Musculoskeletal MRI [1 ed.] 0340906618, 9780340906613

Table of contents :
Cover
Book title
Contents
Foreword
Preface
Acknowledgements
Abbreviations
1. The shoulder girdle
Technique
The rotator cuff
Pathology of the superior rotator cuff
Pathology of the anterior rotator cuff
Miscellaneous pathologies of the rotator cuff
The rotator interval
Pathology of the rotator interval
The long head biceps tendon
Pathology of the long head biceps tendon
The shoulder bursae
Pathology of the shoulder bursae
The capsule and labrum
Pathology of the capsule and labrum
The superior glenoid labrum
Pathology of the superior labrum
Miscellaneous conditions of the glenohumeral joint
The nerves
Pathology of the nerves
The post-operative shoulder
The acromioclavicular joint
Pathology of the acromioclavicular joint
The sternoclavicular joint
Pathology of the sternoclavicular joint and medial clavicle
The scapulothoracic joint
Pathology of the scapulothoracic joint
The thoracohumeral muscles
Pathology of the thoracohumeral muscles
References
2. The elbow
Technique
The bones and joints
Pathology of the bones and joints
The joint capsule
Pathology of the capsule
The ligaments
The muscles and tendons
The bursae
Pathology of the bursae
The nerves
References
3. The wrist and hand
Technique
The distal radioulnar joint
Pathology of the distal radioulnar joint
The radiocarpal and ulnocarpal joints
Pathology of the distal ulna
The carpus
The tendons and muscles of the wrist
The nerves
The carpometacarpal joints
The metacarpophalangeal joints
The proximal interphalangeal joints
The finger extensor tendons
Pathology of the finger extensor tendons
The finger flexor tendons
Pathology of the finger flexor tendons
Miscellaneous tumours and pseudotumours of the wrist and hand
References
4. The hip joint and pelvic girdle
Technique
The hip joint
The hip bursae
The paediatric hip
The post-operative hip
The pelvic bones
Pathology of the pelvic bones
The pelvic muscles
The pelvic nerves
Pathology of the pelvic nerves
References
5. The knee
Technique
The menisci
Pathology of the menisci
The cruciate ligament
The medial capsular structures
Pathology of the medial capsular structures
The posteromedial corner
Pathology of the posteromedial corner
The lateral capsular structures
The posterior capsular area
Pathology of the posterior capsular area
The extensor mechanism
Miscellaneous knee injuries
Miscellaneous knee conditions
Miscellaneous aspects of the paediatric knee
The proximal tibiofibular joint
Pathology of the proximal tibiofibular joint
The post-operative knee
References
6. The ankle and foot
Technique
The distal tibiofibular joint
Pathology of the distal tibiofibular joint
The tibiotalar joint
The flexor tendons
The extensor tendons
The foot
The hind-foot
The mid-foot
The forefoot
Pathology of the forefoot bones
The forefoot nerves
Miscellaneous paediatric foot and ankle conditions
Soft-tissue masses of the ankle and foot
The post-operative ankle and foot
References
7. The joints
Technique
Degenerative pathology of the joints
Inflammatory arthropathy
Crystal arthropathy
Miscellaneous arthropathies
Infection
Tumours and tumour-like lesions
References
8. The limbs
Technique
Anatomy
Pathology of the bones
The bone marrow
Pathology of the bone marrow
Miscellaneous conditions of bone
Pathology of the soft tissues
The peripheral nerves
Pathology of the peripheral nerves
References
9. The spine
Technique
The craniocervical junction
Pathology of the craniocervical junction
The subaxial spine
Degenerative disorders of the subaxial spine
Subaxial spinal deformity
Traumatic disorders of the subaxial spine
Infective disorders of the subaxial spine
Neoplastic disorders of the subaxial spine
Primary spinal tumours
Miscellaneous conditions of the vertebrae
Inflammatory disorders of the subaxial spine
The lumbosacral junction
Pathology of the lumbosacral junction
The sacrum and sacroiliac joints
Pathology of the sacrum and sacroiliac joints
The post-operative spine
References
Index
A
B
C
D
E
F
G
H
I
J
K
L
M
N
O
P
Q
R
S
T
U
V
W
X
Y
Z

Citation preview

Musculoskeletal MRI

Asif Saifuddin Consultant Musculoskeletal Radiologist The Royal National Orthopaedic Hospital NHS Trust Stanmore, UK Honorary Senior Lecturer The Institute of Orthopaedics and Musculoskeletal Research University College London Stanmore, UK Consultant Musculoskeletal Radiologist Medtel UK, The Alliance Medical Imaging Centre and The London Upright MRI Centre London, UK

PART OF HACHETTE LIVRE UK

First published in Great Britain in 2008 by Hodder Arnold, an imprint of Hodder Education, part of Hachette Livre UK, 338 Euston Road, London NW1 3BH http://www.hoddereducation.com Distributed in the United States of America by Oxford University Press Inc., 198 Madison Avenue, New York, NY10016 Oxford is a registered trademark of Oxford University Press

© 2008 Asif Saifuddin All rights reserved. Apart from any use permitted under UK copyright law, this publication may only be reproduced, stored or transmitted, in any form, or by any means with prior permission in writing of the publishers or in the case of reprographic production in accordance with the terms of licences issued by the Copyright Licensing Agency. In the United Kingdom such licences are issued by the Copyright licensing Agency: Saffron House, 6-10 Kirby Street, London EC1N 8TS. Hachette Livre UK’s policy is to use papers that are natural, renewable and recyclable products and made from wood grown in sustainable forests. The logging and manufacturing processes are expected to conform to the environmental regulations of the country of origin. Whilst the advice and information in this book are believed to be true and accurate at the date of going to press, neither the author[s] nor the publisher can accept any legal responsibility or liability for any errors or omissions that may be made. In particular, (but without limiting the generality of the preceding disclaimer) every effort has been made to check drug dosages; however it is still possible that errors have been missed. Furthermore, dosage schedules are constantly being revised and new side-effects recognized. For these reasons the reader is strongly urged to consult the drug companies’ printed instructions before administering any of the drugs recommended in this book. British Library Cataloguing in Publication Data A catalogue record for this book is available from the British Library Library of Congress Cataloging-in-Publication Data A catalog record for this book is available from the Library of Congress ISBN-13 978-0-340-90661-3 1 2 3 4 5 6 7 8 9 10 Commissioning Editor: Project Editor: Production Controller: Cover Design: Indexer:

Gavin Jamieson Francesca Naish Andre Sim Helen Townson Laurence Errington

Typeset in 10 on 12pt Minion by Phoenix Photosetting, Chatham, Kent Printed and bound in Great Britain by MPG Books, Bodmin What do you think about this book? Or any other Hodder Arnold title? Please visit our website: www.hoddereducation.com

To my mother and father: Razia and Ali Anwar Saifuddin You raised me on the ‘straight path’.

And to my wife and children: Saira, Hashim, Zehra, Sahar and Umar Humza You helped to keep me there, once I had reached it.

This page intentionally left blank

Contents

Foreword Preface Acknowledgements Abbreviations 1.

The shoulder girdle Technique The rotator cuff Pathology of the superior rotator cuff Pathology of the anterior rotator cuff Miscellaneous pathologies of the rotator cuff The rotator interval Pathology of the rotator interval The long head biceps tendon Pathology of the long head biceps tendon The shoulder bursae Pathology of the shoulder bursae The capsule and labrum Pathology of the capsule and labrum The superior glenoid labrum Pathology of the superior labrum Miscellaneous conditions of the glenohumeral joint The nerves Pathology of the nerves The post-operative shoulder The acromioclavicular joint Pathology of the acromioclavicular joint The sternoclavicular joint Pathology of the sternoclavicular joint and medial clavicle The scapulothoracic joint Pathology of the scapulothoracic joint The thoracohumeral muscles Pathology of the thoracohumeral muscles References

2.

The elbow Technique The bones and joints Pathology of the bones and joints The joint capsule Pathology of the capsule The ligaments The muscles and tendons The bursae

xi xiii xv xvii 1 1 5 15 24 33 35 37 38 40 42 44 45 52 66 68 71 75 76 79 84 86 90 91 92 93 95 95 97 105 105 107 111 115 117 118 123 135

viii Contents

Pathology of the bursae The nerves References

135 137 142

3.

The wrist and hand Technique The distal radioulnar joint Pathology of the distal radioulnar joint The radiocarpal and ulnocarpal joints Pathology of the distal ulna The carpus The tendons and muscles of the wrist The nerves The carpometacarpal joints The metacarpophalangeal joints The proximal interphalangeal joints The finger extensor tendons Pathology of the finger extensor tendons The finger flexor tendons Pathology of the finger flexor tendons Miscellaneous tumours and pseudotumours of the wrist and hand References

145 145 147 148 149 161 162 183 193 200 204 208 210 211 212 212 215 221

4.

The hip joint and pelvic girdle Technique The hip joint The hip bursae The paediatric hip The post-operative hip The pelvic bones Pathology of the pelvic bones The pelvic muscles The pelvic nerves Pathology of the pelvic nerves References

225 225 228 263 266 272 274 278 282 299 302 304

5.

The knee Technique The menisci Pathology of the menisci The cruciate ligament The medial capsular structures Pathology of the medial capsular structures The posteromedial corner Pathology of the posteromedial corner The lateral capsular structures The posterior capsular area Pathology of the posterior capsular area The extensor mechanism Miscellaneous knee injuries Miscellaneous knee conditions Miscellaneous aspects of the paediatric knee The proximal tibiofibular joint Pathology of the proximal tibiofibular joint The post-operative knee References

309 309 312 327 344 362 364 368 370 373 386 389 393 428 441 452 456 457 459 474

Contents

6.

The ankle and foot Technique The distal tibiofibular joint Pathology of the distal tibiofibular joint The tibiotalar joint The flexor tendons The extensor tendons The foot The hind-foot The mid-foot The forefoot Pathology of the forefoot bones The forefoot nerves Miscellaneous paediatric foot and ankle conditions Soft-tissue masses of the ankle and foot The post-operative ankle and foot References

484 484 487 489 490 508 531 540 540 573 583 584 595 599 601 603 606

7.

The joints Technique Degenerative pathology of the joints Inflammatory arthropathy Crystal arthropathy Miscellaneous arthropathies Infection Tumours and tumour-like lesions References

611 611 616 620 628 632 637 643 656

8.

The limbs Technique Anatomy Pathology of the bones The bone marrow Pathology of the bone marrow Miscellaneous conditions of bone Pathology of the soft tissues The peripheral nerves Pathology of the peripheral nerves References

661 661 662 677 764 766 777 783 856 857 880

9.

The spine Technique The craniocervical junction Pathology of the craniocervical junction The subaxial spine Degenerative disorders of the subaxial spine Subaxial spinal deformity Traumatic disorders of the subaxial spine Infective disorders of the subaxial spine Neoplastic disorders of the subaxial spine Primary spinal tumours Miscellaneous conditions of the vertebrae Inflammatory disorders of the subaxial spine The lumbosacral junction Pathology of the lumbosacral junction The sacrum and sacroiliac joints

889 889 898 904 922 951 1006 1034 1067 1079 1079 1110 1118 1133 1136 1138

ix

x Contents

Pathology of the sacrum and sacroiliac joints The post-operative spine References Index

1142 1160 1177 1191

Foreword

Asif Saifuddin, a prolific contributor to the peer reviewed imaging literature, and Consultant at the renowned Royal National Orthopaedic Hospital in Stanmore, UK, has produced a well-crafted and highly informative text on MR imaging of the axial and appendicular skeleton. Dr. Saifuddin, especially well-known in Europe, has always written and spoken with crispness, clarity and content. The lucidity and learning value of this beautifully produced comprehensive text is based on the cogent bullet points that augment over 4000 illustrations. The appendicular skeleton is discussed in two distinct subtitles: the joints and the limbs, thereby covering joint-imaging, bone marrow, muscle, bone and soft tissue neoplasms, comprehensively. In dealing with the spine in as great a detail as the appendicular skeleton, Dr. Saifuddin’s text is up-to-date in the ever burgeoning field of MR imaging of the musculoskeletal system. Musculoskeletal MR imaging is in its third decade of clinical use. In some regards it is a mature technology routinely and widely used for imaging joints, the spine, evaluation of soft tissue masses and staging of bone sarcomas. In other regards it continues to evolve with changes in magnet strength, pulse sequences, coils and clinical applications. A number of MRI musculoskeletal books have been written for the novice, the expert and those in between as MRI has evolved and knowledge acquired. Dr. Saifuddin’s text in its coverage of pulse sequences, anatomy, findings on joint imaging and musculoskeletal disease states has succeeded in providing us with an up-to-date, easily digestible, practical, informative and richly illustrated book on MR imaging of the musculoskeletal system. As a sole author text, the style throughout is uniform and easy to read. It will serve well all those engaged in musculoskeletal MRI. I anticipate this text being widely read and exhaustively used in daily clinical practice. Murali Sundaram, M.D., FRCR Professor of Radiology, Lerner College of Medicine Consultant Radiologist, Cleveland Clinic Cleveland, Ohio, USA

Preface

‘Then We made the Nutfah (the mixture of male and female sexual fluids) into a clot of congealed blood; then of that clot We made a lump (foetus); then We made out of that lump bones and clothed the bones with flesh; then We developed out of it another (independent) creature. So blessed be Allah, the best of creators!’ The Qur’an: Chapter 23; The True Believers, verse 14. The conception and development of the human embryo, and particularly its musculoskeletal system, was described in The Qur’an in the 7th Century. Now, over 1400 years later, the remarkable technique of magnetic resonance imaging can show us in the most superb detail, the anatomy and pathology of those bones and the ‘flesh that clothes them’. Asif Saifuddin London, April 2008

Acknowledgements

The author has been privileged to work as a Consultant Musculoskeletal Radiologist at The Royal National Orthopaedic Hospital NHS Trust, Stanmore, UK for 14 years. The fact that he has been able to collect the superb range of pathology illustrated within this book is a tribute to the excellence of clinical care provided by the entire staff of the Hospital. Although there is a single author named on the cover of the book, it would not have been possible to complete this task without the valued help of many colleagues and institutions. Foremost amongst these are Dr. Steven James (First RNOHT Lodestone Musculoskeletal Radiology Fellow, now Consultant Radiologist at The Royal Orthopaedic Hospital, Birmingham, UK) and Dr. Sajid Butt (Consultant Radiologist at The Royal National Orthopaedic Hospital, Stanmore, UK), who spent an excessive amount of their free time in proof reading the whole text and suggesting improvements and/or clarifications. Also, thanks to Dr. Paul O’Donnell (Consultant Radiologist at The Royal National Orthopaedic Hospital, Stanmore, UK) for the enthusiasm with which he provided cases from his personal collection of MRI studies. Mention also to Dr. Murali Sundaram of The Cleveland Clinic, Ohio, USA for agreeing to write the Foreword. I also thank Miss Kaline Ali (former Radiology Research Assistant, RNOHT, Stanmore) and the staff of the Library of The Institute of Orthopaedics, Sir Herbert Seddon Teaching Centre at The RNOHT, Stanmore for their efforts in collecting the vast amount of literature reviewed for the book. With regards to institutions, special mention is given to Medtel UK, 64 Harley Street, London, UK and to the MRI staff at The Alliance Medical Imaging Centre, Bulstrode Place, London, UK for their immense support in the preparation of this work, to The London Upright MRI Centre, Newman Street, London, UK and last but by no means least, to the MRI staff at The RNOHT, Stanmore, UK. A list of friends and colleagues who provided cases is given below.

CONTRIBUTORS Dr. Faysal Alyas Consultant Radiologist Queen’s Hospital, Romford, UK

Mr. Tim WR Briggs Consultant Orthopaedic Surgeon RNOHT, Stanmore, UK

Mr. John Angel Consultant Orthopaedic Surgeon (Retired) RNOHT, Stanmore, UK

Dr. Peter Brooks Consultant Radiologist Lister Hospital, Stevenage, UK

Dr. Hifz Aniq Consultant Radiologist Royal Liverpool University Hospital, Liverpool, UK

Mr. Stephen R Cannon Consultant Orthopaedic Surgeon RNOHT, Stanmore, UK

Dr. Sayed Babar Consultant Radiologist Hammersmith Hospital, London, UK

Mr. Adrian Casey Consultant Spinal Neurosurgeon RNOHT, Stanmore, UK

Dr. Philip Bearcroft Consultant Radiologist Addenbrook’s Hospital, Cambridge, UK

Dr. David Connell Consultant Radiologist RNOHT, Stanmore, UK

Dr. Simon Blease Consultant Radiologist Medtel, UK

Dr. Ruth Green Consultant Radiologist RNOHT, Stanmore, UK

xvi Acknowledgements

Dr. Srinivasan Harish Consultant Radiologist Hamilton, Canada

Mr. Sohaib Sait Consultant Orthopaedic Surgeon Darent Valley Hospital, Dartford, UK

Dr. Brian Holloway Consultant Radiologist Royal Free Hospital, London, UK

Dr. Imtiaz Shaikh Consultant Radiologist Bedford Hospital, Bedford, UK

Dr. Richard Hughes Consultant Radiologist Stoke Mandeville Hospital, Aylesbury, UK

Mr. Dishan Singh Consultant Orthopaedic Surgeon RNOHT, Stanmore, UK

Dr. K Jeyapalan Consultant Radiologist Glenfield Hospital, Leicester, UK

Mr. John A Skinner Consultant Orthopaedic Surgeon RNOHT, Stanmore, UK

Dr. Shahid Khan Consultant Radiologist Queen Elizabeth II Hospital, Welwyn Garden City, UK

Mr. Ben A Taylor Consultant Spinal Orthopaedic Surgeon Wellington Hospital, London, UK

Mr. Simon Lambert Consultant Orthopaedic Surgeon RNOHT, Stanmore, UK

Mr. Stuart Tucker Consultant Spinal Orthopaedic Surgeon RNOHT, Stanmore, UK

Dr. Justin Lee Consultant Radiologist Chelsea and Westminster Hospital, London, UK

Dr. Martin Warren Consultant Radiologist Luton and Dunstable Hospital, Luton, UK

Mr. Jan Lehovsky Consultant Spinal Orthopaedic Surgeon RNOHT, Stanmore, UK

Dr. Martin Watson Consultant Radiologist West Middlesex University Hospital, London, UK

Dr. Emer MacSweeney Consultant Neuroradiologist Medtel, UK

Mr. John White Consultant Orthopaedic Surgeon Queen’s Hospital, Romford, UK

Mr. Sayed Mohammed Consultant Spinal Orthopaedic Surgeon Hope Hospital, Salford, UK

Dr. Philip White Consultant Radiologist Torbay Hospital, Torquay, UK

Dr. Thillainayagam Muthukumar Consultant Radiologist RNOHT, Stanmore, UK

Dr. Rick Whitehouse Consultant Radiologist Manchester Royal Infirmary, Manchester, UK

Mr. M Hilali Noordeen Consultant Spinal Orthopaedic Surgeon RNOHT, Stanmore, UK

Dr. David Wilson Consultant Radiologist Nuffield Orthopaedic Centre, Oxford, UK

Dr. Simon Ostlere Consultant Radiologist Nuffield Orthopaedic Centre, Oxford, UK

Dr. Roger Wolman Consultant Rheumatologist and Sports Physician RNOHT, Stanmore, UK

Mr. Rob Pollock Consultant Orthopaedic Surgeon RNOHT, Stanmore, UK

Mr. Tariq Zaman Consultant Orthopaedic Surgeon Ealing Hospital, UK

To anyone missing from this list, I can only offer my sincerest apologies.

Abbreviations

3D ABC ABER AC ACI ACJ ACL ADI ADM AF AIDS AIIS AIOS AITibFL ALIF ALL ALPSA AMBRI

AP APL AS ASAD ASIS ATCCS ATFL ATT ATTL AVFs AVM AVN BF BHT BLC BP BPOP BPTB BVCF CC CFL CFT CHD CHL CID CIND CLC CMC CNL CPN CPPD CS CSF CTS dddd-POS DDH

three-dimensional aneurysmal bone cyst abduction external rotation acromioclavicular autologous chondrocyte implantation acromioclavicular joint anterior cruciate ligament atlantodens interval abductor digiti minimi annulus fibrosus acquired immune deficiency syndrome anterior inferior iliac spine acquired, instability, overstress, surgery anteroinferior tibiofibular ligament anterior lumbar interbody fusion anterior longitudinal ligament anterior labroperiosteal sleeve avulsion atraumatic, multidirectional, bilateral, rehabilitation, inferior capsular shift (if surgery required) anteroposterior abductor pollicis longus ankylosing spondylitis arthroscopic subacromial decompression anterior superior iliac spine acute traumatic central cord syndrome anterior talofibular ligament anterior tibialis tendon anterior tibiotalar ligament arteriovenous fistulae arteriovenous malformation avascular necrosis biceps femoris ‘bucket-handle’ tear biceps–labral complex brachial plexus bizarre parosteal osteochondromatous proliferation bone–patellar tendon–bone benign vertebral compression fracture coracoclavicular calcaneofibular ligament common flexor tendon coracohumeral distance coracohumeral ligament carpal instability dissociative carpal instability non-dissociative collateral ligament complex carpometacarpal joint calcaneonavicular ligament common peroneal nerve calcium pyrophosphate deposition chondrosarcoma cerebrospinal fluid carpal tunnel syndrome dedifferentiated dedifferentiated parosteal osteosarcoma developmental dysplasia of the hip

dGEMRIC DIP DISH DISI DPN DRUJ DTML (Chapter 3) DTML (Chapter 6) ECRB ECRL ECU ED EDB EDL EDM EHB EHL EI EPB EPL ESR FAI FBSS FCL FCR FCU FD FDAL FDB FDL FDP FDS FHB FHL FLAIR FOV FPL FR FS FSE FTRCT GCRG GCSF GCT GCTTS GE GLAD HADD HAGL HIZs IER IGHL IL IMC ITB IVD IVF

delayed gadolinium-enhanced MRI distal interphalangeal diffuse idiopathic skeletal hyperostosis dorsal intercalated segment instability deep peroneal nerve distal radioulnar joint deep transverse metacarpal ligament deep transverse metatarsal ligament extensor carpi radialis brevis extensor carpi radialis longus extensor carpi ulnaris extensor digitorum extensor digitorum brevis extensor digitorum longus extensor digiti minimi extensor hallucis brevis extensor hallucis longus extensor indicis extensor pollicis brevis extensor pollicis longus erythrocyte sedimentation rate femoroacetabular impingement failed back surgery syndrome fibular collateral ligament flexor carpi radialis flexor carpi ulnaris fibrous dysplasia flexor digitorum accessorius longus flexor digitorum brevis flexor digitorum longus flexor digitorum profundus flexor digitorum superficialis flexor hallucis brevis flexor hallucis longus fluid-attenuated inversion recovery field of view flexor pollicis longus flattening ratio fat-suppressed fast spin-echo full-thickness rotator cuff tear giant cell reparative granuloma granulocyte colony-stimulating factor giant cell tumour giant cell tumour of tendon sheath gradient echo glenolabral articular disruption hydroxyapatite deposition disease humeral avulsion of the glenohumeral ligament high-intensity zones inferior extensor retinaculum inferior glenohumeral ligament iliolumbar ligament intermetacarpal iliotibial band intervertebral disc intervertebral foramen

xviii Abbreviations

LCL LF LHBT LPN LST LSTV LTD LTI LTL LUCL MC MCL MCP MFC MFH MFL MGHL MHE MM (Chapter 6) MM (Chapter 8) MPFL MPN MPNST MR MRI MT MTB MTP MTSS NF NHL NOF NP OA OCD OLTs OM OPL OPLL OS PBT PCHA PCL PDW PFFD PID PIN PIP PITibFL PL (chapter 3) PL (chapter 5) PLC (chapter 5) PLC (chapter 9) PLIF PLL PLT PNET POL POLPSA PP PRS PsA PTFJ PTFL PTRCT PTS

lateral collateral ligament ligamentum flavum long head biceps tendon lateral plantar nerve lumbosacral trunk lumbosacral transitional vertebra lunotriquetral dissociation lateral trochlear inclination lunotriquetral ligament lateral band of the UCL metacarpal medial (tibial) collateral ligament metacarpophalangeal medial femoral condyle malignant fibrous histiocytoma meniscofemoral ligament middle glenohumeral ligament multiple hereditary exostoses multiple myeloma myelomatosis medial patellofemoral ligament medial plantar nerve malignant peripheral nerve sheath tumour magnetic resonance magnetic resonance imaging metatarsal mycobacterial tuberculosis metatarsophalangeal medial tibial stress syndrome neurofibromatosis non-Hodgkin’s lymphoma non-ossifying fibroma nucleus pulposus osteoarthritis osteochondritis dissecans osteochondral lesion of the talus osteomyelitis oblique popliteal ligament ossification of posterior longitudinal ligament osteosarcoma peroneus brevis tendon posterior circumflex humeral artery posterior cruciate ligament proton density-weighted proximal focal femoral deficiency prolapsed intervertebral disc posterior interosseus nerve proximal interphalangeal posteroinferior tibiofibular ligament palmaris longus patellar length posterolateral corner posterior ligamentous complex posterior lumbar interbody fusion posterior longitudinal ligament peroneus longus tendon primitive neuroectodermal tumour posterior oblique ligament posterior labrocapsular periosteal sleeve avulsion proximal phalanx post-radiation sarcoma psoriatic arthropathy proximal tibiofibular joint posterior talofibular ligament partial-thickness rotator cuff tear post-traumatic syringomyelia

PTT PVNS RA RBC RCL RCT RI RIC RLTL RSCL RSLL RTA SA SAPHO SBC SCD SCI SCIWORA SCJ SD SE SER SGHL SI SIJ SIPIL SLAC SLAP SLD SLE SLL SOC SONK SP SPGR SPR SSCM SSFP STIR STML STS SUFE T1W T2W T2*W TAFA TB TCL TD TE TFCC THL THR TL TLIF TMT TOS TTD TUBS UCL VEP VISI VMO WD

posterior tibialis tendon pigmented villonodular synovitis rheumatoid arthritis red blood cell radial collateral ligamant rotator cuff tendon rotator interval rotator interval capsule radiolunotriquetral ligament radioscaphocapitate ligament radioscapholunate ligament road traffic accident subacromial synovitis, acne, pustulosis, hyperostosis and osteitis simple bone cyst sickle cell disease spinal cord injury spinal cord injury without radiographic abnormality sternoclavicular joint subdeltoid spin-echo superior extensor retinaculum superior glenohumeral ligament signal intensity sacroiliac joint sacroiliac part of the iliolumbar ligament scapholunate advanced collapse superior labral anteroposterior scapholunate dissociation systemic lupus erythematosus scapholunate ligament synovial osteochondromatosis spontaneous osteonecrosis of the knee sacral plexus spoiled gradient recalled superior peroneal retinaculum split spinal cord malformation steady-state free precession short tau inversion recovery superficial transverse metatarsal ligament soft-tissue sarcoma slipped upper femoral epiphysis T1-weighted T2-weighted T2*-weighted trochlear articular facet asymmetry tuberculosis tibial (medial) collateral ligament trochlear depth echo time triangular fibrocartilage complex transverse humeral ligament total hip arthroplasty tendon length transforaminal lumbar interbody fusion tarsometatarsal thoracic outlet syndrome trochlea–tubercle distance traumatic, unidirectional, Bankart, surgery ulnar collateral ligament vertebral end-plates volar intercalated segment instability vastus medialis obliquus well differentiated

1 The shoulder girdle

TECHNIQUE Conventional MRI1–3 ● ● ●

● ●

the patient lies supine with the arm adducted and in neutral or mild external rotation a dedicated shoulder coil is required for high-resolution imaging a typical shoulder series comprises: ■ coronal oblique T1-weighted (T1W)/proton density-weighted (PDW) fast spin-echo (FSE) sequence; obtained from an axial scout and planned parallel to the supraspinatus tendon (Fig. 1.1), covering the subscapularis anteriorly to the infraspinatus posteriorly ■ coronal oblique fat-suppressed (FS) PDW FSE/T2-weighted (T2W) FSE sequence aligned to the supraspinatus tendon: – the addition of fat suppression improves the diagnosis of full-thickness rotator cuff tears (FTRCTs) and partial-thickness rotator cuff tears (PTRCTs) compared with conventional T2W FSE images4 – similar information may be obtained by the use of a modified short tau inversion recovery (STIR) sequence5 ■ sagittal oblique T2W FSE sequence (with/without fat suppression); obtained from an axial scout and planned perpendicular to the supraspinatus tendon, covering from the scapular neck medially to the deltoid muscle laterally ■ axial T2*-weighted (T2*W) gradient-echo (GE) sequence; covering from the acromion to the inferior glenoid rim ■ additional axial PDW FSE (± FS) sequence technical parameters: field of view 14–16 cm, slice thickness 2–3 mm and matrix 512¥512 for the post-operative shoulder:6 surgical clips/sutures may produce artefact; therefore, avoid the use of GE/FS techniques and use FSE and STIR

Figure 1.1 Axial T2*-weighted gradient-echo image through the supraspinatus muscle showing the plane for coronal oblique imaging of the shoulder, which runs parallel to the tendon (arrows).

2 The shoulder girdle

Additional sequences ● ● ●

the apprehension test position:7 the shoulder is positioned in 90° abduction and maximal tolerable external rotation, which requires an open scanner8 abduction external rotation (ABER):7 the shoulder is positioned in abduction and external rotation with the palm of the hand behind the head both techniques are usually combined with indirect or direct magnetic resonance (MR) arthrography, giving the advantage of: ■ optimal demonstration of the anterior band of the inferior glenohumeral ligament (IGHL) (Fig. 1.2): non-arthrographic MRI in the ABER position has a reported sensitivity and specificity of 94 per cent and 82 per cent for determining the status of the IGHL in patients with anterior instability9 ■ improved assessment of anteroinferior labral injuries and possible improvement of identification of rotator cuff tears10

Figure 1.2 Axial T1-weighted spin-echo fat-suppressed MR arthrogram in the abduction external rotation position showing the anterior band of the inferior glenohumeral ligament (arrow).

Kinematic MRI11,12 ● ●

using a special positioning device, kinematic MRI allows the shoulder to be imaged in the axial plane through internal to external rotation normal findings include: ■ change in morphology and signal intensity (SI) of the anterior glenoid labrum: in internal rotation the labrum is blunted and may show increased SI, while in external rotation the labrum is triangular ■ change in morphology of the anterior capsule

Indirect MR arthrography2,13 ●

● ● ●

involves the intravenous injection of gadolinium followed by 10–15 minutes of shoulder exercise, resulting in enhancement of areas of synovitis or hypervascular repair tissue and a hyperintense joint effusion (Fig. 1.3) coronal oblique, sagittal oblique and axial imaging with T1W spin-echo (SE) FS sequences are performed together with a coronal oblique T2W FSE FS/STIR sequence indirect MR arthrography may improve the detection of rotator cuff tears14 and labral abnormalities the major disadvantage is the lack of joint distension

Direct saline MR arthrography15 ● ●

this involves the intra-articular injection of 12–15 mL normal saline under fluoroscopic control intra-articular position is confirmed by initial injection of 1–2 mL iodinated contrast medium

Technique

Figure 1.3 Indirect shoulder MR arthrogram. Axial T1-weighted spin-echo fat-suppressed image showing hyperintense joint fluid (arrows).

● ●

coronal oblique, sagittal oblique and axial imaging with T2W FSE FS sequences are performed (Fig. 1.4) disadvantages: ■ does not differentiate between native joint fluid and injected joint fluid since both appear hyperintense ■ image resolution is relatively poor compared with T1W SE FS images as used in direct gadolinium MR arthrography

Figure 1.4 Direct saline MR arthrogram. Coronal oblique T2-weighted fast spin-echo fat-suppressed image showing hyperintense joint fluid.

Direct gadolinium MR arthrography2,16,17 ●

this involves the intra-articular injection of 12–15 mL dilute gadolinium/saline mixture (approximately 1:100–200) under fluoroscopic control using an anterior or a posterior approach: ■ the anterior approach is most commonly used but may result in damage to the subscapularis muscle/tendon (Fig. 1.5a), the IGHL or the anteroinferior glenoid labrum ■ the posterior approach does not involve the needle traversing any anterior capsulolabral structures and may be preferable for the assessment of anterior instability ■ imaging should be performed within 30 minutes

3

4

The shoulder girdle

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coronal oblique, sagittal oblique and axial imaging with T1W SE FS sequences (Fig. 1.5b) and/or PDW FSE sequences (Fig. 1.5c) resulting in hyperintense joint fluid differentiates injected from native joint/bursal fluid since the latter remains hypointense

a b

d c

e

f

Figure 1.5 Direct gadolinium MR arthrography. Axial T1-weighted (T1W) spin-echo (SE) fat-supressed (FS) image (a) showing the anterior labrum (arrow) and contrast within the subscapularis tendon and muscle (arrowheads). Coronal oblique T1W SE FS (b) and axial proton density-weighted fast spin-echo (FSE) images (c) showing hyperintense joint fluid (arrows). Coronal T1W SE FS (d) and T2-weighted (T2W) FSE FS (e) images showing low signal intensity (SI) within an extra-articular cyst on T1W (arrow d) and high SI on T2W (arrow e). Coronal T2W FSE FS image (f) showing oedema (arrows) within the humeral head.

The rotator cuff

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addition of a coronal oblique FS T2W FSE/STIR sequence allows assessment of: ■ bursal fluid and extra-articular cystic lesions (Fig. 1.5d, e) ■ the superior surface of the tendon ■ signal abnormality within the tendon and bone oedema (Fig. 1.5f) the ABER position may be added to the standard MR sequences (Fig. 1.2) imaging in the adduction and internal rotation position is performed by placing the palm of the hand behind the back, and aids in the identification of certain anterior labral abnormalities18

THE ROTATOR CUFF ROTATOR CUFF AND SCAPULOHUMERAL MUSCLES Normal anatomy19–21 ● ●

the rotator cuff comprises the supraspinatus, infraspinatus, teres minor and subscapularis muscles/tendons the supraspinatus muscle arises from the supraspinatus fossa of the scapula and inserts via a single large tendon onto the superior facet of the greater tuberosity, just posterior to the bicipital groove (Fig. 1.6a–c): ■ the musculotendinous junction lies within a 15° arc of the 12 o’clock position above the humeral head (Fig. 1.6a) ■ it is innervated by the suprascapular nerve (C5 and C6)

a

b

c

Figure 1.6 Normal anatomy of the supraspinatus muscle and tendon. Coronal proton density-weighted (PDW) fast spin-echo (FSE) image (a) showing the supraspinatus muscle (white arrows) arising within the supraspinatus fossa of the scapula and inserting via its tendon (white arrowhead) into the anterior tubercle of the greater tuberosity (black arrowhead). The musculotendinous junction (black arrow) lies at the level of the mid-sagittal plane through the humeral head. Sagittal PDW FSE image (b) showing the muscle belly (arrow) within the supraspinatus fossa. Sagittal PDW FSE image (c) showing the musculotendinous junction (arrow) at the level of the acromioclavicular joint.

5

6

The shoulder girdle

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the infraspinatus muscle arises from the infraspinatus fossa of the scapula (Fig. 1.7a, b) and inserts via its tendon onto the middle facet of the greater tuberosity, just posterior to the supraspinatus tendon (Fig. 1.7c, d): ■ it has a multipennate configuration with multiple tendons converging to the musculotendinous junction (Fig. 1.7a) ■ the infraspinatus tendon may be fused with the teres minor tendon, and the inferior margin also blends with the joint capsule ■ it is innervated by the distal fibres of the suprascapular nerve after it has passed into the infraspinatus fossa through the spinoglenoid notch the teres minor muscle arises from the middle third of the lateral border of the scapula and inserts via its tendon onto the inferior facet of the greater tuberosity (Fig. 1.8a, b): ■ the muscle is adherent to the posterior joint capsule and is innervated by the axillary nerve

b

a

d

c Figure 1.7 Normal anatomy of the infraspinatus muscle and tendon. Coronal oblique (a) and sagittal oblique (b) proton density-weighted (PDW) fast spin-echo (FSE) images showing the muscle (arrows) arising from within the infraspinatus fossa. The multiple tendons (arrowheads a) are visible. Sagittal oblique PDW FSE image (c) showing the infraspinatus tendon (arrowheads) posterior to the humeral head. Axial T2*-weighted gradient-echo image (d) showing the insertion of the tendon (arrows) into the middle facet of the greater tuberosity (arrowhead).

The rotator cuff

a b Figure 1.8 Normal anatomy of the teres minor muscle and tendon. Coronal oblique (a) and sagittal oblique (b) proton density-weighted fast spin-echo images showing the muscle (arrows) arising from the inferolateral aspect of the scapula inferior to the infraspinatus and inserting via its tendon (arrowhead a) into the posterior facet of the greater tuberosity.

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the subscapularis muscle arises from the anterior surface of the scapula (Fig. 1.9a, b) and inserts via multiple tendons into the lesser tuberosity (Fig. 1.9c–e): ■ superficial fibres extend to the greater tuberosity and contribute to the transverse humeral ligament, which forms the roof of the bicipital groove ■ the muscle is divided into nine bellies, and the most inferior belly may insert onto the humerus separately, distal to the remaining insertion onto the lesser tuberosity ■ occasionally, a belly inserts onto the coracoid process ■ the subscapularis is innervated by the upper and lower subscapular nerves (C5–7)

Additional scapulohumeral muscles ●

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the deltoid muscle (Fig. 1.10a–c) originates from the lateral clavicle, acromion and scapular spine and has a common insertion into the deltoid tubercle on the humeral shaft: ■ it is the strongest abductor of the glenohumeral joint and is innervated by the axillary nerve (C4–5) the teres major muscle originates from the posterior surface of the inferior angle of the scapula and inserts on the medial aspect of the intertubercular groove: ■ it is an internal rotator, adductor and extensor of the humerus and is innervated by the subscapular nerve (C5–7) the coracobrachialis muscle (Fig. 1.10d, e) originates together with the short head of biceps from the tip of the coracoid process and inserts onto the anteromedial surface of the humeral shaft: ■ it is a flexor and adductor of the glenohumeral joint and is innervated by the musculocutaneous nerve (C5–7) the triceps muscle (Fig. 1.10f): the long head of triceps originates from the infraglenoid tubercle and inferior labrum, and inserts together with the two humeral heads into the olecranon process of the ulna: ■ it acts as an extensor and adductor of the glenohumeral joint and is innervated by the radial nerve (C6–8)

MRI anatomy19 ● ● ●

the supraspinatus and infraspinatus tendons are optimally assessed on coronal and sagittal oblique images the normal rotator cuff tendon (RCT) is uniformly hypointense on all pulse sequences increased SI in the tendon on short echo time sequences may be a normal finding due to:22

7

8

The shoulder girdle

a

b

c

d

e

the magic-angle effect results in increased SI of the supraspinatus tendon on T1W/PDW and PDW FSE FS images just medial to its insertion into the greater tuberosity (Fig. 1.11a–c): – it is reported with a prevalence of 5 per cent, may be reduced by external rotation of the arm23 and disappears on T2W FSE images (Fig. 1.11d) ■ interdigitation of muscle fibres with the tendon at the musculotendinous junction, which is most marked if the shoulder is imaged in internal rotation (Fig. 1.12) the subscapularis, infraspinatus and teres minor muscles/tendons are optimally assessed on axial T2*W GE and sagittal oblique T2W FSE sequences: ■ the subscapularis tendon has a normal striated pattern on axial images, with coronal and sagittal oblique PDW/T1W SE images demonstrating multiple tendons ■

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Figure 1.9 Normal anatomy of the subscapularis muscle and tendon. Axial T2*-weighted (T2*W) gradient-echo (GE) (a) and sagittal proton density-weighted (PDW) fast spin-echo (FSE) (b) images showing the muscle (arrows) arising from the anterior scapula. Coronal oblique PDW FSE fat-suppressed (c) and sagittal oblique PDW FSE (d) images showing the multiple tendons (arrows c; arrowheads d). Axial T2*W GE image (e) shows the insertion of the tendon (arrowheads) into the lesser tuberosity.

The rotator cuff

b a

c d

e

f

Figure 1.10 The scapulohumeral muscles. Deltoid: Coronal proton density-weighted (PDW) fast spin-echo (FSE) image (a) showing the acromial origin of the deltoid (arrow). Sagittal PDW FSE image (b) showing the clavicular (arrow) and acromial (double arrows) heads of deltoid. Axial T2*-weighted (T2*W) gradient-echo (GE) image (c) showing the deltoid (arrows). Coracobrachialis: Sagittal PDW FSE image (d) showing the coracobrachialis (arrows) arising from the coracoid process (arrowhead). Axial T2*W GE image (e) showing the coracobrachialis (arrow) lying medial to the short head of biceps tendon (arrowhead). Triceps: Sagittal PDW FSE image (f) showing the origin of the long head of triceps (arrow) from the infraglenoid tubercle.

9

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The shoulder girdle

b a

d c Figure 1.11 The magic-angle effect. Coronal oblique T1-weighted spin-echo (a), proton density-weighted (PDW) fast spinecho (FSE) (b) and PDW FSE fat-suppressed (c) images showing mild increased signal intensity (SI) (arrows) in the supraspinatus tendon due to the ‘magic-angle’ effect. The tendon SI becomes normal on the T2-weighted FSE image (d).

The rotator cuff

a

b

c

d

Figure 1.12 Imaging in internal rotation. Coronal oblique proton density-weighted (PDW) fast spin-echo (FSE) (a), PDW FSE fat-suppressed (FS) (b) and T2-weighted FSE FS (c) images showing increased signal intensity (arrow) in the tendon due to imaging with the shoulder in internal rotation (d).

THE CORACOACROMIAL ARCH Normal anatomy ● ● ●

●

the coracoacromial arch comprises a combination of bony and ligamentous structures beneath which runs the RCT bony: the anterior acromion and acromioclavicular joint (ACJ), which are optimally assessed on a combination of coronal (Fig. 1.13a) and sagittal oblique images (Fig. 1.13b, c) ligamentous: coracoacromial,24 which extends from the superior surface of the coracoid process to the undersurface of the anterior acromion, being optimally assessed on sagittal oblique T2W/PDW FSE images (Fig. 1.14a) but also seen on coronal images (Fig. 1.14b): ■ its thickness varies from 2 mm to 5.6 mm acromial morphology: four types are described based on the sagittal oblique MR appearance:25 ■ type 1 – flat or slightly convex undersurface (23 per cent) (Fig. 1.15a) ■ type 2 – concave undersurface (sloping) (63 per cent) (Fig. 1.15b) ■ type 3 – hooked anterior margin (14 per cent) (Fig. 1.15c) ■ type 4 – convex undersurface; relevance uncertain (Fig. 1.15d) ■ radiographic outlet views are superior to any single sagittal oblique MR image for assessment of acromial shape, but are inferior to the combination of two sagittal oblique slices obtained at the lateral acromial edge and just lateral to the ACJ26

11

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The shoulder girdle

a b

c

Figure 1.13 The coracoacromial arch. Coronal oblique proton density-weighted fast spin-echo (FSE) image (a) showing the normal acromioclavicular joint (ACJ) (arrowhead) and the anterior acromion (arrow). Sagittal oblique T2-weighted FSE images (b, c) showing the normal ACJ (arrow b) and the acromion (arrow c).

b a Figure 1.14 The coracoacromial ligament. Sagittal oblique (a) and coronal oblique (b) proton density-weighted fast spinecho images showing the normal coracoacromial ligament (arrows) running between the coracoid process (arrowhead a) and the acromion (double arrowheads a, b).

The rotator cuff

a

b

c Figure 1.15 Acromial morphology. Sagittal oblique T2-weighted fast spin-echo images showing (a) type 1, (b) type 2, (c) type 3 (arrow) and (d) type 4 acromial morphology.

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d

low-lying acromion; defined on coronal oblique images when the anteroinferior tip of the acromion lies inferior to the plane of the distal clavicle (Fig. 1.16a): ■ may also be due to ACJ separation or instability the lateral acromion angle;27 measured on coronal oblique images (Fig. 1.16b) and has a mean of 78° (range 64–99°): ■ a statistically significant relationship exists between reduced lateral acromion angle and FTRCTs, with all cases of lateral acromion angle 15° medial to the superior aspect of the humeral head on coronal images (Fig. 1.23a) with massive cuff tears, the humeral head articulates with the undersurface of the acromion, resulting in ‘cuff arthropathy’ (Fig. 1.23b, c) the reported MRI sensitivity, specificity and accuracy for FTRCTs are excellent:20 ■ sensitivity 84–96 per cent, specificity 94–98 per cent, accuracy 92–97 per cent ■

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b a

c

Figure 1.23 Massive cuff tear. Coronal oblique T2-weighted (T2W) fast spin-echo (FSE) fat-suppressed (FS) image (a) showing tendon retraction (arrow). Coronal oblique T2W FSE (b) and sagittal proton density-weighted FSE FS (c) images showing superior migration of the humeral head, which is articulating with the acromion.

Partial-thickness rotator cuff tears ●

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PTRCTs involve only part of the vertical depth of the tendon and are subclassified as follows: ■ superior surface – involving only the bursal side of the RCT ■ inferior surface – involving only the articular side of the RCT ■ intra-substance – involving the tendon substance with no communication to the tendon surface arthroscopic grading of PTRCTs:29 1 ■ grade 1 – < ⁄4 depth of the tendon ( ⁄2 depth of the tendon (>6 mm) a particular type of acute, traumatic articular-side PTRCT is termed the ‘rim-rent’ tear:36 ■ it occurs in the anterior cuff at the tendon–bone interface as opposed to the critical zone, and is seen in a younger patient group (mean age ~31 years) ■ in the arthroscopic literature, it is referred to as the ‘PASTA’ lesion (partial articular-side supraspinatus tendon avulsion)

21

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The shoulder girdle

MRI findings ● a focal fluid-filled area of cuff disruption is seen on the bursal side of the cuff (Fig. 1.24a), on the articular side of the cuff (Fig. 1.24b) or within the cuff substance (Fig. 1.24c) ● rim-rent tears appear as a linear, transverse area of fluid SI at the tendon–bone interface (Fig. 1.24d) ● the reported MRI sensitivity, specificity and accuracy for PTRCTs are moderate: ■ sensitivity 35–44 per cent, specificity 85–97 per cent, accuracy 77–87 per cent

MR arthrography of rotator cuff tears2,16,17 ● ●

direct gadolinium MR arthrography improves the differentiation of small FTRCTs from PTRCTs and improves assessment of tear size37 indirect MR arthrography in the ABER position significantly improves the detection of PTRCTs of the supraspinatus tendon14

a b

c Figure 1.24 Partial-thickness rotator cuff tear. Bursal side: Coronal oblique T2-weighted (T2W) fast spin-echo (FSE) fatsuppressed (FS) image (a) showing fluid (arrow) within an irregular defect in the bursal side of the cuff tendon. Articular side: Coronal oblique T2W FSE FS image (b) showing fluid within a defect (arrow) in the articular side of the tendon. Intra-substance: Coronal oblique proton density-weighted (PDW) FSE image (c) showing fluid within the tendon substance. Coronal oblique PDW FSE FS image (d) showing a ‘rim-rent’ tear (arrow) of the supraspinatus tendon.

d

Pathology of the superior rotator cuff

MRI findings ● on direct gadolinium MR arthrography, the undersurface of the normal supraspinatus tendon is smooth to its lateral insertion into the greater tuberosity (Fig. 1.5a) ● an articular-side PTRCT exhibits contrast imbibition part-way into the substance of the tendon (Fig. 1.25a, b) with irregularity of the undersurface of the tendon: ■ most occur at the critical zone, 1cm medial to the tendon insertion ■ the accuracy and specificity of MR arthrography are reported to be 95 per cent and 97 per cent, respectively38 ● bursal-side PTRCTs exhibit partial-thickness, fluid-filled defects on the superior surface of the tendon on T2W FSE/STIR sequences or irregularity of the superior tendon surface: ■ they are not seen on T1W SE FS images ● an FTRCT appears as a focal or diffuse, contrast-filled gap through the whole thickness of the tendon (Fig. 1.25c), with injected gadolinium seen in the subacromial–subdeltoid bursa (Fig. 1.25d)

a

b

c

d

Figure 1.25 MR arthrography of rotator cuff tendon tears. Partial-thickness rotator cuff tear: Coronal oblique (a) and sagittal oblique (b) T1-weighted (T1W) spin-echo (SE) fat-suppressed (FS) images showing a deep partial articular-side RCT involving the infraspinatus (arrows). Full-thickness rotator cuff tear (FTRCT): Sagittal T1W SE FS image (c) showing contrast within an FTRCT (arrows). Coronal oblique T1W SE FS image (d) showing contrast in the subacromial–subdeltoid bursa (arrows).

