig. 12.26).

Osteochondroma Osteochondroma (also termed “ecchondroma” or “cartilaginous exostosis” or “cartilage capped exostosis”) is a common benign tumor of spontaneous onset or which presents secondarily to trauma or radiotherapy. Osteochondromas may be solitary or multiple. Between 70 and 80% of osteochondromas are diagnosed before 20 years of age. They are often located in the metaphysis

Fig. 12.26 Chondromyxoid fibroma in a child. Coronal schematic diagram. Smoothly marginated tumor, no bone marrow or soft tissue edema of the tibial metaphysis.

of the long tubular bones but the pelvis and scapula may also be affected. The most salient feature of an osteochondroma on MRI is that it is in direct contact with the bone marrow space of normal bone (▶ Fig. 12.27 and ▶ Fig. 12.28). There is also cortical continuity between the healthy bone and the osteochondroma. The tumor has a cartilage cap (see ▶ Fig. 12.28).69 If the thickness of this cartilage cap is greater than 2 cm, there is reason to suspect malignant transformation.83 Multiple tumors also present a higher risk of transformation. Other signs of malignant transformation include: ● Pain onset. ● Sudden growth acceleration. On rare occasions, benign ecchondromas may become symptomatic, for example, causing bursitis secondarily to the pressure exerted on adjacent organs. Chronic pressure can also give rise to serous inflammatory fluid accumulation in the adjacent soft tissues (pseudobursae; ▶ Fig. 12.29; see also ▶ Fig. 12.27). These can generally be palpated as a nontender bony mass in proximity to joints. The tumors become inactive when the patient reaches skeletal maturity. The tumor grows in the direction of the diaphysis

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Fig. 12.27 Osteochondroma (cartilaginous exostosis) of the humerus. The patient reported increasingly more painful swelling of the upper arm. Broad-based, humeral spur with fatty marrow–equivalent base, inhomogeneous cartilage cap, and formation of a pseudobursa (arrows) secondary to chronic soft tissue irritation. (a) Coronal STIR sequence. (b) Axial Gd-contrast T1w sequence.

Fig. 12.28 Osteochondroma (cartilaginous exostosis) of the femur. Broad-based femoral spur with fatty marrow–equivalent base, inhomogeneous, large cartilage cap (a, arrow) and formation of a “pseudobursa” (c, arrow). The size of the cartilage cap is suggestive of malignant transformation. (a) Axial PDw fat-saturated TSE sequence. (b) Native T1w sequence. (c) Sagittal PDw fat-saturated TSE sequence.

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12.4 Tumors: Specific Section as a sessile or broad-based osteochondroma or as a pediculate growth (▶ Fig. 12.30). Conventional radiography is used for diagnostic investigation; MRI is adept at assessment of the cartilage cap, with non–fatsuppressed sequences (T2w or PDw contrast) suitable for distinguishing between a cartilage cap and pseudobursa. Multiple osteochondromas are seen in association with hereditary syndromes (multiple cartilaginous exostoses, diaphyseal aclasia). Predilection sites are the knee region (▶ Fig. 12.31) and pelvis. These tumors may cause severe deformities. There are isolated reports of spontaneous regression of osteochondromas.62

Giant Cell Tumor

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Fig. 12.29 Osteochondroma. Schematic diagram. Broad-based femoral spur with fatty marrow in the base, cartilage cap growth zone, and soft tissue irritation with fluid accumulation (pseudobursa).

Giant cell tumors (osteoclastoma) are found in the long tubular bones of mainly the distal femur or proximal tibia but are also encountered in the sacrum and humerus (▶ Fig. 12.32 and ▶ Fig. 12.33). The tumor arises in the epiphysis and can extend into the metaphysis, exhibiting aggressive growth. In rare cases (fewer than 5%), it can even spread to the lungs. It mainly affects men aged 20 to 40 years. The tumor can infiltrate adjacent regions; in the knee, it spreads through the cruciate ligaments into the joint. Patients complain of persistent pain; joint effusion is seen secondarily to tumor infiltration of the joint.

Fig. 12.30 Osteochondroma of the femur. (a) Sagittal T1w image. Painful, hard swelling on thigh. The pedicle and base have mature fatty marrow (arrow). (b) Sagittal PDw fatsat image. (c) Axial PDw fatsat image. The cap and reaction zone have signal pattern isointense to fluid and cartilage (arrow).

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Fig. 12.31 Multiple cartilaginous exostoses (ecchondromas). (a) Conventional radiograph of both knees. Multiple ecchondromas (arrows). (b) Coronal T2*w GRE image of the knee. The tumor base exhibits the same signal intensity as the femoral bone marrow. The narrow cartilage caps have the same signal intensity as the joint cartilage (arrows).

inhomogeneous with areas of hypointensity and hyperintensity.137 Often, hemosiderin is identified, exhibiting low signal intensity on both T1w and T2w images.2 Tumor recurrence is common. Unlike an aneurysmatic bone cyst, this tumor exhibits mainly homogeneous CM enhancement. MRI is generally used to detect tumor recurrence based on the following signs: ● Absorption of bone graft, but this is also seen in association with infection. ● Progressive osteolysis.

Fibrous Bone Tumors Fibrous and Osteofibrous Dysplasia

Fig. 12.32 Differential diagnosis of sacral space-occupying lesion. Relevant findings are, for example, the giant cell tumor and chordoma in middle-aged patients. T1w TSE images. (a) Giant cell tumor. (b) Chordoma. The chordoma is often calcified (arrow).

Giant cell tumors are mainly diagnosed on conventional radiography but MRI is useful for assessment of tumor extension. MRI demonstrates a typical solid, mainly homogeneous, clearly delineated lesion that has generally low signal intensity on T1w images. On T2w sequences, the giant cell tumor may appear

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This disorder results from a developmental anomaly of bone with formation of immature fibrous tissue masses which are classified as tumorlike lesions. These space-occupying masses cause displacement of healthy bone. The condition is seen mainly in adolescents and young adults. The disorder may be monostotic or polyostotic. The polyostotic form may be seen in association with certain syndromes (e.g., Albright’s syndrome: polyostotic fibrous dysplasia in young girls, associated with café-au-lait spots and precocious puberty). The monostotic form typically affects the proximal femur, proximal tibia, mandible, base of skull, and ribs. Lesions are found mainly in the metaphysis and diaphysis. The polyostotic form may affect one entire side of the body or the tubular bones, hands, and feet as well as the pelvis. Diminished physical stability and pathologic fractures can give rise to severe deformities especially of the tubular bones. Radiographs show ground glass, osteolytic lesions surrounded by a sclerotic halo, deformities, and a trabecular pattern following trabecular remodeling. MRI demonstrates a matrix of homogeneous low signal intensity on T1w images and, in the majority of cases, of homogeneous low signal intensity on T2w images as well as slight hyperintensity on fat-saturated images (▶ Fig. 12.34). The sclerotic halo and areas

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Fig. 12.33 Giant cell tumor in proximal humerus. A 38-year-old male patient. (a) Radiograph. (b) T1w image. (c) STIR image. (d) Contrast-enhanced fat-saturated image.

Fig. 12.34 Monostotic fibrous dysplasia in the metadiaphyseal region of the femur. (a) Radiograph. Confluent osteolysis, sclerotic halos, and trabecular thickening. (b) Coronal T2*w GRE image. The process exhibits predominantly, homogeneously high signal intensity, interspersed with signal-void sclerotic halos and trabecular plates.

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Nonossifying Fibroma (Fibrous Cortical Defect, Fibroxanthoma) This developmental anomaly of the periosteal cortex gives rise to a fibrous connective lesion interspersed with fibroblasts, giant cells, and xanthomatous cells, mainly in the metaphysis of the distal femur or distal tibia. The lesion appears in childhood or adolescence and heals by ossification once bone growth is complete. On conventional radiographs, the lesion is typically demonstrated as an eccentric intra- or juxtacortical defect with trabeculations and a thin sclerotic halo; diagnosis is based on these findings. A discrete sclerotic focus may persist once the lesion has resolved. The findings identified on MRI vary in accordance with the age of the lesion (▶ Fig. 12.35). In the early stage, the lesion can be

Fig. 12.35 Nonossifying fibroma. (a) Sagittal T1w image. Heterogeneous lesion of the posterior distal femoral metaphysis with muscle-isointense signal and focal signal obliterations. (b) PDw fatsat image. Heterogeneous increases in signal intensity. (c) Radiograph. Three years later. Shrinkage and increasing sclerosis (arrow).

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of trabecular thickening are devoid of signal on all sequences. A much more inhomogeneous pattern results because of fractures or secondary aneurysmatic bone cysts. Lesions exhibit mainly homogeneous enhancement as well as in around onequarter of cases peripheral ring enhancement. Again, in around one-quarter of cases the adjacent soft tissues show edematous changes with high signal intensity on T2w images as well as CM uptake. Hemorrhage occurs, giving rise to methemoglobin deposits that have high signal on T1w mages as well as fluid–fluid levels.65 Osteofibrous dysplasia is a special type of this condition that affects only the cortex of the fibula or tibia.70

12.4 Tumors: Specific Section

Desmoplastic Fibroma (Desmoid) Desmoid bone tumor is predominantly encountered in the tubular bones of young adults. The tumor appears to be very aggressive (mainly Enneking’s stage 3). Conventional radiographs show metaphyseal, at times very large, poorly marginated, trabeculated, osteolytic lesions. These are frequently associated with cortical erosions and soft tissue infiltration. MRI displays a nonspecific signal intensity pattern of hypointensity on T1w images and hyperintensity on T2w images.96

Intraosseous Lipoma The MRI characteristics of this rare benign tumor are similar to those of soft tissue lipoma. It has two predilection sites: the calcaneus and femoral neck. The tumor exhibits high signal intensity on T1w and intermediate to high signal intensity on T2w sequences (▶ Fig. 12.36). Calcification and cystic changes secondary to fatty necrosis or cystic degeneration may be observed.11,98

Langerhans Cell Histiocytosis (Histiocytosis X) Langerhans cell histiocytosis is a nonmalignant disease of the monocyte macrophage system with proliferation of histiocytes, eosinophilic granulocytes, lymphocytes, and multinucleated giant cells, mainly in the reticuloendothelial system of bone, lymph

nodes, the skin and mucosa, the liver, spleen, lungs, and central nervous system. The bone is the most commonly implicated location, accounting for over 90% of cases. This disease has a broad spectrum of manifestations ranging from single-bone to multiple-bone involvement. The term “Langerhans cell histiocytosis” should be given preference over the former generic term “histiocytosis X” which comprised three different variants of the disease: ● Eosinophilic granuloma (mono-osseous involvement). ● Hand–Schüller–Christian disease (chronic course with multiple-organ and multiple-bone involvement). ● Abt–Letterer–Siwe disease (acute course with multiple organ involvement). Eosinophilic granuloma (mono-osseous involvement) is a tumorlike lesion that is characterized by histiocytic infiltration of the bone marrow. It affects mainly children, adolescents, and young adults, and is more common in men than women. Solitary tumors are more common than multiple lesions. Eosinophilic granuloma can be encountered in the skull, mandible, spinal column, ribs, and the long tubular bones. It is seen less frequently in the clavicle, pelvis, and scapula, and almost never in the bones of the hands and feet. Clinical symptoms include mild pain, swelling, low-grade fever, elevated erythrocyte sedimentation rate, and in its early-stage peripheral eosinophilia. Curettage is curative in the majority of cases. Eosinophilic granuloma develops over four different histopathology phases,25 producing accordingly variable imaging findings. The entire radiographic spectrum of bone destruction described by Lodwick et al may be observed. Eosinophilic granuloma produces equally variable findings on MRI comprising the following phases8: ● Initial phase: The initial phase is dominated by diffuse bone infiltration with poorly defined margins, extensive concomitant bone marrow edema, and a periosteal reaction as well as cortical destruction. ● Intermediate phase: During the transition from the intermediate to the late phase, edema resolves and the lesion appears less aggressive. ● Late phase: In the late phase, the tumor is well delineated and there is no, or only minimal, edema or soft tissue involvement.

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demonstrated at a typical location as an area of slightly increased signal intensity on T1w images (large proportion of lipid laden xanthomatous cells) and as reduced signal intensity on T2w images (hemosiderin, fibrous connective tissue). Once the defect has resolved, areas of sclerosis with low signal intensity or signal void are seen on all sequences. Following absorption of the sclerotic defect, the signal intensity equalizes that of the surrounding normal yellow bone marrow. The signal intensity pattern can at times be very inhomogeneous.96

The signal pattern is nonspecific with low to slightly increased signal intensity on T1w as well as high to very high signal intensity on T2w images. Strong CM enhancement is seen. Findings identified in the various regions include (▶ Fig. 12.37): ● Development of vertebra plana when there is spinal involvement. ● Beveled lesion in the skull due to the different stages of disease of the external and internal table, formation of central sequesters with signal void on all sequences in the late phase. ● Soft tissue involvement, in particular, in the initial phase. If sequesters are detected, the following entities should be included in differential diagnosis: ● Osteomyelitis. ● Fibrosarcoma. ● Osteoid osteoma. ● Intraosseous lipoma. Fig. 12.36 Intraosseous lipoma in the distal femur. Sagittal T1w image. Somewhat polylobulated configuration with septa (arrow).

Osteomyelitis and Ewing’s sarcoma should be borne in mind, in particular, for differential diagnosis in the early phase.

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Initial phase: bone destruction of aggressive appearance, soft tissue component, periosteal reaction, extensive edema

Late phase: sharply marginated lesion, little edema, possible sequester

Beveled lesion in skull base

Vertebra plana

Fig. 12.37 Eosinophilic granuloma. Certain diagnostic pointers of eosinophilic granuloma depending on activity phase and location. Schematic diagram.

This tumor is detected in 80% of cases before age 20 years. Predilection sites are the metaphysis of long tubular bones and posterior parts of the vertebral bodies and, less commonly, the pelvis. On histology, the tumor is seen to contain blood-filled spaces surrounded by granulation tissue, osteoid, and multinucleated giant cells. Calcifications may also be present. Intraosseous lesions expand the cortex, while extraosseous lesions erode the cortex of adjacent bones. The etiology of aneurysmatic bone cysts has not been conclusively elucidated to date. One theory postulates proliferation of vascular tissue secondary to hemorrhage in primary tumors, such as giant cell tumors, chondroblastomas, osteoblastomas, nonossifying fibromas, and chondromyxoid fibromas, as well as unicameral bone cysts, fibrous dysplasia, fibrous histiocytomas, eosinophilic granulomas, and malignant tumors. There may be complete or partial regression of the primary tumor. Patients typically complain of swelling and moderate pain. Curettage and plastic reconstruction suffice as initial treatment. More radical surgical treatment may be needed for any recurrences. On MRI, aneurysmatic bone cysts are often seen to have thin, well-delineated margins, with central areas of high signal intensity on T1w and T2w sequences attesting to the presence of methemoglobin. On T2w images, the tumor has mainly high signal intensity, but often an inhomogeneous signal pattern is observed, possibly reflecting intracystic hemorrhage of different ages.6,157 Septation is also seen. Aneurysmatic bone cyst exhibits strong, mainly, peripheral CM uptake after CM administration (▶ Fig. 12.38). Fluid–fluid

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Fig. 12.38 Aneurysmatic bone cyst in the left ilium. A 22-year-old female patient. Multiloculated, fluid-isointense, space-occupying lesion with peripheral CM enhancement. (a) Coronal T1w sequence. (b) Coronal STIR sequence. (c) Axial T2w sequence. (d) Axial fatsat sequence following CM administration.

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Aneurysmatic Bone Cyst

12.4 Tumors: Specific Section

Juvenile (Unicameral) Bone Cyst Juvenile (unicameral) bone cyst is a cystic cavity filled with a yellow, clear fluid and lined with a membrane. It is typically seen in the metaphyses of tubular bones in children aged 3 to 14 years. Its pathomechanism is unclear. Symptoms manifest only after fractures. The bone cysts arise close to the epiphysis and migrate toward the diaphysis with longitudinal bone growth and declining rate of cystic growth. In adolescents older than 14 years, the bone cysts are seen as smaller, less aggressive, well-delineated lesions (latent cyst). Multiple lesions may be observed. Differential diagnosis should include fibrous dysplasia and aneurysmatic bone cyst. Treatment entails curettage and filling with cortisone injections. The recurrence rate of latent cysts is much lower than that of initial stage cysts. MRI demonstrates a cystic appearance with low signal intensity on T1w images and very high signal intensity on T2w images, with a smooth margin exhibiting low signal to signal void. CM uptake is generally not observed. Gas may accumulate in the cyst and is seen as an air-filled level. MRI is generally not needed for diagnosis of unicameral bone cysts.

Hemangioma Hemangioma is a benign, vascular tumor, often diagnosed as an incidental finding in middle-aged patients. Hemangiomas have a predilection for the vertebral bodies (see Chapter 2.7.3), skull, and facial bones. MRI findings are often specific: the tumor has high signal intensity on T1w as well as on T2w sequences because it contains fat and blood products (methemoglobin).122 Postcontrast images demonstrate CM enhancement. For vertebral hemangiomas, MRI is particularly adept at visualizing obliteration of the subarachnoid space and bone marrow compression.58,81 Hemangiomas of the peripheral skeleton are rarely encountered. On MRI, they manifest as discrete focal lesions with low signal on T1w and high signal intensity on T2w contrast images. Unlike vertebral hemangiomas, they rarely contain fatty matrix components120 and are generally surrounded by a hypointense halo, and often have areas of focal or linear signal obliterations (focal calcifications or thickened bone trabeculae). In rare cases, only an edematous zone, but no tumor, is identified. Conventional radiographs demonstrate mainly osteolytic and, very occasionally, also osteosclerotic lesions.

12.4.2 Soft Tissue Tumors Malignant Soft Tissue Tumors Most malignant soft tissue tumors have poorly delineated margins and often infiltrate the surrounding tissues.111 The majority of malignant soft tissue tumors exhibit an inhomogeneous signal pattern on T2w sequences.111 Destruction of adjacent bones, encasement, and infiltration of neurovascular bundles are suggestive of the malignant nature of a tumor but can also be seen in association with benign lesions.73,93,94,111 Most malignant tumors have higher signal intensity than that of healthy skeletal muscles

on T2w sequences.111 However, the malignant fibrous histiocytoma may exhibit low signal intensity on T2w images. In the following, we describe common malignant soft tissue tumors, of which a number are particularly malignant. Please consult the internet and literature for details of other tumors not discussed here (e.g., skin tumors, rare pathologies).12

Malignant Fibrous Histiocytoma The formerly termed “malignant fibrous histiocytoma” is now mainly designated as undifferentiated pleomorphic sarcoma (not otherwise specified) if line differentiation cannot be identified with the currently available modalities. Some of the former malignant fibrous histiocytomas are now classified as “dedifferentiated liposarcoma” (MDM2 and CDK4 positivity) or as “myxofibrosarcoma” (if more than 10% myxoid composition). Undifferentiated pleomorphic sarcoma is a tumor that may be found in both soft tissues and bones. It is the most common type of malignant soft tissue tumor seen in adults. The mean age of onset in patients is 50 years. The recurrence rate after resection is high (up to 45%). Multiple histologic subtypes have been characterized, with the most important forms having a predominantly histiocytic, fibromatous, or xanthomatous morphology. Undifferentiated pleomorphic sarcoma generally has low to intermediate signal intensity on T1w image and high inhomogeneous signal intensity on T2w images (▶ Fig. 12.39).92,93 The signal intensity pattern is nonspecific. When there is a preponderance of fibromatous components, the malignant fibrous histiocytoma may have low signal intensity on T2w sequences.134,135 This tumor has a relatively intense and, often, inhomogeneous pattern of enhancement. Necrosis is frequently observed.

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levels are frequently identified on T1w image within at least 10 minutes and are thought to be linked to sedimentation of various blood constituents.

Liposarcoma Liposarcoma is a common malignant soft tissue tumor in adults, with predilection age between 40 and 60 years. Liposarcomas tend to be found in the deeper tissue layers of the extremities as well as the retroperitoneum, where they can grow to an enormous size. Four subtypes have been characterized, with the grade of malignancy inversely proportional to the intracytoplasmic fat content and proportional to the number of polymorphic cells127: ● Well-differentiated liposarcoma: Low-grade malignancy (less prone to metastasis); predominantly atypical adipocytes, resembling a lipoma, and traversed by septa; onset in older age; the most common liposarcoma variant; more chronic types are at higher risk of malignancy. ● Myxoid liposarcoma: The most common subtype (40–50% of all liposarcomas) with low-grade malignancy; predominantly lipoblasts of different degrees of maturity; myxoid stromal component (▶ Fig. 12.40 and ▶ Fig. 12.41). ● Round cell dedifferentiated liposarcoma: high-grade malignancy and hypercellular. ● Pleomorphic liposarcoma: high-grade malignancy and bizarre pleomorphic cells. Hypercellular and high-grade malignant tumors may be devoid of normal fatty tissue. Such tumors cannot be distinguished on MRI from other soft tissue sarcomas. Well-differentiated liposarcomas do not take up any, or only minimal, CM. Besides, well-differentiated liposarcoma has smooth

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Fig. 12.39 Malignant fibrous histiocytoma on the thigh. Axial plane. (a) T1w SE image. Hypointense tumor that is slightly hyperintense to muscle. (b) T1w image following CM administration. Inhomogeneous enhancement pattern. (c) T2w TSE image. Inhomogeneous, high signal tumor. (d) Fatsuppressed STIR image. Encasement of a central vessel by the tumor.

margins and cannot be reliably distinguished from a benign lipoma.72,74 Malignancy criteria include a tumor matrix containing CM-enhancing septa and nodules as well as a large tumor diameter. There is broad overlap between benign, atypical, or mixed lipomas.16 Imaging is not able to assure reliable differentiation of these entities. The other liposarcoma types often have poorly delineated margins. Undifferentiated high-grade malignant liposarcomas exhibit intense, inhomogeneously mottled or ring-shaped, contrast enhancement.141 Onset of necrotic areas in the later course is suggestive of an ongoing undifferentiated tumor. Myxoid tumor regions and necrosis have very high signal intensity on T2w images. The liposarcoma recurrence rate is very high.

Synovial Sarcoma This malignant tumor originates in the mesenchymal tissues and mimics the histology of synovial tissue. However, it does not arise from the synovial lining of the joint capsule, and

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only in 10% of tumors is there intra-articular involvement. The tumor is found mainly in young adults. It is a slow-growing tumor occurring mainly in the lower extremities. Metastases and postoperative local recurrence are common. Extensive calcification is observed in one-third of cases, typically along the tumor periphery. The signal pattern on MRI is nonspecific, with low signal intensity on T1w and increased signal intensity on T2w images. The tumor has a lobulated, morphologic appearance with smooth margins, septa, and fluid–fluid levels secondary to hemorrhage.

Fibrosarcoma Fibrosarcomas are malignant soft tissue or bone tumors with a connective tissue matrix. Reflecting this composition, they have heterogeneously low signal intensity on T1w images and high signal intensity on T2w contrast images. A heterogeneous pattern of CM enhancement is observed. A number of different histologic subtypes have been characterized. The term ‘Evans’ tumor’ is used

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12.4 Tumors: Specific Section

Fig. 12.40 Myxoid liposarcoma. (a) Sagittal T1w MR image. The posterior portions of the tumor have high signal intensity, consistent with fat signal. But the anterior tumor portion has low signal intensity. This marked inhomogeneity is suggestive of a diagnosis of myxoid liposarcoma. (b) Axial T1w MR image. Recurrent fatty, high-signal tumor regions as well as inhomogeneous, hypointense zones.

to denote a low-grade fibrosarcoma with myxoid components in young adults.63,68 Myxoid components exhibit a signal intensity pattern very similar to that of fluid on MRI.85 Due to their infiltrative growth pattern, myxofibrosarcomas have characteristic long and uneven protrusions that extend along adjacent intercellular tissue spaces or fascia (tail sign; ▶ Fig. 12.42).85 These tumor extensions must also be resected to prevent recurrences.

Angiosarcoma Angiosarcomas are very rare and often seen in association with chronic lymphedema (see Chapter 16.1), giving rise to Stewart– Treves syndrome, for example, following mastectomy. To date, no specific MRI criteria have been formulated.

Malignant Nerve Sheath Tumor This is a space-occupying lesion with a nonspecific signal intensity pattern similar to that of benign peripheral nerve sheath tumor (see Peripheral Nerve Sheath Tumor [Schwannoma, Neurofibroma] p. 558). Differentiation is not possible on MRI. This rare tumor is also known as “malignant schwannoma,” “neurofibrosarcoma,” or “neurogenic sarcoma.”

Benign Soft Tissue Tumors Lipomas Lipomas are benign soft tissue tumors. They typically have high signal intensity on T1w (▶ Fig. 12.43) and intermediate to high

signal intensity on T2w sequences, reflecting the signal pattern of fatty tissue (see ▶ Fig. 12.3).113 Signal obliteration on fat-saturated native T1w sequences is a reliable diagnostic pointer. The tumor is generally homogeneous on both sequences. This lesion is sharply marginated and may contain fibrous septa. The possibility of a liposarcoma must be contemplated if the tumor exhibits inhomogeneous signal intensity or its margins are not well defined. Lipomas mainly occur in the subcutaneous fatty tissue (superficial lipomas) of the back, shoulder, abdomen, and the extremities. But they can also be found in deeper soft tissue layers (deep-seated lipomas), and are now mainly bigger and less sharply marginated. Regions where deep-seated lipomas occur include the muscles (intra- and intermuscular lipomas), bone (intraosseous lipomas), periosteum (periosteal or parosteal lipomas), and the cortex; they are also seen in association with connective tissue (fibrolipomas), vascular proliferation (angiolipoma), or cartilaginous or bone metaplasia (chondrolipoma, osteolipoma). Depending on the proportion of nonfatty tissue, the imaging scan may also show other structures that are not isointense to fat in the tumor.41 At times, a very heterogeneous pattern, possibly also with inhomogeneous CM enhancement, is observed. Intramuscular lipomas are often interspersed with muscle-isointense, partially striated tissue components (▶ Fig. 12.44). Cytogenetic analysis can now be used for differentiation of the various types of lipoma. The term lipomatosis is used to denote diffuse neoplastic or, possibly, drug-induced (cortisone) reactive fatty tissue

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Fig. 12.41 Myxoid liposarcoma. A 48-year-old male patient with tumor of left thigh, relatively smoothly marginated, virtually fluid-isointense on native images; intense, somewhat inhomogeneous CM enhancement. (a) Coronal T1w image. (b) Coronal STIR image. (c) Axial T2w image. (d) Contrast-enhanced fat-saturated image.

proliferation with a mass effect. This may be found in numerous organs and regions of the body such as the mediastinum, abdomen, pelvis, or the spinal canal (epidural lipomatosis), presenting a risk of neurologic deficits (▶ Fig. 12.45).142 Epidural lipomatosis can be classified as thoracic and lumbar lipomatosis. Unlike lipomas, lipomatosis is nonencapsulated.

Intramuscular Myxoma Intramuscular myxoma is a benign mesenchymal lesion33 with onset mainly between the ages of 50 and 70 years. Pathologically

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altered fibroblasts produce excessive amounts of mucopolysaccharides and are not able to generate normal collagen. The majority of intramuscular myxomas occur in the thigh, although they can also be found in other body regions such as the shoulder, upper arm, or buttocks.33 A link has been identified between multiple intramuscular myxomas and fibrous dysplasia (Mazabraud’s syndrome).33 Intramuscular myxoma is sharply marginated71,112,140 and has lower signal intensity than that of normal muscle on MRI T1w images. The tumor is markedly hyperintense on T2w sequences71, 112,140; as such, the signal pattern resembles that of a cyst.

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12.4 Tumors: Specific Section

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Fig. 12.42 Myxoid fibrosarcoma in superficial compartment. Axial schematic diagram. (a) On T2w contrast image, the tumor and edema have high signal intensity. (b) Tumor enhancement following CM administration (3), superficial (2) and deep tumor infiltration (1) (uneven tumor infiltration: tail sign), but no enhancement of peritumoral edema (4).

Therefore, detection of myxoid tissue in biopsy specimens is not diagnostic of intramuscular myxoma. Differential diagnosis of myxoma on MRI should include neurinoma.

Desmoid Tumor (Extra-Abdominal Desmoid, Aggressive Fibromatosis) Extra-abdominal desmoid tumors are rare soft tissue tumors that arise from fibrous muscle tissue, fascia, or aponeurosis in patients generally aged between 15 and 40 years.121 Desmoid tumors occur mainly in the thighs, upper arms, and gluteal region. The tumor often grows aggressively, infiltrating adjacent tissues. It has irregular margins, and does not metastasize. Multifocal growth is seen. This is often a hypocellular tumor, interspersed with numerous collagen fibers.121,135 There is a high recurrence rate after local resection (between 25 and 68%).121 The main role of MRI is to determine desmoid tumor extension and its spatial relationship to neurovascular bundles. MRI is also useful for early detection of recurrence. The more hypercellular tumor components have homogeneously low signal, that is, isoto hypointense to muscle, on T1w images, but if it has a larger proportion of myxoid or fatty components, it may also be hyperintense to muscle. On T2w images, the hypercellular components may exhibit homogeneously high signal intensity. The fibrous tumor fascicles manifest as variable areas of linear or nodular signal void, mainly arranged in bundles and septa, on T1w and T2w contrast images. As such, the MRI findings are not consistent or specific, but if the fibrous fascicles are very prominent, a tentative diagnosis should be possible (▶ Fig. 12.46, ▶ Fig. 12.47, and ▶ Fig. 12.48).147 It is now thought that this tumor undergoes a specific aging process, with an initial, hypercellular, growth phase being distinguished from an involution phase characterized by tumor shrinkage and higher fibrous tissue content (higher proportion of low signal areas identified on T2w images).145 The commonly encountered recurrences have a much greater tendency to grow; hence, desmoid tumor may also be encountered in the subcutaneous tissues where they have irregular (uneven) borders. Deep fibromatosis includes, apart from aggressive fibromatosis (extra-abdominal fibromatosis), abdominal and intra-abdominal

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However, unlike in the case of cysts, postcontrast images show inhomogeneous CM enhancement in the lesion.112 Myxoid tissues can also be produced by other tumors such as myxoid liposarcoma, myxoid chondrosarcoma, and myxoid malignant fibrous histiocytoma, but also by ganglion cysts.

Fig. 12.43 Intramuscular lipoma of tensor fasciae latae. (a) CT. Hypodense space-occupying lesion in muscle with increase in entire diameter. (b) Axial T1w SE image. Hyperintense space-occupying lesion in muscle (arrow).

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Fig. 12.44 Intramuscular lipoma of the thigh. Fat-equivalent tumor within the thigh muscles with inclusions in peripheral striates muscles. (a) Coronal T1w image. (b) Axial PDw fatsat image.

Fig. 12.45 Thoracic epidural lipomatosis. (a) Sagittal T1w SE image in an adolescent. The high-signal fat accumulation with a spaceoccupying effect in the epidural space of the dorsal spinal canal (arrows) can be clearly identified. Neurologic deficits have already been observed in the patient. (b) Axial T1w SE image in an adult. Crescentic accumulation of fatty tissue (arrow) with indentation of the dural sac.

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12.4 Tumors: Specific Section

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Fig. 12.46 Desmoid tumor (aggressive fibromatosis). (a) T1w MRI. Parts of the tumor exhibit very low signal intensity; the tumor has irregular margins. (b) T2w image. The tumor has predominantly low signal intensity with numerous areas of linear signal-void, consistent with a high proportion of connective tissue.

Fig. 12.47 Desmoid tumor (aggressive fibromatosis). Another patient. Desmoid tumor on upper arm; sagittal plane. (a) T1w image. Inhomogeneous low signal tumor, which is slightly hyperintense to muscle (area probably containing fat), with areas of nodular as well as linear signal void (connective tissue). (b) T2*w GRE image. Inhomogeneous, predominantly hyperintense tumor with signal-void components. (c) Fatsuppressed STIR image. Inhomogeneous tumor with hyperintense (cellular), hypointense (fat-containing), and signal-void (connective tissue) components.

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Fig. 12.48 Desmoid tumor in left thorax. A 61-year-old male patient. Indistinct infiltration of chest wall. (a) Coronal T1w image. (b) Coronal STIR image. (c) Coronal contrast-enhanced image.

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12.4 Tumors: Specific Section fibromatosis. Subsumed under the collective term superficial fibromatosis are the following diseases: ● Palmar fibromatosis (Dupuytren’s contracture). ● Plantar fibromatosis (Ledderhose’s disease). ● Penile fibromatosis (plastic induration of the penis, Peyronie’s disease).

Vascular Tumors Vascular tumors include hemangioma, angiomatosis, hemangioendothelioma, lymphangioma, and angiolipoma.

Hemangioma and Angiomatosis

Fig. 12.49 Hemangioma in right thigh. Coronal fat-suppressed STIR image. The tumor can be identified as a high-signal, garlandlike, space-occupying lesion between the subcutaneous tissue and muscle (arrow).

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Hemangiomas are generally found in the skin and subcutaneous tissues34 as well as in deep soft tissues. In children, hemangiomas often occur in the skeletal muscles22,34 and can result in muscular atrophy.17,156 The predilection sites for hemangiomas are the extremities. While most tumors are well demarcated, they can in some cases involve the entire limb (angiomatosis). A distinction is made between capillary and cavernous subtypes.34 On T1w images, the hemangioma is isointense or slightly hyperintense to muscle.156 If the lesion contains fat, high signal intensity may be observed on T1w sequences. On T2w images, the tumor is seen as a well-delineated area of hyperintensity. Dilated vascular structures can be identified as characteristic garlandlike, high-signal structures (▶ Fig. 12.49). On GRE images, flowing blood with high signal intensity can sometimes be demonstrated in the tumor, depending on the direction of blood flow.25 On T1w and T2w sequences, hypointense fibrotic areas may also be observed. Phlebolith calcifications are characteristic of hemangiomas (▶ Fig. 12.50 and ▶ Fig. 12.51) and are thought to originate from calcified thrombi in the tumor vascular system. These appear as signal-void structures on all MRI sequences. Hemangiomas show moderate to intense enhancement (▶ Fig. 12.52).52

Hemangioendothelioma Hemangioendothelioma is a semi-malignant hemangioma subtype with a high risk of malignant transformation (see ▶ Fig. 12.50).

Fig. 12.50 Hemangioendothelioma of the lower leg and foot. (a) Radiograph of the forefoot. Phlebolith calcifications between the first and second toes. (b) Sagittal contrast-enhanced SE image. Several enhancing, nodular tumor regions (arrows).

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Fig. 12.51 Angioma on the elbow. (a) Sagittal T2w sequence. (b) Coronal STIR sequence. Signal-intense loculated, space-occupying lesion with foci of signal void characteristic of phleboliths (arrow).

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Fig. 12.52 Characteristic hemangioma on the right upper arm. A 27-year-old male patient with garlandlike, fluid-isointense tumor matrix with linear and oval-shaped enhancement as well as areas of reduced signal consistent with phleboliths. (a) Coronal T1w image. (b) Coronal STIR image. (c) Coronal contrast-enhanced image.

Lymphangioma Lymphangiomas produce similar imaging findings to hemangiomas and cannot therefore be reliably distinguished from these entities. But, unlike hemangiomas, no fatty components are identified on T1w images.

Angiolipoma Angiolipoma is demonstrated as a heterogeneous signal pattern but with both low and high signal components on T1w as well as T2w sequences.113 On both sequences, the high-signal areas reflect blood products. Structures resembling vessels are commonly visualized.

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Peripheral Nerve Sheath Tumor (Schwannoma, Neurofibroma) Neurogenic tumors are now classified as peripheral nerve sheath tumors and categorized as schwannomas (formerly also known as neurinoma), neurofibromas, and malignant peripheral nerve sheath tumors. Schwannomas and neurofibromas occur in all age groups but with peak incidence between the ages of 20 and 50 years.34 Schwannomas are mainly solitary; neurofibromas may be solitary or multiple, especially in patients with peripheral Recklinghausen’s disease. Giant neurofibroma (also known as plexiform neurofibroma or elephantiasis neuromatosa) is a special, noticeably large, variant found in patients with peripheral

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12.4 Tumors: Specific Section

Fig. 12.53 Schwannoma of the upper arm. Axial plane. (a) T1w SE image. The tumor has low signal intensity with isolated areas of inhomogeneity. It is located at the periphery between the subcutaneous tissue and muscle, beside the blood vessels; it is round and encapsulated (arrow). (b) Contrast-enhanced image. Intense enhancement with central area of inhomogeneity. (c) T2*w GRE image. Displacement of adjacent vessels (curved arrow). (d) Fat-suppressed STIR image. Very high-signal visualization with slight inhomogeneous pattern.

Recklinghausen’s disease. Schwannomas of the upper extremities typically occur in the flexor region along the large nerve bundles. They grow slowly and are freely movable apart from along the long axis of the implicated nerve. The majority of schwannomas and neurofibromas exhibit slightly inhomogeneous, intermediate signal intensity on T1w images. Very high signal intensity is typically observed on T2w sequences, occasionally also with a very inhomogeneous pattern.131 This is thought to be due to hypo- and hypercellular regions as well as necrotic and fibrotic areas.131 Myxoid components have also been identified. Intense enhancement is observed, including at times at the periphery. Schwannomas are enclosed in a capsule that is mainly hypointense on MR images. They have a characteristic rounded or ovoid shape (▶ Fig. 12.53) and generally occur in the subcutaneous tissues, where they cause indentation of the adjacent muscle, or along the course of larger nerves. Often, a lemon-shaped contour or protrusion is observed

on both sides of an ovoid neurogenic tumor at the junction to the nerve (string sign), with a rind of fat around the tumor (split fat sign) or target-shaped configuration with peripherally higher signal intensity (target sign) (▶ Fig. 12.54 and ▶ Fig. 12.55).9 Malignant nerve sheath tumors cannot be reliably distinguished from benign lesions on MRI.131 They may present as primary tumors or arise secondarily to malignant transformation of a neurofibroma. A sudden increase in the size of a neurofibroma and marked inhomogeneous signal pattern are suggestive of malignant transformation. The terminology used to denote these tumor entities is inconsistent and comprises the following terms: ● Malignant schwannoma. ● Malignant neurilemmoma. ● Nerve sheath fibrosarcoma. ● Neurogenic sarcoma. ● Neurofibrosarcoma.

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but other large joints may also be involved. The patient complains of intermittent pain and swelling. Conventional radiographs show a dense, soft tissue tumor, possibly with bone erosions. On MRI, the tumor has an inhomogeneous signal pattern that is intermediate or hypointense to skeletal muscle on T1w images. On T2w images, the tumor exhibits mainly homogeneously low signal intensity and may have small areas of focal hypointensity on T2*w images, reflecting focal hemosiderin deposits. Diffuse homogeneous enhancement is observed (▶ Fig. 12.57 and ▶ Fig. 12.58). The diffuse growth pattern has been outlined in the chapter describing the knee (see Chapter 7.15.2).

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Fig. 12.54 Neurogenic tumor. Coronal schematic diagram, section through the distal thigh of patient with neurogenic tumor in tibial nerve (3). T2w contrast image. Preserved fat stripe (1) between tumor and muscle (split fat sign), continuity between nerve and tumor (string sign), and target-shaped signal distribution (2) (target sign).

Malignancy criteria: ● Size. ● Poorly defined margins. ● Infiltration of surrounding structures. ● Marked inhomogeneity. The combination of peripheral denervation, muscular atrophy, and a soft tissue mass along a peripheral nerve is suggestive of a nerve sheath tumors.

Muscle tumors are classified in terms of their tissue of origin, with a distinction made between striated (skeletal muscle, leiomyoma) and smooth muscle (rhabdomyoma; ▶ Table 12.9). The signal pattern identified on MRI is nonspecific, with low signal intensity on T1w and increased signal intensity on T2w images. Malignancy criteria (as in the case of other soft tissue sarcomas) are as follows: ● Poorly defined margins. ● Inhomogeneous signal pattern. ● Rapid growth. ● Size. Mixed histology types have been characterized (e.g., with vascular structures: angioleiomyoma or vascular leiomyoma). In the case of the angioleiomyoma, the tumor arises from the muscle cells of the vascular media of veins or often arteries of the hands or feet, in the superficial compartment (above the fascia). Areas of linear, branched calcification and hyperintensity can be detected in the tumor on T2w or STIR images; otherwise, the imaging findings are nonspecific.53

Hibernoma (Brown Lipoma) Giant Cell Tumor of the Tendon Sheath and Tendon Sheath Fibroma Giant cell tumors of the tendon sheath are histologically identical to fibrous tissues, hemosiderin deposits, histiocytes, macrophages, and giant cells,34 and reflect nodular chronic inflammation of the synovial tendon sheath. These tumors occur mainly on the volar aspects of the fingers. Normally, they are not painful but can be painful when exercising. The recurrence rate following resection is 9 to 20%. Malignant transformation can occur. On histology, the tumor produces findings similar to those of pigmented villonodular synovitis. The lesion presents as low signal intensity along the tendon sheath on T1w sequences and has also relatively homogeneously low signal intensity on T2w image125; inhomogeneity caused by fibrotic areas and hemosiderin may be observed.125 Tendon sheath fibromas produce similar histology results (▶ Fig. 12.56).

Pigmented Villonodular Synovitis This disease could be classified as a chronic inflammatory pseudotumor or focal synovial thickening. The tumor has either a diffuse growth pattern along the synovial lining or grows as a round, focal space-occupying lesion. It affects mainly the knee

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This rare benign fatty tissue tumor is composed of multivacuolated fat cells and is highly vascularized. Multivacuolated fat is found in hibernating mammals (Latin: “hibernare” = to hibernate) and is responsible for heat regulation. While adult humans do not have this type of fat, neonates have multivacuolated fat stores in the neck, axillae, intercostal, and mediastinal regions as well as in other parts of the trunk (▶ Fig. 12.59). No multivacuolated fat is stored in the extremities. Multivacuolated fat is particularly rich in mitochondria and well perfused, lending it a brownish macroscopic appearance (brown fat; ▶ Fig. 12.60). Hibernomas are encountered mainly in the neck, axillae, and the scapular region of the shoulder in patients aged 30 to 50 years. Other reported locations include the mediastinum, upper thorax, and, noteworthy, also the thigh and knee region. The clinical manifestations include a slowly growing, asymptomatic, freely movable, bulging space-occupying lesion. Local hyperthermia occurs at times because of the high vascularization. A number of special features should be borne in mind for diagnostic imaging of hibernomas: an intense vascular blush is seen on angiography, and CM enhancement on cross-sectional imaging.25 MRI visualizes a mainly encapsulated, partially septate, moderately inhomogeneous tumor with intermediate signal that

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Myogenic Tumors, Including Angioleiomyoma

12.4 Tumors: Specific Section

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Fig. 12.55 Schwannoma. Peripheral nerve sheath tumor of the ulnar nerve. (a) Axial T1w image. Muscle-isointense to slightly hyperintense tumor. (b) T2w image. High signal intensity and target-shaped configuration. (c) Contrast-enhanced image. High signal intensity and target-shaped configuration. (d) Sagittal T2w image. Inhomogeneous fat saturation. Continuity between the nerve (here the ulnar nerve; arrow) and tumor, which is a typical finding for nerve sheath tumor, can be identified on the image.

is hypointense to subcutaneous fat and hyperintense to muscle on T1w mages, and high signal intensity on T2w images.86,100 Based on the morphologic imaging findings, it is therefore not possible to distinguish between a hibernoma and liposarcoma.118 Hibernomas are positive on PET scans (▶ Fig. 12.61).

Lipomatosis “Lipomatosis” is a collective term denoting various types of fatty tissue proliferation or the presence of multiple lipomas.

Subcutaneous Lipomatosis One such type of lipomatosis is subcutaneous lipomatosis of unknown origin which is often associated with alcoholism and is also known under the following terms: ● Benign symmetrical lipomatosis. ● Launois–Bensaude syndrome. ● Launois–Bensaude–Madelung syndrome. ● Madelung’s fatty neck.

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Fig. 12.56 Tendon sheath fibroma. Tumorlike, space-occupying lesion along the vastus lateralis. Histology: tendon sheath fibroma. (a) T1w image. Areas of inhomogeneous, focal signal obliterations (arrow). (b) T1w image following CM administration. Slight CM enhancement, reflecting fibrous matrix.

This disease was first described by Brodie (1848), followed by Madelung (1888) as well as Launois and Bensaude (1898) who published details of further cases. The condition is characterized by more diffuse or nodular tissue proliferation seen as yellow fat on light microscopy. No capsule is present. Three types have been distinguished in accordance with the implicated body region: ● Type I: neck and nape (true Madelung’s fatty neck). ● Type II: upper arms, upper trunk, upper thoracic aperture (pseudoathletic type). ● Type III: pelvis, medial thigh (gynoid type). A highly symmetrical pattern of fat distribution is observed, often entailing a mixed-type pattern of involvement, with slow growth. Patients at times report familial clusters of lipomas or surgical resection of lipomas in the most diverse body regions. Men, mainly between 30 and 50 years, are affected much more often than women (ratio 30: 1). A higher incidence of this disease is observed in the Mediterranean region and in east European countries. A high percentage of patients are reported to concomitantly suffer from alcoholism, cirrhosis of the liver, and peripheral neuropathy impaired metabolism of uric acid, fat, and glucose, in addition to macrocytic anemia. There is no evidence for the belief that this disease is caused by a developmental anomaly of brown fat cells. The following complications may present depending on the implicated site: ● Tracheal stenosis. ● Dysphagia. ● Sleep apnea. ● Stenocardia. ● Neurovascular compression. Management of anesthesia becomes more difficult due to the increased fatty tissue volume. Therapeutic options include fat

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resection and liposuction but the recurrence growth rate is high. Drug-based treatment with salbutamol can curtail growth. MRI identifies the nodular or more diffuse tissue proliferation as a signal intensity pattern similar to that of mature fat, making it difficult to diagnose subcutaneous lipomatosis.

Macrodystrophia Lipomatosa and Congenital Infiltrative (Aggressive) Lipomatosis This, often congenital, disease involves diffuse fatty tissue proliferation in one body region with infiltration of adjacent organs as well as often concomitant impaired bone growth. Macrodystrophia lipomatosa is associated with lipomatous fatty tissue proliferation in the extremities with impaired growth, in particular hyperplastic skeletal growth. By contrast, in congenital infiltrative (aggressive) lipomatosis, there is extensive fatty tissue proliferation in the region of the facial skull with hyperplasia of the facial bones on the affected body side, enlarged organs, and enlarged teeth (macrodontia) (▶ Fig. 12.62). 90,129

Superficial Soft Tissue Tumors Subsumed under the term “superficial soft tissue tumors” are tumors that occur above the fasciae in the cutis and subcutaneous tissues. The current state of knowledge underlines the merits of separate classification of tumors in this body region: ● The clinical symptoms differ in certain respects from those of more deep-seated tumors (often detected earlier). ● The spectrum of anticipated tumor histology patterns is different. ● The probability of metastasization of malignant lesions is lower.

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a

b

c

d

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12.4 Tumors: Specific Section

Fig. 12.57 Recurrent pigmented villonodular synovitis of the foot. Heterogeneous space-occupying lesion with focal signal-void components, heterogeneous CM enhancement and erosions in the region of the midtarsal joints. (a) Sagittal T1w image. (b) Sagittal STIR image. (c) Sagittal contrast-enhanced image. (d) CT.

There is a large spectrum of potential tumor entities. In one study of 136 patients, the following tumors were detected more than once (number of patients affected in parentheses)18: ● Benign: lipoma (11), hemangioma (7), fibromatosis (5), neurofibroma (2), nodular fasciitis (2), granular cell tumor (2). ● Malignant: spindle cell sarcoma (11), myxofibrosarcoma (9), liposarcoma (8), lymphoma (8), leiomyosarcoma (5), unclassified sarcoma (5), synovial sarcoma (5), anaplastic sarcoma (4), malignant melanoma (2), rhabdomyosarcoma (2). ● Nonneoplastic: Fat necrosis (8), hematoma (4), epidermoid cyst (3).

The tumor dignity cannot be reliably determined on imaging examinations. Diagnostic pointers of malignancy include18: ● Tumor size (the cut-off value given in the literature is 3–5 cm). ● Rapid increase in size. ● High patient age. ● Poorly defined margins. ● Infiltration of adjacent tissue structures (cutis, fascia, etc.). ● Skin thickening. ● Edema of the fascia. ● Necrosis. ● Lobulated shape. ● Hemorrhage.

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Fig. 12.58 Pigmented villonodular synovitis of the knee. CM-enhancing space-occupying lesion with focal signal obliterations in the superior recess of Hoffa’s fat pad. (a) Sagittal native T1w sequence. (b) Sagittal contrast-enhanced T1w sequence. (c) Axial PDw fat-saturated TSE sequence.

12.4.3 Solid Tumors with Cyst-Isointense Signal Pattern Certain solid tumors exhibit a fluid-isointense signal pattern on native MR images. This may be due to necrosis or to a matrix with high water content such as myxoid stroma (high content of hyaluronic acid and immature collagen fibers), cartilaginous matrix, or synovial matrix. Most of these tumors can be differentiated from cystic lesions (ganglion cysts, bursae, dermal cysts [inclusion cysts], seroma, hematoma) through their partially inhomogeneous and partially homogeneous CM enhancement pattern. Tumors with myxoid matrix:

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● ●

●

Benign: myxoma (often intramuscular). Malignant: myxoid liposarcoma, myxoid chondrosarcoma, myxofibrosarcoma, myxoid malignant fibrous histiocytoma (synonym: undifferentiated pleomorphic sarcoma). Other tumors that may exhibit fluid-isointense signal patterns: synovial sarcoma, some metastases, peripheral nerve sheath tumors (schwannoma, neurofibroma), and vascular tumors (hemangioma, lymphangioma).9

Signs pointing to a solid cystoid tumor on native MR images: ● Atypical location. ● Heterogeneous signal intensity.

12.4 Tumors: Specific Section Table 12.9 Overview of myogenic tumors Smooth muscle

Striated muscle

Benign Leiomyoma (cutaneous and deep)

●

Adult rhabdomyoma

●

Angiomyoma (vascular leiomyoma)

●

Genital rhabdomyoma

●

Fetal rhabdomyoma

●

Epithelioid leiomyoma (benign leiomyoblastoma)

●

Intravenous leiomyomatosis

●

Disseminated peritoneal leiomyomatosis

Malignant ●

Leiomyosarcoma

●

Rhabdomyosarcoma (embryonic, alveolar, pleomorphic, mixed)

●

Epithelioid leiomyosarcoma (malignant leiomyoblastoma)

●

Ectomesenchymoma

Fig. 12.60 Multivacuolated brown and univacuolated white or yellow fat. Both fat types arise from differentiation of primitive precursor fat. Brown fat is responsible for fetal heat regulation and regresses in adulthood. In rare cases, brown fat is identified again in adults at the characteristic locations (see ▶ Fig. 12.59a) (high age, wasting diseases, long-term hunger). Brown fat is highly vascularized and innervated. White fat has the following functions: energy reserves, thermoinsulation, water binding, replacement of atrophic tissue, and supporting functions. A distinction is made between the functions of the storage fat, which is greatly influenced by blood, endocrine and neural systems, and the largely unchanging supporting fat found in various fat bodies (orbits, joints, soles of the feet, palms of the hand, cheeks, etc.).75,152 (a) Multivacuolated brown fat. (b) Univacuolated white or yellow fat. Downloaded by: The University of Edinburgh. Copyrighted material.

●

7

Fig. 12.59 Distribution of multivacuolated, brown fat of the human embryo. (a) Anterior view. (b) Posterior view. 1, cervical (in particular in the neck, around the carotid arteries, and the thyroid gland); 2, axillary; 3, intercostal; 4, anterior mediastinum; 5, anterior abdomen; 6, perirenal (in particular renal hilum); 7, urachal; 8, inferior epigastrium; 9, retropubic; 10, suprailiacal; 11, interscapular; 12, deltoid; 13, trapezius; 14, latissimus dorsi.

a

b

Fig. 12.61 Hibernoma on left thigh. Fat-equivalent tumor in the upper thigh muscles. (a) CT. Septation and smooth margins. (b) PET-CT fusion image. Sharp increase in glucose consumption.

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Fig. 12.62 Congenital aggressive lipomatosis. A 20-year-old female patient. Massive fatty tissue proliferation in the right half of the face. Enlargement of the mandible, parotid glands, and the teeth (macrodontia) on the right half of the body. Atrophy of the right masticatory muscles, thought to be caused by mechanical inactivity. (a) CT (soft tissue window). (b) CT (bone window). (c) T1w SE sequence. (d) T2w SE sequence.

● ●

Wall thickening . Thickened septa.

The use of contrast-enhanced sequences facilitates differentiation in such cases.

12.4.4 Metastases Secondary bone and soft tissue tumors account for the vast majority of routinely diagnosed tumors, of which in turn most are bone

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metastases; skin and other soft tissue metastases are rare. No epidemiologic data are presented in this section, with the focus instead on specific MRI findings and on aspects of differential diagnosis. Osteolytic bone metastases have low signal intensity on T1w and high signal intensity on T2w MR images and take up CM. The most sensitive sequences for detection of metastases are fat-suppressed STIR sequences, contrast-enhanced sequences (in particular when using a subtraction technique, albeit only enhancing areas have increased signal intensity on the reformatted image),

12.4 Tumors: Specific Section

Schmorl’s nodes of the vertebral bodies can be distinguished from early-stage vertebral body metastases based on their location close to the end plates, surrounding sclerosis, and no, or only minimal, CM uptake, as well as by consulting previous examination results (hence always compare current with previous radiographic results if available). Hemangiomas of the vertebral bodies generally exhibit high signal intensity on T1w and T2w images because of their high fat content and present a differential diagnostic challenge, at most, with respect to melanotic metastases of malignant melanoma. Bone cysts are brighter on T2w images than metastases and do not take up CM.

MRI is a highly sensitive modality in detecting metastases and should therefore always be used in cases where conventional radiography and bone scintigraphy have not been able to rule out suspected metastasis or explain discrepant findings. For example, early-stage osteolytic metastases can go undetected on both radiography and scintigraphy. Therefore, MRI should be used for patients with malignant underlying disease who are experiencing pain or elevated alkaline phosphatase activity. Skin and other soft tissue metastases are on the whole rare and generally do not constitute an indication for MRI. Anyhow, the diagnosis is deemed highly probable if the patient has a history of underlying tumor disease, and evidence of a recurrent space-occupying lesion in the corresponding soft tissues is supported by the follow-up results of palpation, inspection, ultrasound, and /or CT. This can be confirmed by biopsy and histology, and MRI is generally no more specific in such cases.

12.4.5 Pseudotumors and Tumorlike Substance Deposits, Paget’s Disease Gouty Tophus

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as well as T1w SE sequence for metastases in hematopoietically inactive fatty bone marrow. Metastatic lesions have very low signal intensity (like muscle) compared with edema (weak low signal intensity on T1w images). Conversely, hemorrhagic and melanotic metastases from malignant melanoma exhibit increased signal intensity on T1w images. The more common amelanotic metastases of malignant melanoma have an uncharacteristic increased signal pattern. Predominantly, osteoblastic metastases have low signal intensity on both T1w and T21 sequences. Areas of necrosis have a fluid-isointense signal pattern and do not take up CM. The initial morphologic appearance of a metastatic lesion is that of a round, relatively sharply delineated space-occupying mass which becomes increasingly less well demarcated because of the surrounding edema. In the case of vertebral metastatic fractures, the entire vertebra is generally hypointense on T1w and hyperintense on STIR images and takes up CM. It is often easier to identify bone destruction on CT than on MRI as the latter visualizes only the bone marrow. Since bone does not contain water protons, it is not directly visualized on MRI. Therefore, only CT should be used to investigate suspected fracture. But on the other hand, MRI is frequently able to detect metastases much earlier than CT. Metastasis to the bone marrow is always the initial finding and only later followed by bone destruction due to osteoclast-activating factors. In addition to focal metastasis, a diffuse metastatic pattern is also observed, with inhomogeneously low signal on T1w and mainly inhomogeneously high signal intensity on STIR images. The bone marrow generally exhibits diffuse inhomogeneous, intense contrast enhancement, similar to that seen in multiple myeloma. MRI is adept at demonstrating extraosseous bone growth with infiltration of the surrounding soft tissues since it is able to accurately determine extension of these soft tissue components and the spatial relationship to adjacent tissues. For example, it may be able to accurately pinpoint the vertebral metastases responsible for sudden onset of neurologic deficits by demonstrating extravertebral tumor in the spinal canal and neural foramina. In differential diagnosis, the following factors are suggestive of metastases: ● High patient age. ● Multiple bone lesions. ● Diagnosis of underlying malignant disease. ● Increase in size and number of lesions within short period of time. ● Predilection for areas with hematopoietically active, red bone marrow (increased perfusion).

Deposition of urate crystals in bone and soft tissues can years to decades after onset of gout give rise to crystal-induced inflammatory pseudotumors known as gouty tophi. Differential diagnosis should not present any problem in patients with a typical case history and arthritic signs. However, it may be very difficult to distinguish between solitary tophi and neoplasms. MRI visualizes a muscle-isointense, space-occupying lesion on T1w images, which on T2w contrast sequences is very variable ranging from homogeneously high signal to inhomogeneously low signal intensity. Homogeneous, intense enhancement is observed. As such, MRI is not specific for gouty tophus.155 Dualsource CT is able to accurately differentiate between urate deposits and other calcium salts.

Amyloid Deposition Amyloidosis can give rise to tumorlike amyloid accumulation in bone, manifesting as pseudotumors measuring a few millimeters to centimeters. These lesions are encountered in the periarticular and subchondral regions, especially of the shoulder (see Chapter 3.9.5), hip (see Chapter 6.16), and knee (see Chapter 7.15.6). These pseudotumors have low signal intensity on T1w images and their signal pattern ranges from low through inhomogeneous to high on T2w images. They do not take up CM. The decisive criteria for differential diagnosis of this condition from neoplasms are the location and patient history.

Xanthoma of the Tendons Xanthoma of the tendons is a space-occupying lesion that occurs in the tendons of the hand and elbow, Achilles tendon, patellar tendon, peroneal tendons and plantar aponeurosis of patients with hyperlipoproteinemia. Lipid-laden foam cells are deposited in the tendon causing an inflammatory reaction and nodular mass. MRI demonstrates discrete tendon thickening with multifocal, reticular, almost diffuse rise in signal intensity due to

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Bone and Soft Tissue Tumors in osteodystrophia fibrosa cystica generalisata—Recklinghausen’s disease). The brown color is due to hemosiderin deposits. Conventional radiographs show partially large osteolytic lesions, also with cortical destruction. MRI demonstrates characteristic tumorlike signal intensity, often with soft tissue and, possibly, multiloculated cystoid components and fluid–fluid levels as well as intense enhancement.61

12.4.6 Extramedullary Hematopoiesis

increased fat deposition. The magnitude of the increase in signal intensity is variable and ranges from a muscle-isointense to a fatisointense pattern. Intense enhancement, possibly attributable to inflammation, is observed.108

Hemophilic Pseudotumor Intense bleeding can lead to large space-occupying masses, in particular, in patients with hemophilia. At times it is not easy to distinguish these lesions from real neoplasms. These pseudotumors can cause bone destruction (▶ Fig. 12.63). They are found in soft tissues as well as within bone. Depending on the hemorrhage age areas of high signal intensity may be detected within an inhomogeneous tumor on T1w images due to the presence of methemoglobin. CM enhancement secondary to connective tissue remodeling as well as a fibrous capsule may be observed in older lesions.66

Paget’s Disease (Osteitis Deformans) Paget’s disease (osteitis deformans) can affect the lower extremities, skull, vertebrae, clavicle, humerus, and the ribs; polyostotic involvement is also seen. The disease progresses in different phases that produce characteristic findings on radiographs, ranging from initial osteolytic changes (osteoporosis circumscripta) through mixed changes (intermediate phase) to the typical latestage abnormalities with cortical irregularity, thickening, and an increasingly stringy appearance. MRI visualizes cortical thickening as areas of signal void on T1w and T2w sequences, as well as contrast enhancement. The bone marrow cavity exhibits fatty marrow-equivalent signal intensity.158

Brown Tumor (Osteodystrophia Fibrosa Localisata, Osteoclastoma) This focal or multifocal bone lesion involves discrete bone breakdown due to osteoclast activity and is seen mainly in association with hyperparathyroidism (resorption lesion, mainly

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These typically manifest as large para- and prevertebral, bilateral, symmetrical lesions in the thoracic and sacral spine; at times they may be very large, measuring several centimeters in diameter.47 The majority of these tumors occur in association with myeloproliferative disorders, in particular idiopathic osteomyelofibrosis, as well as hereditary anemia, especially thalassemia major. Such foci are more likely to occur as compensatory mechanisms when the extramedullary hematopoiesis capacity of the liver and spleen is exceeded. The tumors have a space-occupying appearance with histology similar to hematopoietic cells. Various symptoms are observed in accordance with the location e.g. bone marrow compression. These foci are radiosensitive. MR images show an uncharacteristic signal pattern of low signal on T1w and increased signal intensity on T2w contrast images115 as well as focal enhancement.

12.4.7 Chloroma (Granulocytic Sarcoma) Chloroma is an extramedullary aggregate of immature granulopoietic cells with a space-occupying, macroscopic appearance, which often has a green color that changes on coming into contact with the air. This phenomenon is due to the presence of intracellular myeloperoxidase. The tumor occurs mainly in association with the following bone marrow diseases: ● Polycythemia vera. ● Essential thrombocythemia . ● Idiopathic osteomyelofibrosis. ● Chronic myeloid leukemia (in 4% of cases). ● Acute myeloid leukemia (in 8% of cases). The following organs are affected in descending order: Bone. ● Periosteum. ● Soft tissues. ● Lymph nodes. ● Skin. ●

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Fig. 12.63 Hemophilia. Axial PDw SE image with MTC effect in pelvis. Osteolytic, inhomogeneous space-occupying lesion (curved arrows), on the right, with hyperintense, intermediate and hypointense components due to hemorrhage of different age. The spaceoccupying lesion does not exhibit any MTC effect.

Foci of extramedullary hematopoiesis may be encountered in the following organs and structures: ● Pleura. ● Lungs. ● Gastrointestinal tract. ● Chest. ● Skin. ● Dura mater. ● Kidneys. ● Adrenal glands.

12.4 Tumors: Specific Section Solitary and multiple chloromas are encountered. On MR images, chloroma has homogeneously low signal on T1w images and homogeneously high signal intensity on T2w contrast images.50 Intense enhancement and a pronounced peritumoral reaction zone are observed.76

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13.1

Introduction

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13.2

Examination Technique

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Osteoporosis

13.3

Clinical Relevance of Magnetic Resonance Imaging

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References

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Chapter 13

Osteoporosis

13 Osteoporosis S. Grampp, M. Vahlensieck, and H. K. Genant

Generalized osteoporosis is the most common metabolic skeletal disease and is characterized by a reduction in bone mass as well as by structural changes.17,23 In trabecular bone, both the density and structural integrity of the trabecular network are reduced. In cortical bone, increased endosteal, periosteal, and intracortical resorption processes cause thinning and increased porousness. The normal microstructure (microarchitecture) of trabecular bone is composed mainly of an extensive network of rod- (columnar) and platelike trabeculae. Abnormally deep subcortical resorption lacunae are observed in association with osteoporosis, especially on the vertebral bodies. These give rise to trabecular thinning and separation, depriving osteoblasts of the morphologic substrate needed for new bone formation. The initially platelike or columnar trabeculae assume an increasingly thinner, rodlike shape, which, in turn, become perforated and eventually disappear. Microfractures and associated reparative mircocallus formation are increasingly seen during this stage, followed by an ongoing decline in the intertrabecular network. These mechanisms eventually result in reduced bone strength. Various studies have reported that of the measurable parameters, bone mineral density (BMD) had the greatest impact on bone strength.3,11 Osteoporotic fractures occur especially in bone with a high trabecular content, for example, vertebral bodies, femoral neck, and distal radius. There is currently a vast armamentarium of clinical techniques available for diagnosis of osteoporosis and fractures as well as for assessment of the bone mass and fracture risk.17,20,24 The majority of these methods are based on the use of ionizing radiation, where the measured radiation absorption is determined by the BMD. In recent years, magnetic resonance imaging (MRI) has also been used increasingly for diagnosis of osteoporosis, in particular for diagnostic imaging of osteoporotic deformities and fractures. High-resolution techniques have been successfully deployed for direct visualization of the bone structure and permit insights into deformities.36 MRI also plays a pivotal role in demonstration of osteonecrosis (avascular necrosis), as may be observed in association with bisphosphonate therapy.26 Such local complications are seen especially in the mandibles. The new advances in recent years in imaging technologies have also contributed to our understanding of osteoporotic bone loss as well as of bone pathology and physiology in general.25 Quantification of the relaxation times (relaxometry) is being currently studied for reliable diagnosis and monitoring of osteoporosis.21,22, 35,48,52,54,63 To that effect, the effective T2 time (T2*) is generally measured and occasionally expressed as a reciprocal value (1/T2*). So far, MRI just falls short of the required low reproducibility values of less than 2%, as achieved by other methods of quantitative osteoporosis assessment (quantitative computed tomography [CT], Dual spectral absorptiometry).32 Determination of the age of spinal fractures is of clinical relevance, in particular with regard to indication of kyphoplasty with fluid-sensitive sequences, such as short-tau inversion recovery (STIR) sequences. Fractures of different ages are commonly seen

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in advanced osteoporosis, and only the more recent (symptomatic) fractures are treated. The signal intensity exhibited by bone marrow edema on STIR sequences grants insights into the fracture age (see below; ▶ Fig. 13.1).

13.2 Examination Technique 13.2.1 Magnetic Resonance Imaging Insufficiency fractures are the most serious type of complication induced by osteoporosis. As per its definition, such a fracture results from physiologic stress which normally should not cause any damage. Insufficiency fractures occur mainly in the vertebral bodies, proximal femur, distal radius, sacrum, and pubic bone. Frequently, they are subacute, progress slowly, and may develop over weeks or months. While the majority of these fractures can be clearly detected on conventional radiography, a significant number are still missed. MRI can be used for diagnosis of such radiologically occult fractures which are relatively common in older osteoporosis patients (around 10% of cases). Various studies of the proximal femur have attested to the suitability of MRI for detection of such fractures.13, 43,50,51,67 MRI typically visualizes a fracture line as an area of markedly reduced signal intensity (T1 weighted [T1w] sequences). The fracture lines generally have a tortuous course, surrounded by bone marrow edema. These changes in signal intensity are attributed to focal hyperemia and edema, impacted trabecular bone, as well as to bone repair processes. Early diagnosis has major clinical implications since offloading the affected structures can help prevent subsequent complications. Fractures of the sacrum represent a specific type of fractures that are generally occult on conventional radiographs but detected with high specificity on MRI. Often the older patients affected had experienced a minor injury, with pain in the pelvic region. Frequently, a radiograph will show fractures of the anterior pelvic ring but with persistent pain despite treatment, especially in the lower back region. In such settings, MRI demonstrates often uni- or bilateral sacral fracture and, accordingly, complete pelvic ring fracture (▶ Fig. 13.2). In those cases where there is no clinical evidence of a proximal femur fracture, MRI often identifies pelvic fractures or other pelvic disorders (hematoma, muscle or tendon lesions, osteonecrosis) which may explain the symptoms exhibited. Compared with scintigraphy, MRI is endowed with at least similar, or according to some studies even superior, sensitivity for diagnosis of osteoporotic insufficiency fractures of the pelvis, sacrum, the hips, or the long tubular bones.4,5,44 That is true especially within the initial days of trauma (▶ Fig. 13.3). During this period, nuclear medicine examination techniques often do not permit diagnosis. The ability of MRI to distinguish osteoporotic from pathologic, tumor-related vertebral body fractures is also of major clinical relevance1,2,53,65,68: pathologic, tumor-related fractures typically induce changes in the signal pattern throughout the entire marrow of the fractured vertebral body,16,45,49 affecting in particular

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13.1 Introduction

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13.2 Examination Technique

a

b

Fig. 13.1 Fracture age. A 76-year-old female patient with back pain. Osteoporosis with numerous “fish vertebrae” deformities of the lumbar vertebrae and lower thoracic vertebrae. The central height loss in thoracic vertebra T9 exhibits only fat-equivalent signal intensity (white arrows) suggestive of an older fracture. Lumbar vertebra L5 has a low signal fracture line with some surrounding bone marrow edema (black arrows) suggestive of a “moderately” old fracture. Lumber vertebrae L3 and L1 as well as thoracic vertebrae T11 and T12 have large areas of edema pointing to fresh or “moderately fresh” fractures. (a) Sagittal T2w sequence. (b) Sagittal STIR sequence.

the vertebral pedicles and arches.61 These are often accompanied by convex deformity of the anterior and posterior margins of the vertebral bodies. Besides, an additional periosteal soft tissue component with a space-occupying effect on the epidural space, spinal canal, and perispinal region is also frequently observed. Likewise, the adjacent vertebral bodies, as well as the vertebral bodies of more distant spinal segments, often harbor metastases, exhibiting corresponding patchy foci of reduced signal intensity on T1w and increased signal intensity on T2 weighted (T2w) images. Conversely, osteoporotic fractures frequently induce bandlike changes in signal intensity adjacent and parallel to the end plates. However, they may also extend into the center of the vertebral bodies and exhibit a rather complex distribution pattern.31 In the nondeformed portions of the vertebral body, the

bone marrow generally continues to exhibit a normal signal pattern (▶ Fig. 13.4 and ▶ Fig. 13.5). The medullary space of adjacent nonfractured vertebral bodies mainly has normal signal intensity. The fracture gap air marking (signal void on all sequences) as well as intravertebral fluid–fluid levels are suggestive of a benign fracture.6,61 MRI has higher sensitivity than bone scintigraphy and higher specificity than CT for differentiation between osteoporotic and pathologic vertebral body fractures1,2,65; a normal MRI scan rules out the presence of an insufficiency fracture.25 Some studies have demonstrated that intravenous injection of contrast medium (CM) can improve diagnostic imaging of the causes of vertebral body fractures.10,27 Osteoporotic fractures exhibit linear enhancement running parallel to the fracture line (▶ Fig. 13.6), while malignant vertebral body fractures are generally associated

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Osteoporosis

b

Fig. 13.2 Sacral fractures. Older female patient with back pain secondary to minor injury. Already diagnosed pubic bone fracture. CT of the sacrum normal. Bilateral edematous changes as well as signal-void fracture lines of the sacrum due to occult sacral fractures (arrows). (a) Coronal T1w sequence. (b) Coronal PDw fatsat sequence.

Fig. 13.3 Femoral neck fracture. MRI of the hip 8 hours after femoral neck fracture in a 67-year-old female patient. The coronal GRE image shows a subcapital fracture line of low signal intensity (white arrow) with adjacent areas of intermediate to low signal intensity (arrowheads) consistent with edema or hemorrhage.

with patchy, irregular enhancement. Bone marrow regions, which are hyperintense on T2w and hypointense T1w sequences, also generally take up CM (▶ Fig. 13.7). The ability of MRI to distinguish between acute traumatic and osteoporotic insufficiency fractures is limited since both fractures produce local changes in signal intensity due to bleeding and repair processes. Severe bone deformation with marked fragment displacement tends to be seen after acute trauma, while chronic

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deformities of adjacent vertebral bodies, exhibiting a normal bone marrow signal pattern, are mainly seen in association with osteoporosis. The age of a fracture can be estimated using a fatsaturated T2w sequence or STIR sequence. Acute or subacute stages are accompanied by bone marrow edema that slowly regresses (within 6–12 weeks). The changes induced in the bone marrow signal pattern by a nonneoplastic fracture usually revert to normal after a few months, leaving behind only a deformed vertebral body. Apart from the immediate changes in the bone marrow, the effects on the intervertebral disks are also monitored. The more stable and healthier the vertebral body, the more pronounced are the height loss and degeneration of the adjacent intervertebral disk and the more severe the degenerative bone changes, such as spondylophytes and intervertebral osteoarthritis.59 MRI is also used when planning kypho- and vertebroplasty for osteoporotic fractures, for example, for assessment of the risk of additional fractures (multisegmental fractures). The presence of an intravertebral vacuum phenomenon and cortical discontinuity are predisposing factors for formation of extravertebral cement deposits following leakage.47 Since there is an increase in the incidence of fractures of the adjacent spinal segments, regardless of whether or not vertebroplasty was performed,30,33 MRI is the method of choice for follow-up examinations. In addition to measuring the trabecular density and structure, MRI is able to generate high-resolution images of the trabecular microarchitecture. After modification of the computer programs, standard MRI systems can produce images with a resolution of 78 μm × 78 μm × 300 μm of the finger phalanges25 and 78 μm × 78 μm × 700 μm of the distal radius (▶ Fig. 13.8) and calcaneus.34,37, 41 Studies were conducted with field strengths of 1.5 to 7 T.38 The reproducibility achieved with “virtual bone biopsies” at 1.5 T is already enough for implementation of long-term therapeutic

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a

13.2 Examination Technique

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Fig. 13.4 Osteoporotic vertebral body compression fractures. (a) Sagittal T1w SE image a few days after sustaining the fracture. Vertebral body L1 has a “fish vertebrae” deformity (open arrow) and low signal intensity in the bone marrow. The superior end plate of vertebral body T12 is also indented and exhibits low signal intensity (arrows). (b) Sagittal T1w image a few months after sustaining the fractures. The signal pattern of vertebral body T12 is now normal. A small area of reduced signal intensity of vertebral body L1 (open arrow) is consistent with focal sclerosis.

a

b

Fig. 13.5 Benign osteoporotic fracture. (a) Sagittal T2w image. Vertebral body L1 has a wedge-shaped deformity with low signal intensity along the inferior end plate as well as increased signal intensity in the bone marrow region. Vertebral body T12 has a roundish area of increased signal intensity suggestive of an intravertebral hemangioma. (b) Sagittal T1w image. Overall, reduced signal intensity in the fracture region.

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Osteoporosis

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Fig. 13.6 Osteoporotic vertebral compression fracture. (a) Sagittal T1w SE precontrast image. Several compression fractures (arrows) of vertebral bodies L2, L3, and L4. (b) Sagittal T1w SE postcontrast image. Linear enhancement (arrows) parallel to the fracture lines of the respective vertebral bodies. This pattern is characteristic of osteoporotic fractures.

a

b

Fig. 13.7 Metastases of several vertebral bodies. (a) Sagittal T1w SE image. Extensive areas of multisegmental reduced signal intensity in both the vertebral pedicles and dorsal vertebral elements in association with metastatic bronchial carcinoma. (b) Sagittal TIRM (turbo inversion recovery magnitude) image. Corresponding areas seen as regions of high signal intensity, with partially diffuse, partially round, focal lesions.

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13.2 Examination Technique

Fig. 13.8 Visualization of the distal radius with a 1.5 T Signa MRI scanner. High-resolution imaging with a T2*w water-presaturated GRASS sequence (see ▶ Table 1.2), slice thickness of 700 μm, and spatial resolution of 156 μm. Trabecular bone in radius (b–d, closed arrows), ulna (b–d, open), and cortex of both bones (b–d, arrowheads). (a) Coronal section through the distal forearm and the wrist. The levels of the axial sections are marked as white lines. (b) Axial section around 7 mm distal to the cortical end plate of the radius (mean T2* relaxation time in 12 healthy subjects = 18.02 ms). (c) Axial section around 19.6 mm distal to the cortical end plate of the radius (T2* = 21.20 ms). (d) Axial section around 35 mm distal to the cortical end plate of the radius (T2* = 32.50 ms).

imaging of patients.32 Similar measurements were also successfully performed on the proximal femur with a resolution of 254 μm, while demonstrating the positive effect of calcitonin treatment in postmenopausal women.7 Postprocessing of these images using data obtained from CT-based image analysis techniques8,9,14,28,29,41,42,46,66 can yield quantitative parameters such as the bone content of an entire 2D surface area of a section, mean trabecular density, number of trabecular branches, or their preferred spatial orientation. However, a number of pitfalls should be borne in mind when interpreting these parameters: ● Incorrect separation of bone and marrow components. ● Mistakes in the relatively limited spatial resolution. ● Partial volume effects. ● Movement artefacts caused by the relatively long acquisition times of around 10 to 20 minutes. In addition to the aforementioned options, there are other image and structural analysis techniques available but these will not be discussed here in detail as they are still mainly in the experimental stage. They include, among others, the following techniques: ● Morphologic granulometry.6

● ●

Calculation of fractal elements.41 Wavelet processing.57

Since studies have already been successfully carried out in clinical patients,42 it is hoped that in the future quantitative analysis of bone-related morphologic factors can be used for calculation and estimation of the individual fracture risk and for monitoring and quantification of therapeutic benefits.36 It is thought that these applications will exceed the power of bone density measurement alone.

13.2.2 Relaxation Time Measurements and Spectroscopy Because of its low number of free protons, cortical bone—and strictly speaking mineralized trabecular rods too—does not emit any MRI-detectable signal. The relaxation times cannot be measured and are extremely short. The trabecular bone is different. The trabecular bone network contains numerous cellular constituents and fat which account for the principle constituents of the bone marrow. When solid

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bodies are surrounded by a liquid, a thin layer of this liquid adheres to the solid body surface. The same principle applies between the bone marrow (quasiliquid phase) and the solid surface of the bone trabeculae. Hydrogen bonds, ion–dipole interactions, dipole–dipole interactions, and hydrophilic attraction forces give rise to changes in the liquid molecule abutting, or in the vicinity of, the solid surfaces. The bone marrow signal detected on MRI is chiefly determined by the composition of the cellular and fatty constituents. Due to its high fat content, the signal emitted by inactive, yellow, hypocellular bone marrow is higher than that of the hematopoietically active, red, hypercellular marrow. However, since the bone marrow of the adult peripheral skeleton is composed mainly of fatty constituents, the use of fat-selective sequences will prevent signal loss caused by chemical shift. MRI is constrained by the signal-to-noise ratio (SNR) and the spatial resolution and is additionally affected by the presence of hematopoietic marrow. The latter has low contrast compared with fatty marrow. For that reason, the majority of in vivo studies have been carried out on peripheral skeletal regions such as the radius, tibia, and calcaneus.25 These have a high trabecular bone content and yield good results when imaged with small, high-resolution MRI coils. The chief determinant of the feasibility of MRI for quantitative assessment of osteoporosis is whether the number, thickness, and separation of the bone trabeculae (bone density) impact the bone marrow signal and whether the relaxation times can be thus affected. Another issue is whether in settings of altered bone strength or bone elasticity (expressed as the elasticity coefficient [Young’s modulus of elasticity] as an indicator of the potential risk of fracture or of risk assessment) the relaxation times are affected. Myriad experiments have been conducted to clarify these issues. These have revealed that the T1 and T2 relaxation times of bone marrow are not significantly influenced by the bone density.40 The elasticity coefficient is also thought to have only a limited impact on the T2 relaxation time.52 Conversely, both the bone density and elasticity coefficient have a significant impact on the effective T2 time (T2* time). This is due to T2*

Magnetic field B0 Normal bone with high trabecular density Hom Trabeculae

Osteoporotic bone with low trabecular density Hom Trabeculae

Osteoporotic bone with trabecular thinning Hom

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sensitivity to the inhomogeneities in the local magnetic field because of the already mentioned susceptibility fluctuations observed along interfaces, for example, at the interface between the trabeculae and bone marrow. The magnetic susceptibility of trabecular bone is much less than that of the bone marrow. This causes distortion of the magnetic field lines. The magnetic properties of protons within these areas of field inhomogeneity are not included in measurements, thus giving rise to shorter T2 relaxation times throughout the bone marrow. Since there is a preponderance of such interfaces within the trabecular network, any changes in the distance between the individual trabeculae or in trabecular thickness will in turn inevitably give rise to changes in the local magnetic field and, accordingly, in the T2* time measured (▶ Fig. 13.9). Increased trabecular density causes faster relaxation with shorter T2* times.12,40,52 Reduced trabecular density, as seen in particular in osteoporosis and, less so, during the normal aging process, causes slower relaxation with longer T2* times. Measurement of the T2* time appears to be the most promising approach for quantitative assessment of osteoporosis on using MRI. As expected, these parameters are affected by patient age, with prolongation of the T2* time of the lumbar vertebrae at a rate of around 0.3 ms/year in premenopausal women and of up to 0.9 ms/year in postmenopausal women. Besides, a significant difference was identified in the T2* time of the lumbar vertebrae of healthy (15.8 + 2.5 ms) versus osteoporotic subjects (18.8 + 2.8 ms).52,63 That was also corroborated by other studies of the lumbar spine (healthy: 13.4 + 1.9 ms; osteoporotic patients: 19.9 + 3.8 ms).16 That the BMD exerts a major impact on the T2* time was demonstrated by quantitative CT. A good correlation was identified on quantitative MRI between the BMD (r = 0.92) and a rise in 1/T2* of 0.2 s–1 per mg/cm3 hydroxyapatite concentration in vitro. Studies based on these in vitro findings confirmed the results of in vivo experiments, too.54 Measurements, based on the assumption of a linear relationship, performed on the distal radius and proximal tibia of healthy subjects30 found that the decrease in T2*

Fig. 13.9 Homogeneous magnetic field of nontrabecular bone marrow. Increase in the homogeneous magnetic field (Hom) of nontrabecular bone marrow due to low trabecular density and trabecular thickness in association with osteoporosis. This leads to prolongation of the T2* time.

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Osteoporosis

13.3 Clinical Relevance of Magnetic Resonance Imaging

IðTEÞ ¼ I0
e 

TE T2

where I (TE) = signal intensity for specific TE, I0 = signal intensity at time point t0. However, since no rephasing pulse is used in GRE sequences, they are sensitive not only to changes in the T2* time but also to rephasing phenomena (see Chapter 11) arising because of various bone marrow constituents. Both TE and field strength have a major impact on these phasing phenomena.48 Consequently, the T2* time is determined not just by the bone density and architecture but also by the bone marrow cellular constituents, which vary considerably from one individual to another. Other drawbacks are the lack of standardized measurement regions of interest (▶ Fig. 13.10)15,21,22 as well as the normally encountered MRI artefacts. Various solutions have been proposed to overcome these hurdles and are being currently explored. One approach advocates the use of exclusively peripheral measurement sites containing only fatty bone marrow, such as the calcaneus and distal radius, so as to minimize phasing effects. The pros and cons of peripheral measurement sites will not be elaborated on further here. Another proposal is to use fat suppression, in the form of water images, to calculate the T2* time

Fig. 13.10 Proximal tibial epiphysis. Axial GRE image with a 1.5 T Signa MRI scanner. Visualization of the central area of the proximal tibial epiphysis of a healthy female subject showing T2* measurement in the bone marrow region.

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relaxation time in line with rising trabecular bone density was 0.2 s–1 per mg/cm3 and, as such, was almost identical to the in vitro results.37,40 Comparison of trabecular T2* measurements with bone density values of the distal radius obtained with peripheral quantitative CT identified,22 depending on the measurement position, correlation coefficients (r) of between 0.63 and 0.93. The closest relationship between T2* measurements and the BMD identified so far was for the proximal tibia of healthy young women (correlation MRI/2 spectral absorptiometry: r = 0.96).15 Likewise, the proximal femur as the main region of interest was also investigated in recent experiments35; by measuring the T2* times, it was possible to distinguish between postmenopausal women with and without fractures of the proximal femur. In vivo measurements of the T2* relaxation time of the lumbar spinal continue to present a technical challenge because of the relatively low SNR and movement artefacts (breathing and intestinal peristalsis). Despite these technical handicaps, it was possible to detect a decrease in the relaxation time 1/T2* of 0.114 s–1 per mg/cm3 change in trabecular density for the lumbar spine.56 Measurements of the lumbar vertebrae of healthy subjects revealed on average shorter T2* relaxation times (16.8 ms) compared with osteoporotic patients (20.8 ms)64; measurements of the bone marrow of lumbar vertebrae L2–L5 proved most suitable for differentiation between healthy and osteoporotic patients.63 Likewise, isolated measurements carried out on vertebra L4 revealed that osteoporosis patients (19.9 ms) had markedly longer T2* relaxation times compared with those of a healthy control group (13.4 ms).16 The poor reproducibility of T2* measurements continues to be a major problem. No variations of less than 5% have been identified for either short- or long-term reproducibility.15,21,39 This is due to various factors: the T2* time is generally measured on gradientecho (GRE) sequences by conducting a series of measurements with different TE,21 and the T2* time is calculated on the basis of the signal intensity recorded within a certain region of interest while using the following formula:

but, while this is a promising technique, it is time consuming. In addition, the T2* time can also be determined on spectroscopy. Other methods currently under development, and mentioned in the interest of completeness, include interferometry and MAGSUS (measurement von MAGnetic field and SUSceptibility).54 Spectroscopy gives insights into the quantitative composition of the bone marrow with regard to the water and fat content.34 The fat content rises in line with declining bone density. One line of current research focuses on the cortical bone. Just like the trabecular network, the cortex too can lose mass with attendant thinning and porousness. In such cases, the cortical water content can be determined as a correlate of cortical loss.57 However, determination of the bone marrow fat content by chemical-shift analysis for prediction of the bone density has failed to produce any satisfactory findings to date.19

Internet Link

●i

Further information on current research in this area can be found on the website of the National Library of Medicine (PubMed) using the search term “osteoporosis mri.”

13.3 Clinical Relevance of Magnetic Resonance Imaging Conventional MRI is adept at differential diagnosis of osteoporotic fractures and has become a mainstay of clinical routine diagnostic work-ups. The high-resolution methods for mapping the microstructure of bone are still in the experimental stage and need to be further refined to assure, in particular, standardized, automated evaluation in order to compete with the rapid progress made by CT modalities. Quantification of the T2* time has shown promising results for both in vivo and in vitro studies. It is expected that the ongoing

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Osteoporosis developments in hardware and software technology will improve reproducibility in the foreseeable future and underpin the role of MRI in osteoporosis diagnosis. That view is supported by the fact that MRI lends itself to both morphologic (e.g., edema) and quantitative assessment of osteoporosis.

[22] Grampp S, Majumdar S, Jergas M, Newitt D, Lang P, Genant HK. Distal radius: in vivo assessment with quantitative MR imaging, peripheral quantitative CT, and dual X-ray absorptiometry. Radiology. 1996; 198(1):213–218 [23] Grampp S, Steiner E, Imhof H. Radiological diagnosis of osteoporosis. Eur Radiol. 1997; 7(10):11–19 [24] Grampp S, Henk CB, Imhof H. Radiologic method for the diagnosis of osteoporotic and age-related bone changes [in German]. Rontgenpraxis. 1998; 51

[1] Allgayer B, vd Flierdt E, von Gumppenberg S, et al. NMR tomography compared to skeletal scintigraphy after traumatic vertebral body fractures[in German]. Rofo. 1990; 152(6):677–681 [2] Baker LL, Goodman SB, Perkash I, Lane B, Enzmann DR. Benign versus pathologic compression fractures of vertebral bodies: assessment with conventional spin-echo, chemical-shift, and STIR MR imaging. Radiology. 1990; 174 (2):495–502 [3] Black DM, Cummings SR, Genant HK, Nevitt MC, Palermo L, Browner W. Axial and appendicular bone density predict fractures in older women. J Bone Miner Res. 1992; 7(6):633–638 [4] Blomlie V, Lien HH, Iversen T, Winderen M, Tvera K. Radiation-induced insufficiency fractures of the sacrum: evaluation with MR imaging. Radiology. 1993; 188(1):241–244 [5] Brahme SK, Cervilla V, Vint V, Cooper K, Kortman K, Resnick D. Magnetic resonance appearance of sacral insufficiency fractures. Skeletal Radiol. 1990; 19 (7):489–493 [6] Chen Y, Dougherty ER, Totterman SM, Hornak JP. Classification of trabecular structure in magnetic resonance images based on morphological granulometries. Magn Reson Med. 1993; 29(3):358–370 [7] Chesnut CH, Majumdar S, Newitt DC, et al. Effects of salmon calcitonin on trabecular microarchitecture as determined by MRI: results from the QUEST study. J Bone Miner Res. 2005; 20:1548–1561 [8] Chevalier F, Laval-Jeantet AM, Laval-Jeantet M, Bergot C. CT image analysis of the vertebral trabecular network in vivo. Calcif Tissue Int. 1992; 51(1):8–13 [9] Chung H, Wehrli FW, Williams JL, Kugelmass SD. Relationship between NMR transverse relaxation, trabecular bone architecture, and strength. Proc Natl Acad Sci U S A. 1993; 90(21):10250–10254 [10] Cuenold C, Laredo J, Chicheportiche V. Vertebral collapses: distinction between porotic and malignant causes on MR images before and after GdDTPA enhancement. Radiology. 1990; 177(P):240 [11] Cummings SR, Nevitt MC, Browner WS, et al. Study of Osteoporotic Fractures Research Group. Risk factors for hip fracture in white women. N Engl J Med. 1995; 332(12):767–773 [12] Davis CA, Genant HK, Dunham JS. The effects of bone on proton NMR relaxation times of surrounding liquids. Invest Radiol. 1986; 21(6):472–477 [13] Deutsch AL, Mink JH, Waxman AD. Occult fractures of the proximal femur: MR imaging. Radiology. 1989; 170(1, Pt 1):113–116 [14] Durand EP, Rüegsegger P. Cancellous bone structure: analysis of high-resolution CT images with the run-length method. J Comput Assist Tomogr. 1991; 15(1):133–139 [15] Fransson A, Grampp S, Imhof H. Effects of trabecular bone on marrow relaxation in the tibia. Magn Reson Imaging. 1999; 17(1):69–82 [16] Funke M, Bruhn H, Vosshenrich R, et al. Bestimmung der T2*-Relaxationszeit zur Charakterisierung des trabekulären Knochens. Fortschr Rontgenstr. 1994; 161:58 [17] Genant HK, Engelke K, Fuerst T, et al. Noninvasive assessment of bone mineral and structure: state of the art. J Bone Miner Res. 1996; 11(6):707–730 [18] Godersky JC, Smoker WR, Knutzon R. Use of magnetic resonance imaging in the evaluation of metastatic spinal disease. Neurosurgery. 1987; 21(5):676– 680 [19] Gokalp G, Mutlu FS, Yazici Z, Yildirim N. Evaluation of vertebral bone marrow fat content by chemical-shift MRI in osteoporosis. Skeletal Radiol. 2011; 40 (5):577–585 [20] Grampp S, Jergas M, Glüer CC, Lang P, Brastow P, Genant HK. Radiologic diagnosis of osteoporosis. Current methods and perspectives. Radiol Clin North Am. 1993; 31(5):1133–1145 [21] Grampp S, Majumdar S, Jergas M, Lang P, Gies A, Genant HK. MRI of bone marrow in the distal radius: in vivo precision of effective transverse relaxation times. Eur Radiol. 1995; 5(1):43–48

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(7):248–256 [25] Griffith JF, Genant HK. New advances in imaging osteoporosis and its complications. Endocrine. 2012; 42(1):39–51 [26] Haworth AE, Webb J. Skeletal complications of bisphosphonate use: what the radiologist should know. Br J Radiol. 2012; 85(1018):1333–1342 [27] Hosten N, Neumann K, Zwicker C, et al. Diffuse Demineralisation der Lendenwirbelsäule. Fortschr Röntgenstr. 1993; 159:264–268 [28] Jara H, Wehrli FW, Chung H, Ford JC. High-resolution variable flip angle 3D MR imaging of trabecular microstructure in vivo. Magn Reson Med. 1993; 29 (4):528–539 [29] Jensen KS, Mosekilde L, Mosekilde L. A model of vertebral trabecular bone architecture and its mechanical properties. Bone. 1990; 11(6):417–423 [30] Kamano H, Hiwatashi A, Kobayashi N, et al. New vertebral compression fractures after prophylactic vertebroplasty in osteoporotic patients. AJR Am J Roentgenol. 2011; 197(2):451–456 [31] Kazawa N. T2WI MRI and MRI-MDCT correlations of the osteoporotic vertebral compressive fractures. Eur J Radiol. 2012; 81(7):1630–1636 [32] Lam SC, Wald MJ, Rajapakse CS, Liu Y, Saha PK, Wehrli FW. Performance of the MRI-based virtual bone biopsy in the distal radius: serial reproducibility and reliability of structural and mechanical parameters in women representative of osteoporosis study populations. Bone. 2011; 49(4):895–903 [33] Lee KA, Hong SJ, Lee S, Cha IH, Kim BH, Kang EY. Analysis of adjacent fracture after percutaneous vertebroplasty: does intradiscal cement leakage really increase the risk of adjacent vertebral fracture? Skeletal Radiol. 2011; 40 (12):1537–1542 [34] Link TM. Osteoporosis imaging: state of the art and advanced imaging. Radiology. 2012; 263(1):3–17 [35] Link TM, Majumdar S, Augat P, et al. Proximal femur: assessment for osteoporosis with T2* decay characteristics at MR imaging. Radiology. 1998; 209 (2):531–536 [36] Link TM, Majumdar S, Grampp S, et al. Imaging of trabecular bone structure in osteoporosis. Eur Radiol. 1999; 9(9):1781–1788 [37] Majumdar S. Quantitative study of the susceptibility difference between trabecular bone and bone marrow: computer simulations. Magn Reson Med. 1991; 22(1):101–110 [38] Majumdar S. Magnetic resonance imaging for osteoporosis. Skeletal Radiol. 2008; 37(2):95–97 [39] Majumdar S, Genant HK. In vivo relationship between marrow T2* and trabecular bone density determined with a chemical shift-selective asymmetric spin-echo sequence. J Magn Reson Imaging. 1992; 2(2):209–219 [40] Majumdar S, Thomasson D, Shimakawa A, Genant HK. Quantitation of the susceptibility difference between trabecular bone and bone marrow: experimental studies. Magn Reson Med. 1991; 22(1):111–127 [41] Majumdar S, Genant HK, Grampp S, et al. Analysis of trabecular bone structure in the distal radius using high resolution magnetic resonance imaging. Eur Radiol. 1994; 4(6):517–524 [42] Majumdar S, Genant HK, Grampp S, et al. Correlation of trabecular bone structure with age, bone mineral density, and osteoporotic status: in vivo studies in the distal radius using high resolution magnetic resonance imaging. J Bone Miner Res. 1997; 12(1):111–118 [43] Matin P. The appearance of bone scans following fractures, including immediate and long-term studies. J Nucl Med. 1979; 20(12):1227–1231 [44] Meyers SP, Wiener SN. Magnetic resonance imaging features of fractures using the short tau inversion recovery (STIR) sequence: correlation with radiographic findings. Skeletal Radiol. 1991; 20(7):499–507 [45] Modic MT, Masaryk T, Paushter D. Magnetic resonance imaging of the spine. Radiol Clin North Am. 1986; 24(2):229–245 [46] Mosekilde L. Age-related changes in vertebral trabecular bone architecture– assessed by a new method. Bone. 1988; 9(4):247–250 [47] Nieuwenhuijse MJ, Van Erkel AR, Dijkstra PD. Cement leakage in percutaneous vertebroplasty for osteoporotic vertebral compression fractures: identification of risk factors. Spine J. 2011; 11(9):839–848

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References

13.3 Clinical Relevance of Magnetic Resonance Imaging [48] Parizel PM, Van Riet B, van Hasselt BA, et al. Influence of magnetic field

[58] Techawiboonwong A, Song HK, Leonard MB, Wehrli FW. Cortical bone water:

strength on T2* decay and phase effects in gradient echo MRI of vertebral

in vivo quantification with ultrashort echo-time MR imaging. Radiology.