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24

The shoulder girdle

PATHOLOGY OF THE ANTERIOR ROTATOR CUFF Subcoracoid impingement31 ●

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the subcoracoid space is located between the coracoid process and the lesser tuberosity of the humeral head and contains the subscapularis tendon and muscle (Fig. 1.26a), the middle glenohumeral ligament (MGHL), the long head biceps tendon (LHBT) (Fig. 1.26b) and the subcoracoid bursa subcoracoid (anterior/coracohumeral) impingement results from chronic compression of the subscapularis tendon/LHBT between the coracoid process and lesser tuberosity clinically, it produces anterior shoulder pain referred to the upper arm that is maximal on internal rotation and forward flexion

a

b Figure 1.26 The subcoracoid space. Axial T2*-weighted gradient-echo (a) and sagittal T1-weighted spin-echo fatsuppressed MR arthrogram (b) images showing the subscapularis tendon (arrow) lying between the tip of the coracoid process (arrowhead) and the lesser tuberosity (double arrowheads). Note also the long head biceps tendon (black arrow b).

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aetiological factors include reduced coracohumeral distance (CHD), when the coracoid tip lies close to the scapular neck due to idiopathic (developmental), post-surgical or post-traumatic causes: ■ a far lateral projection of the coracoid tip ■ a massive rotator cuff tear resulting in static anterior subluxation of the humeral head the CHD is measured between the tip of the coracoid process and lesser tuberosity: ■ the CHD is reduced in internal rotation and forward elevation ■ using cine MRI, the mean CHD in asymptomatic individuals is 11 mm in maximal internal rotation, reducing to 5.5 mm in symptomatic patients39 using MRI in the conventional external rotation position,40 females are found to have a CHD that is an average of 3 mm less than that in males: ■ a sex-adjusted CHD of 10.5–11.5 mm is significantly related to subcoracoid impingement, but has a poor predictive value (sensitivity 79–84 per cent; specificity 44–59 per cent)

MRI findings ● subcoracoid impingement is best imaged in internal rotation on axial T2*W GE images ● reduced CHD: the mean CHD in symptomatic individuals is 5.5 mm in maximal internal rotation ● subscapularis tendinopathy: the tendon lesion typically occurs 1–2 cm medial to the lesser tuberosity insertion: ■ the tendon appears hyperintense with an abnormal morphology (irregular contour, swollen or thinned) (Fig. 1.27a)

Pathology of the anterior rotator cuff

a

b

Figure 1.27 Subcoracoid impingement. Axial T2*-weighted gradient-echo image (a) showing marked reduction of coracohumeral distance (arrow) and swelling and hyperintensity of the subscapularis tendon. Axial proton densityweighted fast spin-echo image (b) showing cystic change (arrows) in the lesser tuberosity.

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additional features include cystic changes in the lesser tuberosity (Fig. 1.27b) the shape of the coracoid process (round, teardrop, oval) and the morphology of the lesser tuberosity (smooth, protuberant) are not related to the presence of subcoracoid impingement40

Anterosuperior internal impingement41 ●

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this is a rare condition resulting from impingement of the deep surface insertion of the subscapularis and/or the reflection pulley (common humeral insertion of the superior glenohumeral ligament (SGHL) and the coracohumeral ligament) and the superior or anterior glenoid rim it results in anterior shoulder pain maximal in internal rotation and forward flexion

MRI findings ● a partial tear of the deep surface of the subscapularis tendon (Fig. 1.28) is seen ● contact between the subscapularis insertion and the anterosuperior glenoid rim

Figure 1.28 Anterosuperior internal impingement. Axial T2*-weighted gradient-echo image showing increased signal intensity of the deep surface of the subscapularis tendon (arrow) consistent with a deep surface tear.

Subscapularis tendon tears42,43 ● ● ● ●

subscapularis tendon tears are uncommon, with 2–8 per cent of supraspinatus tendon tears involving the subscapularis muscle the incidence of subscapularis involvement increases with the size and chronicity of supraspinatus tears44 conversely, most subscapularis tears (69 per cent) are extensions of supraspinatus tendon tears 27 per cent are partial thickness and 73 per cent complete, while 67 per cent are limited to the cranial third of the tendon

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The shoulder girdle

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isolated tears can occur secondary to acute abduction–external rotation trauma or in elderly patients with recurrent anterior dislocation subscapularis tears are associated with: ■ reduced CDH:45 the mean CHD was 5.0±1.7 mm for subscapularis tears and 10.0±1.3 mm in the control group ■ LHBT abnormalities: subluxation/dislocation in 49 per cent and rupture in 7 per cent

MRI findings ● a poorly defined tendon contour is seen with increased SI on T2W FSE/T2*W GE images (Fig. 1.29a) ● thickening of the distal tendon and tendon discontinuity (Fig. 1.29b–d) ● complete tear: discontinuity or retraction of the tendon from the lesser tuberosity (Fig. 1.30a, b) with associated muscle atrophy (Fig. 1.30c) ● effusion in the subscapularis recess and/or subcoracoid bursa (Fig. 1.30d)

b a

d

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Figure 1.29 Partial subscapularis tendon tear. Axial T2*-weighted (T2*W) gradient-echo (GE) image (a) showing thickening, irregularity and hyperintensity of the distal cranial margin of the tendon (arrow). Coronal short tau inversion recovery (b), sagittal proton density-weighted fast spin-echo (c) and axial T2*W GE (d) images showing discontinuity of the cranial margin of the tendon (arrows), with fluid adjacent to the lesser tuberosity (arrow c).

Pathology of the anterior rotator cuff

b

a

d c Figure 1.30 Complete subscapularis tear with tendon retraction. Axial proton density-weighted fast spin-echo (FSE) (a) and sagittal T2-weighted (T2W) FSE (b) images showing absence of the tendon (arrows) anterior to the lesser tuberosity and tendon retraction (arrowhead a). Sagittal T2W FSE image (c) showing marked atrophy of the subscapularis muscle (arrows). Axial T2*-weighted gradient-echo image (d) showing a distal tear (arrow) with effusion in the subcoracoid bursa (arrowheads).

MR arthrographic findings46 ● the grading system is as follows: ■ grade 0 – normal tendon, homogeneously hypointense (Fig. 1.31a) ■ grade 1 – fraying and SI increase in the cranial portion of the tendon (Fig. 1.31b) ■ grade 2 – tear of the cranial portion of the tendon, while the inferior portion remains attached to the lesser tuberosity ■ grade 3 – a complete tear, with medial tendon retraction ● additional MR arthrographic findings: leak of contrast medium deep to the tendon onto the surface of the lesser tuberosity (Fig. 1.31c): ■ fatty infiltration of the subscapularis muscle and subluxation/dislocation of the LHBT ● sensitivity and specificity with the combination of sagittal and axial images are reported as 91 per cent and 86 per cent, respectively

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The shoulder girdle

b a

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Figure 1.31 MR arthrography of the subscapularis tendon. Axial T1-weighted (T1W) spin-echo (SE) fat-suppressed (FS) image (a) showing the normal subscapularis tendon (arrows). Coronal T1W SE FS image (b) showing fraying (arrow) of the cranial margin of the subscapularis. Axial T1W SE FS image (c) showing injected contrast medium (arrow) deep to the subscapularis tendon. Note also a cyst (arrowhead) within the lesser tuberosity.

FEATURES ASSOCIATED WITH ROTATOR CUFF TEARS Effusion and bursitis ● ●

glenohumeral joint effusion47 is rare in the normal shoulder and is therefore indicative of arthropathy or rotator cuff tear (Fig. 1.22a) subacromial–subdeltoid bursitis:48 ■ in normal individuals, the range of bursal thickness is 0–7 mm (mean 1.3 mm; median 2 mm), with most fluid seen lateral to the ACJ and in the posterior or middle quarter of the bursa ■ in patients with a rotator cuff tear, the range of bursal thickness is 0–8 mm (mean 3.3 mm; median 3 mm), with most fluid seen beneath or medial to the ACJ and in the anterior aspect of the bursa (Fig. 1.19a)

Humeral head cysts49–51 ● ● ●

subchondral humeral head cysts can be seen at various locations, being identified in 70 per cent of patients, seven times more commonly in the posterior humeral head than in the anterior head anterior cysts occur at the insertion of the supraspinatus and/or subscapularis tendons and appear to be associated with rotator cuff tears, being demonstrated in 23 per cent of cases posterior cysts are located in the bare area of the anatomical neck (posterosuperior aspect of the head/neck) and are not related to cuff disease, but may represent a degenerative/ageing phenomenon

Pathology of the anterior rotator cuff

MRI findings ● cysts show intermediate/low SI on T1W images (Fig. 1.32a) and hyperintensity on T2W images (Fig. 1.32b) ● anterior cysts are located in the lesser tuberosity (Fig. 1.32c) or greater tuberosity (Fig. 1.32d) ● cysts may be single or multiple (one to three) and are typically 2–4 mm in size ● 94 per cent of all humeral head cysts communicate with the joint as demonstrated by MR arthrography (Figs 1.31c, 1.32e)

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c d

e

Figure 1.32 Humeral head cysts. Coronal T1-weighted (T1W) spin-echo (SE) (a) and T2-weighted (T2W) fast spin-echo (FSE) (b) images showing a posterior humeral head cyst (arrows). Sagittal oblique T2W FSE image (c) showing subchondral cysts (arrow) in the lesser tuberosity, adjacent to the subscapularis tendon insertion. Axial T2W FSE fat-suppressed (FS) image (d) showing a cyst in the greater tuberosity (arrowhead) with an associated subscapularis tear (arrow). Axial T1W SE FS MR arthrogram (e) showing contrast-filled cysts (arrow) in the posterior aspect of the humeral head.

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The shoulder girdle

Acromioclavicular joint cysts52 ● ●

ACJ cysts occur due to leakage of glenohumeral joint fluid through a massive complete cuff tear into a degenerate ACJ clinically, they present as a painless pseudotumour of the shoulder in middle-aged/elderly patients

MRI findings ● the typical SI characteristics of a cyst are seen on T1W (Fig. 1.33a) and T2W/STIR images (Fig. 1.33b) ● cyst size is reported to range from 1.5 cm to 6 cm (mean 3.27 cm) ● ACJ osteoarthritis (OA) is invariable and the inferior ACJ capsule is ruptured, allowing extension of joint fluid and injected contrast at MR arthrography to enter the cyst (geyser sign) (Fig. 1.33b) ● an extensive rotator cuff tear, with/without tendon retraction, is typically seen (Fig. 1.33b)

a b Figure 1.33 Acromioclavicular joint (ACJ) cyst. Sagittal T1-weighted spin-echo image (a) showing a small intermediate signal intensity cyst (arrow) superior to the degenerate ACJ. Coronal T2-weighted fast spin-echo fat-suppressed image (b) showing extension of fluid through the ACJ (arrow) into the cyst (arrowhead), associated with a massive rotator cuff tear (double arrowheads).

Intramuscular cysts53 ● ● ●

intramuscular cysts represent a collection of joint fluid within a fascial sheath or the substance of a rotator cuff muscle they are reported with a prevalence of ~1 per cent and are always associated with an FTRCT or a PTRCT most cysts are located in the supraspinatus muscle (~55 per cent), the infraspinatus muscle (~30 per cent) or rarely in the subscapularis or teres minor, and there is usually an associated tear of the corresponding RCT

MRI findings ● the cysts are elongated, running along the length of the muscle and measuring 2–4 cm in their long axis and ~2 cm in cross-section ● they show fluid SI on T1W and T2W images (Fig. 1.34a) and may be unilocular or multilocular ● occasionally, a small tail is seen communicating with the RCT and the cyst may fill on MR arthrography (Fig. 1.34b–d)

Pathology of the anterior rotator cuff

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b

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d

Figure 1.34 Intramuscular cyst. Coronal T2-weighted fast spin-echo fat-suppressed (FS) image (a) showing a large cyst (arrow) within the subscapularis muscle. MR arthrography: Coronal T1-weighted (T1W) spin-echo (SE) FS image (b) showing a full-thickness rotator cuff tear (arrow). Sagittal T1W SE FS images (c, d) showing contrast entering the infraspinatus tendon (arrow c) and communicating with an intramuscular cyst (arrow d).

Atrophy of rotator cuff muscles ● ●

atrophy of various cuff muscles is associated with massive FTRCTs often with tendon retraction supraspinatus54 atrophy is optimally assessed on the sagittal oblique view at the base of the medial aspect of the coracoid process, referred to as the ‘Y-view’ (Fig. 1.35a): ■ supraspinatus muscle atrophy may be calculated as the occupation ratio (R): – R = the ratio between the cross-sectional area of the supraspinatus muscle belly and the crosssectional area of the supraspinatus fossa – the mean R in controls and patients with degenerative cuffs is reported to be 0.7 and 0.62 (no significant difference), respectively – the mean R in patients with an FTRCT is 0.44 (Fig. 1.35b) ■ severe atrophy may demonstrate a positive ‘tangent sign’,55 which is positive when the supraspinatus muscle does not extend above a line joining the cranial margins of the scapular body and scapular spine on the Y-view (Fig. 1.35c)

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The shoulder girdle

a

b

d c Figure 1.35 Muscle atrophy. Y-view: Sagittal oblique proton density-weighted (PDW) fast spin-echo (FSE) image (a) at the medial aspect of the coracoid process showing the normal supraspinatus muscle (arrows) filling the supraspinatus fossa. Sagittal oblique PDW FSE image (b) showing atrophy of both the supraspinatus (arrow) and the infraspinatus (arrowheads). Sagittal oblique PDW FSE image (c) showing a positive ‘tangent sign’. Sagittal oblique PDW FSE image (d) showing asymmetrical atrophy of the supraspinatus affecting the superficial portion (arrow) and sparing the deep portion (arrowhead).

supraspinatus atrophy associated with FTRCT is commonly asymmetrical;56 significantly more common on the superficial (fascial) side of the tendon than on the deep (bony) side of the tendon (Fig. 1.35d): – the deep portion of the muscle more commonly undergoes fatty infiltration – asymmetrical atrophy does not result in a change in position of the tendon within the supraspinatus fossa infraspinatus:57 reported in 4.3 per cent of shoulder MRI studies and confined to the infraspinatus in 20 per cent of these: ■ associated infraspinatus tendon tears are seen in 53 per cent of cases, while an anterior FTRCT is present in 90 per cent of cases ■ infraspinatus muscle atrophy can occur with an intact infraspinatus tendon ■

●

Miscellaneous pathologies of the rotator cuff

Chondral defects of the glenohumeral joint ●

chondromalacia of the humeral head or glenoid fossa is reported with a frequency of 29 per cent in patients undergoing arthroscopy for subacromial impingement

MRI findings ● diagnosed by MR arthrography as surface irregularity with partial/full-thickness contrast-filled defects of the articular cartilage more commonly involving the humeral head ● MR arthrography is reported to have an accuracy of 65–77 per cent for humeral lesions and 65–67 per cent for glenoid lesions

MISCELLANEOUS PATHOLOGIES OF THE ROTATOR CUFF Calcific tendinitis58 ● ● ●

● ●

calcific tendinitis of the RCT results from deposition of hydroxyapatite crystals as part of hydroxyapatite deposition disease (HADD) and is a condition of unknown aetiology ~80 per cent of cases involve the supraspinatus tendon, and the condition may be bilateral HADD may also involve the subscapularis tendon, the origins of the long and short heads of biceps (adjacent to the supraglenoid tubercle and coracoid tip, respectively), the pectoralis major tendon insertion into the anterior proximal humeral shaft59 and, less commonly, other tendons and bursae around the shoulder clinically, it presents with acute-onset or chronic pain over the lateral shoulder and upper arm, usually in the fourth to sixth decades of life, though children can be affected60 pathologically, five phases of the disorder are described: ■ first – the silent (asymptomatic) phase in which crystals are deposited in the RCT (most commonly at the critical zone of the supraspinatus) ■ second – the mechanical phase, with increasing size of crystal deposition and rupture into the tendon substance and subsequently deep to the subacromial bursa (sub-bursal rupture) or into the bursa (intrabursal rupture) ■ third – adhesive periarthritis, a chronic stage in which inflammation secondary to the extruded calcifications results in fibrosis of the peri-tendinous soft tissues and chronic symptoms, and may be associated with spontaneous rupture of the degenerated tendon ■ fourth – intraosseous loculation, an infrequent complication in which the extruded calcific material erodes into the greater tuberosity to produce a subcortical cyst ■ fifth – dumbbell loculation, resulting from compression of the semi-solid sub-bursal calcifications by the coracoacromial ligament, causing a dumbbell configuration

MRI findings ● calcification appears as focal areas of low SI or signal void on T1W and T2W SE/GE sequences (Fig. 1.36a, b) ● tendon oedema may be seen on T2W sequences (Fig. 1.36c) ● rarely, associated with cortical erosion of the humerus,61 appearing as a subcortical cyst with surrounding marrow oedema (Fig. 1.36d, e) ● marrow oedema may also occur in HADD in the absence of cortical erosion62 ● rarely, HADD progresses to an FTRCT at the site of calcification63

Rotator cuff strain64 ●

rotator cuff strain is a post-traumatic condition occurring typically in patients 90 per cent of individuals and arises from the lateral aspect of the base of the coracoid process (Fig. 1.40a, b): ■ distally, the CHL forms two major bands: – a larger, lateral band that inserts on the greater tuberosity and the anterior border of the supraspinatus tendon – a smaller, medial band that crosses the LHBT to insert into the lesser tuberosity and the superior fibres of the subscapularis and contributes to the ‘THL’ ■ the CHL is normally surrounded by fat the ‘reflection pulley’ is formed by the SGHL, the medial band of the CHL and the superior fibres of the subscapularis: ■ it functions to stabilise the LHBT as it enters the bicipital groove ■ injuries to this region are termed ‘pulley lesions’ the anatomy of the RI is optimally assessed on direct MR arthrography (Fig. 1.41)69,70

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The shoulder girdle

Figure 1.39 The rotator interval capsule. Sagittal oblique proton density-weighted fast spin-echo image showing the long head biceps tendon (arrow) within the rotator interval (RI) covered by the RI capsule (arrowheads).

a

b

Figure 1.40 The coracohumeral ligament (CHL). Sagittal oblique T2-weighted (T2W) fast spin-echo (FSE) (a) and coronal oblique T2W FSE (b) images showing the CHL (arrows) extending from the coracoid process (arrowhead) into the rotator interval (double arrowheads b).

Figure 1.41 The rotator interval (RI). Sagittal oblique T1-weighted spin-echo fat-suppressed MR arthrogram showing the long head biceps tendon (arrow) within the RI and lying deep to the RI capsule (arrowheads).

Pathology of the rotator interval

PATHOLOGY OF THE ROTATOR INTERVAL Trauma65,66,70 ● ● ●

●

the clinical manifestations of an RI lesion are non-specific and include chronic shoulder pain and multidirectional instability they are termed ‘hidden lesions’, since they may not be identified at arthroscopy injuries to the RI may be caused by repetitive or forceful overhead throwing actions in athletes, occupational injuries from repetitive overhead labour, acute injuries from falls on the outstretched hand or following acute anteroinferior dislocation of the humeral head the various structures of the interval may be injured in isolation or in combination

a

b

Figure 1.42 Acute rotator interval (RI) injury. Sagittal oblique T2-weighted fast spin-echo (FSE) image (a) showing thickening of the RI capsule (arrows). Coronal oblique proton density-weighted FSE fat-suppressed image (b) showing oedema in the RI (arrows) and lack of visualisation of the coracohumeral ligament.

MRI findings ● acute injury: thickening, irregularity and heterogeneous increased SI of the CHL and RIC (Fig. 1.42a) are seen, with oedema and haemorrhage in the RI (Fig. 1.42b) ● chronic injury (Fig. 1.43a–c): irregular thickening and scarring of the CHL and RIC and synovitis within the RI ● LHBT injury (see later) ● pulley lesions: acute injuries may result in tears of the reflection pulley (CHL, SGHL) and anteromedial subluxation of the LHBT: ■ they may be associated with partial/complete tears of the subscapularis tendon or dislocation of the LHBT through an oblique tear of the subscapularis tendon ● associated injuries include: ■ tears of the leading edge of the supraspinatus tendon immediately before its insertion into the greater tuberosity (Fig. 1.43d) ■ tears of the superior distal margin of the subscapularis and superior labral anteroposterior (SLAP) lesions (see later)

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The shoulder girdle

b

a

d c Figure 1.43 Chronic rotator interval (RI) lesion. Coronal oblique T1-weighted spin-echo (a) and sagittal oblique T2-weighted (T2W) fast spin-echo (FSE) (b) images showing irregular thickening and hyperintensity of the coracohumeral ligament (arrow). Sagittal oblique proton density-weighted FSE image (c) showing irregularity and thickening of the RI capsule (arrow). Associated injuries: Coronal oblique T2W FSE fat-suppressed image (d) showing a tear of the leading edge of the supraspinatus (arrow) adjacent to the long head biceps tendon (arrowhead).

MR arthrographic findings71 ● abnormalities of the superior border of the subscapularis tendon are seen ● extra-articular contrast collection through a ruptured RI capsule ● injected fluid may be seen in the subcoracoid space, around the CHL and SGHL or over the superior aspects of the humeral tuberosities ● LHBT subluxation ● the reported sensitivity and specificity of MR arthrography are ~90 per cent

THE LONG HEAD BICEPS TENDON Normal anatomy21 ● ● ●

the biceps brachii muscle comprises two heads, the short head and the long head the short head arises from the anterior aspect of the coracoid process (Fig. 1.44) the LHBT arises from the supraglenoid tubercle and superior labrum (biceps–labral complex), with some fibres also arising from the base of the coracoid process

The long head biceps tendon

Figure 1.44 Normal anatomy of the short head of biceps. Axial T2*-weighted gradient-echo image showing the origin of the tendon (arrow) from the tip of the coracoid process (arrowhead). ●

the LHBT has an intracapsular and extracapsular portion: ■ the intracapsular portion extends from its origin, running deep to the RCT to enter the bicipital groove via the RI ■ its position is stabilised before entry into the bicipital groove by the reflection pulley (CHL and SGHL) ■ rarely, the intracapsular portion of the LHBT may be absent, in which case it arises from the bicipital groove

MRI findings the LHBT is hypointense on all pulse sequences, with its origin identified on coronal and axial images showing the superior labrum (Fig. 1.45a, b)

●

b a

c

Figure 1.45 Normal MR arthrographic anatomy of the long head biceps tendon (LHBT). Coronal (a) and axial (b) T1-weighted (T1W) spin-echo (SE) fat-suppressed (FS) images showing the origin of the tendon (arrow) from the superior labrum (arrowheads). The LHBT (double arrows a) runs deep to the supraspinatus tendon (black arrow a). Axial T1W SE FS image (c) showing the tendon (arrow) within the bicipital groove.

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The shoulder girdle

● ● ●

the tendon runs obliquely over the humeral head deep to the supraspinatus (Fig. 1.45a) it is identified within the RI on sagittal images between the humeral head and the RIC (Figs. 1.39, 1.41) and is covered in the bicipital groove by the THL, seen optimally on axial images (Fig. 1.45c) a small amount of fluid within the tendon sheath is normal

PATHOLOGY OF THE LONG HEAD BICEPS TENDON Tenosynovitis/tendinosis72–74 ●

inflammation of the LHBT is associated with rotator cuff disease in most cases

a

c

e

b

d Figure 1.46 Pathology of the long head biceps tendon (LHBT). Tendinosis: Sagittal oblique T2-weighted (T2W) fast spin-echo (FSE) image showing a swollen hyperintense tendon (arrow) deep to the rotator cuff. Subluxation: Axial T2W FSE fatsuppressed (FS) image (b) showing the LHBT (arrow) lying on the medial ridge of the bicipital groove. Dislocation: Axial proton density-weighted (PDW) FSE image (c) showing the tendon (arrow) lying anteromedial to the humeral head and an empty bicipital groove (arrowhead). Incomplete dislocation: Axial T1-weighted spin-echo FS MR arthrogram (d) showing a coronal split (arrows) in the cranial portion of the subscapularis tendon with dislocation of the LHBT (arrowhead) into the tear. Instability: Axial PDW FSE image (e) showing a shallow bicipital groove (arrow).

Pathology of the long head biceps tendon

MRI findings ● signal increase is seen in the tendon with fusiform tendon enlargement (Fig. 1.46a) ● surface irregularity, synovial adhesions and non-communicating effusion of the tendon sheath

Subluxation/disclocation70,75 ● ●

displacement of the LHBT is associated with tears of the subscapularis muscle and reflection pulley MRI may be able to predict the presence of LHBT instability within the RI:76 ■ the sensitivity, specificity, positive predictive value and negative predictive value are reported as 67 per cent, 90 per cent, 86 per cent and 75 per cent, respectively

MRI findings ● subluxation: the tendon lies on the medial ridge of the bicipital groove (Fig. 1.46b) ● dislocation: the tendon lies anterior to the medial humeral head and the bicipital groove is empty (Fig. 1.46c) ● a defect in the subscapularis apparatus may allow intra-articular entrapment of the LHBT, resulting in incomplete dislocation: ■ MRI shows the LHBT lying within a partially disrupted subscapularis tendon (Fig. 1.46d) ● morphological abnormalities predisposing to instability include an obtuse angle of the intertubercular sulcus (Fig. 1.46e) and a flattened LHBT

Rupture of the long head biceps tendon77 ●

●

● ●

the aetiology of LHBT rupture includes chronic rotator cuff disease, a chronic tear of the leading edge of the supraspinatus tendon allowing impingement of the uncovered LHBT by the undersurface of the acromion LHBT tears are associated with a supraspinatus tear in 96 per cent of cases, an infraspinatus tear in 35 per cent of cases and a subscapularis tear in 47 per cent of cases:78 ■ there is a significant association between supraspinatus and subscapularis tears and LHBT rupture, but not with infraspinatus or teres minor tears acute traumatic rupture is rare partial- (Fig. 1.47) or full-thickness tears of the LHBT tendon are diagnosed by conventional MRI with a reported sensitivity, specificity and accuracy of 52 per cent, 86 per cent and 79 per cent78

MRI findings ● an empty bicipital groove is seen containing chronic scar tissue ● an associated SLAP lesion

Figure 1.47 Partial rupture of the long head biceps tendon (LHBT). Axial T2*-weighted gradient-echo image showing a longitudinal tear (arrow) of the LHBT within the bicipital groove and an associated synovial effusion.

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The shoulder girdle

THE SHOULDER BURSAE Introduction21,79 ● ● ●

shoulder bursae may be classified as communicating or non-communicating communicating include the subscapularis, subcoracoid and peribicipital bursae non-communicating include: ■ the subacromial–subdeltoid (SA-SD) bursa ■ the coracoclavicular (CC) ligament bursae; variably present between the conoid and trapezoid parts of the CC ligament ■ a bursa superior to the ACJ ■ a bursa adjacent to the inferior tip of the scapula (see later) ■ a bursa between the scapula and the ribs (scapulothoracic; see later) ■ various bursae adjacent to the insertion sites of the latissumus dorsi, teres major and pectoralis major muscles

Subacromial–subdeltoid bursa ●

the SA-SD bursa comprises two interconnected portions: ■ the SA bursa, which is located inferior to the acromion and coracoacromial ligament, superior to the RCT and RI, and extends medially as far as the ACJ ■ the SD bursa, which is located between the lateral aspect of the humeral head and the deltoid muscle ■ they communicate with each other, but not with the glenohumeral joint ■ the normal bursa is delineated by a fat stripe seen on coronal oblique T1W/PDW FSE images (Fig. 1.48)

Figure 1.48 The subacromial–subdeltoid bursa. Coronal T1-weighted spin-echo image showing a fat stripe (arrows) deep to the deltoid muscle (arrowhead).

Subscapularis bursa ● ●

the subscapularis bursa represents an anterior extension of the glenohumeral joint between the SGHL and MGHL it is located between the scapular blade and the subscapularis muscle (Fig. 1.49a), sometimes extending above the subscapularis tendon to lie beneath the base of the coracoid process (Fig. 1.49b)

Subcoracoid bursa80,81 ●

the subcoracoid bursa lies between the anterior surface of the subscapularis tendon and the coracoid process (Fig. 1.50a–c) and may communicate with the SA-SD bursa

The shoulder bursae

a Figure 1.49 The subscapularis bursa. Axial short tau inversion recovery (a) and sagittal oblique proton density-weighted fast spin-echo (b) images showing effusion (arrows) within the subscapularis bursa.

b

a b

c

Figure 1.50 The subcoracoid bursa. Coronal oblique T2-weighted (T2W) fast spin-echo (FSE) (a), sagittal oblique T2W FSE fat-suppressed (FS) (b) and axial proton densityweighted FSE FS (c) images showing fluid within a distended subcoracoid bursa (arrows) located anterior to the subscapularis muscle (double arrowheads b, c) and inferior to the coracoid process (arrowheads a, b).

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44

The shoulder girdle

PATHOLOGY OF THE SHOULDER BURSAE Bursitis82 ●

isolated subacromial fluid may be associated with subacromial impingement and supraspinatus tendinosis, or FTRCT or bursal-side PTRCT (Fig. 1.19a) and instability, or in asymptomatic patients may occur following rotator cuff repair83

a b

d

c

Figure 1.51 Subacromial–subdeltoid (SA-SD) bursitis. Axial T2-weighted (T2W) fast spin-echo (FSE) fat-suppressed image (a) showing fluid in the SD bursa (arrows). Sagittal postcontrast T1-weighted (T1W) spin-echo (SE) images (b, c) showing a massively distended SA-SD bursa with synovial enhancement (arrows). Rice body bursitis: Sagittal T1W SE (d) and axial T2W FSE (e) images showing distension of the SA-SD bursa (arrows) and multiple hypointense ‘rice bodies’ due to chronic synovitis (e).

e

The capsule and labrum

●

primary bursitis may result from rheumatoid arthritis (Fig. 1.51a–c) and tuberculous synovitis, possibly with ‘rice body’ formation84

MRI findings ● rice body bursitis: a distended bursa is seen containing multiple small T2W hypointense rice bodies (Fig. 1.51d, e) ● subscapularis bursal fluid may be normal or may be associated with non-specific glenohumeral joint effusions: ■ isolated fluid in the subscapularis bursa may be seen with subacromial impingement ● subcoracoid bursal fluid80 is reported in 0.6 per cent of patients undergoing shoulder MRI: ■ the subcoracoid bursa may be confused with the subscapularis bursa ■ isolated or predominant subcoracoid effusions (Fig. 1.50a–c) are considered abnormal; causes include anterior RCT tears and RI tear81

THE CAPSULE AND LABRUM Glenohumeral joint capsule19,21,85–87 ● ● ●

● ● ● ●

stability of the glenohumeral joint is provided by a combination of static and dynamic factors, with the joint capsule and labroligamentous complex playing a major role the joint capsule extends from the glenoid rim to the anatomical neck of the humerus the anterior capsule:88 three types of capsular insertion are described: ■ type 1 – inserts into the base of the glenoid labrum (Fig. 1.52a) ■ type 2 – inserts into the scapular neck (Fig. 1.52b) ■ type 3 – inserts further medially into the scapula, at the transition between the neck and the body (Fig. 1.52c) the relationship of types 2 and 3 to instability is unclear and they may be acquired following previous anterior dislocation the posterior capsule always inserts into the posterior glenoid rim (Fig. 1.52b) the inferior capsule; in the axillary region, the capsule may be partially fused to the tendon of the long head of triceps at its origin from the infraglenoid tubercle capsular recesses include: ■ the subscapularis; anterior to the scapular blade and deep to the subscapularis muscle (Fig. 1.49) ■ the axillary; between the anterior and posterior bands of the IGHL (Fig. 1.52d) ■ the intertubercular/peribicipital; surrounds the LHBT (Fig. 1.45c)

Glenohumeral ligaments89 ● ●

●

the glenohumeral ligaments represent thickenings of the joint capsule and comprise the SGHL, the MGHL and the IGHL the SGHL arises from the supraglenoid tubercle adjacent to the LHBT, extending anterolaterally to merge with the CHL before its insertion just superior to the lesser tuberosity at the RI: ■ the SGHL gives some stability to the shoulder in adduction and helps to prevent inferior subluxation ■ it is identified on arthroscopy and MR arthrography in 97 per cent and 98 per cent of cases, respectively ■ anatomical variants of the SGHL include a common origin with the LHBT or the MGHL ■ the SGHL is seen on axial and sagittal MRI/MR arthrography as a thick band arising from the supraglenoid tubercle, adjacent to the LHBT, and runs parallel and medial to the coracoid process to insert at the RI (Fig. 1.53a–c) ■ thickening of the SGHL may be associated with absence or underdevelopment of the MGHL (Fig. 1.53d) the MGHL most commonly arises from the anterosuperior labrum, extending inferolaterally, deep to the anterior capsule and subscapularis muscle to insert into the lesser tuberosity, inferior to the SGHL: ■ the MGHL limits external rotation with the arm at 60–90° abduction

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The shoulder girdle

a

b

c

d

Figure 1.52 Capsular insertions. Axial T1-weighted (T1W) spin-echo (SE) magnetic resonance (MR) arthrograms showing the various anterior capsular insertions (arrows): type 1 (a), type 2 (b) and type 3 (c). Note that the posterior capsule (arrowhead b) inserts directly into the posterior labrum. Recesses: Coronal T1W SE fat-suppressed MR arthrogram (d) showing the axillary recess (arrow).

it is seen on axial and sagittal MRI/MR arthrography as a hypointense band between the anterior labrum and the subscapularis muscle (Fig. 1.54) ■ anatomical variations of the MGHL are relatively common:90 – variable origin; from the scapular neck (Fig. 1.55a), or a combined origin with the SGHL (Fig. 1.55b) or IGHL – variable insertion; may blend with the subscapularis tendon before insertion into the humerus (Fig. 1.55c) – variable thickness – the MGHL is absent in 8–30 per cent of cases,21 resulting in a large opening between the joint cavity and the subscapularis recess – rarely, the MGHL is duplicated or has a longitudinal split – the Buford complex has a reported prevalence of 1.5–6.5 per cent and comprises the association of a thickened, cord-like MGHL and an absent anterosuperior labrum (Fig. 1.55d, e) the IGHL has three components: ■ the anterior band originates at the 2–4 o’clock position on the labrum (Fig. 1.56a, b) ■ the posterior band originates at the 7–9 o’clock position on the labrum (Fig. 1.56c) ■ the axillary pouch is a diffuse thickening of the capsule between the anterior and posterior bands (Fig. 1.52d) ■ the anterior band is thicker than the posterior band in 75 per cent of cases ■ the IGHL extends from the anteroinferior labrum to insert into the humeral neck (Fig. 1.56d) ■

●

The capsule and labrum

b a

c

d

Figure 1.53 MR arthrographic anatomy of the superior glenohumeral ligament (SGHL). Sagittal (a) and axial (b) T1-weighted (T1W) spin-echo (SE) fat-suppressed (FS) images showing the SGHL (arrow) arising from the superior labrum (arrowhead). Sagittal T1W SE FS image (c) showing the SGHL insertion (arrow) into the lesser tuberosity (double arrowhead). Sagittal T1W SE FS image (d) showing a thickened SGHL (arrow) and a thin middle glenohumeral ligament (arrowhead).

Figure 1.54 Anatomy of the middle glenohumeral ligament (MGHL). Axial T2*-weighted gradient-echo image shows the MGHL (arrow) arising from the anterior labrum (arrowhead) and lying deep to the subscapularis tendon (double arrowhead).

47

48

The shoulder girdle

b

a

d c

e

it is the major stabiliser of the shoulder joint in 90° abduction and full external rotation, being lax with the shoulder adducted ■ the IGHL is best demonstrated in the ABER position (Fig. 1.2) the spiral glenohumeral ligament,91 also termed the fasciculus obliquus, arises from the infraglenoid tubercle of the glenoid rim and the long head of triceps: ■ it forms a tight communication with the MGHL, extending to fuse with the posterocranial margin of the subscapularis tendon, with which it inserts into the lesser tuberosity ■ it appears on MR arthrography as a thin, hypointense band in the anterior capsule, lying deep to the subscapularis tendon (Fig. 1.57) ■

●

Figure 1.55 Anatomical variants of the middle glenohumeral ligament (MGHL). Axial T2*-weighted gradient-echo image (a) showing the MGHL (arrow) arising from the scapular neck. Sagittal T1-weighted (T1W) spin-echo (SE) fat-suppressed (FS) MR arthrogram (b) showing the MGHL (arrow) arising from the superior labrum (arrowhead). Axial T1W SE FS MR arthrogram image (c) showing the MGHL (arrow) fusing with the subscapularis tendon (arrowhead). The Buford complex: Axial T1W SE FS (d) and sagittal proton densityweighted FSE (e) MR arthrograms show a thickened, cord-like MGHL (arrowheads) and absent anterosuperior labrum (arrow d).

The capsule and labrum

b a

c d Figure 1.56 Normal anatomy of the inferior glenohumeral ligament (IGHL). Coronal (a) and axial (b) T1-weighted (T1W) spin-echo (SE) fat-suppressed (FS) MR arthrograms showing the origin of the anterior band of the IGHL (arrows) from the anteroinferior labrum and its insertion into the humeral neck. Axial T1W SE MR arthrogram (c) showing the origin of the posterior band of the IGHL (arrow) from the inferior labrum (arrowhead). Sagittal T1W SE FS MR arthrogram (d) showing the insertion of the anterior (arrow) and posterior (arrowhead) bands of the IGHL into the humeral neck.

Figure 1.57 The spiral glenohumeral ligament. Sagittal T1-weighted spin-echo fat-suppressed MR arthrogram showing focal thickening (arrow) of the anterior capsule deep to the subscapularis tendon and distinct from the middle glenohumeral ligament (arrowhead).

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The shoulder girdle

Glenoid labrum ● ●

●

●

● ●

the glenoid labrum is a fibrous/fibrocartilaginous structure that attaches to the glenoid rim the anatomical portions of the labrum when viewed en face can be described as a clock face: ■ superior – 12 o’clock ■ anterior – 3 o’clock ■ inferior – 6 o’clock ■ posterior – 9 o’clock the labrum has several functions; it serves as an anchor for the origin of the LHBT and glenohumeral ligaments and also deepens the glenoid articular surface, thereby increasing contact with the humeral head the anterior and posterior labrum are ideally assessed on axial images, appearing as hypointense, triangular structures separated from the underlying bony glenoid by a thin, intermediate-SI layer of articular hyaline cartilage the anterior labrum is typically pointed and is larger than the posterior labrum (Fig. 1.58a) the anterior labrum may also be rounded or blunted, especially when the shoulder is imaged in internal rotation (Fig. 1.58b)

a

c

●

●

b

Figure 1.58 Normal anatomy of the glenoid labrum. Axial T2*-weighted (T2*W) gradient-echo (GE) image (a) showing the normal pointed anterior (arrow) and posterior (arrowhead) labrum. Note the hyperintense hyaline cartilage (small arrows) between the labrum and the bony glenoid. Variants of the anterior labrum: Axial T1-weighted spin-echo MR arthrogram (b) showing a rounded anterior labrum (arrow). Axial T2*W GE image (c) showing globular increased intralabral signal intensity (arrow).

variations in the MR appearance of the arthroscopically normal labrum include:92 ■ increased linear or globular SI in 30 per cent (Fig. 1.58c), due to a combination of fibrovascular tissue, eosinophilic/mucoid degeneration, synovialisation or ossification/calcification ■ deformed or fragmented in 12 per cent ■ complete separation from the glenoid rim in 2 per cent and complete absence in 2 per cent the mean size of the labrum is: ■ 3.8¥3.3 mm anteriorly at the level of the subscapularis bursa ■ 6.1¥5.6 mm anteriorly at the inferior portion of the glenoid rim

The capsule and labrum

Glenohumeral joint21,93 ● ● ● ●

the glenohumeral joint is formed by the humeral head and the glenoid articular surface of the scapula the central portion of the glenoid articular surface is devoid of hyaline cartilage, being termed the ‘bare area’ (Fig. 1.59a, b), and should not be mistaken for a cartilage defect in 75 per cent of cases, the glenoid articular surface has a mean retroversion of 5–7° (Fig. 1.59c, d) greater retroversion may predispose to posterior instability

a b

c

e

d

Figure 1.59 Normal anatomy of the glenohumeral joint. Axial (a) and sagittal (b) T1-weighted spin-echo fat-suppressed (FS) MR arthrogram showing the ‘bare area’ (arrows) of the glenoid articular surface. Axial T2-weighted fast spin-echo FS images (c, d) showing the measurement of glenoid version (double black arrowhead d). Axial T2*-weighted gradient-echo image (e) showing posterior glenoid rim deficiency (arrow).

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The shoulder girdle

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in 25 per cent of cases, the glenoid articular surface has a mean anteversion of 2–10° glenoid anteversion and glenoid hypoplasia may predispose to glenohumeral instability variations occur in the shape of the posteroinferior glenoid rim, which can be demonstrated by MRI;94 subtypes are assessed on the most caudal axial MR image that demonstrates glenoid articular cartilage and include: ■ a normal triangular shape, seen in 28 per cent of cases ■ a ‘lazy-J’ shape, describing a rounded margin, seen in 59 per cent of cases (Fig. 1.59e) ■ a ‘delta’ shape, describing a sharply angulated margin, seen in 13 per cent of cases such glenoid dysplasia (glenoid hypoplasia, posterior glenoid rim deficiency) may predispose to posterior labral tears and posterior instability:95 ■ moderate to severe dysplasia is reported in ~14 per cent of patients, and is significantly associated with the presence of posterior labral tears compared with normal or mildly dysplastic posterior glenoid rims

PATHOLOGY OF THE CAPSULE AND LABRUM GLENOHUMERAL INSTABILITY Classification86,87,96,97 ● ●

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glenohumeral instability may be classified by its aetiology (traumatic, atraumatic or micro-instability) and its direction (unidirectional or multidirectional) traumatic instability is typically unidirectional (~95 per cent anterior, ~3–5 per cent posterior) and usually follows a single episode of dislocation, which may then become recurrent: ■ it is referred to by the acronym TUBS (traumatic, unidirectional, Bankart, surgery) atraumatic instability is typically multidirectional and is commonly seen in individuals with congenital hypermobility syndromes: ■ it is referred to by the acronym AMBRI (atraumatic, multidirectional, bilateral, rehabilitation, inferior capsular shift [if surgery required]) microinstability is typically seen in overhead athletes: ■ it is referred to by the acronym AIOS (acquired, instability, overstress, surgery)

Traumatic anterior instability ●

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traumatic anterior instability follows an episode of anterior subcoracoid dislocation, classically due to a fall on the outstretched hand in a person younger than 35–40 years of age: ■ in older patients, dislocation may result in an acute RCT tear, an avulsion fracture of the greater tuberosity or a tear of the subscapularis muscle and anterior capsule stability of the glenohumeral joint depends on both dynamic and static factors dynamic stabilisers include the rotator cuff muscles static stabilisers include the bony glenoid and hyaline cartilage, the fibrocartilaginous glenoid labrum, the glenohumeral ligaments and the joint capsule pathological lesions associated with anterior traumatic instability comprise a variable combination of soft-tissue and bony injuries

Soft-tissue Bankart injury ●

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the soft-tissue Bankart lesion represents complete avulsion of the anteroinferior glenolabral complex (the antero-inferior labrum and the anterior band of the IGHL) from the scapula and rupture of the scapular periosteum it is the commonest injury, seen in ~74 per cent of patients following anterior dislocation anterior dislocation may result in absence, fraying, detachment or deformity of the anteroinferior labrum

Pathology of the capsule and labrum

MRI findings96 ● a zone of increased SI is seen at the glenolabral junction or an irregular, small (Fig. 1.60a) or absent anteroinferior labrum (Fig. 1.60b) ● conventional MRI is reported to demonstrate 93 per cent of labral tears but only 46 per cent of detached labra98 ● a sensitivity of 78 per cent and a specificity of 89 per cent for both T2*W GE and T2W FSE FS sequences is reported99

a b

c

Figure 1.60 Soft-tissue Bankart lesions. Non-contrast MRI: Axial T2*-weighted (T2*W) gradient-echo (GE) image (a) showing a small anterior labrum (arrow). Axial T2*W GE image (b) showing absence of the anterior labrum (arrow) and thickening of the anterior capsule with stripping of the scapular periosteum (arrowhead). MR arthrography: Axial T1-weighted spin-echo fat-suppressed image (c) showing absence of the anterior labrum (arrow) and stripping of the anterior capsule (arrowhead).

MR arthrographic findings ● an avulsed anteroinferior labrum, leaving a bare anterior glenoid rim (Fig. 1.60c) ● linear contrast medium extending into the labrum, indicating a labral tear ● a blunted labrum, resulting in an altered labral contour ● 96 per cent of labral tears and detachments are demonstrated on axial MR arthrography98 ● addition of the ABER position may increase the sensitivity of MR arthrography for identifying anteroinferior labral tears100

Variants of anterior soft-tissue lesions ●

anterior labroperiosteal sleeve avulsion (ALPSA), also termed the ‘medialised Bankart lesion’, represents an avulsion of the anterior scapular periosteum with the attached anteroinferior glenoid labrum (Fig. 1.61a): ■ it is more common in patients who have suffered recurrent dislocation

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a b Figure 1.61 Anterior labroperiosteal sleeve avulsion (ALPSA). Axial T1-weighted (T1W) spin-echo (SE) fat-suppressed (FS) MR arthrogram (a) showing stripping of the anterior scapular periosteum (arrow) with an attached anteroinferior labrum (arrowhead). Axial T1W SE FS MR arthrogram image (b) showing a chronic ALPSA lesion (arrow) scarred down medially to the anteroinferior scapula.

the chronic lesion typically scars down in an inferior and medially displaced location (Fig. 1.61b) ALPSA rarely occurs in an anterosuperior location101 Perthes’ lesion102 represents a non-displaced tear of the anteroinferior glenoid labrum (Fig. 1.62a), which may be missed on standard MRI sequences (Fig. 1.62b): ■ it is best imaged with a combination of axial and ABER views with intra-articular contrast (Fig. 1.62c) ■ ■

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Figure 1.62 Perthes’ lesion. Proton density-weighted fast spin-echo MR arthrogram (a) showing contrast entering deep to the anterior labrum (arrow). T1-weighted spin-echo fat-suppressed MR arthrograms in the axial position (b) showing a normal anteroinferior labrum (arrow) and in the abduction external rotation position (c) showing contrast medium (arrow) between the displaced anteroinferior labrum (arrowhead) and the underlying bony glenoid.

Pathology of the capsule and labrum

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glenolabral articular disruption (GLAD)103 is caused by impaction of the humeral head against the anteroinferior glenoid and is usually a stable lesion resulting in anterior shoulder pain: ■ it comprises a superficial tear of the anteroinferior labrum, which remains firmly attached to the anterior scapular periosteum ■ there is an adjacent glenoid articular cartilage injury, which may take the form of a cartilaginous flap tear or a depressed osteochondral injury ■ GLAD is best imaged by MR arthrography, which shows extension of contrast material into the labral tear (Fig. 1.63a) and a cartilaginous defect (Fig. 1.63b)

b a Figure 1.63 Glenolabral articular disruption. Axial T1-weighted spin-echo fat-suppressed MR arthrograms (a, b) showing injected contrast medium extending into an anteroinferior labral tear (arrow a) and a glenoid cartilage defect (arrow b).