[49] Porter BA, Shields AF, Olson DO. Magnetic resonance imaging of bone marrow disorders. Radiol Clin North Am. 1986; 24(2):269–289 [50] Quinn SF, McCarthy JL. Prospective evaluation of patients with suspected hip fracture and indeterminate radiographs: use of T1-weighted MR images. Radiology. 1993; 187(2):469–471 [51] Rizzo PF, Gould ES, Lyden JP, Asnis SE. Diagnosis of occult fractures about the hip. Magnetic resonance imaging compared with bone-scanning. J Bone Joint Surg Am. 1993; 75(3):395–401 [52] Rosenthal H, Thulborn KR, Rosenthal DI, Kim SH, Rosen BR. Magnetic susceptibility effects of trabecular bone on magnetic resonance imaging of bone marrow. Invest Radiol. 1990; 25(2):173–178 [53] Sartoris DJ, Clopton P, Nemcek A, Dowd C, Resnick D. Vertebral-body collapse in focal and diffuse disease: patterns of pathologic processes. Radiology. 1986; 160(2):479–483 [54] Schick F, Seitz D, Machann J, Lutz O, Claussen CD. Magnetic resonance bone densitometry. Comparison of different methods based on susceptibility. Invest Radiol. 1995; 30(4):254–265 [55] Sebag GH, Moore SG. Effect of trabecular bone on the appearance of marrow in gradient-echo imaging of the appendicular skeleton. Radiology. 1990; 174 (3, Pt 1):855–859 [56] Sugimoto H, Kimura T, Ohsawa T. Susceptibility effects of bone trabeculae.

2008; 248(3):824–833 [59] Tosun O, Fidan F, Erdil F, Tosun A, Karaoğlanoğlu M, Ardıçoğlu O. Assessment of lumbar vertebrae morphology by magnetic resonance imaging in osteoporosis. Skeletal Radiol. 2012; 41(12):1583–1590 [60] Chen YJ, Chen HY, Hsu HC. Sequential magnetic resonance imaging changes in osteoporotic compression fractures: can it be used as a risk predictor for nonunion? Spine. 2011; 36(26):2363 [61] Vilela P, Nunes T. Osteoporosis. Neuroradiologie. 2011; 53 Suppl. 1: S185–S189 [62] Wehrli FW. Osteoporosis. Proc Soc Magn Reson Med. 1992; 12:115 [63] Wehrli FW, Ford JC, Haddard JG, et al. Can quantitative MR imaging help diagnose osteoporosis? J Magn Reson Imaging. 1993; 175:175 [64] Wehrli FW, Ford JC, Haddad JG. Osteoporosis: clinical assessment with quantitative MR imaging in diagnosis. Radiology. 1995; 196(3):631–641 [65] Wiener SN, Neumann DR, Rzeszotarski MS. Comparison of magnetic resonance imaging and radionuclide bone imaging of vertebral fractures. Clin Nucl Med. 1989; 14(9):666–670 [66] Wu Z, Chung H, Wehrli FW. Sub-voxel tissue classification in NMR microscopic images of trabecular bone. Proc Soc Magn Reson Med. 1993:451 [67] Yao L, Lee JK. Occult intraosseous fracture: detection with MR imaging. Radiology. 1988; 167(3):749–751 [68] Yuh WT, Zachar CK, Barloon TJ, Sato Y, Sickels WJ, Hawes DR. Vertebral com-

Quantification in vivo using an asymmetric spin-echo technique. Invest

pression fractures: distinction between benign and malignant causes with

Radiol. 1993; 28(3):208–213

MR imaging. Radiology. 1989; 172(1):215–218

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bone marrow. J Comput Assist Tomogr. 1995; 19(3):465–471

[57] Tasciyan T, Schweitzer M. Bone density MR images via wavelet processing. Proc Soc Magn Reson Med. 1993:417

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14.1

Introduction

586

14.2

Examination Technique

586

The Sacroiliac Joints

14.3

Anatomy

587

14.4

Causes of Sacroiliitis

595

14.5

Inflammatory Rheumatoid Disorders of the Sacroiliac Joints

595

14.6

Osteoarthrosis Deformans and Juxta-Articular Pneumatocysts

611

14.7

Disseminated Idiopathic Skeletal Hyperostosis

611

14.8

Osteitis Condensans Ilii and Sacri as well as Triangular Hyperostosis Ilii and Sacri

613

14.9

Osteomalacia

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14.10 Pyogenic, Septic Sacroiliitis

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14.11 Tuberculous Sacroiliitis

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14.12 Traumatic Changes

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14.13 Tumor and Tumorlike Conditions of the Joint

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References

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Chapter 14

The Sacroiliac Joints

14 The Sacroiliac Joints M. Bollow, J. Braun, and K.-G. Hermann

14.1 Introduction Magnetic resonance imaging (MRI) of the sacroiliac joints now plays a pivotal role in rheumatology for diagnosis of sacroiliitis following the development of new classification criteria for spondyloarthritis.96 The task of the radiologist is to properly identify early-onset inflammatory changes and distinguish them from abnormalities induced by degenerative, infectious, or tumor processes and trauma.

14.2 Examination Technique

MRI of the sacroiliac joints is carried out with a phased-array coil and the patient in the supine position. The legs are placed on a foam rubber cushion such that the hip and knee joints are flexed at an angle of around 15 degrees. Ideally, a magnetic field strength of 1.5 T is used.

Fig. 14.1 Planning examination to obtain paraxial sections on sagittal overview image, parallel to the long axis of the sacrum. The sections planned on a sagittal scout view run almost parallel to the sacroiliac joint surfaces. Anterior presaturation is used to reduce movement artefacts caused by abdominal wall movement and intestinal peristalsis.

14.2.2 Imaging Planes First, orientational images are acquisitioned in three planes to plan the next examination steps. A sagittal overview image is used to plan sectional orientation, whereas transverse (axial) overview images are used as a second localizer. Taking account of the oblique orientation of the sacroiliac joints, a paraxial (= paracoronal) sectional plane, which is individually tailored to the long axis of the sacrum or the anterior edge of sacral vertebrae S1 and S2, is selected for all sequences. Presaturation pulses are applied anterior and superior to the region of interest (ROI) (▶ Fig. 14.1). To avoid artefacts, a left-to-right phase-encoding direction is used for signal processing. Once optimum section and saturation positions have been identified for the initial measurement, these are used accordingly for all subsequent paraxial sequences. A coronal orientational section can be used additionally for, apart from excellent visualization of sacroiliac joint morphology, any further diagnostic findings in relation to the hip joints and lumbar spine.

14.2.3 Sequences Proposed sequence order (▶ Fig. 14.2): ● Paraxial T1-weighted (T1w) 2D turbo spin-echo (TSE) sequence: ○ TR = 400 ms. ○ TE = 14 ms. ○ Slice thickness = 3 mm. ○ Matrix = 512 × 512. ○ Duration = 3:12 minutes. ● Paraxial cartilage sequence, for example, WATSc sequence (water-selective spoiled 3D GRE [gradient-echo] sequence for cartilage [c = cartilage]) with parallel imaging: ○ TR = 20 ms.

586

TE = 7.1 ms. Slice thickness = 2.4 mm. ○ Matrix = 256 × 512. ○ Flip angle = 20 degrees. ○ Duration = 4:53 minutes. Coronal T1w 3D GRE sequence with fat saturation, for example, THRIVE (T1w high-resolution isotropic volume excitation), following intravenous injection of paramagnetic contrast medium (CM): ○ TR = 6.5 ms. ○ TE = 3.2 ms. ○ Slice thickness = 2 mm. ○ Matrix = 368 × 512. ○ Flip angle = 10 degrees. ○ Duration = 2:38 minutes. Paraxial T1w 3D GRE sequence with fat saturation, for example, THRIVE, following intravenous injection of paramagnetic CM (as late CM phase): ○ TR = 7.8 ms. ○ TE = 3.7 ms. ○ Slice thickness = 2 mm. ○ Matrix = 368 × 512. ○ Flip angle = 10 degrees. ○ Duration = 4:57 minutes. ○ ○

●

●

These parameters are intended for orientational purposes and should be tailored to the equipment used at the respective site. If CM is contraindicated or the patient does not want any intravenous injection, the following native sequences can be used alternatively: ● Paraxial short-tau inversion recovery (STIR) sequence: ○ TR = 4,000 ms.

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14.2.1 Patient Positioning and Coil Selection

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14.3 Anatomy

Fig. 14.2 Standard sequence protocol for MRI examination of the sacrum. Normal findings. (a) Paraxial T1w TSE sequence. (b) Paraxial T2*w 3D GRE sequence (cartilage sequence). (c) Coronal T1w 3D GRE sequence with fat saturation following CM administration. (d) Paraxial T1w 3D GRE sequence with fat saturation following CM administration.

TI = 150 ms. TE = 43 ms. ○ Slice thickness = 3 mm. ○ Matrix = 384 × 384. ○ Duration = 3:30 minutes. Paraxial PDw fat-saturated 2D sequence: ○ TR = 2,160 ms. ○ TE = 14 ms. ○ Slice thickness = 3 mm. ○ Matrix = 512 × 512. ○ Duration = 3:50 minutes. ○ ○

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14.3 Anatomy 14.3.1 General Anatomy Since it is a rigid articulation with restricted movement, the sacroiliac joint is classified as an amphiarthrodial articulation composed of a diarthrosis and synarthrosis. The joints that extend along the ear-shaped, curved articular surface of the ilium and sacrum comprise the following components: ● Iliac and sacral joint cartilage. ● Joint cavity. ● Two to three layers of hypovillus synovial membrane composed of overlying synovial cells and found primarily in the vicinity of the anterior and, to a lesser extent, also of the posterior joint capsule.36,48

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The Sacroiliac Joints Joint capsule composed of taut fibrous fibers that originate directly from the pelvic periosteum.8,22,36,99,102,111,120

The exclusively hyaline cartilage layer of the sacral surface measures 2 to 3 mm in thickness, whereas the predominantly fibrocartilage layer covering the iliac surface is only around 1 mm thick (▶ Fig. 14.3 and ▶ Fig. 14.4).22,36,79,99,102 The joint capsule is reinforced anteriorly by the anterior sacroiliac ligaments (see ▶ Fig. 14.4) and posteriorly by the interosseous sacroiliac ligaments (▶ Fig. 14.5), which fan out in the retroarticular space that is rich in fatty and connective tissue, as well as by the posterior sacroiliac ligaments (see ▶ Fig. 14.5), sacrospinous ligament, and the sacrotuberous ligament.111,120,121 The joint is divided into a superoposterior fibrous, a synarthrotic portion (see ▶ Fig. 14.4 and ▶ Fig. 14.5), and an inferoanterior diarthrotic portion that increases in size as it runs in a superoinferior direction (see ▶ Fig. 14.4). The sacroiliac joints36,57,111 are innervated by dorsal branches of spinal nerves S1 to S2. The posterior ligamentous complex also receives dorsal branches of spinal nerves S3 to S4. After exiting from the posterior sacral foramina, the dorsal branches of spinal nerves S1 to S4 pierce the posterior ligamentous complex while

giving off tiny branches to the sacral origin of the gluteus maximus and continue as the medial cluneal nerves to the skin. The sacroiliac joints22 receive their blood supply from the branches of the iliolumbar artery, lateral sacral arteries, and the superior and inferior gluteal arteries.

14.3.2 Special Magnetic Resonance Imaging Anatomy On MRI, hyperintense tissue interspersed with punctate to linear areas of low signal intensity is identified in the posterosuperior retroarticular space on T1w sequences (▶ Fig. 14.6); this signal pattern corresponds to the fatty, highly vascularized connective tissue, which is traversed by the interosseous sacroiliac ligaments.1,14,15,16,50,83 The anteroinferior cartilaginous compartment of the sacroiliac joints shows characteristic MRI morphology (see ▶ Fig. 14.6): the iliac and sacral cartilage, which is surrounded by a signal-void cortical rim and is smoothly outlined, exhibits homogeneous intermediate signal intensity on T1w sequences. The periarticular

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5 6

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Fig. 14.3 Anatomic specimens of the sacroiliac joint. (a) Macromorphologic transverse section of an anatomic specimen of the pelvis at the level of the sacral vertebrae S2 to S3. At this caudal level, the cartilaginous portion of the sacroiliac joints extends anteriorly to posteriorly between the sacrum and ilium. In the anatomic specimen, the joint cavity is visualized between the around 3-mm-wide sacral (black arrow) and the around 1-mm-wide iliac joint cartilage (black arrowhead). The joint capsule is reinforced anteriorly by the anterior sacroiliac ligaments (white arrow) and posteriorly by the posterior sacroiliac ligaments (white arrowhead). (b) Histology section of a middle portion of the sacroiliac joint, azan stain (magnification: 150-folds). The joint cavity (arrow) is limited by the around 2- to 3-mm-wide hyaline, sacral-sided joint cartilage and the around 1-mm-wide cartilaginous, iliac joint cartilage. In terms of morphology, the iliac fibrocartilage, which is interspersed with collagen fibers, functions as an enthesis; hence, the sacroiliac joints are classified as entheseal joints. 1, ilium; 2, sacrum; 3, sections of the iliac vessels; 4, iliac joint cartilage; 5, compact bone; 6, sacral joint cartilage.

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Fig. 14.4 Anatomy of the sacroiliac joints. Direct comparison of anatomic specimen and MR images in the paraxial plane. (a) Anatomic section through the cartilaginous compartment of the sacroiliac joints. (b) Cartilage sequence corresponding to (a). (c) Section through the fibrous compartment of the sacroiliac joints, and retroarticular space. (d) T1w sequence corresponding to (c). The interosseous ligaments, which are contiguous with the posterior joint capsule and fan out between the ilium and sacrum, can be identified as a hypointense to signalvoid, punctate to linear substrate in the fatty connective tissue of the retrospatial space. (e) Histology section through retroarticular space of anatomic specimen, hematoxylin and eosin stain. Anterior and posterior views of the joint cartilage. The interosseous ligaments penetrate the cortical margins of the sacrum and ilium and are therefore classified as “entheses.” (f) Partial section from (e). The anterior joint capsule fuses with the periosteum of the sacrum and ilium and is therefore classified as an enthesis. Detailed histology image of the anterior joint capsule, hematoxylin and eosin stain, demonstrates the transition of the fibrous joint capsule to the pelvic periosteum (arrows). The delicate synovial membrane (asterisk) is situated beneath the fibrous joint capsule. (g) Partial section from (e). The posterior joint capsule merges with the interosseous ligaments.

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bone marrow regions have an intermediate to hyperintense signal pattern, reflecting their fat content.40 On cartilage-specific GRE sequences, the joint can be identified as a smoothly outlined area of homogeneous hyperintensity that contrasts sharply with the subchondral and juxta-articular bone marrow regions. Areas of linear hypointense signal between the iliac fibrocartilage and the sacral hyaline cartilage are caused by the different magnetic susceptibility profiles of the two cartilage types (▶ Fig. 14.7).125 Small, triangular areas of signal void on the iliac side of the anterior joint capsule (see ▶ Fig. 14.7) reflect physiologic iliac hyperostosis, caused by adaptation to the pressure exerted here on the sacroiliac joints in the upright position.36,37 Unlike the adult MRI morphology of the sacroiliac joints, children and adolescents have cartilaginous connections between the sacroiliac joints and the neuroforamina of the sacral alae at the level of the sacral intervertebral disks (▶ Fig. 14.8).19 These junctions correspond to the segmental apophyses, which arise from the costal ossification centers of the sacral segments S1 to S3 and are incorporated into the sacral alae.36,68 After fusion with the corresponding transverse processes, the ossification centers of S1 to S3 form the lateral sacral elements. The S1 to S3 costal ossification centers are incorporated into the articular surface of each sacral ala. These segmental apophyses of the sacral alae undergo a progressive ossification process between the ages of 9 and 16 years. However, there are significant differences in the aging process between children with “open,” purely cartilaginous segmental apophyses (11.3 ± 2.3 years) on the one hand (see ▶ Fig. 14.8 and ▶ Fig. 14.15) and children with both partial (▶ Fig. 14.9) and completely “closed” segmental apophyses (14.8 ± 1.7 years) on the other hand.19 In women, ossification of the segmental apophyses of the sacral alae, presenting on average at 14.5 ± 1.5 years, is significantly earlier than in men, presenting at 16.0 ± 1.2 years.19 The lateral apophyses of the sacral alae in children can be identified as a halo located medially between the sacroiliac joint and the sacral marrow (see ▶ Fig. 14.9 and ▶ Fig. 14.15), which exhibits intermediate and, in cartilage-specific sequences, hyperintense signal pattern on T1w sequences.19 These lateral apophyses, which are enchondral ossification centers or growth plates, undergo progressive ossification between the ages of 9 and 17

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years. Trapezoidal ossification centers are observed in these lateral apophyses at an average age of 14.7 ± 1.6 years at the interfaces between the sacroiliac joints and the segmental apophyses of the sacral alae (see ▶ Fig. 14.9). Ossification occurs significantly earlier in girls than in boys.19 The lateral sacral apophyses may also persist beyond adolescence (▶ Fig. 14.10). The joint cartilage of normal sacroiliac joints, which is avascular and nourished by diffusion, does not take up CM.14,15,16 Slight linear enhancement of the anterior joint capsule (see ▶ Fig. 14.15) can be viewed as a physiologic manifestation.16,18

14.3.3 Variants Familiarity with the normal MRI anatomy of the sacroiliac joints is particularly important in settings of pelvic asymmetry or anatomic variants to avoid misdiagnosis. The paraglenoid sulcus is formed by the anterior attachment of the joint capsule36,100 and may present as a small contour variant (see ▶ Fig. 14.6d, ▶ Fig. 14.6e, and ▶ Fig. 14.6f) or large bony recess (▶ Fig. 14.11). In rare cases, an “upper” ilium-sided paraglenoid sulcus is also seen.36 Besides, around 10% of the normal variants observed18,101 are lumbosacral transition vertebrae, corresponding to lumbarization or hemilumbarization of the first sacral vertebral body (▶ Fig. 14.12) or to sacralization or hemisacralization of the fifth lumbar vertebral body (▶ Fig. 14.13). The assimilation joints associated with sacralization of the fifth lumbar vertebral body may be a cartilaginous-synchondral or fibrous connection (see ▶ Fig. 14.13) and develop peripheral sclerosis in response to increased mechanical stress. Likewise, inflammatory processes may be identified in patients with spondyloarthritis, since the synchondral connections contain fibrocartilage. Uni- or bilateral accessory joints (▶ Fig. 14.14) may present as fibrous or entheseal fibrocartilaginous connections between the posterior superior iliac spine and the sacral crest or between the iliac tuberosity and the sacral tuberosity.18

14.3.4 Enthesis Organ The term “enthesis” denotes the insertion sites of tendons, ligaments, joint capsules, or fasciae on bone.47 The enthesis reduces

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Fig. 14.5 Anatomy of the lumbosacral junction. (a) Anatomic specimen. (b) T1w TSE sequence of the lumbosacral junction just above the sacroiliac joints. In addition to the interosseous ligaments (arrow), the taut sacrospinous ligaments are demonstrated (arrowheads). Since only limited motion of the sacroiliac joints is permitted because of this taut ligamentous fixation, these joints are classified as an amphiarthrosis.

14.3 Anatomy

the stress exerted at these transitional sites on the bone11 by distributing the biomechanical energy generated. In doing so, they are at risk for repetitive microtraumatic effects. Disorders of the enthesis may arise in association with traumatic, endocrinologic, metabolic, degenerative, as well as inflammatory processes. Acute inflammation of the enthesis is termed “enthesitis.” Two types of enthesis can be distinguished based on its structure and location:

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Fig. 14.6 Normal MRI anatomy (adult). MRI anatomy of a 34-year-old male volunteer on a T1w 2D TSE sequence (on the left, in each case) and a T1w 3D WATSc sequence (cartilage sequence; on the right, in each case), showing in each case cranial (a) to caudal (f) sections. (a) Section 1 (cranial). (b) Section 2. (c) Section 3. (d) Section 4. 1, gluteus maximus; 2, gluteus medius; 3, gluteus minimus; 4, iliacus; 5, psoas; 6, piriformis; 7, common iliac artery; 8, common iliac vein; 9, inferior gluteal artery and vein; C, coccyx; I, ilium; L, fifth vertebral body L5; M, lateral sacral mass; S, sacrum with four sacral vertebral bodies and, in each case, four neuroforamina, showing nerve roots S1 to S4. Asterisk, sacral plexus; the sacral branches S1 to S3 exit from the pelvic sacral foramina of the sacrum and together with the lumbosacral trunk (portions of the fourth and fifth lumbar branches) form the sacral plexus, from which the sciatic nerve arises as the major nerve. Arrows, internal iliac artery and vein. Curved arrows, median sacral artery. Angulated arrows, inferior paraglenoid sulcus (synonym: juxta-articular sulcus): Insertion of the fibrous anterior joint capsule at the ilium and sacrum; less commonly, a superior sulcus is also identified. Open arrows, fibrous compartment of the sacroiliac joints; fatty retroarticular space traversed by the low-signal interosseous ligaments. Arrowheads, cartilaginous compartment of the sacroiliac joints, which exhibits intermediate signal intensity on T1w images and a hyperintense signal pattern on T2w images.

Fibrous type: Fibrous entheses are characterized by dense fibrous connective tissue at the tendon– or ligament–bone interfaces.97 They are typically encountered at the metaphyses and diaphyses of long tubular bones. Fibrocartilaginous type: The majority of entheses, such as the tendon insertions at the epiphyses of long tubular bones,10 have a fibrocartilaginous structure, with a transition zone of

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Fig. 14.6 (continued) Normal MRI anatomy (adult). (e) Section 5. (f) Section 6 (caudal).

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Fig. 14.7 Normal MRI anatomy (adolescent). Paraxial fat-saturated T1w GRE sequence following CM administration. Normal MRI anatomy of the sacroiliac joints of a 14-year-old boy. The iliac fibrocartilage (white arrows) is separated by a hypointense halo from the sacral hyaline cartilage (black arrows) due to the differences in magnetic susceptibility. Physiologic hyperostosis on the ilium, bilateral (arrowheads) point to the maximum-pressure zones in the joint region.

Fig. 14.8 Normal MRI anatomy (adolescent). Water-selective fatsaturated cartilage sequence. Normal MRI anatomy of the sacroiliac joints of an 11-year-old boy. Broad cartilaginous junctions (arrows) of the joints to the disk remnants of the sacrum (arrowheads). These junctions correspond to the segmental apophyses, which arise from the costal ossification centers of the sacral segments S1 to S3 and are incorporated into the sacral ala.

fibrocartilage at the bone attachment.97 Fibrocartilaginous entheses consist of four zones91: ○ Type I tendon composed of fibrocytes and collagen fibers. ○ Type II zone composed of chondrocytes and collagen fibers of uncalcified or sesamoid fibrocartilage. ○ Cartilage–bone transition zone known as a tidemark.

○

Type II zone composed of chondrocytes and collagen fibers of uncalcified or periosteal fibrocartilage.

A distinction is made between the classic entheses, such as the Achilles tendon insertion, and the functional entheses, where the tendons do not insert directly into the bone but rather, given

14.3 Anatomy

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Fig. 14.9 Normal MRI anatomy (adolescent). Asymptomatic 15-year-old boy. (a) Water-selective, fat-saturated cartilage sequence of the middle portion of joint. Ossification of the lateral apophyses of the sacral alae seen as hypointense area (arrows). The segmental apophyses of the sacral alae appear narrower than that in ▶ Fig. 14.8. (b) In the inferior joint regions, the interfaces between the sacroiliac joints and the segmental apophyses manifest as hypointense, trapezoidal areas (arrows); the cartilage signal pattern of the later sacral apophysis can still be identified as a hyperintense line (arrowheads).

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Fig. 14.10 Persistent apophysis. A 61-year-old man. (a) Paraxial T1w TSE sequence. Persistent bone marrow–equivalent apophysis of the lateral sacral apophysis (arrowheads), juxta-articular–sacral on the right, surrounded by a cartilage-isointense apophyseal plate rim. (b) Paraxial T1w WATSc sequence parallel to section in a (cartilage sequence). Signal pattern of persistent apophyseal plate (arrowhead) and bone marrow–equivalent demonstration of the apophyseal center. (c) Coronal T1w 3D GRE sequence with fat saturation following CM administration. No apophyseal CM enhancement (arrowhead).

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Fig. 14.12 Hemilumbarization of the first sacral vertebral body S1, right, as normal variant. A 31-year-old man with hemilumbarization of the first sacral vertebral body, left, causing pelvic asymmetry. (a) Paraxial T1w TSE sequence. (b) Paraxial T1w WATSc sequence (cartilage sequence). (c) Coronal T1w 3D GRE sequence with fat saturation following CM administration.

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Fig. 14.11 Paraglenoid sulcus. A 32-year-old woman with prominent paraglenoid sulcus (arrows). (a) The paraglenoid sulcus can be clearly identified on the coronal fat-saturated T1w GRE sequence. (b) The paraglenoid sulcus can masquerade as erosive lesions in the paraxial plane.

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14.5 Inflammatory Rheumatoid Disorders of the Sacroiliac Joints

Fig. 14.13 Hemisacralization of lumbar vertebral body L5, bilateral, normal variant. A 30-year-old woman. (a) Overview radiograph of the sacroiliac joints showing assimilation joints (arrowheads). (b) Paraxial T1w TSE sequence. Hemisacralization of lumbar vertebra L5, bilateral, with cartilage- or disk-isointense assimilation joint, left (arrowhead), and a cortex-isointense assimilation joint, right (arrow). (c) Paraxial T1w WATSc sequence parallel to section in (b) (cartilage sequence). Disk-isointense signal pattern of assimilation joint, left (arrowhead), and peripheral sclerosis of the assimilation joint, right (arrow). (d) Coronal T1w 3D GRE sequence with fat saturation following CM administration. The assimilation joints manifest as delicate cartilaginous synchondroses (arrowhead) or as an irregular plate with peripheral sclerosis (arrow).

the close anatomic relationship, progress from tendons to bony protuberances (hypomochlia). The functional enthesis organ is formed in proximity to synovial bursae between a sesamoid fibrocartilage layer on the tendon itself and a periosteal fibrocartilage layer on the bone. The third group of entheses is known as entheseal joints11; the sacroiliac joint is a typical example of the entheseal joints. The entheseal insertion of the iliac-sided articular fibrocartilage (see ▶ Fig. 14.3) spreads across the entire iliac articular surface into the subchondral bone, which is highly vascularized and owing to the relatively thin cortex is susceptible to inflammatory joint processes.11 In addition, the entheseal transitions of the sacroiliac joint capsules to the periosteum are predilection sites for inflammatory processes or mechanical, stress-related damage. Familiarity with the enthesitis concept has contributed to an understanding of the pathogenesis and pathomorphology of spondyloarthritis,64 with its classic simultaneous juxtaposition of osteodestructive and osteoproliferative changes.

14.4 Causes of Sacroiliitis The causes of sacroiliitis cover a broad differential diagnostic spectrum of inflammatory and rheumatic entities, in addition to spondyloarthritis already described. Sacroiliitis may also be associated with infectious, granulomatous, and metabolic disorders. Neurogenic, degenerative, and tumor disorders as well as trauma and postactinic lesions can mimic sacroiliitis (▶ Table 14.1).

14.5 Inflammatory Rheumatoid Disorders of the Sacroiliac Joints 14.5.1 Spondyloarthritis Inflammation of one or both sacroiliac joints, that is, sacroiliitis, is the principal symptom of spondyloarthritis. The term “spondyloarthritis” comprises a group of rheumatic disorders,

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Fig. 14.14 Accessory joints. A 53-year-old man. (a) Overview radiograph of the sacroiliac joints showing delicate accessory joints with peripheral sclerosis (arrowheads). (b) Coronal T1w 3D GRE sequence with fat saturation following CM administration. Cartilaginous aspect of the accessory joints, seen within the retroarticular space as a delicate synchondrosis (arrowheads), with peripheral sclerosis between the posterior superior iliac spine and sacral dorsum. (c) Paraxial T1w TSE sequence showing the cartilaginous accessory joints as low signal intensity (arrowheads). (d) Paraxial T1w WATSc sequence parallel to section in (c) (cartilage sequence), with disk-isointense signal pattern exhibited by the left assimilation joint (arrowhead) and peripheral sclerosis of the right assimilation joint (arrow).

manifesting clinically as inflammatory changes in the region of the axial skeleton, tendon insertions, and joints as well as in other regions of the body outside the musculoskeletal system, such as the eye, skin, intestines, and the blood vessels.70 A relationship has been documented between spondyloarthritis and the major histocompatibility complex class 1 molecule human leukocyte antigen (HLA)-B27.26 For example, in one study, 83% of HLA-B27-positive patients with rheumatic disorders were affected by sacroiliitis.67 Whereas 5 to 10% of the normal Caucasian population is HLA-B27-positive, 70 to 95% of patients with spondyloarthritis, or, in particular, patients with ankylosing spondylitis, are found to be HLA-B27-positive.94 HLA-B27 constitutes a risk factor for the onset of sacroiliitis and chronicity of spondyloarthritis. In principle, a distinction is made between predominantly axial and predominantly peripheral types of spondyloarthritis: ● The axial types include, in addition to the classic ankylosing spondylitis23,55,118—sometimes called “Bechterew’s disease”— the nonradiographic type (nr-axSpA). Subsumed under this term are, besides the early types, also many abortive processes, which, while associated with clinical signs, do not result in any structural abnormalities, even after many years.

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As regards the peripheral types, a distinction is made between psoriatic arthritis or spondyloarthritis in association with psoriasis,115,119 spondyloarthritis with chronic inflammatory bowel disease,56,78 and spondyloarthritis secondary to infection of the urogenital or intestinal tract (reactive arthritis, e.g., Reiter’s disease)72,74 and undifferentiated spondyloarthritis,39,127 which is not associated with such specific clinical symptoms.

Whereas the prevalence of ankylosing spondylitis in Europe is thought to be in the region of 0.3 to 0.5%,25 the prevalence of all spondyloarthritis types at around 1 to 2%25 is the same as that for rheumatoid arthritis. The main symptom exhibited by patients with spondyloarthritis is chronic back pain, often presenting as classic inflammatory back pain. The principal symptoms of inflammatory back pain are slow onset, together with morning stiffness, lasting over 3 months in young patients. Inflammatory back pain improves on movement and generally deteriorates at rest.109 Since over 80% of patients with ankylosing spondylitis respond well to treatment with nonsteroidal anti-inflammatories, this response is also interpreted as a diagnostic pointer.

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14.5 Inflammatory Rheumatoid Disorders of the Sacroiliac Joints Often, ankylosing spondylitis is diagnosed only after 5 to 10 years after onset of the initial symptoms.45 This delay is due to the fact that the New York Criteria for Diagnosis of Ankylosing Spondylitis (▶ Table 14.2), which were modified in 1984, call for evidence of sacroiliitis on conventional radiographs and, as such, cannot be applied for early diagnosis.118 In 2009, the Assessment of SpondyloArthritis International Society (ASAS) published new classification criteria,96 whereby patients below the age of 45 years with chronic back pain of more than 3-month duration can be classified as patients with spondyloarthritis if, in line with the clinical symptoms, they meet one of the following two conditions: ● Sacroiliitis identified on imaging studies plus at least one spondyloarthritis parameter. ● HLA-B27-positive plus at least two spondyloarthritis parameters.

Disease group

Examples

Inflammatory rheumatoid disorders

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Spondyloarthritis

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Juvenile idiopathic arthritis (types IV and V)

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SAPHO syndrome (= PAO syndrome, CRMO)49

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Behçet’s disease

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Familial Mediterranean fever

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Pyogenic/septic sacroiliitis

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Tuberculosis

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Sarcoidosis

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Brucellosis

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Syphilis

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Whipple’s disease

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Primary/secondary hyperparathyroidism77

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Hypoparathyroidism

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Intestinal bypass operations

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Gout

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Chondrocalcinosis = Pseudogout

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Polychondritis

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Ochronosis

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Gaucher’s disease

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Multicentric reticulohistiocytosis

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Cushing’s disease

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Fluorosis

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Vinyl chloride disease

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Hemiplegia

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Paraplegia

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Tetraplegia

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Osteoarthrosis deformans

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Disseminated idiopathic skeletal hyperostosis

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Osteitis condensans ilii and sacri/triangular hyperostosis ilii and sacri

Table 14.2 Modified New York criteria for ankylosing spondylitis118

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Paget’s disease

Clinical criteria

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Bone metastases

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Primary malignant bone tumors

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Lymphoma

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Tuberculous sclerosis

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Arteriovenous malformations

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Occult sacral fractures

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Sacral joint disruption

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Radiogenic sacroiliitis or osteoradionecrosis (following radiotherapy of gynecologic or urologic malignant tumors)

Infectious disorders

Metabolic and storage diseases

Neurogenic paraosteoarthropathy mimicking sacroiliitis

Degenerative disorders mimicking sacroiliitis

Tumor and tumorlike lesions mimicking sacroiliitis

Trauma and radiotherapy mimicking sacroiliitis

The spondyloarthritis parameters comprise the following: Inflammatory back pain. ● Arthritis. ● Enthesitis (heel). ● Uveitis. ● Dactylitis. ● Psoriasis. ● Crohn’s disease or ulcerative colitis. ● Good response to nonsteroidal anti-inflammatories. ● Positive family history of spondyloarthritis. ● HLA-B27. ● Elevated cross-reactive protein (CRP) levels. ●

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Table 14.1 Disorders associated with or mimicking sacroiliitis

Evidence of sacroiliitis is deemed to have been produced on imaging if the MRI results are well correlated with active (acute) inflammation, consistent with spondyloarthritis-associated sacroiliitis, or there is definitive radiographic evidence of sacroiliitis based on the modified New York criteria (see ▶ Table 14.2). If well-defined structural lesions in the sacroiliac joints can already be identified on radiographs, that is, radiographic grade II bilateral or grade III uni- or bilateral sacroiliitis,32 the term “ankylosing spondylitis” is also used. If there is (still) no radiographic evidence of changes, this early stage is classified as “nonradiographic axial spondyloarthritis” (nr-axSpA). These ASAS criteria have been

Criteria

Radiographic criteriaa

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Inflammatory back pain

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Restricted motion of the lumbar spine (≤ 5 cm in Schober’s test)

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Restricted respiratory excursion (≤ 2.5 cm in fourth intercostal space)

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Sacroiliitis score ≥ 2 bilateral

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Sacroiliitis score 3–4 uni- or bilateral

Note: Score 0, no changes; Score 1, suspected changes; Score 2, minor abnormalities; Score 3, pronounced changes; Score 4, ankylosis. aDiagnosis

is conclusive if one radiographic criterion associated with at least one clinical criterion has been met. A probable diagnosis is possible if all three clinical criteria or only radiographic criteria are met.

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14.5.2 Juvenile Spondyloarthritis The term juvenile idiopathic arthritis denotes rheumatoid arthritis, with onset during childhood. Several subtypes have been characterized: ● Type I: Systemic juvenile idiopathic arthritis. ● Type II: Juvenile rheumatoid factor–positive polyarthritis. ● Type III: Juvenile rheumatoid factor–negative polyarthritis. ● Type IV: Juvenile idiopathic oligoarthritis. ● Type V: Juvenile idiopathic arthritis with enthesitis.27 ● Type VI: Juvenile psoriatic arthritis.108,117 These subtypes are categorized after 6-month disease duration. Juvenile arthritis is not classified within the first 6 weeks to 6 months of disease onset. Juvenile idiopathic arthritis of the axial skeleton, including the sacroiliac joints, often involves enthesitis and juvenile psoriatic arthritis; hence, these two subtypes V and VI are important parameters for diagnosis of sacroiliitis. A prospective clinical radiology study of 185 children with rheumatic disorders demonstrated that CM-enhanced MRI of the sacroiliac joints can be used as a clinically relevant modality for diagnosis of juvenile sacroiliitis (▶ Fig. 14.15 and ▶ Fig. 14.16).18,19 If the modified New York criteria have been met, the term “juvenile ankylosing spondylitis” can also be applied for children (see also ▶ Fig. 14.19).

14.5.3 Magnetic Resonance Imaging Findings for Inflammatory Rheumatoid Sacroiliitis More importance is now ascribed by the ASAS international group96 to MRI evidence of sacroiliitis than had previously been the case for formulation of classification criteria for axial spondyloarthritis. This is because, in many countries, the indication for drug-based treatment of spondyloarthritis with tumor necrosis factor (TNF) blockers is based on MRI-documented active inflammation of the sacroiliac joints, in particular, in the case of the nonradiographic type. Based on numerous MRI studies of sacroiliitis,1,13,14,16,19,21,82,126 the ASAS group has formulated definitions for the various sacroiliitis findings95; these are explained below. In general, a distinction is made between the changes associated with active (acute) inflammation and structural lesions (i.e., chronic changes) (▶ Table 14.3).

Enthesitis of the Articular Iliac-Sided Fibrocartilage Enthesitis of the iliac-sided fibrocartilage (▶ Fig. 14.17, ▶ Fig. 14.18, ▶ Fig. 14.19, and ▶ Fig. 14.20; see also ▶ Fig. 14.15 and ▶ Fig. 14.16) is, in compliance with the enthesitis concept of spondyloarthritis, the first inflammatory change or evidence of onset of inflammation of the sacroiliac joints in spondyloarthritis.21,82 These changes can be reliably detected as enhancing halos in thin slices on T1w and fat-saturated 3D sequences after CM administration, even if no, or only incipient, juxta- and periarticular osteitis is manifested so far. The use of CM is recommended

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for diagnosis of sacroiliitis, since these early changes cannot be detected on native sequences, including a STIR sequence.

Juxta- and Periarticular Osteitis The term “juxta-articular or periarticular osteitis” (▶ Fig. 14.21; see also ▶ Fig. 14.15, ▶ Fig. 14.16, ▶ Fig. 14.17, ▶ Fig. 14.18, ▶ Fig. 14.19, and ▶ Fig. 14.20) refers to bone marrow regions close to the joints that are seen to take up CM on postcontrast T1w sequences, manifesting as hypointensity on native T1w images and hyperintensity on STIR sequences. Unlike erosions, osteitis does not result in discontinuity of the juxta-articular cortical rims. Ahlström et al1 reported similar signal changes and interpreted them as “early inflammatory processes of the subchondral regions of the sacroiliac joints.” Histopathology studies conducted by a Japanese group107 involving open biopsy of patients with earlystage ankylosing spondylitis detected “subchondral inflammatory granulation tissue with cartilaginous and osseous metaplasia.” Likewise, reports by Dihlmann et al38 of “subchondral chondroid aggressive proliferative metaplasia” concord with MRI and histomorphology studies carried out by the present authors. These comparative studies of MRI and immunohistology of patients with sacroiliitis20,24 revealed that T cells and macrophages were the predominant sacroiliitis-associated cells in the early stages of spondyloarthritis. Analysis of joint biopsies revealed angiogenesis in the joint space in around 60% of patients with MRI-documented active sacroiliitis.20 This angiogenesis may be the reason for enhancement of the joint space and juxta-articular bone marrow following CM administration (see ▶ Fig. 14.20g and ▶ Fig. 14.20h). However, osteitis is not to be interpreted as a single diagnostic finding but rather as an inflammatory manifestation of calcified fibrocartilage and, as such, as one phenotype of enthesitis. One important aspect to bear in mind when imaging a patient with clinically suspected sacroiliitis is that following CM administration, these areas of osteitis continue to exhibit marked, protracted rising signal enhancement after the initial CM intensive-uptake phase. To ensure reliable diagnosis, it is therefore important to administer CM early on and obtain delayed images at the end of the entire examination. Periarticular osteitis (visualized in at least two contiguous slices) is the only finding that has been specified by the ASAS group for definition of active sacroiliitis, in the same way as it is required within the framework of the classification of nonradiographic axial spondyloarthritis.95,96 However, doubt is cast on that definition in view of the early findings of enthesitis, as described above.

Capsulitis Inflammatory changes of the anterior or posterior capsule (see ▶ Fig. 14.15, ▶ Fig. 14.17, and ▶ Fig. 14.20) are characterized by thickening and enhancement following CM administration. However, the pericapsular soft tissues continue to be normal, with, at most, slight concomitant edema. The joint capsules fuse anteriorly with the periosteum of the ilium and sacrum, thus reflecting the anatomic entheseal structure (see ▶ Fig. 14.4). At times, capsulitis can therefore spread to the medial and lateral periosteum (see ▶ Fig. 14.15).63 Capsule enhancement continues to the cartilaginous, iliac-sided articular enthesis.

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formulated as classification rather than as diagnostic criteria but are often used in practice for diagnostic purposes. MRI plays a pivotal role, in particular, in nr-axSpA, since detection of active periarticular inflammation on MRI is decisive for correct classification.95

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14.5 Inflammatory Rheumatoid Disorders of the Sacroiliac Joints

Fig. 14.15 Juvenile idiopathic arthritis with enthesitis. A 13-year-old boy with HLA-B27–associated juvenile idiopathic arthritis and type IV enthesitis. His parents reported severe uveitis and a positive paternal family history of ankylosing spondylitis. The boy had experienced severe inflammatory back pain of the left side over the previous weeks. (a) Conventional radiographs of the sacroiliac joints. No pathologic changes. Wavy joint contours due to nonossification of the apophyses of the sacral alar segments (arrows). (b) Native T1w TSE sequence. Smoothly outlined joint contours, bilateral, with disk-isointense signal pattern. A poorly defined hypointense or muscle-isointense juxta-articular halo (arrow) can be identified in the bone marrow in the left ilium. (c) Cartilage-specific native opposed-phase T2*w GRE sequence in a section position identical to that of (b). Slight extension of the left joint space into the posterior third (asterisk), continuing into the left posterior joint capsule (white arrowhead). The anterior joint capsules present as dots of hyperintensity (open arrow). The apophyses of the sacral alar segments (vertical arrows) and the lateral sacral alae (horizontal arrows) appear normal. (d) STIR sequence. Thickening and hyperintensity of the left posterior joint capsule (the white arrowheads help compare both joint capsules); otherwise, no other diagnostic abnormalities seen. The anterior joint capsules manifest, as in the T2*w GRE sequence, as hyperintense dots (open arrows). Narrow hyperintense, sacral-sided halos beside the joints (horizontal arrows) and in proximity to the segmental apophyses, reflecting physiologic proliferation or growth zones (columnar cartilage) at the cartilage–bone interfaces. Only retrospectively on comparing both sides on postcontrast images can a hyperintense halo be identified in the juxta-particular region of the left ilium. Therefore, the STIR sequence does not contribute to diagnosis of sacroiliitis at this early stage. (e) Opposed-phase T1w GRE sequence corresponding to sections in (b), (c), and (d), 3 minutes following CM administration. Intensive CM enhancement of enthesis organ of the iliac fibrocartilage (open arrow), with appearance of a narrow halo of juxta- articular iliac bone marrow, left (white horizontal arrow), attesting to early juxta-articular osteitis, extending to the joint capsules (arrowheads), causing capsulitis, as well as to the posterior iliac periosteum (black arrow) in the form of periostitis. The anterior joint capsule, right (white vertical arrow), shows linear enhancement, which is deemed physiologic in children.

599

a

b

c

d

Fig. 14.16 Juvenile idiopathic arthritis with enthesitis. A 16-year-old girl with HLA-B27–associated juvenile idiopathic arthritis and type IV enthesitis. The patient had experienced inflammatory back pain, on the right, over the previous 6 weeks. While on the native T1w TSE sequences and native cartilage sequences, it was not possible to detect any pathologic changes in the sacroiliac joints (not illustrated), in the paraxial T1w 3D sequences (a, b) and the coronal THRIVE sequences (c) following CM administration, it was possible to discern discrete enthesitis of the iliac fibrocartilage in the anterior third of the right sacroiliac joint, with adjacent discrete osteitis of the iliac bone marrow (a–c, arrowheads); this can be termed “sacroiliitis circumscripta.” (a) Paraxial T1w 3D THRIVE sequence following CM administration. (b) Paraxial T1w 3D THRIVE sequence following CM administration. (c) Coronal T1w 3D THRIVE sequence following CM administration. (d) A more posterior section of the coronal sequence following CM administration. Also seen is florid enthesitis of the ligamenta flava in vertebral segment L5/S1, right (arrowhead).

Table 14.3 MRI findings in association with inflammatory rheumatoid sacroiliitis Active inflammation

600

Structural lesions

●

Enthesitis of the articular fibrocartilage

●

Erosions

●

Juxta- and periarticular osteitis

●

Subchondral sclerosis

●

Capsulitis

●

Periarticular fat accumulation

●

Enthesitis of the interosseous ligaments

●

Transarticular bone buds/bridges

●

Ankylosis

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The Sacroiliac Joints

14.5 Inflammatory Rheumatoid Disorders of the Sacroiliac Joints

Erosions The following types of erosion have been characterized: ● Inflammatory active erosions that take up CM. ● Postinflammatory residual “smoothed” erosions that do not take up CM (see ▶ Fig. 14.22). Erosions (see also ▶ Fig. 14.17, ▶ Fig. 14.18, ▶ Fig. 14.19, ▶ Fig. 14.20, and ▶ Fig. 14.21) are first encountered on the iliacsided fibrocartilage, and only later, they are seen on the

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Fig. 14.17 Nonradiographic axial spondyloarthritis. A 30-year-old HLA-B27-positive male patient with most severe inflammatory back pain (VAS 10), left, with a history of various complaints over the previous 6 months. Evidence of iliac-sided florid enthesitis of the articular fibrocartilage, left, anterior capsular enthesitis, left (c, arrows), as well as extensive left iliac- and sacral-sided, juxta- and periarticular osteitis and enhancement of the joint space in the left sacroiliac joint as well as anterior capsulitis. Tiny, beadlike iliac- and sacral-sided erosions (c, arrowheads) are demonstrated in the right sacroiliac joint, but these can be conclusively identified only on postcontrast images. Evidence of florid enthesitis of the interosseous ligaments in the connective tissue retroarticular space (d, e, arrows); this exhibits low signal intensity on native T1w sequences and, following CM administration, shows intense enhancement. The tissue cylinder taken during therapeutic intra-articular cortisone injection into the left sacroiliac joint (g, h) is representative of the cartilage– bone interface of the left sacroiliac joint. Dense cellular collagen connective tissue can be identified between the trabecular columns and the hyaline joint cartilage of the bone marrow space. The majority of these cells are the result of recruitment of activated local connective tissue cells. Numerous vessels (h, asterisk) can be detected between the inflamed tissue. At the blurred transition zone between connective tissue and hyaline cartilage tissue (g, h, arrowheads), the destructive nature of the inflamed tissue can be identified: infiltration of the cartilage has resulted in lacuna formation within the cartilage tissue. Activated chondrocytes with enlarged halos can be identified in the hyaline cartilage. Further immunohistology tests (not illustrated here) also detected the presence of lymphoplasmacytic cellular and hypercellular inflamed tissue and, in addition to numerous plasma cells, several CD8 + T lymphocytes and many CD68 + macrophages. (a) Paraxial T1w TSE sequence. (b) Paraxial T1w WATSc sequence (cartilage sequence). (c) Paraxial T1w 3D THRIVE sequence with fat saturation following CM administration. b, connective tissue; h, hyaline joint cartilage; I, lacuna; s, trabecular column.

sacral-sided counterpart, too. They result in discontinuity of the juxta-articular cortex, but continuity with the internal joint space or with the joint cartilage is preserved. Large (at least 2 mm) or confluent erosions manifest as pseudodistension of the joint space. Small erosions (maximum 1 mm in diameter) can often be reliably identified only following CM administration. On histology studies, erosions are seen as destructive, fibrous lymphoplasmacellular inflammatory connective tissue infiltrates at the cartilage–bone transition zone.20,24,63

601

Fig. 14.17 (continued) Nonradiographic axial spondyloarthritis. (d) Partial image section showing a cranial slice from the paraxial T1w TSE sequence. (e) Partial image section showing a cranial slice from the paraxial T1w 3D THRIVE sequence following CM administration (parallel to d). (f) Quadrant-based activity score of 16 left and 4 right: the activity of, in each case, one of the four quadrants, right, resulted from enhancement of the erosions and the posterior joint capsule. The large increase in signal intensity of the periarticular bone marrow of all four quadrants following CM administration, left, resulted from florid osteitis and was therefore confirmed with a score of 4, in each case, following extension of over 66% of each quadrant surface area. Here, the results of semiquantitative evaluation of floridity are as follows: 0, no florid inflammatory changes; 1, floridity ≤ 10% of the quadrants (joint space, erosions, capsule; no osteitis); 2, osteitis 11 to 33% of the quadrant; 3, osteitis 34 to 66% of the quadrant; 4, osteitis > 66% of the quadrant. The chronicity score on the right was II and on the left 0. (g) Gold stain, magnification 40-fold. (h) Gold stain, magnification 100-fold.

602

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The Sacroiliac Joints

a

b

c

d

1

4 1

1 4

3

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14.5 Inflammatory Rheumatoid Disorders of the Sacroiliac Joints

4 4

e

Fig. 14.18 Nonradiographic axial spondyloarthritis. A 19-year-old HLA-B27-positive man with inflammatory back pain and variable vascular pain (VAS 7) over previous 8 weeks but no radiographic sign of sacroiliitis. Evidence of iliac-sided florid enthesitis of the articular fibrocartilage (arrows), bilateral. Bilateral formation of beadlike, iliac-sided erosions (b, arrowheads), from which a bilateral chronicity score of II can be calculated. Attesting to floridity, juxta- and periarticular osteitis of the right sacrum and left ilium as well as posterior sacrum has produced an activity score of 12 on the left and of 10 on the right. (a) Paraxial T1w 2D TSE sequence. (b) Paraxial T1w 3D WATSc sequence (cartilage sequence). (c) Paraxial T1w 3D THRIVE sequence following CM administration. (d) Coronal T1w 3D THRIVE sequence following CM administration. (e) Quadrant-based activity score of 12 on the left and of 10 on the right. For the results of semiquantitative evaluation of floridity, see ▶ Fig. 14.17(f).

603

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The Sacroiliac Joints

Fig. 14.19 Juvenile ankylosing spondylitis. A 15-year-old HLA-B27-positive boy with inflammatory back pain over previous 5 years. CT (a) shows a mixed range of findings for the sacroiliac joint, with subchondral iliac-sided sclerosis and iliac-sided beadlike erosions, giving rise to partial pseudodistension of the joints. Transarticular bone bridges observed only in isolated cases (a, arrow) (CT score III, bilateral). Correlating with the CT morphology, MRI (b–e) also demonstrates characteristic mixed findings for the sacroiliac joint, with subchondral sclerosis (hypointense iliac halos on a native T1w sequence [b]) and confluent iliac-sided erosions with ensuing pseudodistention of the joints, producing a bilateral chronicity score of III. The postcontrast images (d, e) show bilateral enhancement of erosions and of the right articular fibrocartilage. Besides, discrete periarticular osteitis can be delineated following CM administration. (a) CT section through the sacroiliac joints. (b) Paraxial T1w TSE sequence. (c) Paraxial T1w WATSc sequence (cartilage sequence). (d) Paraxial T1w 3D THRIVE sequence following CM administration. (e) Coronal T1w 3D THRIVE sequence following CM administration. (f) Quadrant-based activity score. A bilateral score of 6 was calculated.

604

14.5 Inflammatory Rheumatoid Disorders of the Sacroiliac Joints

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Fig. 14.20 HLA-B27-positive ankylosing spondylitis. A 26-year-old female patient with radiographic diagnosis of ankylosing spondylitis (radiography score III, left), with intermittent inflammatory back pain on the left side over previous 7 years as well as bilateral persistent exacerbation of these complaints over preceding 6 months. CT (a, b) shows characteristic mixed findings for the left sacroiliac joint, comprising subchondral sclerosis (S), pseudodilated erosions (arrows), and transarticular bone bridges (angulated arrows): CT score III, left. The area of sclerosis, adjacent to the capsule, on the right anterior ilium, beside the unremarkable right joint space, is consistent with physiologic hyperostosis at this typical location (h). MRI (c-g) shows evidence of left iliac subchondral sclerosis (S), with hypointensity evident on all sequences. The anterior zone of low signal intensity beside the capsule on the right ilium is consistent with physiologic hyperostosis at this typical location (h). Whereas the contours of the right sacroiliac joint are of a normal size and smooth, those of the left joint are irregular due to transarticular bone bridges (d, e, angulated arrows) and, to some extent, confluent and, as such, pseudodilated erosions (d-g, arrows). These erosions exhibit intermediate signal on T1w sequences and high signal on T2*w sequences and STIR sequence, with intense enhancement following CM administration. Attesting to juxta-articular fat accumulation (F), areas of high signal intensity are seen in the periarticular bone marrow on T1w images and of low signal intensity on opposed-phase T2*w images. Only on CM-enhanced sequences, there is conclusive evidence of pathologic changes of the iliac fibrocartilage of the right sacroiliac joint. The articular fibrocartilage (g, open arrow) and right joint capsules (g, arrowheads) undergo intense enhancement, reflecting the early stages of entheseal sacroiliitis with capsulitis. The periarticular iliac bone marrow, right, and the periarticular sacral bone marrow, left, show high, steep enhancement consistent with discrete osteitis (g, asterisk). These inflammatory bone marrow abnormalities can also be detected on the STIR sequence (e, asterisk); by contrast, there is no evidence of inflammation of the right iliac fibrocartilage on the STIR sequence. (a) Transverse CT section of the middle third of joint (level S2). (b) Transverse CT section of inferior third of joint (level S3/S4). (c) T1w SE sequence. (d) T2*w GRE sequence, using opposed-phase technique.

605

The Sacroiliac Joints

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Fig. 14.20 (continued) HLA-B27-positive ankylosing spondylitis. (e) STIR sequence. (f) T1w GRE sequence in opposed-phase technique before intravenous injection of Gd-DTPA 0.1 mmol/kg body weight. (g) T1w GRE sequence in opposed-phase technique 3 minutes following CM administration. (h) Quadrant-based semiquantitative activity score of 8 on the right and of 4 on the left. The activity score of 2 for the upper outer right quadrant resulted from juxta-articular, iliac-sided enhancement, in association with osteitis. The activity score of 1 in the upper inner right quadrant results from enhancement of the joint capsule. The increase in signal intensity of the periarticular bone marrow in the lower outer right quadrant is due to iliac-sided osteitis, with extension across less than 66% of the quadrant, and is therefore assigned a score of 3. The inflammatory activity of, in each case, 1 in the lower left quadrants resulted from posterior capsulitis and enhancement of erosions. The chronicity score is 0 on the right and III on the left.

606

14.5 Inflammatory Rheumatoid Disorders of the Sacroiliac Joints

Subchondral sclerosis (see ▶ Fig. 14.20, ▶ Fig. 14.21, and ▶ Fig. 14.22) develops as a reaction of the periarticular bone to inflammation and is seen as a rim of low signal intensity or signal void on all sequences. It shows no rise in signal intensity following CM administration. Sclerotic changes are observed mainly on the iliac side during the early stages of sacroiliitis, appearing only later

on the sacral side, too. As sclerosis progresses, the joints become increasingly more blurred because of increasing periarticular fat deposition, which cannot be distinguished from sclerosis, especially on fat-saturated sequences. Since fat deposition makes it harder, or even impossible, to detect subchondral sclerosis, only non–fat-saturated sequences can be used to that effect. MRI is vastly superior to computed tomography (CT) in detection of subchondral sclerosis.

a

b

c

d

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Subchondral Sclerosis

Fig. 14.21 Ankylosing spondylitis. A 42-year-old HLA-B27-positive male patient with 10-year history of intermittent flares of inflammatory back pain. On current examination, the patient reported only moderate back pain (VAS 4). Radiography demonstrated (a) characteristic mixed findings for the sacroiliac joint, bilateral, with subchondral sclerosis, transarticular bone bridges, as well as erosions leading to narrowing, and in some cases obliteration, of the joint spaces (radiography score III). MRI (b–e) demonstrates similar findings to the overview radiograph, with likewise mixed findings for the sacroiliac joint (bilateral chronicity score III), with periarticular fat accumulation and subchondral sclerosis, discrete transarticular bone bridges (c, arrowheads), and, in some cases, confluent erosions that take up CM with ensuing pseudodistension (e, arrowheads) of the joints. The serrated contours of both narrowed sacroiliac joints are caused by juxtaposition of multiple beadlike, smoothed erosions and multiple peri- and transarticular bone buds, that is, by the simultaneous presence of osteodestructive erosive lesions and osteoproliferative new bone formation. If there is evidence of discrete osteitis of the anterior inner quadrant (d, arrowheads) and CM-enhancing erosions (e, arrowhead), a quadrant-based activity score of 4 is assigned to the right and 5 to the left. (a) Overview radiograph of the sacroiliac joints. (b) Paraxial T1w TSE sequence. (c) Paraxial T1w WATSc sequence (cartilage sequence). (d) Paraxial T1w 3D THRIVE sequence with fat saturation following CM administration.

607

The Sacroiliac Joints sacroiliac joints with ensuing joint space narrowing (see ▶ Fig. 14.21). In terms of histomorphology, these ankylosis manifestations are caused by peri- and intra-articular new bone formation,20,24 as occurring in settings of fibrocartilaginous metaplasia and, as such, as chondral ossification.

Ankylosis

Fig. 14.21 Ankylosing spondylitis. (continued) (e) Coronal T1w 3D THRIVE sequence with fat saturation following CM administration.

Periarticular Fat Accumulation The periarticular bone marrow exhibits patchy to diffuse fat accumulation, consistent with the replacement of the hematopoietically active bone marrow by exclusively fatty marrow. The areas of periarticular fat accumulation (▶ Fig. 14.23; see also ▶ Fig. 14.20, ▶ Fig. 14.21, and ▶ Fig. 14.22, as well as ▶ Fig. 14.27 and ▶ Fig. 14.28) are caused by esterification of fatty acids in the inflamed periarticular regions of bone marrow.85 Fat accumulation is more pronounced on the sacral compared with the iliac side and is one of the structural changes induced by sacroiliitis but can also be seen increasingly following a good response to anti-inflammatory treatment.112 In elderly patients, it is not always possible to differentiate between this postinflammatory fat accumulation and physiologic bone marrow fat deposition (conversion).40 Analogous to the physiologic bone marrow fat deposition seen in settings of marrow conversion, postinflammatory periarticular fat accumulation exhibits a hyperintense signal pattern on T1w sequences. Since on STIR sequences, the fat protons do not contribute to signal intensity because of the decay of their longitudinal magnetization, periarticular fat accumulation exhibits a hypointense to signal-void signal pattern. Such decreases in signal intensity are also observed on sequences with selective fat suppression. With progressive chronicity of sacroiliitis, fat accumulation tends to become more diffuse, covering the entire former joint space after complete ankylosis (phantom joint).

608

Enthesitis of the Interosseous Ligaments Because of the anatomic extra-articular location of the interosseous ligaments, enthesitis of these structures within the retroarticular space is viewed as a separate disease entity; enthesitis—inflammation of the insertion sites of tendons, ligaments, and muscles (▶ Fig. 14.24; see also ▶ Fig. 14.17)—is one of the classification criteria essential for diagnosis of spondyloarthritis.96 Enthesitis of the interosseous ligaments resulting from dorsal capsulitis may be detected within the retroarticular space in settings of sacroiliitis. However, enthesitis of the retroarticular space and/or inflammatory changes in tendons, ligaments, and/or muscles63,82 may also present independently of rheumatoid sacroiliitis. For example, if patients with complete ankylosis of the sacroiliac joints clinically experience inflammatory low back pain, again this may be due to florid enthesitis of the interosseous ligaments in the retroarticular space.

14.5.4 Staging and Scoring Magnetic Resonance Imaging Chronicity Score Based on the results of a prospective study of 125 patients16 as well as a prospective follow-up study of 66 patients to monitor treatment efficacy,17 an MRI chronicity score was defined for sacroiliitis using native sequences (▶ Table 14.4 and ▶ Fig. 14.25, ▶ Fig. 14.26, ▶ Fig. 14.27, and ▶ Fig. 14.28). This five-level scoring system is tailored to the modified New York criteria.32,118

Periarticular Bone Buds and Transarticular Bone Bridges

Magnetic Resonance Imaging Activity Score

The CT morphology of periarticular bone buds and transarticular bone bridges is better than that of MRI, thanks to its direct hyperdense visualization (on MRI, they can only be identified indirectly as areas of signal void; see ▶ Fig. 14.20, ▶ Fig. 14.21, and ▶ Fig. 14.22, as well as ▶ Fig. 14.26 and ▶ Fig. 14.27). On MRI, ankylosing signs manifest as low-signal to signal-void areas of transarticular discontinuity of the joint cartilage; they can increase in size and numbers over time. Transarticular bone bridges lead to irregular joint space narrowing and eventually to ankylosis. These areas of ankylosis exhibit low signal intensity on all sequences and due to secondary fat accumulation (see above) may acquire an intermediate to hyperintense signal pattern. Periarticular bone buds may also manifest as serrated contours of the

A quadrant-based semiquantitative scoring system was developed to determine the (disease) activity score as a replacement for the time-consuming, semiquantitative method used in dynamic testing.63 To that effect, the sacroiliac joint was divided into four quadrants (▶ Fig. 14.29). Using a T1w fat-saturated 3D sequence (e.g., THRIVE), pathologic increases in signal intensity were semiquantitatively evaluated in and around each quadrant of the sacroiliac joint following CM administration (▶ Table 14.5; see ▶ Fig. 14.17, ▶ Fig. 14.18, ▶ Fig. 14.19, and ▶ Fig. 14.20). It must be pointed out that the focus here was on evaluation of a volume rather than on analysis of an individual slice. As such, inflammatory changes must be present in two or more individual slices to avoid misinterpretations due to partial volume effects.

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e

As the osteoproliferative processes triggered by periarticular bone buds and transarticular bone bridges progress, they eventually result in the terminal stages of sacroiliitis, involving partial to complete ankylosis of the sacroiliac joints (see ▶ Fig. 14.23, ▶ Fig. 14.27, and ▶ Fig. 14.28). Now, the former structure of the joint can be detected only as a phantom joint, since it has merged with the surrounding iliac and sacral bone marrow.

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14.5 Inflammatory Rheumatoid Disorders of the Sacroiliac Joints

Fig. 14.22 Ankylosing spondylitis. HLA-B27-positive 35-year-old male man with a 10-year history of inflammatory back pain. From the radiograph (a), a bilateral radiography score of III is assigned on detection of mixed findings for the sacroiliac joint, in accordance with Dihlmann, with simultaneous triad of subchondral sclerosis, erosions with pseudodistention, and transarticular bone bridges and bone buds. MRI (b–e) demonstrates similar findings to the overview radiograph, with likewise mixed findings for the sacroiliac joint (bilateral chronicity score III) and subchondral sclerosis, discrete ankylosis (d, arrow), and confluent smoothed erosions, with resultant pseudodistension of the joints. An iliac bulge on the left sacroiliac joint was identified as an anatomic variant (c, arrowhead). Only minor pain was reported at the time of examination. Hence, there was no evidence of relevant CM uptake or measurable inflammatory activity (quadrant-based bilateral activity score of 0). (a) Overview radiograph. (b) Paraxial T1w TSE sequence. (c) Paraxial T1w WATSc sequence (cartilage sequence). (d) Paraxial T1w 3D GRE sequence with fat saturation following CM administration. (e) Coronal T1w 3D GRE sequence with fat saturation following CM administration.

609

a

b

c

d

e

Fig. 14.23 Ankylosing spondylitis. A 48-year-old HLA-B27-positive male patient with a 30-year history of ankylosing spondylitis. At the time of examination, the patient experienced only minor back pain (VAS 2.) Radiographs (a) show complete ankylosis of both sacroiliac joints (radiography score IV). MRI (b–e), like radiography, demonstrates complete bone fusion of both sacroiliac joints (bilateral chronicity score IV) with residual cartilage, left (c, arrowheads). Following CM administration, there is no evidence of CM-enhancing structures or, as such, of any acute inflammatory changes (bilateral activity score 0). (a) Overview radiograph of the sacroiliac joints. (b) Paraxial T1w TSE sequence. (c) Paraxial T1w WATSc sequence (cartilage sequence). (d) Paraxial T1w 3D THRIVE sequence with fat saturation following CM administration. (e) Coronal T1w 3D THRIVE sequence with fat saturation following CM administration.

610

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The Sacroiliac Joints

14.7 Disseminated Idiopathic Skeletal Hyperostosis

Table 14.4 MRI staging (scoring) of chronic changes in association with sacroiliitis, modified after Bollow et al14 Chronicity score

Description

0

No chronic inflammatory changes

I

Mild subchondral sclerosis with well-defined joint contours and up to two erosions per section, normal joint width Isolated transarticular bone bridges (see ▶ Fig. 14.25)

II

Moderate subchondral sclerosis, with blurring of no more than one-third of the joint space More than two erosions per section, no confluence, normal joint width (see ▶ Fig. 14.26) Isolated transarticular bone bridges

III

Pronounced periarticular sclerosis, with blurring of more than one-third of the joint space And/or pseudodistension of the joint space due to confluent erosions And/or discrete transarticular bone buds, with joint space narrowing (see ▶ Fig. 14.27)

IV

Definitive ankylosis of more than one-quarter of the joint space Joint space can be identified only as a phantom joint filled with fatty marrow–like tissue (see ▶ Fig. 14.28)

The activity grades for the four joint quadrants were totaled; the maximum value per joint is 16. If only native sequences are available for a patient, as an alternative, the sacroiliitis activity score can be calculated from the extent of periarticular osteitis by using STIR sequences or fat-saturated PDw sequences. Using this approach, it was revealed that STIR images were able to detect around 95% of bone marrow edema–equivalent lesions compared with contrast-enhanced sequences.4 However, since this method did not permit assessment of inflammatory changes of the joint capsules or enthesis organs, the alternative semiquantitative activity score had to be amended accordingly (▶ Table 14.6).

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Fig. 14.24 Enthesitis of the interosseous ligaments. A 28-year-old male patient with diagnosis of ankylosing spondylitis and inflammatory back pain. (a) Paraxial T1w TSE sequence. Enthesitis of the interosseous ligaments can be identified in the fatty connective tissue of the retroarticular space superior and posterior to the cartilaginous compartment of the sacroiliac joints (arrows). This disorder has fully displaced the fatty tissue and manifests as low signal intensity on native T1w sequences, with poor delineation versus the surrounding compact halos. (b) Paraxial STIR sequence. Osteitis of the sacral and iliac bone marrow as a concomitant manifestation of florid enthesitis of interosseous ligaments (arrowheads).

Sacroiliitis can be diagnosed with MRI if a chronicity score of at least 2 has been calculated. A chronicity score of 1 can also be calculated for degenerative changes of the sacroiliac joints and is therefore not conclusive proof of sacroiliitis. If an activity score of more than 1 has not been calculated for any of the four quadrants of a joint (contrast-enhanced method) and there is no evidence of chronic changes, only a diagnosis of suspected sacroiliitis (borderline finding) may be issued. MRI follow-up examination around 6 months later is recommended in such cases.

14.6 Osteoarthrosis Deformans and Juxta-Articular Pneumatocysts Pneumatocysts are benign, nitrogen-containing juxta-articular bone cysts seen in the region of the sacroiliac pelvis (▶ Fig. 14.30), in association with arthritic changes of the sacroiliac joints (▶ Fig. 14.31),43 and with vacuum phenomena within sacroiliac joints (see ▶ Fig. 14.30). The water-equivalent signals identified on T2-weighted (T2w) images and STIR sequences are interpreted as the liquefied aggregate state of nitrogen, similar to the fluid accumulations observed in degenerative intervertebral disks with vacuum phenomena.33,76

14.7 Disseminated Idiopathic Skeletal Hyperostosis Disseminated idiopathic skeletal hyperostosis is one of the most common causes of nonrheumatoid enthesopathy and can be seen as a link between mechanical, stress-related, and metabolic causes.51,104 Disseminated idiopathic skeletal hyperostosis syndrome of the spine was first reported by Forestier and RotesQuerol,46 who described flowing anterolateral calcification of the anterior longitudinal spinal ligament92 and/or of the posterior longitudinal spinal ligament,93 encompassing more than four vertebral bodies but with preservation of the intervertebral disk height, absence of vacuum phenomena, and absence of

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Fig. 14.26 Chronicity score II. For description, see ▶ Table 14.4. (a) Schematic diagram of findings. (b) Paraxial T1w WATSc sequence (cartilage sequence). (c) Paraxial T1w TSE sequence.

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Fig. 14.27 Chronicity score III (mixed findings for the sacroiliac joint). For description, see ▶ Table 14.4. (a) Schematic diagram of findings. (b) Paraxial T1w WATSc sequence (cartilage sequence). (c) Paraxial T1w TSE sequence.

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Fig. 14.25 Chronicity score I. For description, see ▶ Table 14.4. (a) Schematic diagram of findings. (b) Paraxial T1w WATSc sequence (cartilage sequence). (c) Paraxial T1w TSE sequence.

14.8 Osteitis Condensans Ilii and Sacri as well as Triangular Hyperostosis Ilii

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Fig. 14.28 Chronicity score IV (phantom joint). For description, see ▶ Table 14.4. (a) Schematic diagram of findings. (b) Paraxial T1w WATSc sequence (cartilage sequence). (c) Paraxial T1w TSE sequence.

Fig. 14.29 Four-quadrant method. Schematic diagram. The joint space divides each joint into two iliac and two sacral quadrants. A virtual horizontal line, which is generally tangent with the inferior border of the first sacral neuroforamen, divides the articular surface into two and, in turn, divides each joint into two separate anterior and two posterior quadrants.

peripheral sclerosis. Conversely, disseminated idiopathic skeletal hyperostosis of the sacroiliac joints manifests as bridging osteophytes of the anterior joint capsules but without narrowing of the cartilaginous joint compartment. These bridging osteophytes can be clearly visualized on both MRI and CT (▶ Fig. 14.32).

14.8 Osteitis Condensans Ilii and Sacri as well as Triangular Hyperostosis Ilii and Sacri Differential diagnosis is challenging when trying to distinguish between inflammatory rheumatoid sacroiliitis and uni- and/or bilateral osteitis condensans ilii and sacri as well as triangular hyperostosis ilii and sacri. These two terms refer to the same disease entity but at different stages of the disease process. Whereas “osteitis condensans ilii and sacri” denotes a still-active stage of stress-related osteitis, with edema-equivalent increases in signal intensity identified in the bone marrow on MRI (▶ Fig. 14.33), “triangular hyperostosis ilii and sacri” is used to describe the subsequent sclerotic stage of osteitis. The morphology identified on radiography and CT is characterized by ovoid to triangular areas of osteosclerosis on the iliac and sacral aspects of the joint, with

Score

Description

0

No changes

1

Increases in signal intensity only in the joint space, joint capsule, or within erosions (maximum 10% of the quadrant surface area)

2

Slight increases in signal intensity in the periarticular bone marrow (11–33% of the quadrant surface area)

3

Moderate increases in signal intensity in the periarticular bone marrow (34–66% of the quadrant surface area)

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Sharp increases in signal intensity in the periarticular bone marrow (> 66% of the quadrant surface area)

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Table 14.5 Semiquantitative MR activity evaluation. CM-based semiquantitative activity score (four-quadrant method)

Table 14.6 Alternative semiquantitative MRI activity score using native examination protocol. STIR-based semiquantitative activity score (fourquadrants method) Score

Description

0

No changes

1

Slight increases in signal intensity in the periarticular bone marrow (up to 33% of the quadrant surface area)

2

Moderate increases in signal intensity in the periarticular bone marrow (34–66% of the quadrant surface area)

3

Sharp increases in signal intensity in the periarticular bone marrow (> 66% of the quadrant surface area)

no longer an evidence of a dominant bone marrow edema–equivalent signal pattern on MRI (▶ Fig. 14.34). Osteitis condensans ilii and sacri87,124 may also be an exaggerated response by the ilium to the gravitational pressure exerted on it in the upright position37; an increased incidence of this disorder is also observed secondary to pregnancy-mediated “pelvic stress”62,100 or in athletic activities exerting increased shear forces on the sacroiliac joints (e.g., football, hockey, tennis).35 Although unlike spondyloarthritis, osteitis condensans ilii and sacri is not associated with the HLA-B27 antigen,110 some patients with osteitis condensans ilii and sacri report back pain that meets the criteria for inflammatory back pain. Osteosclerosis induced by triangular hyperostosis ilii and sacri extends to the sacroiliac joint but often does not alter the joint space.66,103

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Fig. 14.30 Juxta-articular pneumocyst. A 29-year-old man with minor low back pain. MRI of the pelvis visualizes an ovoid structure in the juxtaarticular anterior ilium in the region of the right sacroiliac joint, which exhibits low signal-to-signal void on T1w sequences (a, c, arrowheads). On STIR sequences (b, d), this manifests as a central area of signal void, surrounded by a water-equivalent peripheral halo. In the paraxial plane images (a, b, arrows), a second, smaller, cystoid lesion can be seen in the left juxta-articular posterior ilium in the region of the left sacroiliac joint. On the STIR sequence, this exhibits hyperintense, water-equivalent signal intensity. On CT (e), this structure in the right anterior juxta-articular ilium is seen as an air- or nitrogen-containing cyst, which is diagnosed as a juxta-articular pneumocyst (white arrowhead). Inferior to the anterior right joint capsule, a nitrogen-containing blister-like structure can be identified (black arrowhead). There is no evidence of a direct connection between the pneumatocysts and the sacroiliac joint space. (a) Paraxial T1w TSE sequence. (b) Paraxial STIR sequence. (c) Axial T1w TSE sequence. (d) Axial STIR sequence. (e) Axial CT section parallel to (c) and (d).

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14.8 Osteitis Condensans Ilii and Sacri as well as Triangular Hyperostosis Ilii

Fig. 14.31 Degenerative capsular ossification and juxta-articular pneumocyst. A 49-year-old man with minor, but chronic, deep low back pain (VAS 3) on the right side. Based on the overview radiograph of the pelvis, right sacroiliitis is suspected because of extensive sclerosis (a, arrow). This sclerosis is imputed to anterior capsular ossification, right (b–d, arrows) in association with osteoarthrosis deformans of the sacroiliac joints. On the right juxta-articular iliac side, a round structure with peripheral sclerosis is identified, with punctate hypointensity at its center and, following CM administration (e), punctate enhancement (b–e, arrowheads). This structure is initially thought to be an osteoid osteoma but on CT (not illustrated) is found to be an air- or nitrogen-containing cyst, thus diagnostic of a juxta-articular pneumocyst. (a) Overview radiograph. (b) Paraxial T1w TSE sequence. (c) Paraxial T1w WATSc sequence (cartilage sequence). (d) Paraxial T1w 3D GRE sequence with fat saturation following CM administration. (e) Coronal T1w 3D GRE sequence with fat saturation following CM administration.

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Fig. 14.32 Disseminated idiopathic skeletal hyperostosis of the sacroiliac joints. A 40-year-old male patient with sporadic back pain. The radiograph demonstrates ossification of the right sacrospinous ligament and the symphysis joint (a, arrows) as well as of the joint capsules of both sacroiliac joints (a, arrowheads). MRI visualizes (b–d) normal and smoothly outlined sacroiliac joints (S). The anterior capsule–ligamentous complex shows bridging osteophytes (b–d, arrowheads), which exhibit high signal intensity on all sequences, leading to triangular fat accumulation in the region of the sacral bone marrow (f). No evidence of enhancement following CM administration (not illustrated). On the CT image (e), arrowheads point to the ossified joint capsules of the sacroiliac joints. (a) Overview radiograph. (b) T1w TSE sequence. (c) T2*w GRE sequence in opposed-phase technique. (d) STIR sequence. (e) Axial CT.

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14.8 Osteitis Condensans Ilii and Sacri as well as Triangular Hyperostosis Ilii

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Fig. 14.33 Osteitis condensans ilii and sacri. A 47-year-old HLA-B27–negative woman (multiparous) with 4-year history of persistent back pain following the birth of her last child (a–d). An external MRI preliminary examination was conducted (e) 6 months after the birth of her last child. The radiograph shows an area of typical triangular sclerosis, periarticular caudal asymmetrical, in proximity to both sacroiliac joints in the ilium and the sacrum (a, arrowheads). MRI visualizes enhancing sacral and iliac bone marrow isointense osteitis in the region of the anterior and inferior sacral and iliac segments of the right sacroiliac joint, reflecting osteitis condensans ilii and sacri (b–d, black arrows). Anterior inferior osteitis condensans sacri is identified on the left (b–d, black arrowheads). An area of unenhanced low signal intensity seen in the right ilium (b–d, white arrowheads) has already undergone sclerosis, consistent with the sclerosis zones seen on the radiograph showing triangular hyperostosis ilii, right. An MRI preliminary examination performed 3 months previously showed still relatively fresh areas of osteitis on a coronal STIR sequence (e, arrowheads), but not yet exhibiting signs of sclerosis. (a) Overview radiograph. (b) Paraxial T1w TSE native sequence. (c) Paraxial T1w 3D THRIVE sequence following CM administration. (d) Coronal T1w 3D THRIVE sequence following CM administration. (e) Coronal STIR sequence.

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Fig. 14.34 Triangular hyperostosis ilii and sacri. A 48-year-old woman (multiparous) with inflammatory back pain (VAS 6). (a) Overview radiograph. Area of caudal symmetrical triangular sclerosis in the region of both sacroiliac joints. (b) Axial CT of the lumbar spine with view of the sacroiliac joints. Zone of homogeneous sclerosis in the anterior inferior region of the sacroiliac joints. A conspicuous finding is the vacuum phenomena in the joint space of both sacroiliac joints. (c) Paraxial native T1w TSE sequence. Evidence of hypointense sacral and iliac zones in the region of the anterior and inferior segments of the sacroiliac joint, bilateral, consistent with triangular hyperostosis ilii and sacri. (d) Paraxial T1w 3D THRIVE sequence following CM administration, corresponding to (c). No evidence of CM enhancement of the area of sclerosis. Enhancement of the anterior sacroiliac joint capsules, reflecting capsulitis (arrowheads).

However, in rare cases, erosive types of disease are manifested, which masquerade as sacroiliitis on clinical examination and radiography. The changes are typically located in the vicinity of the inferior anterior sacroiliac joint region (loco typico) (see ▶ Fig. 14.33 and ▶ Fig. 14.34). In-depth analyses of changes to the anterior joint regions are crucial in differentiating between stress-related changes and rheumatoid sacroiliitis. Based on the observations of the present authors, analogous to erosive intervertebral osteochondrosis (Modic changes type I–III81), osteitis

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condensans comprises an acute inflammatory stage, a postinflammatory stage of degenerative fat deposition, and the radiographically identifiable sclerotic stage of triangular hyperostosis ilii and sacri. Furthermore, concomitant enthesitis of the interosseous ligaments in the retroarticular space is observed (see ▶ Fig. 14.34). On MR images, areas of osteosclerosis associated with triangular hyperostosis ilii and sacri exhibit low signal intensity on both T1w and T2w sequences. They may have a hyperintense halo on STIR sequences, which, following CM

14.10 Pyogenic, Septic Sacroiliitis

e

f

administration, may show enhancement on T1w images and can thus be interpreted as a residual stage of resolved osteitis condensans. By virtue of the typical location, it is easier to distinguish inflammatory rheumatoid sacroiliitis from osteitis condensans88 on CT than on MRI, in particular, if vacuum phenomena are also identified in the sacroiliac joint space (see ▶ Fig. 14.34). Vacuum phenomena are not found in association with rheumatic inflammatory sacroiliitis.

14.9 Osteomalacia A distinction can be made between inflammatory rheumatoid sacroiliitis and the changes induced in the sacroiliac joints by osteomalacia or rickets, in association with, as yet undiagnosed, impaired vitamin D metabolism, since in settings of osteomalacia, the sacroiliac joints may be surrounded by uncalcified osteoid halos similar to the joint space distension caused by sacroiliitis (▶ Fig. 14.35).77 Furthermore, patients with osteomalacia may report clinical symptoms of inflammatory back pain. Looser’s pseudofractures may also be detected on radiographs and MRI in association with osteomalacia (see ▶ Fig. 14.35e).

14.10 Pyogenic, Septic Sacroiliitis Septic sacroiliitis, which is generally unilateral, is acute in about 50% of cases and subacute and chronic in about another 50% of cases2,6,12,30,31,34,41,44,65,75,84,105,113 and often results in progressive immobilizing symptoms, with referred pain in the back, gluteal region, hip, and even abdomen. Localizing the clinical findings to the sacroiliac joints can be challenging. The predisposing factors and portals of entry associated with the mainly hematogenous

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Fig. 14.34 Triangular hyperostosis ilii and sacri. (continued) (e) Cranial slice of the slice pack used for the paraxial T1w 3D THRIVE sequence following CM administration. Intense CM enhancement of the retroarticular space (arrowheads) attesting to florid enthesitis of the interosseous ligaments. This stress-mediated enthesitis was thought to have been the cause of the inflammatory back pain. (f) Coronal T1w 3D THRIVE sequence following CM administration. Hypointense triangular hyperostosis ilii and sacri, bilateral, consistent with the areas of sclerosis seen on the radiograph and CT. The arrowheads point to the area of enthesitis of the interosseous ligaments in the posterosuperior retroarticular space.

septic sacroiliitis are skin infections, tonsillitis, trauma, and pregnancy.3,29,42 The main pathogens implicated in acute courses of disease, accompanied by high temperatures, are Staphylococcus aureus, streptococci, and Enterobacter. The subacute and chronic form of sacroiliitis often has few symptoms and is mainly caused by mycobacteria5,61,69,86,89,122and Brucella.53,58,73 Infectious sacroiliitis was a rarely described disease entity prior to the 1970s, but a marked increase has been reported in recent times among intravenous drug users,52,54,58,90 imputed primarily to Pseudomonas aeruginosa, Staphylococcus aureus, and streptococci. The latency period between onset of symptoms and diagnosis is, on average, between 7 days for acute courses of disease and over 6 weeks for subacute courses. However, isolation of the causative pathogen from a positive blood culture is rare. Conventional overview radiographs are often normal during the initial 2 to 4 weeks.31,34,41,54,58,73,80,105 On MRI,28,60,71,73,98,114, 123 the following findings may be observed in pyogenic or septic sacroiliitis (▶ Fig. 14.36): on T1w images, the joint exhibits low signal intensity, whereas on T2w and STIR sequences as well as on T1w sequences it has high signal intensity following CM administration. These signal changes first extend across the capsule, destroying it, and then to the subperiosteal regions of the ilium and/or sacrum. The disease spreads anteriorly in the later course to the intermuscular peripelvic fatty tissue and the iliopsoas muscles and/or posteriorly to the gluteal muscles. There is generally concomitant diffuse inflammatory infiltration of the periarticular sacral and/or iliac bone marrow. This phenomenon is similar to lava eruption, hence the term “lava columnar phenomenon.”114 Late-stage septic sacroiliitis may be accompanied by joint pyarthrosis, with joint distension, and phlegmonous infiltration of bone, periosteum, and muscles as well as intraarticular sequestration and abscess formation, exhibiting intense peripheral enhancement.

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Fig. 14.35 Sun-deficiency osteomalacia, with involvement of the sacroiliac joints. A 16-year-old Turkish girl who had migrated to Germany from her country of origin only 2 years previously and continued to wear traditional long garments and headscarves, thus giving rise to vitamin D deficiency due to lack of sun exposure. This eventually resulted in osteomalacia, with clinical symptoms of deep “inflammatory” low back pain (VAS 6), in particular at rest but also on exertion, radiating into the legs and toes. No evidence of elevated inflammatory parameters. The patient’s symptoms were relieved after taking nonsteroidal anti-inflammatories and following 4-week vitamin D supplementation. The sacroiliac joints appeared to be expanded to a width of 12 mm on a native T1w sequence (normal width: 3–4 mm). On the sacral side, they were surrounded by a rim of high signal intensity (a, black arrowheads); this finding corresponded to linear fat deposition at the growth plate or apophysis of the lateral sacral alae. Likewise, the apophyses between sacral vertebra S1 and the sacral alae (a, white arrowheads) exhibit marked thickening. Closer analysis of the cartilage sequences reveals linear structures of low signal intensity at the center of the joint, indicating the joint cavity region (b, arrowheads). Following CM administration (c, d), hyperintense halos can also be identified on both the sacral and iliac sides, beside the central cartilaginous joints structures, which appear normal. These are thought to be the cause of the joint expansion observed on the native T1w sequence. These are broad halos of uncalcified osteoids. The apophyses of the iliac crest, apophyses of the greater femoral trochanter, and the epiphyseal plates of the proximal femur are also slightly enlarged but only to a slight extent, compared with the sacroiliac osteoid deposits. External MRI examination performed 4 months earlier had demonstrated bone marrow edema-equivalent osteitis in the right sacral alae containing Looser’s pseudofractures (e, arrowheads), which could no longer be seen in the present MRI a few weeks after vitamin D supplementation. (a) Paraxial T1w TSE sequence. (b) Paraxial T1w WATSc sequence (cartilage sequence). (c) Paraxial T1w 3D GRE sequence with fat saturation following CM administration.

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14.13 Tumor and Tumorlike Conditions of the Joint caverns (▶ Fig. 14.37) and is frequently accompanied by spondylodiscitis, with psoas abscesses and saponification.7,9,69,89,106,116,122 Noteworthy for differential diagnosis of tuberculous sacroiliitis versus inflammatory rheumatoid sacroiliitis is that in settings of tuberculous sacroiliitis, there is never any evidence of characteristic necrosis and saponification in and around the joint or any infiltration of the surrounding muscles.114

14.12 Traumatic Changes

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d

Diagnosis of the sequelae of trauma to the pelvic skeleton, with involvement of the sacroiliac joints, is the preserve of conventional radiography and CT. MRI STIR sequences and fat-saturated sequences are able to visualize occult fractures and stress fractures following CM administration, based on the hyperintense signal pattern exhibited by bone bruises (▶ Fig. 14.38 and ▶ Fig. 14.39). The fracture line can often be delineated as a hypointense linear structure within the bone marrow edema– equivalent signal pattern and can extend into the neuroforamina or have a garland-like configuration. MRI is superior to CT for detection of concomitant neurovascular injuries secondary to sacral fractures and for demonstrating traumatic sacroiliac joint disruptions (▶ Fig. 14.40).

14.13 Tumor and Tumorlike Conditions of the Joint

e

Fig. 14.35 (continued) Sun-deficiency osteomalacia, with involvement of the sacroiliac joints. (d) Coronal T1w 3D GRE sequence with fat saturation following CM administration. (e) Coronal T2w TSE sequence with fat saturation (baseline examination prior to vitamin D supplementation).

14.11 Tuberculous Sacroiliitis Unlike pyogenic or septic sacroiliitis, tuberculous sacroiliitis is often characterized by periarticular abscess formation or bone

MRI and CT play an equal role in diagnostic imaging of tumor type and tumor extension (▶ Fig. 14.41, ▶ Fig. 14.42, and ▶ Fig. 14.43) of tumorlike lesions that alter and infiltrate the sacroiliac joints and the surrounding regions. Since tumors affecting the sacroiliac joint can mimic the symptoms of “inflammatory back pain,” most patients are initially referred for MRI examination to investigate the possibility of sacroiliitis. MRI is able to visualize any tumor infiltration of the bone marrow and soft tissues as well as the lumbosacral plexus and sciatic nerve, whereas, on the other hand, CT is adept at demonstration of bone destruction and at differentiating between osteolytic and osteoplastic processes. CT and MRI sectional imagings are also able to detect any “inflammatory” involvement of the sacroiliac joints in Paget’s disease.59 With few exceptions, diagnostic imaging alone is unable to determine the type of tumor involved, and hence a biopsy is needed for histologic confirmation. MRI and CT are useful in selecting the biopsy access routes.

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Fig. 14.36 Septic sacroiliitis. A 32-year-old male patient with drug dependence, who had experienced right septic sacroiliitis following hematogenous dissemination of staphylococci. (a) Paraxial T1w TSE sequence. The right sacroiliac joint exhibits high signal intensity; the joint space borders are poorly outlined. The periarticular decreases in signal intensity extend across the capsule, destroying it, and extending anteriorly as a diffuse pattern to the lliopsoas muscles and posteriorly to the gluteal muscles as well as to the sacral and iliac bone marrow; this manifestation is termed “lava columnar phenomenon.” (b) Paraxial STIR sequence. Areas of hypointensity observed on T1w sequence now appear hyperintense. (c) Paraxial T1w TSE sequence with fat saturation following CM administration. Intense enhancement of the destroyed right sacroiliac joint and infiltration of surrounding structures. The anterior structures and linear posterior substrates, which continue to exhibit low signal or are devoid of signal following CM administration and extend into the former right joint space, are sequesters.

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14.13 Tumor and Tumorlike Conditions of the Joint

Fig. 14.37 Tuberculous sacroiliitis or tuberculous osteoarthritis of the right sacroiliac joint. A 35-year-old Tunisian male patient with miliary tuberculosis. (a) Axial CT of the sacroiliac joints. Destruction of the sacral articular surface, right, of the anterior joint segment due to bone caverns extending into the right lateral sacral mass. Calcification anterior to the bone cavern is consistent with saponification of abscess. (b) Paraxial native T1w TSE sequence. Diffuse hypointensity of the right lateral sacral mass adjacent to the discrete and smoothly outlined hypointense structure of the anterior sacral articular surface. The right joint space is extended compared with the left side. (c) Paraxial STIR sequence. Diffuse bone marrow edema–equivalent signal pattern in the right sacrum, with isolated small bone caverns. The hyperintense tissue masses in the joint space were interpreted as tuberculous empyema that had spread continuously, while destroying the anterior joint capsule, to the iliacus, now sitting as a cap over the joint space (lava column phenomenon). (d) Paraxial section through the middle of the sacroiliac joint on T1w SPIR sequence, with fat saturation following CM administration. (e) Cranial slice of the paraxial slice pack used in the T1w SPIR sequence, with fat saturation following CM administration. Delineation of the hypointense abscess formation in the iliopsoas, in the extended joint space and sacrum. Intense peripheral enhancement of abscesses or caverns, with diffuse infiltration of the muscles.

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Fig. 14.38 Radiologically occult sacral fracture. A 55-year-old female patient with low back pain. MRI of the sacroiliac joints demonstrates, in addition to bone marrow edema–equivalent signal pattern of the left sacral ala, the clear fracture line (a, arrowheads) of an insufficiency fracture secondary to postmenopausal osteoporosis. (a) T1w TSE sequence. (b) STIR sequence. (c) T1w fatsat TSE sequence following CM administration.

Fig. 14.39 Insufficiency fractures. A 50-year-old female patient who had an MRI scan following clinically and scintigraphically suspected bilateral florid sacroiliitis. Bilateral insufficiency fractures of the sacral alae with associated bone marrow edema–equivalent osteitis as well as a fracture through sacral vertebra S2 (a, arrowheads). (a) Paraxial T1w TSE sequence. (b) Paraxial T1w 3D GRE sequence with fat saturation following CM administration.

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14.13 Tumor and Tumorlike Conditions of the Joint

Fig. 14.40 Fracture of the right sacral ala and disruption of the right sacroiliac joint. Images of an 18-year-old female patient with fracture of the right sacral ala and disruption of the right sacroiliac joint, clinically accompanied by sacral plexus lesion, right. The fracture line through the right sacral alae (a–d, arrows), whose morphology is well visualized on CT but poorly visualized on MRI, extends into the right neuroforamen S1/S2. Based on CT morphology, a number of fragments (f), which on MRI are masked by concomitant hematoma, can be identified in the anterior region. Likewise, the spinous process can be visualized only on CT. The nerve bundle exiting on the right from neuroforamen S1/S2 shows clear signs of contusion on MRI compared with CT (c–f, open arrows), whereas the intact nerve bundles on the left can be well differentiated (c–f, angulated arrows). In particular, the absence of the normally high signal intensity associated with the cerebrospinal fluid on the right on T2*w sequences is interpreted as evidence of severance of the nerve bundle (e, f). Furthermore, on the T2*w sequences, a fresh hematoma (h) can be clearly identified; this had masked the neurovascular bundle of the internal iliac vessels (e, f, tailed arrows) on the right. On the left, these neurovascular structures show high contrast on T2*w sequences (e, f, arrowheads). The left sacroiliac joint has a normal width of 3.5 mm, whereas the right sacroiliac joint is around 8 mm because of disruption and hyperintense hemorrhage (c–f, asterisk). In summary, MRI proved to be inferior to CT in demonstrating fracture lines and fragments but was superior in detecting nerve damage and details of sacroiliac joint disruption. (a) Transverse CT at the level of the first sacral vertebral body S1. (b) Transverse CT at the level of sacral the second vertebral body S2. (c) Transverse PDw image at the level of the first sacral vertebral body S1. (d) Transverse PDw image at the level of the second sacral vertebral body S2.

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Fig. 14.40 (continued) Fracture of the right sacral ala and disruption of the right sacroiliac joint. (e) Paraxial section through the sacroiliac joints at the level of the first sacral vertebral body S1, using a T2*w GRE sequence in opposed-phase technique. (f) Paraxial section through the sacroiliac joints at the level of the second sacral vertebral body S2, using a T2*w GRE sequence in opposed-phase technique.