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humeral avulsion of the glenohumeral ligament (HAGL)104 represents an isolated tear of the anterior IGHL from its humeral attachment, usually associated with a severe dislocation: ■ it is reported in 7.5–9.4 per cent of patients with anterior dislocation, usually in male patients involved in contact sports (e.g. rugby) or those with first-time dislocation over the age of 35 years ■ associated injuries include a tear of the subscapularis tendon insertion and dislocation of the LHBT ■ 20 per cent are associated with avulsion of bone from the humerus, referred to as bony HAGL ■ MRI demonstrates inhomogeneity or frank disruption of the anterior capsule at the humeral insertion, with fluid anterior to the shoulder ■ MR arthrography may show a ‘J-shaped’ configuration to the anterior IGHL, rather than the normal ‘U-shape’ on coronal images105 (Fig. 1.64a), and extravasation of contrast through the capsular defect (Fig. 1.64b, c) non-classifiable injuries97 are those that cannot be classified into the above categories on arthroscopy, typically in the setting of chronic anterior instability and reported in ~20 per cent of cases:106 ■ MRI/MR arthrography demonstrates a swollen IGHL complex without clear distinction between labrum, IGHL and scapular periosteum (Fig. 1.65) MR arthrography can classify the various types of anteroinferior labroligamentous injuries with a sensitivity of 77–88 per cent, a specificity of 91 per cent and an accuracy of 84–89 per cent:106 ■ Bankart, ALPSA and Perthes’ lesions are correctly classified in 80 per cent, 77 per cent and 50 per cent of cases, respectively, whereas non-classifiable lesions were correctly identified in 83 per cent of cases

Injury to other anterior soft-tissue structures ●

the anterior capsule may be stripped from the scapular neck (Fig. 1.66a): ■ capsular injury in the absence of a Bankart lesion manifests as capsular thickening with adjacent increased SI (Fig. 1.66b) ■ MR arthrography may show elongation of the inferior and anteroinferior capsule in recurrent anterior dislocation107 (Fig. 1.66c, d)

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Figure 1.64 Humeral avulsion of the glenohumeral ligament. MR arthrography: Coronal oblique T1-weighted (T1W) spinecho (SE) fat-suppressed (FS) image (a) showing a ‘J-shaped’ configuration (arrow) of the anteroinferior capsule. Axial (b) and coronal (c) T1W SE FS images showing extracapsular leak of injected contrast medium (arrows).

Figure 1.65 Non-classifiable labral injury. Axial T1-weighted spin-echo fat-suppressed MR arthrogram showing a grossly swollen anteroinferior labrum (arrow).

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the subscapularis tendon108 undergoes thinning and elongation in recurrent anterior dislocation (Fig. 1.66e): ■ the mean thickness and cross-sectional area of the subscapularis tendon in affected shoulders are 6.5 mm and 388.6 mm2, respectively, compared with 8.5 mm and 547.9 mm2

Pathology of the capsule and labrum

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Figure 1.66 Anterior soft-tissue injury. Capsule: Axial T1-weighted (T1W) spin-echo (SE) fat-suppressed (FS) MR arthrogram (a) showing anterior capsular stripping (arrowhead) associated with a soft-tissue Bankart lesion (arrow). Axial T2*-weighted gradient-echo image (b) showing a normal anterior labrum with thickening and hyperintensity of the anterior capsule (arrow). Coronal (c) and axial (d) T1W SE MR arthrograms showing a patulous anterior capsule (arrows). Subscapularis tendon: Axial T1W SE FS MR arthrogram (e) showing elongation and thinning of the tendon (arrows).

Bone lesions following anterior dislocation ●

the Hill–Sachs deformity (Broca lesion) results from an impaction fracture of the posterolateral humeral head against the anteroinferior glenoid rim during anterior dislocation, and may be cartilaginous or osteocartilaginous: ■ its incidence based on arthroscopy following first-time anterior dislocation is reported as 47–100 per cent

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Figure 1.67 The Hill–Sachs defect. Coronal proton densityweighted fast spin-echo (FSE) (a) and axial T2*-weighted (T2*W) gradient-echo (GE) (b) images showing a shallow defect (arrows) in the posterolateral humeral head. Axial T2*W GE image (c) showing a deeper defect (arrow) that runs parallel to the bony glenoid. Coronal (d) and axial (e) T1-weighted spinecho fat-suppressed MR arthrograms showing a contrast-filled posterolateral defect (arrows). Axial T2*W GE image (f) showing the normal shallow groove (arrow) at the level of the anatomical neck of the humerus. Axial T2-weighted FSE fatsuppressed image (g) showing an acute impaction injury (arrow) of the posterolateral humeral head with adjacent marrow oedema (arrowheads).

Pathology of the capsule and labrum

the lesion may range from a shallow, mainly chondral defect to a deep osteochondral lesion defects that involve less than one-third of the humeral head circumference (Fig. 1.67a, b) are regarded as prognostically insignificant ■ larger lesions, particularly if oriented parallel to the glenoid (Fig. 1.67c) are more likely to result in repeated subluxation and dislocation the bony Bankart lesion represents an avulsion fracture of the anteroinferior rim of the glenoid during anterior dislocation: ■ large fractures (>7 mm fragment width) may result in recurrent instability and preclude arthroscopic repair ■ ■

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MRI findings ● the Hill–Sachs lesion appears as a defect in the posterolateral humeral head (Fig. 1.67a–c), best identified on axial images at or just above the level of the coracoid process, at which level the humeral head is normally round: ■ the lesion fills with contrast on MR arthrography (Fig. 1.67d, e) ■ a Hill–Sachs defect must be differentiated from the normal humeral groove on the posterolateral aspect of the humerus109 (Fig. 1.67f), which arises >2 cm from the top of the humeral head ■ the Hill–Sachs deformity lies in a more cephalad position, usually in the top 2 cm of the humeral head ■ an acute lesion may be associated with bone bruising (Fig. 1.67g), while purely cartilaginous lesions are difficult to identify110 ■ MRI is reported to have a sensitivity, specificity and accuracy of 97 per cent, 91 per cent and 94 per cent, respectively, for the detection of Hill–Sachs lesions ● the bony Bankart lesion is best identified on axial images through the inferior glenoid (Fig. 1.68a, b): ■ a fracture that results in an anteroposterior glenoid dimension above the mid-glenoid notch that is greater than that below, as assessed on sagittal oblique images (Fig. 1.68c), is considered clinically relevant

Posterior instability85–87,111 ● ● ● ● ●

posterior dislocation is uncommon and usually results from violent muscle contraction associated with an epileptic seizure or electric shock it may also result from recurrent micro-trauma, as seen in, for example, swimmers and throwers pathological lesions are a combination of soft-tissue trauma to the posterior labrum/capsule and the humeral head soft tissue: the reverse Bankart lesion,112 which occurs at the 6–10 o’clock position of the labrum bony: ■ the reverse Hill–Sachs lesion (hatchet deformity), an impaction fracture of the lesser tuberosity ■ the reverse bony Bankart lesion, an impaction fracture of the posterior glenoid rim ■ an avulsion fracture of the lesser tuberosity ■ chronic remodelling of the posterior glenoid rim may occur in patients with recurrent posterior dislocation

MRI findings ● the reverse Bankart lesion: the findings are as for a Bankart lesion, except involving the posterior labrum (Fig. 1.69a) ● may be better identified using double oblique axial MR arthrography than the conventional axial plane113

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Figure 1.68 Bony Bankart lesion. Axial T1-weighted spin-echo (a) and coronal proton density-weighted fast spin-echo (FSE) fat-suppressed (FS) (b) images showing a fracture (arrows) of the anteroinferior bony glenoid. Sagittal T2-weighted FSE FS image (c) showing the fracture (arrow) resulting in reduction in size of the inferior glenoid articular surface.

excessive posterior translation of the humeral head on axial images (Fig. 1.69b):114 ■ 4.9 mm vs 0.7 mm in controls ■ the degree of posterior humeral translation is greater on MR arthrography the reverse Hill–Sachs lesion: seen on axial images as an impaction fracture of the lesser tuberosity (Fig. 1.69c)

Variants of posterior soft-tissue lesions ● ●

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isolated tears of the teres minor and the posterior capsule115 (Fig. 1.70a) the Bennett lesion116 is an extra-articular avulsion injury of the posterior capsule caused by traction of the posterior band of the IGHL, typically seen in overhead throwing athletes: ■ it may result in the development of a crescent-shaped region of mineralisation at the posteroinferior aspect of the glenoid rim, at the insertion of the posterior capsule/posterior band of the IGHL (Fig. 1.70b), and sclerosis of the posterior glenoid posterior labrocapsular periosteal sleeve avulsion (POLPSA)117 is avulsion of the posterior scapular periosteum, which remains attached to the capsule and posterior glenoid labrum: ■ the labrum is usually not torn, but may be degenerate ■ POLPSA may represent an acute form of Bennett lesion

Pathology of the capsule and labrum

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Figure 1.69 Posterior instability. Reverse Bankart lesion: Axial T1-weighted spin-echo fat-suppressed MR arthrogram (a) showing contrast (arrow) between the posterior glenoid labrum and the bony glenoid. Axial proton density-weighted fast spinecho MR arthrogram (b) showing a tear (arrow) of the posterior labrum and posterior subluxation of the humeral head (arrowhead). Reverse Hill–Sachs lesion: Axial T2*-weighted gradient-echo image (c) showing a chronic impaction fracture (arrow) of the lesser tuberosity lying medial to the bicipital groove (arrowhead).

humeral avulsion of the posterior band of the IGHL118 may occur in isolation or combined with posterior or, rarely, anteroinferior labrocapsular abnormalities, or may be associated with multidirectional instability: ■ MR arthrography demonstrates a medial insertion of the posterosuperior joint capsule (Fig. 1.70c) and avulsion of the posterior band of the IGHL (Fig. 1.70d, e)

Atraumatic instability97 ● ●

atraumatic instability is usually multidirectional and seen in patients with congenital hypermobility, who typically have bilateral involvement it may also be seen in throwing/overhead athletes, involving the throwing arm

MRI findings ● a capacious subscapularis recess is seen with excessive labroligamentous laxity (Fig. 1.71) and absence of the MGHL ● in non-athletes, the anteroinferior labrum is typically normal, whereas in athletes the labrum may be hypoplastic or torn, or show evidence of degenerative change, manifest as swelling and increased SI

Micro-traumatic instability97 ● ●

micro-traumatic instability is thought to result from chronic trauma to the capsular structures in throwers/overhead athletes (e.g. tennis, swimming) typically unilateral, affecting the dominant arm

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Figure 1.70 Variations of posterior soft-tissue injury. Axial T1-weighted (T1W) spin-echo (SE) fat-suppressed (FS) MR arthrogram (a) showing a rupture of the teres minor tendon (arrow) and osteochondral injury (arrowhead) to the lesser tuberosity. The Bennett lesion: Axial T2*-weighted gradientecho image (b) showing crescentic low signal intensity (arrow) posterior to the glenoid rim consistent with capsular calcification. Avulsion of the posterior band of the inferior glenohumeral ligament (IGHL). MR arthrography: Axial proton density-weighted (PDW) fast spin-echo (FSE) image (c) showing medial insertion of the posterior capsule (arrow). Coronal T1W SE FS (d) and axial PDW FSE (e) images showing avulsion of the posterior band of the IGHL (arrows).

pathologically, repetitive abduction and external rotation results in anterior capsular damage and instability: ■ repetitive overhead activity associated with abduction, flexion and internal rotation can result in posterior capsular injury and subsequent posterior instability

MRI findings ● laxity of the anterior and posterior capsule is seen ● labral injury: degeneration/fraying, labral tears and detachment, and SLAP lesions (see later) ● rotator cuff injury from secondary impingement

Pathology of the capsule and labrum

Figure 1.71 Multidirectional instability. Axial T1-weighted spin-echo fat-suppressed MR arthrogram showing capacious subscapularis (arrowhead) and posterior (double arrowheads) capsular recesses and an intact anterior glenoid labrum (arrow).

LESIONS ASSOCIATED WITH SHOULDER INSTABILITY Paralabral cyst119 ● ●

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paralabral cysts can develop in association with a glenoid labral tear, due to the passage of joint fluid through a tear into the adjacent soft tissues they are reported in 2.3 per cent of shoulder MRI studies and may arise in a variety of locations:120 ■ superior location – 45 per cent (Fig. 1.72a) ■ posterior location – 45 per cent (Fig. 1.72b) ■ anterior location – 10 per cent (Fig. 1.72c) ■ inferior cysts are rare (Fig. 1.72d) cyst extension into the suprascapular (Fig. 1.72a) and/or spinoglenoid (Fig. 1.72e) notch may cause compression neuropathy of the suprascapular nerve121 (see later) rarely, a cyst arising from the inferior glenoid labrum extends into the quadrilateral space, compressing the axillary nerve122 paralabral cysts may present as an intra-articular mass123

MRI findings ● the lesions are hypointense to muscle on T1W (Fig. 1.72a) and hyperintense on T2W (Fig. 1.72b–e) images ● well-defined, lobulated margins, with a reported mean diameter of 2.2 cm ● cysts may show a tail-like extension to the labrum (Fig. 1.72f) MR arthrographic findings ● paralabral cysts usually do not fill with intra-articular contrast medium (Fig. 1.72b) and may be missed on FS T1W images (Fig. 1.5d)

Occult fracture of the humeral head124,125 ● ●

a non-displaced avulsion injury of the greater tuberosity may occur following anterior dislocation it typically occurs in patients over age 35–40 years suffering acute shoulder trauma/dislocation and presents as a rotator cuff tear, being reported in 1.3 per cent of shoulder MR studies

MRI findings ● oedema in the greater tuberosity, with reduced marrow SI on T1W (Fig. 1.73a) and increased SI on T2W/STIR (Fig. 1.73b) images ● a thin, hypointense fracture line may be evident on T1W images (Fig. 1.73a)

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Figure 1.72 Paralabral cysts. Coronal oblique T1-weighted spin-echo image (a) showing a cyst (arrow) in the suprascapular notch. Axial proton density-weighted fast spin-echo (FSE) MR arthrogram (b) showing a noncommunicating posterior labral cyst (arrow). Axial T2*-weighted (T2*W) gradient-echo (GE) image (c) showing an anterior labral cyst (arrow). Sagittal T2-weighted FSE image (d) showing a multiloculated inferior cyst (arrows). Axial T2*W GE image (e) showing a cyst (arrow) extending into the spinoglenoid notch. Axial T2*W GE image (f) showing a posterior paralabral cyst (arrow) with a tail-like extension (arrowhead) to the labrum.

Pathology of the capsule and labrum

b a Figure 1.73 Occult humeral head fracture. Coronal T1-weighted spin-echo (a) and axial T2*-weighted gradient-echo (b) images showing a hypointense fracture line (arrow a) and associated marrow oedema (arrow b).

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the lesion is optimally identified on T2W FSE FS/STIR images126 an acute FTRCT or PTRCT may be present in older patients, with a reported incidence of 54 per cent (100 per cent in those aged >70 years)127

Axillary nerve injury128 ●

the axillary nerve may be injured during anterior dislocation, resulting in weakness of the deltoid muscle, with a reported incidence of 43 per cent129

MRI findings ● features of instability/previous anterior dislocation ● denervation changes in deltoid, with hyperintensity on T2W/STIR in the subacute phase (Fig. 1.74a) and atrophy/fatty replacement on T1W images in the chronic phase (Fig. 1.74b)

a b Figure 1.74 Axillary nerve injury. Acute: Coronal short tau inversion recovery image (a) demonstrates mild denervation oedema of the deltoid (arrow) with an associated occult humeral head fracture (arrowhead). Chronic: Coronal oblique T1-weighted spin-echo image showing atrophy (long arrow) and fatty replacement (arrow) of the deltoid muscle with an associated minor Hill–Sachs defect (arrowhead).

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THE SUPERIOR GLENOID LABRUM Normal anatomy19,21 ● ● ●

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the superior labrum is optimally assessed on coronal oblique images, appearing as a triangular structure with a low SI on all pulse sequences (Fig. 1.75a–e) anatomical variants of the superior labrum include the sublabral recess and the sublabral foramen the sublabral recess (sulcus) represents a recess between the biceps–labral complex (BLC) and the superior glenoid rim: ■ it extends from the origin of the SGHL to the attachment of the LHBT, though it may extend posterior to the latter ■ it appears on MR arthrography as contrast medium between the superior labrum and the glenoid margin, being differentiated from a labral tear by its smooth outline and orientation, running superomedially (Fig. 1.75c, d) ■ the recess is identified in ~74 per cent of shoulders and is typically seen on the most anterior coronal oblique images demonstrating the superior labrum four types of superior labral attachment to the glenoid rim have been described:130 ■ type 1 – the superior labrum is firmly attached to the superior aspect of the glenoid rim (23 per cent) ■ type 2 – the superior labrum shows a recess of 2 mm or less in depth (19 per cent) (Fig. 1.75c) ■ type 3 – the superior labrum shows a recess of >2 mm but 5 mm) (33 per cent) the sublabral foramen (hole) represents a defect in the attachment between the anterosuperior portion of the labrum (1 o’clock to 3 o’clock position) and the adjacent glenoid rim anterior to the BLC: ■ it is present in 8–12 per cent of individuals and appears on MR arthrography as contrast medium between the anterosuperior labrum and the glenoid rim (Fig. 1.75f), being differentiated from a labral tear by its smooth medial margin ■ it may have an associated thickened MGHL the BLC comprises:131 ■ the superior portion of the glenoid labrum and the proximal portion of the LHBT ■ the LHBT has a combined origin from the supraglenoid tubercle and the superior labrum three types of BLC are described:131 ■ type 1 – the LHBT is firmly attached to the superior aspect of the glenoid rim (Fig. 1.76a) ■ type 2 – the LHBT is attached several millimeters medial to the glenoid rim (Fig. 1.76b) ■ type 3 – the superior labrum is shaped like a meniscus with a large sublabral recess projecting under the labrum and over the cartilaginous portion of the glenoid rim (similar to a type 4 superior labral attachment)

The superior glenoid labrum

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Figure 1.75 The normal superior glenoid labrum. Coronal oblique T1-weighted (T1W) spin-echo (SE) (a) and T1W SE fatsuppressed (FS) (b) MR arthrograms showing the normal triangular superior glenoid labrum (arrows). Sublabral recess: Coronal oblique T1W SE FS MR arthrograms (c, d, e) showing type 2 (arrow c), type 3 (arrow d) and type 4 (arrow e) superior labral attachment. Sublabral foramen: Axial T1W SE FS MR arthrogram (f) showing contrast (black arrow) between the anterosuperior labrum (arrowhead) and the glenoid rim (white arrow).

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Figure 1.76 Normal anatomy of the biceps–labral complex (BLC). Coronal oblique T1-weighted spin-echo MR arthrogram (a) showing a normal type 1 BLC firmly attached to the bony glenoid (arrow). Coronal oblique T2-weighted fast spin-echo fat-suppressed image (b) showing a type 2 BLC (arrow) arising medial to the glenoid margin.

PATHOLOGY OF THE SUPERIOR LABRUM Superior labral anteroposterior lesion31,97 ● ●

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the SLAP lesion is an injury of the superior labrum that extends in an anterior-to-posterior direction SLAP lesions are relatively common in athletes, usually resulting from a repetitive traction or torsion injury to the biceps tendon (types 1 and 2) or a fall onto the outstretched arm or flexed elbow (types 3 and 4) SLAP tears involve the 11–3 o’clock position on the labrum, terminating anteriorly at or above the midglenoid notch and posteriorly extending to just behind the LHBT origin they are classified into four main types: ■ type 1 – superior labral degeneration and fraying (Fig. 1.77a, b); non-traumatic, relatively common in older individuals and may be asymptomatic ■ type 2 – avulsion of the superior glenoid labrum and LHBT from the glenoid rim (Fig. 1.77c, d); the commonest type ■ type 3 – a ‘bucket-handle’ tear of the superior labrum with a preserved biceps anchor (Fig. 1.78e); the avulsed labrum may be displaced inferiorly between the humeral head and the glenoid articular surface ■ type 4 – extension of a ‘bucket-handle’ labral tear into the proximal LHBT (Fig. 1.78f) additional classification usually represents a combination of a type 2 SLAP lesion with other injuries: ■ type 5 – associated and continuous with a Bankart lesion (classically seen in athletes with traumatic anterior instability) ■ type 6 – a flap tear of the superior labrum ■ type 7 – anterior extension into the MGHL additional types include those with associated posterior labral tears or RI lesions

MRI findings ● abnormal morphology and hyperintensity of the superior labrum are seen on coronal oblique images (Fig. 1.77a, b) ● a linear (Fig. 1.77c) or globular (Fig. 1.77d) area of increased SI between the superior labrum and glenoid rim132 ● a displaced labral fragment ● conventional MRI is reported to have sensitivity, specificity and accuracy of 66–85 per cent, 75–83 per cent and 70–83 per cent, respectively, for the diagnosis of SLAP lesions133

Pathology of the superior labrum

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Figure 1.77 Superior labral anteroposterior lesions. Type 1: Coronal oblique T1-weighted spin-echo (a) and T2-weighted (T2W) fast spin-echo (FSE) fat-suppressed (FS) (b) images showing irregularity, blunting and hyperintensity of the superior labrum (arrows). Type 2: Coronal oblique T2W FSE FS images (c, d) showing linear (arrow c) and globular (arrow d) regions of increased signal intensity within the superior labrum.

MR arthographic findings134,135 ● ●

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there is marked fraying of the articular aspect of the labrum (Fig. 1.78a), consistent with a type 1 lesion an irregular contrast collection within the labrum (Fig. 1.78b, c) represents a type 2 SLAP lesion and can be differentiated from a sublabral recess by the orientation (lateral and superior extension) and shape (irregular rather than smooth, with relatively wide separation from the glenoid rim) biceps anchor avulsion a vertical tear with a horizontal component separating the labrum from the biceps anchor (Fig. 1.77d) with/without an inferiorly displaced ‘bucket-handle’ fragment (type 3) (Fig. 1.78e) extension of the tear into the biceps tendon fibres (type 4) (Fig. 1.78f) MR arthrography is reported to have sensitivity, specificity and accuracy of 82–89 per cent, 91–98 per cent and 90 per cent for the diagnosis of SLAP lesions a 66–76 per cent concordance between MR arthrography and arthroscopic classification of SLAP type is reported differentiation between a SLAP lesion and a sublabral recess can also be suggested by the width of T2W high SI on coronal oblique images:136 ■ a width of at least 2 mm on MRI and 2.5 mm on MR arthrography has a specificity of 89 per cent and 85 per cent, respectively, but a sensitivity of only 39 per cent and 46 per cent ■ the sensitivity and specificity of T2W high SI posterior to the BLC are 54 per cent and 74 per cent, respectively, for MRI, and 69 per cent and 54 per cent, respectively, for MR arthrography

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Figure 1.78 Superior labral anteroposterior lesions, MR arthrography. Type 1: Coronal oblique T1-weighted (T1W) spinecho (SE) fat-suppressed (FS) image (a) showing irregularity and fraying (arrow) of the superior labrum. Type 2: Coronal oblique (b) and axial (c) T1W SE FS images showing a vertical linear collection of contrast (arrow b) within the superior labrum and displacement of the labrum (arrow c) from the glenoid rim. Type 3: Coronal oblique T1W SE FS image (d) showing a vertical and horizontal collection of contrast (arrow) separating a labral fragment (arrowhead) from the biceps anchor (double arrowheads). Coronal oblique T1W SE FS image (e) showing an inferiorly displaced ‘bucket-handle’ labral fragment (arrow). Type 4: Coronal oblique T1W SE FS image (f) showing extension of the tear into the long head biceps tendon (arrows).

Miscellaneous conditions of the glenohumeral joint

a

c

b

Figure 1.79 180–360° labral tear. Axial (a, c) and coronal oblique (b) proton density-weighted fast spin-echo fatsuppressed images showing extensive injury to the anterior (arrow a), posterosuperior (arrow b) and inferior (arrow c) labrum.

180–360° labral tears137 ● ● ●

tears of the glenoid labrum may be categorised as anterior, posterior, superior or inferior 180–360° labral tears are uncommon and represent tears that involve more than two quadrants of the labrum they are typically reported in young, athletic male patients (mean age 28 years), usually with an acute precipitating injury

MRI findings ● 180–360° tears are suggested by the presence of either extensive posterior labral pathology or multiple sites of labral pathology (Fig. 1.79a–c) ● the findings may be subtle and include the presence of labral cysts

MISCELLANEOUS CONDITIONS OF THE GLENOHUMERAL JOINT Adhesive capsulitis138–141 ●

●

adhesive capsulitis is a condition of unknown aetiology that results in painful restriction of shoulder movements, particularly external rotation (frozen shoulder), and is most commonly seen in middle-aged women (40–60 years) pathologically, adhesive capsulitis results in synovitis, thickening and contraction of the joint capsule and synovium, particularly involving the axillary recess and RI

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a

b

d

c

f

e Figure 1.80 Adhesive capsulitis. Coronal T1-weighted (T1W) spin-echo (SE) (a) and short tau inversion recovery (b) images showing synovitis (arrows) within the axillary recess. Arrowheads (a) show the measurement of axillary recess synovial thickening. Sagittal T2-weighted (T2W) fast spin-echo (FSE) image (c) showing abnormal tissue (arrows) within the rotator interval (RI). Sagittal T2W FSE image (d) showing abnormal tissue (arrow) encasing the biceps anchor (arrowhead). Coronal (e) and sagittal (f) post-contrast T1W SE images showing enhancement within the axillary recess (arrow e) and RI (arrowheads f). Arrowheads (f) show the measurement of RI capsular thickness.

Miscellaneous conditions of the glenohumeral joint

MRI findings ● thickening of the synovium and capsule in the axillary recess is measured as the synovial thickness perpendicular to the humeral neck in the coronal oblique plane138 (Fig. 1.80a, b): ■ the mean thickness in patients with adhesive capsulitis is 9.0±2.2 mm, compared with 0.4±0.7 mm in normal shoulders142 ■ axillary recess synovial thickening >8 mm is seen in ~85 per cent of patients with adhesive capsulitis ● abnormal soft-tissue thickening within the RI139 (Fig. 1.80c); measured on post-contrast T1W sagittal images (Fig. 1.80f): the mean thickness in adhesive capsulitis patients is 8.4±2.8 mm, compared with 0.6±0.8 mm in normal shoulders:142 ■ RI synovial thickening of >5 mm is seen in ~92 per cent of adhesive capsulitis patients ● abnormal soft tissue encasing the biceps anchor (Fig. 1.80d) ● variable enhancement of the capsule and synovium within the axillary recess and RI140 (Fig. 1.80e, f) MR arthrographic findings143,144 ● thickening of the CHL is seen: 4.4 mm vs 2.7 mm in controls; CHL thickness >4 mm has a sensitivity of 59 per cent and a specificity of 95 per cent ● thickening of the RI capsule: 7.1 mm vs 4.5 mm in controls; RI capsule thickness >7 mm has a sensitivity of 64 per cent and a specificity of 86 per cent ● reduced volume of the axillary recess ● synovitis at the superior border of the subscapularis tendon ● complete obliteration of the fat triangle between the CHL and the coracoid process, with reported sensitivity of 32 per cent and specificity of 100 per cent ● narrowing of the RI: 7.45 mm vs 8.48 mm in controls ● thickening of the joint capsule and synovium: 2.97 mm vs 1.86 mm in controls ● on coronal oblique T2W images,145 an axillary recess capsule thickness of at least 3 mm has sensitivity, specificity and accuracy of 79 per cent, 100 per cent and 89 per cent, respectively, for the humeral side of the recess and 93 per cent, 86 per cent and 89 per cent, respectively, for the glenoid side

Focal articular cartilage lesions of superior humeral head146 ●

humeral head chondromalacia is a rare cause of post-traumatic shoulder pain and typically occurs along the superior surface of the posterior humeral head, medial to the expected location of a Hill–Sachs lesion

MRI findings ● a defect in the articular cartilage that may fill with contrast medium on MR arthrography ● in acute cases, there may be associated bone bruising in the adjacent humeral head

Osteochondral defect of the glenoid fossa147 ●

osteochondral defect of the glenoid articular surface is commonly associated with previous anterior dislocation or subluxation and is also reported as a rare injury in elite throwing athletes148

MRI findings ● a multiloculated cyst is seen in the subchondral bone mimicking a subchondral cyst (Fig. 1.81a) ● a single osteochondral fragment/intra-articular loose body ● signs of previous anterior dislocation: anterior labral tear (Fig. 1.81b) and a redundant capsular insertion ● may mimic the GLAD lesion149

Osteochondritis dissecans of humeral head150 ●

a very rare lesion that typically involves the anterosuperior portion of the humeral head

MRI findings ● combined injury to the articular cartilage and underlying bone

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a

b

Figure 1.81 Osteochondral defect of the glenoid fossa. Coronal oblique T1-weighted spin-echo (a) and axial T2*-weighted gradient-echo (b) images showing a subarticular cyst (arrows) of the glenoid and an anterior labral tear (arrowhead b).

Obstetric brachial plexus palsy151,152 ●

this may be associated with soft-tissue and bony deformities of the glenohumeral joint

MRI findings ● soft tissue: ■ blunting of the anterior and posterior labrum is seen ■ atrophy of the rotator cuff muscles is universal, with the subscapularis and infraspinatus being most severely affected153 ■ cuff muscle atrophy correlates with the presence of glenohumeral joint incongruence, increased glenoid retroversion and internal rotation contracture ● bony: ■ deformity of the glenoid articular surface, which may be retroverted (Fig. 1.82a), convex or biconcave, or may have a posteroinferior pseudoglenoid (Fig. 1.82a) ■ flattening of the humeral head (Fig. 1.82b) ● joint position: ■ posterior subluxation or disclocation (Fig. 1.82a) ■ the humeral head may articulate with the pseudoglenoid

a

b

Figure 1.82 Obstetric brachial plexus palsy, MR arthrography. Axial T1-weighted (T1W) spin-echo (SE) fat-suppressed (FS) image (a) showing glenoid retroversion and a posteriorly subluxed humeral head, which is articulating with a pseudoglenoid (arrow). Coronal T1W SE FS image (b) showing flattening of the medial part of the humeral head (arrow).

The nerves

THE NERVES Normal anatomy154,155 ●

the suprascapular nerve is a mixed motor and sensory nerve that carries pain fibres from the glenohumeral and ACJ and provides motor supply to the supraspinatus and infraspinatus muscles: ■ it arises from the superior trunk of the brachial plexus (C5–6) and runs laterally, deep to the trapezius and parallel to the omohyoid muscle, entering the suprascapular fossa through the suprascapular notch (Fig. 1.83a) and giving off a branch to supraspinatus

b a

d c

e

Figure 1.83 Anatomy of the nerves. Suprascapular nerve: Coronal proton density-weighted (PDW) fast spin-echo (FSE) image (a) showing the suprascapular fossa (arrow). Axial T2*-weighted gradient-echo image (b) showing the spinoglenoid fossa (arrow). Axillary nerve/quadrilateral space: Coronal oblique PDW FSE image (c) showing the quadrilateral space bounded by the teres minor (short arrow), the teres major (long arrow) and the humeral shaft (arrowhead). Axial PDW FSE (d) and sagittal T2-weighted FSE (e) images showing the axillary nerve and posterior circumflex humeral artery (arrows).

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it then winds around the lateral border of the scapular spine to reach the infraspinatus fossa, providing a branch to the infraspinatus muscle ■ consequently, lesions of the nerve at the level of the suprascapular notch involve both the supraspinatus and the infraspinatus, whereas lesions in the spinoglenoid notch (Fig. 1.83b) involve the infraspinatus only the axillary nerve originates from the posterior cord of the brachial plexus (C6–7), runs anterior to the subscapularis muscle, then turns posteriorly to enter the quadrilateral space, together with the posterior circumflex humeral artery (PCHA): ■ the borders of the quadrilateral space are (Fig. 1.83c–e) the humeral shaft (lateral), the long head of triceps (medial), the teres minor muscle (superior) and the teres major muscle (inferior) ■ the axillary nerve provides motor supply to the teres minor and deltoid muscles, and sensory innervation to the shoulder and upper arm the subscapular nerves: the upper and lower subscapular nerves arise from the posterior cord of the brachial plexus and supply the subscapularis muscle ■

●

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PATHOLOGY OF THE NERVES Suprascapular nerve entrapment154,155 ●

causes of suprascapular nerve entrapment include scapular fractures, shoulder dislocation, tumour, and compression by the suprascapular ligament during shoulder movement: ■ ganglion/paralabral cyst: cysts associated with posterosuperior labral tears usually extend into the spinoglenoid notch, causing denervation oedema/atrophy of the infraspinatus muscle (Fig. 1.84a–c) ■ intraneural ganglia of the suprascapular nerve:156 suprascapular neuropathy may also be caused by the rare intraneural ganglia of the nerve, which are shown to have connections with the glenohumeral joint through posterior labrocapsular complex tears ■ varicosities in the spinoglenoid notch157 may result in nerve compression and infraspinatus muscle atrophy, with MRI demonstrating varicosities measuring ~6–10 mm in size (Fig. 1.84d)

Acute brachial neuritis (Parsonage–Turner syndrome)158–160 ● ●

●

Parsonage–Turner syndrome is a self-limiting condition of unknown aetiology it is also termed ‘acute brachial neuritis’ or ‘neuralgic amyotrophy’, and is an uncommon condition manifest clinically by: ■ sudden onset of severe shoulder pain with spontaneous resolution within 1–3 weeks ■ followed by weakness of at least one shoulder girdle muscle, most commonly the supraspinatus or infraspinatus, or occasionally the deltoid or subscapularis ■ bilateral involvement is reported in 33 per cent of patients ■ recovery usually takes a few months, but may take years incidence of nerve involvement in Parsonage–Turner syndrome:160 ■ involvement of the suprascapular nerve is reported in 97 per cent of cases, with 50 per cent being limited to this nerve ■ involvement of the axillary nerve is reported in 50 per cent of cases, with only 3 per cent being limited to this nerve ■ only 3 per cent have involvement of the subscapular nerve, but not in isolation

MRI findings acute stage: muscle oedema is seen on T2W/STIR images due to denervation (Fig. 1.85a, b) ● chronic stage: muscle atrophy and fatty replacement are best appreciated on T1W images (Fig. 1.85c–e) ● use of whole-body turbo STIR MRI showing unilateral involvement of the shoulder girdle muscles improves the specificity, allowing differentiation from other conditions such as polymyositis161 ●

Pathology of the nerves

a b

c

d

Figure 1.84 Suprascapular nerve compression. Paralabral cyst: Coronal T1-weighted spin-echo (a), axial proton densityweighted fast spin-echo (FSE) (b) and sagittal T2-weighted FSE (c) images showing a lobulated spinoglenoid notch cyst (arrows) with associated denervation oedema/atrophy (arrowheads b, c) of the infraspinatus muscle. Enlarged spinoglenoid notch veins: Axial T2*-weighted gradient echo image (d) showing varicose veins (arrow) in the spinoglenoid notch and atrophy of the infraspinatus muscle (arrowheads).

Quadrilateral space syndrome162 ● ●

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this a clinical syndrome caused by compression of the axillary nerve and PCHA in the quadrilateral space clinical features include shoulder pain radiating to the arm in a non-dermatomal manner, with symptoms aggravated by forced abduction and external rotation, and tenderness over the lateral aspect of the quadrilateral space dynamic compression may occur in the ABER position, while causes of static compression/damage include proximal humeral or scapular fractures, posteroinferior paralabral cysts, hypertrophy of the teres minor muscle, fibrous bands (commonest cause) and other mass lesions in the quadrilateral space155,156

MRI findings ● selective denervation changes (acute: oedema; chronic: atrophy) of the teres minor (usually) and/or deltoid muscles (Fig. 1.86a–c) are seen ● however, isolated denervation of the teres minor is reported in 3 per cent of shoulder MRI studies, of which none showed a lesion in the quadrilateral space:163 ■ alternative causes include rotator cuff injuries and traction injuries to the axillary nerve ● occlusion of the PCHA in abduction can be demonstrated by MR angiography: ■ however, this finding is also present in 80 per cent of asymptomatic volunteers164

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a

c

e

b

d

Figure 1.85 Acute brachial neuritis (Parsonage–Turner syndrome). Acute stage: Coronal proton density-weighted (PDW) fast spin-echo (FSE) fat-suppressed image (a) demonstrates oedema of the supraspinatus (arrows). Sagittal T2-weighted (T2W) FSE image (b) shows oedema of the supraspinatus (arrowheads) and infraspinatus (arrows). Chronic stage: Coronal (c) and axial (d) PDW FSE and sagittal oblique T2W FSE (e) images showing atrophy of the supraspinatus (arrows c, e) and infraspinatus (arrowheads d, e) with an intact rotator cuff tendon (long arrow c).

The post-operative shoulder

b a

c

Figure 1.86 Quadrilateral space syndrome. Coronal oblique proton density-weighted (PDW) fast spin-echo (FSE) image (a) shows chronic atrophy of the deltoid muscle (arrowheads). Coronal oblique PDW FSE (b) and T2-weighted FSE fatsuppressed (c) images showing varicosities (arrows) within the quadrilateral space.

THE POST-OPERATIVE SHOULDER Introduction165–168 ●

the surgical procedures most commonly performed in the shoulder include: ■ subacromial decompression for impingement/PTRCT ■ rotator cuff repair ■ repair for glenohumeral instability

Arthroscopic subacromial decompression ●

●

arthroscopic subacromial decompression (ASAD) is the current treatment of choice for chronic extrinsic impingement of the RCT, the aim of which is to increase the space available for the cuff tendons between the acromion and the humeral head the surgical technique for ASAD includes diagnostic arthroscopy, resection of the coracoacromial ligament and subacromial bursa, anterior and posterior acromial resection (acromioplasty), resection of any significant ACJ osteophytes and, if required, resection of the distal clavicle (Mumford procedure)

MR findings: normal ● change in morphology of the acromion: ■ usually from a hook or curve (type 3) to a flatter, slightly shortened configuration (type 1) ■ non-visualisation of the anterior third of the acromion (Fig. 1.87a) ● decreased SI in the acromion on T1W and T2W images due to fibrosis of the acromial marrow

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a b

c d

e

f

Figure 1.87 Normal appearances following arthroscopic subacromial decompression. Coronal T1-weighted (T1W) spinecho (SE) image (a) showing absence of the anterior acromion (arrow). Sagittal oblique proton density-weighted fast spin-echo (FSE) image (b) showing absence of the coracoacromial ligament with replacement by scar tissue (arrow). Axial T2*-weighted (T2*W) gradient-echo (GE) image (c) showing metallic artefact (arrows) in the subacromial space. Mumford procedure: Coronal T1W SE (d) and axial T2*W GE (e) images showing resection of the distal clavicle (arrows). Coronal oblique T2W FSE fat-suppressed image (f) showing fluid (arrow) in the subacromial space at the site of the excised subacromial bursa. ● ● ● ●

absence of the coracoacromial ligament insertion into the acromion, with replacement by fat, scar tissue (Fig. 1.87b) or metallic artefact (Fig. 1.87c) widening of the ACJ by 1–2 cm following a Mumford procedure (Fig. 1.87d, e) fluid at the site of the resected subacromial bursa in 100 per cent of cases (Fig. 1.87f) residual tendon changes (tendinosis) are still apparent

The post-operative shoulder

MRI findings: abnormal ● residual impingement due to subacromial (Fig. 1.88) or ACJ osteophytes ● the reliability of MRI for the assessment of residual bony impingement is reported as: ■ sensitivity 64–84 per cent, specificity 82–87 per cent and accuracy 74 per cent ● continuing bony impingement from subacromial spurs or acromioclavicular joint osteophytes is optimally assessed on sagittal T2W FSE images

Figure 1.88 Recurrent post-subacromial decompression impingement. Sagittal oblique T1-weighted spin-echo image showing continued impingement on the cuff by residual subacromial osteophyte (arrow).

Rotator cuff repair ● ● ● ● ●

●

●

techniques used for rotator cuff repair depend on the type, size and location of the tear bursal-side PTRCT: ASAD with debridement of the tendon small articular-side PTRCT: tendon debridement ± acromioplasty deep articular-side PTRCT: tears >50 per cent depth may be treated as small FTRCTs FTRCT: open or arthroscopically assisted (mini-open) repair, which comprises splitting of the deltoid muscle, debridement of unhealthy cuff tissue, side-to-side suturing of the tendon (for small FTRCTs), reattachment of the tendon to the greater tuberosity with sutures (for distal RCT tears) and possible associated acromioplasty/Mumford procedure massive FTRCT may be irreparable, in which case tendon transfers may be performed: ■ massive subscapularis tears may be treated by split pectoralis major transfer ■ massive supraspinatus tears may be treated by latissimus dorsi tendon transfer biceps tenodesis may be indicated in the presence of associated LHBT pathology (atrophy/hypertrophy, partial tears >25 per cent of tendon width, tendon subluxation), particularly in younger patients

MRI findings: normal ● ● ●

● ● ●

intermediate or low T1W SI in the tendon due to granulation tissue or fibrosis increased T2W SI due to granulation tissue, which should not reach fluid SI and cannot be differentiated from residual tendinosis regular or irregular tendon morphology: ■ only 10 per cent of asymptomatic patients have normal tendon morphology after cuff repair ■ small FTRCTs measuring 8 mm on average can be seen in asymptomatic patients, compared with recurrent tears in symptomatic patients, which measure on average 3.4 cm mild superior subluxation of the humeral head, with/without marrow oedema that can persist for up to 5 years fluid in the SA-SD bursa, which is a non-specific finding and may extend into the ACJ (geyser sign), and glenohumeral joint effusion a non-watertight seal is common after successful cuff repair and MR arthrographic contrast may therefore leak through a defect in a well-healed cuff, and through arthroscopy portals

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● ● ● ●

artefacts from surgical tacks/sutures many surgical fixation devices are biodegradeable and are not seen on conventional radiography, but the remaining bioabsorbable screw and tunnel can be seen on MRI (Fig. 1.89a) osteolysis may be seen around suture anchors and may double in size by 6 months post-operatively holes around absorbable anchors fill with bone by 2 years

MR findings: abnormal ● MRI/MR arthrographic criteria for recurrent FTRCT include: ■ a fluid/contrast-filled full-thickness cuff defect (Fig. 1.89b) and/or non-visualisation of part of the cuff tendon ■ the most specific sign is complete absence of the cuff tendon ■ most re-tears occur at the tendon–bone junction or approximately 1.5 cm proximal to this ■ the position of the musculotendinous junction is unreliable as a secondary sign of cuff tear, since the tendon may have been mobilised (usually for tears >3 cm) ● recurrent PTRCT is difficult to diagnose on standard MRI: ■ focal high SI in the cuff tendon may be due to granulation tissue or fluid trapped between sutures ■ the diagnostic accuracy is increased with MR arthrography, which can show extension of contrast into the partial articular-side cuff defects ● the prevalence of tendon re-rupture following repair of FTRCT is reported as ~58 per cent:169 ■ however, not all re-ruptures are clinically relevant ■ re-ruptures are significantly more common in patients with intermediate/poor clinical outcomes, with surgically demonstrated two-tendon or three-tendon tears or with pre-operative fatty degeneration of the supraspinatus muscle ■ re-ruptures are also significantly larger in these subgroups ● diagnostic performance of MRI in the assessment of recurrent cuff tears: ■ sensitivity and specificity reported as 100 per cent and 87 per cent, respectively, for combined PTRCT and FTRCT ■ sensitivity and specificity reported as 83 per cent and 83 per cent, respectively, for PTRCT ● the diagnostic performance of MR arthrography in the assessment of recurrent FTRCT is reported as:170 ■ supraspinatus: sensitivity, specificity and accuracy 86–90 per cent, 59–89 per cent and 71–90 per cent, respectively ■ infraspinatus: sensitivity, specificity and accuracy 79–100 per cent, 94–100 per cent and 90–100 per cent, respectively ■ subscapularis: sensitivity, specificity and accuracy 90–91 per cent, 92–100 per cent and 92–96 per cent, respectively

a b Figure 1.89 Post-operative changes. Axial proton density-weighted fast spin-echo (FSE) MR arthrogram (a) showing the site of a bioabsorbable screw (arrow). Recurrent full-thickness rotator cuff tear: Coronal oblique T2-weighted FSE image (b) showing fluid (arrow) through the full thickness of the repaired supraspinatus tendon.

The post-operative shoulder

Complications of arthroscopic subacromial decompression and tendon repair ●

● ● ●

deltoid detachment from the acromial insertion is a potential complication following open rotator cuff repair, due to violation of the deltoid insertion and overlying fascia: ■ MRI demonstrates retraction of the deltoid muscle with fluid in the gap and deltoid atrophy in chronic cases acromial fracture, frozen shoulder, deep infection, dislocation, heterotopic ossification, hardware displacement axillary nerve injury may occur if the deltoid split incision is carried >5 cm below the acromion LHBT rupture/dislocation

Surgery for glenohumeral joint instability ● ● ●

●

a wide variety of techniques are available for anterior/multidirectional instability, both open and arthroscopic open techniques are classified as anatomical or non-anatomical anatomical techniques are the most commonly performed and are repairs that maintain the normal anatomy of the shoulder: ■ Bankart repair: suture anchors are passed through holes drilled in the anterior glenoid at approximately the 3, 4 and 5 o’clock positions, with reattachment of the torn labrum, capsule and anterior band of the IGHL non-anatomical techniques are most commonly used for revision surgery and may be soft-tissue or osseous: ■ soft-tissue techniques include: – Putti–Platt: shortening of the anterior capsule and subscapularis muscle – Magnusson–Stack: transfer of the subscapularis tendon from the lesser to the greater tuberosity – inferior capsular shift: used for primary treatment of multidirectional instability and as an adjunct to a Bankart repair ■ osseous techniques include: – Bristow–Helfet: transfer of the tip of the coracoid process with the attached tendons to the scapular neck/anteroinferior glenoid

MR findings: normal ● following a Bankart repair: paramagnetic artefacts in the anterior glenoid rim (Fig. 1.90a), anterior capsular thickening/nodularity (2–4 mm) and thickening/irregularity of the labrum and glenohumeral ligaments: ■ mild superior subluxation of the humeral head due to capsular tightening ● following a Putti–Platt repair: marked thickening of the distal subscapularis tendon ● following inferior capsular shift: a small axillary pouch (Fig. 1.90b), thickening of the anteroinferior capsule (Fig. 1.90c) and low SI artefact in the anterior capsule and subscapularis tendon (Fig. 1.90d) MR findings: abnormal ● recurrent labral detachment/capsular stripping, which is optimally assessed with MR arthrography in the ABER position

Post-operative complications following surgery for instability ● ● ● ●

recurrent instability and re-tear migration of surgical bioabsorbable tacks or suture anchors, which may result in articular cartilage damage and early OA, or in loose body formation bioabsorbable tacks can also produce synovitis misplacement of tacks or sutures may result in nerve injury: ■ the axillary nerve may be damaged as it crosses the inferolateral aspect of the subscapularis muscle and the anteroinferior glenohumeral joint capsule ■ the suprascapular nerve may be injured in the spinoglenoid notch by a posteriorly placed suture anchor

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a

b

c

d

Figure 1.90 Normal appearances following anterior capsular repair. Axial T1-weighted spin-echo fat-suppressed MR arthrogram (a) following Bankart repair showing metallic artefact (arrow) in the anterior bony glenoid rim. Inferior capsular shift: Coronal proton density-weighted (PDW) fast spin-echo (FSE) image (b) showing contraction of the axillary recess (arrow). Sagittal oblique PDW FSE images (c, d) showing thickening of the anteroinferior capsule (arrows c) and metallic artefact in the subscapularis tendon (arrows d).

THE ACROMIOCLAVICULAR JOINT Normal anatomy171–173 ● ● ● ●

the ACJ is a diarthrodial, synovial joint formed by articulation between the distal clavicle and the anteromedial aspect of the acromion the inferior margins of the clavicle and acromion are usually aligned (Fig. 1.91a), but in approximately 20 per cent of cases the inferior margins are incongruent (Fig. 1.91b) in the axial plane, the articular surface of the acromion is angled anteromedially (Fig. 1.91c) the inclination of the ACJ in the coronal plane is variable: ■ the clavicle overrides the acromion in 49 per cent of cases ■ there is vertical alignment in 27 per cent of cases (Fig. 1.91a) ■ the clavicle underrides the acromion in 3 per cent of cases ■ the joint is incongruous in 21 per cent of cases

The acromioclavicular joint

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b

c

d

e

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Figure 1.91 Normal anatomy of the acromioclavicular joint (ACJ). Coronal oblique T1-weighted spin-echo images (a, b) showing the ACJ with normal alignment (a) and malalignment (b) of the inferior surfaces of the acromion and distal clavicle. Axial T2*-weighted (T2*W) gradient-echo (GE) image (c) showing the normal ACJ (arrow). Axial T2*W GE image (d) showing the anterior capsule (arrow). Coronal oblique proton density-weighted fast spin-echo image (e) showing the normal superior (arrow) and inferior (arrowhead) acromioclavicular ligaments.

the joint is lined by fibrocartilage and possesses a meniscus (articular disc) that usually undergoes degeneration by the second decade of life the normal width of the joint is 1–3 mm the joint is stabilised by a combination of ligaments and muscles ligaments include the acromioclavicular (AC) and the CC: ■ the AC ligaments support the thin capsule (Fig. 1.91d), the largest being the superior AC ligament (Fig. 1.91e); the inferior AC ligament is absent in ~50 per cent of cases ■ the CC ligament comprises conoid and trapezoid components, forming a V-shaped ligament with its apex arising from the coracoid process and its base at the undersurface of the distal acromion (Fig. 1.92a, b): – the conoid ligament lies posteromedial and the trapezoid ligament lies anterolateral

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a

b Figure 1.92 The coracoclavicular (CC) ligament. Coronal proton density-weighted fast spin-echo (FSE) image (a) through the acromioclavicular joint showing the trapezoid (arrowhead) and conoid (arrow) components of the CC ligament. Sagittal oblique T2-weighted FSE image (b) showing the CC ligament (arrow).