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14.13 Tumor and Tumorlike Conditions of the Joint

Fig. 14.41 Metastasis from an anaplastic thyroid gland carcinoma. Osteolytic lesion of the left sacral ala extending into the joint from metastasis of an anaplastic thyroid gland carcinoma in a 60-year-old woman who had complained of deep low back pain, on the left side. (a) Axial CT section. (b) Axial CT section parallel to that in (a). (c) Native T1w TSE sequence. (d) T1w TSE sequence following CM administration. (e) STIR sequence.

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Fig. 14.42 Metastases from a prostate carcinoma. A 77-year-old male patient with back pain who was referred for MRI examination because of radiographically suspected bilateral sacroiliitis with ankylosis. Disseminated, and in some cases confluent, bone lesions with destruction of the right sacroiliac joint (b–d, arrows). The lesions were osteoplastic metastases of hitherto undiagnosed prostate carcinoma. A sacral-sided, on T1w sequences hyperintense and on fat saturation hypointense, focus, on the left, consistent with the hemangiolipoma (b–d, arrowheads). (a) Pelvic overview. (b) Native paraxial T1w TSE sequence. (c) Paraxial T1w 3D GRE sequence with fat saturation following CM administration. (d) Coronal T1w 3D GRE sequence with fat saturation following CM administration.

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e

f

Fig. 14.43 Nodular sclerosing type Hodgkin’s lymphoma. A 54-year-old HLA-B27-positive male patient with inflammatory low back pain, right, over the previous 4 weeks and with a positive paternal family history of ankylosing spondylitis was referred for MRI of the sacroiliac joints. An inhomogeneous hypointense signal pattern with muscle-isointense areas of destruction was identified in the posterior portion of the right ilium on native T1w sequences (a, b), extending into the right sacroiliac joint. Following CM administration, these muscle-isointense areas exhibit homogeneous enhancement with infiltration of the right sacrum, with destruction of the compact bone and extension into the joint space (c–e, arrowheads). CT (f, g) images demonstrate, in addition to extensive sclerosis of the right ilium and mild sclerosis of the right sacral ala, compression of the right sacroiliac joint and osteolytic lesions, destroying the compact bone in the posterior right ilium (f, arrowheads). On histology, these are found to be infiltration of the bone and joint by modular sclerosing-type Hodgkin’s lymphoma. (a) Native paraxial T1w TSE sequence (sectional plane 1). (b) Native paraxial T1w TSE sequence (sectional plane 2). (c) Paraxial T1w 3D THRIVE sequence, parallel to that in (a), following CM administration. (d) Paraxial T1w 3D THRIVE sequence parallel to that in (b), following CM administration. (e) Coronal T1w 3D THRIVE sequence following CM administration. (f) Axial CT through the sacroiliac joints (level 1).

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g

1379–1390

Fig. 14.43 (continued) Nodular sclerosing type Hodgkin’s lymphoma. (g) Axial CT through the sacroiliac joints (level 2).

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[1] Ahlström H, Feltelius N, Nyman R, Hällgren R. Magnetic resonance imaging of sacroiliac joint inflammation. Arthritis Rheum. 1990; 33(12):1763–1769 [2] Ailsby RL, Staheli LT. Pyogenic infections of the sacroiliac joint in children. Radioisotope bone scanning as a diagnostic tool. Clin Orthop Relat Res. 1974 (100):96–100 [3] Almoujahed MO, Khatib R, Baran J. Pregnancy-associated pyogenic sacroiliitis: case report and review. Infect Dis Obstet Gynecol. 2003; 11(1):53–57 [4] Althoff CE, Feist E, Burova E, et al. Magnetic resonance imaging of active sacroiliitis: do we really need gadolinium? Eur J Radiol. 2009; 71(2):232–236 [5] Augé B, Toussirot E, Wendling D. Tuberculous rheumatism presenting as spondyloarthropathy. J Rheumatol. 1999; 26(10):2288–2289 [6] Avila L. Primary pyogenic infection of the sacro-iliac articulation. A new approach to the joint. J Bone Joint Surg. 1941; 23:922 [7] Bell GR, Stearns KL, Bonutti PM, Boumphrey FR. MRI diagnosis of tuberculous vertebral osteomyelitis. Spine. 1990; 15(6):462–465 [8] Bellamy N, Park W, Rooney PJ. What do we know about the sacroiliac joint? Semin Arthritis Rheum. 1983; 12(3):282–313 [9] Benchakroun M, El Bardouni A, Zaddoug O, et al. Tuberculous sacroiliitis. Four cases. Joint Bone Spine. 2004; 71(2):150–153 [10] Benjamin M, Ralphs JR. Fibrocartilage in tendons and ligaments–an adaptation to compressive load. J Anat. 1998; 193(Pt 4):481–494 [11] Benjamin M, McGonagle D. The anatomical basis for disease localisation in seronegative spondyloarthropathy at entheses and related sites. J Anat. 2001; 199(Pt 5):503–526 [12] Biedermann K, Schneider KTM, Kleinert B, Huch A. Pyogenic sacroiliitis. Case report and review of a rare complication in the puerperium [in German]. Gynakol Rundsch. 1984; 24(3):145–152 [13] Blum U, Buitrago-Tellez C, Mundinger A, et al. Magnetic resonance imaging (MRI) for detection of active sacroiliitis–a prospective study comparing conventional radiography, scintigraphy, and contrast enhanced MRI. J Rheumatol. 1996; 23(12):2107–2115 [14] Bollow M, König H, Hoffmann C, Schilling A, Wolf KJ. Initial findings using dynamic magnetic resonance tomography in the diagnosis of inflammatory diseases of the sacroiliac joint [in German]. RoFo Fortschr Geb Rontgenstr Nuklearmed. 1993; 159(4):315–324 [15] Bollow M, Braun J, König H, et al. Dynamic magnetic resonance tomography of the sacroiliac joint: diagnosis of the early stages of a sacroiliitis [in German]. Rontgenpraxis. 1994; 47(3):70–77 [16] Bollow M, Braun J, Hamm B, et al. Early sacroiliitis in patients with spondyloarthropathy: evaluation with dynamic gadolinium-enhanced MR imaging. Radiology. 1995; 194(2):529–536 [17] Bollow M, Braun J, Taupitz M, et al. CT-guided intraarticular corticosteroid injection into the sacroiliac joints in patients with spondyloarthropathy: indication and follow-up with contrast-enhanced MRI. J Comput Assist Tomogr. 1996; 20(4):512–521

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15.1

Introduction

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15.2

Examination Technique

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The Jaws and Periodontal Apparatus

15.3

Anatomy

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15.4

Special Disorders

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15.5

Clinical Relevance of Magnetic Resonance Imaging 643 References

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Chapter 15

The Jaws and Periodontal Apparatus

15 The Jaws and Periodontal Apparatus 15.1 Introduction The intra- and extraoral techniques used in conventional and digital radiography are the mainstay of dental radiology, which, in particular, with the advent of corresponding software packages, have been supplemented in the preoperative setting by dental computed tomography (CT), volume CT, and increasingly also by dental magnetic resonance imaging (MRI).11 Furthermore, detailed assessment of the jaws should be an integral part of evaluation for all patients undergoing other diagnostic investigations where the lower half of the face is also imaged. Thanks to optimal visualization of the soft tissues on the MR image, it is now possible to gain a better insight into changes in bone marrow and vitality of dental pulp as well as to improve differentiation between pathologic inflammatory and blastomous processes, especially those extending into the paranasal sinuses. In settings of severe atrophy of the alveolar ridge, MRI is also superior to CT in distinguishing the alveolar canal from the surrounding, rarefied trabeculae.28 As in other regions of the body, it is also easier to evaluate the activity of neoplastic and inflammatory processes as well as any soft tissue component following intravenous injection of contrast medium (CM).17 Likewise, MRI provides for better demonstration of ingrowth of augmentation materials and assessment of pulp vitality.13,20 It is also adept at visualization of neurovascular bundle irritation following extraction of a wisdom tooth.21

Internet Links

●i

The homepages of the following institutions and journals provide useful information on the topic of “MRI of the jaws and periodontal apparatus”: ● German Society for Dentistry, Oral Medicine and Orthodontics (DGZMK). ● Germany Society of Radiology. ● International Association of Dentomaxillofacial Radiology. ● European Academy of Dentomaxillofacial Radiology. ● International Association for Dental Research. ● Radiological Society of North America. ● Dentomaxillofacial Radiology. ● Oral Surgery Oral Medicine Oral Pathology Oral Radiology. ● SEDENTEXCT.

15.2 Examination Technique 15.2.1 Equipment and Coils The use of low-field scanners has been recommended by one working group to reduce the magnetic artefacts caused by crowns, pins, and implants. These susceptibility artefacts can adversely affect evaluation of the imaging results if they are not confined to the dental crown alone but also impact the root.12 However, on the other hand, it is well known that preference should be given to the signal-to-noise ratio afforded by high-field

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scanners in the interest of enhanced spatial resolution, which is of paramount importance in this body region. It should also be noted that open scanning systems are more appropriate for patients with mild claustrophobia. It has been posited that differences in the magnetic susceptibility profiles of bone versus soft tissues, or even more so between soft tissues and air, cause magnetic field inhomogeneities, which, in turn, result in a certain amount of image distortion in the frequency-encoding direction, generally in the image plane at 0.3 mm and 0.2 T.12 The measurement accuracy of dental MRI, in any case at 1 T, has proved to be equal to that of dental CT and direct osteometry with measurement inaccuracies of less than 1 mm observed, and was adequate for evaluation of the alveolar canal of up to 1.5 T.7,22,25 While it had no clinical relevance, microleakage of amalgam fillings was observed at 3 T.35 A publication by Tymofiyeva et al gives an overview of MRI compatibility with the materials used in dentistry.34 No thermal damage to dental prosthetics was observed on using field strengths of up to 3 T; however, a spacer should be placed between the oral mucosa and any orthodontic appliances.15 The benefits conferred by the enhanced image quality on using surface coils should be weighed up in the individual case against the drawbacks of a massive decrease in signal intensity in deeper regions of interest and attendant inability to achieve homogeneous fat suppression. Likewise, the use of surface coils should be eschewed when subsequent dental reconstruction is planned because of poor penetration depth, as will be explained later. Besides, comparison of the right with the left side can often prove insightful, as in other body regions. If extensive changes are present, several imaging planes may be needed to evaluate the entire lesion.19 In general, the best results are achieved with multichannel head-neck coils. The patient is placed in the supine position and instructed not to swallow during data acquisition. This, on the one hand, prevents movement artefacts and, on the other hand, air—hypointense on all sequences—is replaced with saliva, which permits visualization of the likewise hypointense dental margins.32 In experimental studies, the oral cavity was even filled with water or MRI contrast agent for the duration of data acquisition to assure direct visualization of the teeth and jaws after 3D reconstruction and intensity inversion. As with dental CT, this can be used for any orthodontic purposes.26 In the meantime, studies have also been carried out using high-resolution sequences during in vivo caries diagnostic imaging.2,33 Foam cushion wedges are used to secure the patient’s head in the coil and thus minimize movement artefacts.

15.2.2 Imaging Plane Axial sections are acquired parallel to the occlusion axis; these are not oriented toward the hard palate but are instead positioned at an angle of 90 degrees to the (imaginary) dental axes in the upper and lower jaws (different slope!). The scope of examination includes, on the one hand, the floor of the maxillary sinus as far as those portions of the dental crown no longer surrounded by

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15.2.3 Sequences In terms of the sequences selected, turbo spin-echo sequences are recommended for T1 and T2 weighting as they are least susceptible to metallic artefacts.29 A slice thickness of 1 mm has proved beneficial, but for assessment of the periodontal apparatus a slice thickness of 2 to 3 mm is suitable, provided that multiplanar reconstruction is not planned.28,32 A fat-suppression presaturation pulse can be applied as deemed necessary.14 The use of T1 weighted (T1w) TFE sequences (turbo field-echo sequences) should be contemplated if the sequences hitherto employed are unable to assure satisfactory anatomic visualization. The large susceptibility artefacts on GRE sequences improve visualization of the cortical margins of the alveolar ridge and alveolar canal as well as cysts and tumors. Intravenous CM injection is indicated when exploring perfusion in association with a pathologic process or assessing pulp vitality.20

15.3 Anatomy 15.3.1 General Anatomy On axial sections, the body of mandible is shaped like a horseshoe, while on sagittal slices it appears L-shaped because of its position versus the ascending mandibular ramus. The size of the mandibular angle increases with age, especially in edentulous patients. The bony portion of the periodontal apparatus comprises the dental alveoli in which the dental roots are secured by means of Sharpey’s fibers. On the inner surface of the mandibular ramus, the inferior alveolar nerve with corresponding artery enters the alveolar canal (▶ Fig. 15.1), first coursing parallel to the ramus, before turning anteriorly at the

mandibular angle and exiting opposite the first premolar through the mental foramen into the soft tissues of the cheek. The medial portion of the body of mandible, not accommodating the alveolar canal, is known as the symphysis. On its inner surface is situated the origin of the geniohyoid and genioglossus muscles and the anterior digastric bellies. The mylohyoid fans out like a diaphragm between both inner surfaces of the body of mandible. The spatial relationship of the maxillary molars (premolars) to the maxillary sinus alveolar recess is variable. The median configuration shows the nasopalatine canal coursing parallel to the nasopalatine vessels and nerve. A rounded to heart-shaped cyst may be found here as a normal variant. To denote the spatial relationships between the individual teeth, a number of additional terms has been incorporated into the nomenclature normally employed for other body regions (see ▶ Fig. 15.1b and ▶ Fig. 15.1d)22: ● The term mesial denotes changes occurring closer to the front teeth and distal those farther away. ● Buccal or vestibular refers to contact surfaces facing toward the oral vestibule. ● Palatal means situated in the upper jaw facing the oral cavity, while lingual means situated in the mandible and, likewise, facing the oral cavity. ● Occlusal denotes structures adjacent to the occlusal plane (masticatory level) and apical more distant ones. ● Approximal denotes the surfaces of adjacent teeth facing each other. ● The buccolingual inclination is the angle by which the mandibular alveolar process deviates from the perpendicular.

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the alveolar ridge and, on the other hand, the corresponding sections of the dental crown in the mandible to just below the alveolar canal (in the presence of cysts or tumors as far as the lower margin of the alveolar process). The software programs normally used in dental CT for visualization of real buccolingually (= orthoradial) oriented sections can also be used if equipment compatibility is assured. Based on a line drawn through the middle of an imaginary dental row on the axial slice, the software programs developed for dental radiology compute sections perpendicular to this line (= orthoradial) (similar to slices of cake) as well as parallel panoramic sections. The number of sections to be reconstructed and the distance between them can be chosen at will. These dental reconstructions give an overview of the jaw as normally afforded by the orthopantomography images used in oral surgery. The coronal imaging plane is next used for slice acquisition, in particular, when aimed at delineation of anatomic or pathologic structures. The sagittal imaging plane is suitable only in exceptional cases, such as for medial processes. It is easier to differentiate between the alveolar canal and impacted teeth or pathologic processes on using parasagittal sections parallel to the alveolar ridge in the posterior region.21 Fitting patients with prosthetic devices with MRI contrast agent markers improves orientation during preimplant imaging assessment.12

A two-digit numbering system is used to indicate the position of a tooth: ● The first digit represents the quadrant number. It starts with 1 in the maxillary right quadrant and, while using the traditional “patient’s view,” moves counterclockwise to 4, in the right mandibular quadrant. ● The second digit uses the numbers 1 to 8 to represent the position of each tooth in the alveolar process. It starts with the mesial front tooth; hence, the position “28” represents the left maxillary wisdom tooth. Primary teeth numbering uses as first digit the numbers 5 to 8 (“73” thus represents the left mandibular primary canine).

15.3.2 Special Magnetic Resonance Imaging The cortex, dentin, and dental cement appear hypointense on all sequences. The dental pulp and neurovascular bundle in the alveolar canal are isointense to muscle on T1w sequences and hyperintense on T2 weighted (T2w) sequences. The fatty marrow is hyperintense on both sequences; therefore, fat-suppression techniques should preferably be used to distinguish the hyperintense alveolar canal from the hypointense bone marrow. MRI can be used to that effect prior to extraction of wisdom teeth, without exposure to radiation of the mainly young patients.8,24 Following CM administration, viable dental pulp exhibits an increase in signal intensity. The pulp cavity is widest in adolescents and continues to reduce in size in the course of time.

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Fig. 15.1 Anatomy of the jaws and periodontal apparatus. (a) Axial T1w image showing the alveolar canal where it enters the ramus of mandible (arrow). Nasopalatine canal (arrowhead). (b) Axial T1w image showing the alveolar canal in the alveolar process (asterisk) and genioglossus (arrowheads). Mesial (curved black arrow), distal (curved white arrow), buccal (open black arrow), and lingual (open white arrow). (c) Coronal T2w image. Overview of the masticatory muscles and the mylohyoid (black arrowhead). Masseter (black arrow), medial pterygoid (white arrowhead), lateral pterygoid (white arrow), temporalis (white curved arrow), and susceptibility artefact following aneurysmal clipping (asterisk). (d) Fatsuppressed coronal T1w image. Anterior digastric belly (asterisk). Occlusal (arrow) and apical (arrowhead) in mandible.

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The following sections now elaborate on only a number of different indications.

For an overview of dental developmental anomalies, odontogenic and nonodontogenic cysts and tumors, and issues related to periodontology and implantology, please consult the relevant general dental radiology literature.16,27,36

15.4.1 Periodontitis If inflammatory processes extend beyond the pulp cavity and spread via the apical foramen at the apex of the root into the

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Fig. 15.2 Periodontitis. Inflammatory periapical change in tooth 25. (a) Axial fat-suppressed T1w sequence. Periapical signal change (arrow). Susceptibility artefact caused by crowns at the front (arrowhead). (b) Axial fat-suppressed T1w sequence following CM administration. Increase in signal intensity (arrow) with pathologic marrow cavity signal distal to that.

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Fig. 15.3 Postextraction changes. Granulation tissue on the alveolar ridge 2 months after extraction of tooth 27. (a) Axial STIR (short-tau inversion recovery) sequence. Hyperintensity distal to tooth 26. (b) Axial T1w image. Hypointensity in the empty alveolus. (c) Axial T1w image with fat suppression following CM administration. Diffuse CM enhancement in the region of tooth 27. Slight CM enhancement also in the pulp cavity attesting to vitality; can be identified for teeth 11–13 (arrows).

surrounding region, such changes will be detected on radiographs and CT images only after the adjacent bone has been resorbed and a well-defined periapical granuloma has formed. However, the patient will have experienced symptoms much earlier. The underlying causes of the clinical symptoms can be identified on T2w sequences as discrete hyperintense bone marrow signal surrounding the root, reflecting edema and inflammatory changes (▶ Fig. 15.2).10 A history of any previous surgery should be explored, as postoperative granulation tissue can mimic such changes (▶ Fig. 15.3). Following tooth extraction, the postextraction alveoli are filled with blood that is slowly eliminated and replaced with granulation tissue. In the course of weeks, bony callus is gradually formed, initially with disorganized trabeculae that later assume a more regular pattern. It is therefore normal to see hyperintense granulation tissue at the tooth extraction site

for the duration of around the subsequent 3 months (see ▶ Fig. 15.3). If periodontitis is not treated in immunocompetent patients, it can lead to formation of a radicular cyst around the root, with displacement of the adjacent trabecular or even cortical bone (▶ Fig. 15.4).

15.4.2 Osteitis and Osteomyelitis If virulent pathogens succeed in overcoming the patient’s immune system or antibiotic treatment proves to be inadequate or is initiated too late, inflammatory changes will continue to unfold within the bone marrow. The sensitivity of MRI in detecting inflammatory bone abnormalities is thought to be equal to that of scintigraphy. The specificity of MRI is superior, thanks to better soft tissue contrast and higher spatial resolution.37

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Fig. 15.4 Radicular cyst. Axial T2w sequence. Homogeneous hyperintense lesion in front mandible causing ballooning of the buccal cortex.

Fig. 15.5 Osteitis. STIR sequence. Four months after extraction of tooth 36, increasing pain and swelling. The empty alveoli are not yet covered with bone. Diffuse hyperintensity of the marrow cavity and the buccal soft tissues.

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Fig. 15.6 Osteomyelitis. Chronic recurrent symptoms 2 years after removal of implants in the right mandible. (a) Axial T2w sequence. Diffuse hypointense marrow cavity signal of the right mandible with thickening of the buccal and lingual cortex. (b) Coronal T2w sequence with fat suppression. Extensive soft tissue changes around the more hyperintense right mandibular ramus.

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Disease course: Acute stage: In the acute stage, the signal intensity is reduced on T1w images and increased on T2w images (▶ Fig. 15.5). The region of interest is poorly delineated versus the surrounding area, with, in particular peripheral, enhancement on postcontrast images. Concomitant soft tissue infiltration around the bone can be clearly visualized on T2w images, together with hyperintense necrosis. Chronic stage: In the chronic stage, the aforementioned osteomyelitic changes are identified on all sequences surrounded by hypointense sclerotic halos whose size is determined by the potency of the patient’s immune response. The surrounding soft tissues are also commonly affected (▶ Fig. 15.6).

15.4.3 Osteoradionecrosis and Bisphosphonate-Induced Osteonecrosis of the Jaw Tumor patients are at high risk of osteoradionecrosis following radiotherapy, in particular if they have poor oral hygiene and suboptimal dental status. Radiotherapy results in a reduction in the number of osteocytes, in the activity of osteoblasts, number of blood vessels, and the quality of ground substance deposition. This in turn is associated with diminished bone repair and increased microvascularization.5,31 Bisphosphonates may be administered to curtail the resurgence in bone remodeling in settings of osteolytic skeletal metastases,

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Fig. 15.7 Bisphosphonate-induced osteonecrosis of the jaw. The patient had been prescribed bisphosphonates due to mastocytosis and experienced pain in the right mandible. A long-term ulcer had not healed 2 years after tooth extraction. (a) Axial fat-suppressed T2w image. Reduced signal intensity in the molar region of the right mandible. A hypointense sequester can be identified within an area of discrete hyperintensity. (b) Parasagittal STIR image. Mesial to distal extension.

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Fig. 15.8 Submucosal retention cyst and odontogenic keratocystic tumor. (a) Coronal fat-suppressed T1w sequence following CM administration. The medial submucosal retention cyst continues to be hypointense, with only discrete increase in signal intensity at the periphery (arrowheads). The odontogenic keratocystic tumor has displaced the alveolar ridge, infiltrating the maxillary sinus and taking up some CM (arrows). (b) Axial T2w sequence. Smoothly outlined, loculated, vesicular bulging of the alveolar ridge; medial to it is the submucosal retention cyst in the maxillary sinus (arrows).

multiple myeloma, or osteoporosis.1,3 Even in healthy persons, the masticatory forces and associated repetitive microtrauma cause tissue damage, which, however, is continually repaired in healthy bone tissue and replaced with new tissue. If this remodeling process is compromised by the prescribed treatment regimen, there is a risk of mandibular necrosis, causing pain to the patient and becoming a therapeutic challenge. Typical manifestations include poor wound healing after tooth extraction, deep pockets, and, in particular periodontal, structural rarefaction with accentuated lamina dura identified on radiography. Sequesters may present in the later course (▶ Fig. 15.7).

15.4.4 Dentogenic Sinusitis Inflammatory changes of the periodontal apparatus can cause reactive mucosal swelling and mucous retention in the adjacent maxillary sinus alveolar recess. While these can be identified on both radiography and CT, only MRI is able to differentiate between these two entities and blastomous processes. Nontumorous mucosal thickening appears hypointense on T1w and hyperintense on T2w images, with moderate CM uptake. Submucosal retention cysts show only minimal CM enhancement (▶ Fig. 15.8). Tumors tend to exhibit intermediate signal intensity on T2w sequences.

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Fig. 15.9 Sinus lift. (a) Axial T1w sequence with fat suppression. Homogeneously hypointense augmentation material on the floor of the left maxillary sinus. (b) Axial T1w sequence with fat suppression following CM administration. Slight enhancement of the augmentation material and only very delicate oral mucosa.

The signal intensity seen in association with mucous retention is determined by its age as well as its water and protein content.30 Initially, such secretions contain up to 95% water and 5% macromolecular protein, with long T1 and T2 relaxation time. As the secretions become thicker, with a protein content of between 5 and 25%, there is clear evidence of a shorter T1 relaxation time and increase in signal intensity on T1w sequences. From a protein content of 35 to 40%, there is a sharp rise in direct crosslinking between the protein molecules and dipole–dipole dephasing. This shortens the T2 relaxation time to such an extent that the secretions appear hypointense on both T1w and T2w sequences. However, there is never any increase in signal intensity following CM administration, thus making it possible to distinguish secretions from tumor.

15.4.5 Pulp Vitality In the event of single tooth loss because of trauma, for endodontologic or other reasons, a devitalized tooth can be replaced with a less needed adjacent tooth so as to try to establish a connection between the vessels of the tooth bed and the pulp via the apical foramen. To date, attempts have been made to demonstrate the vitality of such tooth transplants with laser Doppler techniques, but this can be challenging due to the absence of spatial resolution.23 That obstacle has now been surmounted on using MRI as a tool to evaluate the signal intensity of the pulp cavity following CM administration and, based on the presence or absence of perfusion, draw conclusions on pulpal vitality (see ▶ Fig. 15.3c).20

15.4.6 Implantology In the event of single or multiple tooth loss, fixed implants can be fitted in the alveolar process and then a fixed dental prosthesis is mounted on the implant. If the edentulous phase lasts for some time, bone loss will result from the lack of loading, negatively impacting both the quality of the trabecular bone and the vertical and horizontal dimensions of the alveolar ridge. Preoperative

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assessment of the bone status is therefore performed with radiography or CT, and the anticipated spatial relationship between the implant to be fitted and the existing anatomic structures (alveolar canal, maxillary sinus, and paranasal sinus floor) determined.6 In some patients, differentiation between the cortical margin of the alveolar canal and the surrounding trabecular bone is so poor that MRI should be used to that effect.18 In settings of severe bone atrophy, the alveolar ridge must be filled with bone prior to fitting the implant (iliac crest, hydroxyapatite). Several terms are used to denote this surgical technique: ● Sinus lift. ● Sinus floor elevation. ● Alveolar ridge augmentation. The augmentation material manifests initially as being more dense and heterogeneous than normal bone on radiography and CT. Impaired healing is identified on CT only in the late stage following sequestration. After just a few weeks of implantation, MRI is able to detect on all sequences within the slightly heterogeneously hypointense augmentation material an increase in signal intensity as a sign of restored angiogenesis (▶ Fig. 15.9 and ▶ Fig. 15.10).4,13 Only then are there prospects for successful implant fixation.

15.4.7 Differentiation between Solid and Cystic Changes In settings of extensive jawbone lesions, MRI can provide for better tissue typing, thus facilitating preoperative management.9 Physiologic variants, such as exostoses and tori, can be distinguished from actual, space-occupying masses requiring treatment (▶ Fig. 15.11). Thanks to good soft tissue differentiation, a distinction can be made between cystic and solid components (▶ Fig. 15.12). MR angiography (MRA) is adept at assessing extension of highly vascularized lesions (▶ Fig. 15.13). Optimized neurovascular bundle evaluation also makes it easier to classify

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Fig. 15.10 Sinus lift. Other patient. (a) Axial T2w image. Impaired healing on the right, with central hyperintensity, susceptibility artefact on the left. (b) Coronal T1w image with fat suppression following CM administration. Heterogeneous enhancement, right, susceptibility artefact, left.

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Fig. 15.11 Palatal torus. Young female patient had felt a hard swelling in her palate. (a) Sagittal T1w sequence. Bone-isointense protrusion of the hard palate. (b) Coronal T2w sequence with fat suppression. The fatty marrow of this normal variant appears hypointense.

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Fig. 15.12 Hemorrhagic bone cyst. Osteolysis of the front mandible was an incidental finding in a young girl undergoing dental examination. (a) Axial T2w image. Fluid-isointense, but nonresorptive, lesion causing displacement of the roots. (b) Axial T1w image with fat suppression. Discrete peripheral CM enhancement.

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Fig. 15.13 Maxillary hemangioma. Unilateral, elastic swelling of the soft palate. (a) Axial T1w sequence. Smoothly outlined, homogeneous, isointense to muscle, protrusion of the left alveolar ridge to the oral cavity. The distance between the teeth is somewhat increased compared with the contralateral side. (b) Coronal T1w sequence with fat suppression. Intense CM enhancement with preserved oral mucosa and no swelling of the maxillary mucosa. Phleboliths (arrows) manifesting as areas devoid of signal. (c) MRA. Extensive vascularization.

neural neoplasms (▶ Fig. 15.14). The topographic relationship between neoplasms of the jaw and the adjacent structures, infiltration of the bone marrow, and any involvement of the orbits, base of skull, and paranasal sinuses are characterized before instigating antineoplastic treatment (▶ Fig. 15.15).

15.5 Clinical Relevance of Magnetic Resonance Imaging Although radiography and CT give insights into the likely dignity of a process, they do not permit histology-based diagnosis, nor should that be attempted. In addition to exact determination of a

lesion or of its relationship to existing structures as can be done with these modalities, in the preoperative setting it may also be of interest to determine which components are cystic and which are blastomous. It is here that MRI with superior soft tissue resolution comes into play. Detailed assessment of the bone marrow and of vascularization is also the preserve of MRI.

Clinical Interview

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Clinical interview with Prim. Prof. Ingeborg M. Watzke, President of the Austrian Society of Oral and Maxillofacial Surgery, Board of Directors: Maxillofacial Surgery: SMZ Ost Donauspital Vienna, Langobardenstraße 122, A-1220 Vienna.

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Fig. 15.14 Schwannoma of the inferior alveolar nerve. Pain and hyperesthesia of the left mandible. (a) Axial T1w image. Bulging of the left inferior alveolar nerve (arrow) at the mandibular foramen. (b) Parasagittal T2w image. Spindle-shaped course (arrowheads). Medial pterygoid (curved white arrow), lateral pterygoid (curved black arrow).

Question: “What role do X-rays play for you?” Answer: “They are very important. Around 95% of our patients need an X-ray before starting treatment.” Question: “For which clinical manifestations or constellation of findings are false-positive MRI results most commonly encountered? ” Answer: “In the case of abscesses, especially in the oral cavity or neck region, their extension is often overestimated.” Question: “For which disorders or constellation of findings do you encounter false-negative MRI results most often and why were diagnostic measures continued in such cases?”

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Answer: “We rarely encounter false-negative MRI results assuming that patients are referred only after taking a precise history and thorough clinical examination.” Question: “For which clinical manifestations can MRI be omitted and for which is the modality overly used?” Answer: “For the above reasons we avoid referring patients with suspected abscesses in the region of the mouth, jaw, or face for an MRI scan.” Question: “What impact do you think that the radiology results have on your further management of the patient?” Answer: “In most cases, it is further corroboration of the clinical diagnosis made based on the patient history.”

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Fig. 15.15 Maxillary rhabdomyosarcoma. Bulging of the maxilla in a 2-year-old girl. (a) Axial T2w sequence. The alveolar ridge of the left maxilla has been displaced by a tumor. The masticatory muscle boundary has been preserved. Expanded pulp cavity of primary teeth (arrowheads), anlagen of the permanent teeth (arrows); medial pterygoid (curved white arrow), masseter (curved black arrow). (b) Fat-suppressed T1w sequence following CM administration. The tumor that shows intense CM enhancement has caused ballooning of the ipsilateral maxillary sinus and ethmoid, filling the adjacent nasal cavity and elevating the orbital floor, following spread of tooth pathogen (arrow). (c) Parasagittal T2w sequence. The orbital floor cannot be delineated; so far no infiltration of the intraorbital fatty tissue.

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in relation to cystic processes of the mandible in dental MRI [in German].

imaging and quantification of carious lesions and dental pulp in vivo. Magn

RoFo Fortschr Geb Rontgenstr Nuklearmed. 2003; 175(1):67–69 [20] Kress B, Buhl Y, Anders L, et al. Quantitative analysis of MRI signal intensity as a tool for evaluating tooth pulp vitality. Dentomaxillofac Radiol. 2004; 33 (4):241–244 [21] Kress B, Gottschalk A, Anders L, et al. High-resolution dental magnetic resonance imaging of inferior alveolar nerve responses to the extraction of third molars. Eur Radiol. 2004; 14(8):1416–1420 [22] Markiewicz H, Kubani M, Stelmaszczyk W, et al. Magnetic resonance imaging in dental implant planning - an application attempt. In:

Res Mat Phys Biol Med. 2009; 22(6):365–374 [34] Tymofiyeva O, Vaegler S, Rottner K, et al. Influence of dental materials on dental MRI. Dentomaxillofac Radiol. 2013; 42(6):20120271 [35] Yilmaz S, Misirlioglu M. The effect of 3 T MRI on microleakage of amalgam restorations. Dentomaxillofac Radiol. 2013; 42(8):20130072 [36] Youssefzadeh S, Gahleitner A, Bernhart D, Bernhart T. Conventional dental radiography and future prospectives [in German]. Radiologe. 1999; 39 (12):1018–1026 [37] Zynamon A, Jung T, Hodler J, et al. Das Magnetresonanzverfahren in der Diagnostik der Osteomyelitis. Fortschr Röntgenstr. 1991; 155:513–517

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[9] Fujita M, Matsuzaki H, Yanagi Y, et al. Diagnostic value of MRI for odontogenic

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Other Disorders and Diagnoses

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Other Aspects of Magnetic Resonance Imaging of the Musculoskeletal System

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References

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Chapter 16

Appendix

16 Appendix M. Vahlensieck

16.1.1 Differential Diagnosis of Swollen Extremities on Magnetic Resonance Imaging Diffuse swelling of one or more extremities can at times present a diagnostic challenge. The diagnostic procedures employed include, in addition to clinical examination, invasive techniques such as phlebography (venography). However, magnetic resonance imaging (MRI) is a noninvasive diagnostic modality that can be used in such settings.15

Venous Edema Venous edema is caused by venous stasis in association with thrombosis, chronic venous insufficiency, heart failure, etc., and depending on the underlying cause, it may be uni- or bilateral. Venous edema manifests as pitting, compressible swelling, affecting also the dorsum of hand or foot. Chronic courses lead to induration. The following findings are seen on MRI: ● Diffuse muscle edema with increased signal intensity on T2 weighted (T2w) images. ● Increased signal intensity of the subcutaneous tissues, too. ● Following contrast medium (CM) administration, enhancement of the muscle compartment. ● Cross-sectional enlargement of the muscle compartment.

Lymphedema Lymphedema manifests as indurated, noncompressible, generally unilateral swelling with involvement of the dorsum of hand or foot. A distinction is made between primary and secondary forms with different stages (reversible swelling, irreversible swelling, elephantiasis). On T2w MR images, the following signs are observed: ● Marked increase in signal intensity of the subcutaneous tissues with accentuation of the subcutaneous fibrous connective tissue (honeycomb pattern; ▶ Fig. 16.1). ● Normal signal intensity of the muscles. ● Marked thickening of the subcutaneous tissues but generally no increase in muscle compartment cross-section. ● Enhancement of the subcutaneous tissues following CM administration.

Lipoid Edema Lipoid edema causes noncompressible bilateral swelling, but without involvement of the dorsum of hand or foot. It is a form of lipomatous hypertrophy that mainly affects obese women older than 20 years. The following signs are identified on MRI: ● Massive increase in subcutaneous fat with normal visualization of the muscle compartment. ● Normal signal intensity.

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Mixed forms with different degrees of severity of the above-mentioned patterns are commonly seen. Other causes of swelling of the extremities, such as angioma or Sudeck’s disease, can generally be ruled out on the basis of the patient history as well as the clinical and morphologic criteria.

16.1.2 The Skin, Subcutaneous Tissues, and Fascia Soft Tissue Infections Cellulitis There is one type of skin and subcutaneous infection that gives rise to the clinical picture of erysipelas. This condition is mainly caused by streptococci and is also known as “cellulitis.” It results in discrete skin thickening as well as in inflammatory edema of the subcutaneous tissues. These changes can be clearly identified on sectional imaging. On MRI, they appear as areas of high signal intensity, especially on fat-suppressed T2w images. Differential diagnosis should include lymphedema. Cellulitis generally encompasses the entire circumference of an extremity and has a honeycomblike arrangement. However, the edema pattern seen in settings of cellulitis is more localized and indistinct (▶ Fig. 16.2).

Fasciitis Fasciitis is a soft tissue infection that has spread to the muscle fasciae or predominantly affects this region (▶ Fig. 16.3). Fasciitis is associated with more severe symptoms than those caused by cellulitis alone. Fascial thickening can be identified on sectional imaging, with more intense enhancement on postcontrast images.

Necrotizing Fasciitis Fulminant courses of disease lead to extensive necrotization of the fascia, termed “necrotizing fasciitis.” Emergency surgery is called for since only timely debridement can reduce the high fatality rate. Several pathogens are known to cause this condition,43 often manifesting as mixed infection attributable to the resident skin and mucosal flora. Clostridium perfringens infection typically leads to gas accumulation. In recent times, group A streptococci has been increasingly implicated in this infection; among the systemic complications of necrotizing fasciitis imputed to group A streptococci is streptococcal toxic shock syndrome with multiorgan failure.25,30 Fournier gangrene is an eponymous term for fasciitis of the perineum first described in 1883. Predisposing factors for development of necrotizing fasciitis include: ● Wasting diseases. ● Immunodeficiency. ● Chronic renal failure. ● Diabetes. ● Alcoholism. ● Other forms of drug abuse. ● Undernutrition.

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16.1 Other Disorders and Diagnoses

Fig. 16.1 Mamma carcinoma and massive lymphedema of the left forearm. Axial MRI. This female patient has severe swelling of the skin and subcutaneous tissues due to fluid accumulation (arrows, honeycomb pattern), with low signal intensity on the T1w image, high signal intensity on the T2*w and fat-suppressed image. No abnormal fluid accumulation of the muscles. (a) T1w SE sequence. (b) T2*w GRE sequence. (c) Fat-suppressed STIR sequence.

Men are affected more often than women. Apart from the perineum, the extremities and the neck region are frequently involved. Clinical symptoms include severe pain, crepitation in cases of gas-forming necrotizing fasciitis, as well as skin discoloration and vesiculation in the late stages. Other signs are fever, leukocytosis, and clouding of consciousness or even shock in the later stages.6,26,32 Pronounced thickening of the fascia with irregular central areas of fluid-equivalent necrosis can be seen on sectional imaging.5,7, 29,39,45 Concomitant myositis or myonecrosis of the adjacent muscles manifests in the later stages. Soft tissue infections caused by anaerobic bacteria generally give rise to gas accumulation in soft tissues which is readily identifiable on overview radiographs. CT is superior to MRI for detection of gas in suspected anaerobic infection.

Eosinophilic Fasciitis (Fasciitis Panniculitis Syndrome) Thickening of the fascia is also observed on sectional imaging in cases of chronic disease of the fascia of rheumatic etiology. This disease is characterized as being “sclerodermalike” and is accompanied by eosinophilia, hypergammaglobulinemia, and accelerated blood sedimentation rate. This constellation of findings is termed “eosinophilic fasciitis” (fasciitis panniculitis syndrome).1 Patients notice slow, progressive thickening of the skin, in particular of the arms and lower legs. Other symptoms include increasing muscle weakness. While the exact etiology is unknown, intensive athletic exercise is thought to be the trigger in certain cases.28 Diagnosis is confirmed on deep skin or muscle biopsy. The disease is treated with corticosteroids.

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Fig. 16.2 Fasciitis and cellulitis. Schematic diagram of the axial plane. (a) Cellulitis (erysipelas) with skin thickening and subcutaneous edema. (b) Fasciitis with skin thickening, subcutaneous edema, and fascial thickening. (c) Differential diagnosis versus lymphedema identified no thickening of the skin or fasciae. Subcutaneous edema is homogeneous, often affecting extensive parts or the entire circumference of the implicated extremity. (d) Necrotizing fasciitis with skin thickening, subcutaneous edema, fascial thickening, necrosis, and concomitant myositis.

Fig. 16.3 Fasciitis. Calf pain of sudden onset, slowly progressing. Increasing signs of inflammation. Axial STIR image. Fluid-equivalent signal intensity along the lower leg fascia, in the subcutaneous fatty tissue as well as in parts of the calf muscles as a sign of fasciitis. Still no sign of necrosis.

Fig. 16.4 Chronic soft tissue inflammation of the upper arm stump following amputation with fistula formation. Extensive soft tissue infection with diffuse increase in signal intensity on STIR image, signal-void foreign body or bone abrasion (b, arrow) and clear evidence of fistula formation (c, arrow). This female patient had suffered from pain and, over the previous weeks, had purulent secretions from the fistula opening. No bone involvement. (a) Axial STIR image. (b) Coronal T1w image. (c) Coronal CM enhanced image.

On MRI, increased signal intensity is identified on T2w images and intense CM uptake by the thickened subcutaneous and deep muscle fascia. Skin thickening is also observed.

Fistula Formation A soft tissue fistula may develop in settings of chronic soft tissue infections or osteomyelitis. Fistula duct extension can be determined on fistulography, but in most cases this can also be accomplished on sectional imaging. In general, enhancement of the fistula duct is seen on postcontrast MR images (▶ Fig. 16.4).

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Fatty Tissue Diseases Lipoatrophy Lipoatrophy (circumscribed lipoatrophy) is the term used to describe more or less severe, discrete, loss of subcutaneous fatty tissue which occurs for generally unknown reasons. The patient history often points to an impact injury in this region. This condition may also be observed in association with subcutaneous injections. The clinically manifested tissue indentation engenders anxiety in the patient, and the disease is mainly misinterpreted as muscle atrophy.

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Fatty Tissue Necrosis Fatty tissue necrosis may be encountered in association with various diseases, such as collagenosis, myeloproliferative syndromes, pancreas disorders, and trauma (bruises, contusion, laceration), or may present without any apparent cause. Predilection sites are the subcutaneous tissues above bony protuberances and the mammae. While in most cases fatty tissue necrosis is not

accompanied by any clinical symptoms, symptoms such as the following may be observed in other situations: ● Indurated mass. ● Changes in the overlying skin due to retraction or thickening. ● Pain. ● Feeling of tightness. On MRI, various changes can be identified in accordance with the stage of fatty tissue necrosis. For example, in the early stage an edematous pattern with swelling and areas of poorly defined, streaked, or extensive signal intensity changes and CM uptake can be observed. In some cases, the fatty tissue exhibits nodular lobulation, while liquefaction with cystic components may be rarely observed (colliquation secondary to saponification; ▶ Fig. 16.6).36 Longstanding fatty tissue necrosis tends to manifest as a discrete, racemose, lobulated mass interspersed with hypointense septa, with fat-equivalent signal intensity on T1w images and high signal intensity on T2w images, particularly high signal intensity on fat-suppressed images, and no CM uptake (▶ Fig. 16.7 and ▶ Fig. 16.8).13 Dystrophic, also ring-shaped, calcification is common. In settings of malnutrition, in particular undernutrition such as kwashiorkor or anorexia nervosa, increased lipolysis can give rise to CM-enhancing fatty tissue edema, which can also manifest as fatty bodies containing structural fat, such as orbital fat. Fat-suppressed MR images are best for visualization of edema; intense CM uptake may be observed.14

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MR sectional imaging is able to localize tissue loss to the subcutaneous fat (▶ Fig. 16.5).

Detection of Changes of the Skin and Subcutaneous Tissues on Magnetic Resonance Imaging in Association with Skin Diseases Fig. 16.5 Circumscribed lipoatrophy. This male patient noticed increasing indentation of the left gluteal region over the previous months. MRI was performed to rule out muscular dystrophy. Axial T1w SE image. Loss of substance of the subcutaneous fat, left; asymmetrical gluteal muscles. The cause of this could not be established from the patient’s history.

a

Thickening of the skin may be observed on MRI and is associated with several skin diseases, for example: ● Scleroderma. ● Other forms of collagenosis. ● Pachyderma.

b

Fig. 16.6 Colliquation in association with fatty tissue necrosis. Male patient with slightly painful mass of unknown origin on the lower leg. No recollection of trauma. (a) Axial T1w sequence. (b) Axial PDw fatsat sequence. Edema of the subcutaneous fatty tissue (black arrow), central, fluidequivalent mass, consistent with colliquation (white arrow) in association with fatty tissue necrosis.

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Fig. 16.8 Gluteal fatty tissue necrosis. Coronal STIR sequence. Young female athlete. Increasing gluteal pain of sudden onset, bilateral. No sign of inflammation. Slow improvement over the ensuing course. Edematous changes of the subcutaneous fat, bilateral gluteal, consistent with spontaneous liponecrosis.

16.1.3 Chronic Sports Injuries

Fig. 16.7 Gluteal fatty tissue necrosis. Young woman with gluteal symptoms of spontaneous onset, left. No trauma, metabolic or other diseases. On STIR contrast image, very high signal intensity lesion in the subcutaneous fatty tissue, left, no space-occupying effect. Narrowing of the subcutaneous fatty tissue halo. The symptoms improved and fully resolved in the later clinical course. Based on the patient history as well as the localization and the signal intensity this is thought to be a case of spontaneous fatty tissue necrosis (liponecrosis). (a) T1w sequence. (b) STIR sequence.

● ● ●

Scleredema adultorum of Buschke. Scars. Stiff skin syndrome.24

Inflammatory skin diseases (see Chapter 16.1.2) cause thickening of the skin and subcutaneous connective tissue septa with CM enhancement and reduction in the volume of the subcutaneous fat lobules.

Soft Tissue Detected on Magnetic Resonance Imaging Following Radiotherapy Radiation-induced edema of the soft tissues is seen within the radiation field in patients undergoing radiotherapy. This edema can be identified as a diffuse increase in signal intensity on T2w, and especially on STIR, images of the skin, subcutaneous tissues, and intramuscular septa. This persists from a few months to several years after termination of radiotherapy, in particular in the intramuscular septa. It can be distinguished from tumor recurrence based on the absence of a space-occupying effect as well as the preserved anatomy of the underlying structures.35

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With the growing trend among the population to engage in sporting activities, physicians are increasingly encountering injuries resulting from sports-associated overloading. Depending on the type of overloading implicated, a broad spectrum of different disorders and syndromes can present in a single region, as illustrated in ▶ Fig. 16.9 by way of example for the elbow region. ▶ Table 16.1 lists a number of common types of overloading injuries, classified in terms of the body region affected. There is a particularly high incidence of many of these injuries when engaging in certain types of sports, and these have their own specific terminology.17,34,42 As such, these disorders are classified on the basis of the types of sports involved. The terms usually employed by sports medicine doctors are shown in italics in the table. Many of these overloading syndromes have an MRI correlate. To interpret the MR images, it is therefore vital to take a history of any sporting activity and be familiar with the pattern of injuries normally encountered. Table 16.1 gives an overview of such injuries. The MRI signs and visible changes are explained in the various sections of this chapter.

Iliotibial Band (Tract) Syndrome Iliotibial band (tract) syndrome is a special type of overuse injury in that it can present in body regions very far apart. It often occurs in distance runners. The iliotibial band is a thickened fibrous bundle of the fascia lata running along the outer aspect of the thigh from the ilium to the lateral tibial condyle. It receives fibers from the gluteus maximus and the tensor fasciae latae muscles. Distance runners may develop insertional tendinopathy at the iliac crest, trochanteric bursitis, or tendinitis and bursitis in the knee region due to repetitive strain (▶ Fig. 16.10).

Snapping Phenomena Sports injuries also include temporary dislocation or subluxation of tendons or nerves known as “snapping phenomena.” These can cause pain and popping/clicking sounds and can at times be

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Exostosis (overuse injury) Medial epicondylitis (golfer’s elbow) Lateral epicondylitis (tennis elbow)

Elbow nerve inflammation

Lateral ligament tear

Olecranon wear

Chondromalacia/radial head fracture

Osteoarthritis Medial ligament strain Olecranon spur

Coracobrachialis insertion strain

Osteochondrosis

Supinator syndrome Biceps insertion strain

a

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Subluxation of radial head (pulled elbow) b

Fig. 16.9 Elbow region. Schematic diagram of the elbow region depicting the variable nature of sports-associated overloading injuries. (a) Anterior view. (b) Posterior view.

Table 16.1 Some common chronic sports injuries Body region

Type of sport

Shoulder

Throwing sports (especially baseball) Posterior extension injury of the rotator cuff Traction injury of the biceps and triceps insertion ( thrower’s exostosis) Anterior capsular laxity Anterior impingement of the rotator cuff (thrower’s arm) Fatigue fracture of the proximal humeral epiphysis (little leaguer’s shoulder)

Elbow

Wrist

Injury

Swimming

Impingement syndrome (swimmer’s shoulder)

Tennis

Impingement syndrome (often subscapularis, infraspinatus) Instability

Weightlifting

Osteolysis of the distal clavicle

Ice hockey

Secondary acromioclavicular osteoarthritis following subluxation

Gymnastics

Impingement syndrome Muscle sprain (wrestler’s shoulder)

Golf

Impingement syndrome (golfer’s shoulder)

Throwing sports

Ulnar nerve compression syndrome/subluxation Median nerve compression syndrome Radial nerve compression syndrome Contracture Medial epicondylitis Pronator teres syndrome Ulnar lateral instability Olecranon spur

Golf

Medial epicondylitis (golfer’s elbow)

Squash

Elbow spur

Badminton

Coronoid process spur

Tennis

Lateral epicondylitis (tennis elbow) Epicondylar apophysitis (little leaguer’s elbow)

Weightlifting, fencing

Insertional tendinopathy of the triceps on the olecranon

Cycling

Ulnar nerve compression syndrome (handgrip paralysis)

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Appendix

Body region

Hand/Finger

Hip

Knee

Ankle

Foot

Type of sport

Injury

Gymnastics

Compression syndrome Ganglion cysts Instability Chondromalacia Triangular fibrocartilage complex injuries

Rowing

Peritendinitis Myotendinitis of the radial extensors

Polo

Chondromalacia of the pisiform

Golf

Peritendinitis

Rock-climbing

Annular ligament injury

Handball

Median nerve paresis (typical: thenar atrophy) Ulnar collateral ligament injury—metacarpophalangeal joint of the thumb (scorer’s thumb)

Boxing

Bursitis of the third metacarpal head (“Quentitia” bursitis, boxer’s fist)

Fencing

Finger flexor tendonitis (trigger finger)

Water skiing

Deep radial nerve paralysis

Pitching

Impingement due to prominent styloid process of the third metacarpal or styloid (carpe bossu, carpal boss)

Bowling

Perineural fibrosis (neuroma) of ulnar digital nerve of the thumb (bowler’s thumb)

Repetitive “hip flexion”

Iliopsoas tendinopathy of the lesser trochanter Nerve compression syndrome due to muscle hypertrophy

Running, rowing

Iliotibial band syndrome

Riding

Adductor sprain

Jumping

Patellar tendinitis (10% tibial, 65% patellar) Quadriceps tendinitis (25% jumper’s knee)

Cross-country skiing

Peroneal nerve compression of the fibular head

Swimming

Anserine bursitis (breaststroker’s knee)

Running

Bursitis Iliotibial band syndrome

Tennis, ball sports, running

Tendinitis of the Achilles tendon

Jogging

Tibial stress reactions

Poor footwear

Achilles tendon bursitis

Various types of sports

Plantar fasciitis Tarsal tunnel syndrome (tibialis posterior nerve)

detected during MRI functional imaging of a joint in different positions based on dislocation of tendons or a nerve. A snapping hip is a relatively common type of snapping phenomenon seen in the hip region where, in the external type, the thickened posterior margin of the iliotibial band or the anterior margin of the gluteus maximus slides over the greater trochanter, giving rise to secondary trochanteric bursitis. In the internal or deep type of snapping hip, the iliopsoas tendon slides over the iliopectineal eminence. Other snapping phenomena have been described for the wrist (see Chapter 5.10) and elbow (see Chapter 4.7.2).

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16.2 Other Aspects of Magnetic Resonance Imaging of the Musculoskeletal System 16.2.1 Magic Angle Phenomenon Certain tissues, such as cartilage and tendons, exhibit a different (anisotropic) signal pattern when their orientation relative to the main magnetic field is changed. This is due to the dependence of the T2 relaxation time on the spatial orientation of the tissue.8,9,18 Because of the particular spatial arrangement of the collagen

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Table 16.1 continued

16.2 Other Aspects of Magnetic Resonance Imaging of the Musculoskeletal System

3cos2@  1 where ∂ = angle between the main magnetic field (B0) and a vector of neighboring protons.

Ilium Insertional strain

Trochanteric bursitis

Inflammatory irritation of the lateral femoral condyle

Fig. 16.10 Iliotibial band. Schematic diagram illustrating the iliotibial band and its vulnerable sites when subjected to overloading in distance runners or rowers.

A decrease in spin–spin coupling prolongs the T2 relaxation time. The spin–spin coupling is minimal for (3 cos2∂ – 1) = 0, as occurs for ∂ = 55 and 125 degrees. These angles are known as the “magic angle.” The orientation of the collagen fibrils does not affect the T1 and T2* relaxation times. The effect on the T2 time is more pronounced at a higher field strength. The prolongation of the T2 relaxation time of tendons can be relatively marked. Longitudinally oriented tendons (∂ = 0 degrees) have T2 times of 250 s. When positioned at 55 degrees relative to the main magnetic field, T2 times of up to 22 ms are measured.18 That effect means that tendons positioned at an angle of 55 degrees to the main magnetic field exhibit an artificial increase in signal intensity on sequences with a relatively short TE.16 That effect is most pronounced on proton density-weighted (PDw) images but is scarcely noticeable on sequences with TE well above 22 ms and the tendons appear hypointense regardless of their orientation. This phenomenon has major clinical implications since an increase in the signal intensity of tendons can be caused by inflammation, hemorrhage, or partial tears. If there is any diagnostic uncertainty, the possibility of an artificial increase in signal intensity induced by the magic angle phenomenon should be ruled out with an additional strong T2w sequence or by applying an magnetization transfer contrast (MTC) pulse. The MTC pulse can suppress this anisotropic effect. The body regions hitherto known to be affected by this phenomenon are as follows: ● Rotator cuff insertion in the shoulder. ● Flexor tendons of the ankle. ● Wrist tendons (▶ Fig. 16.11).16

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fibers in tendons and cartilage, the spin–spin coupling of protons is negatively affected by the orientation of the magnetic field because of dipole interactions. This is expressed by the following formula:

These orientation-induced changes in signal patterns can also be observed for hyaline joint cartilage38 but are of virtually no significance for clinical diagnosis. At most, in certain orientations, the normally visible hyaline cartilage layers can no longer be identified. Other tissues, such as the kidneys, muscles, or white matter, are not subject to anisotropy of the relaxation times when positioned differently relative to the magnetic field. The occurrence of magic angle effects depends on the orientation of the main magnetic field. For vertical magnetic fields, for example, in open

Fig. 16.11 Magic angle phenomenon. Wrist, axial plane. Identical parameters (PDw SE sequence, TR = 1,800 ms, TE = 20 ms), same window setting, similar section through the carpal tunnel. In the flexed position, higher signal intensity exhibited by the flexor tendons due to the magic angle phenomenon (arrows). (a) The hand is stretched and parallel to the main magnetic field (longitudinal axis of the scanner). (b) The arm was flexed at the elbow such that the lower arm was at an angle of 40 to 50 degrees relative to the orientation of the main magnetic field.

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Appendix

16.2.2 Use of Dedicated Systems Dedicated MRI systems are compact scanners designed to image only specific portions of the body without enclosing the entire body. They are based on permanent or resistive magnets with relatively low field strengths (around 0.2–0.3 T). However, dedicated systems with higher field strengths (up to 1.5 T) have also been introduced in the meantime. A scanner with a 1,000 kg permanent magnet and 0.18 T magnetic flux density has been specially designed for diagnostic imaging of the extremities (ARTOSCAN, manufacturer: Esaote Biomedica, Genua, in Germany: Lunar Deutschland). Another scanner is being marketed by the firm Magna-LAB under the name “Magna-SL.” It operates at 0.3 T and lends itself to motion studies, thanks to its open design. Dedicated systems have the advantage of low production and operating costs as well as reduced space requirement compared with the expensive high field scanners based on superconductors. The drawbacks are the lower signal-to-noise ratio (SNR) and the inability to perform whole-body imaging.44 For example, the ARTOSCAN scanner design does not permit imaging of the shoulder or hip. The lower SNR leads to images with either lower spatial resolution or higher noise level which, if unacceptable, can be offset by longer acquisition times for image generation (=lower patient throughput). The theoretically expected value of a 5- to 16-fold lower SNR afforded by an 0.2 T scanner compared with a 1 T system is reduced in practice to a value of 3 by making technical improvements with smaller readout gradients and lower receiver bandwidths.35 The T1 and T2 relaxation times are 40 to 50% shorter at 0.2 T compared with 1 T. Chemical shift artefacts are comparable. In terms of image quality, dedicated systems are susceptible to geometric distortion by several pixels. Because of the low receiver bandwidth, the minimum TE of dedicated systems is over 20 ms.41 The experiences gained on using the ARTOSCAN system for imaging the joints have demonstrated that satisfactory results were obtained in around 90% of cases of diagnostic imaging of the knee.12,22 Positive experiences have also been reported for diagnostic imaging of the wrist,23 ankle, elbow, and the peripheral tubular bones.19 Comparative studies of the wrist have attested to satisfactory diagnostic reliability of dedicated systems in detecting 90% of pathologic lesions in general10 and, in particular, occult wrist fractures.11 However, tumors exceeding the relatively small measurement field as well as grading of fractures, which has implications for treatment and prognosis, proved to be a challenge. Patients with persistent complaints but no evidence of a pathologic lesion when imaged with a dedicated system should be scanned again with a high field system.10 Comparison of a dedicated system with a 1.5 T high field system for meniscus imaging attested to similarly high accuracy (concordance: 98.7%) but with significantly lower diagnostic reliability.33 Dedicated systems did not prove satisfactory in detecting anterior cruciate ligament tears, being able only to identify direct signs of rupture (discontinuity). Detection of indirect signs was deemed unreliable.4

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Dedicated systems, like open systems, are suitable for claustrophobic patients. However, only minor differences were found on comparing the acceptance of various MRI systems among nonclaustrophobic patients.21 In recent times, the advent of dedicated systems has increasingly raised issues regarding professional and occupational interests for the diagnostic radiologist.12,31 In view of the aforementioned drawbacks, it is likely that the main focus in the future will continue to be on the development and use of whole-body systems, which are also able to meet the frequent requests for orthopaedic examination of the spine as well as the shoulder and hip. With the development of conductor materials able to assure high temperature superconductivity, it may be possible to dispense with the expensive and cumbersome practice of having to cool down the superconductors with liquid helium. Accordingly, this could help to reduce the procurement and operating costs of these high field scanners.

16.2.3 Use of 3 Tesla Systems Thanks to the ongoing advances in MRI technology, 3 T systems are now routinely used, with attendant clinical benefits. A higher SNR can be expected in principle because of the high field strength. This has already been exploited in neuroradiology and spectroscopy to save time or improve spatial resolution. Similarly positive experiences have been reported by publications for studies of the musculoskeletal system.27 However, it should be noted that the T1 relaxation times are 30 to 45% longer at 3 T, and the T2 times are up to 10% shorter. That means that certain parameters must be brought into line with the 3 T boundary conditions to assure optimum image contrast. Another shortcoming is that the permissible limits for the specific absorption rates—in particular, on turbo spin-echo (TSE) sequences—are reached sooner, and this can in some cases considerably prolong the measurement time. In the meantime, a number of techniques have been developed to overcome such obstacles and increase 3 T attractiveness for many applications. Such techniques include parallel imaging, variable refocusing techniques (permit lower specific absorption rate), coils, and direct digitization in the coil (helps to reduce electronic noise, i.e. improves SNR). The development of multichannel transmit/receive coils has been particularly advantageous. These can be used to drastically reduce high frequency radiation compared with the body coil (generally used to that effect) for the same sequences. This in turn provides for a much shorter measurement time with, at the same time, higher resolution. These benefits of higher isotropic resolution can be exploited not only for 2D but also 3D images, making, for example, 3D images of the knee less susceptible to pulsation artefacts (▶ Fig. 16.12). Whether, in addition to enhanced signal or potentially higher resolution, 3 T scanners can bestow the clinical advantage of higher sensitivity and specificity than that afforded by 1.5 T systems must yet be demonstrated by systematic studies. Besides, susceptibility to artefacts increases in line with the field strength, with, in particular, more pronounced susceptibility effects. Older 3 T systems had the drawback that, especially on TSE sequences, the permissible limits for the specific absorption rate were reached sooner with attendant prolongation of the measurement time. These obstacles can be surmounted using novel techniques such as parallel imaging (SENSE [sensitivity encoding], GRAPPA

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high field systems (see Chapter 16.2.4 p. 657), such signal patterns are observed accordingly at other sites.

a

b

c

d

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16.2 Other Aspects of Magnetic Resonance Imaging of the Musculoskeletal System

Fig. 16.12 MR images of the knee at 3 T. Sagittal PDw fatsat images. Fewer pulsation artefacts in 3D measurement technique. (a) 2D measurement technique with 0.4 mm × 0.4 mm × 3.0 mm resolution and 3:04 min measurement time (slice 1). (b) 2D measurement technique with 0.4 mm × 0.4 mm × 3.0 mm resolution and 3:04 min measurement time (slice 2). (c) 3D measurement technique with sagittal reformatting (slice 1). 0.62 mm3 isotropic dataset reformatted to 3 mm slice thickness, 6:38 min measurement time. (d) 3D measurement technique with sagittal reformatting (slice 2). 0.62 mm3 isotropic dataset reformatted to 3 mm slice thickness, 6:38 min measurement time.

[generalized autocalibrating partially parallel]) and variable flip angle refocusing techniques (FAS [flip angle sweep], Hyperecho) and, to an extent, the measurement times can even be shortened. Off-center imaging is also now used in the meantime on a large scale.

16.2.4 Use of Open High Field Systems These MRI scanners are particularly suitable for claustrophobic or very obese patients (▶ Fig. 16.13). Thanks to the open design,

patients feel less enclosed and are rarely anxious.3 The open space can also be used for obtaining cinematographic motion images. Practically unhindered movement of the extremities allows for motion studies of even the shoulder and hip in real time.2 1 T systems with vertically oriented magnetic field and special coils (solenoid coils) produce excellent SNR, which is superior to I T systems with a horizontal magnetic field and is on a par with that of 1.5 T systems.20 When interpreting the images, it is important to bear in mind that magic angle artefacts can manifest in body regions different from those seen in association

657

Appendix

a

b

c

Fig. 16.14 Magic angle artefact. Artificial laminar increase in signal intensity of the proximal patellar ligament because of the magic angle on sagittal T1w TSE and PDw fatsat images (a, b, arrows) in vertically oriented magnetic field of an open high field system (Panorama). On using strong T2 weighting (120 ms) with short ED, the ligament appears normal since virtually no further occurrence of magic angle artefacts (c, arrow). (a) Sagittal T1w TSE sequence. (b) Sagittal PDw fatsat sequence. (c) Strong T2w sequence (120 ms) with short ED.

with a horizontally oriented main magnetic field. Predilection sites include the menisci at the transition to the pars intermedia, the patellar ligament (▶ Fig. 16.14), and the cartilage of the femoral condyles and retropatellar space (▶ Fig. 16.15).

16.2.5 Use of Open Spinal Systems for Upright Imaging The introduction of increasing numbers of open and dedicated systems has also seen the advent of open design scanners where patients can be imaged while sitting down (upright MRI). This

658

open design even permits a certain degree of hyperextension and flexion, and accordingly functional imaging of the lumber spine. Such examinations have the advantage over radiographs in that they are able to visualize position-related intervertebral disk dislocations or functional stenosis due to soft tissues (e.g., ligamentum flavum hypertrophy).40

Internet Link

●i

More information on this topic can be obtained using the search terms “upright mri images.”

Downloaded by: Collections and Technical Services Department. Copyrighted material.

Fig. 16.13 Open high field MRI “Panorama” (manufacturer: Philips Medizinsysteme, Hamburg, Germany). With 1 T magnetic flux density and vertical field line orientation of the main magnetic field (with kind permission of Praxisnetz Radiologie and Nuklearmedizin Bonn Bad Godesberg, RheinSieg).

16.2 Other Aspects of Magnetic Resonance Imaging of the Musculoskeletal System [13] Canteli B, Saez F, de los Ríos A, Alvarez C. Fat necrosis. Skeletal Radiol. 1996; 25(3):305–307 [14] Demaerel P, Dekimpe P, Muls E, Wilms G. MRI demonstration of orbital lipolysis in anorexia nervosa. Eur Radiol. 2002; 12 Suppl 3:S4–S6 [15] Duewell S, Hagspiel KD, Zuber J, von Schulthess GK, Bollinger A, Fuchs WA. Swollen lower extremity: role of MR imaging. Radiology. 1992; 184(1): 227–231 [16] Erickson SJ, Cox IH, Hyde JS, Carrera GF, Strandt JA, Estkowski LD. Effect of tendon orientation on MR imaging signal intensity: a manifestation of the “magic angle” phenomenon. Radiology. 1991; 181(2):389–392 [17] Feuerstake G, Zell J. Sportverletzungen. Ulm: Fischer; 1997 [18] Fullerton GD, Cameron IL, Ord VA. Orientation of tendons in the magnetic field and its effect on T2 relaxation times. Radiology. 1985; 155(2):433–435 [19] Gehardt P, Golder W, Kersting-Sommerhoff B, et al. [MR tomography of the extremities using the hemibody system ARTOSCAN. Initial experiences and expectations]. Rontgenpraxis. 1994; 47:4 [20] Ham K, Warntjes M, Gulpers S. Comparison of image quality between open and cylindrical systems. Poster as presented at ISMRM 2004. Available at: http://cds.ismrm.org/ismrm-2004/Files/001581.pdf [21] Heuck A, Bonél H, Huber A, Müller-Lisse GU, Sittek H, Reiser M. Acceptance of

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high field whole body MRI equipment, open MRI systems dedicated extremity scanners by patients. Radiologe. 1997; 37(10):778–784 [22] Kersting-Sommerhoff B, Gerhardt P, Golder W, et al. MR of the knee joint: first results of a comparison of 0.2 T specialized system and 1.5 T high field

Fig. 16.15 Magic angle artefact. Axial PDw fatsat image in vertical main magnetic field of open high field MRI. The medial cartilage layer (arrow) appears to be brighter than the lateral or that of the patellar ridge. This variation in signal pattern is thought to be caused by the magic angle phenomenon.

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field strength (1.0 Tesla)]. Radiologe. 1997; 37(10):773–777

660

Index Achilles tendon 361, 362, 364, 365, 382

abductor digiti minimi 365

– bursitis 409, 413

abductor hallucis 362, 403 abscess – Brodie's 375, 383, 501 – epidural 68 – focal bone, sacroiliac joint 263 – intermedullary 41 – intraosseous 54 – intraspinal 68 – muscles 455 – para-/intraspinal soft tissue 52, 54 – paravertebral 53 – sacral 263 Abt–Letterer–Siwe disease 547 acceleration trauma, spine 59 accessory bones – foot 370, 372, 416, 416, 418 –– fractures 370 – talus 367 accessory joints, sacroiliac 590, 596 accessory muscles 454 – foot and ankle 416, 419 – lower leg 416 – peroneus quartus 417, 421

– bursae protecting 410 – disorders 382 –– postoperative status 387 – ganglion cyst 392, 406

–– See also bone marrow, distribution patterns –– active/inactive, distribution 31, 475, 477–479 –– signal intensity, intervertebral disks 31

– bone marrow edema 373 – chronic sports injuries 653 – clinical interview 417 – clinical relevance of MRI 417 – examination technique 358 –– coil selection 358

– nodules 387, 392

– intervertebral disks 31, 39, 44, 50

–– contrast media 359

– overloading, apophysitis due to 370

– segmental apophyses of sacral

–– patient positioning 358

– pain (achillodynia) 406

alae 590

–– pitfalls 415

– tears 382, 390

– ulnar collateral ligament 160

–– full-thickness 386, 390–391

– vertebral bodies 31

–– partial 385

aggressive fibromatosis 553, 555

– fractures

– tendinitis 383

Ahlbäck's disease 325, 327

–– of bony prominences 373

– tendinopathy 383, 390, 409

alar ligaments 39

–– stress 371

– xanthomas 411

alar plicae 334–335, 335, 340

–– talus 367

acromioclavicular joint 87, 91, 94, 129

Albright's syndrome 544

– hemophilic arthropathy 409

– anatomy 92

aleukemic myelosis

– impingement, see talocrural joint

– disorders 129

(osteomyelosclerosis) 493, 494

–– sequences and parameters, protocols 358, 358, 416

– indirect MR arthrography 10

– distal clavicle edema 127, 130

algodystrophy 374

– ligament injuries 395

– fat pad 92, 92

ALPSA lesion 110, 117–118

– loose joint bodies 406, 416

– ligament injuries 129

alveolar canal 635, 636

– lower joint, see subtalar joint

– normal variants 137, 137

alveolar ridge 637, 640

– magic angle phenomenon 416

acromion 85, 87, 91

– augmentation 640, 640–641

– nerve compression syndrome 402

– anatomy and variants 87, 93, 95

amphiarthrodial articulation 587–588,

– osteoarthritis 406

– cartilaginous exostosis 96 – coracoacromial ligament

590

– osteochondral injuries 367

amphiarthrosis 182

– osteochondritis dissecans 367

amyloid arthropathy

– pitfalls in image interpretation 415

– hook-shaped 85, 96

– hip 267, 268

–– accessory muscles 416, 419

– ossification centers 139

– knee 333

–– signal patterns of anatomic

– persistent ossification center 137

– shoulder 124

–– synchondritis 137, 139

amyloid deposition 567

– rheumatoid arthritis 406

– straight-shaped 96, 96

amyloidosis 53, 567

– sarcoidosis 505

acromioplasty 135

– bone marrow 495

– sprains 419

– status after 135

– pseudotumors 567

– subchondral cysts 409

acronyms

– supra-acetabular 272

– shoulder, changes 124

– syndesmotic tilting 358

– fast MRI methods 6, 9

anaerobic glycolysis 445–446

– tendon disorders 379

acetabular labrum

– GRE techniques, different

anaerobic infections 649

– upper joint, see talocrural joint

anatomy, see specific joints/bone/

ankle mortise 359, 397

– wrist 223, 228 accessory posterior sesamoids (fabellae) 347 accessory soleus 417, 420 accessory tendons – biceps tendon 137 – iliacus tendon 272, 278 acetabular fossa 236 – fat pad 237

– age-related changes 258, 261

attachment 93, 95

manufacturers 4, 6

– anatomic variants 258, 261

activity score, sacroiliac joint 608, 613

– anatomy 237

acute immunodeficiency syndrome

– clock face 234, 236, 259 – cysts 261, 264–265 – degenerative changes 254, 259, 261 –– in hip dysplasia 251, 254 – detachment 259, 264

(AIDS) 495 acute inflammatory demyelinating polyradiculoneuropathy 40 acute transverse myelitis, multiple sclerosis vs 40

muscles anconeus 153, 158 Anderson's lesion 55

structures 415

ankylosing spondylitis 55, 596 – sacroiliac joint 596, 604–605, 607, 609–610

Andrew's lesion 111, 117, 119

–– diagnosis 597

aneurysmal (aneurysmatic) bone cysts,

–– HLA-B27-positive 595, 604–607,

see bone cysts

609–610

aneurysms, popliteal vessels 343

–– Hodgkin's lymphoma 629

– examination technique 234

adamantinoma 535

angiography

– injuries 257

–– juvenile 598, 604

additive T1/T2 contrast 10

– femoral head fractures 252

–– New York criteria (modified)

adenosine diphosphate (ADP) 19, 444

– magnetic resonance, see magnetic

– labral syndrome 261–262 – lesions 257, 276 – mucoid degeneration 264

adenosine triphosphate (ATP) 19, 444–

resonance angiography (MRA)

for 597 – spine 55, 57

angioleiomyoma 560

ankylosis

– tears 259, 263

adhesions

angiolipoma 558

–– causes 259

– fibrous, temporomandibular

– scarred, anterior cruciate

angioma 558

–– complex 259, 264 – thickness 258 – triangular 258 acetabular ligament 236–237 acetabulum 236

445

ligament 305 – temporomandibular joint 434, 439, 441 adhesive capsulitis (frozen shoulder) 124

angiomatosis 557, 557

joint 435, 435 – foot 378

angiosarcoma 535, 551

– sacroiliac joint 608, 610, 612–613

anisotropic dataset 15

annular ligament

ankle 358

– of fingers 208, 210

– See also foot, lower leg, specific

– of radius 152, 153

– See also hip

adiabatic high-frequency pulses 19

– anatomy 236, 237

adipose tissue, see fatty tissue

– accessory muscles 416, 419

anserine bursa 337

adolescents, sacroiliac joint

– anatomy 359

anserine bursitis 340

–– See also subtalar joint, talocrural

anterior cruciate ligament (ACL) 301,

– clock face 234, 236, 259 – fractures 251, 257

anatomy 590, 592–593

anatomic structures

–– tears/lesions 161

–– avulsion 255–256

aerobic glycolysis 445

– impingement, see femoroacetabular

Agati's disease 191

–– specific MRI anatomy 361

– absorption cysts 349, 349, 350

age-related changes, see degenerative

–– subtalar joint 360

– anatomy 283, 284, 286, 288, 289, 301

–– talocrural joint 359

– avulsion, bone marrow edema 304,

impingement (FAI) – teardrop figure 254 – tumors 523 Achilles bursitis 409, 413

changes/diseases

joint

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A

301

– acetabular labrum 258, 261

– apophysitis 370

– bone marrow 30, 475–476

– arthritis 406

– components 283

– bone disorders 367

– ganglion cysts 341, 342, 342

305

661

Index

– instability 310 – lesions 301, 301 – mucinous degeneration 306, 306

structures, upper arm – position, shoulder examination 85, 86

– postoperative changes 307, 308–309

Armstrong classification system 407

– reconstruction 307–308, 308–309

artefacts

–– bone tunnel positioning 308, 309

– chemical shift, see chemical shift

–– complications 308–309

artefact

arthrosis deformans, wrist 197

bacterial myositis 458, 459–461

articular disk

Baker's cyst 332, 336, 338, 344

– acromioclavicular 87

Bankart's lesion 110, 117–118

– shoulder 87

– bony 110

– TMJ, see temporomandibular joint

– reverse 113

(TMJ)

basivertebral veins 31

articularis (muscle) 349

Batson's valveless venous plexus 31, 50 Baxter's nerve 404

– CSF flow 41

ARTOSCAN 656

– tears 301–303

– etching 5

aseptic necrosis, see avascular necrosis

–– acute 301

– in GRE technique 4–5, 5

–– bone bruises (subchondral) 302, –– bone marrow edema 506

basilic vein 158

– wrist 182–183, 184–185

– scarred adhesions 305

303–304

– entrapment 404, 406

(osteonecrosis)

Bechterew's disease 596

– knee, line (truncation) 347

Askin tumor 532

Bennet's lesion 114, 117

– magic angle, see magic angle

atlas 33

Bennett's classification 105

atrophy, see specific structures

biceps anchor

avascular necrosis (osteonecrosis) 497,

– injury 114

phenomenon

–– chronic (historic) 305

– metal

–– diagnostic signs 303

–– prosthesis imaging 21

–– direct signs (MRI) 301, 303

–– spinal surgery 69–70

– carpal bones 191

–– indirect signs (MRI) 301–302, 302,

– motion, spine 41

– femoral head, see femoral head

– pulsatile flow, popliteal artery 347

– foot 369, 371

– anlage variants 137

303, 303, 304, 305

497

– tears, partial 104, 108 biceps brachii (biceps muscle) 147, 153, 163

–– isolated 301

– spinal examination 41

– humeral head 124, 127–128

– pulley lesion 105, 112

–– partial 305, 305

– truncation 41

– jaws, bisphosphonate-induced 638,

– short and long heads 153

–– PCL tears vs 307

–– knee 347

–– recurrent 308

– wrist 224

– juvenile, see juvenile osteonecrosis

biceps tendon 154

–– sensitivity 301, 304

arterial MRA 14

– knee, see knee

– accessory 137

–– stump retraction with

arteriovenous shunt 15

– lunate, see lunate

– aplasia 137

arthritis

– metatarsal (Köhler II disease) 369,

entrapment 305, 306 –– tangents and angle 305

– ankle and foot 406

639

369

biceps insertion strain 653

– dislocation 105, 109, 112 – distal 163 –– insertion tendinopathy 161, 164,

– thickening 306

– bacterial, see bacterial arthritis

– MRI diagnostic role 574

anterior fibulotalar ligament 359, 360

– bone marrow 504

– scaphoid 191, 194, 197

– rupture and disorders 397, 398

– hip, see hip, arthritis

– shoulder 124, 124, 127–128

–– retraction 161

anterior labral complex, disorders 110

– knee 282

– spontaneous

–– rupture 161, 162–163

anterior labroligamentous periosteal

– osteoarthritis, see osteoarthritis

–– femoral condyle 325, 327

–– tears 178

sleeve avulsion (ALPSA) 110, 117–

– psoriatic 596

–– lunate (Kienböck's disease), see

– double 137, 137

118

– rheumatoid, see rheumatoid arthritis

lunate

166

– labrum complex with 92, 93

– sacroiliac joint 263

–– scaphoid 191, 194, 197

– long head of 87, 90, 91, 94

– septic, see septic arthritis

–– wrist 191

–– anatomy 90, 92

– shoulder 122

– talus 367, 368

–– fluid in tendon sheath 137

– temporomandibular joint 435

– toes 415

–– tears 104, 107–108

– healthy, appearance 57

arthrography

– wrist, see wrist

–– tendinitis 102

– hematoma, whiplash injury 60

– magnetic resonance, see magnetic

avulsion fractures, see fracture(s),

–– transverse ligament tear 104

anterior lateral ligament, ankle and foot 359 anterior longitudinal ligament (spine) 39

– posttraumatic changes 57

resonance arthrography

avulsion

– proximal, disorders

– tears 57, 59–60

– three-compartment, wrist 205

avulsion injuries

–– chondromatosis 106, 112

– whiplash injuries 58, 60

– triangular fibrocartilage

– anterior cruciate ligament 304, 305

–– osteochondromatosis 106, 112

– fractures, see fracture(s), avulsion

–– pulley lesions 105, 111

arthropathy

– gastrocnemius medialis 385, 391

–– tears 104

anterior sacroiliac ligament 588, 588

– amyloid, see amyloid arthropathy

– humerus 127, 129

–– tendinitis 102

anterior syndesmotic ligament 397

– calcium pyrophosphate crystal,

– knee flexors 269

– pulley lesions 105, 111

– meniscus, see meniscus (menisci),

–– classification (Habermeyer) 105,

anterior meniscofemoral ligament of Humphrey 283, 288, 289

anterior tibiofibular ligament 359, 360, 398 – lesions 397, 398

complex 208

temporomandibular joint 436, 437 – defect arthropathy 100 – hemophilic, see hemophilic

knee

110

– muscles and tendons 463, 464

–– tears 105, 111

– posterior cruciate ligament 306

– pulley mechanism 105, 109

– synovial, knee 328

– shoulder 127, 129–130

– short head 87, 94

arthroscopy 350

–– glenoid labrum 110–111, 119

– tears 104, 107–108

anulus fibrosus 39, 44, 44

– bone marrow edema 504, 506

axial plane, see transverse (axial) plane

–– bucket-handle, SLAP lesion 119

– degenerative changes 44, 44

– temporomandibular joint 440

axillary nerve 136

–– elbow 156

– tears/fissures 44, 45

– wrist 205

– compression 108, 114

–– partial, of biceps anchor 104, 108

aplastic anemia 492, 493

arthrosis, see osteoarthritis

axis (cervical spine) 33

– tendinitis 102

apophysitis

– early-onset

axonotmesis 456

– ankle 370

–– hip 261

– calcaneal 370, 372

–– knee 317

– elbow 165

– elbow 163, 168, 169–170

– foot 370

– femoropatellar 318

apparent diffusion coefficient

– knee, see knee, arthrosis

anterior tibiotalar ligament 360 anterior transverse ligament of knee 283, 284, 288, 288

(ADC) 475

arthropathy

– mixed-type femoroacetabular

bicipital aponeurosis 161, 163 bicipital bursitis 161, 165

B

bicipitoradial bursa 155, 157

back pain, chronic (inflammatory) 596,

biochemical MRI, spine 30

601, 603–605, 621 bacterial arthritis, see septic arthritis

– bursitis 168 bisphosphonate-induced osteonecrosis 639

– hip 263, 266

– jaws 638

– radioulnar 197, 200

– sacroiliac joint 263

block vertebrae, see vertebrae

– shoulder, see shoulder, arthrosis

bacterial infections

blood supply

– sternoclavicular joint 134

– diabetic foot syndrome 408

– sacroiliac joint 588, 591

arcuate ligament 169

– wrist 197

– septic sacroiliitis 619, 622

– scaphoid 204

– lesions 312

– zygapophysial joints 47, 49–50

– temporomandibular joint 435

– spine 31

arachnoid membrane, herniation 66

impingement 260

arachnoiditis, see spinal arachnoiditis ARCO classification, avascular necrosis 240

662

arm, see forearm, specific anatomic

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– grafts and problems of 308–310

Index – osteonecrosis (avascular

–– vertebral bodies 52

– foot 371

–– scapula 477, 478

blood vessels

– knee 322, 504, 506

–– shoulder 121, 137, 137, 478

– signal intensities 519

–– ACL injuries 302, 303–304, 322

–– skull 477, 477

– tumors 530

–– chondral damage 318, 322

–– spine 475, 476, 477, 480–481

blood viscosity 483

–– medial collateral ligament

–– sternum 477

– polycythemia vera 483, 486

necrosis) 497, 497 – plasma cell proliferation (myeloma) 488, 489–491

–– tibia 478

– postradiation changes 497, 500

Blumensaat's line 305

–– patella dislocation 322

–– vertebral bodies 31, 476, 477

– radiochemotherapy effects 528

body coil imaging, bone tumors 516

–– PCL tears 307, 322

– edema, see bone marrow edema

– reconversion 478, 479, 483, 483–

body-array coils, pelvis

– resolution 322

– essential thrombocythemia 483

– sacroiliac joint trauma 621, 624

– examination techniques,

examination 234

attachment 311

bone

– spinal 59

– accessory, see accessory bones

bone buds, periarticular (sacroiliac

– bruise, see bone bruise

joint) 605, 607, 608, 609, 612

sequences 474

484, 485, 523 – salt-and-pepper pattern 488 – sarcoidosis 504, 505

– fatty (yellow) 30, 31, 475–476, 519

– sclerotic skeletal dysplasia 492, 492

–– distribution patterns, see above

– septic arthritis 504

– contusion, see bone bruise

bone cysts 567

–– post-transplant 496, 496

– serous atrophy 493

– cortical 37, 519

– aneurysmal (aneurysmatic) 548

–– reconversion to hematopoietic 478,

– sickle-cell anaemia 479, 485

–– destruction, bone tumors 523

–– ilium 548, 548

–– osteoporosis 574

–– tibia 520, 520

–– serous atrophy 493

–– relaxation times short 579

–– vertebral/spine 72, 73

–– signal intensity 476, 579

– storage diseases 494

– cysts, see bone cysts

– hemorrhagic, mandible 642

–– spinal tumor distribution and 71,

–– Gaucher's disease 494, 496

– density 574, 580

– juvenile (unicameral) 549

– disorders, see bone disorders

bone disorders

– fatty replacement 492, 501

– structure 31

– edema 496

– ankle 367

–– postradiation change 497, 499

– systemic mastocytosis 483, 487

–– See also bone marrow edema

– foot 367, 369

– fibrosis 493

– T1/T2 relaxation times 580

– erosions, shoulder 122

– shoulder 124

–– idiopathic osteomyelofibrosis 493,

– thalassemia 481

– fragments, spinal cord

– talus 367

479, 483, 483–484, 485, 523

72

494

– signal-to-noise ratio (SNR) 580 – skeletal dysplasia 481, 492

– stress reaction 42

– trabecular bone, magnetic fields 580,

– temporomandibular joint 436

–– pancytopenia 483

– healing 69, 70

bone marrow 29, 30, 474

– focal diseases 496

– transient osteoporosis 497, 499

–– abnormal, signs 70

– active, see bone marrow,

– generalized disorders 478

– transplant 495

– GRE technique 5, 8

–– changes after 495, 496, 496

compression 65

–– per primam 69

hematopoietic

580

–– per secundam 70

– acute leukemia 485, 488

– hematopoietic (red) 30, 475–476

– trauma 504

–– spine 69

– age-related changes, see age-related

–– clavicle (adult) 130, 134

–– See also bone bruise

–– distribution patterns, see above

–– in bone bruise 504, 506

– infarcts 494, 497, 497, 498

changes

–– acute 497

– amyloidosis 495

–– fatty replacement 492, 501

–– in fractures 508

– inflammation 50

– anatomy 475

–– in adults, distribution 475, 475, 476

–– in occult fractures 504, 507

– lymphoma, primary 77, 535

–– general anatomy 475

–– polycythemia vera 483, 486

–– in stress fractures 509, 509, 510–

– malformations, spinal 37

–– specific MRI anatomy 476

–– post-transplant 496, 496

– metastases, see under bone tumors

– arrested hyperpneumatization 477,

–– signal intensity 476, 579

– microfractures 574

482

–– spinal tumor distribution and 71,

511 – vertebral bodies, diffuse disease 31 – vertebral body end plates 41

– microstructure 574

– biopsy 486, 488

– necrosis 481, 501

– black 495

–– Waldenström's disease 492

– radiochemotherapy effects 528

– bone infarction 497, 497, 498

–– white cell infiltration, leukemia 485

– sclerotic in tumors, signal intensity

– carpal bones 186

– hypercellularity 483

– after arthroscopy 504, 506

– cell infiltration 478, 481

– hyperplasia 479, 483

– femur, slipped capital femoral

–– in lymphoma 486

–– uncontrolled 481

–– mast cells 483

– hypoplasia 492

– foot and ankle 374

–– plasma cells 488, 489–491

–– chemotherapy-induced

–– talar osteonecrosis 367, 368

patterns 518 – sequestered, chronic osteomyelitis 501 – spongy (cancellous/trabecular), see bone, trabecular

–– platelets 483

– stress reactions, foot 371

–– red cells (polycythemia vera) 483

– trabeculae, separation, bone

–– white cells (leukemia) 485, 485

density 580

– clinical relevance of MRI 509

72

changes 493 –– panmyelopathy (aplastic anemia) 492, 493 – in-phase and opposed-phase

– zygapophyseal joint changes 48 bone marrow edema 42, 48, 54, 55, 61, 496, 496

epiphysis 249, 250

–– talus/talocrural joint 373 – fractures 508 –– occult, osteoporosis 574 – hand –– rheumatoid arthritis 222

– trabecular 37, 579, 580

– components 30

–– bone marrow, magnetic fields 580,

– constituents, signal intensities 476

– inactive, see bone marrow, fatty

–– T2* time affected by 581

– infarction, knee 328, 329

–– density decrease 580, 580

– contusion, spinal 59

– inflammation 50, 500

– hip

–– density increase 580

– density, T2* time (effective T2

– iron deposition 495

–– cam impingement 260

– ischemia 497

–– osteoarthritis 265

580

–– microarchitecture 574, 576, 579

time) 580, 580

imaging 29

–– ulnocarpal impaction syndrome 194–195

–– microfracture 371

– development 475, 477

– malignancies involving 29, 485

–– transient osteoporosis 242

–– osteoporosis 574

– diffuse lymphoma infiltration 486

– metastases to 567

– knee

–– relaxation time measurement 579

– diffuse plasma cell infiltration 488,

– MRI indications 509

–– ACL tears/avulsion 304, 305, 322,

–– T2* relaxation times 580, 580, 581

490

– MRI interpretation 476

506

– tumors, see bone tumors

– displacement 481

– MRI principle and signals 579

–– blunt trauma causing 322

– tunnels, ACL reconstruction 308, 309

– distribution patterns (active/inactive

– multiple myeloma 488, 489–491

–– cartilage damage 317, 322

– myeloproliferative diseases 486

–– cartilage lesions 320

–– clavicle 130, 134, 477

–– benign/semimalignant 483

–– osteonecrosis 330

–– femur 475, 477, 479

–– malignant 485

–– shifting 324

bone bruise 318, 504

–– hip 271

– noninfectious inflammatory

– lunate, Kienböck's disease 191

– carpal bones 199

–– humerus 477, 477

– cause and features 322

–– knee 475–476

– osteomyelitis

– elbow 163

–– panmyelopathy 492, 493

–– acute 500, 500, 504

– osteomyelitis 500, 501

– femoral 303

–– pelvis 476, 477

–– chronic 501, 501

– postradiation change 499

– vertebral body end plates 41 bone bridges, transarticular (sacroiliac joint) 605, 607, 608, 609, 612

marrow) 30, 475, 476

diseases 504

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Blount's disease 328

– noninfectious inflammatory diseases 504

663

Index

brachialis muscle 147, 153

– stress fractures 509, 510

– tears 163

– tumors 412

bone marrow edema syndrome 374,

brachialis tendon 154

calcareous tendinitis, rotator cuff 100,

brachioradialis muscle 147, 154

389

104

cartilage capped exostosis, see osteochondroma cartilage–bone grafts, knee 321, 321– 322 cartilaginous exostoses, see

– See also osteoporosis, transient

Brainard's disease 191

calcification

bone mineral density (BMD),

bright disk sign 31, 31

– bone infarction 497

– knee 345, 346

osteochondroma

broad resonance signal, saturation 11

– cortical osteoid osteoma 537

cartilaginous lesions 11

bone scintigraphy

Brodie's abscess 375, 383, 501

– knee 348

– degrees of severity 11

– avascular necrosis of femoral

bronchoalveolar carcinoma, metastases

– meniscal 300

– imaging modalities 11

– phlebolith 557, 557–558

– magnetization transfer contrast 11,

osteoporosis 574

head 240

to femur 10

– sunburst, malignant bone

– hip stress fractures 254

brown fat 560, 565

– transient osteoporosis of hip 242

brown lipoma 560

bone tumors 516

brown tumor 568

– See also specific tumor types

buccolingual inclination 635

– benign 530, 535

bucket-handle tears

– benign vs malignant 516

– biceps tendon, SLAP lesion 119

–– diffusion weighting 518

– glenoid labrum 115, 119

calf muscle

– anatomic variants 69

–– dynamic MRI 516, 518

– menisci (knee) 288, 291, 291, 292,

– healthy, phosphorus spectroscopy 20

caudal variants 33

– lipoma 17, 18

cellular infiltration, marrow, see bone

–– signal intensity patterns 518, 519

292, 293, 293–294, 296

tumors 524 – traumatic myositis ossificans 465, 466 calcium pyrophosphate crystal arthropathy, TMJ 436, 437

– biopsy planning 527

Buford complex 87, 89, 136

calf pain 650

– chemotherapy response,

bursae

calvaria, bone marrow distribution

monitoring 527, 527, 529

– elbow 155

patterns 477, 477

12 – stage I 11 – T2 relaxation time 11 cartilaginous tumors 530, 539 cauda equina 32, 40–41 – adhesions to dural sac 40

marrow cellulitis 648, 650 cephalic vein 147, 158

– curative surgical strategies 520, 522

– gluteus minimum region 268–269

cam impingement 250, 254, 258–260

– elbow 171

– hip 277–278

capitate 195, 212

– examination technique 516

– indirect MR arthrography 11

– anatomy 182–183, 187, 189–190

cervical ligament (ankle) 360

–– sequences and parameters 516

– knee 336, 337

– carpal coalition 198

cervical spinal cord 40

– extension 522

– subacromial-subdeltoid 87

– displacement 206

– butterfly 39, 40

–– cortical destruction 523

–– disorders 109

capsular osteoma, knee 319

cervical spine

–– epiphyseal 523

bursitis

capsulitis

– anatomy (MRI) 32

–– intra-articular 523

– Achilles 409, 413

– adhesive (frozen shoulder) 124

–– joints 32–33

–– intramedullary 522

– bicipital 161, 165

– sacroiliac joint 598, 599, 601, 605

– fusion 36

–– neurovascular bundle

– elbow 155, 157, 168, 175

carbon spectroscopy 21

– MRI protocols 30

– foot 409, 413

cardiac cycle 13, 14

– multiple sclerosis 40, 41

–– periosteal reaction 523, 524, 574

– hip 272

carpal bones 183–184, 187, 189

– rheumatoid arthritis 56

–– soft tissue 524

– iliopsoas 267, 277

– avascular necrosis 191

– spinal canal 23

–– transcompartmental 524

– iliotibial 340

– bone bruise 199

– vertebrae 32–33, 40

infiltration 524

cerebrospinal fluid (CSF) flow artefacts 41

– extraosseous component 525

– knee 339, 339

– bone marrow space 186

Charcot foot 407, 409

– femur 545–547

– olecranon 161, 168, 175

– coalition 198

Charcot–Marie–Tooth disease 409, 411

– fibrous 544, 545–547

– prepatellar 339, 339

– general anatomy 182

chemical exchange 12

– foot 411

– radiohumeral 168

– instability 198

chemical exchange saturation transfer

– hand and wrist 214

– subacromial-subdeltoid bursa 109

– ligaments between 183, 184

– malignant 529, 530

– talocrural joint 409, 413

– nutrient vessel entry points 225, 229

chemical shift

– metastases 516, 529, 566

– trochanteric 268

(CEST), spine 30

– occult fracture 199, 202

– hydrogen spectroscopy 16

–– amelanotic 567

– traumatic lesions 199

– of tetramethylsilane 17

–– differential diagnosis 567

C

carpal boss/bossing 225, 228

– of the second kind 5

carpal collapse 198

chemical shift artefact

–– morphologic appearance 567

C sign 378

carpal tunnel 188, 189, 209

– spine 41

–– MRI sensitivity 567

Caffey's disease 328

– median nerve and flexor

– wrist and hand 224

–– osteoblastic 567

calcaneal apophysitis 369–370, 372

–– osteogenic sarcoma 517

calcaneal bursa 361

carpal tunnel syndrome 209, 212, 223

–– osteolytic 566–567

calcaneal cyst, stress-associated 373,

– causes 210

–– hemorrhagic and melanotic 567

379

tendons 209

chemical shift imaging (spectroscopic imaging) 17 – T2* time measurement 581

– congenital anomalies and 210

– two-dimensional 20

– perineoplastic edema 527

calcaneal lipoma 373

– diagnosis and MRI 210–211

chemical shift sequence

–– extraosseous tumor vs 525

calcaneal process

– postoperative MRI 211, 212

– bone marrow 474

– postoperative fibrosis and

– anterior, coalition with

carpe bossu 225, 228

– Gaucher's disease 494

carpometacarpal joints 182

chemical-selective saturation

– necrotic vs viable tissue 526, 526

edema 528

navicular 378, 386, 389

– recurrence 522, 528

– pseudarthrosis and fracture 373, 376

– first 182

– shoulder 130, 134

calcaneal tendon, see Achilles tendon

cartilage

chemotherapy

– signal intensity patterns 518, 519

calcaneal tuberosity 361, 410

– CHESS (chemical-selective

– bone marrow changes 493

– spine, see spine

calcaneonavicular coalition 378, 378,

– staging 520

389

saturation) 7 – damage, knee, see knee

–– Enneking's 520, 521, 522

calcaneus 360, 361, 364–365

– elbow 155

–– TNM 522, 522

– bone marrow edema 395

– fracture 504

bone tunnels, ACL reconstruction 308,

– cuboid, coalition 386

– hyaline joint, see hyaline joint

309

– lipomas 412, 414

cartilage

(CHESS) 6, 6, 17

–– patterns 527–528 – bone/soft tissue tumor response, monitoring 527, 527, 529 – failure, bone/soft tissue tumor volume increase 527, 527 – muscle changes 460

bony erosions, shoulder 122

– peroneal trochlea 389, 395

– imaging 11

– myeloablative high-dose 495

boomerang configuration 283

– stress fracture 375, 377–378

– regeneration 320

CHESS (chemical-selective

bow tie configuration, menisci 288

–– migrating 373, 380

cartilage cap, osteochondroma 541,

brachial artery 156

– stress reaction 377

542–543

saturation) 6, 6, 17 children

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brachial fascia 447

– sacrum, insufficiency fractures 511

382, 497

664

– talus coalition 323, 378, 378, 387–

– pyogenic spondylitis 52

Index

hematopoietic – bone marrow edema, foot 374 – congenital hip dysplasia 251, 251, 252 – epiphyseal plate fractures, leg 375 – intervertebral disks 39, 50

claustrophobia 656–657

conjoined nerve roots 38, 38

– bipartite 371, 374

clavicle 91

connective tissue tumors 530

– persistent ossification centers 371

– bone marrow distribution

contrast angiography 14, 15

cyclops lesion (syndrome) 309, 309,

pattern 477

contrast dynamic enhancement 9

341

– distant, edema 127, 130

– hip rheumatoid arthritis 264

cyst(s)