●

– the two segments are separated by fat or a bursa – the trapezoid ligament is the primary restraint to posterior displacement of the clavicle – the conoid ligament is a primary restraint to anterior and superior displacement muscle attachments to the ACJ include the trapezius and the deltoid

PATHOLOGY OF THE ACROMIOCLAVICULAR JOINT Osteoarthritis174 ● ● ● ●

OA of the ACJ is a common finding on shoulder MRI studies and is the commonest cause of ACJ pain however, ACJ OA is present in 82 per cent of asymptomatic individuals undergoing shoulder MRI175 conversely, 98 per cent of patients with symptomatic ACJ OA also have some form of internal derangement of the shoulder on MRI176 MRI is much more sensitive than radiography in identifying and staging ACJ OA174

MRI findings177 ● joint space narrowing is seen with subchondral irregularity (Fig. 1.93a) and cyst formation (Fig. 1.93b) ● capsular thickening and oedema/synovitis (Fig. 1.93c) with/without joint effusion (Fig. 1.93d) ● osteophyte formation (Fig. 1.93e), resulting in a bulky joint (Fig. 1.93f) ● hyperintensity of the distal clavicle (Fig. 1.93g) and/or acromion (Fig. 1.93h) ● relationship between MRI findings and symptoms: hyperintensity of the distal clavicle is statistically more common in patients with ACJ pain,178 while capsular thickening is predictive of a good response to injection of local anaesthetic into the ACJ179

Distal clavicular osteolysis180,181 ● ● ●

distal clavicle osteolysis may be post-traumatic or stress induced the preceding trauma may be mild or may involve traumatic separation of the ACJ (incidence reported as 1–21 per cent) post-traumatic osteolysis occurs after a variable interval (2 weeks to several years) following an acute episode of trauma

Pathology of the acromioclavicular joint

a

b

c

d

e

f Figure 1.93 Osteoarthritis of the acromioclavicular joint (ACJ). Axial T1-weighted (T1W) spin-echo (SE) image (a) showing loss of joint space and subchondral irregularity. Coronal oblique proton density-weighted (PDW) fast spin-echo (FSE) fatsuppressed (FS) image (b) showing subchondral cyst formation (arrow). Coronal oblique PDW FSE FS images (c, d) showing superior capsular thickening (arrow c) and a joint effusion (arrow d). Coronal oblique T1W SE image (e) showing inferior osteophyte formation (arrows). Sagittal oblique T2-weighted (T2W) FSE image (f) showing a bulky ACJ (arrow) due to osteophytes. (continued)

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g Figure 1.93 (continued) Axial T2W FSE FS image (g) showing oedema (arrow) in the distal clavicle. Coronal T2W FSE FS image (h) showing oedema in the acromion (arrow). ● ●

h

stress-induced osteolysis is described in manual workers and athletes (particularly weight-lifters) clinically, patients present with pain and swelling of the ACJ and a palpable lump, mimicking a tumour

MRI findings ● marrow oedema of the distal clavicle (always) (Fig. 1.94a, b) with/without oedema of the adjacent acromion and a subchondral distal clavicular fracture line ● cortical irregularity or erosion of the distal clavicle (always) (Fig. 1.94a, b) with/without erosion of the adjacent acromion

a

c

b

Figure 1.94 Distal clavicular osteolysis. Coronal oblique T1-weighted spin-echo (a) and short tau inversion recovery (b) images showing oedema and cortical erosion of the distal clavicle (arrowhead) and joint effusion (arrow). Axial T2*-weighted gradient-echo image (c) showing a widened joint space (arrowhead) and subchondral erosion (arrow).

Pathology of the acromioclavicular joint

● ● ●

joint space widening, capsular thickening, effusion (Fig. 1.94c) and intra-articular bone fragments fibrosis in the ACJ with low SI on T1W and T2W images hyperintensity of the distal clavicle has also been reported with an incidence of 12.5 per cent in patients undergoing shoulder MRI and in most cases is of no clinical relevance182 (Fig. 1.95): ■ however, increased T2W SI of the distal clavicle in patients with chronic ACJ pain and no other radiological abnormality of the joint may be clinically significant, possibly representing early distal clavicular osteolysis ■ such patients respond to resection of the distal clavicle

Figure 1.95 Coronal oblique proton density-weighted fast spin-echo fat-suppressed image showing hyperintensity of the distal clavicle (arrow).

Acromioclavicular joint cysts52 ● ● ●

ACJ cysts are typically related to massive rotator cuff tears (see above) and may present as a soft-tissue tumour rarely, an ACJ cyst extends into the trapezius muscle to form an intramuscular ganglion183 a juxta-articular myxoma may also mimic a cyst of the ACJ184

Trauma172,173 ●

ACJ dislocation accounts for >10 per cent of all shoulder injuries and can be graded as follows: ■ type 1 – a sprained but intact AC ligament ■ type 2 – a disrupted AC ligament and sprained but intact CC ligament ■ type 3 – disruption of both the AC and the CC ligament ■ subtypes of type 3 include: – type 4 – posterior displacement of the clavicle into the trapezius muscle – type 5 – vertical separation of the clavicle from the scapula – type 6 – inferior displacement of the clavicle

MRI findings ● type 1: there are no specific features, since SI abnormalities (oedema due to synovitis) around the ACJ are common in the absence of trauma ● type 2: disrupted AC ligament and oedematous but intact CC ligament (Fig. 1.96) with oedema in the adjacent clavicle and acromion ● type 3: disruption of both the AC and the CC ligament with haemorrhage and oedema seen in the CC space, and possible detachment of deltoid and/or trapezius from the distal end of the clavicle ● type 4: axial images show posterior displacement of the distal clavicle into the trapezius ● type 5: disruption of the deltoid and trapezius insertions and superior displacement of the distal clavicle ● type 6: inferior displacement of the distal clavicle beneath the acromion or the coracoid process

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Figure 1.96 Coronal oblique proton density-weighted fast spin-echo image showing swelling and poor definition of the coracoclavicular ligament (arrow) consistent with a sprain.

THE STERNOCLAVICULAR JOINT Normal anatomy171 ● ●

the sternoclavicular joint (SCJ) is a diarthrodial joint formed by articulation between the medial end of the clavicle and the superolateral margin of the manubrium (Fig. 1.97a) joint integrity is dependent on the joint capsule and adjacent ligaments, which include: ■ the intra-articular disc ligament: attached to the joint capsule and may be complete or incomplete, passing between the clavicle and manubrium, thereby dividing the joint into two cavities (Fig. 1.97b) ■ the anterior and posterior sternoclavicular (capsular) ligaments: thickenings of the joint capsule anterosuperiorly and posteriorly, running between the medial clavicular epiphysis and the manubrium ■ the interclavicular ligament: connects the superomedial aspect of each clavicle to the capsular ligaments and upper sternum (Fig. 1.97b) ■ the costoclavicular ligament: extends from the superior aspect of the first rib to the rhomboid fossa on the inferior surface of the medial clavicle

b a Figure 1.97 Normal anatomy of the sternoclavicuar joint. Coronal T2*-weighted (T2*W) gradient echo (GE) image (a) showing the joint (arrow) formed by the medial clavicle (arrowhead) and the manubrium sterni (double arrowhead). Coronal T2*W GE image (b) showing the intra-articular disc ligament (arrow) and the interclavicular ligament (arrowheads).

Pathology of the sternoclavicular joint and medical clavicle

PATHOLOGY OF THE STERNOCLAVICULAR JOINT AND MEDIAL CLAVICLE Osteoarthritis185 ● ●

SCJ OA usually presents in the sixth decade, resulting in painful swelling for months or years however, asymptomatic changes of OA may be present in 50 per cent of individuals in the fourth decade and in >90 per cent after 60 years of age

MRI findings ● joint space narrowing is seen with subchondral cyst formation ● osteophytosis: most commonly from the inferomedial margin of the clavicle (Fig. 1.98a) ● subchondral sclerosis: most marked in the inferomedial clavicle but also affects the manubrium ● capsular thickening and joint effusion (Fig. 1.98b)

b a Figure 1.98 Osteoarthritis of the sternoclavicular joint (SCJ). Coronal T1-weighted spin-echo image (a) showing erosion of the cortical margins of the SCJ, a small inferior clavicular osteophyte (arrow) and generalised capsular thickening (arrowheads). Coronal T2-weighted fast spin-echo fat-suppressed image (b) showing a joint effusion (arrow).

Osteitis condensans claviculi185,186 ● ●

an uncommon condition of unknown aetiology that may result from repetitive stress and is almost completely limited to women of childbearing age clinically, results in pain and swelling of several months’ duration that may be referred to the ipsilateral shoulder and aggravated by arm abduction

MRI findings ● low SI is seen on T1W (Fig. 1.99a) and T2W (Fig. 1.99b) images in the inferior medial aspect of the clavicle ● associated marrow oedema (Fig. 1.99b) and adjacent soft-tissue oedema ● variable marrow and soft-tissue enhancement may be seen following gadolinium (Fig. 1.99c) ● a normal appearance of the SCJ and adjacent manubrium differentiates the condition from OA

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The shoulder girdle

a

c

b

Figure 1.99 Osteitis condensans claviculi. Coronal T1-weighted (T1W) spin-echo (SE) (a) and T2-weighted fast spin-echo fat-suppressed (FS) (b) images show sclerosis in the inferomedial clavicle (arrows) and adjacent marrow oedema (arrowhead b). Axial post-contrast T1W SE FS image (c) showing enhancement in the medial clavicle and adjacent soft tissues (arrow).

THE SCAPULOTHORACIC JOINT Normal anatomy187 ● ●

the scapulothoracic joint is formed by ‘articulation’ between the scapula and the posterolateral chest wall, but is not a true joint since it has no articular surfaces the associated muscles that attach the scapula to the chest wall include: ■ the trapezius, which has descending, transverse and ascending parts: – the descending part originates from the occipital protruberance and ligamentum nuchae and inserts into the lateral clavicle (Fig. 1.100a) – the transverse part originates from the transverse processes of C7–T3 and inserts into the medial acromion and lateral scapular spine – the ascending part originates from the spinous processes of T3–12 and inserts into the medial scapular spine (Fig. 1.100b) ■ the rhomboids: – rhomboid minor originates from the spinous processes of C6 and C7 – rhomboid major originates from the spinous processes of T1–4 – both insert into the medial border of the scapula ■ the levator scapulae originates from the transverse processes of C1–4 and inserts into the superior angle of the scapula ■ the serratus anterior comprises superior, middle and inferior parts: – originates from the anterior aspects of the first to ninth ribs and inserts into the anterior aspect of the medial border of the scapula (Fig. 1.100c) ■ the pectoralis minor originates from the third to fifth ribs and inserts into the medial border of the coracoid process and occasionally into the humerus

Pathology of the scapulothoracic joint

a b

c

Figure 1.100 Normal anatomy of the scapulothoracic muscles. Trapezius: Coronal proton density-weighted (PDW) fast spinecho (FSE) image (a) showing the insertion of the descending part (arrow) into the lateral clavicle. Sagittal oblique PDW FSE image (b) showing the medial clavicular and scapular spine insertions (arrowheads). Serratus anterior: Axial T1-weighted spin-echo image (c) showing the serratus anterior (arrowheads) inserting into the medial scapula (arrow).

PATHOLOGY OF THE SCAPULOTHORACIC JOINT Scapulothoracic crepitus188 ●

●

scapulothoracic crepitus is also termed ‘scapulothoracic syndrome’, or ‘grating’ or ‘snapping’ scapula and is a condition of various aetiologies, including: ■ an osseous lesion: osteochondroma (arising from the deep scapula or outer rib), malunited rib or scapular fracture, hooked superomedial angle of the scapula, Luschka’s tubercle (any bony prominence of the superomedial angle of the scapula) ■ a soft-tissue lesion: bursitis, atrophied or fibrotic muscle, anomalous muscle insertions ■ incongruence of the scapulothoracic articulation: scoliosis and kyphosis asymptomatic scapulothoracic crepitus may be physiological, being reported in 31 per cent of normal individuals

MRI findings ● these are consistent with the underlying aetiology, the commonest osseous cause being a small osteochondroma (Fig. 1.101)

Scapulothoracic bursitis188,189 ●

two major (anatomical) and four minor (adventitial) bursae are described for the scapulothoracic articulation

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The shoulder girdle

Figure 1.101 Scapulothoracic crepitus. Sagittal T1-weighted spin-echo image showing a small osteochondroma (arrow) arising from the deep surface of the scapular blade.

●

●

● ●

the major bursae: ■ the infraserratus bursa: lying between the serratus anterior muscle and the chest wall and bordered by the origin of the serratus anterior laterally and the rhomboid muscles medially ■ the supraserratus bursa: lying between the subscapularis muscle and the serratus anterior and bordered laterally by the axilla and medially by the insertion of the serratus anterior the minor bursae: ■ an infraserratus bursa at the inferior angle of the scapula ■ the infraserratus and supraserratus bursae at the superomedial angle of the scapula ■ a trapezoid bursa at the medial base of the scapular spine, deep to the trapezius scapulothoracic bursitis is due to inflammation of minor (adventitial) bursae, affecting two main sites: the superomedial (commonest) and the inferior angle of the scapula clinically, it may present as a palpable, painless soft-tissue mass mimicking a tumour

MRI findings ● a cystic structure is seen lying between the serratus anterior and the chest wall (Fig. 1.102a, b), typically measuring 5–12 cm ● it may contain areas of haemorrhage ● spontaneous resolution is reported in all cases over a period of several weeks

a

b

Figure 1.102 Scapulothoracic bursitis. Axial T1-weighted spin-echo (a) and short tau inversion recovery (b) images showing a cystic mass (arrows) between the chest wall and the serratus anterior (arrowheads).

Pathology of the thoracohumeral muscles

THE THORACOHUMERAL MUSCLES Normal anatomy187 ●

●

the pectoralis major has an extensive origin from the anterior chest/abdominal wall: ■ the clavicular part originates from the anterior surface of the medial two-thirds of the clavicle ■ the sternocostal part originates from the sternum/manubrium and the costal cartilage of the first to sixth ribs ■ a small abdominal part originates from the external oblique muscle fascia ■ it has a common insertion via its tendon into the lateral rim of the intertubercular groove (Fig. 1.103): – the tendon measures 5–15 mm in length and approximately 5 cm in craniocaudal dimension – its superior margin is at the level of the quadrilateral space – its inferior margin lies just above the deltoid tubercle the latissimus dorsi is an adductor, internal rotator and extensor of the shoulder joint, with an extensive origin from the spine, ilium, ribs and scapula: ■ the vertebral part originates from the spinous processes of T7–12 ■ the iliac part originates from the thoracolumbar fascia and iliac crest ■ the costal part originates from the 10th to 12th ribs ■ the scapular part originates from the inferior angle of the scapula ■ inserts into the floor of the intertubercular groove of the humerus (Fig. 1.103)

Figure 1.103 Anatomy of the thoracohumeral muscle insertions. Axial T1-weighted spin-echo image showing insertion of the pectoralis muscle tendon (arrow) into the anterior humerus, the musculotendinous junction (arrowhead) and the muscle (black arrows). The insertion of the latissimus dorsi (double arrowheads) is seen just medial to the pectoralis major.

PATHOLOGY OF THE THORACOHUMERAL MUSCLES Pectoralis major rupture190,191 ● ●

●

pectoralis major rupture is a rare injury almost always confined to male athletes, typically performing weight-lifting/bench-pressing, water skiing, wrestling or American football tears may be: ■ partial, usually at the musculotendinous junction and treated conservatively ■ complete, usually at the tendon–bone interface and treated surgically clinically, patients present with sudden pain in the arm and shoulder, bruising and variable loss of function

MRI findings ● acute partial tears exhibit oedema and haemorrhage with a variable degree of muscle fibre discontinuity at the musculotendinous junction

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The shoulder girdle

● ●

acute complete tears of the tendon–bone interface show discontinuity of the tendon, haemorrhage and periosteal stripping chronic tears show fibrosis and scarring

Calcific tendinitis of the pectoralis major tendon59 ●

calcific tendinitis is a rare condition presenting with acute-onset anterior shoulder/arm pain and spontaneous resolution, possibly mimicking a bone or soft-tissue sarcoma

MRI findings ● an oedematous mass at the site of tendon insertion (Fig. 1.104a) ● possible cortical destruction and adjacent marrow oedema ● tendon calcification is optimally demonstrated on CT (Fig. 1.104b)

a

b Figure 1.104 Calcific tendinitis of the pectoralis major tendon. Axial short tau inversion recovery image (a) showing an oedematous mass (arrows) at the insertion of the tendon. Note also cortical erosion and marrow oedema in the humerus. Axial CT image (b) showing tendon calcification (arrow).

Poland’s anomaly192 ● ●

Poland’s syndrome/anomaly is a rare congenital anomaly resulting in the absence of the sternal head of the pectoralis major muscle associated abnormality of the pectoralis minor, serratus anterior and latissimus dorsi may be present

MRI findings ● there is absence of the respective muscles, which may be bilateral

Latissimus dorsi tendinosis/tear193 ● ● ●

acute avulsion or chronic overuse injury (with degeneration) of the humeral insertion of the latissimus dorsi is a rare occurrence that may present as an upper arm/humeral pseudotumour overuse injuries may occur in sports such as volleyball, while acute avulsion can be seen in basketball clinically, patients present with upper limb/shoulder girdle discomfort, with pain on adduction and on palpation of the proximal medial humeral shaft

MRI findings ●

tendinosis manifests as tendon thickening and inhomogeneous tendon SI on all pulse sequences

References

similar though milder changes may be seen to involve the pectoralis major and teres major tear of the tendon with haemorrhage in the latissimus dorsi and teres major cortical reaction at the tendon insertion to the humerus with associated marrow oedema enhancement of SI changes within both the tendon and the adjacent bone following contrast

● ● ● ●

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2 The elbow

TECHNIQUE Conventional MRI1–3 ● ●

● ● ● ● ●

●

for high-resolution imaging of the elbow joint, a surface coil is essential the optimal imaging position: ■ supine: with the arm in the anatomical position by the side, thereby minimising forearm rotation and optimising coronal imaging of the collateral ligaments and tendons ■ prone: with the arm overhead (‘Superman’ position), thereby placing the elbow in the isocentre of the magnet and improving image quality: – however, this position results in significant forearm pronation, which may reduce the ability to assess ligaments and tendons in a true coronal plane sequences include axial, coronal and sagittal axial images are planned from a sagittal scout perpendicular to the long axis of the humerus, radius and ulna with the arm fully extended, covering from the distal humeral metaphysis to the radial tuberosity coronal images are planned from an axial scout parallel to a line joining the two epicondyles (Fig. 2.1a) sagittal images are obtained perpendicular to coronal images (Fig. 2.1a) sequences include: ■ T1-weighted (T1W) spin-echo (SE) or proton density-weighted (PDW) fast spin-echo (FSE), for anatomical detail ■ fat-suppressed (FS) PDW FSE or T2-weighted (T2W) FSE/short tau inversion recovery (STIR), for bone and soft-tissue oedema ■ T2*-weighted gradient-echo (GE) images may provide optimal imaging of the collateral ligaments technical parameters: field of view (FOV) 12–14 cm, matrix 256¥192 or 256¥256, slice thickness: ■ axial: 3–4 mm with 1 mm inter-slice gap ■ sagittal and coronal: 3 mm with 0.2 mm inter-slice gap

Additional sequences ●

● ●

the collateral ligaments may be optimally assessed on a coronal oblique plane:4 ■ using a 20° posterior angulation in relation to the humeral shaft from a sagittal scout with the elbow extended (Fig. 2.1b) or using a true coronal plane with the elbow flexed approximately 20° the lateral ulnar collateral ligament (UCL) is optimally demonstrated using high-resolution intermediateweighted sequences or with magnetic resonance (MR) arthrography5 optimal positioning for the distal biceps tendon: the flexion, abduction, supination position:6,7 ■ the patient lies prone, with 180° shoulder abduction and 90° elbow flexion ■ a sagittal localiser of the flexed elbow is obtained and slices perpendicular to the proximal radius are planned (Fig. 2.1c) ■ allows the distal biceps tendon to be imaged in continuity from the musculotendinous junction to the radial tuberosity (Fig. 2.1d)

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a

b

c Figure 2.1 Elbow imaging techniques. Axial proton density-weighted (PDW) fast spin-echo (FSE) image (a) showing imaging planes for coronal and sagittal sequences. Sagittal PDW FSE image (b) showing the posterior oblique plane for optimal imaging of the collateral ligaments. Flexion, abduction, supination position: Sagittal localiser (c) and resulting PDW FSE image (d) showing the distal biceps tendon (arrows) extending to the radial tuberosity (arrowhead).

d

MR arthrography8,9 ● ●

●

●

elbow MR arthrography may be performed as an indirect or a direct technique indirect MR arthrography:10 an intravenous gadolinium injection followed by immediate (vascular phase) and delayed (late phase – 5–10 minutes post-injection) imaging with FS T1W SE images: ■ indications: assessment of cartilage defects, loose bodies and ligament tears direct MR arthrography using either: ■ saline and T2W FSE FS images or ■ dilute gadolinium and T1W SE FS images in the coronal, sagittal and axial planes (Fig. 2.2): – also include a coronal T2W FSE FS/STIR sequence for assessment of marrow oedema and extraarticular fluid ■ the joint is entered under fluoroscopic control via a lateral approach into the radiocapitellar joint or a posterior approach into the olecranon fossa ■ intra-articular position is confirmed with iodinated contrast medium, following which approximately 5–10 ml dilute gadolinium/saline is injected indications: assessment of intra-articular loose bodies, unstable osteochondritis dissecans (OCD), partial deep surface tears of the collateral ligaments and symptomatic synovial plicae

The bones and joints

Figure 2.2 Coronal T1-weighted spin-echo fat-suppressed direct gadolinium MR arthrogram showing hyperintense contrast within the joint (arrows).

THE BONES AND JOINTS Normal anatomy1–3,11 ● ● ●

the elbow joint comprises three articulations between the distal humerus and the proximal radius and ulna: the ulnohumeral, the radiocapitellar and the proximal radioulnar compartments approximately 150° of elbow flexion occurs at the ulnohumeral joint approximately 75° of pronation and 85° of forearm supination occur at the radiocapitellar and proximal radioulnar joints

The ulnohumeral joint ● ●

● ●

the ulnohumeral joint comprises the articulation between the trochlea of the distal humerus and the greater sigmoid notch of the ulna (Fig. 2.3a, b) the greater sigmoid (trochlear) notch lies between the olecranon and the coronoid processes of the proximal ulna (Fig. 2.3c): ■ it is divided into anterior and posterior portions by a transverse central bony trochlear ridge ■ the trochlear ridge lacks articular cartilage and measures approximately 2–3 mm wide and 3–5 mm in height: – it is reported to be present in 81 per cent of elbow MRI studies of normal volunteers (Fig. 2.3d) and should not be mistaken for a central osteophyte or olecranon stress fracture ■ adjacent to the central trochlear ridge, sagittal MR images give the appearance of a groove in the articular surface of the ulna, the ‘trochlear groove’ (Fig. 2.3e, f), which should not be mistaken for a chondral defect during elbow extension, the tip of the olecranon inserts into the olecranon fossa of the distal humerus (Fig. 2.3g) during elbow flexion, the tip of the coronoid inserts into the coronoid fossa of the distal humerus (Fig. 2.3g)

The radiocapitellar joint ● ● ●

the radiocapitallar joint is formed by the capitellum of the distal humerus and the radial head (Fig. 2.4a) during elbow flexion, the radial head inserts into the radial fossa of the distal humerus (Fig. 2.4b) the ‘pseudodefect’ of the capitellum (Fig. 2.4c, d) represents an irregularity of the articular surface, where the anteriorly placed capitellum intersects the posteriorly located lateral epicondyle

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b a

c

d

Figure 2.3 Anatomy of the ulnohumeral joint. Coronal T1-weighted (T1W) spin-echo (SE) fat-suppressed (FS) MR arthrogram (a) and sagittal proton density-weighted (PDW) fast spin-echo (FSE) image (b) showing the ulnohumeral joint (arrows). Sagittal PDW FSE image (c) showing the trochlear notch (arrowheads) lying between the coronoid (short arrow) and olecranon (long arrow) processes of the proximal ulna. Sagittal PDW FSE image (d) showing the trochlear ridge (arrow). (continued)

The bones and joints

f

e

g

Figure 2.3 (continued) Sagittal PDW FSE image (e) and T1W SE FS MR arthrogram (f) showing the trochlear groove (arrows). Sagittal T2*-weighted gradient-echo image (g) showing the olecranon (arrow) and coronoid (arrowhead) fossae of the distal humerus.

●

contrast medium may fill the pseudodefect on MR arthrography (Fig. 2.4e, f), which should not be mistaken for an osteochondral defect, which lies more anteriorly

The proximal radioulnar joint ● ● ●

the proximal radioulnar joint is formed by the articulation between the radial head and the lesser sigmoid (semilunar) notch of the proximal ulna (Fig. 2.5a, b) approximately 240° of the outer circumference of the radial head is covered by hyaline cartilage, while the anterolateral one-third of the radial head is not covered by hyaline cartilage distal to the radial head are the radial neck and radial tuberosity (Fig. 2.5c)

The humeral epicondyles ● ● ●

the medial and lateral humeral epicondyles are extracapsular structures (Fig. 2.6) the medial epicondyle gives origin to the anterior and posterior bands of the UCL and the common flexor tendon (CFT) the lateral epicondyle gives origin to the lateral ligament complex and common extensor origin

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a b

c d

e

f

Figure 2.4 Anatomy of the radiocapitellar joint. Coronal (a) and sagittal (b) proton density-weighted (PDW) fast spin-echo (FSE) images showing the radiocapitellar joint (arrows) and the radial fossa (arrowhead b) of the distal humerus. Coronal (c) and sagittal (d) PDW FSE images showing the ‘pseudodefect’ of the capitellum (arrows). Coronal (e) and sagittal (f) T1-weighted spin-echo fat-suppressed MR arthrograms showing contrast medium (arrows) filling the pseudodefect of the capitellum.

Pathology of the bones and joints

b

a

Figure 2.5 Anatomy of the proximal radioulnar joint. Coronal (a) and axial (b) proton density-weighted (PDW) fast spin-echo (FSE) images showing the proximal radioulnar joint (arrows) and the sigmoid notch (arrowhead b) of the proximal ulna. Coronal PDW FSE image (c) showing the radial neck (arrows) and tuberosity (arrowhead).

c

Figure 2.6 Coronal proton density-weighted fast spin-echo image showing the medial (arrow) and lateral (arrowhead) humeral epicondyles.

PATHOLOGY OF THE BONES AND JOINTS Panner’s disease1,11,12 ● ● ●

Panner’s disease represents osteochondrosis of the humeral capitellum it typically affects boys aged 7–12 years, during the period of active ossification of the capitellar epiphysis clinically, it presents with pain and swelling, with tenderness over the lateral elbow

MRI findings ● reduced T1W signal intensity (SI) and increased T2W SI are seen in the capitellum

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a

b

Figure 2.7 Osteochondritis dissecans of the humeral trochlea. Coronal (a) and sagittal (b) proton density-weighted fast spin-echo images showing fragmentation and irregularity of the trochlear articular surface (arrows).

● ●

irregularity of the capitellar articular surface with a low SI subchondral line consistent with avascular necrosis joint effusion

Osteochondritis dissecans1,3,12 ● ● ●

● ● ●

OCD of the elbow most commonly involves the humeral capitellum, being only rarely reported to involve the radial head and trochlea13 (Fig. 2.7a, b) it usually affects boys aged 12–15 years, by which time the capitellar epiphysis is almost completely ossified OCD is considered to be due to trauma associated with sporting activities resulting in repetitive overuse of the elbow; therefore, it typically involves the dominant arm of young male baseball pitchers and young female gymnasts it most commonly affects the anterolateral aspect of the capitellum and is rarely bilateral clinically, it presents with pain and swelling, with tenderness over the lateral elbow classification:12 ■ type Ia – intact articular cartilage with stable subchondral bone ■ type Ib – intact articular cartilage with unstable subchondral bone ■ type II – cartilage fracture with collapse or partial displacement of subchondral bone ■ type III – loose cartilaginous fragments within the joint

MRI findings14 ● early stages may show only marrow oedema (Fig. 2.8a); later, focal low T1W SI and high T2W SI with surrounding sclerosis is seen (Fig. 2.8b, c) ● signs of an unstable lesion include a lesion surrounded by cysts (Fig. 2.8d) or a complete rim of hyperintense fluid on T2W images between the lesion and underlying bone marrow: ■ an enhancing rim between the lesion and surrounding bone on post-contrast MRI ■ extension of injected contrast around the lesion on MR arthrography ■ an osteochondral loose body (Fig. 2.8e, f) ● enhancement of the lesion indicates that it is viable with a good blood supply ● reliability of MRI in the identification of loose bodies:15 in a comparative study with arthroscopy as the gold standard, non-arthographic MRI has sensitivity and specificity of 88–100 per cent and 20–60 per cent, respectively: ■ MRI is much more accurate in the diagnosis of loose bodies in the posterior joint compartment

Pathology of the bones and joints

a b

c

d

f e Figure 2.8 Osteochondritis dissecans (OCD) of the humeral capitellum. Coronal T2-weighted (T2W) fast spin-echo (FSE) fat-suppressed (FS) image (a) showing oedema (arrow) in the capitellum. Coronal T1-weighed (T1W) spin-echo (SE) (b) and T2W FSE FS (c) images showing the OCD (arrows), with intermediate signal intensity (SI) on T1W and high SI on T2W. Note the thin sclerotic margin on T1W (arrow b) and the focal cartilage defect on T2W (arrowhead c). Sagittal T2*-weighted gradient-echo image (d) showing the anteriorly located OCD (arrowhead) with associated subchondral cyst formation (arrow). Osteochondral loose body: Sagittal T1W SE FS (e) and axial proton density-weighted FSE (f) MR arthrograms showing osteochondral fragments (arrows) in the coronoid recess anterior to the humerus.

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a

b

c

d Figure 2.9 Elbow fractures. Olecranon stress fracture: Sagittal T2-weighted fast spin-echo (FSE) fat-suppressed (FS) image (a) showing a hypointense stress fracture line (black arrow) in the olecranon with associated marrow oedema. A small loose body (white arrow) is also present. Occult radial fracture: Sagittal proton density-weighted (PDW) FSE image (b) showing a transverse band of oedema (arrow) through the radial neck. Coronal PDW FSE FS image (c) showing a cortical fracture (arrow), an impacted transverse fracture line (black arrowhead) and bone bruising (white arrowhead) in the capitellum. Sagittal PDW FSE FS image (d) showing a traumatic joint effusion (arrow).

Stress fracture of the olecranon process16 ●

stress fractures of the olecranon process of the ulna are described in professional baseball players and javelin throwers and affect the posteromedial aspect of the olecranon, resulting in posterior medial elbow pain

MRI findings ● marrow oedema is seen in the posteromedial olecranon, indicative of stress response ● a focal hypointense line extending to the cortex, indicative of stress fracture with associated oedema (Fig. 2.9a) ● occasionally, oedema is present within the radial head, while the UCL is always intact

Avulsion fracture of the ulnar sublime tubercle17 ● ● ●

the sublime tubercle is the tip of the medial aspect of the base of the coronoid process of the ulna avulsion injury of the sublime tubercle is described in baseball players clinically, it presents with acute-onset medial elbow pain during throwing

The joint capsule

MRI findings ● a small avulsion fracture of the tip of the sublime tubercle is optimally demonstrated on GE sequences ● it may be associated with a mid-substance injury to the UCL

Occult fractures MRI may demonstrate occult elbow fractures in both children and adults in children, MRI has demonstrated occult fractures in 22–57 per cent and soft-tissue injuries in 62 per cent of patients with traumatic elbow effusions in adults, MRI has demonstrated occult fractures in 47–100 per cent and soft-tissue injuries in 16–24 per cent of patients with traumatic elbow effusions (Fig. 2.9b–d): ■ most patients without fractures had post-traumatic bone bruising utility of MRI in paediatric elbow fractures:18 MRI is useful in assessing radiographically identified fractures and may demonstrate radiographically occult injuries including: ■ transphyseal fracture extension, extension along the physis, bone bruising, associated ligament/muscle injury ■ however, additional MRI findings may not change patient management

● ● ●

●

THE JOINT CAPSULE Normal anatomy1,19 ● ●

●

the joint capsule invests all three elbow articulations to form a single continuous joint space and comprises two layers: a deep synovial lining and a superficial fibrous layer intracapsular fat pads; three major fat pads are located between the two layers of the capsule: ■ the anterior capitellar and trochlear fat pads are located within the corresponding fossae (Fig. 2.10a, b) ■ the posterior fat pad lies within the olecranon fossa (Fig. 2.10b) capsular attachments: ■ anterior to the distal humerus at the superior margin of the coronoid and radial fossae and to the coronoid process of the ulna (Fig. 2.10c) ■ posterior to the distal humerus just proximal to olecranon fossa

b a

c

Figure 2.10 Intra-articular fat pads and capsule. Sagittal proton density-weighted (PDW) fast spin-echo (FSE) image (a) showing the capitellar fat pad (arrow). Sagittal PDW FSE image (b) showing the trochlear (arrow) and olecranon (arrowhead) fat pads. Sagittal T2*-weighted gradient-echo image (c) showing the anterior capsular attachments (arrows).

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medial to the medial margin of the olecranon and trochlear notch lateral, along the lateral margin of the trochlear notch and annular ligament capsular recesses;8 five are recognised: ■ the anterior humeral recess is located anteriorly and comprises the coronoid and radial fossae recesses (Fig. 2.11a) ■ the olecranon recess is the largest and is found along the posterior margin of the joint, having three components: superior (Fig. 2.11b), medial and lateral (Fig. 2.11c) ■ the annular (peri-radial) recess is located anteriorly, where the capsule passes beneath the annular ligament (Fig. 2.11d) ■ ■

●

a

b

c

d

e

Figure 2.11 Joint capsular recesses. Axial (a, c, d), sagittal (b) and coronal (e) T1-weighted spin-echo fat-suppressed MR arthrograms showing the anterior humeral recess (arrow a), the superior olecranon recess (arrow b), the medial (arrowhead c) and lateral (arrow c) olecranon recesses, the annular (arrows d) and radial collateral ligament (arrowhead d) recesses and the ulnar collateral ligament recess (arrow e).

Pathology of the capsule

the medial collateral ligament and lateral collateral ligament (LCL) recesses are extensions of the olecranon recess along either side of the olecranon process and are limited by the UCL (Fig. 2.11e) and the radial collateral ligament (RCL) (Fig. 2.11d) synovial folds (plicae)8 are reported to be present in 86 per cent of cadaver elbows20 and are demonstrated in 48 per cent of conventional MRIs and 81 per cent of MR arthrograms:21 ■ commonly located in the dorsal/dorsolateral/lateral aspect of the radiocapitellar joint20 (Fig. 2.12a, b) ■ other synovial plicae include the synovial fold of the superior lateral olecranon recess (Fig. 2.12c) and folds within the medial or LCL recesses (Fig. 2.12d) ■

●

a

c

b

d

Figure 2.12 Synovial plicae. Sagittal T2*-weighted gradient-echo (a) and T1-weighted (T1W) spin-echo (SE) fatsuppressed (FS) (b) MR arthrograms showing the posterolateral synovial plica (arrows) in the posterior aspect of the radiocapitellar joint. Axial T1W SE FS MR arthrogram (c) showing the superior lateral olecranon recess synovial plica (arrow). Coronal T1W SE FS MR arthrogram (d) showing the radial collateral ligament recess synovial plica (arrow).

PATHOLOGY OF THE CAPSULE Painful snapping elbow and synovial fold syndrome21–25 ● ● ●

a snapping sensation at the elbow is not uncommon and can be due to extra-articular or intra-articular causes extra-articular causes include subluxation of the medial head of triceps or the ulnar nerve intra-articular causes include synovial folds,21,22 a torn/redundant annular ligament23 and loose bodies

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The elbow

● ● ●

elbow synovial fold syndrome24 is a condition that presents with symptoms suggestive of a loose body, in which a thickened plica may prevent full elbow extension snapping plicae may also be associated with chondromalacia of the anterolateral radial head25 clinically, there may be a history of previous trauma, and snapping typically occurs at 90–110° of flexion

MRI findings ● conventional MRI studies are usually reported as showing no abnormality ● non-contrast MRI with the use of microscopy coils has been reported to show synovial folds21 MR arthrographic findings24 ● in patients with elbow synovial fold syndrome, a thickened plica in the olecranon recess has been demonstrated, with mean thickness 3.1 mm (range 2–5 mm)

THE LIGAMENTS THE MEDIAL COLLATERAL LIGAMENT Normal anatomy1,26,27 ● ●

●

●

●

the medial (ulnar) collateral ligament comprises three distinct components: the anterior (oblique) bundle, the posterior bundle and the transverse bundle the anterior bundle28 accounts for most of the stability against valgus and internal rotatory stress and is optimally demonstrated on coronal MR images; it arises from a broad-based origin on the anteroinferior aspect of the medial epicondyle: ■ interdigitation of fat within the proximal ligament may result in increased focal SI (Fig. 2.13a, b), a phenomenon that is reduced by imaging in the 20° posterior coronal oblique plane4 ■ it inserts into the sublime tubercle at the medial aspect of the base of the coronoid process of the ulna; the insertion is variable, being at the joint margin (Fig. 2.13c) or up to 2–4 mm distal to the joint line (Fig. 2.13d) ■ a slightly more distal insertion may mimic a partial avulsion of the ligament the posterior bundle is a secondary stabiliser against valgus and internal rotatory stress at 120° elbow flexion and represents a fan-shaped thickening of the posterior capsule, originating from the posterior surface of the medial epicondyle and inserting on the medial aspect of the olecranon process of the ulna: ■ it is optimally demonstrated on axial MR images (Fig. 2.13e) the transverse bundle is also termed the ‘ligament of Cooper’ and represents a thickening of the medial capsule between the coronoid process and the tip of the olecranon process: ■ it does not contribute to joint stability and is not routinely identified on MRI anatomical variants: an accessory (extra) bundle of the UCL is identified in approximately 25 per cent of individuals and extends from the posteromedial aspect of the capsule to the transverse bundle

PATHOLOGY OF THE ULNAR COLLATERAL LIGAMENT Ulnar collateral ligament tears2,3,26,27,29,30 ● ● ● ●

injury to the UCL results in valgus instability of the elbow and may occur following a fall on the outstretched hand, elbow dislocation, or actions such as weightlifting most are full-thickness tears of the anterior bundle; partial-thickness tears most commonly involve the deep surface of the anterior bundle injury most commonly occurs in the mid-substance, followed by avulsion from the ulnar attachment and rarely from the epicondylar attachment clinically, UCL injury manifests with signs and symptoms of medial elbow instability, including medial elbow pain and opening of the joint on valgus stress: ■ symptoms of ulnar neuropathy may also be present

The ligaments

a

c

e

●

b

d

Figure 2.13 Anatomy of the ulnar collateral ligament. Coronal T2*-weighted gradient-echo image (a) showing the anterior bundle of the ulnar collateral ligament (UCL) (arrow) inserting into the sublime tubercle (arrowhead) of the ulna. Coronal proton density-weighted (PDW) fast spin-echo (FSE) image (b) showing fat (arrow) within the proximal ligament. Coronal T1-weighted spin-echo fat-suppressed MR arthrograms (c, d) showing the normal insertion of the anterior bundle of the UCL (arrow c) into the sublime tubercle and insertion more distally (arrow d). Axial PDW FSE image (e) showing the posterior bundle of the UCL (arrows).

the differential diagnosis includes medial epicondylitis, flexor–pronator tendon tears, flexor–pronator fascial compression syndrome, valgus extension overload syndrome and ulnar neuropathy

MRI findings ● a full-thickness tear manifests as focal discontinuity of the ligament, which is replaced by T2W hyperintensity due to oedema and haemorrhage (Fig. 2.14a)

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The elbow

b a Figure 2.14 Ulnar collateral ligament (UCL) injury. Coronal T2*-weighted gradient-echo image (a) showing rupture (arrow) of the anterior bundle of the UCL. Coronal proton density-weighted fast spin-echo MR arthrogram (b) showing the ‘T-sign’ (arrows).

● ● ●

partial-thickness tears manifest as abnormal morphology (thickening, laxity) and increased SI of the UCL with periligamentous oedema acute tears may be associated with lateral compartment (radiocapitellar) bone bruises MRI is reported to have sensitivity and specificity of: ■ 100 per cent for the diagnosis of full-thickness tears of the anterior bundle ■ 57 per cent and 100 per cent, respectively, for partial-thickness tears of the anterior bundle

MR arthrographic findings9 ● complete tears show extravasation of injected contrast medium at the site of ligament rupture ● partial deep surface tears are optimally demonstrated by coronal MR arthrography: ■ demonstrates irregularity of the deep surface of the ligament ■ extension of contrast medium beneath the ulnar attachment of the ligament producing the ‘T-sign’ (Fig. 2.14b) ● sensitivity and specificity for partial thickness tears improves to 86 per cent and 100 per cent with MR arthrography ● indirect MR arthrography demonstrates focal enhancement at the site of the tear10

Valgus extension overload syndrome27,29 ● ●

this is a common condition in throwing athletes pathologically, the anterior bundle of the UCL is intact but attenuated due to repetitive microtrauma from the overhead throwing action: ■ the posteromedial olecranon tip impinges on the medial aspect of the olecranon fossa during the early and late acceleration phases of throwing ■ posteromedial olecranon impingement leads to the development of medial olecranon osteophytes and chondromalacia of the posteromedial trochlea ■ osteophytes may fracture and become intra-articular loose bodies

MRI findings the findings are of attenuation and redundancy of the anterior bundle of the UCL ● posteromedial trochlear chondromalacia (Fig. 2.15) ● intra-articular loose bodies in the posterior compartment of the joint ●

The ligaments

Figure 2.15 Posteromedial olecranon impingement. Axial T2-weighted fast spin-echo image showing osteoarthritis of the medial aspect of the humeroulnar joint with posteromedial trochlear chondromalacia (arrow).

THE LATERAL COLLATERAL LIGAMENT Normal anatomy1,26,27 ● ● ●

●

●

the LCL comprises three distinct components: the RCL, the annular ligament and the lateral band of the UCL (LUCL) the RCL originates from the lateral epicondyle of the humerus and inserts into the fibres of the annular ligament, being optimally visualised on coronal MR images (Fig. 2.16a) the annular ligament is a thick, fibrous band that completely encircles the radial head and stabilises the proximal radioulnar joint: ■ its anterior portion attaches to the anterior margin of the sigmoid notch, while the posterior portion divides into several bands that attach into the posterior margin of the sigmoid notch ■ it is optimally visualised on axial MR images (Fig. 2.16b, c) the LUCL, together with the annular ligament, provides most of the stability against varus and external rotatory stress: ■ it is present in 90 per cent of individuals and originates from the lateral epicondyle of the humerus together with the RCL, extending distally and obliquely to insert into the supinator crest of the proximal ulna ■ it is optimally visualised on coronal high-resolution PDW (Fig. 2.16d) or direct MR arthrography (Fig. 2.16e) images as an oblique hypointense structure running posterior to the radial neck5 anatomical variants: an accessory LCL is occasionally identified and extends from the annular ligament to the supinator crest

PATHOLOGY OF THE LATERAL COLLATERAL LIGAMENT Radial collateral ligament insufficiency26,27 ● ●

●

RCL insufficiency results in varus instability, which is less common than valgus instability varus stress may occur as an acute injury or due to elbow dislocation or subluxation: ■ post-operatively due to excessive release of the common extensor tendon or radial head excision ■ rarely, as a repetitive stress injury RCL tears are most commonly full thickness from the proximal attachment

Posterolateral rotatory instability26,27 ●

●

posterolateral rotatory instability is due to an LUCL tear with an intact annular ligament and results in: ■ posterior subluxation/dislocation of the radial head relative to the capitellum ■ secondary rotatory subluxation of the ulnohumeral joint LUCL tears most commonly occur at the lateral epicondylar attachment and less commonly in midsubstance

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b

a

c

e

●

d

Figure 2.16 Anatomy of the lateral collateral ligament. Coronal proton density-weighted (PDW) fast spin-echo (FSE) image (a) showing the radial collateral ligament (arrows) extending from the lateral epicondyle to the annular ligament. Axial PDW FSE (b) and T1-weighted (T1W) spin-echo (SE) fatsuppressed (FS) (c) MR arthrograms showing the anterior (arrow) and posterior (arrowhead) attachments of the annular ligament. Coronal PDW FSE (d) and T1W SE FS MR arthrogram (e) images showing the lateral ulnar collateral ligament (arrowheads d; arrows e) running obliquely, posterior to the radial neck.

clinically, manifests as chronic lateral elbow pain with a catching or snapping sensation on elbow movement

MRI findings ● discontinuity of the LUCL from its proximal attachment is optimally seen on coronal images ● posterior subluxation of the radial head with the arm supinated and elbow extended, optimally assessed on sagittal images (Fig. 2.17a)

The muscles and tendons

b

a Figure 2.17 Lateral collateral ligament injuries. Posterolateral rotatory instability: Sagittal proton density-weighted fast spin-echo image (a) showing posterior subluxation of the radial head relative to the capitellum and soft-tissue swelling (arrow) posterior to the radial head/neck at the site of the lateral band of the ulnar collateral ligament. Annular ligament tear: Axial T1-weighted spin-echo fat-suppressed MR arthrogram (b) showing escape of contrast medium (arrow) from the posterior radioulnar joint consistent with rupture of the posterior annular ligament.

Annular ligament abnormalities ● ●

a loose annular ligament may be a cause of snapping elbow24 tears of the annular ligament occur with subluxation or dislocation of the proximal radioulnar joint and may be demonstrated on MR arthrography by escape of joint fluid from the region of the torn ligament (Fig. 2.17b)

THE MUSCLES AND TENDONS THE ANTERIOR COMPARTMENT Normal anatomy1 ● ● ●

the anterior compartment muscles include the brachialis and the biceps, both of which flex the elbow the brachialis muscle arises from the anterior surface of the distal humerus (Fig. 2.18a, b) and inserts via its tendon into the base of the coronoid process of the ulna and the ulnar tuberosity (Fig. 2.18c) the biceps muscle lies superficial to the brachialis within the distal arm: ■ the distal biceps tendon7 forms 6–7 cm above the elbow joint and runs through the anterior aspect of the cubital fossa (Fig. 2.18d, e) to insert into the posterior aspect of the radial tuberosity (Fig. 2.18f) ■ the ventral surface of the tendon is flattened and the tendon rotates through 90° before its insertion ■ it is separated from the anterior aspect of the radial tuberosity by the bicipitoradial bursa ■ the distal biceps tendon gives rise to the bicipital aponeurosis (Fig. 2.18g), which blends with the fascia covering the flexor–pronator group of muscles and may prevent proximal migration of the tendon following complete tendon rupture

PATHOLOGY OF THE ANTERIOR COMPARTMENT MUSCLES Distal biceps tendon rupture7,29 ●

distal biceps tendon rupture is classically associated with sports that utilise weight training, and accounts for 3–10 per cent of biceps tendon ruptures

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The elbow

b

a

c d

e

g

f

Figure 2.18 Anatomy of the anterior compartment muscles. Brachialis: Sagittal (a) and axial (b) proton density-weighted (PDW) fast spin-echo (FSE) images showing the brachialis muscle (arrows) and tendon (arrowheads) lying anterior to the distal humerus. Axial PDW FSE image (c) showing the tendon insertion (arrow) into the ulnar tuberosity. The distal biceps tendon: Sagittal (d) and axial (e) PDW FSE images showing the tendon (arrows) lying anterior to the brachialis. Note the flat ventral surface. Axial PDW FSE image (f) showing the tendon insertion (arrow) into the radial tuberosity. Axial PDW FSE image (g) showing the tendon (arrow) with its attachment to the bicipital aponeurosis (arrowhead).