– hematopoietic bone marrow 130,

contrast media 9

– absorption, anterior cruciate

134

– benign vs malignant tumors 517

ligament 349, 349, 350

–– bone marrow and 30, 31

– osteolysis 127

– knee, special features 344

claw hand 170, 177

– diffusion 11

– aneurysmal bone, see bone cysts

– sacroiliac joint anatomy 590, 592–

claw-foot deformity 392

– elbow examination 147–148

– Baker's 332, 336, 338, 344

– bone marrow 31, 474

– acetabular labrum 261, 264–265

clear cell chondrosarcoma 533

– hip/pelvis imaging 234

– bone, see bone cysts

– spinal cord injuries 64

cleft sign 295

– in systemic mastocytosis 484

– calcaneal, stress-associated 373, 379

chloroma 486, 568

clivus, bone marrow distribution

– knee examination 282

– epithelial, see epidermal cysts

– lower leg, ankle and foot 359

– epithelioid, see epidermal cysts

593

chondral damage, knee, see knee, cartilage damage

patterns 477, 482 Clostridium perfringens infection 648

– sacroiliac joint examination 586, 587, 608

chondroblastoma 540

coalition

– highly aggressive 541, 541

– calcaneonavicular 378, 378, 389

– shoulder imaging 85

chondrocyte implantation, autologous,

– carpal bones 198

– spinal imaging 30

– cartilaginous 386

– temporomandibular joint

knee cartilage damage 321, 321

– ganglion, see ganglion cysts – glenoid labrum 122, 123 – greater tubercle of humerus 129, 132 – hand and wrist 216 – inclusion, hand 213

chondrolysis, diffuse acute, in SCFE 250

– classification 376, 386

chondroma (enchondroma) 539

– complete/incomplete 376

– wrist and finger examination 182

– meniscal 299, 300

– calcified, shoulder 123, 124

– fibrous 386

contrast-enhanced GRE 4–5, 5

– MRI, differential diagnosis 217, 499

– femur 540, 540

– talocalcaneal 378, 378, 387–389

conus medullaris 35, 39

– mucoid, foot 413

–– magnetization transfer contrast 12,

– tarsal 376, 386, 419

– low-level 39

– nerve-root sheath 38, 38

coil selection

Cooley's anemia 481

– paralabral 123

– foot 413

– ankle and foot 358

coracoacromial arch 87

– parameniscal 299, 300

– knee 344

– bone tumors 516

– aggressive 96

– posterior glenoid labrum 123

– MRI findings 540, 540

– elbow 146

– anatomy 93, 94

– radicular 637, 638

– periosteal (juxtacortical) 540, 541

– hip and pelvis examination 234

coracoacromial ligament 93, 94–95

– rupture 217

– shoulder 123, 124

– jaws and periodontal apparatus 634

– thickened 96, 97

– signal, shoulder 122

chondromalacia, patella 312, 317

– knee 282

coracobrachialis 91

– solid tumors with cyst-isointense

chondromatosis

– lower leg 358

– insertion strain 653

– biceps tendon 106, 112

– sacroiliac joint 586

coracohumeral ligament 98

– subchondral, see subchondral cysts

– knee 333

– shoulder 84

– anatomy 93, 95

– submucous retention, jaws 639, 639

–– secondary 334

– temporomandibular joint 426

coracoid impingement 100, 105–106

– synovial, see synovial cyst

– synovial, see synovial

– wrist and finger 182

coracoid process 91, 93, 94

– tubercle (shoulder) 129, 132

coil technology, hydrogen

– avulsion fracture 127, 130

– tumors, signal intensity pattern 519

– stress reaction 128, 131

cystic adventitial degeneration – knee region 343

13

chondromatosis chondromyxoid fibroma 541, 541

spectroscopy 17

examination 429

signal pattern vs 564

chondropathy 317

collateral ligaments

coronal plane

– knee 317, 317

– ankle, see medial collateral ligament

– elbow 146, 148–149

– popliteal artery 343, 343–344

– hip and pelvis 234, 234, 238

cystoid tumors, signal patterns 564

chondrosarcoma 532, 537

(ankle)

– clear cell 533

– elbow, see elbow

– ilium 536

– fingers 208

– knee 286, 288

– pelvis 532, 536

– knee, see lateral collateral ligament,

– muscle examination 444

– tibia 537

medial collateral ligament

– jaws and periodontal apparatus 635

– oblique, temporomandibular

D dark-star sign 458

Chopper-Dixon method 7

–– anatomy 283–284

chordochondral sarcoma 533

–– injuries 310

– sacroiliac joint 586

chordoma

– ulnar, contusion trauma and

– shoulder 84, 84, 87, 90

dedicated MRI systems 656

joint 429, 429

de Quervain's tenovaginitis stenosans 219, 224–225, 229

– spine 28, 32, 34–35

– advantages/disadvantages 656

– spine 76, 77

colliquation 651, 651

– subtalar joint 364, 366

deep infrapatellar bursa 336, 337

chronic myeloid leukemia 485

compartment syndrome 467, 467

– talocrural joint 364, 366

deep lateral sulcus sign 303, 305

chronic recurrent multifocal

compartment(s), muscle, see muscle

– wrist and fingers 186, 187–188, 192

deep peroneal nerve, compression 405

cortical bone, see bone

defect arthropathy 100

coxa saltans (snapping hip) 270

degenerative changes/diseases, see age-

– sacral 544

osteomyelitis (CRMO) 56, 58 chronic regional pain syndrome (CRPS) 374, 497 chronic venous insufficiency, dermatofibrosis 385 chronicity score, sacroiliitis 608, 611, 612–613

tear 209, 228, 230

compartments compartmental classification, tumor extension 524, 526 complex regional pain syndrome

cranial variants 33

– hand 188

cross relaxation 11

– hip 254

cross talk 234

–– See also acetabular labrum

computed tomography (CT),

cruciate ligaments

– intervertebral disks, see

cine loop 427–428

quantitative, bone marrow density

– fingers 208

cinematic MRI examinations 21

effect 580

– knee, see anterior cruciate ligament

– See also dynamic MRI – cine mode 21

related changes

creatine kinase reaction 444–445, 467

compression, see nerve compression

(CRPS) 374, 497

condyle, see specific condyles (e.g. femoral condyle)

intervertebral disks –– anulus fibrosus 44, 44

(ACL), posterior cruciate ligament

–– nucleus pulposus 44

(PCL)

– knee 318

– femoropatellar joint 22

congenital anomalies

cubital patella 173

–– anterior cruciate ligament 306, 306

– shoulder 86

– shoulder 129, 132

cubital tunnel, ulnar nerve

–– menisci, see meniscus (menisci),

– spine 29

– spinal, see spine

– temporomandibular joint

congenital hip dysplasia 251, 251, 252

cuboid bone 364–365

– mandibular condyle 436, 437, 440

congenital infiltrative (aggressive)

cuboid tunnel 388, 393

– sacroiliac joint 611, 615

cuboid tunnel syndrome 388, 393

– shoulder 130, 133

cuneiform 364–365

– spine 41

examination 427 – very fast sequences 21 circumscribed lipoatrophy 650, 651

lipomatosis 566 – lipomatosis 562

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– bone marrow, see bone marrow,

damage 170

knee

665

Index

437 – wrist 188–189

DISI (dorsal intercalated segment instability) 206

–– ulnar collateral ligament 159, 160

E

– collateral ligament(s), anatomy

ecchondroma, see osteochondroma

–– radial (lateral) 151, 152–153

– zygapophysial joints 47, 48

disk(s)

echinococcosis 53, 55

–– ulnar (medial) 151, 152, 228, 230

delayed gadolinium-enhanced MRI of

– articular, see articular disk

echo distance (ED) 3

– contusions 160

– intervertebral, see intervertebral

echo spacing 3

– dislocation 163, 167

echo time (TE), see TE (echo time)

–– staging 163

echo train length (ETL) 3

– effusion, without fracture 162

ED (echo distance) 3

– epicondylitis, see epicondylitis

diskitis, postoperative 66

edema

– examination techniques 146

dislocation, see specific joints

– bone 496

–– axial (transverse) plane 146, 150–

deltoid muscle 91, 94

dissection, Baker's cyst 336, 338–339

– bone marrow, see bone marrow

– atrophy 108

disseminated idiopathic skeletal

cartilage (dGEMRIC) 11 – spine 30 delayed-onset muscle soreness (DOMS) 461, 461 deltoid ligament, see medial collateral ligament (ankle)

– axillary nerve course and 136 – fibrous tear 109, 115 – insertion into humerus 138, 140

disks – temporomandibular, see temporomandibular joint (TMJ)

hyperostosis 611, 616 distal (second) intersection syndrome 219

edema – distant clavicle 127, 130

–– coronal plane 146, 148–149 –– flexed abducted supinated

– lipoid 648 – muscles 454, 455, 457, 458, 461, 468

denervation, see muscle(s), denervation

– spine 29

– perineoplastic, see perineoplastic

Denis' three-column model 59

doorstop sign 135, 136

dens 32, 39

dorsal intercalated segment instability

– rheumatoid arthritis 54, 56

(DISI) 206

–– contrast media 147

– Hoffa's fat pad 313, 313, 340

– modified 7, 9

myeloma 489

151 –– coils 146

– dural sac, postoperative 65

Dixon technique

demineralization, multiple

edema

view 154, 154–156 –– MR arthrography 147, 151 –– patient positioning 146 –– planes and sequences 146, 147

– soft tissue, radiation-induced 652

–– sagittal plane 146, 147–148

– spinal cord 63, 64

–– standard MR tomography 146

dental alveoli 635

dorsal intercarpal ligament 183

– subcutaneous 468

–– STIR sequence 147

dental implants 640

dorsal radiotriquetral ligament 183

– tumor recurrence vs 528, 530

–– TSE sequences 146

dental MRI 634

double anterior horn sign 293, 294

– venous 648

– false-positive MRI results 176, 178

dental prosthesis, fixed 640

double posterior cruciate ligament

Eden–Lange–Hybbinette opera-

– fluid in joint space 155

dental pulp 635

sign 293

tion 134, 136

– fractures at 162–163, 166–167, 178

– See also teeth

double-echo GRE 6

effective echo time 3

–– concomitant injuries 163

effective T2 time, see T2* time (effective

–– occult 163, 167, 176

– vitality 637, 640

double-fat plane 110

dental radiology 634

double-line sign

dentistry, materials, MRI

– bone infarction 497

effusion

– golfer's 158, 653

– osteonecrosis 124, 241

– elbow 162

– indications for MRI 146

dentogenic sinusitis 639

–– femoral head 241, 241–242

– hip 263, 263, 266

– internet links and internet research

depth-resolved surface-coil

DRESS (depth-resolved surface-coil

– joint, transient osteoporosis 497

compatibility 634

spectroscopy (DRESS) 19, 20 dermatofibrosis, chronic venous insufficiency 385

spectroscopy) 19, 20 Duchenne's muscular dystrophy 456, 457

T2 time)

– ganglion cyst 178

on 146

– shoulder 124, 137, 138

– lifting injury, biceps tendon tear 156

– subacromial-subdeltoid bursa 109,

– limitations of MRI 158

115–116

– loose joint bodies 166, 168, 172, 178

dermatomyositis 457, 457

Dupuytren's disease 220, 401, 557

– subcoracoid recess 137, 138

– muscles 152

desmoid bone tumor 547

dural sac 39

– wrist 189

–– anterior group 153

desmoid tumors (soft tissue) 553, 555–

– anatomy 32

elasticity coefficient 580

–– lateral (radial) group 154

– cauda equina adhesions to 40

elbow 146

–– medial group 154

– edema, postoperative after disk

– anatomy 147, 149

–– posterior group 153

–– blood vessels 156

– neoplasms/neoplasm-like

556 – extra-abdominal 553 desmoplastic fibroma 547

surgery 65

diabetic foot syndrome 406, 408–410

– empty, spinal arachnoiditis 69

–– bones 154

– bacterial infections 408

– posterior, tear 60

–– bursae 155, 157

–– bone 171

– bone marrow edema 374

DWI, see diffusion-weighted imaging

–– joint cartilage 155, 157

–– soft tissue 172

– osteomyelitis 408–409, 410 – pathogenesis 407 – sensory neuropathy 407 – staging/classification 407–408 – ulcer sites 407 diabetic neuro-osteoarthropathy 406 – classification 407 dialysis, chronic 53 – amyloid arthropathy in hip 267, 268

(DWI) DWIBS (diffusion-weighted body suppression) 13 dynamic MRI, see cinematic MRI examinations – benign vs malignant tumors 516, 518 – chemotherapy response in tumors 528

changes 171

–– ligaments 149

– neuropathies 168, 176–177

–– muscles, see elbow, muscles

– osteochondritis 166

–– nerves 155

–– secondary 170

–– normal variants 154

– osteochondritis dissecans 166, 171

–– overlapping effect 154

– Panner's disease 167, 171

–– recesses 155

– pitfalls in image interpretation 173

–– tendons 152

– plicae (synovial folds) 168, 173–175,

– angioma 558

178

– annular ligament, lesions/tears 161

– post-therapy findings 173

– stress fractures (hip) 257

– contrast-enhanced investigations 9

– apophysitis 165

– pseudodefects 154–155, 157

diaphyseal aclasia 543

–– bone marrow 474

– arthrosis 163, 168, 169–170

– pulled 653

diastematomyelia 36, 36

–– spine 30

– biceps tendon (distal), see biceps

diffuse idiopathic skeletal hyperostosis

– temporomandibular joint

tendon, distal

– radioulnar synostosis 168, 173 – snapping triceps 161

– bone bruise 163

– space-occupying lesions 170

dynamic phosphorus spectroscopy 21

– bursitis 155, 157, 168, 175

– subluxation 163, 167

dyskinesia, femoropatellar joint 312

– cartilage damage 168

–– staging 163

diffusion-weighted imaging (DWI) 13

dysplasia

– chronic sports injuries 653, 653

– tennis 158, 158, 159, 464, 653

– bone marrow 475

– fibrous, see fibrous dysplasia

– clinical interview 176

– traumatic lesions 162, 166–167

– chemotherapy response in

– hip, see hip, dysplasia

– clinical relevance of MR

– triceps tendon, see triceps tendon

(DISH) 611, 616 diffusion-weighted body suppression (DWIBS) 13

tumors 528

examination 427

– skeletal, see skeletal dysplasia

tomography 173, 176

electrocardiography (ECG), gated-

– spine 29

– spinal 33

– collateral ligament lesions 159, 163

– tumors 518

dysplasia epiphysealis hemimelica

–– age-related changes 160

electromyogram (EMG) 456

–– radial collateral ligament 160, 161

elephantiasis neuromatosa 558

digital subtraction angiography (DSA) 14

666

dipolar coupling 12

(Trevor's disease) 379, 389

–– tears 160–161

inflow technique 13, 14

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– temporomandibular joint 430, 436,

Index Ewing's sarcoma 524, 531

– acetabular fossa 237

– spine 74, 75

– acromioclavicular joint 92, 92

en face image, hip 234, 235

– staging, MRI role 531, 535

– foot, see foot

–– MRI advantages 240

enchondroma 539

Ewing's sarcoma tumor family 532

– Hoffa's, see Hoffa's fat pad

–– necrotic zone 240–241, 241

– See also chondroma

examination techniques, see specific

– knee, lesions 340

–– secondary, disorders causing 239

– suprapatellar (quadriceps) 341, 342

–– staging 239–240

fat presaturation pulse, spine 29

–– surgical treatment 241, 243–244

fat saturation

–– transient osteoporosis link 242

extensor digitorum brevis 361

– GRE sequence, sacroiliac joint 586

– epiphysis

extensor digitorum longus,

– TSE sequence, bone marrow 474

–– cartilage, in hip dysplasia 251, 251–

tears 98, 102

– femur 540, 540 – knee 344

anatomic regions extensor carpi ulnaris tendon, tendinitis/peritendinitis 220, 225

endocrine myopathy 468 energy metabolism, in muscles, see muscle(s)

disorders 395

Enneking's compartmental classification 524, 526

extensor hallucis brevis 361

fat signal, shift, see chemical shift artefact

–– Mitchell's signal pattern, necrotic regions 240–241

252 –– Perthes' disease 246, 247–248

Enneking's stage 520, 521, 522, 526

extensor hallucis longus, disorders 395

fat suppression (sequences) 6

entheseal joint 592

extensor muscles, foot 394

– See also STIR sequence

– sacroiliac 588–589, 590, 592

extensor pollicis brevis, tendon

– chemical-selective saturation 6

– fractures 252

–– slipped, see slipped capital femoral epiphysis (SCFE)

– Chopper-Dixon method 7

–– subchondral 253

– classic 592

extensor pollicis longus, tendinitis 219

– elbow examination 146

– hyaline cartilage 238

– fibrocartilaginous 591

extensor tendons

– hip 235

– impaired perfusion 263

– fibrous 591

– fingers 154, 186, 187

– hydrogen spectroscopy 17

– ligamentum teres, see ligamentum

– functional 592

– foot 394

– modified Dixon technique 7, 9

enthesis organ 590

– hand and wrist 184, 185–187

– short-tau inversion recovery 7

enthesitis 591, 595

– thumb 154

– spine 29

– Perthes' disease 243, 247–248

– articular iliac-sided

external auditory meatus 428, 428

– T2* time measurement 581

– roof, fractures 251

external magnetic field (B0) 2

– water excitation 7

femoral neck

extramedullary hematopoiesis 568

fat-water phantom, TSE sequence 3

– bone defects 271, 276

extremities, dedicated MRI

fatigue fractures, see fracture(s), fatigue

– cam impingement (decreased

inflammation 219

enthesis 590

fibrocartilage 598, 601, 603–604 – interosseous ligaments (sacroiliac) 608, 611 – juvenile idiopathic arthritis with 598, 599–600

systems 656

entrapment – Baxter's nerve 404, 406 – sural nerve 406

offset) 250, 254, 258–259

extremity coil 358, 516

fatty replacement, bone marrow, see

F

fatty tissue

fabellae (accessory posterior

– necrosis 651, 651

– plica 267, 268

–– gluteal 652

– transcortical synovial

enthesopathy, see insertional tendinopathy

fatty acids, oxidation 445

teres of femoral head – ossification centers 248, 252

bone marrow – diseases 650 sesamoids) 347

– fractures 251, 576 –– occult 251, 257 – lateral, decreased offset (pistol grip deformity) 254, 259

eosinophilic fasciitis 649

failed back surgery syndrome 65

– tumors 519, 530, 560

eosinophilic granuloma 547, 548

false-positive/negative MRI results

–– See also lipoma, liposarcoma

femoral nerve, compression 274 femoral shaft fractures 508, 508

– vertebra plana 73, 74

– elbow 176, 178

–– signal intensities 518–519

epicondylitis 158

– foot and ankle 417

fat–muscle interface, signal intensities,

– histology 158

– hip 252, 276

– lateral (tennis elbow) 158, 158, 159,

– jaws 644

femoral bone tunnel 308, 309

– knee 350

femoral condyle

– medial (golfer's elbow) 158, 653

–– meniscus 297

– arthroscopy, bone marrow

– radial humerus 158, 158, 159

– shoulder 139

464, 653

GRE technique 7

edema 504, 506

herniation 271, 276

femoral spur 542–543 femoroacetabular impingement (FAI) 254 – cam impingement 250, 254, 258– 260 – iliopsoas impingement 257

– ulnar humerus 158

– spinal 78

– bone bruises 504

– ischiofemoral impingement 256

epidermal cysts

– temporomandibular joint 440–441

– hollowed-out depression 305

– mixed-type impingement 258, 260

– foot 413, 413

– wrist 228–229

– lateral, osteochondral compression

– other types 256

– hand 213

fasciae 446, 447

epidermal inclusion cysts, foot 413

– disorders 648

– magic angle artefact 658, 659

– subspine impingement 256, 260

epidural abscess 68

– thickening 648–649

– medial, cartilage damage 317

femoropatellar arthrosis 318

epidural fat 31

fasciitis 648, 650

– normal depression 305

femoropatellar joint

epidural fibrosis 65, 66–67

– eosinophilic 649

– ossification 344

– dyskinesia 312

– recurrent disk herniation with 67

– necrotizing 648, 650

– osteonecrosis, spontaneous

– maltracking 312, 313

– recurrent prolapse vs 65

fasciitis panniculitis syndrome 649

epidural hematoma, postoperative 69

fast spin-echo sequence 2

femoral head

– normal gliding/tracking 312

epidural lipomatosis 552, 554

– See also turbo spin-echo (TSE)

– anatomy 236, 237

– osteoarthritis 312

– angiography 252

femur

– avascular necrosis 238, 241–242

– bone marrow distribution 475, 477,

– spine 49, 51 epidural venous plexus 31 epiphyseal plate, asymmetry 349 epiphyseal–diaphyseal angle, femoral 249, 249 epiphysis, tumor extension 523 epiphysitis, metatarsal base 370, 371

sequence – temporomandibular joint examination 427

fracture 319

idiopathic 325, 327

–– ARCO classification 240

– pincer impingement 254, 258, 260

– MRI cinematography 22

479

fast STIR sequence 7

–– bilateral 243

– bone outgrowths 345, 346

fat

–– causes 238–239, 250

– chondroma 12, 13

– deposition, muscle atrophy in

–– classification 239–240

– fibrous bone tumors 545–547

shoulder 107, 107, 113

–– development after fractures 252

– fractures 508, 508

epithelioid cell granulomas 504

– epidural 31

–– double-line sign 241, 241–242

– metastases 72, 516, 517

erosions

– in tumors, signal intensity

–– early diagnosis important 239

–– fast STIR sequence 10

– sacroiliac joint 601, 601, 602–607 – shoulder 122

patterns 518–519 – multivacuolated, brown 560, 565

–– Ficat and Arlet's staging 239–240

– osteochondroma 542–543

–– idiopathic juvenile, see Perthes'

– osteogenic sarcoma, necrotic vs

– styloid process 225

– signal vectors, GRE sequences 6

erysipelas 648, 650

– subcutaneous, see subcutaneous fat

–– idiopathic/primary 239

– osteoid osteoma 538

essential thrombocythemia 483

– univacuolated, white (yellow) 560,

–– localization and extension

– osteosarcoma 524

etching artefact 5 ETL (echo train length) 3

565 fat pad(s)

disease

parameters 240

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Ellman's classification, rotator cuff

viable tissue 526, 526

– trochlear groove, patella gliding over 312

667

Index – tumors 517

– flexors, T2 relaxation times 453, 454

–– ligaments 360–361

– sesamoids 371, 373, 419

fibrocartilage

– giant cell tumor of tendon

–– muscles 361

– sole 365

– ankylosis 378

– stress reactions and fractures 371

– apophysitis 370

– synchondritis 370–371

– triangular, complex, see triangular

– ligaments 208

– avascular necrosis 369, 371

– synostoses 376, 378

–– annular (ring pulleys) 208, 210

– bone disorders 367, 369

–– secondary 378

fibroma

–– collateral 208

– bone marrow edema syndrome 374,

– chondromyxoid 541, 541

–– cruciate 208

fibrocartilage complex (TFCC)

382

– synovitis 406 – tarsal coalitions 376, 386, 419

– desmoplastic 547

– rheumatoid nodules 214

– bursitis 409, 413

–– calcaneonavicular 378, 378, 389

– nonossifying 544, 546

– snapping 220

– cartilage deformity 379

–– talocalcaneal 378, 378, 387–389

– tendon sheath 560, 562

– subluxations/dislocations 208, 209–

– Charcot 407, 409

– tendinitis, insertional 384

fibromatosis – aggressive (desmoid tumors) 553, 555

210

– chondromas 413

– tendon disorders 379

– subungual tumors 212–213, 216

– chronic osteomyelitis 501

–– inflammation 379

– tendon sheaths 185–186, 208

– chronic sports injuries 653

–– tears 379, 385–386

– tendons 185–186, 186–187, 189

– clinical interview 417

–– thickening 379

– forearm 177

–– anatomy 185, 185, 186, 186–187

– clinical relevance of MRI 417

– transient osteoporosis 374

– palmar (Dupuytren's disease) 220,

–– flexor tendon, disorders 220, 226

– diabetic, see diabetic foot syndrome

– tumors 411

–– tears 220, 227

– epidermal inclusion cysts 413

–– bone 411

– penile (Peyronie's disease) 402, 557

–– tenovaginitis of flexor tendon 223

– epiphysitis 370, 371

–– soft tissue, malignant 413

– plantar 401, 403–405, 557

– trigger 220, 226

– examination technique 358

–– subungual 413

fibrosarcoma 535, 550

fistula, soft tissue 650, 650

–– coil selection 358

– ulcers, diabetic 407

– myxoid 549–550, 553

FLASH sequence, knee joint 282

–– contrast media 359

– xanthomas 411

fibrosis

flexible rectangular coil, knee

–– patient positioning 358

footprint tear 101, 106, 132

–– sequences and parameters,

forearm

– deep 553

401, 557

– bone marrow, see bone marrow

examination 282

– epidural, see epidural fibrosis

flexor digitorum brevis 362, 365

– muscles, see muscle(s)

flexor digitorum longus 361, 362, 364,

– postoperative 528, 530

396

protocols 358, 358, 359

– fibromatosis 177

– extensor tendons/muscles 394

– lymphedema 649

– false-positive MRI 417

– muscle anatomy 447–449, 453

– scar 455

– accessory 417

– fat pads

– muscle compartments 524, 525

fibrotic tissue, in tumors, signal

– tears and disorders 392

–– diseases 402

– muscle denervation 456

– tendovaginitis 392

–– obesity 405

– tendon disorders 218

fibrous bone tumors 544

flexor digitorum profundus 453

– flexion (plantar and dorsal) 361

–– distal dorsoradial 219

– femur 545–547

flexor digitorum superficialis 453

– flexor tendons, deep, see tibialis

forefoot

fibrous cortical defect 544

flexor hallucis longus muscle 362, 365,

intensity patterns 518–519

– knee 345, 346

392, 396

posterior tendon

– anatomy 365, 367

–– courses 390, 396

– examination technique

fibrous dysplasia 544

– disorders 392

–– disorders 390

–– patient positioning 358

– monostotic 544, 545

– in posterior impingement 399, 401

– fractures 373, 376

–– sequences and parameters 359,

– polyostotic 544

– tears 394

–– accessory bones 370

fibrous lunotriquetral coalition 196,

flexor pollicis longus tendon, recurrent

–– middle foot 405

– ganglion cysts 411, 413

198, 201

359–360

–– occult 371

– hemangioendothelioma 557

flexor retinaculum

–– pediatric 375

four-quadrant method 601, 611, 613,

– bulging, carpal tunnel syndrome 212

–– stress 371

– foot 361, 362

– ganglion cysts 411, 413

Fournier gangrene 648

fibula 359

– wrist/hand 190, 209

– giant cell tumor of tendon

fracture hematoma 508

– anatomy, sagittal sections 364

flexor tendon sheath, fingers 208

– occult fracture 507

– pitfalls in interpretation 226, 229

– hemangioendothelioma 557

– stress fracture 377, 509

flexor tendons

– hemophilic arthropathy 409

–– acetabular 255–256

fibulocalcaneal ligament 359, 360–361,

– deep, foot 390, 396

– ligament injuries 395

–– coracoid process 127, 130

fibrovascular reaction, spondylodiscitis 52, 54 fibroxanthoma 544

399

tears 220, 227

sheath 412

613

fracture(s), see specific bones – avulsion 509

– fingers 154, 185, 186–187, 189, 192

–– Lisfranc injury 398, 419

–– knee 322, 322

– tears 398, 399

–– disorders 220

– lymphedema 648

–– rectus femoris, inferior iliac

fibulotalar joint, indirect MRI

–– in carpal tunnel 209

– magic angle phenomenon 416

–– tears 220, 227

– mucoid cysts 413

–– wrist 200

arthrography 10

spine 256

fibulotalar ligament 360–361, 415

– hand and wrist 154, 184, 185–188

– nerve compression syndrome 402

– bone marrow edema 508

Ficat's staging, avascular necrosis of

–– disorders 220

– neutral position 358

– burst 62, 64

fluid sign 76, 78

– osteoarthritis 406

–– thoracolumbar 57

field of view (FOV)

fluid–fluid levels 520

– osteochondral injuries 369

– compression

– shoulder 84

– bone cysts 73, 73, 549

– osteoid osteoma 411, 414

–– knee 319

– temporomandibular joint 427

– bone/soft tissue tumors 520, 529,

– osteomyelitis 374

–– osteoporotic 576, 577–578

– pigmented villonodular

–– spine 489

femoral head 239–240

– wrist 182

568

synovitis 563

–– vertebral bodies 59, 61–62, 577–578

fingers 182

– giant cell tumor 74

– See also hand

– patellar dislocation with fracture 323

– pitfalls in image interpretation 415

– fatigue 509

– anatomy (MRI) 186–187, 190, 192

fluoroquinolones, Achilles tendon

–– accessory bones and sesamoids 416

–– hip 252

–– accessory muscles 416, 419

– healing

– chronic sports injuries 653

tear 382, 390

– Dupuytren's disease 220

foot 358

– plantar fascia diseases 400

–– fibrous union 204

– epidermal cysts 213

– See also ankle, forefoot, specific

–– See also plantar fascia

–– partial union 204

– pseudobursae 411

– impression, humeral head 114, 125,

– examination technique 182 –– coil selection 182 –– patient positioning 182

anatomic structures – accessory bones 370, 372, 416, 416, 418

– pseudotumor 395 – rheumatoid arthritis 406

128 – in seronegative

–– sequences and parameters 182

– accessory muscles 416, 419

– sensory neuropathy

– flexion and extension 185–186,

– anatomy 359

–– diabetic, see diabetic foot syndrome

– insufficiency 252, 509, 574

–– flexor aspect 361

–– nondiabetic 348, 419

–– osteoporosis 574

186–187

668

sheath 213, 216 – glomus tumors 212, 217

spondyloarthropathy 56

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– iliac, see iliac fibrocartilage – menisci (knee) 283, 288

Index –– sacrum 59, 61, 253, 258

–– rupture 217

– tear 113, 117, 118–119, 121

– steady-state 4, 5

–– sternum 511

GARD (glenoid rime articular divot)

–– anterior 121, 123

– T2* time (effective T2 time)

lesion 111, 118

–– bucket-handle 115, 119

measurement 581

– occult 251, 504

Garré's osteomyelitis 56

–– classification 117

– temporomandibular joint 426

–– carpal bones 199, 202

gastrocnemius bursae 336, 337

–– GLAD lesions 111, 118

– ultrathin axial slices, knee (meniscal

–– elbow 163, 167, 176

gastrocnemius medialis

–– imaging modality sensitivity/

–– femoral neck 251, 257

– avulsion 385

–– fibula 507

–– tennis leg 385, 391

–– partial 121

grafts

–– foot 373

– Duchenne's muscular dystrophy 456

– traumatic lesions 110, 119

– ACL and PCL reconstruction 308, 309

–– hip 251

– ganglion cyst 343

glenoid labrum ovoid mass (GLOM)

–– complications 308–310

–– knee 322

gastrocnemius–semimembranosus

–– osteochondral/subchondral 504

bursa 336, 336, 337

–– osteoporosis 574

– fluid 338

–– pelvic 251

gated-inflow technique 13, 14

–– pisiform 202

Gaucher's disease 494, 496

–– scaphoid 203

genioglossus 636

– osteochondral compression,

Gerdy's tubercle 311, 311, 337

knee 319

specificity 123

sign 117 glenoid labrum–biceps tendon complex 92, 93 glenoid rime articular divot (GARD) lesion 111, 118 GLOM (glenoid labrum ovoid mass) sign 117

tears) 297 – wrist and fingers 182

– autologous cartilage–bone, knee 321, 321 – Matti–Russe graft 205, 206 – osteochondral allograft, knee 322 – tendon, Achilles 387 granulocyte colony-stimulating factor (G-CSF) 479, 481

ghost images 41

glomus bodies 212

granulocytic sarcoma 486, 568

– osteoporotic, see osteoporosis

ghost sign 295

glomus tumors 217

granuloma

– overloading, see fracture(s), stress

giant cell tumor 543

– fingers and hand 212

– eosinophilic, see eosinophilic

– pathologic

– bone 543, 544–545

– toes 413

–– osteoporotic fractures vs 574

– humerus 545

gluteal fatty tissue necrosis 652

– epithelioid cell 504

–– spine 489

– in Hoffa's fat pad 341, 341

gluteal tendons, insertional

GRASS sequence 6

– stress 509

– of tendon sheath 560

–– calcaneal 373, 377–378, 380

–– finger 213, 216, 218

gluteus maximus

– knee joint 282

–– distal fibula 377

–– foot 412

– enthesis, insertional

grayscale matrix 2

–– distal tibial metaphysis 375

–– knee 341, 341

–– elbow 163

– sacral 544

– myotendinitis 465

–– fibula 509

– spine 74, 75

gluteus medius 268

greater trochanter

–– foot 371, 373, 375, 377–378

GLAD (glenolabral articular disruption)

– insertional tendinopathy 268, 270

– discontinuity, fractures 508

gluteus minimus

– insertional tendinopathy of gluteal

–– hip 252, 257

lesion 111, 118, 122

tendinopathy 268

tendinopathy 270, 272–273

granuloma

– distal radius 579

GRE technique, see gradient-echo (GRE) technique

–– insufficiency 252

– posterior 114

– bursa 268–269

–– metatarsals 373, 381, 510

Glaser fissure 428

– insertional tendinopathy 268, 270

Guillain–Barré syndrome 40

–– migrating (foot) 373, 380

glenohumeral joint 86, 87

glycogen storage disease 446

Guyon's canal 189, 211, 212

–– pelvis 257

– MR arthrography 86

glycogenosis 446

– ganglion cyst in 211, 213–214

–– pitfalls in image interpretation 509

glenohumeral ligaments 87, 87, 93, 95

glycolysis 445, 446

–– spinal 59, 61

– anatomy 89

glycosaminoglycans 520

–– talar 373, 380

– disorders 112

golfer's elbow 158, 653

–– tibia 375, 509

– inferior, discontinuity 119

gout

frozen shoulder 124

– variants 89, 90

– knee 334

glenoid avulsion glenohumeral

– toes 415

ligament (GAGL) lesion 112

G

gouty tophi 334, 415, 567

tendons 268

H Habermeyer's classification 102, 105, 110 HAGL (humeral avulsion glenohumeral ligament) lesion 112, 119

glenoid fossa 87, 117

gracilis syndrome 270, 273

Haglund's exostosis 410

gadolinium 9

glenoid labrum 87, 87, 89, 117

gradient reversal 4

Haglund's heel 384, 409

– benign vs malignant tumors 516

– anatomy 87, 88, 91

gradient-echo (GRE) technique 4

hallux valgus 415, 417

– magnetic resonance arthrography 9

– anterior 87

– acronyms, manufacturers 4, 6

halo sign 458

– spinal imaging 30

–– variants 89

– artefacts 4–5, 5

Hamada's classification 100, 103

GAGL (glenoid avulsion glenohumeral

– avulsion injuries 110–111, 119

– basic technique 4

hamate, hamulus of 213

– cysts 122, 123

– bone marrow 5, 8, 474

– fracture 203

ganglia

– disorders 110

– circuit diagrams 5

– hammering pressure, damage 221

– nerve roots 38

–– anterior labral complex 110, 118,

– contrast and parameter changes 4–5

hamatolunate impingement 197

– contrast-enhanced 4–5, 5

hamstrings

– cortical destruction in bone

– insertional tendinopathy 269, 271

ligament) lesion 112

– space-occupying lesion in shoulder 108

119 –– arm positioning for MRI 119

ganglion cysts 214

–– diagnostic criteria for MRI 117

– Achilles tendon 387, 392

–– inferior ligament complex 112, 119

– double-echo 6

– elbow 173, 178

–– MRI sensitivity 121

– dynamic contrast-enhanced 9

– foot 411, 413

–– posterior labrum complex 113, 119

– fat and muscle

– gastrocnemius medialis 343

–– superior labral complex, see SLAP

–– proton spectra 4, 6

tumors 523, 524

– tears, insertional tendinopathy and 267, 269 hamulus of hamate, see hamate, hamulus of hand, see fingers, thumb, wrist

–– signal intensities 7

– anatomy 182, 183–185

– knee 309, 341, 342–343

– instability 110

– fat and water, signal vectors 5, 6, 29

–– special MRI anatomy 186

–– cruciate ligaments 341, 342, 342

– normal variants 87, 89, 136

– jaws and periodontal apparatus 635

–– tendons and tendon sheaths 184,

–– extra-articular 342

– partial aplasia 87, 89

– knee joint 9, 282, 289

–– Hoffa's fat pad 341–342

– posterior 87

– multiplanar reformatting 5

– chronic polyarthritis 217, 221–222

–– intra-articular 342, 342, 342

–– cysts 123

– opposed-phase 474

– chronic sports injuries 653

– wrist 218–219

–– hypertrophy, congenital

– oscillation period 5, 7

– degenerative changes 188

– hand 214, 218, 220

–– Guyon's canal narrowing 211, 213– 214

lesions

malformations 129, 132 –– tears 111, 119

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– nonunion (pseudarthrosis) 203, 205

185–187

– phase shifts 4

– Dupuytren's disease 220, 401, 557

– sacroiliac joint 586, 587, 588, 592

– ganglion cysts 214, 220 – glomus tumors 212

–– intraosseous 214, 216, 218–219

– superior

– shoulder joint 8, 84

–– lunate 219

–– injuries, see SLAP lesions

– spine 29

– lymphedema 648

–– radial volar septate 219

–– insertion, variants 116, 121

– spoiled 4, 5

– rheumatoid arthritis 222, 225

669

Index – reverse 126, 128

– synovial membranes, disorders 217

hindfoot

– tendon disorders 218, 223

– chronic osteomyelitis 501

–– knee flexors 269, 271

– scar tissue at 309

– tumors 212, 214

– patient positioning for

–– rare types 270

– space-occupying lesion 564

–– types 269

– tears 302, 340

examination 358

272–273

– loose joint body in superior recess 326

–– soft tissue 215

hip 234

– internet links and research 234

Hoffa's recess 340, 564

– vascular diseases 221

– See also acetabulum, femoral head,

– joint capsule 238

hollow foot 384

–– diseases 266

Honda's sign 59 humeral avulsion glenohumeral

Hand–Schüller–Christian disease 547

pelvis

hard palate, swelling 641

– amyloid arthropathy 267, 268

– labral lesions, see acetabular labrum

head and neck coil 427

– anatomy 236, 237, 258, 278

– neurovascular compression

– jaws and periodontal apparatus 634

–– ball-and-socket joint 236

syndrome 270, 274, 274

heel spurs 400, 417

–– bursa 277–278

– osteoarthritis 267

– dorsal 384

–– ligaments 238

–– early-onset 261, 265

– aseptic osteonecrosis 124, 127–128

– plantar 401

–– sectional 238–239

– osteoid osteoma 275, 539, 539

– high-riding 100, 103

heel, pain 403, 404

– arthritis 262

– osteomyelitis 262

– impingement 125, 128

hemangioendothelioma 535, 557, 557

–– early-onset osteoarthritis 261, 265

– pain 247, 259, 271, 273–275, 497

– impression fractures 114, 125, 128

hemangioma 549, 557

–– rheumatoid 264, 277

– Perthes' disease, see Perthes' disease

– posterolateral contour, variants 137

– foot 413

–– Salmonella 266

– pigmented villonodular

humeroradial joint 147

– maxillary 643

–– septic arthritis 262

– peripheral skeleton 549

– arthrosis, early-onset 261, 265

– pitfalls in image interpretation 271

humerus

– spine 72, 73

– avascular necrosis, see femoral head,

–– accessory iliacus tendon 272

– bone marrow distribution

– thigh 557

avascular necrosis

synovitis 270

–– bursitis 272

ligament (HAGL) lesion 112, 119 humeral glenoid joint 87 humeral head

humeroradial plica 168, 174–175

pattern 477, 478

– upper arm 558

– bone defects 271, 276

–– hematopoietic bone marrow 271

– capitulum

– vertebral body 37, 72, 73, 549, 567

– bursitis 272

–– supra-acetabular fossa 272

–– osteochondritis dissecans 166, 171

hematoma

– chronic sports injuries 653

–– transcortical synovial

–– pseudodefects 154, 157

– after disk surgery 65, 69

– clinical interview 276

– muscles, see muscle(s)

– clinical relevance of MRI 276

– spinal cord compression 65

– compression syndrome 270, 274,

hematopoiesis 475

274

– extramedullary 568

– degenerative changes 254

hemilaminectomy, intraspinal abscess

– dislocation

after 68 hemilumbarization, sacral vertebral body 594 hemisacralization, lumbar vertebral body 590, 595

herniation 271, 276

– giant cell tumor 545

– prosthetic implants 236–237

– greater tubercle

–– MRI use 236

–– avulsion injuries 127, 129

–– periarticular fluid collection 236–

–– cysts 129, 132

237

–– congenital 251, 251, 252

– rheumatoid arthritis 264, 277

–– high, dysplasia with 251, 253

– septic arthritis 262

– dysplasia 251

– slipped capital femoral epiphysis, see

–– adults 251, 253–254 –– congenital 251, 251, 252

– deltoid muscle insertion 138, 140

– plicae (synovial folds) 266, 268

– lesser tubercle, avulsion injuries 127, 129 – osteochondroma 542 – osteomyelitis 502

slipped capital femoral epiphysis

– osteosarcoma 534

(SCFE)

–– chondroblastic 532

hemivertebrae, congenital 37

– effusion 263

– snapping (coxa saltans) 270, 654

–– telangiectatic 522, 531, 534

hemophilia 53

–– septic 263, 266

– synovial effusion, reactive

Humphrey, anterior meniscofemoral

– elbow (secondary arthrosis) 165, 170

– examination techniques 234

– pelvis 568

–– axial plane 234, 238–239

– synovial membranes, diseases 266 – synovial osteochondromatosis 266,

irritative 250

ligament 283, 288, 289 hyaline cartilaginous end plate,

– shoulder 123

–– coil selection 234

hemophilic arthropathy

–– contrast media 234

– foot and ankle 409, 412

–– coronal plane 234, 234, 238

– knee 331, 333

–– oblique axial sequence 235

hemophilic pseudotumors 568, 568

–– patient positioning 234

– trauma 251

– hip 236

hemorrhage

–– planes 234, 234

– tumors 270

– knee 282, 290, 317, 324

– muscles, see muscle(s)

–– radial MRI 234, 235

–– extension into joint 523, 523

–– See also knee, cartilage damage

– signal intensities 519

–– sagittal plane 234, 234

– valgus deformity 253

– orientation-induced changes in

hemosiderin deposits 568

–– sequences and parameters 234

hip bone (coxal bone) 236

– bone marrow 481, 495

–– special sequences 234

hip tract syndrome 274

– sacroiliac joint 588

– foot and ankle 409

– false-positive/negative MRI

histiocytoma, malignant fibrous 528,

hydrogen (1H) spectra 16–17

– hip 271 – knee 331, 332 – shoulder 123

findings 252, 276 – fractures, see acetabulum, femoral head, femoral neck

267 – transient osteoporosis 242, 245–246, 497, 499

529, 535, 549, 550 histiocytosis X (Langerhans' cell histiocytosis) 73, 74, 547

disks 39 hyaline joint cartilage 32 – elbow 155, 157 – femoral head 238

signal patterns 655

hydrogen (1H) spectroscopy 16, 17, 18–19 – coil technology 17

– wrist and hand 213

–– dislocated, status after 256

HIV infection 495

– myositis 446

hemosiderosis 495

–– false-positive findings 252

HLA-B27 595

– relaxometry 18

hereditary sensorimotor

–– fatigue 252

Hodgkin's lymphoma 488, 496, 629

– subcutaneous fatty tissue 19

–– femoral head development

– spinal involvement 77

– suppression techniques 17

Hoffa fracture 302

– volume selection techniques 17, 19–

neuropathy 409, 411 hernias, muscle 463, 464

after 252

20

HF (MR) signal 2

–– insufficiency 252

Hoffa's disease (Hoffitis) 341

HF pulse, see high-frequency (HF) pulse

–– occult 251

Hoffa's fat pad 288, 306, 306, 334

hydromyelia 40

hibernoma 560, 565

–– posttraumatic 251

– anatomy 340

hyperparathyroidism 568

high-field scanners 634, 656

–– stress 252, 257

– diseases involving 341

hypertrophy, muscle, see muscle(s)

– indications for 656

– impingement, see femoroacetabular

– edema 313, 313, 340

hyperuricemia 415, 416

– ganglion cyst 341–342

hypothenar hammer syndrome 221,

– open, use 657, 657, 658

impingement (FAI)

high-frequency (HF) pulse 2, 4

– indications for MRI 234, 276

– giant cell tumor 341, 341

– adiabatic, spectroscopy 19

– inflammatory diseases 262

– inflammatory pannus tissue 340

– insertional tendinopathy 267

– lesions 340

–– at greater trochanter 269, 271

– local arthrofibrosis 341

high-resolution volume coil, knee examination 282 Hill–Sachs lesion 126, 128

–– gluteal tendons 268, 270

227 hypotrophy, muscles 454, 455

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–– bone 214

670

–– gluteus maximus enthesis 270,

– rheumatoid nodules 214

Index

I

inflammatory back pain 596, 601, 603–

idiopathic osteomyelofibrosis 493, 494

inflammatory myopathy 457

–– postoperative 30, 49

iliac fibrocartilage 588, 592

inflammatory pseudotumors,

–– postoperative status 52

– osteomyelitis 637, 638

–– posttraumatic 56, 65

– osteoradionecrosis 638

–– protrusion 45, 46–47

– solid vs cystic changes 640

–– recurrent, epidural fibrosis vs 65,

– submucous retention cyst 639, 639

– enthesitis 598, 601, 603–604 iliacus tendon, accessory 272, 278 iliofemoral ligament 237, 238 iliopectineal bursa (iliopsoas bursa) 277

rheumatoid arthritis 214 inflammatory rheumatoid disorders, sacroiliac joints, see sacroiliac joint

–– migration 45, 47 –– MRI protocols 30

infrapatellar plica 334–335, 335, 340 infraspinatus muscle 91, 94

65 –– recurrent, epidural fibrosis with 65,

– odontogenic keratocystic tumor 639, 639 – osteitis 637, 638

– tumors 643 – vascular lesions 640, 643

iliopsoas bursa 277

– atrophy 107, 113

iliopsoas bursitis 267, 277

– tears 103

–– recurrent, postoperative 65, 65, 66

– hip 238

iliopsoas impingement 257

insertional tendinopathy 101

–– sequester 45, 47

– knee 328

iliopsoas tendon

– elbow

–– subligamentous 45, 47

– sacroiliac joint 588, 589, 590, 592

– accessory iliacus tendon 272, 278

–– biceps tendon (distal) 161, 164, 166

–– transligamentous 45

– shoulder, see shoulder

– insertional tendinopathy 270, 273

–– triceps tendon 161, 166

– osteoporosis 576

– talocrural joint 359

iliotibial band (tract), see iliotibial tract

– foot/ankle/lower leg 370–371, 384

– postoperative changes 65

– temporomandibular joint 428, 428

–– peroneus brevis tendon 390

–– after herniation 30, 49

– tibiofibular, ganglion cysts 342

–– tibialis anterior tendon 395, 397

–– complications 65

joint(s), see specific joints

– hip 267, 270–271

–– epidural hematoma 69

– dedicated MRI systems 656

iliotibial bursa 336, 337

–– gluteal tendons 268, 270

–– normal images after surgery 65

– spine 32

iliotibial bursitis 337, 340

–– gluteus maximus enthesis 270,

–– recurrent herniation and epidural

Jones' fracture 390

(band) iliotibial band (tract) syndrome 652, 655

iliotibial tract (band) 284, 286

66–67

fibrosis 65, 66–67

272–273

joint capsule

Junghans motion segment 47

– injuries 311, 311

–– gracilis (gracilis syndrome) 270, 273

– posttraumatic changes 56

juvenile (unicameral) bone cyst 549

iliotibial tract (band) syndrome 311,

–– iliopsoas, calcification 270, 273

– prolapse, see intervertebral disks,

juvenile ankylosing spondylitis 598,

312

– knee

herniation

604

ilium 236, 238

–– flexors 269, 271

– revascularization 44

juvenile chronic arthritis 55

– anatomy 587, 588–589

–– quadriceps 315

–– after degenerative changes 50, 53

juvenile flatfoot 377

– aneurysmatic bone cyst 548, 548

– shoulder 108

– spinal cord compression 65

juvenile idiopathic arthritis 598

– bulge 609

–– pectoralis major 108, 114

– spondylodiscitis 49, 53–54

– with enthesitis 598, 599–600

– chondrosarcoma 536

–– rotator cuff 101

– structure 44, 44

juvenile osteochondrosis deformans,

– fractures, fatigue 253

intercarpal arthrodesis 194

– vascularization 50

image-guided in vivo spectroscopy

intercondylar notch, meniscal fragment

– zygapophysial joint

(ISIS) 20

in 293, 294

interrelationship 47

impingement

interferometry 581

– hamatolunate 197

intermedullary abscess 41

(neuroforamina) 37

– hip, see femoroacetabular

intermetacarpal joint 182

intramedullary cavity,

impingement (FAI) – shoulder 94, 97 –– See also rotator cuff, subacromial impingement –– humeral head 125, 128 impingement syndrome 94, 97

intervertebral foramina

osteosarcomas 529

interosseous bursa 155 interosseous sacroiliac ligament 588, 589

– See also osteochondritis – capitulum of humerus 167, 171 – knee 328, 328 juvenile spondyloarthritis 598, 599– 600 juxta-articular osteitis 598, 606–607

intraosseous lipoma 547, 547

juxta-articular pneumatocysts,

inversion recovery sequence 7

interosseous talocalcaneal

– muscles, pitfalls 468

ligament 359–360, 360, 364, 365

see Perthes' disease juvenile osteonecrosis 167

intramuscular myxoma 552

– enthesitis 608, 611

ischemic necrosis, see avascular

sacroiliac joint 611, 614–615

K

– shoulder 94, 97, 130

interosseous tibiofibular ligament 397

– talocrural, see talocrural joint

interspinous ligaments 39

ischial tuberosity

Kahler's disease, see multiple myeloma

– ulnar 196, 199

– tear 60

– flexors, avulsion 269

keratoacanthoma 413

implantology 640

interval lesion 98

– pain, insertional tendinopathy 269

Kienböck's disease 191

in-phase imaging, spine 29

intervertebral disks 39, 44

ischiofemoral impingement 256

– See also under lunate

in-phase TE 5, 7

– See also anulus fibrosus, nucleus

ischiofemoral ligament 237, 238

Kim's lesion 114

inclusion body myositis 457, 457

pulposus

necrosis

ischium 236

Klippel–Feil syndrome 36, 37

inclusion cyst, hand 213

– age-related changes 31, 39, 44, 50

Iselin's disease 369

knee 282

indirect MR arthrography, see magnetic

– anatomy 32, 39, 39

isotropic dataset 15

– See also specific anatomic structures

resonance arthrography

– bulging 45, 45–46

– bone marrow and intervertebral

– cartilaginous end plates 44, 44

disks 30, 31

– ACL lesions, see anterior cruciate

– bright disk sign 31, 31

infancy

ligament (ACL)

J

– advantages of MRI 351

– degenerative changes 39, 44, 52

jaws 634

– amyloid arthropathy 333

–– differential diagnosis 53

– See also mandible, maxilla

– anatomy 282

–– localization 46

– anatomy 635

–– axial plane 77, 284

infarction

–– revascularization 50, 53

–– general 635, 636

–– bursae 336, 336

– bone, see bone, infarcts

– height 39, 44

–– specific MRI 635

–– coronal plane 286, 288

– spinal cord 41

– herniation 39, 45, 45, 46

– bisphosphonate-induced osteonecro-

–– general anatomy 282

infections, see bacterial infections

–– broad-based 45

– HIV 495

–– classification 45

– clinical interview 643

–– ligaments 283–284, 315

– soft tissue 648

–– diagnosis, features for 46

– clinical relevance of MRI 643

–– sagittal plane 287, 288

inferior alveolar nerve,

–– disk material location 45, 47

– disorders 636

–– sectional anatomy 284, 284–287

–– extrusion 45, 46–47

– examination techniques 634

–– specific MRI anatomy 284

inferior extensor retinaculum 360

–– focal 45, 47

–– equipment and coils 634

– anterior arthrofibrosis, localized

inferior iliac spine, avulsion

–– focal extrusion 45, 47

–– imaging planes 634

–– focal protrusion 45, 46–47

–– sequences 635

–– localization 47

– false-positive/negative MRI 644

– arthrofibrosis (diffuse) 309

–– lumbar spine 46–47

– indications for MRI 634

– arthrosis 318

– congenital hip dysplasia 251, 251, 252

Schwannoma 644

fractures 256 inflammation, bone marrow 500

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605, 621

sis 638, 639

–– lateroposterior 311

(cyclops syndrome) 309, 309, 341 – arthritis 282

671

Index –– development, signs 318

– joint capsule, changes 328

knuckle pads 221

–– sacroiliac joint 588, 588–589

–– early-onset 317

– juvenile avascular necrosis 328

Köhler I disease 369

–– shoulder 87, 88–89, 89, 93

–– radiographically occult 318

– juvenile osteonecrosis 328, 328

Köhler II disease 369, 369–370

–– spinal 39

– avascular necrosis 326, 328, 330

– lateral capsular ligament

Köhler's disease 328

–– wrist 182, 183, 206

Köhler–Mouchet's disease (scaphoid

– diseases, see specific ligaments,

–– spontaneous idiopathic of femoral condyle 325, 327

– ligament lesions, see individual ligaments

– bone bruises 322, 504, 506

– limitations of MRI 350

– bone marrow 476

– lipohemarthrosis 323

–– edema, see bone marrow edema

– lipoma arborescens 332, 334

–– infarction 328, 329

– loose joint bodies 291, 318–319, 320,

– bone trauma 322

326

avascular necrosis) 191, 194, 197 kyphoplasty 71, 576

anatomic regions – signal intensities 519 ligamentum teres of femoral head 236, 237, 238

L

– degenerative changes 261, 265

labral plica 267, 268

– tears 261

labral recess 263

line artefacts, see truncation artefacts

– bursitis 339, 339

– magic angle phenomenon 288

labral syndrome 261–262

lipoatrophy 650

– capsular osteoma 319

– menisci, see meniscus (menisci),

labral tears, see acetabular labrum

– circumscribed 650, 651

labrum, see acetabular labrum, glenoid

lipohemarthrosis, knee 323

– cartilage (chondral) damage 317, 318, 320, 322 –– autologous cartilage–bone grafts 321, 321 –– autologous chondrocyte implantation 321, 321 –– classification 317, 317–318, 320 –– osteochondral allograft 322

knee – nerve compression syndrome 342

labrum–biceps tendon complex 92, 93

– osteochondral allograft 322

Langerhans' cell histiocytosis 73, 74,

– osteochondral autologous graft 321, 321 – osteochondral compression fracture 319 – osteochondral damage 318

–– traumatic 320

– osteochondral flake fracture 319,

– cartilage balding 331 – cartilage flake fractures 319 – cartilaginous exostoses 345, 346 – children, special features 344

320 – osteochondritis dissecans, see osteochondritis dissecans – osteonecrosis, see knee, avascular necrosis

– chondromatosis 333

– patella dislocation, see patella

– chondropathy 317, 317

– PCL lesions, see posterior cruciate

– chronic sports injuries 653

ligament (PCL)

– chronic synovitis 318

– pigmented villonodular

– clinical interview 350

synovitis 329, 331, 564

– clinical relevance of MRI 350 – collateral ligament injuries, see

labrum

– osteoarthritis, early-onset 317

–– postoperative MRI 321 –– treatment 320

– pitfalls in image interpretation 288, 345

547 lateral capsular ligament injuries, knee 311, 311, 312

lipoid edema 648 lipoma 499, 551 – brown 560 – calcaneal 412, 414 – calf muscle 17, 18 – intramuscular 553–554

lateral collateral ligament (LCL, knee)

– intraosseous 547, 547

– anatomy 284, 286

lipoma arborescens

– bursa 336, 337

– knee 332, 334

– injuries 311

– shoulder 124

lateral gastrocnemius bursa 336, 337

lipomatosis 551, 561

lateral hyperpressure syndrome 313

– benign symmetrical 561–562

lateral ligament (elbow), tear 653

– congenital infiltrative

lateral ligament complex (talocrural joint) 359, 360

(aggressive) 562, 566 – epidural, see epidural lipomatosis

– injuries 397

– subcutaneous 561

lateral patella plica 335

lipomyelocele 36, 36

lateral patellar retinaculum 284, 314,

lipomyelomeningocele 36

315

liponecrosis 651, 652

lateral plantar nerve 362

liposarcoma 549

– first branch, compression 404, 406

– dedifferentiated 549

–– absorption cysts 349, 349, 350

lateral pterygoid 428–429, 636

– myxoid 549, 551–552

–– accessory posterior sesamoids 347

– inferior head 428, 428–429

– pleomorphic 549

cruciate ligament (ACL), posterior

–– articularis (muscle) 349

– superior head 428, 428

– round cell dedifferentiated 549

cruciate ligament (PCL)

–– bi-/tri-/multipartite patella 347

lateral subluxations syndrome 313

– well-differentiated 549

– degenerative diseases 318

–– calcification 348

lateral–medial patella subluxation 313

Lisfranc injury 398, 406, 419

– embryology 334

–– dorsal defect in patella 347, 349

Launois–Bensaude syndrome 561–562

Lisfranc joint 398

– enchondroma 344

–– increased signal intensity, meniscus

lava columnar phenomenon 619, 622

Lisfranc joint ligamentous

collateral ligaments – cruciate ligament lesions, see anterior

– epiphyseal plate asymmetry 349

periphery 345, 346

– examination technique 282

–– line (truncation) artefacts 347

–– 3D display of MRI data 14, 16

–– meniscomeniscal ligament 348, 349

–– 3Tesla images 656, 657

–– popliteal artery pulsatile flow 347

–– axial plane, radial acquisition 16

– plicae 334, 335

–– coil selection 282

– prosthesis, magnetic resonance

–– magnetization transfer contrast 12

neurography 23, 24

Ledderhose's disease (plantar fibromatosis) 221, 401, 403–405 leg, see lower leg, specific anatomic structures Legg–Calvé–Perthes disease, see Perthes' disease

complex 398 Lister's tubercle 191, 219 lithotripsy, shock wave, shoulder 131 little leaguer's elbow 158 little leaguer's shoulder 128, 131 loose joint bodies

leiomyosarcoma, lower leg 530

– ankle 406, 416

–– patient positioning 282

– referred pain 350

leprosy 409

– elbow 166, 168, 172, 178

–– sequences and parameters 4, 9, 282

– rheumatoid arthritis 328, 330

lesser trochanter, iliopsoas, insertional

– knee 291, 318–319, 320, 326

– extensor mechanism 284

– sarcoidosis 332, 333, 505

– false-positive/negative MRI 350

– subchondral bone cysts 331, 333

Letterer–Siwe disease 547

– femoropatellar joint dyskinesia 312

– subchondral cysts 318

leukemia

– shoulder 123 – wrist 197

tendinopathy 273

– rotator cuff calcareous tendinitis 100, 104

– fibrous cortical defect 345, 346

– synovial compartments 334

– acute 485, 488

– fractures 322, 323

– synovial fluid 290

– chronic myeloid 485

Looser's pseudofractures 619, 620–621

–– avulsion 322, 322

– synovial membrane changes 328

– shoulder involvement 134

low back pain 28

–– occult 322

– synovial plicae (folds) 334

leukoerythroblastic anemia

– inflammatory (chronic) 596, 601,

–– osteochondral compression 319

–– embryological origin 334

– ganglion cysts, see ganglion cysts

– synovial popliteal cysts 336

Levin classification 408

– red flags 28

– gout 334

–– dissection 336, 338–339

ligamenta flava 39

low-field scanners 634

– hemophiliac arthropathy 331, 333

– tendonitis 315, 316

– healthy vs injured 57

lower arm, see forearm

– hyaline joint cartilage 282, 290, 324

– transient osteoporosis 324, 499

ligamentous plica, hip 267, 268

lower leg 358

–– See also knee, cartilage (chondral)

– tumors/tumorlike lesions 282, 344

ligaments, see individual ligaments

– See also ankle

– vascular diseases 343

– anatomy

– accessory muscles 416

–– damage 317

knee flexors 269

–– elbow 149

– anatomy 359

– iliotibial tract (band) syndrome 311,

– avulsion 269

–– foot 360–361

–– deep flexor compartment 361

– insertional tendinopathy 269, 271

–– hip 238

–– extensor group of muscles 360

knot of Henry 364, 392, 396

–– knee 283–284, 315

–– lateral group of muscles 361

damage

312 – indications for MRI 282, 351

672

injuries 311, 311

(osteomyelosclerosis) 493, 494

603–605, 621

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–– secondary 328

Index

– chronic venous insufficiency 385 – Duchenne's muscular dystrophy 456 – epiphyseal plate fractures 375

magic angle phenomenon 12, 12, 654, 655 – artefacts in open high field systems 658, 658

– femur chondroma 12, 13 – knee joint 12, 289 – magic angle phenomenon 12, 12, 655

medial ligament complex (talocrural joint) 359, 360 medial patellar plica 335, 335–336 – types 335

– examination technique 358

– femoral condyle 658, 659

– shoulder joint 12, 12

medial patellar retinaculum 314, 315

–– coil selection 358

– foot and ankle 416

– subtraction method 12

medial patellofemoral ligament 314,

–– contrast media 359

– implications 655

– tissues with strong effect 12

–– sequences and parameters,

– knee 288

– tumor recurrence vs postoperative

protocols 358

–– meniscus 658, 658

fibrosis 528, 529–530

315 medial plantar nerve 362 medial pterygoid 428, 636

– leiomyosarcoma 530

– principle/explanation 654

MAGSUS 581

medial subluxation syndrome 313

– malignant fibrous histiocytoma 529

– shoulder 92

malignant fibrous histiocytoma 528,

median artery, persistent 223

– muscle anatomy 448, 451–452, 453

– wrist and hand 187, 224, 655

– muscle compartments 524, 525

Magna-SL 656

– peripheral arterial occlusive

magnetic field

disease 15 – pitfalls in image interpretation 415 – shin splint syndrome 375 – tendon disorders 382, 387 – transient ischemia 345

529, 535, 549, 550 malignant melanoma, metastases 519, 567

median nerve – developmental variants 209 – elbow 156

– dedicated MRI systems 656

malignant nerve sheath tumor 551

–– entrapment 176

– tissue orientation change, effect, see

malleolar sulcus 389

–– lesions 168

malleolus, lateral 389

– severed 202

mandible

– wrist 189

– body 635

–– compression 209, 212

magic angle phenomenon magnetic resonance angiography (MRA) 13

lumbar spinal cord 40

– arterial 13, 14

– hemorrhagic bone cyst 642

medulloblastoma, metastases 484

lumbar spine

– chemotherapy response in

– osteolysis 642

melanoma, malignant, metastases 519,

– anatomy (MRI) 34–35 – bone marrow distribution

tumors 528

mandibular angle 635

567

– contrast-enhanced 14, 15

mandibular condyle 428

meningitis, spinal 41

– gated-inflow technique 13, 14

– bifid 429, 430

meningocele 66

– compression fractures 62

– indications 13

– degenerative changes 436, 437, 440

meniscal homologue 183, 185

– congenital variants 33

– neurovascular bundle infiltration by

– disk displacement and 432

meniscectomy 298

– malpositions 434, 435

meniscofemoral ligaments 288, 289

– mouth closed 429

meniscoids 47

– mouth opening 429

meniscomeniscal ligament 348, 349

patterns 480

– disk herniation 46–47 – fusion 36, 49 – MRI protocols 30

tumors 524 – peripheral arterial occlusive disease 15

– osteoporosis 568

– phase contrast 14, 14

– restricted translation 432, 432

meniscotibial ligament 283

– spinal canal 23

– vascular injuries, spinal 58

mandibular neck, fractures 437, 439

meniscus (menisci), knee

– synovial cyst 48, 50

– vascularized jaw lesions 640

– classification 437–438

– anatomy 282, 282, 290

– T2* relaxation time

magnetic resonance arthrography 9

mandibular ramus 635, 636

–– axial plane 284–285

– acetabular labral variants 259

marching cleft sign 295, 295

–– coronal plane 286, 288

– direct 9

masseter 428, 636

–– sagittal plane 287, 288, 288

–– elbow 147

mast cell proliferation 483, 487

– anterior horns 283, 288

lumbosacral junction, anatomy 590

–– glenohumeral joint 86

masticatory muscles 428, 636

–– basal (root) tear 296

lumbosacral transition vertebrae 590,

–– hip and pelvis 235

mastocytosis, systemic 483, 487

–– double, sign 293, 294

– elbow examination 147, 151

Matti–Russe graft 205, 206

–– tears 291

–– ulnar collateral ligament

maxilla 635

– bow tie 288

– rhabdomyosarcoma 645

– cysts 299, 300

measurements 581 lumbar vertebral body, hemisacralization 590, 595

594–595 lunate 182 – avascular necrosis (Kienböck's

lesions 160 – hip and pelvis 235

maxillary hemangioma 643

– degenerative changes 290, 290, 299

–– stage I 192, 193–194

– hip stress fractures 254

maxillary sinus lift 640, 640–641

–– calcification 290

–– stage II 192, 193

– indirect 9

maximum intensity projection

–– fraying 290, 290, 297

–– stage III 192, 193, 195

–– advantages 11

–– stage IV (chronic) 193, 194, 196

–– ankle joint 10

Mazabraud's syndrome 552

– detachment 292

–– treatment 194

–– bursae 11

McArdle's syndrome 446

– discoid (variant) 298, 298

– changes 189

–– elbow 149, 151

McLaughlin's fracture 114

–– incomplete 298–299

– intraosseous ganglion cyst 219

–– hip and pelvis 235

medial alar plica 284

–– tears 299

lunate malacia 191

–– shoulder 11, 85, 86

medial calcaneal nerve 362

– dislocation 292, 301, 301

lunotriquetral coalition 196, 198, 201

– lower leg, ankle and foot 359

medial capsular ligament (knee) 283

– false-positive/negative results 297

– incomplete (coalescence) 198

–– talar osteochondral lesions 367

medial collateral ligament (ankle) 359,

– flipped, sign 293, 294

lunotriquetral ligament 182, 187, 188

– NaCl solution injection 85, 148

– disorders 205

– shoulder 85, 86

– instability 395

–– at periphery, artefacts 345, 346

lymphangioma 558

–– glenohumeral joint 86

– segments 395

– lateral

lymphedema 648, 649

– temporomandibular joint 440

medial collateral ligament (MCL, knee)

–– anatomy 282, 283, 283, 286

– differential diagnosis 650

– wrist and finger 182

– anatomy 283, 283, 286, 288, 310

–– bucket-handle tear 294

lymphoma

magnetic resonance imaging (MRI)

– bursa 336, 337

–– deformed 298

disease) 191, 191, 192, 193, 196

– diffuse infiltration of bone

(MIP) 14

360, 362

–– maceration 290

– hyperintensity 290, 290

– bursitis 341

–– discoid 298–299

magnetic resonance myelography 21

– injuries 310, 310

–– displacement, ACL tear 302, 303

– Hodgkin's, see Hodgkin's lymphoma

magnetic resonance neurography 21

–– concomitant injuries 311

–– horizontal tear 291

– non-Hodgkin 488

– knee prosthesis 23, 24

–– findings 310

–– pars intermedia 288, 346

– primary, of bone 77, 535

magnetic resonance spectroscopy

–– grades 310, 311

–– tears 294, 296, 296

–– signs (MRI), sensitivity/

– lesions 290

marrow 486

– secondary, spinal 77

techniques, see techniques (MRI)

(MRS), see spectroscopy magnetization

specificity 311

–– diagnostic accuracy of MRI 296, 298

M

– longitudinal 2

– superficial and deep layers 288–289

–– interpretation of MRI 297

– transverse 2, 2

– tears 301–302, 322, 504

–– prediction of outcome of

macrodystrophia lipomatosis 562

magnetization transfer contrast

medial gastrocnemius bursa 336, 337

Madelung's deformity 197 Madelung's fatty neck 561–562

(MTC) 11, 11 – cysts, hand and wrist 217

medial ligament (elbow), strain 653

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–– superficial flexor compartment 361

treatment 297 –– therapeutic relevance of MRI 297 –– validity of MRI 296

673

Index – spinal 76, 78–79

– accessory, see accessory muscles

– medial

–– carcinomas with 76

– acute overload 461

–– anatomy 283, 283–284, 286

–– vertebral bodies 76, 78–79, 574,

– advantages of MRI 470

–– basal (root) tear 296, 296

– anatomy 446, 447

453 –– type II (fast-twitch) 445, 453, 453, 453 – fibrosis 454, 455, 465

–– bucket-handle tear 293–294

metatarsal(s)

–– functional 453

–– cysts 299

– compression syndrome 405, 407

–– specific MRI anatomy 453

–– shoulder 108

–– horizontal tear 291–292

– stress reactions/fractures 373, 381,

–– variants/developmental anoma-

– fusion 454

–– incomplete discoid 299

510

lies 454, 468

– hemorrhage/hematoma 462, 462, 464

–– longitudinal tear 291, 293

metatarsalgia 415, 416, 419

– aplasia (congenital absence) 454

–– oblique tear 291

– Morton's (neuroma) 405, 407, 419

– atrophy 454, 455, 456

– hernias 463

–– radial tear 295

metatarsophalangeal joint

–– chronic rotator cuff tear 99

– hyperplasia 454

–– tears 291, 293

– fibrous scar thickening 414

–– fatty 107, 113

– hypertrophy 454, 454, 455, 455

– meniscocapsular separation 292

– sesamoids 371, 373, 415

–– full-thickness tears 463

– hypoplasia 454

– mucoid degeneration 290, 290

methemoglobin, tumors with 519

–– grading 99–100

– hypotrophy 454, 455

– ossification and calcification 300

Meyerding grading system 33

–– inactivity causing 107

– infective necrosis 455

– parameniscal cysts 299, 300

microfractures 504

–– muscular dystrophy 456

– inflammatory myopathy 457

– pars intermedia 283, 288, 346

midcarpal joint 182, 184

–– shoulder, see shoulder,

–– See also myositis

–– magic angle artefact 658, 658

midfoot, chronic osteomyelitis 501

–– narrowed, missing, deformed 293,

Mitchell's signal pattern, necrotic

294

regions 240–241

supraspinatus muscle

– injuries, classification 463

– avulsion 463, 464

– irreversible damage 455

– biopsy 445, 454, 457, 469

– ischemic necrosis 455

– chemotherapy-associated

– lipomatous transformation 457

– posterior horns 283

mitochondrial disease 446

–– tear 291

mitochondrial myopathy 446

– postoperative changes 297

mixed weighted sequence 4

– chronic overload 464

– myotonic disorders 456

–– meniscal suture 297

Modic stages

–– See also myositis ossificans

– necrosis 454, 455

–– meniscectomy 298

– mixed forms 43

–– myotendinitis 464, 465

– neuropathies affecting 455

–– partial resection 297

– stage I 41, 42, 44

– clinical relevance of MRI 469

– normal MRI 453, 454

– ring (variant) 298

– stage II 42, 43–44

– compartment syndrome 467, 467

– pathological abnormalities 444

– structure 283, 288

– stage III 43, 43

– compartments, see muscle

– patterns on MRI imaging 454, 454

– subluxation (extrusion) 301, 301

modified Dixon (mDixon) technique 7,

– suture 297

9

changes 460

compartments – contusion 461, 468

– MR spectroscopy 444

– physiologic activity 453 – pitfalls of image interpretation 454,

– tears 290, 350

– See also Dixon technique

– damage, overload causing 461

–– basal (root) 296, 296, 301

mortise plane 358

– delayed-onset soreness 461, 461

–– denervation findings 468

–– bucket handle 288, 291, 291, 292,

Morton's metatarsalgia (neuroma) 405,

– denervation 455–456, 456, 468

–– inversion recovery sequences 468

–– acute to subacute 456

–– signal variations, superficial

292, 293, 293–294, 296

407, 419

468

–– cleavage 290

mosaicplasty 321

–– chronic 456

–– closed 290

motion artefacts, spine 41

–– misinterpretation 468

– proton spectra 6

–– complex 296

motion MRI, see cinematic MRI

–– reversible 456

– pseudohypertrophy 454, 455

– diagnostic MRI 453

– radiotherapy-associated changes 460

– disorders 454, 454

– renervation 456

– dystrophy, see muscular dystrophy

– sarcoidosis 458

– edema 454, 455, 457, 458, 461, 468

– scar fibrosis 455

– energy demands 445

– secondary myopathy 467

mucoid cysts, foot 413

– energy metabolism 444

– signal intensities 7, 453–454, 519

mucoid degeneration

–– fatty acid oxidation 445

– strain 461

–– horizontal 291–292

– acetabular labrum 264

–– glycolysis 445

– strain-related injury 461

–– longitudinal 292, 292–293, 296

– menisci (knee) 290, 290

–– muscle fiber types 445

– supernumerary 454

–– MRI signs 292

– temporomandibular disk 430, 431

– energy metabolism impairment 446

– tears 462, 462

–– oblique 291

multi-echo SE sequence, turbo spin-

–– glycogenosis 446

–– full-thickness 462

–– mitochondrial disease 446

–– partial (fiber bundle) 462, 463

–– degenerative 290, 290, 291 –– diagnosis results (MRI) 297 –– discoid 299 –– displaced fragments 292, 293–295 –– flap 291, 291–292 –– fragment in intercondylar notch 293, 294

–– parrot-beak 295, 295

examinations MRI subtraction technique, arthritis of hand 222 MTC, see magnetization transfer contrast (MTC)

echo (TSE) sequence vs 2–3

muscles 468

–– radial 295, 295

multiplanar reformatting 5, 15

–– muscular dystrophy 446

– trauma, repetitive 465

–– traumatic, see below

multiple cartilaginous exostoses 543,

–– myositis 446

– traumatic myopathy, see traumatic

–– validity of MRI 296 – traumatic tears and avulsions 291,

544 multiple myeloma 488, 489, 491

–– spectroscopy 446 –– spinal muscular atrophy 446

myopathy – treatment monitoring 469

– diffuse pattern 488, 490

– examination technique (MRI) 444

– tumorlike lesions 464

–– complex 296

– spinal involvement 74, 76, 489–491

–– axial plane 444

– tumors 468

–– detachment 296

– staging and clinical course 490–491,

–– coils 468

–– classification 560

– exercise 445

–– differential diagnosis 454–455

296

–– dislocation after 301, 301

491

–– longitudinal 291

multiple sclerosis

–– ATP levels 444

– variant insertions 454

–– transverse (radial) 295

– differential diagnosis 40

–– energy metabolism 444–445, 445

muscular dystrophy 446, 456

metacarpal bones

– spinal cord 40, 41

–– MRI signal intensity 453–454

– Duchenne's 456, 457

– ligaments between 184

muscle cells, rhabdomyolysis 467–468

–– T2 relaxation times 453, 454

– progressive 456

– osteoid osteoma 215

muscle compartments 446, 447, 467,

– fat deposition, in muscular

musculoskeletal tumors 530

– tendons and ligament at level of 187

674

576, 578

–– type I (slow-twitch) 445, 453, 453,

524, 525

metastases 566

– compartment syndrome 467, 467

– See also specific tumors

– forearm 524, 525

dystrophy 456–457 – fiber bundle tears (partial tears) 462, 463

– See also bone tumors, soft tissue tumors – primary 530

– bone, see bone tumors

– lower leg 524, 525

– fiber tears 462, 462

– femur 10, 72, 516, 517

– thigh 524, 525

–– shoulder 109, 115

myelofibrosis 493, 494–495

– in bone marrow 567

– upper arm 524, 525

– fiber types 445, 453, 453

myelography, magnetic resonance 21

– osteoplastic 37

muscle(s) 444

–– diagnostic MRI 453

myelomalacia 64

– skeletal 71, 72

– abscess 455

myelocele 36

myelomeningocele 36, 36

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– magic angle artefact 658, 658

Index – conjoined 38, 38

Osborne's ligament 152

– benign/semi-malignant 483

– ganglia 38

oscillation period, GRE sequences 5, 7

– idiopathic osteomyelofibrosis 493

– sheath cysts 38, 38

Osgood–Schlatter's disease 315, 328,

osteochondroma (ecchondroma) 541, 542–543 – femur 542–543 – foot 379

– malignant 485

nerve(s), signal intensities 519

mylohyoid 635, 636

neural foramina, anatomy 32

ossification

– humerus 542

myocytes, energy metabolism 444

neurofibroma 558

– femoral condyle 344

– multiple 543, 544

myogenic tumors 560, 565

– giant (plexiform) 558

– meniscal 300

– pseudobursae due to 541, 542–543

myopathy, see specific muscle disorders

neuroforamina 37

– sacroiliac joint 611, 611, 615–616

osteochondromatosis

– endocrine 468

– narrowing/stenosis 38, 48, 51, 65

– traumatic myositis ossificans 465,

– biceps tendon 106, 112

– secondary 467

neurogenic tumor 559, 560–561

– traumatic, see traumatic myopathy

neurography, magnetic resonance 21

ossification centers

– hip 266, 267

myositis 446

neuroma, Morton's 405, 407, 419

– acromion, see acromion

– primary idiopathic 266

– chronic, lipomatous

neuropathies

– cuneiform 371

– secondary 266, 267

– elbow 168, 176–177

– femoral head 248, 252

– shoulder 124, 126

transformation 457

340

466

– elbow 165, 170

– idiopathic 457, 457

– foot

– patella 347–348

osteochondrosis, spine 51

–– polymyositis 457, 457, 458

–– diabetic, see diabetic foot syndrome

– persistent

osteoclastoma, see giant cell tumor

– inclusion body 457, 457

–– nondiabetic 348

–– acromion 137, 137, 139

osteodystrophia fibrosa localisata 568

– infectious 457

– muscle damage 455

–– cuneiform 371

osteofibrous dysplasia 544

–– bacterial 458, 459–460

– obturator 270, 274

– sacral 590

osteogenic sarcoma 517

–– pyogenic 458, 459–461

– periarticular, knee 342

– secondary 475

– chemotherapy response,

–– viral 458, 458

neuropraxia 455

osteitis

myositis ossificans

neurotmesis 456

– jaws 637, 638

– necrotic vs viable tissue 526, 526

– traumatic 464, 466

neurovascular bundles

– juxta-/periarticular (sacroiliac

osteoid osteoma 535

– types 465

– ankle 361

myotendinitis 464, 465

– infiltration, tumor extension 524

myotonic disorders 456

neurovascular compression syndrome,

myxofibrosarcoma 549–550, 553

hip 270, 274

joints) 598, 606–607 osteitis condensans ilii and sacri, sacroiliac joint 613, 617–618 osteitis deformans (Paget's disease) 37,

monitoring 527, 527

– cortical type 537, 538–539 – femur 538 – foot 411, 414 – giant, see osteoblastoma – hip 275, 539, 539

myxoid matrix 520, 564

Nex signal excitations 17

myxoma, intramuscular 552

non-Hodgkin lymphoma 488

osteoarthritis

– intra-articular type 539, 539

nonossifying fibroma 544, 546

– ankle 406

– medullary (trabecular) type 538

N

notchoplasty 309

– early-onset

– metacarpal bone 215

notochord remnants 37

–– hip 261, 265

– spinal 73, 74, 535

nail bed 216

nuclear Overhauser effect 19

–– knee 317

– subperiosteal type 538

nasopalatine canal 635, 636

nucleus pulposus 39, 44, 44

– femoropatellar joint 312

– tibia 538

navicular 365, 396

– bulging 39, 45

– foot 406

osteolysis, clavicle 127

– anatomic variants 390

– degenerative changes 44

– sacroiliac joint 611

osteoma 539

– coalition with anterior calcaneal

– positive pressure 44

– talocrural joint, secondary 409, 412

– posterior supratrochlear bone 172

– temporomandibular joint 436, 438

– shoulder 124

– wrist 197

osteomalacia

osteoarthrosis deformans, sacroiliac

– sacroiliac joint 619, 620

process 378, 386, 389 necrosis – avascular, see avascular necrosis (osteonecrosis)

O oarsman's wrist/forearm 219

568

joint 611

– sun-deficiency 619, 620

– bone 481, 501

oblique sagittal plane, see sagittal plane

osteoblastoma 539

osteomyelitis 408, 497

– fatty tissue 651, 651, 652

obturator externus bursa 272, 277–278

– pseudomalignant 539

– acute, bone marrow 500, 500, 504

– muscles 454, 455

obturator membrane 237

– spinal 73

– chronic 501–503

necrotic tissue, viable tissue vs 526,

obturator nerve, compression 274

osteochondral injuries

–– bone marrow 501, 501 – chronic recurrent multifocal

obturator neuropathy 270, 274

– ankle 367

necrotizing fasciitis 648, 650

occult fractures, see fracture(s), occult

– classification 369

Neer's stages, impingement 95–96

odontogenic keratocystic tumor 639,

– foot 369

526

neoarthrosis 100

639

nerve compression syndrome

olecranon 147

(CRMO) 501 – diabetic foot syndrome 408, 410

– knee 318

– foot 374

– talocrural joint 367, 368

– hip 262

– ankle 402

– notch in joint surface 155, 173

– talus 367, 368, 416

– jaws 637, 638

– elbow 168, 176

– persistent bone center 173

osteochondritis, see juvenile

– plasma cell 501, 503

– foot 402

– synovial tunnel, transverse

– hip 270, 274, 274

groove 154

osteonecrosis

– tibia 375, 385

– elbow 166

osteomyelosclerosis 493, 494 osteonecrosis, see avascular necrosis

– knee 342

– wear 653

– posttraumatic, talus 367

– shoulder 108, 114

olecranon bursa 155, 157

– secondary, elbow 170

– wrist, see wrist

olecranon bursitis 161, 168, 175

– spontaneous, talus 367

nerve compression/entrapment

Ollier's disease 540

osteochondritis dissecans

– axillary nerve 108, 114

omarthrosis, see shoulder, arthrosis

– elbow 166, 171

– deep peroneal nerve 405

onion-skin phenomenon 531–532, 535

– etiology 324

– diffuse, in systemic mastocytosis 483

– femoral nerve 274

open high field scanners 657, 657, 658

– knee 324

osteopetrosis 492, 492

– intermetatarsal nerve 405

opposed-phase imaging, spine 29

–– atypical 327

osteophytes 48

– median nerve (wrist), see carpal

opposed-phase TE 5, 7

–– secondary, avascular necrosis

tunnel syndrome

orthopantomography 437, 440

with 326

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myeloproliferative diseases 483, 486

(osteonecrosis) osteonecrosis, juvenile, see juvenile osteonecrosis osteopenia 501

– coracoid process 101 – foot 406

– obturator nerve 274

os peroneum 370

–– staging 324, 325

– knee 317, 318

– sciatic nerve 274

os tibiale externum syndrome 371, 372

–– types 324

– metacarpal 201

– sural nerve 406

os triangulare 184

–– types IV and V 324, 326

– sternoclavicular arthrosis 134

– tibial nerve 343, 403

os trigonum 371

– talus/ankle 367, 368–369

– temporomandibular joint 437, 437–

–– See also tarsal tunnel syndrome

os trigonum syndrome 399, 401

– temporomandibular joint 437

nerve roots 38

os triquetrum secundarium 184

438 osteophytosis, shoulder arthrosis 131

675

Index pain

– Ewing's, see Ewing's sarcoma

osteoporosis 574

– Achilles tendon 406

– osteogenic, see osteogenic sarcoma

– clinical relevance of MRI 581

– back, chronic (inflammatory) 596,

SE sequence, see spin-echo (SE)

601, 603–605, 621

– examination techniques and diagnosis 574

– discogenic 46

sensory neuropathy, foot, diabetic, see

T1-weighted sequence, see spin-echo (SE) sequence T2-weighted sequence, see spin-echo

–– See also T2* time (effective T2 time)

– heel 403, 404

–– high-resolution MRI 574, 576, 581

– hip 247, 259, 271, 273–275, 497

septic arthritis, see bacterial arthritis

talocrural joint, see ankle

–– image and structural analysis 579

– knee 350

seronegative spondyloarthropathy, see

tears (muscles/tendons), see specific

–– MRI 574, 581

– shoulder 115

–– postprocessing, CT data 579

– wrist 191

–– quantitative assessment 580–581

palatal torus 641

–– relaxation time measurements 579

palmar fibromatosis (Dupuytren's

–– spectroscopy 581

disease) 220, 401, 557

–– T2* time 579, 580, 580, 581

Palmer classification 209, 211

– fractures 78, 574

panmyelopathy 492, 493

–– acute traumatic vs osteoporotic 576

Panner's disease 167, 171

–– blastomous vs, vertebral body 59,

pannus tissue, foot/ankle 406

61, 63

patella, fat pad under, see Hoffa's fat

–– bone tumors vs 574

pad

–– compression 576, 577–578

pelvis, see hip

–– femoral neck 576

periodontal apparatus, see entries

–– fish vertebrae deformity 575, 577 –– fluid sign 76, 78

beginning dental, jaws pitfalls in image interpretation, see

–– insufficiency 574

individual anatomic regions

diabetic foot syndrome

spondyloarthropathy short-tau inversion recovery, see STIR sequence shoulder, see specific anatomic structures – biceps tendon disorders, see biceps tendon – dislocation, see glenoid labrum, disorders – glenoid labrum disorders, see glenoid labrum – impingement syndrome, see rotator cuff – instability, see shoulder, dislocation – muscle atrophy, see supraspinatus muscle

–– metastases vs 576, 578

plantar aponeurosis, see plantar fascia

– rotator cuff disorders, see rotator cuff

–– occult 574

plasmacytoma, see multiple myeloma

spectroscopic imaging, see chemical

–– pathologic fractures vs 574, 577–

plicae, see specific plicae

578 –– pelvic ring 574, 576 –– sacrum 574

spectroscopy

– intervertebral disks, see

– hydrogen, see hydrogen (1H)

intervertebral disks – meniscus, see meniscus (menisci),

–– spinal 59, 61, 63, 76, 79, 568, 577

knee

–– spinal, age determination 574, 575

– spine, see spine

–– vertebral bodies 76, 78–79

prosthesis MRI, hip, see hip

– generalized 574

proton spectroscopy, see hydrogen

– in rheumatoid arthritis 55 – intervertebral disks 576

shift imaging

postoperative appearance/changes

–– risk, assessment 580

spectroscopy pulley lesions, see under biceps tendon

spectroscopy – phosphorus, see phosphorus (31P) spectroscopy spin-echo (SE) sequence, turbo (fast), see turbo spin-echo (TSE) sequence spine, see vertebral bodies – degenerative changes/conditions, Modic stages, see Modic stages

– kyphoplasty, MRI for planning 576

– disks, see intervertebral disks

– microstructural changes 574

R

– fractures, see vertebral bodies

recess(es), shoulder

– postoperative changes, disks, see

– quantitative assessment 574 – trabecular bone microarchitecture 574, 576

– subcoracoid, see subcoracoid recess

– trabecular density low 580, 580

– sublabral, see sublabral recess

– trabecular thinning 580

relaxation times, see T1 relaxation time,

– transient –– bone marrow 497

T2 relaxation time revascularization, intervertebral disks, see intervertebral disks

–– foot 374 –– hip 242, 245–246, 497, 499

rheumatoid disorders, sacroiliac joints, see sacroiliac joint

–– knee 324, 499 – vertebroplasty, MRI for planning 576

rotator cuff, see infraspinatus muscle,

– neuroforamina, see neuroforamina intervertebral disks – posttraumatic changes, fractures, see spine, fractures – rheumatoid arthritis, see rheumatoid arthritis

changes spur, see osteophytes – heel, see heel spurs

– chondroblastic 532 – extraosseous 531 – femur 524 – parosteal (juxtacortical) 529 – periosteal 531, 532–533 – periosteal reaction 529, 531, 532 – skip lesion (daughter metastases) 516, 517, 529 – telangiectatic 531, 534–535 osteosynthesis materials, MRI and 70 overloading injuries, sports 652, 653 owl sign 41

stress fractures, see fracture(s), stress subchondral bone bruises, see bone bruise

S

subcoracoid bursa, glenoid labrum

sacroiliac joint, inflammatory

superficial soft tissue tumors, see soft

disorders, see glenoid labrum rheumatoid disorders, see sacroiliitis

– ankylosing spondylitis, see ankylosing spondylitis – spondyloarthritis, see spondyloarthritis sacroiliitis, see sacroiliac joint, inflammatory rheumatoid disorders – ankylosing spondylitis, see ankylosing spondylitis

P

– inflammatory rheumatoid, see

Paget's disease 37, 568

sarcoma

sacroiliac joint

temporomandibular joint (TMJ) – condylar head, see mandibular condyle – disk disorders, internal derangement, see disk displacement (below) – trauma, fractures, see mandibular neck, fractures tendinopathy – insertional, see insertional tendinopathy – noninsertional, see tendinitis tendinosis, see tendinitis tendon insertion lesions, see insertional tendinopathy tendon sheath, see peritendinitis, tenosynovitis – giant cell tumors, see giant cell tumor tendon(s), see specific tendons – accessory, see accessory tendons tendovaginitis, see tenosynovitis TFCC, see triangular fibrocartilage complex (TFCC) three-dimensional rendering, see three-dimensional display, MRI trabecular bone, see bone transient osteoporosis, see osteoporosis, transient traumatic lesions/changes – bone marrow, see bone marrow – meniscus, see meniscus (menisci), knee – spine, see spine traumatic myopathy, see specific conditions under 'muscles' triangular fibrocartilage complex

– trauma, see spine, posttraumatic

muscle, teres minor subacromial impingement

techniques teeth, see entries beginning dental

– spondylodiscitis, see spondylodiscitis

subscapularis muscle, supraspinatus – impingement, subacromial, see

muscles/tendons techniques (MRI), see specific

triangular disk, see ulnar triangular disk

osteosarcoma 518, 529 monitoring 527, 527

(SE) sequence

– spondylitis, see spondylitis

osteoradionecrosis, jaws 638 – chemotherapy response,

676

sequence

T

tissue tumors superior labral complex lesions, see SLAP lesions surgery, see postoperative appearance/ changes synovial folds, see plicae synovial osteochondromatosis, see osteochondromatosis synovitis, pigmented villonodular, see pigmented villonodular synovitis

(TFCC), see ulnar triangular disk TSE sequence, see turbo spin-echo (TSE) sequence tumorlike substance deposits, amyloid, see amyloidosis tumors, see specific anatomic structures

U ulnar fibrocartilage complex, see triangular fibrocartilage complex (TFCC) ulnar triangular disk, see triangular fibrocartilage complex (TFCC) ulnar triangular fibrocartilage complex, see triangular fibrocartilage complex (TFCC) ulnocarpal complex, see triangular fibrocartilage complex (TFCC) upper leg, see femur, thigh

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osteoplastic metastases 37

Index

vertebrae, see spine vertebral bodies, see spine, vertebrae

vertebral body end plates, bone and bone marrow changes, see Modic stages

W wrist, see hand – avascular necrosis, spontaneous,

– nerve compression syndrome –– median nerve, see carpal tunnel syndrome –– ulnar nerve, see Guyon's canal

lunate, see lunate

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V

677

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