The muscles and tendons

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● ● ●

it is usually due to a single traumatic event, with ruptures typically occurring at 1–2 cm proximal to the radial tuberosity, where there is commonly a zone of tendon hypovascularity associated with the development of degenerative hypoxic tendinopathy ruptures may be partial or complete and rarely occur at the musculotendinous junction if the bicipital aponeurosis remains intact, little or no tendon retraction occurs, in which case tears may be difficult to identify clinically, ruptures are seen in the dominant arm of men aged 40–60 years: ■ the muscle contracts proximally with elbow flexion with associated marked weakness of flexion and supination, and a soft-tissue mass may be present in the antecubital fossa

MRI findings ● complete rupture: detachment of the tendon from the radial tuberosity is seen with proximal retraction of the biceps muscle (Fig. 2.19a, b) and increased T2W SI in the antecubital fossa due to oedema and haemorrhage (Fig. 2.19b): ■ additional features: marrow oedema in the radial tuberosity due to micro-avulsion and fluid within the bicipitoradial bursa ● partial rupture:31 increased intratendinous T2W SI (Fig. 2.19c): ■ bicipitoradial bursitis and radial tuberosity marrow oedema are seen in ~50 per cent of cases ● a pseudotumour of the distal biceps muscle has been described following chronic complete distal biceps tendon rupture32

a

c

b

Figure 2.19 Distal biceps tendon rupture. Complete rupture: Axial T1-weighted spin-echo image (a) showing absence of the tendon in the antecubital fossa (arrow). Sagittal T2-weighted (T2W) fast spin-echo (FSE) fat-suppressed (FS) image (b) showing retraction of the tendon (arrow) and muscle with surrounding oedema and haemorrhage. Partial rupture: Axial T2W FSE FS image (c) showing increased signal intensity within the distal biceps tendon (arrowhead) and fluid within the bicipitoradial bursa (arrow).

Distal biceps tendinopathy ● ●

distal biceps tendinopathy results from repetitive mechanical impingement of the poorly vascularised distal tendon between the radius and the ulna it may precede tendon rupture

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MRI findings ● swelling and hyperintensity of the distal tendon (Fig. 2.20a, b) are seen ● chronic biceps tendinopathy may be associated with: ■ osseous proliferation at the radial tuberosity (Fig. 2.20c) ■ supinator muscle oedema and bursitis in the region of the distal tendon (bicipitoradial or interosseous)

b

c

a Figure 2.20 Distal biceps tendinopathy. Sagittal T1-weighted (T1W) spin-echo (SE) (a) and axial T2-weighted fast spinecho (b) images showing swelling and hyperintensity of the tendon (arrows). Axial T1W SE image (c) showing bony proliferation at the radial tuberosity (arrowhead).

THE POSTERIOR COMPARTMENT Normal anatomy1 ● ●

●

●

the posterior compartment muscles include the triceps, the anconeus and the anconeus epitrochlearis the triceps muscle comprises medial, lateral and long heads, which blend together to form a single musculotendinous unit that inserts via the triceps tendon into the tip of the olecranon process of the ulna (Fig. 2.21a–c): ■ rarely, part of the medial head inserts into the medial epicondyle, where it can compress the ulnar nerve ■ the tendon is separated from the olecranon process by the olecranon bursa ■ the muscle functions to extend the elbow the anconeus muscle arises from the posterior portion of the lateral epicondyle (Fig. 2.21d) and inserts into the posterolateral surface of the proximal ulna: ■ it covers the lateral aspect of the radial head and annular ligament (Fig. 2.21e) but has little role in stabilising the elbow joint the anconeus epitrochlearis muscle is an accessory muscle present in 3–28 per cent of elbows: ■ it replaces the cubital tunnel retinaculum, arising from the medial epicondyle and inserting into the tip of the olecranon process of the ulna

The muscles and tendons

b

a

d

c

e

Figure 2.21 Anatomy of the posterior compartment muscles. Triceps: Sagittal proton density-weighted (PDW) fast spin-echo (FSE) image (a) showing the triceps tendon (arrowhead a) inserting into the olecranon process (arrow). Axial (b) and coronal (c) PDW FSE images showing the triceps tendon (arrowhead) and the medial (long arrow b) and lateral (short arrow b) heads of triceps. Anconeus: Axial PDW FSE images (d, e) showing the origin of the anconeus (arrow d) from the posterior aspect of the lateral epicondyle and the muscle (arrow e) lying posterolateral to the proximal radioulnar joint.

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PATHOLOGY OF THE POSTERIOR COMPARTMENT MUSCLES Triceps tendon rupture29 ●

● ●

triceps tendon rupture is a rare injury that may occur following a direct blow or a fall on an outstretched hand: ■ it is also associated with sports requiring repetitive elbow extension and may be associated with radial head fracture risk factors predisposing to triceps tendon ruptures include renal insufficiency, hyperparathyroidism, Marfan’s syndrome, osteogenesis imperfecta tarda, olecranon bursitis and use of corticosteroids full-thickness tears are more common than partial-thickness tears and typically occur at the insertion into the olecranon process

MRI findings ● full-thickness tears appear as a fluid-filled discontinuity of the tendon from the olecranon process ● partial-thickness tears appear as a fluid-filled partial defect within the triceps tendon (Fig. 2.22a, b) with surrounding oedema ● rarely, an avulsion fracture of the tip of the olecranon may occur (Fig. 2.22c, d)

a

b

c

d

Figure 2.22 Triceps tendon injuries. Partial rupture: Sagittal proton density-weighted (PDW) fast spin-echo (FSE) (a) and coronal PDW FSE fat-suppressed (FS) (b) images showing a partial-thickness area of increased tendon signal intensity (arrows). Olecranon avulsion: Sagittal T1-weighted spin-echo (c) and coronal PDW FSE FS (d) images showing a small avulsion fracture (arrows) of the olecranon tip.

The muscles and tendons

Triceps tendon subluxation33 ● ● ●

the medial head of the triceps muscle or tendon may dislocate over the medial epicondyle, resulting in snapping during elbow flexion or elbow extension from the flexed position clinically, this manifests as painless or painful elbow snapping, with/without ulnar neuropathy predisposing factors include a congenital or acquired prominent medial head of triceps, an accessory triceps tendon and developmental or post-traumatic cubitus varus

MRI findings34 ● dislocation may be demonstrated by imaging the elbow in extension followed by full flexion ● a subluxing or dislocating medial head of triceps and/or ulnar nerve is identified medial or anterior to the medial epicondyle in the flexed position

Anconeus epitrochlearis oedema35 ●

●

the anconeus epitrochlearis (accessory anconeus) muscle typically measures 2.5¥2¥1 cm and is located in the posteromedial aspect of the elbow, forming the roof of the cubital tunnel, where it may result in ulnar nerve compression oedema of the anconeus epitrochlearis, of uncertain aetiology, has also been reported as a potential cause of medial elbow pain

MRI findings ● increased muscle SI is seen on T2W FSE FS/STIR images

THE MEDIAL COMPARTMENT Normal anatomy1 ●

● ● ●

● ● ●

● ●

the medial compartment muscles include the pronator teres and the four superficial flexors (flexor carpi radialis, palmaris longus, flexor carpi ulnaris [FCU] and flexor digitorum superficialis [FDS]) (Fig. 2.23a), which function to flex the wrist and pronate the forearm the pronator teres arises mainly from the medial humeral epicondyle (humeral head) (Fig. 2.23b) and the medial aspect of the coronoid process (ulnar head) the superficial flexor muscles and part of the pronator teres arise from the medial epicondyle via the CFT (Fig. 2.23c–e) the CFT normally appears diffusely hypointense on all pulse sequences: ■ however, it may show thickening and intermediate SI on T1W and T2W images in the absence of symptoms of medial epicondylitis36 the FDS also arises from the proximal radius the FCU has two heads arising near the cubital tunnel, from the medial part of the CFT and the medial aspect of the olecranon (Fig. 2.23f) a fibrous arch termed the ‘arcuate ligament’ (Osborne’s band or the cubital tunnel retinaculum) runs between the two heads and forms the roof of the cubital tunnel: ■ it is absent in 23 per cent of cases the palmaris longus is absent in 13 per cent of cases the deep flexor muscles include flexor digitorum profundus (FDP) and the flexor pollicis longus, both of which originate from the proximal ulna, distal to the cubital tunnel

PATHOLOGY OF THE MEDIAL COMPARTMENT MUSCLES AND TENDONS Medial epicondylitis29,30,36 ● ●

medial epicondylitis is also termed ‘golfer’s elbow’ other sports associated with this injury include racket and throwing sports, bowling, archery, weightlifting and swimming

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b

a

d

c

f

e

Figure 2.23 Anatomy of the medial compartment muscles. Common flexor muscles: Axial proton density-weighted (PDW) fast spin-echo (FSE) image (a) at the level of the radial head showing the pronator teres (single white arrowhead), the flexor carpi radialis and palmaris longus (double white arrowhead), the flexor digitorum superficialis (black arrowhead), the flexor carpi ulnaris (black arrow) and the flexor digitorum profundus (white arrow). Pronator teres: Axial PDW FSE image (b) at the level of the humeral condyles showing the pronator teres muscle (arrowhead) and its origin from the medial epicondyle (arrow). Common flexor origin: Coronal PDW FSE fat-suppresed (c) and axial (d) and sagittal PDW FSE (e) images showing the common flexor tendon (arrows) arising from the medial epicondyle (arrowheads). Flexor carpi ulnaris: Axial PDW FSE image (f) showing the two heads of flexor carpi ulnaris (arrows) and the arcuate ligament (arrowhead) passing between them.

The muscles and tendons

● ● ●

it may be associated with lateral epicondylitis and ulnar nerve symptoms pathologically, it results from flexor tendinosis due to repetitive valgus and flexion movements, with changes being most commonly identified in the pronator teres and the flexor carpi radialis tendons clinically, it is usually seen in athletes with chronic medial elbow pain and point tenderness over the common flexor origin

MRI findings36 ● tendinosis manifests as increased SI and swelling at the common flexor origin adjacent to the medial epicondyle, best seen on coronal and axial images (Fig. 2.24a–c) ● in the relatively acute stage of symptoms, MRI may be normal ● additional features: increased SI within the medial epicondyle and adjacent muscles ● increased T2W SI within the tendon and in the surrounding muscles is specific for symptomatic medial epicondylitis ● in the skeletally immature, medial epicondylitis must be differentiated from avulsion of the medial epicondylar apophysis ● common flexor tendon tears may also occur: ■ full-thickness tears of the tendon appear as a fluid-filled gap at the tendon–epicondyle attachment (Fig. 2.24d) ■ partial-thickness tears manifest as thinning of the tendon with surrounding fluid

b

a

d c Figure 2.24 Common flexor tendon injury. Medial epicondylitis: Coronal T1-weighted spin-echo (a), T2-weighted fast spin-echo (FSE) fat-suppressed (FS) (b) and sagittal proton density-weighted (PDW) FSE FS (c) images showing hyperintensity and swelling (arrows) at the common flexor origin (arrowheads). Complete rupture: Coronal PDW FSE image (d) showing a fluid-filled gap (arrows) at the common flexor origin.

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a

b

d

c

f

e

g

h

The muscles and tendons

●

fluid SI changes around/within the tendon may also be due to recent corticosteroid or anaesthetic injections

MR arthrographic findings10 ● indirect MR arthrography shows enhancement at the site of tendinopathy and within the epicondyle

THE LATERAL COMPARTMENT Normal anatomy1 ●

●

●

●

muscles of the lateral compartment can be divided into three components: the superficial group, the common extensors and the supinator, which all function to extend the wrist joint and supinate the forearm the superficial group includes the brachioradialis and the extensor carpi radialis longus (ECRL): ■ the brachioradialis originates from the supracondylar ridge of the humerus (Fig. 2.25a) and inserts into the radial styloid ■ the ECRL originates from the supracondylar ridge of the humerus distal to the brachioradialis (Fig. 2.25a) and inserts into the base of the second metacarpal the common extensor group includes the extensor carpi radialis brevis (ECRB), extensor digitorum, extensor digiti minimi and extensor carpi ulnaris (Fig. 2.25b): ■ the ECRB, extensor digitorum, extensor digiti minimi and extensor carpi ulnaris all arise from the lateral epicondyle via the common extensor tendon (Fig. 2.25c–e) the supinator has a bulky deep component and a slim superficial component: ■ it arises from the anterior aspect of the lateral epicondyle and the supinator crest of the ulna and extends distally and laterally to insert into the radial shaft (Fig. 2.25f, g) ■ the posterior interosseous nerve lies between the superficial and deep components of the supinator, which can occasionally be differentiated by the presence of a thin layer of fat (Fig. 2.25h)

PATHOLOGY OF THE LATERAL COMPARTMENT MUSCLES AND TENDONS Lateral epicondylitis29 ● ●

lateral epicondylitis is the commonest cause of sports-related elbow pain; it is also termed ‘tennis elbow’ it may also be an occupational injury associated with carpentry and with the playing of various musical instruments, including drums and string instruments (violin and cello)

Figure 2.25 (opposite) Anatomy of the lateral compartment muscles. Superficial extensors: Axial proton density-weighted (PDW) fast spin-echo (FSE) image (a) at the level of the humeral epicondyles showing the brachioradialis (arrowhead) and extensor carpi radialis longus (ECRL) (arrow) muscles. Superficial and common extensor muscles: Axial PDW FSE image (b) at the level of the radial head showing the brachioradialis (double white arrowheads), the ECRL and extensor carpi radialis brevis (ECRB) (large white arrowhead), the extensor digitorum (white arrow), the common extensor tendon (black arrow) and the extensor carpi radialis tendon (black arrowhead). Coronal PDW FSE image (c) showing the common extensor tendon (arrowhead) arising from the lateral epicondyle, and the ECRL (double arrowhead), ECRL and ECRB (short arrow) and supinator (long arrow) muscles. Axial (d) and sagittal (e) PDW FSE images showing the common extensor tendon (arrows) arising from the lateral epicondyle (arrowheads). Supinator: Sagittal (f) and axial (g) PDW FSE images showing the supinator (arrows) and its origin from the supinator crest (arrowhead g). Axial T1-weighted spin-echo image (h) showing the superficial (arrow) and deep (arrowhead) components of the supinator, which are separated by a thin fat stripe (double arrowhead).

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The elbow

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●

pathologically, it results from repetitive varus stress at the common extensor origin causing tendinosis, tendinitis, tenosynovitis and partial/complete tears, which most commonly affect the ECRB and extensor digitorum tendons at the lateral epicondyle clinically, it is most commonly seen in the 40–60-year age group and presents with chronic lateral elbow pain and point tenderness over the lateral epicondyle

MRI findings ● tendinosis manifests as swelling and increased intratendinous SI on T1W/PDW FSE (Fig. 2.26a) and T2W images (Fig. 2.26b), with the greatest SI abnormality involving the region of the ECRB tendon ● partial tears manifest as tendon thinning with associated adjacent fluid SI (Fig. 2.26c, d) ● full-thickness tears manifest as a complete fluid-filled gap at the tendon–epicondyle interface ● associated features include oedema in the adjacent lateral epicondyle and increased T2W SI in the anconeus muscle (Fig. 2.26d): ■ fluid in the radiohumeral bursa and injuries of the LUCL MR arthrographic findings ●

indirect MR arthrography shows enhancement at the site of tendinopathy and within the epicondyle10

b a

d

c

Figure 2.26 Lateral epicondylitis. Coronal proton density-weighted fast spin-echo (FSE) (a) and T2-weighted FSE fat-suppressed (b) images showing increased signal intensity in the common extensor tendon (arrows). Coronal (c) and axial (d) short tau inversion recovery images showing fluid (arrows) within the common extensor tendon consistent with a partial tear and mild oedema of the anconeus muscle (arrowhead d).

Pathology of the bursae

THE BURSAE Normal anatomy19 ● ● ●

●

the elbow/cubital bursae include the bicipitoradial, the interosseous bursa and the olecranon bursa the bicipitoradial bursa37 covers the anterior aspect of the radial tuberosity, lying between the tuberosity and the distal biceps tendon insertion, and functions to reduce friction between these two structures the interosseous bursa is identified in approximately 20 per cent of cases and is located in the medial aspect of the antecubital fossa, adjacent to the biceps tendon and brachialis muscle: ■ it occasionally communicates with the bicipitoradial bursa the olecranon bursae: three posterior bursae are reported: ■ the superficial olecranon lies in subcutaneous tissues between the skin and the olecranon process ■ the deep intratendinous bursa lies within the substance of the triceps near its insertion into the olecranon ■ the deep subtendinous bursa lies deep to the triceps tendon near its insertion

PATHOLOGY OF THE BURSAE Bicipitoradial (cubital) bursitis37,38 ●

●

cubital bursitis results in enlargement of the bursa and may result from: ■ chronic mechanical trauma due to repetitive elbow supination and pronation ■ infection or inflammatory arthropathy ■ tumour-like lesions: synovial chondromatosis, lipoma arborescens39 clinically, patients present with a mass in the antecubital fossa, which may be painful, and restricted elbow movement: ■ the enlarged bursa may result in compression of adjacent nerves, including the superficial or deep branches of the radial nerve, but not the median nerve

MRI findings ● a lobulated mass is seen in the antecubital fossa with partial or complete envelopment of the distal biceps tendon (Fig. 2.27a, b) ● the mass is hypointense to muscle on T1W (Fig. 2.27a) and hyperintense on T2W/STIR (Fig. 27b) ● it has a smooth or irregular outline with internal septa (Fig. 2.27c) and/or heterogeneous hypointensity due to chronic synovitis (Fig. 2.27d, e) ● variable rim enhancement is seen following gadolinium (Fig. 2.27f), the degree of enhancement being related to the degree of active synovitis ● localised cortical bone resorption has been described in cubital bursitis complicating rheumatoid arthritis40

Olecranon bursitis41 ● ●

●

●

olecranon bursitis may be classified as aseptic or septic aseptic olecranon bursitis is associated with repetitive trauma, inflammatory arthropathy, obesity, prolonged pressure against the elbow in patients on haemodialysis (dialysis elbow) and trauma (elbow fracture, triceps tendon tear) septic bursitis accounts for approximately 33 per cent of cases of olecranon bursitis and may be posttraumatic or occur in immunocompromised patients, with 90 per cent of cases due to Staphylococcus aureus clinically, patients present with a soft posterior elbow mass, which may be painful

MRI findings ● there is a lobulated mass deep to the skin and superficial to the triceps tendon that is hypointense to muscle on T1W (Fig. 2.28a) and hyperintense on T2W (Fig. 28b, c) ● the mass shows rim enhancement following gadolinium

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The elbow

a

b

c

d

e

f

Figure 2.27 Bicipitoradial bursitis. Sagittal T1-weighted (T1W) spin-echo (SE) (a) and short tau inversion recovery (b) images showing a lobulated lesion (arrows) anterior to the biceps tendon (arrowhead a) in the antecubital fossa. Axial T2-weighted (T2W) fast spin-echo (FSE) fat-suppressed image (c) showing internal septa (arrow). Axial T2W FSE images showing partial (d) and complete (e) envelopment of the biceps tendon (arrows) by the bursa (arrowheads) and heterogeneous low signal intensity due to chronic synovitis and ‘rice bodies’ (e). Axial post-contrast T1W SE image (f) showing rim enhancement of the bursa (arrows) anterior to the biceps tendon (arrowhead). ● ● ●

associated features include elbow joint effusions, surrounding soft-tissue oedema, thickening of the triceps tendon and marrow oedema in the olecranon no single feature discriminates aseptic from septic bursitis however, marked soft-tissue oedema, increased lobulation, olecranon marrow oedema and thickening of the triceps tendon are more suggestive of infection

The nerves

c

b a Figure 2.28 Tubercular olecranon bursitis. Sagittal T1-weighted spin-echo (a), sagittal short tau inversion recovery (b) and axial T2-weighted fast spin-echo (c) images showing a large lobulated cystic mass in the posterior distal arm extending to the olecranon process.

THE NERVES THE RADIAL NERVE Normal anatomy1,42,43 ●

● ●

●

the radial nerve is a continuation of the posterior cord of the brachial plexus at the level of the elbow joint; it runs within the radial tunnel, a space that is ~5 cm in length, extending from the capitellum proximally to the supinator muscle distally and bounded by the brachioradialis anterolaterally, the brachialis anteromedially and the capitellum posteriorly (Fig. 2.29a) at the proximal margin of the supinator, it divides into two major branches (Fig. 2.29b): the posterior interosseous nerve (PIN) and the superficial radial nerve the PIN passes between the superficial and deep heads of supinator and extends distally in the posterior compartment of the forearm together with the posterior interosseous artery: ■ the proximal edge of the superficial head of supinator may form a fibrous arch, the arcade of Frohse, through which the nerve passes; this is present in 35–65 per cent of individuals and may be seen on MRI as a low SI band overlying the supinator muscle (Fig. 2.29c) ■ in the elbow region, the nerve innervates the common extensor and anconeus muscles the superficial radial nerve passes distally between the supinator and brachioradialis (Fig. 2.29d) and provides sensory innervation to the dorsal soft tissues of the forearm and hand

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The elbow

a

b

d c Figure 2.29 Anatomy of the radial nerve. Axial proton density-weighted (PDW) fast spin-echo (FSE) image (a) at the level of the humeral epicondyles showing the radial nerve (white arrow) lying deep to the extensor carpi radialis longus (arrowhead) and superficial to the brachialis (black arrow). Axial PDW FSE image (b) at the level of the capitellum showing the superficial radial nerve (arrow) and posterior interosseous nerve (arrowhead). Axial PDW FSE image (c) showing the arcade of Frohse (arrowheads) at the proximal edge of the superficial head of supinator (arrow). Axial PDW FSE image (d) showing the superficial branch of the radial nerve (black arrow) running between the brachioradialis (arrowhead) and the supinator (white arrow).

PATHOLOGY OF THE RADIAL NERVE Posterior interosseous nerve syndrome29,42,43 ● ● ●

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●

PIN syndrome is also termed ‘supinator syndrome’ and results from compression of the PIN five possible sites of compression are described, the commonest being the tendinous proximal edge of the superficial head of supinator (arcade of Frohse) others include the anterior capsule of the radiocapitellar joint, small vessels from the recurrent radial artery that cross the nerve (the leash of Henry), the fibrous edge of the ECRB muscle and the distal margin of the supinator other causes of compression neuropathy include tumours, ganglion cysts, radiocapitellar synovitis, biciptoradial bursitis, radial head trauma (fractures/dislocations) and iatrogenic, following internal fixation of the proximal radius clinically, PIN syndrome manifests with slow onset of pain (without significant sensory loss) and loss of motor function in muscles innervated by the PIN, mainly the extensor group of muscles, resulting in wrist drop

MRI findings ● denervation oedema/atrophy of the supinator and extensor muscles (Fig. 2.30a–c) is observed ● the underlying cause (Fig. 2.30a–c)

The nerves

a b

c

Figure 2.30 Supinator syndrome. Proximal forearm lipoma: Sagittal (a) and axial (b) T1-weighted spin-echo images showing the hyperintense lipoma (arrows) lying deep to the brachioradialis. Denervation atrophy of the extensor muscle group (arrowheads) indicates chronic compression of the posterior interosseous nerve. Radiocapitellar synovitis: Axial T2-weighted fast spin-echo image (c) showing a joint effusion (black arrowhead) and denervation oedema of the supinator–extensor muscle group (white arrows).

Radial tunnel syndrome29,42–44 ● ● ●

radial tunnel syndrome is due to compression of the PIN in the radial tunnel pathologically, it results from dynamic stress caused by passive compression from repeated elbow flexion, pronation and supination clinically, it manifests as activity-related, radial-side forearm pain with no motor loss, pain on resisted supination of the forearm and pain on resisted middle finger extension: ■ relief of symptoms may be associated with injection of local anaesthetic into the radial tunnel ■ it is associated with lateral epicondylitis in ~5 per cent of cases

MRI findings ● these may be optimally demonstrated with the forearm pronated ● the muscle denervation pattern depends on the site of compression: ■ denervation of the triceps, anconeus, brachioradialis and ECRL indicates radial nerve compression before its division into the PIN and superficial radial nerves ■ denervation changes are most commonly seen in the supinator (44 per cent) or the proximal forearm muscles (12 per cent ) ■ isolated oedema of the pronator teres is a rare occurrence (4 per cent) ● a mass lesion may be seen along the route of the PIN

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The elbow

THE MEDIAN NERVE Normal anatomy1,42,43 ● ● ●

● ●

the median nerve is formed from branches of the medial and lateral cords of the brachial plexus at the level of the humeral epicondyles, it runs between the pronator teres and the brachialis (Fig. 2.31a) within the antecubital fossa, the nerve lies deep to the bicipital aponeurosis and medial to the biceps tendon and brachial artery (Fig. 2.31b) and extends distally between the two heads of pronator teres (in 80 per cent of individuals) it innervates the pronator teres and the common flexor muscles, and gives rise to the anterior interosseous nerve at the inferior border of the pronator teres in the absence of fat, the median nerve is difficult to visualise on axial MR images

b a Figure 2.31 Anatomy of the median nerve. Axial proton density-weighted (PDW) fast spin-echo (FSE) image (a) at the level of the humeral epicondyles showing the median nerve (white arrow) lying deep to the pronator teres (black arrowhead) and superficial to the brachialis (black arrow). Axial PDW FSE image (b) showing the position of the median nerve (white arrow) in the antecubital fossa where it lies medial to the biceps tendon (black arrowhead) and brachial artery (white arrowhead).

PATHOLOGY OF THE MEDIAN NERVE Pronator syndrome42,43 ● ●

pronator syndrome is due to compression of the median nerve at the elbow or in the proximal forearm four potential sites of compression are described: ■ the supracondylar process of the humerus (avian spur): a bony prominence arising from the anteromedial aspect of the distal humerus, 5–7 cm proximal to the medial epicondyle and present in approximately 3 per cent of individuals: – a fibrous band (the ligament of Struthers) may extend from the spur to the medial epicondyle, forming a fibro-osseous tunnel through which the median nerve and occasionally the brachial artery pass – this is the least common site of compression ■ a thickened bicipital aponeurosis or an accessory fibrous band associated with a third head of biceps ■ between the humeral (superficial) and ulnar (deep) heads of pronator teres: the commonest site of compression neuropathy, due to fibrous bands (found in 50 per cent of individuals) or prolonged pronation of the forearm ■ at the FDS muscle: the second commonest site of compression neuropathy, due to a fibrous band arising 2 cm distal to the pronator teres muscle

The nerves

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●

other causes of compression neuropathy include an accessory bicipital aponeurosis, intra-articular entrapment following closed reduction of elbow dislocation, aberrant vessels and accessory muscles (the accessory head of flexor pollicis longus [Gantzer’s] muscle and palmaris profundus) clinically, patients experience pain in the volar aspect of the elbow and forearm that is exacerbated by exertional activities (repetitive pronation and grasping), and paraesthesia in the thumb to middle fingers

MRI findings ● technique: the FOV must cover from the distal one-third of the arm to the FDS in the forearm ● denervation oedema/atrophy of the flexor–pronator muscle group and evidence of the underlying cause: ■ a low SI band due to the ligament of Struthers or a soft-tissue mass

THE ULNAR NERVE Normal anatomy1,42,43 ● ● ●

●

the ulnar nerve arises from the medial cord of the brachial plexus proximal to the elbow, the nerve runs posterior to the medial epicondyle (Fig. 2.32a) at the level of the elbow joint, the nerve runs through the cubital tunnel (Fig. 2.32b): ■ the floor of the cubital tunnel is formed by the posterior bundle of the UCL ■ the roof is formed by the cubital tunnel retinaculum (arcuate ligament) ■ within the cubital tunnel, the nerve is surrounded by fat ■ distally, the nerve passes between the two heads of FCU (Fig. 2.32c) in the proximal forearm, the ulnar nerve innervates the FCU and the medial part of the FDP muscle

a

b

c

Figure 2.32 Anatomy of the ulnar nerve. Axial proton densityweighted (PDW) fast spin-echo (FSE) image (a) at the level of the humeral epicondyles, showing the ulnar nerve (arrow) lying posterior to the medial epicondyle (arrowhead). Axial PDW FSE image (b) at the level of the cubital tunnel showing the ulnar nerve (arrow) lying deep to the cubital tunnel retinaculum (arrowhead). Axial PDW FSE image (c) distal to the cubital tunnel showing the ulnar nerve (arrow) lying between the two heads of flexor carpi ulnaris.

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The elbow

PATHOLOGY OF THE ULNAR NERVE Cubital tunnel syndrome42,43 ●

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● ●

sites of potential compression of the ulnar nerve in the elbow and proximal forearm region include: ■ just proximal to the elbow joint by the medial head of triceps ■ in the cubital tunnel: the commonest site ■ less commonly, by Osborne’s fascia (a fibrous band connecting the proximal edge of the FCU to the medial epicondyle) and the deep flexor–pronator aponeurosis, through which the ulnar nerve exits the cubital tunnel cubital tunnel syndrome is the commonest neuropathy of the ulnar nerve at the elbow and may be classified as: ■ physiological, due to the normal decrease in volume of the cubital tunnel during elbow flexion ■ acute or subacute external compression, following direct force applied to the cubital tunnel ■ chronic compression, due to mass lesions including bursae, medial elbow ganglia45 (accounts for 8 per cent of cases, is the third most common cause and is almost always associated with osteoarthritis), inflammatory synovitis, osteophytes and loose bodies, joint deformity such as cubitus valgus and an accessory muscle, the anconeus epitrochlearis two age ranges are described: 20–30 years (typically post-traumatic) and 50–60 years (typically associated with osteoarthritis) clinically, cubital tunnel syndrome manifests as paraesthesia along the ulnar aspect of the hand and the little and ring fingers, medial elbow and forearm pain, and weakness of the muscles innervated by the ulnar nerve

MRI findings ● swelling and/or hyperintensity of the ulnar nerve within the cubital tunnel is seen on T2W FSE FS images;46 this should be distinguished from an engorged deep recurrent ulnar vein, which lies just lateral to the ulnar nerve in the cubital tunnel ● denervation of muscles on the ulnar side of the forearm and hand, including the FCU and FDP ● any underlying cause such as osteophytes, synovitis or soft-tissue masses ● indirect MR arthrography may demonstrate perineural enhancement10

Ulnar nerve subluxation/dislocation ● ● ●

●

subluxation/dislocation of the ulnar nerve may be asymptomatic and is reported in 10–16 per cent of individuals it may lead to secondary friction neuritis and ulnar neuropathy ulnar nerve dislocation may be secondary to: ■ congenital absence, tear or laxity of the arcuate ligament ■ a hypoplastic trochlea or post-traumatic cubitus valgus it may also be associated with snapping triceps syndrome – dislocation of the medial head of triceps over the medial epicondyle

MRI findings ● a dislocated ulnar nerve is optimally visualised on axial images ● a subluxing nerve is optimally visualised with the elbow imaged in flexion ● an absent arcuate ligament may be noted

REFERENCES 1 2

Kijowski R, Tuite M, Sanford M. Magnetic resonance imaging of the elbow. Part I. Normal anatomy, imaging technique, and osseous abnormalities. Skeletal Radiol 2004; 33: 685–97. Chung CB, Stanley AJ, Gentili A. Magnetic resonance imaging of elbow instability. Semin Musculoskelet Radiol 2004; 9: 67–76.

References

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29 30

Cunningham PM. MR imaging of trauma: elbow and wrist. Semin Musculoskelet Radiol 2006; 10: 284–92. Cotten A, Jacobson J, Brossmann J et al. Collateral ligaments of the elbow: conventional MR imaging and MR arthrography with coronal oblique plane and elbow flexion. Radiology 1997; 204: 806–12. Carrino JA, Morrison WB, Zou KH, Steffen RT, Snearly WN, Murray PM. Lateral ulnar collateral ligament of the elbow: optimization of evaluation with two-dimensional MR imaging. Radiology 2001; 218: 118–25. Guiffre BM, Moss MJ. Optimal positioning for MRI of the distal biceps brachii tendon: flexed abducted supinated view. AJR Am J Roentgenol 2003; 182: 944–6. Chew ML, Guiffre BM. Disorders of the distal biceps brachii tendon. Radiographics 2005; 25: 1227–37. Cotten A, Jacobson J, Brossmann J, Hodler J, Trudell D, Resnick D. MR arthrography of the elbow: normal anatomy and diagnostic pitfalls. J Comput Assist Tomogr 1997; 21: 516–22. Sahin G, Demirtas M. An overview of MR arthrography with emphasis on the current technique and applicational hints and tips. Eur J Radiol 2006; 58: 416–30. Bergin D, Schweitzer ME. Indirect magnetic resonance arthrography. Skeletal Radiol 2003; 32: 551–8. Stoane JM, Poplausky MR, Haller JO, Berdon WE. Panner’s disease: X-ray, MR imaging findings and review of the literature. Comput Med Imaging Graph 1995; 19: 473–6. Kobayashi K, Burton KJ, Rodner C, Smith B, Caputo AE. Lateral compression injuries in the pediatric elbow: Panner’s disease and osteochondritis dissecans of the capitellum. J Am Acad Orthop Surg 2004; 12: 246–54. Patel N, Weiner SD. Osteochondritis dissecans involving the trochlea: report of two patients (three elbows) and review of the literature. J Pediatr Orthop 2002; 22: 48–51. Bowen RE, Otsuka NY, Yoon ST, Lang P. Osteochondral lesions of the capitellum in pediatric patients: role of magnetic resonance imaging. J Pediatr Orthop 2001; 21: 298–301. Dubberley JH, Faber KJ, Patterson SD et al. The detection of loose bodies in the elbow: the value of MRI and CT arthrography. J Bone Joint Surg [Br] 2005; 87-B: 684–6. Schickendantz MS, Ho CP, Koh J. Stress injury of the proximal ulna in professional baseball players. Am J Sports Med 2002; 30: 737–41. Salvo JP, Rizio III L, Zvijac JE, Uribe JW, Hechtman KS. Avulsion fracture of the ulnar sublime tubercle in overhead throwing athletes. Am J Sports Med 2002; 30: 426–31. Pudas T, Hurme T, Mattila K, Svedström E. Magnetic resonance imaging in pediatric elbow fractures. Acta Radiol 2005; 46: 636–44. Fowler KA, Chung CB. Normal MR imaging anatomy of the elbow. Radiol Clin North Am 2006; 44: 553–67. Duparc F, Putz R, Michot C, Muller JM, Freger P. The synovial fold of the humeroradial joint: anatomical and histological features, and clinical relevance in lateral epicondylalgia of the elbow. Surg Radiol Anat 2002; 24: 302–7. Fukase N, Kokubu T, Fujioka H, Iwama Y, Fujii M, Kurosaka M. Usefulness of MRI for diagnosis of painful snapping elbow. Skeletal Radiol 2005; 35: 797–800. Huang GS, Lee CH, Lee HS, Chen CY. A meniscus causing painful snapping of the elbow joint: MR imaging with arthroscopic and histologic correlation. Eur Radiol 2005; 15: 2411–14. Aoki M, Okamura K, Yamashita T. Snapping annular ligament of the elbow joint in the throwing arms of young brothers. Arthroscopy 2003; 19: E4–7. Awaya H, Schweitzer ME, Feng SA et al. Elbow synovial fold syndrome: MR imaging findings. AJR Am J Roentgenol 2001; 177: 1377–81. Antuna SA, O’Driscoll SW. Snapping plicae associated with radiocapitellar chondromalacia. Arthroscopy 2001; 17: 491–5. Potter HG, Ho ST, Altchek DW. Magnetic resonance imaging of the elbow. Semin Musculoskelet Radiol 2004; 8: 5–16. Kaplan LJ, Potter HG. MR imaging of ligament injuries to the elbow. Radiol Clin North Am 2006; 44: 583–94. Munshi M, Pretterklieber ML, Chung CB et al. Anterior bundle of ulnar collateral ligament: evaluation of anatomic relationships by using MR imaging, MR arthrography, and gross anatomic and histologic analysis. Radiology 2004; 231: 797–803. Kijowski R, Tuite M, Sanford M. Magnetic resonance imaging of the elbow. Part II. Abnormalities of the ligaments, tendons, and nerves. Skeletal Radiol 2005; 34: 1–18. Ouellette H, Kassarjian A, Tretreault P, Palmer W. Imaging of the overhead throwing athlete. Semin Musculoskelet Radiol 2005; 9: 316–33.

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31 Williams BD, Schweitzer ME, Weishaupt D et al. Partial tears of the distal biceps tendon: MR appearance and associated clinical findings. Skeletal Radiol 2001; 30: 560–4. 32 Qureshi SS, Puri A, Agarwal M, Merchant NH, Sheth T, Jambhekar N. Unusual late sequel of ruptured distal tendon of biceps brachii mimicking a soft-tissue tumor. Skeletal Radiol 2004; 33: 417–20. 33 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-A: 239–47. 34 Spinner RJ, Hayden FR Jr, Goldner RD. Imaging the snapping triceps. AJR Am J Roentgenol 1996; 167: 1550–1. 35 Jeon IH, Fairbairn KJ, Neumann L, Wallace WA. MR imaging of edematous anconeus epitrochlearis: another cause of medial elbow pain? Skeletal Radiol 2005; 34: 103–7. 36 Kijowski R, De Smet AA. Magnetic resonance imaging findings in people with medial epicondylitis. Skeletal Radiol 2005; 34: 196–202. 37 Skaf AY, Boutin RD, Dantas RWM 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: 111–16. 38 Yamamoto T, Mizuno K, Soejima T, Fujii M. Bicipital radial bursitis: CT and MR appearance. Comput Med Imaging Graph 2001; 25: 531–3. 39 Doyle AJ, Miller MV, French JG. Lipoma arborescens in the bicipital bursa of the elbow: MRI findings in two cases. Skeletal Radiol 2002; 31: 656–60. 40 Taira H, Yoshida S, Takasita M, Tsumura H, Torisu T. Localized cortical bone absorption induced by cubital bursitis in rheumatoid arthritis. Orthopedics 2002; 25: 860–1. 41 Floemer F, Morrison WB, Bongartz G, Ledermann HP. MRI characteristics of olecranon bursitis. AJR Am J Roentgenol 2004; 183: 29–34. 42 Bordalo-Rodrigues M, Rosenberg ZS. MR imaging of entrapment neuropathies at the elbow. Magn Reson Imaging Clin N Am 2004; 12: 247–63. 43 Kim S, Choi J-Y, Huh Y-M et al. Role of magnetic resonance imaging in entrapment and compressive neuropathy: what, where, and how to see the peripheral nerves on the musculoskeletal magnetic resonance image. Part 2. Upper extremity. Eur Radiol 2007; 17: 509–22. 44 Ferdinand BD, Rosenberg ZS, Schweitzer ME et al. MR imaging features of radial tunnel syndrome: initial experience. Radiology 2006; 240: 161–8. 45 Kato H, Hirayama T, Minami A, Iwasaki N, Hirachi K. Cubital tunnel syndrome associated with medial elbow ganglia and osteoarthritis of the elbow. J Bone Joint Surg [Am] 2002; 84-A: 1413–19. 46 Britz GW, Haynor DR, Kuntz C et al. Ulnar nerve entrapment at the elbow: correlation of magnetic resonance imaging, clinical, electrodiagnostic, and intraoperative findings. Neurosurgery 1996; 38: 458–65.

3 The wrist and hand

TECHNIQUE Routine MRI1–3 ● ●

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●

optimal MR imaging of the wrist requires a high-field magnet (1.5 T) and a dedicated wrist coil patient position: the patient may be supine with the arm by the side, the elbow extended, the forearm pronated and the palm of hand resting on the tabletop: ■ excessive ulnar or radial tilt should be avoided, since the resulting images may mimic the presence of carpal instability ■ alternatively, the ‘Superman’ position may be used, but this can be difficult to maintain standard imaging planes: ■ coronal images are planned from an axial scout parallel to a line running through the scaphoid, lunate and triquetrum (Fig. 3.1a) ■ sagittal images are planned perpendicular to the coronal plane ■ axial images should cover from just proximal to the distal radioulnar joint (DRUJ), to just distal to the metacarpal (MC) bases standard sequences: ■ coronal T1-weighted (T1W) spin-echo (SE) or proton density-weighted (PDW) fast spin-echo (FSE), for anatomical detail ■ coronal PDW/T2-weighted (T2W) FSE fat-suppressed (FS), for detection of bone marrow oedema and the triangular fibrocartilage (TFC) complex ■ coronal T2*-weighted (T2*W) gradient-echo (GE), for assessment of the TFC complex and carpal ligaments ■ sagittal T1W or PDW FSE, for assessment of carpal alignment ■ axial T1W or PDW FSE with T2W/PDW FSE FS, for assessment of tendons and the carpal tunnel ■ three-dimensional GE sequences can also be used: – provide very thin sections with the ability to reconstruct images – optimal imaging of carpal ligaments technical parameters: ■ a small field of view, ideally 8–10 cm ■ a high-resolution matrix ■ slice thickness 3 mm

Additional sequences ● ●

sagittal oblique imaging4 along the length of the volar extrinsic carpal ligaments has been described axial oblique imaging5 of the intrinsic ligaments following arthrography has recently been described (Fig. 3.1b, c):

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a b

c

■

Figure 3.1 Axial proton density-weighted (PDW) fast spinecho (FSE) image (a) showing the plane for coronal imaging of the wrist. Coronal PDW FSE images (b, c) showing the scan planes for axial oblique imaging of the scapholunate (b) and lunotriquetral (c) ligaments.

the addition of axial oblique images increases sensitivity and specificity for the diagnosis of scapholunate ligament (SLL) and lunotriquetral ligament (LTL) tears compared with the coronal and true axial plane alone

MR arthrography6–9 ● ● ● ●

●

●

● ●

direct and indirect techniques are described direct MR arthrography involves intra-articular injection of dilute gadolinium followed by imaging with a combination of T1W SE FS and T2W FSE FS sequences6,7 it can be performed as single- (radiocarpal), double- (radiocarpal and mid-carpal, or radiocarpal and DRUJ) or triple- (radiocarpal, mid-carpal and DRUJ) compartment arthrography injection sites and suggested volumes include: ■ radiocarpal (3–4 ml): radioscaphoid space injection, directed away from the SLL ■ mid-carpal (3–4 ml): into the scaphocapitate or triquetrohamate spaces ■ DRUJ (1–2 ml): into the proximal aspect of the joint indications: ■ TFC tear: single-compartment radiocarpal injection ■ suspected ulnar detachment of the TFC: radiocarpal and DRUJ injections ■ chronic occult wrist pain or instability syndromes: triple-compartment injection in the normal radiocarpal injection, contrast fills the dorsal recess of the joint and communication with the pisotriquetral joint occurs in 34–70 per cent of cases, while injection distal to the scaphoid tubercle may result in filling of the mid-carpal compartment in the normal wrist mid-carpal injection, contrast normally fills the scapholunate and lunotriquetral spaces but is limited from entering the radiocarpal space by an intact SLL and LTL indirect MR arthrography involves intravenous injection of gadolinium, followed by passive or active wrist exercise and imaging with a combination of T1W SE FS and T2W FSE FS sequences8,9

The distal radioulnar joint

THE DISTAL RADIOULNAR JOINT Normal anatomy1,10,11 ● ●

●

the DRUJ is formed between the distal ulna and the sigmoid notch of the distal radius (Fig. 3.2a, b): ■ the sigmoid notch is a medial depression in the distal radius static stabilisers of the joint include: ■ the distal radioulnar ligaments: volar and dorsal ligaments, which have a striated appearance on MRI, are variably demonstrated on coronal and axial MR images due to their oblique course (Fig. 3.2c); occasionally, the ulnar attachment is not seen ■ the interosseous membrane and TFC complex ■ the sigmoid notch of the radius dynamic stabilisation is afforded by the pronator quadratus (Fig. 3.2d), and the extensor and flexor carpi ulnaris (FCU) muscle tendons

b

a

d c Figure 3.2 Normal anatomy of the distal radioulnar joint (DRUJ). Coronal (a) and axial (b) proton density-weighted (PDW) fast spin-echo (FSE) images showing the normal DRUJ (arrows) and the sigmoid notch of the radius (arrowhead b). Axial T2*-weighted gradient-echo image (c) showing the volar (arrow) and dorsal (arrowhead) radioulnar ligaments. Axial PDW FSE image (d) showing the pronator quadratus muscle (arrowheads).

●

the relationship between the distal ulna and the sigmoid notch is dependent on wrist position: ■ neutral: the distal ulna sits within the sigmoid notch ■ prone: the ulnar head moves dorsally (Fig. 3.3a) ■ supine: the ulnar head moves in the volar direction (Fig. 3.3b)

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a

b

c

d

Figure 3.3 Axial T1-weighted (T1W) spin-echo (SE) images of the distal radioulnar joint (DRUJ) in the prone position (a) showing slight dorsal deviation of the ulnar head (arrow) and in the supine position (b) showing slight volar deviation of the ulnar head (arrow). Axial T1W SE image (c) showing the radioulnar line method for assessing DRUJ alignment. Axial T1W SE image (d) showing the epicentre method for assessing DRUJ alignment.

●

the normal relationship can be assessed on axial images using a variety of techniques: ■ in the neutral position: using the radioulnar line (Mino) method, where the ulnar head position is normal if it lies between two lines, as shown in Fig. 3.3c ■ in the prone position: using the pronation congruity method, where the position is normal if there is congruity between the ulnar head and the sigmoid notch ■ in the supine position: using the epicentre method (Fig. 3.3d), where a perpendicular line is drawn from a line joining the centre of the ulnar styloid process and the centre of the ulnar head to the sigmoid notch; the joint position is normal if this line is in the middle of the sigmoid notch

PATHOLOGY OF THE DISTAL RADIOULNAR JOINT Distal radioulnar joint instability1,12,13 ● ● ●

●

the aetiology of DRUJ instability includes disruption of the TFC complex, fracture of the distal radius or ulnar styloid, and inflammatory processes such as rheumatoid arthritis (RA) dorsal instability is more common than volar instability clinically, DRUJ instability manifests as ulnar-sided wrist pain, swelling and deformity, difficulty with grip and forearm rotation and prominence of the ulnar head: ■ however, abnormal relationships of the DRUJ are not uncommon in asymptomatic individuals14 optimal assessment may be made by axial imaging of both wrists in the neutral, prone and supine positions, with the arms above the head, using a head or neck coil

The radiocarpal and ulnocarpal joints

MRI findings ● there is an abnormal relationship of the distal ulna with respect to the sigmoid notch (Fig. 3.4a, b) ● dorsal instability may be associated with a tear of the volar radioulnar ligament (Fig. 3.4b)

b

a Figure 3.4 Distal radioulnar joint (DRUJ) subluxation. Sagittal T1-weighted spin-echo (a) and axial T2*-weighted gradientecho (b) images showing dorsal subluxation of the ulnar head relative to the distal radius (arrows). Note the absence of the volar radioulnar ligament and fluid in the DRUJ (arrowhead b).

THE RADIOCARPAL AND ULNOCARPAL JOINTS Introduction ● ●

the radiocarpal joint is formed by the articulation between the distal radius and the adjacent scaphoid and lunate the ulnocarpal joint is formed by the distal ulna, the TFC complex and the adjacent lunate and triquetrum

THE DISTAL RADIUS Normal anatomy10,12,13 ●

●

●

● ●

the distal radius has two concave depressions in its articular surface that articulate with the scaphoid and lunate (Fig. 3.5a): ■ the scaphoid fossa is triangular in shape and the lunate fossa is rectangular the radial inclination describes the angulation of the distal radial articular surface with reference to a line drawn perpendicular to the long axis of the radius on an anteroposterior radiograph (coronal MRI) (Fig. 3.5b); normal values are ~15–35° (mean ~23°) the palmar tilt describes the volar angulation of the distal radial articular surface with reference to a line drawn perpendicular to the long axis of the radius on a lateral radiograph (sagittal MRI) (Fig. 3.5c); normal values are 0–20° (mean 12° in women and 9° in men): ■ any degree of dorsal tilt is considered abnormal the radial styloid is located at the distal radial tip of the radius (Fig. 3.5d) the dorsal surface of the distal radius has a bony prominence called Lister’s tubercle, which separates the second and third extensor tendon compartments (Fig. 3.5e)

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b a

d c

e

Figure 3.5 Normal anatomy of the distal radius. Coronal proton density-weighted (PDW) fast spin-echo (FSE) image (a) showing the biconcave distal radial articular surface with a small intervening ridge (arrow). Coronal (b) and sagittal (c) PDW FSE images showing assessment of the radial inclination (b) and palmar tilt (c) of the distal radial articular surface. Coronal PDW FSE image (d) showing the radial styloid (arrow). Axial PDW FSE image (e) showing Lister’s tubercle (arrow).

THE DISTAL ULNA Normal anatomy10,12,13 ● ●

the distal ulna comprises the ulnar head and ulnar styloid (Fig. 3.6a, b) ulnar variance, also termed ‘radioulnar index’ or ‘Hulten variance’, refers to the relative lengths of the distal radius and ulna: ■ neutral variance: the articular surfaces are of equal length ■ positive variance: the ulnar articular surface is distal to the radial articular surface (Fig. 3.6c) ■ negative variance: the ulnar articular surface is proximal to the radial articular surface (Fig. 3.6d)

The radiocarpal and ulnocarpal joints

b

a

d

c Figure 3.6 Distal ulnar anatomy. Sagittal (a) and axial (b) proton density-weighted (PDW) fast spin-echo (FSE) images showing the ulnar head (white arrow a) and ulnar styloid process (black arrows). Ulnar variance: Coronal T1-weighted spin-echo images (c, d) showing positive (c) and negative (d) ulnar variance.

● ●

ulnar variance is dependent on forearm position, being greatest with forearm pronation and the wrist gripped and least with forearm supination ulnar variance can be assessed with MRI, though measurements of ulnar variance may not be accurate

PATHOLOGY OF THE DISTAL RADIUS Distal radial fractures15 ●

MRI of distal radial fractures may show features not evident on radiography, including: ■ extension into the DRUJ (Fig. 3.7a) and radiocarpal joint (Fig. 3.7b, c) and occult carpal bone fractures ■ soft-tissue injury is reported in 48 per cent of cases, including SLL rupture (Fig. 3.7a), TFC complex rupture (Fig. 3.7a), extensor carpi ulnaris (ECU) tenosynovitis and dorsal radiocarpal ligament rupture

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a b

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Figure 3.7 Distal radial fracture. Coronal short tau inversion recovery images (a, b) showing a distal radial fracture (arrows) extending into the distal radioulnar joint and radial articular surface. Note also scapholunate ligament rupture (arrowhead a) and ulnar avulsion of the triangular fibrocartilage (double arrowhead a). Axial T2*-weighted gradient-echo image (c) showing the hyperintense fracture line (arrow) extending to the articular surface.

Madelung deformity16 ●

●

Madelung deformity is a developmental growth disturbance due to asymmetrical closure of the distal radial physis, which may be idiopathic, associated with a variety of syndromes or post-traumatic in nature clinically, idiopathic (primary) Madelung deformity presents in childhood/adolescence with wrist pain, deformity and weakness

MRI findings ● there is a fixed pronated deformity of the distal radius, with a physeal bar that bridges the metaphysis and epiphysis of the radius on the volar aspect of the ulnar facet ● ligamentous abnormalities include an anomalous volar ligament and hypertrophy of the volar radiotriquetral and short radiolunate ligaments

THE RADIOCARPAL AND ULNOCARPAL LIGAMENTS Introduction ● ● ●

the wrist ligaments can be classified as extrinsic or intrinsic, volar or dorsal extrinsic ligaments originate in the forearm and insert into the carpal bones intrinsic ligaments are confined to the carpus and represent capsular thickenings, appearing as hypointense bands on all MR pulse sequences (see later)

The radiocarpal and ulnocarpal joints

THE VOLAR EXTRINSIC LIGAMENTS Normal anatomy13,17–19 ●

●

the five volar extrinsic ligaments are considered to be the most important stabilisers of the wrist joint, preventing ulnar translocation of the carpus and supporting the intra-articular ligaments in controlling carpal motion the radioscaphocapitate ligament (RSCL) is the most radial and superficial of the extrinsic ligaments: ■ it is an oblique ligament originating from the volar surface of the radial styloid (Fig. 3.8a) that runs across the scaphoid waist (Fig. 3.8b) to insert into the head of the capitate ■ it also inserts via a fibrous band into the volar aspect of the distal pole of the scaphoid and plays an important role in preventing rotatory subluxation of the scaphoid

a b

c

d

e

Figure 3.8 Anatomy of the volar extrinsic carpal ligaments. Coronal T2*-weighted (T2*W) gradient-echo (GE) image (a) showing the radioscaphocapitate ligament (RSCL) (arrow) arising from the radial styloid (arrowhead). Coronal T1-weighted spin-echo fat-suppressed MR arthrogram (b) showing the RSCL (arrow) and the radiolunotriquetral ligament (RLTL) (arrowhead). Coronal T2*W GE image (c) showing the RLTL (arrowheads) arising from the radial styloid (arrow) and inserting into the lunate and triquetrum. Sagittal T2*W GE image (d) showing the radioscapholunate ligament (arrow). Coronal T2*W GE image (e) showing the ulnotriquetral ligament (arrow) extending from the triangular fibrocartilage (arrowhead) to the triquetral (double arrowheads).

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●

● ●

the radiolunotriquetral ligament (RLTL) arises from the radial styloid on the ulnar side of the RSCL ligament (Fig. 3.8b) and runs obliquely across the wrist, inserting into the volar ridge of the lunate and distally into the volar surface of the triquetrum (Fig. 3.8c): ■ it is a major stabiliser of the wrist and also inserts into the volar surfaces of the interosseous SLL and LTL at the ‘confluence zone’ ■ it is routinely visualised on coronal and sagittal images (Fig. 3.8b, c) the radioscapholunate ligament (RSLL) is the deepest volar extrinsic ligament, arising from the volar rim of the radius at the junction of the scaphoid and lunate fossae: ■ superficial fibres insert into the scaphoid and lunate bones and deep fibres merge with the SLL ■ it is a relatively vascular structure, accounting for its normal increased signal intensity (SI) compared with other wrist ligaments (Fig. 3.8d) the ulnolunate ligament originates from the mid-third of the TFC/volar radioulnar ligament and inserts into the volar aspect of the lunate (see later) the ulnotriquetral ligament originates from the mid-third of the TFC/volar radioulnar ligament and inserts into the volar invagination of the triquetrum (Fig. 3.8e)

PATHOLOGY OF THE VOLAR EXTRINSIC LIGAMENTS Ligament tears ● ● ●

injury to the RSCL usually occurs following a fall on an outstretched hand and may be associated with scapholunate dissociation (SLD)4 injury to the RSCL, RLTL and RSLL usually occurs at the radial attachment avulsion fractures of the ulnotriquetral ligament may occur following excessive wrist extension and radial deviation and are usually associated with LTL tears and ulnar-sided wrist instability

MRI findings ● ligament disruption manifests as thickening, thinning, elongation or absence, with increased T2W SI and surrounding fluid ● chronic injuries may be associated with ganglion cyst formation MR arthrographic findings ● injected contrast medium leaks through defects in the ligament/capsule (Fig. 3.9)

Figure 3.9 Pathology of the volar extrinsic carpal ligaments. Sagittal T1-weighted spin-echo fat-suppressed MR arthrogram showing disruption of the radioscaphocapitate (black arrowhead) and radiolunotriquetral (arrow) ligaments with leakage of injected contrast medium into the volar soft tissues of the wrist (white arrowhead).

The radiocarpal and ulnocarpal joints

THE DORSAL EXTRINSIC LIGAMENTS Normal anatomy13,17–19 ●

●

the dorsal extrinsic ligaments comprise: ■ the radiotriquetral (radiocarpal) ligament (Fig. 3.10), which represents a dorsal capsular thickening composed of one to three fascicles, arising from Lister’s tubercle (84 per cent of cases) or the radial styloid and inserting into the dorsal rim of the triquetrum, but also into the lunate ■ the ulnotriquetral (ulnocarpal) ligament, which arises from the dorsal radioulnar ligament and extends to the dorsal aspect of the triquetrum injury to the radiotriquetral ligament commonly involves the insertional fibres

Figure 3.10 The dorsal extrinsic ligaments. Coronal T2*-weighted gradient-echo image showing the dorsal radiotriquetral ligament (arrows).

The collateral ligaments ● ●

the radial collateral ligament (RCL) (Fig. 3.11) arises from the tip of the radial styloid and inserts into the radial aspect of the scaphoid waist and flexor carpi radialis (FCR) tendon the ulnar collateral ligament (UCL) is not a prominent structure and merges with the tendon sheath of the ECU, thus forming part of the TFC complex: ■ it represents a capsular thickening that arises from the ulnar styloid and inserts into the triquetrum and is not clearly visualised as a separate structure on MRI

Figure 3.11 The collateral ligaments. Coronal T1-weighted spin-echo fat-suppressed MR arthrogram showing the radial collateral ligament (arrow) extending from the radial styloid to the scaphoid.

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THE TRIANGULAR FIBROCARTILAGE COMPLEX Normal anatomy1,2,13,20 ● ●

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●

the TFC complex stabilises the DRUJ and forms a cushion for the ulnocarpal joint components of the TFC complex include: ■ the central (articular) disc (TFC) ■ the volar and dorsal radioulnar ligaments ■ the ulnolunate and ulnotriquetral ligaments ■ the meniscal homologue (ulnocarpal meniscus) ■ the UCL and the tendon sheath of the ECU the TFC appears on MRI as a low SI structure with smooth margins located between the distal ulna and the carpus, and may be demonstrated optimally using microscopy coils: ■ on coronal images, it appears triangular with its apex at the radial attachment (Fig. 3.12 a, b) ■ on sagittal images, it appears biconvex with thicker peripheral margins (Fig. 3.12c) ■ on axial images, it appears triangular with its apex at the ulnar styloid (Fig. 3.12d) ■ the TFC originates from the ulnar border of the distal radius between the sigmoid notch and the distal articular surface, where it separates the radiocarpal joint from the DRUJ ■ it is attached to the hyaline cartilage of the distal radius, resulting in a normal increased SI zone between it and the bone (Fig. 3.12b) ■ it extends to the ulnar styloid, where two types of attachment are described: – 1 – to both the fovea at the base of the ulnar styloid and the tip of the ulnar styloid (Fig. 3.12e); this type of ulnar attachment is sometimes referred to as the triangular ligament – 2 – less commonly, a broad-based striated fascicle attaching along the length of the ulnar styloid ■ the ulnar attachments of the TFC may be obscured by intervening loose vascular connective tissue (termed the ‘ligamentum subcruentum’), which manifests as relatively increased SI on T1W and T2W images (Fig. 3.12f, g) ■ the dorsomedial margin of the TFC is also attached to the ECU tendon and meniscus homologue by fibrous bands ■ the TFC is thicker (~5 mm) at its margins than centrally (~2 mm), the thickness being inversely proportional to ulnar length ■ the thickened dorsal and volar margins of the TFC are also referred to as the dorsal and volar radioulnar ligaments, which stabilise the DRUJ the meniscus homologue lies on the volar side of the wrist (Fig. 3.12h), arising from the dorsoulnar corner of the radius, in common with the dorsal radioulnar ligament, and inserting into the triquetrum, separating the pisotriquetral joint from the radiocarpal joint

b a Figure 3.12 Anatomy of the normal triangular fibrocartilage (TFC). Coronal proton density-weighted (PDW) fast spin-echo (FSE) (a) and T2*-weighted (T2*W) gradient-echo (GE) (b) images of the wrist showing the hypointense TFC (arrows). Note the hyperintense cartilage (arrowhead b) separating the TFC from the radius. (continued)

The radiocarpal and ulnocarpal joints

d

c

f

e h

g

Figure 3.12 (continued) Sagittal PDW FSE image (c) showing the TFC (arrow) and ulnotriquetral ligament (arrowhead). Axial T2*W GE image (d) showing the TFC (arrows). Coronal T1-weighted (T1W) spin-echo (SE) fat-suppressed (FS) MR arthrogram (e) showing the foveal (arrowhead) and the ulnar styloid (arrow) attachments of the TFC. Coronal PDW FSE (f) and T2*W GE (g) images showing intermediate signal intensity vascular connective tissue (arrows) obscuring the ulnar attachment of the TFC. Coronal T1W SE FS MR arthrogram (h) showing the meniscal homologue (arrow) and fluid in the prestyloid recess (arrowhead).

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the pre-styloid recess is an extension of the radiocarpal joint lying just distal to the ulnar styloid, representing a fluid-filled space located between the TFC and the meniscus homologue (Fig. 3.12h) asymptomatic degenerative change is a common finding with age, seen in 38–55 per cent of individuals in the third to fourth decades and 100 per cent in the sixth decade: ■ it tends to affect the central portion of the articular disc (a relatively avascular zone) and may progress to a degenerative tear ■ asymptomatic communicating defects have been reported in 46 per cent of wrists; 69 per cent are bilateral and most occur on the radial side of the disc ■ non-communicating defects are reported in 27 per cent of asymptomatic discs ■ it manifests as intermediate SI on T1W SE/PDW FSE images without increased SI on T2W/short tau inversion recovery (STIR) images (Fig. 3.13) changes in morphology of the TFC complex occur between neutral, supine and prone positioning:21 ■ no change occurs in the shape of the TFC or radial portions of the radioulnar ligaments ■ the TFC is horizontal in the neutral position and tilted to align with the proximal carpal row in pronation and supination ■ the ulnar attachment of the TFC changes orientation from coronal in neutral to sagittal in supination and pronation ■ the meniscal homologue appears smaller in supination and pronation ■ the ECU tendon is centred in its groove in neutral and pronation, but subluxes in supination

a

b

Figure 3.13 Triangular fibrocartilage (TFC) degeneration. Coronal proton density-weighted fast spin-echo (a) and short tau inversion recovery (STIR) (b) images showing mild increased signal intensity (SI) within the TFC (arrow a) but no increased SI on STIR.

PATHOLOGY OF THE TRIANGULAR FIBROCARTILAGE COMPLEX Triangular fibrocartilage complex tears22–24 ● ● ●

TFC complex tears manifest clinically as non-specific, ulnar-sided wrist pain, crepitus and weakness in relation to sports injuries, they occur following a rapid twisting mechanism with ulnar loading, as seen in racket sports, golf and gymnastics, and may be associated with distal radial fractures TFC complex tears are classified according to the system of Palmer into: ■ type 1 – traumatic injury: – IA – central perforation (Fig. 3.14a) – IB – ulnar avulsion with/without distal ulnar/ulnar styloid fracture (Fig. 3.14b–d) – IC – distal avulsion from carpal attachment to lunate or triquetrum – ID – radial avulsion with/without sigmoid notch fracture ■ type 2 – degenerative injury (represents the progressive stages of ulnocarpal impaction syndrome): – IIA – TFC thinning and degeneration, predominantly on the ulnar side (Fig. 3.15a) – IIB – TFC thinning and degeneration with lunate or ulnar chondromalacia

The radiocarpal and ulnocarpal joints

b a

d

c Figure 3.14 Traumatic triangular fibrocartilage (TFC) complex tears. Central perforation: Coronal T1-weighted (T1W) spinecho (SE) fat-suppressed MR arthrogram (a) showing a central perforation (arrow) of the TFC with injected contrast entering the distal radioulnar joint (arrowhead). Ulnar-side TFC tear: Coronal T1W SE (b) and short tau inversion recovery (c) images showing disruption of the TFC with excessive fluid around the ulnar attachment and ulnar styoid process (arrows). Sagittal T1W SE image (d) showing avulsion of the TFC from the foveal attachment (arrow).

●

– IIC – TFC perforation with lunate or ulnar chondromalacia (Fig. 3.15b) – IID – TFC perforation with lunate or ulnar chondromalacia and LTL rupture (described in 70 per cent of cases) – IIE – TFC perforation with lunate or ulnar chondromalacia, LTL rupture and osteoarthritis (OA) degenerative defects are more common than traumatic defects

MRI findings ● no MRI features reliably differentiate degenerative from traumatic tears, the diagnosis being dependent on a history of acute injury, while positive ulnar variance may indicate a type 2 lesion ● TFC tears manifest as discontinuity and/or fragmentation of the normally hypointense TFC disc ● traumatic tears (central perforations) occur most commonly on the radial side of the disc, 2–3 mm from the radial insertion and are commonly slit-like (Fig. 3.14a) ● intermediate SI on T1W and high SI on T2W may be seen within the tear due to fluid

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a

b Figure 3.15 Degenerative triangular fibrocartilage (TFC) complex tears. Coronal T2*-weighted (T2*W) gradient-echo (GE) image (a) showing positive ulnar variance and degenerative thinning of the TFC (arrow). Coronal T2*W GE image (b) showing positive ulnar variance (arrowhead) and a degenerative tear of the TFC (arrow). ●

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ulnar-side tears may be associated with fluid in the DRUJ (non-specific) (Fig. 3.15a) and proximal to the location of the pre-styloid recess: ■ they may then be associated with subluxation of the ulnar head MRI is reported to have sensitivity, specificity and accuracy of 89 per cent, 92 per cent and 90 per cent, respectively, compared with surgical findings however, the sensitivity, specificity and accuracy for ulnar-side tears are less and reported as 17 per cent, 79 per cent and 64 per cent, respectively:25 ■ sensitivity may be improved by imaging the wrist in maximal ulnar abduction

MR arthrographic findings ● direct MR arthrography demonstrates hyperintense fluid within the tear (Figs 3.14a, 3.16a, b) with extension into the DRUJ bursa ● the reported sensitivity, specificity and accuracy of indirect MR arthrography are 100 per cent, 77 per cent and 93 per cent26 ● degenerative change in the TFC disc should not be mistaken for a tear

b a Figure 3.16 Direct MR arthrography of triangular fibrocartilage (TFC) tears. Coronal (a) and axial (b) T1-weighted spinecho fat-suppressed images showing ulnar avulsion of the TFC complex, manifest as hyperintense contrast medium between the TFC and the ulnar styoild (arrowhead a) and leak of contrast medium proximal to the ulnar styloid (arrows). The disc is intact.

Pathology of the distal ulna

PATHOLOGY OF THE DISTAL ULNA Ulnar impaction syndrome6,12,22,24 ●

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ulnar impaction syndrome is also known as ulnar abutment or ulnocarpal loading and is a degenerative condition most commonly occurring with positive ulnar variance, though it is occasionally seen in the setting of neutral or negative ulnar variance the commonest predisposing factors include congenital positive ulnar variance, and secondary positive ulnar variance due to: ■ distal radial fracture, premature closure of the distal radial physis or previous radial head resection clinically, it manifests with ulnar-side wrist pain, swelling and limitation of movement MRI may be useful in establishing the diagnosis when radiographs are normal

MRI findings ● early: fibrillation of the ulnar head and the ulnar carpus cartilage is seen ● bone hyperaemia manifests as marrow oedema in the ulnar head, the ulnar aspect of the lunate (Fig. 3.17a) and the adjacent triquetrum that may resolve following ulnar shortening

b a

d c Figure 3.17 Ulnar abutment. Coronal T1-weighted (T1W) spin-echo (SE) image (a) showing oedema and sclerosis of the ulnar side of the lunate (arrow). Coronal T2*-weighted gradient-echo image (b) showing degenerative change in the triangular fibrocartilage (TFC), lunate chondromalacia (arrow) and cyst formation in the lunate (arrowhead). Coronal T1W SE (c) and short tau inversion recovery (d) images showing oedema in the ulnar head and lunate, subchondral cyst in the lunate (arrow) and a degenerative tear of the TFC (arrowhead).

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progression to marrow sclerosis and subchondral cystic change (Fig. 3.17b–d) degenerative tear of the TFC complex (Fig. 3.17d) end-stage: rupture of the LTL

Ulnar impingement syndrome22,24 ● ●

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ulnar impingement syndrome is caused by a short distal ulna that impinges on the distal radius proximal to the sigmoid notch a short ulna is most commonly due to surgical resection of the distal ulna: ■ other causes include negative ulnar variance and post-traumatic premature fusion of the distal ulnar physis clinically, it manifests as ulnar-side wrist pain that is exacerbated by forearm supination and pronation

MRI findings ● a short ulna is seen with impingement against the distal radius proximal to the sigmoid notch ● characteristic scalloping of the ulnar side of the distal radial metaphysis ● shortening of the ulna may result in secondary deformity of the TFC complex

Ulnocarpal impaction syndrome secondary to ulnar styloid non-union22,24 ● ●

●

ulnar styloid fractures may be isolated or more commonly associated with distal radial fracture symptomatic non-union of the ulnar styloid may result from: ■ loose body formation with irritation of the proximal ulnar side of the carpus ■ impingement of the ECU tendon or TFC complex injury two types of ulnar styloid non-union are described: ■ type 1 non-union – affecting only the tip of the styloid process, leaving the DRUJ and TFC complex intact ■ type 2 non-union – associated with subluxation of the DRUJ and ulnar avulsion of the TFC complex (Palmer type 1B lesion)

MRI findings ● ●

a non-united ulnar styloid fragment chondromalacia of the ulnar carpus, with associated TFC complex and DRUJ injuries

Ulnar styloid impaction syndrome5,22,24 ● ●

ulnar styloid impaction syndrome is ulnar-sided wrist pain due to impaction between an excessively long ulnar styloid (>6 mm) and the adjacent triquetrum pathologically, single or repetitive trauma results in bone contusion, chondromalacia and synovitis: ■ a single traumatic event may result in dorsal triquetral fracture, while chronic impaction may produce lunotriquetral instability

MRI findings there is a prominent ulnar styloid ● chondromalacia of the ulnar styloid and adjacent triquetrum, with associated marrow oedema ● LTL tear ●

THE CARPUS THE BONES AND JOINTS Normal anatomy10,27 ● ●

the carpus comprises two rows of four bones each the proximal row comprises the scaphoid, lunate, triquetrum and pisiform (Fig. 3.18a, b)

The carpus

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a

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Figure 3.18 Anatomy of the carpal bones. Proximal carpal row: Coronal (a) and axial (b) proton density-weighted (PDW) fast spin-echo (FSE) images showing the scaphoid (Sc), lunate (Lu), triquetral (Tr) and pisiform (Pi). Distal carpal row: Coronal PDW FSE (c) and axial T2*-weighted gradient-echo (d) images showing the trapezium (Tr), trapezoid (T), capitate (Ca) and hamate (Ha).

the distal row comprises the trapezium, trapezoid, capitate and hamate (Fig. 3.18c, d) three smooth arcs are described with normal radiocarpal and intercarpal alignment: ■ 1 – the proximal articular margins of the proximal carpal row ■ 2 – the distal articular margins of the proximal carpal row ■ 3 – the proximal articular margins of the distal carpal row disruption of these arcs is seen with ligament rupture and carpal instability the two carpal rows are separated by the mid-carpal joint, which comprises three compartments: ■ laterally, the scaphotrapezoid-trapezial (triscaphe) and scaphocapitate ■ centrally, the capitolunate ■ medially, the hamatotriquetral the central column of the wrist comprises the lunate and capitate: ■ with normal alignment, in the sagittal plane, a line can be drawn through the long axis of the distal radius, lunate, the capitate and the third MC (Fig. 3.19a) the lunocapitate angle is measured on sagittal images; it is formed by the intersection of a line drawn along the long axis of the lunate and a line drawn along the long axis of the capitate, the normal angle being 3 mm) ■ stage IV – as stage III, with associated secondary OA SLAC represents the end-stage of scapholunate instability and is classified into four stages: ■ stage 1 – isolated OA between the radial styloid and scaphoid ■ stage 2 – progression to radioscaphoid OA ■ stage 3 – mid-carpal OA at the capitolunate joint, with proximal migration of the capitate into the widened scapholunate gap and reduced carpal height ■ stage 4 – pan-carpal OA

MRI findings ● the features of an SLL tear are seen (Fig. 3.32)

The carpus

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sagittal images show abnormal alignment of the radius, lunate and capitate: ■ dorsiflexion of the lunate and proximal displacement of the capitate (Fig. 3.34a) with volar rotation of the scaphoid (rotatory subluxation) (Fig. 3.34b) ■ abnormal scapholunate (>70°; normal 30–60°) and capitolunate (>30°; normal 0–30°) angles coronal images:43 normally, the most volar portion of the lunate is seen two to three slices posterior to the proximal pole of the scaphoid: ■ in DISI, volar slide of the lunate on the radial articular surface results in the volar surface being identified before or at the same time as the proximal pole of the scaphoid (Fig. 3.34c), apparent enlargement of the lunate and associated ulnar slide of the bone with increased scapholunate distance (Fig. 3.34d) dorsal tilt of the lunate may be simulated on MRI mimicking the DISI configuration, depending on wrist position44 (Fig. 3.35): ■ in the neutral position, the mean capitolunate, scapholunate and radiolunate MR angles are approximately 14°, 7° and 19° larger than measurements from lateral radiographs

a

c

b

d

Figure 3.34 Dorsal intercalated segment instability. Sagittal T1-weighted (T1W) spin-echo (SE) images through the lunate (a) and scaphoid (b) showing dorsal tilt of the lunate (radiolunate angle 23°) and volar flexion of the scaphoid (radioscaphoid angle 68°). The scapholunate angle measures 91°. Coronal T1W SE image (c) through the volar aspect of the wrist showing the volar surface of the lunate (arrow) appearing at the same time as the proximal pole of the scaphoid (arrowhead). Coronal T1W SE image (d) showing ulnar slide of the lunate (arrow) and increased scapholunate distance (arrowhead).

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a

Figure 3.35 Simulated dorsal intercalated segment instability. Coronal T1-weighted scout image (a) showing the wrist imaged in ulnar deviation. Sagittal T2*-weighted gradient-echo image (b) showing the resulting dorsal tilt of the lunate.

■ ■

b

with 15° ulnar deviation, the mean capitolunate, scapholunate and radiolunate MR angles are approximately 32°, 17° and 37° larger than measurements from lateral radiographs with 15° radial deviation, measurements on MR and radiographs are equivalent

Lunotriquetral dissociation13,27 ●

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●

LTD has a variable aetiology and may be associated with the latter stages of perilunate instability, resulting from tears of the LTL and secondary stabilisers, or the latter stages (IID and IIE) of ulnocarpal impaction clinically, it presents with ulnar-side wrist pain and a motion-associated click LTD results in volar flexion and slight dorsal translation of the lunate, with associated mild volar shift of the distal carpal row: ■ this results in the VISI pattern of instability ■ the volar flexion of the lunate results in reduction of the scapholunate angle LTD may be staged in a similar way to SLD, eventually resulting in mid-carpal OA (stage IV)

MRI findings ● sagittal images show volar tilt of the lunate and increased capitolunate angle (Fig. 3.36a) with an abnormal scapholunate angle (2 mm and radiolunate contact of 3 at the hook of hamate is indicative of CTS bowing of the flexor retinaculum, secondary to increased pressure or volume within the CT, is optimally evaluated at the level of the hook of hamate, where the retinaculum should be straight (Fig. 3.46b) or slightly convex (Fig. 3.48d): ■ bowing is assessed by dividing the palmar displacement of the flexor retinaculum by the distance between the hook of hamate and the tubercle of the trapezium (Fig. 3.48e) ■ the normal bowing ratio is 0–0.15 (mean: 0.05), while in CTS the bowing ratio is 0.14–0.26 (mean: 0.18), which is possibly one of the most specific signs of CTS causes of median nerve compression include nerve sheath tumours, fibrolipomatous hamartoma, ganglion cyst, fracture, OA and flexor tenosynovitis (Fig. 3.44a–d) occasionally, muscle oedema and atrophy are seen ■

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Figure 3.48 Carpal tunnel syndrome. Axial T2-weighted fast spin-echo (FSE) image (a) showing hyperintensity of the median nerve (arrow). Flattening ratio (FR) of the median nerve: Axial proton density-weighted (PDW) FSE images at the level of the distal radioulnar joint (b) and the hook of hamate (c) showing measurement of the FR. Flexor retinacular bowing: Axial T2*-weighted gradient-echo image (d) showing the normal slightly convex flexor retinaculum (arrowheads). Axial PDW FSE image (e) showing measurement of flexor retinaculum bowing.

The nerves

Fibrolipomatous hamartoma58 ● ● ●

fibrolipomatous hamartoma is now termed ‘lipomatosis of nerve’ and most commonly involves the median nerve pathologically, it comprises increased fatty tissue interspersed between thickened nerve bundles, with endoneural and perineural fibrosis clinically, lipomatosis of nerve presents as swelling with/without symptoms of neural compression; 27–66 per cent of individuals have macrodactyly of the involved region, which if present at birth is termed ‘macrodystrophia lipomatosa’

MRI findings ● serpiginous low SI structures are seen representing thickened nerve fascicles (Fig. 3.49a, b) ● the surrounding fat is evenly distributed between the nerve fascicles, appearing hyperintense on T1W (Fig. 3.49a, b) and hypointense on STIR (Fig. 3.49c)

a

b

c

Figure 3.49 Lipomatosis of the median nerve. Axial (a) and coronal T1-weighted spin-echo (b) and short tau inversion recovery (c) images showing fatty infiltration and enlargement of the median nerve (arrows).

THE ULNAR NERVE Normal anatomy32,56,57 ● ●

●

the ulnar nerve, together with the ulnar artery, runs within Guyon’s canal (the ulnar tunnel) Guyon’s canal is located superficial and to the ulnar side of the flexor retinaculum, though its position is dependent on wrist position: ■ with the hand in a neutral position, the ulnar nerve usually lies medial to the hook of hamate (the hamulus) ■ however, its position may vary from a point 7 mm ulnar to the hamulus to a point 2 mm radial to the hamulus ■ flexion and extension of the wrist induce ulnar and radial displacement of the nerve, respectively the canal is approximately 1.5 cm long and has the following boundaries: ■ anterior: the superficial transverse (volar) carpal ligament (Fig. 3.50a) ■ posterior: the deep transverse carpal ligament (flexor retinaculum) (Fig. 3.50b)

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c

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Figure 3.50 Anatomy of Guyon’s canal and the ulnar nerve. Axial proton density-weighted (PDW) fast spin-echo (FSE) image (a) showing the superficial transverse carpal ligament (arrowhead) overlying the ulnar artery (short arrow) and ulnar nerve (long arrow). Axial PDW FSE image (b) showing the deep transverse carpal ligament (white arrow) posterior to the ulnar artery (short black arrow) and ulnar nerve (long black arrow) and the pisiform bone (Pi). Axial PDW FSE image (c) showing the hook of hamate (arrowhead) lying posterolateral to the ulnar artery (short arrow) and ulnar nerve (long arrow).

medial: the pisiform bone and pisohamate ligament (Fig. 3.50b) posterolateral and distal: the hook of hamate (Fig. 3.50c) the canal is divided longitudinally into three zones, related to the bifurcation of the ulnar nerve: ■ zone 1 – just before the bifurcation of the nerve, the area being triangular with a mean width of 11 mm and a mean depth of 7 mm ■ zone 2 – contains the deep motor branch at the pisohamate hiatus (between the pisiform and hamate bones), an area that measures ~13 mm by ~4 mm ■ zone 3 – lies distally and contains the sensory branch only proximal to Guyon’s canal, the nerve provides sensory innervation to the dorsal ulnar head and the hypothenar eminence within Guyon’s canal, the nerve divides into superficial sensory and deep motor branches (in 77 per cent of cases) the superficial branch supplies: ■ the palmaris brevis muscle, a thin subcutaneous muscle that arises from the flexor retinaculum and palmar aponeurosis and inserts into the skin on the ulnar side of the hand ■ sensation to the little finger and the ulnar half of the ring finger the deep motor branch curves laterally around the hook of hamate and passes under a fibrotendinous arch (the pisohamate hiatus) to innervate the hypothenar muscles (Fig. 3.51a, b), the adductor pollicis (Fig. 3.51c), the third and fourth lumbricals and all of the interossei less commonly, the nerve bifurcates into radial and ulnar trunks, or trifurcates the hypothenar muscles include: ■ the ADM, which usually has two bellies, originating from the pisiform, the FCU tendon and the pisometacarpal and pisohamate ligaments and inserting into the ulnar side of the base of the fifth PP and the adjacent extensor mechanism (Fig. 3.51a, b) ■ the flexor digiti minimi brevis originates from the hamulus, the adjacent flexor retinaculum and the radial part of the pisiform and inserts with the ADM (Fig. 3.51a, b) ■ the opponens digiti minimi has two layers, superficial (originating from the hamulus and inserting into the ulnar side of the distal fifth MC shaft) and deep (originating from the ulnar aspect of the flexor retinaculum and inserting into the ulnar side of the proximal fifth MC shaft) (Fig. 3.51a, b) ■

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The nerves

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Figure 3.51 Anatomy of the hypothenar eminence. Axial (a) and coronal (b) proton density-weighted (PDW) fast spin-echo (FSE) images showing the abductor digiti minimi (short arrow) originating from the pisiform (black arrowhead b), the flexor digiti minimi brevis (double arrowheads) and the opponens digiti minimi (long arrow). Axial PDW FSE image (c) showing the transverse head of the adductor pollicis muscle (arrow).

the adductor pollicis has two heads, the oblique and the transverse: ■ the oblique head originates from the volar surfaces of the second and third MC bases and adjacent carpal bones ■ the transverse head originates from the volar surface of the third MC shaft ■ both insert into the medial side of the base of the thumb PP, together with the first palmar interosseous muscle muscle variants are present in Guyon’s canal in 22–35 per cent of individuals: ■ most commonly, accessory ADM muscles (see above) ■ also recognised are accessory palmaris muscles, anomalous flexor digiti minimi muscles and duplicate tendons of the FCU accompanied by splitting of the ulnar nerve ■ bilateral muscle variants are seen in ~50 per cent of cases

PATHOLOGY OF THE ULNAR NERVE Ulnar tunnel syndrome32,56,57 ●

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ulnar tunnel syndrome represents a compressive neuropathy of the ulnar nerve within Guyon’s canal and commonly affects those taking part in sports such as cycling (handlebar palsy), martial arts and racket sports: ■ it may also affect workers using vibrating tools or may be due to mass lesions in the ulnar tunnel ■ other causes include fracture of the hook of hamate, pisotriquetral OA, an os hamuli proprium (bipartite hamulus), dislocation of the pisiform, and systemic conditions as for CTS clinically, presentation is dependent on the site of compression; three different zones are described within the canal: ■ zone 1 – compression just proximal to or within the canal before the bifurcation of the nerve; results in combined motor and sensory deficit ■ zone 2 – compression of the deep motor branch at the pisohamate hiatus; results in motor weakness ■ zone 3 – compression of the sensory branch only at the distal end of the canal (least common site); results in sensory deficit affecting the palmar aspect of the hand only

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MRI findings ● the findings are of the cause of compression, including: ■ anomalous muscles ■ mass lesions and ganglia (Fig. 3.52a, b) ● muscle oedema (Fig. 3.52a) and atrophy of the denervated muscles

b a Figure 3.52 Pathology of the ulnar nerve. Coronal T2*-weighted gradient-echo (a) and axial T2-weighted fast spin-echo (b) images showing a ganglion cyst (arrows) in Guyon’s canal and mild denervation oedema of the hypothenar muscles (arrowhead a).

THE CARPOMETACARPAL JOINTS THE THUMB CARPOMETACARPAL JOINT Normal anatomy59 ● ● ●

the first carpometacarpal (CMC) joint comprises the articulation between the distal surface of the trapezium and the base of the first MC the joint is stabilised by a combination of ligaments, surrounded by tendons and the thenar muscles four main ligaments contribute to first CMC joint stability: ■ the anterior oblique ligament is a short, thick band running from the palmar tubercle of the trapezium to the base of the thumb MC (Fig. 3.53a) with superficial and deep (intra-articular) components ■ the dorsal radial ligament arises from the dorsoradial aspect of the trapezium and inserts onto the adjacent portion of the thumb MC base (Fig. 3.53b), being reinforced by the APL tendon ■ the posterior oblique ligament runs from the dorsoulnar tubercle of the trapezium to the ulnar tubercle of the thumb MC base ■ the intermetacarpal (IMC) ligament runs from the ulnar aspect of the thumb MC to the radial aspect of the base of the index finger MC (Fig. 3.53c)

PATHOLOGY OF THE FIRST CARPOMETACARPAL JOINT Trauma59 ● ● ●

acute injury to the first CMC joint usually occurs following an axial load with flexion of the thumb MC resulting in dorsal dislocation, following a direct blow, or associated with a fracture to the base of the MC clinically, it presents with pain and focal tenderness deep to the thenar eminence MRI can demonstrate ligament injury

The carpometacarpal joints

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c

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Figure 3.53 Anatomy of the thumb carpometacarpal joint. Sagittal proton density-weighted fast spin-echo image (a) showing the anterior oblique ligament (arrow). Coronal T2*-weighted (T2*W) gradient-echo (GE) image (b) showing the dorsal radial ligament (arrow) supported by the tendon of the abductor pollicis longus (arrowhead). Coronal T2*W GE image (c) showing the intermetacarpal ligament (arrow). MC, metacarpal; Tr, trapezium.

MRI findings ● MRI most commonly shows injury to the superficial anterior oblique ligament (~90 per cent of cases), typically at or adjacent to the distal insertion: ■ tears may be partial or complete, with/without stripping of the periosteum from the thumb MC base ● dorsal radial ligament injury occurs in ~80 per cent of cases, usually from the proximal aspect ● additional features: bone marrow oedema on either side of the joint and soft-tissue haematoma ● chronic ligament injury manifests as laxity and thickening of the involved ligaments and may be associated with OA of the joint, manifest as joint space loss, marginal osteophytes, subchondral sclerosis and cyst formation

THE SECOND TO FIFTH CARPOMETACARPAL AND INTERMETACARPAL JOINTS Normal anatomy60 ●

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the CMC articulations are formed between the distal surfaces of the trapezoid, capitate and hamate with the adjacent bases of the index, middle, ring and little finger MCs: ■ trapezoid with index finger MC, capitate with middle finger MC, and hamate with ring and little finger MCs ■ an additional articulation between the capitate and the ring finger MC base is commonly present the CMC joints are supported by an assortment of ligaments and tendons

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six CMC ligaments: ■ the dorsal common CMC ligaments extend from the dorsal aspects of the distal-row carpal bones to the dorsal aspects of the bases of the index to little finger MCs; thick bands optimally demonstrated on sagittal MR images (Fig. 3.54a) ■ the palmar common CMC ligaments extend from the palmar aspects of the distal-row carpal bones to the palmar aspects of the bases of the index to little finger MCs (Fig. 3.54a); not routinely seen on MRI since they are very thin structures ■ the pisometacarpal ligament extends from the dorsal aspect of the pisiform to the bases of the dorsal aspects of the ring and little finger MCs; routinely demonstrated on sagittal (Fig. 3.23a) and axial (Fig. 3.54b) images running on the ulnar side of the hook of hamate ■ the RCL extends from the dorsoradial aspect of the trapezoid to the dorsoradial aspect of the index finger MC ■ the capito-third ligament extends from the ulnar side of the capitate to the ulnar side of the middle finger MC (Fig. 3.54c) ■ the UCL extends from the dorsoulnar aspect of the hamate to the dorsoulnar aspect of the little finger MC the RCL, capito-third ligament and UCL are consistently visualised on coronal MR images

a b

d c Figure 3.54 Anatomy of the carpometacarpal (CMC) joints. Sagittal T2*-weighted (T2*W) gradient-echo (GE) image (a) showing the dorsal (arrow) and volar (arrowhead) common CMC ligaments between the capitate (C) and the base of the third metacarpal (MC). Axial T2*W GE image (b) showing the pisometacarpal ligament (arrow) running adjacent to the hook of hamate (HH). Coronal T2*W GE image (c) showing the capito-third ligament (arrow) running between the capitate (C) and the third MC base. Axial T2*W GE image (d) showing the dorsal (arrows) and volar (arrowheads) intermetacarpal ligaments.

The carpometacarpal joints

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three IMC ligaments: ■ the IMC ligament: a thin structure extending between the dorsal aspect of the index to the little finger MC, commonly visualised on axial images (Fig. 3.54d) ■ the palmar IMC ligament: a thin structure extending between the palmar aspect of the index to the little finger MC, commonly visualised on axial images (Fig. 3.54d) ■ the interosseous IMC ligament: comprises anterior and posterior bands linking the bases of the MCs, commonly visualised on axial images tendons: comprise four insertions into the MC bases: ■ the FCR longus (Fig. 3.55a) and ECRL (Fig. 3.55b) tendons into the palmar and dorsal base of the index finger MC, respectively ■ the ECRB into the base of the middle finger MC ■ the ECU into the base of the little finger MC (Fig. 3.55c)

PATHOLOGY OF THE SECOND TO FIFTH CARPOMETACARPAL AND INTERMETACARPAL JOINTS Trauma60 ● ● ● ●

a

injury to the CMC and IMC joints is usually due to large torsional forces applied to the hand CMC joint dislocations most commonly result in dorsal displacement of the MCs and most commonly involve the little finger, followed by the index, middle and ring fingers they may be radiographically subtle MRI findings of ligament injuries are not yet described in the literature

b

c

Figure 3.55 Anatomy of the carpometacarpal joints. Sagittal T2*-weighted (T2*W) gradient-echo (GE) image (a) showing the flexor carpi radialis longus tendon (arrows). Sagittal T2*W GE image (b) showing the extensor carpi radialis longus tendon (arrows). Coronal T2*W GE image (c) showing the extensor carpi ulnaris tendon (arrow).

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THE METACARPOPHALANGEAL JOINTS Normal anatomy45,46,48,49,61 ● ●

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the MCP joints are unicondylar joints, which allow a degree of rotation and radial/ulnar deviation as well as flexion/extension the joint capsule is attached proximally to an elevated crest surrounding the head of the MC and distally to a ridge separating the concave articular surface of the PP from the shaft of the PP: ■ it is optimally demonstrated on sagittal MR images in the presence of effusion or on direct MR arthrography the collateral ligaments are situated on the radial (RCL) and ulnar (UCL) sides of each MCP joint and blend with and reinforce the capsule: ■ they comprise two bands, the main (proper) collateral ligaments and the accessory collateral ligaments ■ the main collateral ligaments arise in a depression on the radial and ulnar sides of the MC head and insert on the base of the PP; they are optimally demonstrated on axial MR images with the joint flexed or on coronal images with the joint extended (Fig. 3.56a) ■ the accessory collateral ligaments arise in a slightly more palmar location than the main collateral ligaments and insert into the base of the PP; they are optimally visualised on axial images with the joint extended (Fig. 3.56b) the palmar (volar) plate is a dense, fibrous structure lying on the palmar surface of the joint between the accessory collateral ligaments, to which it is fused (Fig. 3.56b); it is also attached firmly to the base of the PP: ■ a small joint recess is present between the distal palmar plate and its phalangeal attachment, optimally visualised on sagittal images (Fig. 3.56c) the deep transverse metacarpal (interglenoid) ligament (DTML) comprises thin, fibrous bands that connect the adjacent palmar plates: ■ the lumbrical muscles and the digital nerve and vessels are located on the palmar aspect of the DTML ■ the interosseous muscles and tendons are located on the dorsal aspect of the DTML ■ the DTML is optimally visualised on axial images with the joint extended (Fig. 3.56d) the extensor hood comprises the sagittal bands, the transverse fibres and the extensor muscles/tendons: ■ the sagittal bands are thin bands that extend from the common extensor tendon to the junction of the palmar plate and the DTML: – they run between the main collateral ligaments and the interosseous tendons and are demonstrated on axial images (Fig. 3.56d) ■ the transverse fibres form a triangular lamina distal to the sagittal bands and extend between the extensor and interosseous tendons; they are demonstrated on axial images with the joint extended (Fig. 3.56e) ■ the extensor muscles/tendons of the index and little fingers form part of the extensor hood of these digits muscles and tendons: ■ the digital flexor tendons comprise deep and superficial muscle tendons that extend across the joint: ■ the tendon sheath position in relation to the palmar plate is maintained by the A1 pulley, which is attached to the junction of the palmar plate and the DTML and is demonstrated on axial images with the joint extended (Fig. 3.56b) ■ the seven interosseous muscles and tendons comprise three palmar and four dorsal: – the palmar interossei originate from the second, fourth and fifth MCs and act to flex the MCP joints and extend the interphalangeal joints – the dorsal interossei originate from the adjacent MCs; the first and second lie on the radial sides of the second and third MCs, the third and fourth lie on the ulnar sides of the third and fourth MCs, and all act to abduct the fingers, flex the MCP joints and extend the interphalangeal joints

The metacarpophalangeal joints

a

b

c

d

e Figure 3.56 Anatomy of the metacarpophalangeal (MCP) joints. Coronal proton density-weighted (PDW) fast spin-echo (FSE) fat-suppressed (FS) image (a) showing the main collateral ligaments (arrowheads) and the interosseous tendons (arrows). Axial PDW FSE FS image (b) showing the extensor tendon (white arrowhead), the flexor tendon (black arrowhead), the accessory collateral ligaments (black arrows), the volar plate (large white arrow) and the A1 pulley (small white arrow). Sagittal PDW FSE FS image (c) showing the volar plate (long arrow), the extensor tendon (short arrow) and the flexor tendons (arrowheads). MP, middle phalanx; PP proximal phalanx. Axial PDW FSE FS image (d) showing the sagittal bands (white arrows), the interosseous tendons (white arrowheads) and the deep transverse metacarpal ligament (black arrowheads). Axial PDW FSE FS image (e) just distal to the MCP joint showing the transverse fibres (arrowheads) attached to the extensor tendon (arrow).

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– the interossei lie dorsal to the DTML and insert into the PP and extensor hood; they are demonstrated on axial and coronal images with the joint extended (Fig. 3.57a, b) the four lumbrical muscles originate from the deep flexor muscles/tendons at the level of the midpalmar region and lie palmar to the DTML, running on the radial side of the corresponding MCP joint to insert into the distal extensor mechanism – they act as flexors of the MCP joints and extensors of the interphalangeal joints and are demonstrated on axial images (Fig. 3.57a)

a

b Figure 3.57 Anatomy of the intrinsic muscles of the hand. Axial proton density-weighted (PDW) fast spin-echo (FSE) image (a) showing the interosseous (arrows) and lumbrical (arrowheads) muscles. Coronal PDW FSE image (b) showing the dorsal interossei (arrows).

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additional anatomical findings in the first MCP joint include: ■ a strong tendinous insertion of the adductor pollicis into the base of the PP and the volarplate/sesamoid complex (Fig. 3.58a) ■ some fibres of the APL contribute to the adductor aponeurosis, which covers the UCL (Fig. 3.58b)

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Figure 3.58 Anatomy of the first metacarpophalangeal joint. Coronal T2*-weighted gradient-echo image (a) showing the ulnar collateral ligament (UCL) (short arrow), the radial collateral ligament (long arrow) and the insertion of the abductor pollicis longus (arrowhead). Coronal proton density-weighted fast spin-echo (b) image showing the UCL (arrow) lying deep to the adductor aponeurosis (arrowhead).

The metacarpophalangeal joints

PATHOLOGY OF THE METACARPOPHALANGEAL JOINTS AND INTRINSIC MUSCLES Trauma45,46 ●

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dislocation of the MCP joint is an uncommon injury that results from forced hyperextension resulting in dorsal displacement and may be classified as simple or complex: ■ in simple injuries, the volar plate is not interposed within the joint and treatment is conservative ■ in complex injuries, interposition of the volar plate may prevent reduction of the joint and treatment is surgical in the setting of chronic joint pain/disability,62 the commonest injury demonstrated is to the collateral ligaments, usually on the radial side and optimally visualised on contrast-enhanced axial T1W images with the fingers flexed: ■ associated lesions include injury to the extensor hood, interosseous tendon, volar plate and, rarely, an osteochondral lesion gamekeeper’s thumb12,63 is an injury to the first MCP joint UCL that is commonly caused by skiing accidents (skier’s thumb): ■ it results from violent hyperabduction of the thumb MCP joint, which results in partial or complete rupture of the UCL, usually from its distal attachment, with/without associated bony avulsion ■ following complete UCL rupture, the UCL may remain deep to the adductor aponeurosis and retraction may be minimal ■ alternatively, severe retraction of the UCL may result in interposition of the adductor aponeurosis and a superficial location of the UCL (Stener lesion), which requires surgical management

MRI findings ● MCP dislocation: MRI demonstrates the integrity and location of the volar plate ● a collateral ligament tear may be seen with a lateral/medial deviation injury and MCP flexion (Fig. 3.59a, b) ● gamekeeper’s thumb (Fig. 3.59c): ■ an undisplaced UCL tear appears as a discontinuity and thickening of an otherwise normally located ligament ■ in a displaced UCL tear, the UCL is retracted to the proximal margin of the adductor aponeurosis and appears as a rounded/stump-like low SI mass: – fluid is seen around the adductor aponeurosis and there may be soft-tissue oedema or haemorrhage, joint effusion and bone bruising ● MR arthrography is more sensitive and accurate in the demonstration of both acute and chronic UCL injuries63

Intrinsic muscles64 ● ●

disorders of the intrinsic muscles of the hands may be due to primary muscle disease, or more commonly secondary to nerve injury MRI may demonstrate the features of muscle injury, including: ■ denervation oedema or atrophy secondary to nerve injury, the pattern of muscle involvement indicating the site of the nerve damage

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Figure 3.59 Pathology of the metacarpophalangeal (MCP) joints. Coronal proton density-weighted fast spin-echo fatsuppressed image (a) showing a chronic injury to the second MCP joint radial collateral ligament (RCL) (arrow), which is thickened and hyperintense. Coronal T2*-weighted gradient-echo image (b) showing an injury of the thumb RCL (arrow) associated with a fracture of the proximal phalanx (arrowhead). Coronal short tau inversion recovery image (c) showing a rupture of the first MCP joint ulnar collateral ligament (arrow).

THE PROXIMAL INTERPHALANGEAL JOINTS Normal anatomy45,46,65 ● ● ●

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the PIP joint is a bicondylar hinge joint stabilised by surrounding soft tissues, particularly the collateral ligaments and the volar plate dynamic stability is maintained by the extensor mechanism, the flexor tendons and the retinacular ligaments the collateral ligament complex comprises the collateral ligament proper and the accessory collateral ligament: ■ the collateral ligament proper arises at the dorsolateral aspect of the PP head and inserts at the volar and lateral aspects of the base of the middle phalanx ■ the accessory collateral ligament arises at the same site as the collateral ligament proper and inserts into the volar plate ■ the collateral ligament complex is optimally visualised on coronal images (Fig. 3.60a) the volar plate is a thick, fibrocartilaginous structure that forms the palmar aspect of the PIP joint capsule; it is attached to the PP by two lateral bands called the checkrein ligaments and extends distally to attach firmly to the volar aspect of the middle phalanx: ■ it prevents hyperextension of the PIP joint and is optimally visualised on sagittal images (Fig. 3.60b) the extensor apparatus (Fig. 3.60b, c) provides dorsal stability to the PIP joint and comprises a central slip that inserts onto the dorsal tubercle of the middle phalanx, and medial and lateral slips that are connected by the retinacular ligaments

The proximal interphalangeal joints

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c

Figure 3.60 Anatomy of the proximal interphalangeal (PIP) joint. Coronal proton density-weighted (PDW) fast spin-echo (FSE) fat-suppressed (FS) image (a) showing the collateral ligament complex of the PIP joint (arrowheads). Sagittal PDW FSE FS image (b) showing the volar plate (arrow), the flexor tendons (double arrowhead) and the insertion of the central slip onto the dorsum of the middle phalanx (arrowhead). Axial PDW FSE FS image (c) showing the central slip (arrow) and the lateral/medial slips (arrowheads).

PATHOLOGY OF THE PROXIMAL INTERPHALANGEAL JOINTS Trauma45,46 ● ●

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the PIP joint is the most commonly injured joint in the hand; injury results in coronal or sagittal instability coronal instability occurs following abduction or adduction forces on the extended joint; three patterns of injury are described: ■ ligament sprain, partial ligament tear or complete ligament tear ■ complete ligament tears are usually associated with complete or partial avulsion of the volar plate from the middle phalanx ■ MRI findings: – discontinuity, detachment or thickening of the ligament with increased T2W SI, peri-articular oedema and swelling sagittal instability occurs following hyperextension or rotational axial compression of the joint: ■ hyperextension lesions are divided into three types: – type 1 – avulsion of the volar plate from the base of the middle phalanx, or less commonly from its proximal attachment, resulting in hyperextension or pseudo-boutonnière deformity, respectively

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– type 2 – volar plate injury plus injury to the collateral ligament complex resulting in dorsal subluxation of the middle phalanx – type 3 – fracture-dislocation of the volar base of the middle phalanx resulting in a stable injury (40 per cent of the articular surface involved) with resulting dorsal subluxation; the latter requires open reduction and internal fixation compression–rotation injury of the semi-flexed PIP results in volar subluxation of the middle phalanx with unilateral disruption of the collateral ligament and partial/complete disruption of the volar plate: – there may be an associated lesion of the extensor apparatus – if untreated, the injury may result in a chronic boutonnière deformity with PIP flexion and DIP extension MRI findings: – depend on the grade of the lesion – oedema and swelling of the volar plate with detachment and soft-tissue oedema – intra-articular fracture of the volar base of the middle phalanx and joint deformity

THE FINGER EXTENSOR TENDONS Normal anatomy45,46,49,65 ● ●

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the extensor tendons, at the level of the MCP joints, are stabilised over the dorsum of the MCs by the extensor hood distal to the MCP joints, the tendons of the extrinsic and intrinsic muscles fuse to form the dorsal apparatus, comprising the central slip and the medial/lateral slips (bands) (Fig. 3.60c): ■ the central slip inserts on the base of the middle phalanx (Fig. 3.60b) the fusion of fibres from the intrinsic tendons to the medial/lateral slips forms the conjoined tendons, which converge distally to form the terminal tendon, which inserts into the distal phalanx the extensor mechanism is optimally assessed on sagittal and axial MR images (Fig. 3.61)

a

Figure 3.61 Anatomy of the finger extensor mechanism. Axial T2*-weighted (T2*W) gradient-echo (GE) image (a) through the middle phalanx showing the conjoined tendons (arrowheads) and the triangular ligament (arrow). Sagittal T2*W GE image (b) showing the insertion of the terminal tendon into the dorsum of the distal phalanx (arrow).

b

Pathology of the finger extensor tendons

PATHOLOGY OF THE FINGER EXTENSOR TENDONS Trauma45,46,49 ● ●

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extensor tendon injury may be classified as open or closed open injuries are classified into eight zones (zone 1=DIP joint; zone 8=distal forearm): ■ odd-numbered zones correspond to articular areas; thus, injuries in these regions may be associated with articular disruption ■ laceration of the tendon in zone 1 results in a flexion deformity of the distal phalanx (open mallet deformity) ■ laceration of the central slip in zone 3 can result in boutonnière deformity (flexion of the PIP and hyperextension of the DIP) ■ injury in zone 5 may result in rupture of the extensor digitorum communis tendon and the sagittal bands, resulting in tendon subluxation/dislocation ■ MRI findings: – partial thickness tears appear as areas of increased SI in a portion of the tendon on T1W and T2W images – complete tears appear as an area of complete tendon disruption, fraying of the tendon ends and hyperintense fluid/haemorrhage within the gap closed injuries include mallet finger, boutonnière deformity and subluxation/dislocation of the extensor tendon: ■ mallet finger is usually due to acute, forced hyperflexion of the extended DIP joint and is associated with avulsion fracture of the dorsal base of the distal phalanx or disruption of the terminal extensor tendon without fracture: – clinically, it manifests as a flexion deformity of the DIP joint and, if left untreated, the injury may progress to a ‘swan neck’ deformity (hyperextension of the PIP joint)

a

b

c

Figure 3.62 Extensor tendon injury. Axial proton densityweighted fast spin-echo fat-suppressed image (a) showing tenosynovitis (arrows) of the extensor tendons at the metacarpophalangeal level. Sagittal (b) and axial (c) T2*-weighted gradient-echo images showing fluid around the displaced extensor mechanism (arrows) associated with an intra-articular fracture of the base of the middle phalanx (arrowhead b).

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boutonnière deformity occurs following a forced flexion injury to the extended PIP joint resulting in avulsion of the central slip into the middle phalanx subluxation/dislocation of the extensor tendon occurs secondary to rupture of the sagittal bands of the extensor hood, most commonly ulnar subluxation of the middle finger MRI findings: – tenosynovitis (Fig. 3.62a) – disruption and increased SI of the affected portion of the extensor mechanism (Fig. 3.62b, c)

THE FINGER FLEXOR TENDONS Normal anatomy46,47,49,65 ● ● ● ● ● ● ● ●

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the digital flexor tendons pass through the carpal tunnel before spreading out in the palm of the hand towards their respective fingers each finger has two flexor tendons, the FDS and the FDP (Fig. 3.63a, b) the FDS tendon splits at the distal MC, passes around the FDP tendon and reunites deep to the FDP tendon at the level of the PIP joint to insert into the mid-portion of the middle phalanx the FDP tendon inserts into the volar aspect of the distal phalanx from the MC neck to the distal phalanx, each tendon runs along a fibro-osseous canal within a synovial sheath the floor of the canal is formed by the volar aspect of the respective bone and the volar plate at each joint level the fibrous portion of the canal is formed by five annular pulleys (A1–5) and three cruciform pulleys (C1–3) the annular pulleys (Fig. 3.63c) are focal transverse thickenings of the tendon sheath: ■ A1 – spans the volar plate of the MCP joint to the PP base (Fig. 3.56b) ■ A2 – arises from the volar aspect of the PP base and extends to just proximal to the neck of the PP ■ A3 – located at the level of the PIP joint ■ A4 – located at the mid-portion of the middle phalanx ■ A5 – located at the level of the DIP the cruciform pulleys are crossing fibres between the annular pulleys: ■ C1 – located between A2 and A3 ■ C2 – located between A3 and A4 ■ C3 – located between A4 and A5 the pulley system functions to stabilise the flexor tendons during finger flexion

PATHOLOGY OF THE FINGER FLEXOR TENDONS Trauma46,47,49 ● ●

flexor tendon injuries may be classified as open or closed injuries, and injuries to the pulley system open injuries comprise lacerations most often involving the mid-substance of the tendon and are classified into five zones: ■ zone 1 – the distal insertion of the FDP to the distal insertion of the FDS ■ zone 2 – the distal insertion of the FDS to the distal palmar fold ■ zone 3 – the proximal part of the A1 pulley to the distal part of the flexor retinaculum ■ zone 4 – the carpal tunnel ■ zone 5 – the forearm proximal to the flexor retinaculum ■ the thumb has three zones: – T1 – extends from the A2 pulley to the FPL tendon insertion – T2 – extends between the A1 and A2 pulleys – T3 – extends between the distal wrist crease and the A1 pulley

Pathology of the finger flexor tendons

b

a

c

MRI findings: – partial or complete tendon disruption – complete disruptions may be associated with tendon retraction – associated findings include tenosynovitis (Fig. 3.64a–c), subluxation or dislocation of the tendon, and pulley lesions closed injuries include avulsions of the FDP and FDS tendons and are classified into four types: ■ type 1 – retraction of the tendon into the palm ■ type 2 – retraction of the tendon to the PIP joint ■ type 3 – avulsion of a bony fragment, which is held in place by the A4 pulley ■ type 4 – a type 3 lesion with additional avulsion of the FDP tendon from the bone fragment ■

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Figure 3.63 Anatomy of the finger flexor tendons. Sagittal T2*-weighted (T2*W) gradient-echo (GE) (a) and axial proton densityweighted fast spin-echo (b) images at the metacarpal level showing the flexor digitorum superficialis (short arrows) and flexor digitorum profundus (long arrows) tendons. Sagittal T2*W GE image (c) showing the location of the A2–5 pulleys.

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Figure 3.64 Flexor tenosynovitis. Sagittal short tau inversion recovery (a), axial T2-weighted fast spin-echo image at the metacarpal level (b) and axial T1-weighted spin-echo image at the middle phalanx level (c) showing effusion in the ring finger flexor tendon sheath (arrows b, c) and increased signal intensity within the flexor tendon (arrowhead b).

the commonest injury is termed ‘jersey finger’ and represents an avulsion of the FDS and FDP tendons from their respective insertions: – it is due to sudden hyperextension and usually involves the ring finger isolated avulsion of the FDS tendon is rare and is usually associated with FDP rupture MRI findings: – tendon disruption with/without retraction (Fig. 3.65a) – peri-tendinous oedema (Fig. 3.65b)

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b

Figure 3.65 Flexor tendon injury. Coronal T1-weighted spin-echo image (a) showing closed rupture of the index finger flexor tendon with minor retraction (arrow) in a patient with rheumatoid arthritis. Axial proton density-weighted fast spin-echo fat-suppressed image (b) showing oedema around the index finger flexor tendons (arrows).

Miscellaneous tumours and pseudotumours of the wrist and hand

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pulley injuries are particularly associated with activities such as rock climbing: ■ the injury begins at the distal aspect of the A2 pulley ■ complete rupture can extend to involve the A3 and A4 pulleys and, rarely, the A1 pulley ■ MRI findings: – displacement of the flexor tendon from the underlying phalanx (bow-stringing sign) shown on sagittal images obtained during forced flexion – axial images may show fluid/haemorrhage between the flexor tendon and underlying bone

MISCELLANEOUS TUMOURS AND PSEUDOTUMOURS OF THE WRIST AND HAND SURFACE LESIONS OF BONE Introduction66 ● ●

proliferative periosteal processes include florid reactive periostitis, bizarre parosteal osteochondromatous proliferation (BPOP), periostitis ossificans, turret exostosis and subungual exostosis they represent a related group of disorders that may have as a common precursor a focus of subperiosteal haemorrhage, the different lesions representing different stages of healing

Florid reactive periostitis66 ● ● ● ●

florid reactive periostitis is a rare, benign lesion most commonly affecting the small bones of the hands and feet it is also referred to as parosteal fasciitis, panniculitis ossificans, benign fibro-osseous pseudotumour, pseudomalignant osseous tumour of soft tissue, nodular fasciitis and pseudosarcomatous fibromatosis clinically, it usually presents in the second to third decades, with a history of trauma in 10–50 per cent of cases sites of involvement in decreasing order of frequency include the PP, the middle phalanx, the MC and the distal phalanx

MRI findings67 ● a soft-tissue para-osseous mass with a low SI rim and associated soft-tissue oedema, possibly with associated adjacent bone marrow oedema

Bizarre parosteal osteochondromatous proliferation66 ● ● ● ● ●

BPOP is also termed ‘Nora’s lesion’ and appears radiologically as a well-defined, calcified or ossified lesion arising from the cortex ~55 per cent of cases arise in the hand, usually involving the PP or middle phalanx clinically, it presents in the third to fourth decades as a painless, slowly enlarging swelling, usually without a history of trauma pathologically, BPOP is differentiated from an osteochondroma by the lack of continuity of the lesion with the medulla of the underlying bone most lesions are 0.5–3.0 cm in size

MRI findings ● a lobulated mass is seen arising on the surface of the bone, with SI characteristics depending on the degree of maturation and calcification/ossification of the lesion ● an immature lesion may show intermediate T1W SI (Fig. 3.66a), increased T2W/STIR SI (Fig. 3.66b, c) and enhancement following contrast (Fig. 3.66d) ● a heavily calcified BPOP typically has intermediate/low SI on all pulse sequences (Fig. 3.66e), whereas the presence of mature ossification results in central marrow SI (Fig. 3.66f) ● marrow invasion is not seen, though, rarely, cortical invasion and marrow and soft-tissue oedema may be present

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a

d

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e

f

Figure 3.66 Bizarre parosteal osteochondromatous proliferation. Immature: Axial T1-weighted (T1W) spin-echo (SE) image (a) showing an intermediate signal intensity (SI) mass (arrows) arising from the volar surface of the ring finger metacarpal (MC). Axial T2-weighted fast spin-echo (b) and short tau inversion recovery (c) images showing increased SI within the lesion (arrows). Axial post-contrast T1W SE image (d) showing heterogeneous enhancement (arrows). Mature: Coronal T2*-weighted gradient-echo image (e) showing reduced SI due to calcification (arrow). Coronal T1W SE image (f) showing a lesion (arrow) arising from the MC (arrowheads) with increased central SI due to marrow fat.

Periostitis ossificans66 ● ●

periostitis ossificans is rare in the hand and is similar to myositis ossificans, though occurring in a periosteal location radiologically, it is characterised by the typical peripheral zoning pattern of soft-tissue mineralisation

MRI findings ● soft-tissue and medullary oedema is seen (Fig. 3.67a, b) together with periosteal reaction (Fig. 3.67c) ● as the lesion progresses, the typical peripheral mineralisation may be demonstrated as a low SI ring (Fig. 3.67d)

Turret exostosis66 ● ●

turret exostosis is a rare complication of minor hand trauma that is thought to result from ossification of a subperiosteal haematoma, most commonly involving the middle phalanx or PP clinically, there is almost always a history of trauma, with progressive symptoms over the next few months

Miscellaneous tumours and pseudotumours of the wrist and hand

a b

d

c

Figure 3.67 Periostitis ossificans. Axial T1-weighted spin-echo (a) and coronal short tau inversion recovery (b) images showing both medullary (arrows) and soft-tissue (arrowheads b) oedema involving the little finger metacarpal. Sagittal T2*weighted (T2*W) gradient-echo (GE) image (c) showing irregular periosteal reaction (arrows). Axial T2*W GE image (d) showing a low signal intensity ring (arrows) due to peripheral mineralisation.

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radiologically, as with other post-traumatic lesions, there is initially soft-tissue swelling followed by slowly maturing juxta-cortical bone formation terminating in the development of a dome-shaped, ossified lesion

MRI findings ● these depend on the stage at which imaging is performed ● the mature lesion appears as a well-defined bony mass protruding from the cortex of the phalanx (Fig. 3.68a, b)

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a

Figure 3.68 Turret exostosis. Coronal (a) and axial (b) T1-weighted spin-echo images showing a turret exostosis (arrows) arising from the base of the little finger middle phalanx.

SOFT-TISSUE MASSES Introduction68,69 ● ●

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soft-tissue masses of the wrist, hand and fingers may be non-neoplastic, benign or a malignant neoplasm (least common) in a review of 134 consecutive soft-tissue masses of the hand and wrist:69 ■ 27 per cent were cysts (ganglion, synovial or peri-tendon) ■ 25 per cent were soft-tissue tumours (most commonly lipoma, haemangioma or giant cell tumour of tendon sheath [GCTTS]) ■ 23 per cent were non-neoplastic tendon disorders (most commonly involving the extensor tendons) ■ 6 per cent were secondary to inflammatory arthropathy (most commonly non-specific synovitis) ■ only two cases were sarcomas the MRI findings of common soft-tissue tumours are as described in Chapter 7

Dupuytren’s contracture68 ● ●

Dupuytren’s contracture represents a proliferation of fibrous tissue within the palmar aponeurosis of the hand, most commonly affecting the fourth ray clinically, patients usually present in the sixth to seventh decades with nodules in the distal palm crease that eventually progress to flexion contractures

MRI findings ● hypointense fibrous nodules or cords arise from the palmar aponeurosis, extending distally and superficially parallel to the flexor tendons ● the cords terminate in the superficial tissues at the level of the distal MC ● highly cellular lesions may be relatively hyperintense on T2W images

Giant cell tumour of tendon sheath65,66,70 ● ● ●

GCTTS represents the localised, nodular form of extra-articular pigmented villonodular synovitis and is the second commonest soft-tissue mass of the wrist and hand, after ganglion cyst 67 per cent of all cases of GCTTS occur in this region clinically, it usually presents as a slowly growing, painless mass in the third to fourth decades, with a slight female predominance

Miscellaneous tumours and pseudotumours of the wrist and hand

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pathologically, the lesion more commonly occurs on the volar aspect of the first three digits, though lateral and circumferential locations are also reported, as is multifocal disease: ■ GCTTS arises from the synovium of the tendon sheaths, the small joints or the bursae of the hand and is typically a multilobular mass surrounded by a collagenous capsule

MRI findings ● pressure erosion of the underlying bone is reported in 23 per cent of cases (Fig. 3.69a, b); the lesion may present radiologically as an intraosseous lesion71 that expands the bone in 11 per cent of cases ● the tumour is round or oval and is located eccentrically to the tendon, or partially or completely encasing the tendon (Fig. 3.69c, d) ● GCTTS typically has intermediate T1W SI (Fig. 3.69e), variable T2W SI depending on the degree of cellularity (Fig. 3.69d) and increased SI on STIR (Fig. 3.69f)

a

b

c

Figure 3.69 Giant cell tumour of tendon sheath. Coronal T1-weighted (T1W) spin-echo (SE) image (a) showing an intermediate signal intensity (SI) mass (arrow) causing marked erosion of the adjacent thumb metacarpal (MC) (arrowhead). Sagittal (b) and axial (c) T1W SE images showing a lobulated mass (arrows) arising from and surrounding the flexor tendon (arrowhead c) and resulting in pressure erosion of the underlying MC (arrowhead b). Sagittal T2-weighted fast spin-echo fat-suppressed image (d) showing a mass with areas of both low/intermediate SI (arrow) and high SI (arrowhead). (continued)

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The wrist and hand

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g

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f

Figure 3.69 (continued) Coronal T1W SE (e), short tau inversion recovery (f) and T2*-weighted gradient-echo (GE) (g) images showing a lesion (arrows) arising from the flexor carpi ulnaris tendon with areas of low SI that are most prominent on the GE sequence (arrowheads g).

areas of low SI are commonly identified, most prominently on T2*W GE images (Fig. 3.69g) enhancement is seen following contrast MRI has been used for pre-operative staging of GCTTS72

Glomus tumour68 ● ● ●

glomus tumours are small hamartomas of the neuromyoarterial apparatus of the glomus body and account for ~5 per cent of soft-tissue tumours of the hand they are most commonly located at the finger tip, either in the pulp space or under the nail clinically, they most commonly present in the fourth to fifth decades as exquisitely painful lesions with symptoms that are affected by changes in temperature: ■ disappearance of pain following application of a tourniquet proximally is diagnostic (the Hildreth sign)

MRI findings ● if the lesion is large enough, it may cause smooth pressure erosion of the adjacent bone (Fig. 3.70a) ● these small tumours are typically of low/intermediate SI on T1W images (Fig. 3.70a, b) and homogeneously hyperintense on T2W/STIR (Fig. 3.70c, d), showing uniform enhancement following contrast

References

b a

c

d

Figure 3.70 Glomus tumour. Axial T1-weighted (T1W) spin-echo (SE) image (a) showing a lesion (arrows) causing pressure erosion (arrowheads) of the underlying bone. Sagittal T1W SE (b), axial T2-weighted fast spin-echo fat-suppressed (c) and sagittal short tau inversion recovery (d) images showing a glomus tumour (arrows) located deep to the thumb nail.

REFERENCES 1 2 3 4 5 6 7 8 9

Zanetti M, Saupe N, Nagy L. Role of MR imaging in chronic wrist pain. Eur Radiol 2007; 17: 927–38. Sofka CM, Potter HG. Magnetic resonance imaging of the wrist. Semin Musculoskelet Radiol 2001; 5: 217–26. Weinberg EP, Hollenberg GM, Adams MJ, Tan RK, Lechner RT. High-resolution outpatient imaging of the wrist. Semin Musculoskelet Radiol 2001; 5: 227–34. Adler BD, Logan PM, Janzen DL et al. Extrinsic radiocarpal ligaments: magnetic resonance imaging of normal wrists and scapholunate dissociation. Can Assoc Radiol J 1996; 47: 417–22. Robinson G, Chung T, Finlay K, Friedman L. Axial oblique MR imaging of the intrinsic ligaments of the wrist: initial experience. Skeletal Radiol 2006; 35: 765–73. Cerezal L, Abascal F, Garcia-Valtuille R, Del Pinal F. Wrist MR arthrography: how, why, when. Radiol Clin North Am 2005; 43: 709–31. Sahin G, Demirtas M. An overview of MR arthrography with emphasis on the current technique and applicational hints and tips. Eur J Radiol 2006; 58: 416–30. Bergin D, Schweitzer ME. Indirect magnetic resonance arthrography. Skeletal Radiol 2003; 32: 551–8. Schweitzer ME, Natale P, Winalski CS, Culp R. Indirect wrist MR arthrography: the effects of passive motion versus active exercise. Skeletal Radiol 2000; 29: 10–14.

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10 Yu JS, Habib PA. Normal MR imaging anatomy of the wrist and hand. Radiol Clin North Am 2006; 44: 569–81. 11 Ekenstam F. Osseous anatomy and articular relationships about the distal ulna. Hand Clin 1998; 14: 161–4. 12 Rosner JL, Zlatkin MB, Clifford P, Ouellette EA, Awh MH. Imaging of athletic wrist and hand injuries. Semin Musculoskelet Radiol 2004; 8: 57–79. 13 Zlatkin MB, Rosner J. MR imaging of ligaments and triangular fibrocartilage complex of the wrist. Radiol Clin North Am 2006; 44: 595–623. 14 Pan CC, Lin YM, Lee TS, Chou CH. Displacement of the distal radioulnar joint of clinically symptom-free patients. Clin Orthop Relat Res 2003; 415: 148–56. 15 Spence LD, Savenor A, Nwachuku I, Tilsley J, Eustace S. MRI of fractures of the distal radius: comparison with conventional radiographs. Skeletal Radiol 1998; 27: 244–9. 16 Cook PA, Yu JS, Wiand W et al. Madelung deformity in skeletally immature patients: morphologic assessment using radiography, CT, and MRI. J Comput Assist Tomogr 1996; 20: 505–11. 17 Brown RR, Fliszar E, Cotten A, Trudell D, Resnick D. Extrinsic and intrinsic ligaments of the wrist: normal and pathologic anatomy at MR arthrography with three-compartment enhancement. Radiographics 1998; 18: 667–74. 18 Connell D, Page P, Wright W, Hoy G. Magnetic resonance imaging of the wrist ligaments. Australas Radiol 2001; 45: 411–22. 19 Theumann NH, Pfirrmann CW, Antonio GE et al. Extrinsic carpal ligaments: normal MR arthrographic appearance in cadavers. Radiology 2003; 226: 171–9. 20 Pfirrmann CWA, Zanetti M. Variants, pitfalls and asymptomatic findings in wrist and hand imaging. Eur J Radiol 2005; 56: 286–95. 21 Pfirrmann CW, Theumann NH, Chung CB, Botte MJ, Trudell DJ, Resnick D. What happens to the triangular fibrocartilage complex during pronation and supination of the forearm? Analysis of its morphology and diagnostic assessment with MR arthrography. Skeletal Radiol 2001; 30: 677–85. 22 Cerezal L, Del Pinal F, Abascal F. MR imaging findings in ulnar-sided wrist impaction syndromes. Magn Reson Imaging Clin N Am 2004; 12: 281–99. 23 Bencardino JT, Rosenberg ZS. Sports related injuries of the wrist: an approach to MRI interpretation. Clin Sports Med 2006; 25: 409–32. 24 Coggins CA. Imaging of ulnar sided wrist pain. Clin Sports Med 2006; 25: 505–26. 25 Haims AH, Schweitzer ME, Morrison WB et al. Limitations of MR imaging in the diagnosis of peripheral tears of the triangular fibrocartilage of the wrist. AJR Am J Roentgenol 2002; 178: 419–22. 26 Haims AH, Schweitzer ME, Morrison WB et al. Internal derangement of the wrist: indirect MR arthrography versus unenhanced MR imaging. Radiology 2003; 227: 701–7. 27 Schmitt R, Froehner S, Coblenz G, Christopoulos G. Carpal instability. Eur Radiol 2006; 10: 2161–78. 28 Timins ME. Osseous anatomic variants of the wrist: findings on MR imaging. AJR Am J Roentgenol 1999; 173: 339–44. 29 Stabler A, Glaser C, Reiser M, Resnick D. Symptomatic fibrous lunato-triquetral coalition. Eur Radiol 1999; 9: 1643–6. 30 Pfirrmann CW, Theumann NH, Chung CB, Trudell DJ, Resnick D. The hamatolunate facet: characterization and association with cartilage lesions—magnetic resonance arthrography and anatomic correlation in cadaveric wrists. Skeletal Radiol 2002; 31: 451–6. 31 Theumann NH, Pfirrmann CW, Chung CB, Antonio GE, Trudell DJ, Resnick D. Pisotriquetral joint: assessment with MR imaging and MR arthrography. Radiology 2002; 222: 763–70. 32 Blum AG, Zabel J-P, Kohlmann R et al. Pathologic conditions of the hypothenar eminence: evaluation with multidetector CT and MR imaging. Radiographics 2006; 26: 1021–44. 33 Karantanas A, Dailiana Z, Malizos K. The role of MR imaging in scaphoid disorders. Eur Radiol 2007; [Epub ahead of print]. 34 Cerezal L, Abascal F, Canga A, Garcia-Valtuille R, Bustamante M, Del Pinal F. Usefulness of gadolinium enhanced MR imaging in the evaluation of the vascularity of scaphoid non-unions. AJR Am J Roentgenol 2000; 174: 141–9. 35 Alam F, Schweitzer ME, Li XX, Malat J, Hussain SM. Frequency and spectrum of abnormalities in the bone marrow of the wrist: MR imaging findings. Skeletal Radiol 1999; 28: 312–17. 36 Nakamura K, Patterson RM, Moritomo H, Viegas SF. Type I versus type II lunates: ligament anatomy and presence of arthrosis. J Hand Surg [Am] 2001; 26-A: 428–36.

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37 Barakat MS, Schweitzer ME, Morrison WE, Culp RW, Bordalo-Rodrigues M. Reactive carpal synovitis: initial experience with MR imaging. Radiology 2005; 236: 231–6. 38 Robertson PL, Page PL, McColl GJ. Inflammatory arthritis-like and other MR findings in wrists of asymptomatic subjects. Skeletal Radiol 2006; 35: 754–64. 39 El-Noueam K, Schweitzer M, Blasbalg R et al. Is a sub-set of wrist ganglia the sequela of internal derangements of the wrist joint? MR imaging findings. Radiology 1999; 212: 537–40. 40 Nahra ME, Bucchieri JS. Ganglion cysts and other tumor related conditions of the hand and wrist. Hand Clin 2004; 20: 249–60. 41 Nguyen V, Choi J, Davis KW. Imaging of wrist masses. Curr Probl Diagn Radiol 2004; 33: 147–60. 42 Theumann NH, Etechami G, Duvoisin B et al. Association between extrinsic and intrinsic carpal ligament injuries at MR arthrography and carpal instability at radiography: initial observations. Radiology 2006; 238: 950–7. 43 Totterman SM, Seo GS. MRI findings of scapholunate instabilities in coronal images: a short communication. Semin Musculoskelet Radiol 2001; 5: 251–6. 44 Zanetti M, Hodler J, Gilula LA. Assessment of dorsal or ventral intercalated segmental instability configurations of the wrist: reliability of sagittal MR images. Radiology 1998; 206: 339–45. 45 Clavero JA, Alomar X, Monill JM et al. MR imaging of ligament and tendon injuries of the fingers. Radiographics 2002; 22: 237–56. 46 Clavero JA, Golano P, Farinas O, Alomar X, Monill JM, Esplugas M. Extensor mechanism of the fingers: MR imaging–anatomic correlation. Radiographics 2003; 23: 593–611. 47 Bencardino JT. MR imaging of tendon lesions of the hand and wrist. Magn Reson Imaging Clin N Am 2004; 12: 333–47. 48 De Maeseneer M, Van Roy P, Jacobson JA, Jamadar DA. Normal MR imaging findings of the midhand and fingers with anatomic correlation. Eur J Radiol 2005; 56: 278–85. 49 Ragheb D, Stanley A, Gentili A, Hughes T, Chung C. MR imaging of the finger tendons: normal anatomy and commonly encountered pathology. Eur J Radiol 2005; 56: 296–306. 50 Anderson SE, Steinbach LS, De Monaco D, Bonel HM, Hurtienne Y, Voegelin E. ‘Baby wrist’: MRI of an overuse syndrome in mothers. AJR Am J Roentgenol 2004; 182: 719–24. 51 De Lima JE, Kim HJ, Albertotti F, Resnick D. Intersection syndrome: MR imaging with anatomic comparison of the distal forearm. Skeletal Radiol 2004; 33: 627–31. 52 Aguiar ROC, Gasparetto EL, Escuissato DL et al. Radial and ulnar bursae of the wrist: cadaveric investigation of regional anatomy with ultrasonographic-guided tenography and MR imaging. Skeletal Radiol 2006; 35: 828–32. 53 Hsu C-Y, Lu H-C, Shih TTF. Tuberculous infection of the wrist: MRI features. AJR Am J Roentgenol 2004; 183: 623–8. 54 Parellada AJ, Morrison WB, Reiter SB et al. Flexor carpi radialis tendinopathy: spectrum of imaging findings and association with triscaphe arthritis. Skeletal Radiol 2006; 35: 572–8. 55 Timins ME. Muscular anatomic variants of the wrist and hand: findings on MR imaging. AJR Am J Roentgenol 1999; 172: 1397–401. 56 Bordalo-Rodrigues M, Amin P, Rosenberg ZS. MR imaging of common entrapment neuropathies at the wrist. Magn Reson Imaging Clin N Am 2004; 12: 265–79. 57 Kim S, Choi J-Y, Huh Y-M et al. Role of magnetic resonance imaging in entrapment and compressive neuropathy: what, where, and how to see the peripheral nerves on the musculoskeletal magnetic resonance image. Part 2. Upper extremity. Eur Radiol 2007; 17: 509–22. 58 Marom EM, Helms CA. Fibrolipomatous hamartoma: pathognomonic on MR imaging. Skeletal Radiol 1999; 28: 260–4. 59 Connell DA, Pike J, Koulouris G, Van Wettering N, Hoy G. MR imaging of thumb carpometacarpal joint ligament injury. J Hand Surg [Br] 2004; 29-B: 46–54. 60 Theumann NH, Pfirrmann CW, Chung CB, Antonio GE, Trudell DJ, Resnick D. Ligamentous and tendinous anatomy of the intermetacarpal and common carpometacarpal joints: evaluation with MR imaging and MR arthrography. J Comput Assist Tomogr 2002; 26: 145–52. 61 Theumann NH, Pfirrmann CWA, Drape J-L, Trudell DJ, Resnick D. MR imaging of the metacarpophalangeal joints of the fingers. Part 1. Conventional MR imaging and MR arthrographic findings in cadavers. Radiology 2002; 222: 437–45. 62 Theumann N, Pessis E, Lecompte M et al. MR imaging of the metacarpophalangeal joints of the fingers: evaluation of 38 patients with chronic joint disability. Skeletal Radiol 2005; 34: 210–16.

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63 Ahn JM, Sartoris DJ, Kang HS et al. Gamekeeper thumb: comparison of MR arthrography with conventional arthrography and MR imaging in cadavers. Radiology 1998; 206: 737–44. 64 Andreisek G, Kilgus M, Burg D et al. MRI of the intrinsic muscles of the hand: spectrum of imaging findings and clinical correlation. AJR Am J Roentgenol 2005; 185: 930–9. 65 Horcajadas AB, Lafuente JL, de la Cruz Burgos R et al. Ultrasound and MR findings in tumour and tumourlike lesions of the fingers. Eur Radiol 2003; 13: 672–85. 66 James SLJ, Davies AM. Surface lesions of the bones of the hand. Eur Radiol 2006; 16: 108–23. 67 Ehara S, Nishida J, Abe M et al. Magnetic resonance imaging of pseudomalignant osseous tumour of the hand. Skeletal Radiol 1994; 23: 513–16. 68 Teh J, Whiteley G. MRI of soft tissue masses of the hand and wrist. Br J Radiol 2007; 80: 47–63. 69 Capelastegui A, Astigarraga E, Fernandez-Canton G, Saralegui I, Larena JA, Merino A. Masses and pseudomasses of the hand and wrist: MR findings in 134 cases. Skeletal Radiol 1999; 28: 498–507. 70 Peh WCG, Wong Y, Shek TWH, Ip W-Y. Giant cell tumour of the tendon sheath: a pictorial essay. Australas Radiol 2001; 45: 274–80. 71 De Schepper AM, Hogendoorn PCW, Bloem JL. Giant cell tumours of the tendon sheath may present radiologically as intrinsic osseous lesions. Eur Radiol 2007; 17: 499–502. 72 Kitagawa Y, Ito H, Amano Y, Sawaizumi T, Takeuchi T. MR imaging for preoperative diagnosis and assessment of local tumor extent on localized giant cell tumour of tendon sheath. Skeletal Radiol 2003; 32: 633–8.

4 The hip joint and pelvic girdle

TECHNIQUE Conventional MRI1–5 ●

● ● ●

●

for the assessment of non-specific hip/groin/pelvic pain, a phased array torso coil provides optimal images: ■ a combination of T1-weighted (T1W)/proton density-weighted (PDW) fast spin-echo (FSE) and short tau inversion (STIR)/T2-weighted (T2W) fast spin-echo (FSE) fat-suppressed (FS) sequences in the coronal and axial planes, with sagittal T2W FSE images through the symptomatic side for the assessment of unilateral hip pain when internal derangement is suspected, the symptomatic hip should be imaged using a surface coil placed over the femoral head technical parameters: field of view (FOV) 14–18 cm, slice thickness 3–4 mm, matrix 256¥256 sequences and planes: ■ coronal and axial T1W SE/PDW FSE sequence for anatomical detail ■ coronal and axial STIR/T2W FSE FS sequence for marrow and soft-tissue oedema ■ sagittal PDW FSE/T2W FSE sequence the use of a limited coronal STIR sequence in the assessment of chronic hip pain has been described;6 a normal appearance of the hips on coronal STIR images excludes pathology with no requirement for additional images: ■ abnormality on STIR is relatively non-specific and requires addition of other sequences for diagnosis

Additional sequences ● ● ●

both diffusion-weighted MRI7 and proton MR spectroscopy8 have been used for the assessment of femoral head avascular necrosis (AVN) diffusion-weighted MRI:7 the apparent diffusion coefficient of a femoral head with AVN is markedly greater than that of the normal femoral head proton MR spectroscopy8 has shown significant differences in the lipid and water components in the epiphyseal marrow of normal-looking hips with contralateral AVN compared with those without AVN

MR arthrography4,9–11 ● ●

●

hip MR arthrography may be either direct or indirect direct MR arthrography involves the intra-articular injection of 5–25 ml dilute gadolinium (1:100–200) under fluoroscopic control: ■ addition of local anaesthetic can help determine whether symptoms are arising from the hip various joint puncture techniques are described; a femoral neck puncture site is associated with a significantly greater volume of extra-articular contrast leak but less discomfort than a femoral head puncture site12

226

The hip joint and pelvic girdle

●

● ●

●

imaging sequences: planes are as for conventional hip MRI: ■ coronal, axial and sagittal T1W SE FS images, for assessment of intra-articular soft-tissue structures (Fig. 4.1a) ■ coronal STIR or T2W FSE FS, for assessment of marrow oedema and extra-articular fluid collections/cysts (Fig. 4.1b) ■ oblique axial/sagittal and oblique coronal planes also described: – the oblique axial/sagittal plane is planned from a coronal scout and angled along the length of the femoral neck (Fig. 4.1c) – the oblique coronal plane is planned from a sagittal scout and angled along the iliac blade (Fig. 4.1d) high-resolution images of the hip are obtained by the use of a surface coil located over the femoral head technical parameters: FOV 14–18 cm, matrix 256¥256: ■ T1W/PDW SE FS images: 3 mm slice thickness ■ T2*-weighted gradient-echo (GE) images: can obtain 1.5 mm slice thickness additional techniques described include: ■ radial images of the labrum using GE images13 are reported to increase the sensitivity of labral pathology compared with the oblique coronal and oblique axial planes in cadavers ■ dedicated water-excitation three-dimensional double-echo steady-state sequence14 ■ imaging during continuous leg traction15 to separate the femoral and acetabular articular cartilage can improve the assessment of hyaline cartilage

a

b

c Figure 4.1 Direct MR arthrography of the hip. Coronal T1-weighted (T1W) spin-echo (SE) fat-suppressed (FS) image (a) showing hyperintense contrast medium outlining the intraarticular soft-tissue structures. Coronal T2-weighted fast spinecho (FSE) FS image (b) showing marrow oedema (arrow) in the acetabulum, not seen in (a). Coronal T1W SE FS image (c) showing the plane for oblique axial/sagittal imaging running parallel to the femoral neck. Sagittal T1W SE FS image (d) showing the plane for oblique coronal imaging running parallel to the ilium.

d

Technique

●

●

inadvertent administration of excess gadolinium results in a ‘black’ contrast effect on MR arthrography16 (Fig. 4.2); if the study is repeated several hours later, the gadolinium may have become sufficiently diluted to produce normal MR arthrogram images indications: assessment of the acetabular labrum and intra-articular loose bodies, and identification of acetabular/femoral cartilage defects

a

b

Figure 4.2 Coronal T1-weighted spin-echo fat-suppressed (FS) (a) and T2-weighted fast spin-echo FS (b) direct MR arthrograms following inadvertent injection of undiluted gadolinium resulting in a ‘black’ contrast effect (arrows).

●

indirect MR arthrography4,11,17 is the intravenous injection of gadolinium followed by a minimum of 5 minutes’ passive hip motion and a delay of 20 minutes before imaging, resulting in a small, hyperintense joint effusion: ■ imaging parameters are as for direct MR arthrography ■ indirect MR arthrography produces little joint distension, but shows synovial enhancement (Fig. 4.3) and has been used to demonstrate: – early cartilage loss manifesting as subchondral enhancement – extra-articular soft-tissue disorders – labral pathology when direct MR arthrography not possible

MR neurography18 ● ●

MR neurography uses a combination of high-resolution coronal and axial T1W SE and T2W FSE FS/fast STIR sequences it may be used to identify morphological abnormalities of the lumbosacral plexus or nerve oedema

b a Figure 4.3 Coronal (a) and axial (b) T1-weighted spin-echo fat-suppressed indirect MR arthrograms showing capsular enhancement (arrows) of the right hip indicative of synovitis. Compare with the normal left hip.

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THE HIP JOINT THE ACETABULUM Normal anatomy5,19,20 ● ● ● ●

● ● ●

the acetabulum is formed from the ilium superiorly, the ischium posteriorly and the pubic bone anteriorly (Fig. 4.4a) it is almost hemispherical and ellipsoid in cross-section with its long axis in the superoinferior direction the articular surface has an inverted horseshoe shape or a three-quarter moon shape (referred to as the lunula or lunate) it is wider posteriorly than anteriorly and is covered by hyaline cartilage, which is thickest anterosuperiorly (~2 mm) and thinnest posteromedially (~1 mm): ■ the outer rim of the lunula is covered by the fibrocartilage of the acetabular labrum in the centre of the acetabulum is a concavity (the acetabular fossa or pulvinar) that is lined by synovium and contains fibro-fatty tissue and branches of the obturator artery and nerve (Fig. 4.4b, c) anteroinferiorly, the bony acetabular rim is deficient, producing the acetabular notch (Fig. 4.4d) which is bridged by the transverse acetabular ligament (Fig. 4.4d, e) the ligamentum teres arises from the transverse acetabular ligament and inserts on the fovea capitis (centralis) of the femoral head (Fig. 4.4f, g): ■ the ligamentum teres contains the foveal artery, a small branch of the obturator artery

PATHOLOGY OF THE ACETABULUM Acetabular stress fractures21,22 ●

reported predisposing causes include: ■ insufficiency fractures occur in the elderly due to associated osteoporosis, rheumatoid arthritis (RA), hyperparathyroidism, previous radiotherapy or corticosteroid use: – in the setting of previous malignancy, they present with severe, mechanical-type hip pain that may simulate recurrent disease21 ■ fatigue fractures22 in military recruits are reported in 6.7 per cent of cases being investigated for femoral neck stress fractures and may involve the acetabular roof or the anterior column

a

Figure 4.4 Normal MR anatomy of the acetabulum. Sagittal proton density-weighted (PDW) fast spin-echo (FSE) image (a) showing the bony constituents of the acetabulum, the pubic bone (arrow) anteriorly, the ilium (arrowhead) superiorly and the ischium (double arrowhead) posteroinferiorly. (continued)

The hip joint

b

d

c

e

g f Figure 4.4 (continued) Coronal (b) and axial (c) PDW FSE images showing the acetabular fossa (arrow) filled with fat. Sagittal T1-weighted (T1W) spin-echo (SE) fat-suppressed (FS) MR arthrogram (d) showing the acetabular notch (arrow) bridged by the transverse acetabular ligament (arrowheads). Axial PDW FSE MR arthrogram (e) showing the transverse acetabular ligament (arrows). Coronal (f) and axial (g) T1W SE FS MR arthrograms showing the ligamentum teres (arrows) arising from the fovea capitis (white arrowheads) and inserting into the transverse acetabular ligament (black arrowhead f).

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The hip joint and pelvic girdle

MRI findings ● linear reduced marrow signal intensity (SI) is seen at the site of the fracture (Fig. 4.5a) with surrounding marrow oedema (Fig. 4.5b) ● acetabular fractures in patients with previous malignant disease typically arise in the supra-acetabular region and are curvilinear in orientation (~90 per cent of cases), or less commonly oblique: ■ associated sacral insufficiency fractures are reported in 13 per cent of cases

a

b

Figure 4.5 Acetabular stress fracture. Coronal T1-weighted spin-echo (a) and short tau inversion recovery (b) images showing a hypointense fracture line (arrow a) in the acetabular roof and surrounding marrow oedema (arrowheads b).

Acetabular dysplasia23,24 ● ●

acetabular dysplasia in the adult hip is defined by a centre-edge angle (of Wiberg) of less than 20° on anteroposterior radiography; a similar measurement can be made on coronal MRI of the hip (Fig. 4.6) the association of labral pathology with acetabular dysplasia has been termed ‘acetabular rim syndrome’

Figure 4.6 Acetabular dysplasia. Coronal T1-weighted spinecho image showing measurement of the centre-edge angle of Wiberg.

The hip joint

●

two types of acetabular anatomical abnormalities are recognised and predispose to labral degeneration, acetabular cartilage defects and eventually premature osteoarthritis (OA): ■ type 1 – the acetabulum and femoral head are incongruent, the acetabulum being shallow and vertical in orientation: – the labrum plays a role in weight-bearing and becomes hypertrophied, degenerate and torn, the tears usually involving the lateral (superior) labrum – perilabral cyst formation may occur ■ type 2 – the acetabulum and femoral head are congruent and the acetabular roof is short: – stress occurs at the osseous rim, resulting in rim fragmentation, os acetabuli and intraosseous cyst formation – acetabular cartilage defects occur at the chondrolabral interface

MRI findings ● there is enlargement of the acetabular labrum with increased intralabral SI due to myxoid degeneration, fraying and marginal fissuring (Fig. 4.7a) ● superolateral labral tear (Fig. 4.7b) and anterosuperior chondromalacia (Fig. 4.7c) ● intraosseous cyst formation (Fig. 4.7a, d) and os acetabuli (Fig. 4.7e, f) ● conventional MRI of the acetabular labrum and articular cartilage has demonstrated elongation of the labrum (mean length 10.9 mm compared with 6.4 mm in control hips) and chondromalacia at the labral–chondral transition zone in 89 per cent of cases, the latter correctly identified in 89 per cent of cases (compared with arthroscopy)24

THE ACETABULAR LABRUM Normal anatomy9,19,20,25 ● ● ● ● ● ●

the acetabular labrum is attached to the acetabular rim and the lunula and serves to deepen the acetabular socket by more than 20 per cent it comprises fibrocartilage and has a triangular cross-section, merging with the acetabular hyaline cartilage at the ‘transition zone’ the labrum has small vessels within its periphery at the junction with the acetabulum, but otherwise is avascular, though surrounded by vascularised synovium within the joint recesses it has a variable width (range 1–17 mm), being widest in its anterior quadrant (mean 5.5 mm), thickest in the posterosuperior segment (mean 5 mm) and thinnest anteroinferiorly along the superior weight-bearing portion of the joint, the labrum covers a 5–18° arc over the femoral head the labrum blends with the transverse acetabular ligament inferiorly at the margins of the acetabular notch; a cleft is formed at the junction of the labrum and ligament, mimicking a tear

MRI findings ● the labrum is typically triangular in cross-section and uniformly hypointense on all pulse sequences (in 44–56 per cent of cases) due to its fibrocartilaginous nature (Fig. 4.8a–c) ● variations of labral shape and SI have been reported in asymptomatic individuals:26 ■ 80 per cent of labral segments have a triangular cross-section, while 13 per cent are rounded, 7 per cent are irregular and 1 per cent are not identified26 ■ the labrum may appear blunted/rounded (Fig. 4.8d), irregular or flat (Fig. 4.8e) due to degenerative change or small tears ■ a portion of the labrum may be absent in 1–14 per cent of individuals, most commonly in the anterosuperior location ■ intermediate/high intralabral SI is reported in ~55 per cent of volunteers on conventional T1W SE/PDW FSE images ■ increased T2W SI is described in 37 per cent of cases, most commonly in the superior labrum (87 per cent); SI changes may be linear, curvilinear or globular and may extend to the labral margin, being attributed to mucoid degeneration ■ variations in morphology and SI are more common with increasing age and may therefore be degenerative phenomena

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The hip joint and pelvic girdle

b

a

c d

f

e Figure 4.7 Acetabular dysplasia. Coronal T1-weighted (T1W) spin-echo (SE) image (a) showing marked hypertrophy and hyperintensity of the superolateral labrum (arrow) with an associated acetabular cyst (arrowheads). Coronal T1W SE fatsuppressed MR arthrogram (b) showing labral hypertrophy and tear manifest as linear high signal intensity (arrow) within the labral substance. Sagittal proton density-weighted fast spin-echo (FSE) image (c) showing acetabular chondromalacia (arrow). Coronal short tau inversion recovery image (d) showing intraosseous acetabular cyst formation (arrow). Coronal T1W SE image (e) showing an os acetabuli (arrow). Axial T2-weighted FSE image (f) in a patient with bilateral acetabular dysplasia showing an os acetabuli (arrow) on the right and an acetabular cyst (arrowhead) on the left.

The hip joint

a b

c

d

e

Figure 4.8 Normal MR anatomy of the acetabular labrum. Coronal T2-weighted fast spin-echo (FSE) (a), sagittal (b) and axial (c) proton density-weighted FSE images showing various portions of the acetabular labrum (arrows). Coronal T1-weighted spin–echo fat-suppressed images (d, e) showing a blunted (arrow d) and flattened irregular (arrow e) labrum.

MR arthrographic findings ● the labrum is optimally demonstrated on direct MR arthrography (Fig. 4.9a–c) ● at the labrochondral transition zone, intermediate/high SI articular cartilage extends deep to the labrum (Fig. 4.9d), mimicking a labral tear ● sublabral sulci are described in an anterosuperior (presence disputed) and posteroinferior location and rarely anterointerior and posterosuperior27

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The hip joint and pelvic girdle

a

b

d Figure 4.9 Normal direct MR arthrographic anatomy of the acetabular labrum. Coronal (a), axial (b) and sagittal (c) T1-weighted spin-echo fat-suppressed (FS) images showing the normal hypointense triangular form of the labrum (arrows). Coronal T2-weighted fast spin-echo FS image (d) showing hyperintense articular cartilage (arrow) undercutting the labrum at the labral–chondral transition zone.

c

●

●

the anterosuperior sublabral sulcus appears as a small, fluid-filled cleft between the labrum and the underlying hyaline cartilage with smooth, well-defined margins (Fig. 4.10a): ■ in the differentiation between this and a labral tear, it is suggested that a tear is present if contrast extends for more than 50 per cent depth across the labrum20 ■ a tear is likely to have irregular margins the posteroinferior sublabral sulcus is reported in 22.4 per cent of cases and can mimic a partial posteroinferior labral detachment (Fig. 4.10b)

b a Figure 4.10 Sublabral recesses. Coronal (a) and axial (b) T1-weighted spin-echo fat-suppressed MR arthrograms showing the anterosuperior (arrow a) and posteroinferior (arrow b) sublabral recesses.

The hip joint

PATHOLOGY OF THE ACETABULAR LABRUM Acetabular labral tears1–3,5,9,10,20,25 ●

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●

●

the aetiology of acetabular labral tears includes: ■ trauma, associated with hyperextension and external rotation injury to the hip, usually involving the anterosuperior labrum, or axial loading of the flexed hip resulting in posterior labral injury ■ posterior hip dislocation (rarely with anterior dislocation) ■ acetabular dysplasia (see previous) pathologically, acetabular labral tears can be classified in various ways: ■ most simply, the labrum may become detached (type 1 tear) or torn (type 2 tear); detachment accounts for ~90 per cent of labral tears: – labral detachments occur at the labral–cartilaginous junction, whereas tears occur within the substance of the labrum ■ according to aetiology, tears may be degenerative, dysplastic, traumatic or idiopathic: – degenerative tears are associated with chronic inflammatory arthropathies – dysplastic tears are associated with acetabular dysplasia (see previous) – traumatic tears are typically isolated to a particular region of the labrum, usually the anterior labrum (associated with minor trauma and without dislocation) ■ a more detailed morphological classification recognises four types: – radial flap tears account for 57 per cent of cases and involve the free margin of the labrum, resulting in a discrete flap – radial fibrillated tears account for 22 per cent of cases and are associated with degenerative change with irregularity of the free margin of the labrum – peripheral longitudinal tears account for 16 per cent of cases and occur at the junction of the labrum and the acetabular rim: ◆ these are more likely to become unstable and displaced, resulting in a bucket-handle fragment – unstable tears account for 5 per cent and are identified at arthroscopy rather than by any particular MR characteristics the location of a labral tear can be described in terms of the four quadrants of the acetabulum: anterior, anterosuperior, posterosuperior and posterior: ■ most pathology occurs in the anterosuperior quadrant, though tears extend into other quadrants in ~30 per cent of cases or occur at multiple separate sites in ~7 per cent (usually the anterior and posterior quadrants) clinically, labral tears present with mechanical hip pain that is exacerbated by hip flexion and internal rotation, clicking, locking and catching

MRI findings ● labral tears manifest as linear high SI extending from the articular side of the labrum through the base or into the labral substance (Fig. 4.11a), with/without abnormal labral morphology (Fig. 4.11b): ■ focal SI confined to the labrum represents intra-substance degeneration ● using an optimised MR technique, 95–96 per cent of labral tears can be identified28 MRI arthrographic findings ● labral detachment manifests as the presence of contrast medium between the labrum and the acetabular bony rim (Fig. 4.11c, d) with/without labral displacement (Fig. 4.11e, f), suggesting the presence of a bucket-handle fragment ● labral tears manifest as the presence of intra-substance contrast material (Fig. 4.7b) ● additional features of labral abnormality include deformity or blunting, and loss of the perilabral recess due to labral hypertrophy (Fig. 4.11b) ● an MRI/MR arthrographic staging system for labral pathology has been described:29 ■ stage 0 – normal, triangular, homogeneously low SI labra with a normal perilabral recess ■ stage 1 – labra with increased intra-substance SI that does not reach the labral surface ■ stage 2 – labra with contrast material extending into them and involving the labral surface ■ stage 3 – labra that are detached from the acetabulum

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f Figure 4.11 Acetabular labral tear. MRI: Sagittal proton density-weighted (PDW) fast spin-echo (FSE) image (a) showing a tear (arrow) through the base of the anterior labrum. Coronal T2-weighted FSE fat-suppressed (FS) image (b) showing labral hypertrophy, intra-substance high signal intensity (arrow) and obliteration of the superior perilabral recess. MR arthrography: Axial T1-weighted (T1W) spin-echo (SE) FS (c) and coronal PDW FSE (d) images showing non-displaced labral detachments manifest as the presence of contrast medium (arrows) between the labrum and the underlying acetabular rim. Axial T1W SE FS image (e) showing extensive contrast medium (arrow) between the labrum and the acetabular rim with lateral labral displacement. The labrum (arrowhead) also appears enlarged and hyperintense. Coronal T1W SE FS image (f) showing a detached and inferiorly displaced superior labrum (arrowhead).

The hip joint

stages 1–3 are subdivided into A and B; B-type labra are hyertrophied with loss of the perilabral recess only type 2 and type 3 labra correlate with tears associated features: chondral lesions are identified in ~30 per cent of cases of labral detachment or tears and are usually located anterosuperiorly in the acetabulum, adjacent to the site of labral pathology direct MR arthrography using a small FOV has reported sensitivity and specificity of 92 per cent and 100 per cent, respectively, for the identification of labral tears30 a recently described finding on direct MR arthrography that should not be confused with acetabular labral pathology is the presence of tubular intraosseous tracking of injected contrast medium:31 ■ this is reported with an incidence of 15 per cent and invariably occurs at the posterior–anterior margins of the acetabular fossa, appearing as a thin (~1 mm) intraosseous extension of injected contrast medium, commonly with a clubbed termination ■ the length of such tracks is 0.4–1.7 cm (mean 1.1 cm) ■ it is thought to represent contrast extension along nutrient foramina of the acetabular fossa, and is seen with equal frequency in symptomatic and asymptomatic hips ■ ■

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Paralabral cysts2,20 ● ● ● ●

paralabral cysts occur when a labral tear passes through the capsule allowing escape of joint fluid; they are especially seen with labral detachment they are associated with OA, acetabular dysplasia (Fig. 4.12a, b) and acute/remote trauma, and are usually 1–2 cm in diameter, though they may enlarge to 3–4 cm cysts are typically extra-articular and may erode the adjacent bone, while large paralabral cysts may compress the femoral nerve and present with leg pain32 anterior paralabral cysts must be differentiated from iliopsoas bursitis: ■ paralabral cysts are typically located lateral to the iliopsoas tendon while bursae are located medially

MRI findings ● cysts are hypointense on T1W (Fig. 4.12c) and hyperintense on T2W images (Fig. 4.12d), usually occurring at the superolateral acetabular margin ● occasionally, they have heterogeneous low T2W SI due to the presence of gelatinous/mucinous material, debris or proteinaceous fluid ● they may fill with contrast medium at MR arthrography (Fig. 4.12e), and continuation with the labral tear may be seen

Femoroacetabular impingement9,20,33–35 ● ● ●

●

femoroacetabular impingement (FAI) is a cause of early hip OA in an otherwise normal hip, or may be associated with pre-existing pathological processes two types of FAI are described: pincer (due to acetabular causes) and cam (due to femoral causes)34 pincer (acetabular)-type FAI usually affects middle-aged, physically active women and occurs when the femoral head–neck junction contacts the acetabular rim: ■ it is usually the result of a condition such as acetabular anteversion or retroversion, coxa profunda or acetabular protrusion ■ initially, the femoral head–neck morphology is normal, but extra-articular osseous prominences may develop later at the acetabular rim and along the anterior femoral neck, resulting in labral tear or degeneration, occasionally with cyst formation and posteroinferior acetabular chondromalacia cam (femoral)-type FAI usually presents in young, physically active men and is due to abnormal prominence of the anterior femoral head–neck junction: ■ causes include insufficient femoral head–neck offset (‘pistol-grip deformity’) secondary to subtle displacement of the femoral epiphysis or frank slipped upper femoral epiphysis (SUFE), developmental dysplasia of the hip (DDH), Perthes’ disease and AVN of the femoral head, or it may occur as a post-traumatic deformity ■ it results in premature contact between the femoral head–neck junction and the acetabular rim on flexion–adduction and internal rotation ■ it leads to abrasion/avulsion of the anterosuperior acetabular cartilage from the labrum and subchondral bone with eventual tear/detachment of the anterosuperior labrum

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Figure 4.12 Acetabular labral cyst. Coronal short tau inversion recovery (STIR) (a) and axial T2-weighted (T2W) fast spin-echo (FSE) (b) images in a patient with acetabular dysplasia and secondary osteoarthritis showing a combined paralabral and intraosseous cyst (arrows). Axial T2W FSE fat-suppressed (FS) (c) and coronal STIR (d) images showing a hyperintense lobulated cystic mass (arrows) arising from the anterosuperior labrum. Coronal T1-weighted spin-echo FS direct MR arthrogram (e) showing filling of a paralabral cyst (arrow).

clinically, pain is produced by hip flexion and internal rotation, which constitutes a positive impingement test

MRI findings36 ● acetabular: ■ tears of the anterosuperior labrum (Fig. 4.13a) usually occur on the articular side of the labrum, with possible acetabular labral cyst formation

The hip joint

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Figure 4.13 Femoroacetabular impingement. Coronal proton densityweighted (PDW) fast spin-echo (FSE) image (a) showing an anterosuperior labral tear (arrow). Note the prominence of the femoral head–neck junction (arrowheads). Sagittal PDW FSE fat-suppressed (FS) image (b) showing subchondral sclerosis (arrow) and acetabular chondromalacia (arrowhead). Coronal T2-weighted FSE image (c) showing marrow oedema in the anterosuperior acetabulum (arrow). Sagittal PDW FSE image (d) showing anterosuperior acetabular chondral injury manifest as cartilage thinning and subchondral cyst formation (arrow) with associated prominence of the femoral head–neck junction (arrowheads). Axial oblique PDW FSE image (e) showing a dysplastic bump (arrow) on the anterior aspect of the femoral neck and associated thickening of the iliofemoral ligament (arrowhead). Axial PDW FSE image (f) showing fibrocystic change (arrow) at the anterior femoral head–neck junction. Coronal PDW FSE FS image (g) showing marrow oedema (arrow) associated with a femoral neck cyst (arrowhead).

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lesions of the labrochondral transition zone are most commonly seen in an anterosuperior (50 per cent) or anterosuperior/superolateral (36 per cent) location ■ acetabular (Fig. 4.13b) (39 per cent) and femoral head (20 per cent) chondromalacia ■ marrow SI changes (Fig. 4.13b, c) or subchondral cyst formation (Fig. 4.13d) (oedema/sclerosis depending on stage), typically in the anterosuperior aspect of the acetabulum ■ acetabular retroversion/anteversion, coxa profunda and rim osteophytes in pincer-type FAI femoral: ■ prominence of the femoral head–neck junction (femoral head–neck offset) (Fig. 4.13a, d), which is optimally assessed on an oblique axial image parallel to the femoral neck (Fig. 4.13e); manifests as a dyplastic femoral neck bump just lateral to the physeal scar ■ femoral neck subcortical cysts (24 per cent) (Fig. 4.13f) and marrow oedema in the femoral neck associated with fibrocystic change37 (Fig. 4.13g) ■ additional features include femoral head oedema, capsular thickening/synovitis and thickening of the iliofemoral ligament (Fig. 4.13e) ■

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MRI arthrographic findings ●

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abnormal morphology of the anterior femoral head–neck junction is reported to be present in 93 per cent of cases and is optimally assessed on oblique axial/sagittal plane images: ■ it is measured in terms of the alpha-angle (Fig. 4.14a), an angle of >55° being closely associated with symptoms of cam-type FAI anterosuperior acetabular cartilage defect manifests as contrast medium entering a defect in the cartilage and is reported to be present in 95 per cent of cases anterosuperior labral tear is reported to be present in 100 per cent of cases (Fig. 4.14b) the triad of the above three findings is present in 88 per cent of cases38 fibrocystic change at the anterosuperior femoral neck (Fig. 4.13f, g)39 is demonstrated in up to 33 per cent of patients with FAI and occurs at the junction of the femoral head and neck: ■ the mean diameter of the cysts is 5 mm (range 3–15 mm) ■ dynamic MRI with hip flexion demonstrates a close relationship between cystic change and anterosuperior acetabular rim

a b Figure 4.14 Femoroacetabular impingement. Axial T1-weighted spin-echo fat-suppressed (FS) MR arthrogram (a) showing measurement of the alpha-angle (double-headed arrow) and a small bony prominence at the anterior femoral head–neck junction (black arrow). Coronal proton density-weighted fast spin-echo FS direct MR arthrogram (b) showing an anterosuperior labral tear (arrow).

The hip joint

THE JOINT CAPSULE Normal anatomy2,5,9,19,20 ● ● ●

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the hip joint is enveloped by a thick, fibrous capsule comprising a deep circular layer, the zona orbicularis and a superficial longitudinal layer the fibres of the zona orbicularis are located posteriorly and inferiorly (Fig. 4.15a) proximally, the capsule attaches to the acetabular rim: ■ along the anterior and posterior joint margins, the capsule inserts at the base of the labrum, creating a small perilabral recess (Fig. 4.15b) ■ superiorly, the capsule inserts several millimeters above the labrum, creating a larger perilabral recess (Fig. 4.15c) distally, the capsule attaches anteriorly to the intertrochanteric line and posteriorly 1–2 cm proximal to the intertrochanteric crest (Fig. 4.15b) in 10–15 per cent of individuals, the capsule communicates directly with the iliopsoas bursa the capsule is lined by a highly vascularised synovium that provides blood supply to the femoral head in adults the capsule is reinforced by three extracapsular ligaments: the iliofemoral, pubofemoral and ischiofemoral the iliofemoral ligament (of Bigelow) is an ‘inverted Y’-shaped structure arising from the anterior inferior iliac spine (AIIS) and inserting into the anterior intertrochanteric line of the femoral neck (Fig. 4.15d, e): ■ its function is to prevent hip hyperextension during standing and to resist excessive external rotation the pubofemoral ligament arises from the superior pubic ramus and inserts into the anterior intertrochanteric line, blending with the iliofemoral ligament (Fig. 4.15f): ■ it functions to resist hyperabduction and extension the ischiofemoral ligament arises from the ischial portion of the acetabular rim, inserting into the posterior femoral neck (blending with the zona orbicularis) and the greater trochanter (Fig. 4.15f): ■ it functions to prevent hyperextension and excessive internal rotation

PATHOLOGY OF THE JOINT CAPSULE Synovium-based disorders ●

there are various synovium-based disorders of the hip joint, including inflammatory, infective, depositional and tumour-like conditions; these are dealt with in Chapter 7

Capsular laxity and trauma35 ●

●

capsular laxity may be seen in patients with a condition such as Marfan’s or Ehler–Danlos syndrome, who may show rotational instability of the hip on clinical examination, thought to be due to laxity or dysfunction of the anterior capsule and iliofemoral ligament: ■ this may be amenable to surgical plication or thermal capsulorrhaphy ■ MRI arthrographic findings: – thickening of the iliofemoral ligament, with irregularity of the undersurface on oblique axial images – capsular laxity may be associated with ligamentum teres hypertrophy capsular injury: traumatic rupture of the iliofemoral ligament has been described in American football players following posterior hip subluxation, posterior acetabular rim fracture and haemarthrosis: ■ less commonly, posterior capsular injury occurs

Adhesive capsulitis40 ● ●

adhesive capsulitis of the hip joint is an uncommon entity that is either idiopathic or is associated with other pathologies, most commonly synovial osteochondromatosis clinically, it typically affects middle-aged women, who present with unexplained, painful restriction of joint motion, and is characterised at arthroscopy by reduced range of movement and capsular fibrosis with haemorrhagic, fibrinous debris: ■ a previous history of trauma is occasionally elicited

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e Figure 4.15 Normal anatomy of the hip capsule. Coronal T1-weighted (T1W) spin-echo (SE) fat-suppressed (FS) MR arthrogram (a) showing the zona orbicularis (arrows). Axial oblique proton density-weighted (PDW) fast spin-echo (FSE) MR arthrogram (b) showing the anterior (arrow) and posterior (white arrowhead) perilabral recesses and the insertion of the capsule into the anterior and posterior aspects of the femoral neck (black arrowheads). Coronal T1W SE FS MR arthrogram (c) showing the superior perilabral recess (arrow). Coronal PDW FSE (d) and sagittal T1W SE FS (e) MR arthrograms showing the iliofemoral ligament (arrowheads) arising from the anterior inferior iliac spine (arrows). Axial PDW FSE MR arthrogram (f) showing the pubofemoral ligament (long arrows) and the ischiofemoral ligament (short arrow), which blends with the zona orbicularis (arrowhead).

The hip joint

MRI findings ● in the few reported cases, no specific MRI features have been demonstrated ● joint effusion and labral tears or acetabular chondromalacia are occasionally seen ● reduction of capsular volume has not been demonstrated at arthrography

MISCELLANEOUS PATHOLOGIES OF THE HIP JOINT Cartilage lesions of the hip14,20,28,41 ● ●

subtle, radiographically occult cartilage lesions of the femoral head or acetabulum may be a cause of undiagnosed chronic hip pain the femoral and acetabular articular cartilage can be assessed on a combination of sagittal, axial and coronal conventional MR images or on MR arthrography

MRI findings ●

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cartilage defects can be graded in a similar manner to other joints: ■ grade 0 – normal ■ grade 1 – chondral softening, no contour defect ■ grade 2 – cartilage defect 50 per cent depth ■ grade 4 – full-thickness defect with subchondral bone involvement on high-resolution PDW FSE images, cartilage defects appear as areas of increased SI28 (Fig. 4.16a) grade 4 lesions may be associated with subchondral marrow SI changes in the acetabular rim or femoral head (Fig. 4.16b) subchondral cyst formation is also recognised in advanced cases (Fig. 4.16c) the accuracy of conventional MRI using high-resolution PDW FSE sequences is reported as approximately 85 per cent for both acetabular and femoral head cartilage

MRI arthrographic findings ● a contrast-filled defect is seen within the femoral head or the acetabular (most commonly anterosuperior region) cartilage (Fig. 4.16d) ● the reported accuracy of MR arthrography for detection of cartilage defects is approximately 75 per cent

Snapping hip syndrome2,3,20,42 ● ● ● ●

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snapping hip syndrome is a rare condition caused by sudden movement of various tendons over adjacent bony structures aetiology: trauma, inflammatory and degenerative arthopathy; also, young athletes with no evidence of underlying hip pathology it may be classified as external, internal or intra-articular external (lateral) is the commonest type and is due to snapping of a thickened iliotibial tract or gluteus maximus over the greater trochanter with hip flexion: ■ it may be associated with greater trochanteric bursitis and the diagnosis is usually made clinically, without the need for imaging internal (anterior) usually occurs with hip extension due to snapping of the iliopsoas tendon over the AIIS, the iliopectineal eminence or a bony ridge on the lesser trochanter: ■ it may be associated with iliopsoas bursitis ■ internal snapping may less commonly be due to the iliofemoral ligament intra-articular is due to internal derangement such as a labral tear, loose body or redundant synovial fold: ■ patients may complain of clicking and pain is a major symptom clinically, patients present with painful snapping of the hip, which is unilateral in approximately 90 per cent of cases: ■ localised groin swelling is present in 60 per cent and reduced range of joint movement is seen in all cases

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Figure 4.16 Cartilage lesions of the hip. Sagittal proton density-weighted fast spin-echo (FSE) image (a) showing fullthickness increased signal intensity (SI) (arrow) in both the acetabular and the femoral head articular cartilage consistent with grade 3 lesions. Sagittal T2-weighted FSE image (b) showing reactive subchondral marrow SI change (arrow) in the anterior acetabular rim consistent with grade 4 chondromalacia. Coronal T1-weighted (T1W) spin-echo (SE) image (c) showing subchondral cyst formation (arrows) in the femoral head and acetabulum. Sagittal T1W SE fat-suppressed MR arthrogram (d) showing contrast medium (arrow) filling a defect in the anterior acetabular articular cartilage.

● ●

most cases can be investigated by radiography/ultrasonography (particularly dynamic) and CT however, when no cause is demonstrated, MRI can usually identify the underlying pathology

MRI findings ● the findings are of the underlying pathological process, including OA, synovitis, iliopsoas bursitis or a possible bone or soft-tissue tumour ● tendinopathy or fibrosis affecting the iliotibial tract, iliopsoas tendon, rectus femoris or gluteus maximus

Traumatic rupture of the ligamentum teres35,43 ● ● ●

the ligamentum teres extends from the fovea capitis of the femoral head to the transverse acetabular ligament and is optimally demonstrated on axial and coronal MR arthrography (Fig. 4.4f, g) trauma to the ligamentum teres may occur following severe injury, including hip dislocation or twisting injuries without dislocation injuries to the ligamentum teres are considered to be the third commonest intra-articular hip problem in athletes

The hip joint

● ●

clinically, patients present with deep anterior groin pain of mechanical nature and catching, locking or giving way, and experience pain on flexion and internal rotation ligament rupture may be complete or partial and may be isolated or associated with labral tears, chondral injury or loose bodies

MRI findings ● these have been only rarely reported ● MR arthrography may demonstrate avulsion of the ligament from its femoral origin ● partial tears may manifest as swelling and hyperintensity of the ligament (Fig. 4.17) ● however, the MR appearance of the arthroscopically normal ligament has not been studied in detail

Figure 4.17 Sprain of the ligamentum teres. Coronal T1-weighted spin-echo fat-suppressed MR arthrogram showing thickening and increased intra-substance signal intensoty in the ligamentum teres (arrow) consistent with a partial tear.

Hip dislocation44 ● ● ● ●

hip dislocation is a relatively rare injury; posterior dislocation is three times more common than anterior dislocation it also occurs twice as commonly in males early findings after dislocation include rupture of the iliofemoral ligament, labral tear, intra-articular loose bodies, bone contusions and muscle injury late findings include osteonecrosis of the femoral head, intra-articular loose bodies (Fig. 4.18) and capsular injury

MRI findings ● the findings are as above

Rapidly destructive osteoarthritis (coxarthrosis)45,46 ● ● ● ●

rapidly destructive OA is a disorder of unknown aetiology characterised by rapid chondrolysis (>2 mm or 50 per cent joint space in 1 year) clinically, there is destruction of the hip joint within months of the onset of symptoms; the condition typically occurs in women aged 60–70 years it is usually unilateral and differs from typical OA by the relative absence of osteophytes and the presence of femoral head collapse it may be predisposed to by subchondral insufficiency fracture of the femoral head in the setting of osteoporosis

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b

a Figure 4.18 Previous hip dislocation. Sagittal T2*-weighted gradient-echo image (a) showing loose bodies (arrow) anterior to the femoral neck. Axial proton density-weighted fast spin-echo direct MR arthrogram (b) showing the intra-articular location of the loose body (arrow).

MRI findings ● femoral head and acetabular marrow oedema in 100 per cent and 83 per cent of cases respectively (Fig. 4.19a); oedema commonly extends into the femoral neck but is most prominent in the weight-bearing region of the femoral head ● collapse at the weight-bearing portion of the femoral head in 92 per cent (Fig. 4.19b) ● superolateral subluxation of the femoral head in 67 per cent of cases ● small marginal osteophytes from the acetabular rim and femoral neck ● abnormality of the subchondral aspect of the femoral head: ■ a low SI subchondral line consistent with a fracture (Fig. 4.19c) ■ a diffuse low SI region on all pulse sequences (Fig. 4.19d, e) ■ subchondral cysts in the weight-bearing surface of the femoral head and acetabulum ● significant joint effusion/synovitis is seen in all cases (Fig. 4.19a, e) ● oedema in the adjacent soft tissues is present in 33 per cent of cases (Fig. 4.19e)

THE FEMORAL HEAD AND NECK Normal anatomy2,19,20 ● ● ●

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the femoral head approximates two-thirds of a sphere and is covered with hyaline cartilage except over the fovea capitis (Fig. 4.20a, b) the head lies superior, medial and anterior to the femoral shaft and femoral condyles femoral head anteversion is approximately 12° in the adult hip and is measured as the angle between a line drawn parallel to the femoral neck and a line drawn through the posterior cortices of the femoral condyles on axial images the femoral head–shaft angle (superior inclination) is approximately 125° in the adult hip and is measured as the angle between a line drawn along the femoral neck and a line drawn along the femoral shaft on a coronal image (Fig. 4.20c) joint articular cartilage: the cartilage of the acetabular lunula is thickest anterosuperiorly (~2 mm) and thinnest posteromedially (~1 mm), while the cartilage of the femoral head is thickest superiorly, medially and posteriorly (~2.5 mm)

The hip joint

a

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d

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e

Figure 4.19 Rapidly destructive coxarthrosis. Coronal T2-weighted (T2W) fast spin-echo (FSE) fat-suppressed (FS) image (a) showing complete loss of joint space, and acetabular and femoral head/neck oedema. Coronal T1-weighted (T1W) spin-echo (SE) image (b) showing marked bilateral femoral head collapse (arrows). Coronal T1W SE image (c) showing a subchondral hypointense line (arrow). Coronal proton densityweighted FSE (d) and T2W FSE FS (e) images showing diffuse subchondral hypointensity (white arrows) and joint effusion (arrowheads) with peri-articular soft-tissue oedema (black arrows e).

PATHOLOGY OF THE FEMORAL HEAD AND NECK Osteonecrosis47,48 ● ● ●

osteonecrosis of the femoral head most commonly affects patients in third to fifth decades of life and may be traumatic or atraumatic in aetiology traumatic follows femoral neck fracture or hip dislocation atraumatic may be classified as direct or indirect: ■ direct causes account for 10 per cent of cases and include radiotherapy, dysbaric osteonecrosis (caisson disease), infiltrative lesions of the femoral neck (myeloproliferative disorders, lymphoma and leukaemia), metabolic disorders such as Gaucher’s disease, sickle cell anaemia and thalassaemia

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Figure 4.20 Anatomy of the femoral head. Coronal (a) and axial (b) proton density-weighted fast spin-echo (FSE) images showing the spherical cartilage-covered femoral head and the central fovea capitis (arrowheads). Coronal T2-weighted FSE image (c) showing measurement of the femoral head–neck angle (double-headed arrow).

indirect causes account for 90 per cent of cases and include corticosteroid use, alcohol and tobacco abuse, chronic renal failure and chronic inflammatory disorders such as RA and systemic lupus erythematosus there are various radiological classifications, of which that by Ficat and Arlet is the most commonly used: ■ stage 1 – normal radiographs ■ stage 2 – sclerosis or cystic change without subchondral fracture ■ stage 3 – crescent sign (subchondral collapse) and/or step-off in the contour of subchondral bone ■ stage 4 – secondary OA with joint space narrowing and osteophytes rapid screening with a single coronal T1W SE sequence is highly sensitive and specific for the diagnosis of osteonecrosis ■

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MRI findings ● in early-stage osteonecrosis (1 and 2) the typical features are: ■ a region of normal fat SI with a surrounding hypointense band on T1W images (band pattern) (Fig. 4.21a) ■ a ‘double-line’ sign on T2W images (Fig. 4.21b), which comprises a high SI line due to hypervascular granulation tissue and a hypointense line due to reactive osteoblastic activity at the margin of the lesion

The hip joint

a b

c

d

e

f

g

Figure 4.21 Osteonecrosis of the femoral head. Coronal T1-weighted (T1W) spin-echo (SE) image (a) showing the ‘double-band’ sign (arrow) of early osteonecrosis. Coronal T2-weighted (T2W) fast spin-echo (FSE) image (b) showing the ‘double-line’ sign (arrow) of early osteonecrosis. Coronal T1W SE image (c) showing intralesional reactive change (arrow). Coronal T1W SE (d) and short tau inversion recovery (e) images showing femoral head and neck oedema (arrows). Coronal T1W SE image (f) showing early collapse of the femoral head consistent with grade 3 osteonecrosis. Sagittal T2*-weighted gradient-echo image (g) showing secondary osteoarthritis consistent with grade 4 osteonecrosis. (continued)

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h i Figure 4.21 (continued) Coronal post-contrast T1W SE fat-suppressed image (h) showing rim enhancement (arrow) of the necrotic lesion. Coronal T2W FSE image (i) showing a joint effusion (arrows) associated with grade 3 osteonecrosis.

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with advancing disease, reactive intralesional and extralesional abnormalities are identified:49 ■ intralesional reactive changes appear as areas of intermediate SI on T1W (Fig. 4.21c) and are most commonly seen in stage 4 disease ■ extralesional reactive changes appear as intermediate SI on T1W (Fig. 4.21d) and hyperintensity on T2W/STIR (Fig. 4.21e) images and correspond to marrow oedema around the boundary of the lesion; most commonly seen in stage 3 disease ■ irregularity of the femoral head contour due to partial collapse (Fig. 4.21f) and secondary OA (Fig. 4.21g) following gadolinium: rim enhancement at the margins of the necrotic area is a very common finding (Fig. 4.21h), while enhancement of reactive intralesional and extralesional areas is also identified joint effusion49,50 (Fig. 4.21i) is more commonly seen in stage 3 disease than in stage 1 bone marrow oedema50–53 (Fig. 4.21d, e) is significantly more common in stage 3 disease than in stage 1 and correlates with the presence of pain: ■ in corticosteroid-induced osteonecrosis, the presence of bone marrow oedema correlates strongly with subsequent collapse of the femoral head52 ■ the presence of marrow oedema also correlates with a greater volume of femoral head necrosis53 ■ the presence of oedema associated with a double-line sign predicts a poor response to core decompression compared with the presence of the double-line sign only MRI can predict the likelihood of femoral head collapse54 based on the area of the femoral head involved by the necrotic lesion: ■ in cases where 50 per cent involvement is associated with collapse in 83 per cent of cases ■ the location of lesions involving 4 mm or its length is >12.5 mm

Subchondral insufficiency fracture of the femoral head60 ●

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subchondral insufficiency fractures mainly affect elderly patients (seventh to ninth decades) with osteoporosis, but are also described in renal transplant patients and may be associated with obesity but not with corticosteroid use clinically, patients present with spontaneous onset of hip pain, and the condition usually results in a requirement for total hip arthroplasty (THR)

MRI findings ● ● ●

a low SI line is seen in the subchondral bone that may be parallel to the articular surface (Fig. 4.24a) or may have a serpentine morphology diffuse femoral head and neck oedema on T2W/STIR images (Fig. 4.24b) the condition may progress to collapse of the articular surface and rapid destruction of the hip joint61

a b Figure 4.24 Subchondral insufficiency fracture. Sagittal proton density-weighted (PDW) fast spin-echo (FSE) MR arthrogram (a) showing a subchondral low signal intensity fracture line (arrow) filled with contrast medium. Coronal PDW FSE fat-suppressed MR arthrogram (b) showing extensive femoral head and neck marrow oedema.

Osteochondral injury of the femoral head1,62 ●

●

osteochondral injury is most commonly associated with previous hip dislocation: ■ anterior dislocation is associated with posterolateral osteochondritis dissecans ■ posterior dislocation is associated with anterior femoral head osteochondritis dissecans (most common) it is also reported in high-level athletes, who present with persistent groin pain; it is located in the anteromedial aspect of the femoral head and is more common in males

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The hip joint and pelvic girdle

MRI findings ● a focal area of subchondral bone marrow oedema is seen occupying 10–25 per cent of the femoral head ● the oedema does not extend across the midline ● there is no evidence of femoral head collapse, though irregularity of the overlying cartilage may be seen

Occult hip fracture63,64 ● ●

several studies have demonstrated the value of MRI in the assessment of patients in whom there is a clinical suspicion of hip fracture but plain radiographs are normal65,66 in these cases, MRI may show various features, including: ■ a radiographically occult femoral fracture involving the neck, intertrochanteric region or greater trochanter ■ a radiographically occult pelvic fracture involving the acetabulum or pubic bone ■ a muscle injury with/without an associated fracture

MRI findings ● occult femoral neck fractures appear as linear areas of low SI surrounded by a variable amount of bone marrow oedema (Fig. 4.25a, b)

a b Figure 4.25 Occult femoral neck fracture. Low-field open MRI: Axial T1-weighted spin-echo image (a) showing a hypointense fracture line (arrow) in the inferomedial aspect of the femoral neck. Coronal short tau inversion recovery image (b) showing oedema (arrow) around the fracture.

Stress fracture of the femoral neck1–3 ●

stress/fatigue fractures of the femoral neck are common sport-related injuries, more frequently seen in females

MRI findings ● ● ● ● ●

a poorly defined area of reduced SI is seen on T1W images (Fig. 4.26a) with increased SI on T2W FSE/STIR images (Fig. 4.26b) within this area, a stress fracture manifests as a linear hypointense line that commonly extends to the cortical margin, typically to the medial femoral neck (Fig. 4.26b, c) increased T2W SI in the fracture site may indicate haemorrhage within the fracture surrounding soft-tissue oedema a healed fracture manifests as a region of medullary sclerosis (Fig. 4.26d)

The hip joint

a

b

d

c Figure 4.26 Stress fracture of the femoral neck. Coronal T1-weighted (T1W) spin-echo (SE) image (a) showing marrow oedema (arrows) in the femoral neck. Coronal short tau inversion recovery (b) and sagittal T2*-weighted gradient-echo (c) images showing a hypointense fracture line (arrows) in contact with the medial femoral neck cortex and oedema (arrowheads) around the fracture. Coronal T1W SE image (d) showing a healed fracture manifest as an area of low signal intensity due (arrow) to marrow sclerosis.

THE GREATER TROCHANTER Normal anatomy67,68 ●

●

the greater trochanter arises from the lateral aspect of the femoral neck and comprises four facets: anterior, lateral, superoposterior and posterior: ■ the anterior is located on the anterolateral surface of the trochanter (Fig. 4.27a) ■ the lateral is located most laterally on the trochanter (Fig. 4.27a) ■ the superoposterior forms the most cranial part of the trochanter (Fig. 4.27b, c) ■ the posterior is the most posterior aspect of the trochanter (Fig. 4.27a) three trochanteric bursae are described: ■ the trochanteric bursa is also termed the ‘subgluteus maximus bursa’ and is located immediately posterior to the posterior facet of the trochanter, appearing as a thin, hypointense line on axial images (Fig. 4.27d) ■ the subgluteus medius bursa is located between the lateral facet and the gluteus medius tendon (Fig. 4.27e) ■ the subgluteus minimus bursa is located anterior to the anterior facet and medial to the tendon of the gluteus minimus (Fig. 4.27f)

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The hip joint and pelvic girdle

b

a

d c

f

e Figure 4.27 Anatomy of the greater trochanter. Axial proton density-weighted (PDW) fast spin-echo (FSE) image (a) showing the anterior (black arrowheads), lateral (short black arrows) and posterior (long white arrows) facets. Sagittal (b) and coronal (c) PDW FSE images showing the superoposterior facet (arrows). Note the insertion of the main tendon of the gluteus medius (arrowhead b). Axial PDW FSE image (d) showing the thin trochanteric bursa (arrow) located posterior to the posterior facet. Coronal PDW FSE image (e) showing the position of the subgluteus medius bursa (arrow) located between the lateral facet and the lateral tendon of the gluteus medius (arrowheads). Axial PDW FSE image (f) showing the subgluteus minimus bursa (arrow) located medial to the main tendon of the gluteus minimus (arrowhead). (continued)

The hip joint

h

g

i

j

Figure 4.27 (continued) Axial (g) and coronal (h) PDW FSE images showing the gluteus minimus (arrows) and gluteus medius (arrowheads) muscles. Coronal PDW FSE image (i) showing the main tendon of the gluteus medius (arrowhead) inserting into the posterosuperior facet (arrow). Axial PDW FSE image (j) showing the insertion of the lateral tendon of the gluteus medius (arrows) into the lateral facet. ●

abductor muscle insertions into the greater trochanter include the gluteus minimus and the gluteus medius, which represent the ‘rotator cuff ’ of the hip joint: ■ both muscles arise from the lateral aspect of the iliac blade (Fig. 4.27g, h) ■ the gluteus minimus attachment has two distinct components: a main tendon, which inserts into the anterior facet (Fig. 4.27f), and a muscular insertion into the ventral and superior aspect of the hip joint capsule ■ the gluteus medius attachment is divided into three parts: – the main tendon arises from the central posterior portion of the muscle and inserts into the posterosuperior facet (Fig. 4.27b, i): – the lateral part of the tendon inserts into the lateral facet (Fig. 4.27e, j) – the anterior part of the tendon blends with the gluteus minimus tendon and is not identified as a separate structure

PATHOLOGY OF THE GREATER TROCHANTER Greater trochanteric pain syndrome68 ● ●

this is a relatively common condition, often synonymous with trochanteric bursitis69 it most commonly occurs between the fourth and sixth decades of life and is four times more common in women

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The hip joint and pelvic girdle

● ●

clinically, it presents with chronic pain and tenderness over the lateral aspect of the hip, with exacerbation of the pain by lying on the affected hip and climbing stairs pathologically, it is most commonly due to tendinosis (~62 per cent) or a tear (~45 per cent) of the gluteus medius insertion into the lateral facet:

a b

c d

e

f

Figure 4.28 Gluteus medius pathology. Coronal proton density-weighted (PDW) fast spin-echo (FSE) fat-suppressed (FS) (a) and axial PDW FSE (b) images showing thickening and hyperintensity of the gluteus medius tendon insertion (arrows) and fluid in the subgluteus maximus bursa (arrowheads a). Coronal (c) and axial (d) T2-weighted (T2W) FSE FS images showing fluid (arrows) at the insertion site of the gluteus medius tendon and discontinuity of the tendon fibres, consistent with a complete tear. Coronal T2W FSE FS image (e) showing oedema and atrophy of the gluteus medius muscle (arrows). Coronal T2W FSE FS image (f) showing fluid in the subgluteus maximus (arrowheads) and subgluteus medius (arrows) bursae.

The hip joint

gluteus medius tears may be complete (~20 per cent) or partial (~40 per cent), with involvement of gluteus minimus seen in approximately one-third of cases ■ associated trochanteric bursitis is rare hydroxyapatite deposition may occur around the hip joint, most commonly in the gluteus maximus: ■ in the gluteus medius and minimus tendons, hydroxyapatite deposition may result in calcific tendinosis, which may be idiopathic or associated with systemic disorders ■

●

MRI findings68–70 ● gluteus medius tendinosis appears as thickening and hyperintensity of the tendon on PDW FSE/T2W images, with an intact tendon and muscle fibres (Fig. 4.28a, b) ● partial tears appear as a focal discontinuity of the tendon ● complete tears appear as retraction of the tendon end from the lateral facet with intervening fluid (Fig. 4.28c, d) ● associated features include: ■ atrophy and oedema of the muscle (Fig. 4.28e) ■ fluid within the subgluteus medius bursa appears as a focal area of PDW/T2W hyperintensity superior to the greater trochanter (Fig. 4.28f) ■ fluid in the subgluteus maximus bursa appears as a focal area of PDW/T2W hyperintensity lateral to the greater trochanter (Fig. 4.28a, f) ● the accuracy of MRI for the diagnosis of abductor tendon tears is reported to be 91 per cent ● calcific tendinosis appears as a region of muscle oedema adjacent to the greater trochanter with small focal areas of signal void due to calcification

Greater trochanteric bursitis68,71,72 ● ● ● ●

trochanteric bursitis is predominantly seen in middle-aged women and results from inflammation of the subgluteus maximus bursa, typically in association with tendinopathy of the hip abductors clinically, it presents with non-specific lateral hip or thigh pain true bursitis of the greater trochanteric bursa has been described with RA71 the greater trochanteric bursa is the commonest reported site of bursal involvement in tuberculosis72

MRI findings ● two patterns are described:72 fluid-filled bursal distension with wall and septal enhancement following gadolinium (Fig. 4.29a–d), and multiple small abscesses

Morel–Lavallee lesion73 ● ● ● ●

the Morel–Lavallee lesion is a post-traumatic fluid collection dissecting through the subcutaneous tissues in the trochanteric region and proximal thigh, related to the fascia lata and iliotibial band it results from a shearing trauma that separates the superficial and deep fascia with consequent collection of interfascial blood and/or lymphatic fluid this eventually leads to the formation of a subcutaneous cystic structure filled with sterile haemolymphatic or serosanguinous fluid and lined by a fibrous capsule clinically, it presents with a soft, fluctuant lateral hip/thigh mass following a history of trauma; delayed presentation may mimic a soft-tissue tumour: ■ it is most commonly seen in high-speed road traffic accidents and may be associated with acetabular and pelvic fractures

MRI findings ● a cystic mass is found in the subcutaneous perifascial planes lateral to the hip (Fig. 4.30a–c) or in the proximal thigh (Fig. 4.30d, e) ● it is usually well defined and oval in shape, with variable SI depending on the cyst contents (Fig. 4.30a–e) ● it may also contain fluid–fluid levels (Fig. 4.30f) and partial or complete septation

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The hip joint and pelvic girdle

a

b

d c Figure 4.29 Greater trochanteric bursitis. Axial T1-weighted (T1W) spin-echo (SE) (a), T2-weighted fast spin-echo (b) and coronal short tau inversion recovery (c) images showing a massively distended trochanteric bursa (arrows) lying deep to the gluteus maximus muscle (arrowheads a, b). Axial post-contrast T1W SE image (d) showing enhancement of the thickened wall (arrows).

●

the lesion is typically surrounded by a hypointense fibrous capsule and has been classified into six subtypes: ■ type I – have signal characteristics of a simple cyst, hypointense on T1 and homogeneously hyperintense on T2/STIR ■ type II – have signal characteristics of subacute haematoma, homogeneous hyperintensity on T1W and T2W/STIR (Fig. 4.30a–e) ■ type III – have signal characteristics of an organising haematoma, intermediate SI on T1W with heterogeneous SI on T2W/STIR, including areas of hypointensity due to haemosiderin deposition, with patchy enhancement post-contrast ■ type IV – longstanding lesions showing a pattern of perifascial dissection and closed fatty-tissue laceration, with/without a serous/haemorrhagic fluid collection ■ type V – perifascial pseudonodular appearance, with occasional irregular enhancement and skin retraction ■ type VI – correspond to an infected lesion, with a thick, irregular, enhancing wall, internal septation and perilesional inflammatory reaction/oedema

The hip joint

a

b

c d

e

f

Figure 4.30 Morel–Lavallee lesion. Coronal T1-weighted (T1W) spin-echo (SE) (a), axial T2-weighted (T2W) fast spin-echo (FSE) fat-suppressed (FS) (b) and coronal short tau inversion recovery (c) images showing a well-defined blood-filled bursa (arrows) overlying the tensor fascia lata (arrowheads a, c). Morel–Lavallee lesion of the proximal thigh: Coronal (d) and axial (e) T1W SE images showing a lesion (arrows) dissecting between the subcutaneous fat and the deep fascia. Axial T2W FSE FS image (f) showing a fluid level.

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The hip joint and pelvic girdle

b a Figure 4.31 Anatomy of the lesser trochanter. Coronal (a) and axial (b) proton density-weighted fast spin-echo images showing the position of the lesser trochanter (arrows).

THE LESSER TROCHANTER Normal anatomy74 ● ● ●

the lesser trochanter arises at the medial aspect of the femoral neck–shaft junction just distal to the level of the greater trochanter (Fig. 4.31) it has three distinct facets, allowing for tendinous insertions, and is the site of insertion of the iliopsoas tendon the lesser trochanteric bursa lies between the psoas tendon and the lesser trochanter

PATHOLOGY OF THE LESSER TROCHANTER Trauma ●

acute avulsion may be associated with sports, while avulsion of the lesser trochanter in an adult should raise the suspicion of a pathological fracture due to underlying malignant infiltration75

Lesser trochanteric bursitis76 ●

lesser trochanteric bursitis is a rare condition presenting with anterior hip/groin pain

MRI findings ● fluid is seen within a bursa adjacent to the lesser trochanter (Fig. 4.32)

Figure 4.32 Lesser trochanteric bursitis. Axial T2-weighted fast spin-echo image showing fluid within a bursa (arrows) overlying the lesser trochanter (arrowhead).

The hip bursae

THE HIP BURSAE THE ILIOPSOAS BURSA Normal anatomy2,77 ● ● ● ●

the iliopsoas bursa is also termed the ‘iliopectineal bursa’ and is the largest bursa in the human body; it is present in 98 per cent of hips it arises due to a protrusion of synovial lining between the iliofemoral and pubofemoral ligaments a normal communication with the hip joint is reported in 10–15 per cent of individuals when distended with fluid, the bursa can extend from the iliac fossa superiorly to just above the lesser trochanter inferiorly

PATHOLOGY OF THE ILIOPSOAS BURSA Iliopsoas bursitis77,78 ●

●

iliopsoas bursitis is most commonly associated with chronic hip arthropathy (degenerative or inflammatory) and may be idiopathic or post-traumatic: ■ overuse injury in sports: irritation of the iliopsoas tendon as it moves over the iliopectineal eminence of the femoral head ■ other causes include infection, pigmented villonodular synovitis, synovial osteochondromatosis and gout clinically, it is more common in women, typically occurring in the fourth to eighth decades: ■ in athletes, it presents with groin pain that is exacerbated by hip extension ■ when complicating chronic arthropathy (OA, RA), it commonly presents as a non-tender, palpable mass

MRI findings ● a fluid SI mass, typically 5–6 cm in size, located posteromedial to the iliopsoas muscle, anterior to the hip joint and posterolateral to the femoral vessels (Fig. 4.33a–c) ● it is hypointense on T1W (Fig. 4.33a) and hyperintense on T2W/STIR images (Fig. 4.33b, c), usually with homogeneous SI ● a thin or occasionally irregularly thickened bursal wall may be seen that enhances following contrast ● communication with the hip joint is optimally identified on axial images (Fig. 4.33a) ● a hip joint effusion may be seen, with evidence of underlying hip pathology (e.g. OA, RA)

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The hip joint and pelvic girdle

b

a

c

Figure 4.33 Iliopsoas bursitis. Axial T1-weighted gradient-echo image (a) showing the hypointense bursa (arrowheads) and its communication with the hip joint (arrow). Axial T2-weighted (T2W) fast spin-echo (FSE) image (b) showing the relationship of the bursa (arrowheads) lying deep to the femoral artery (arrow). Sagittal T2W FSE image (c) showing the relationship between the bursa (arrowheads) and the iliopsoas tendon (arrow).

THE OBTURATOR EXTERNUS BURSA Normal anatomy79 ● ●

the obturator externus bursa is a potential bursa that lies between the tendon of the obturator externus and the posterior hip capsule it is thought to arise secondary to the protrusion of synovium between the ischiofemoral ligament and the zona orbicularis (Fig. 4.34a)

PATHOLOGY OF THE OBTURATOR EXTERNUS BURSA Obturator externus bursitis79 ●

obturator externus bursitis is associated with underlying hip pathology, including OA, synovial osteochondromatosis, pigmented villonodular synovitis and tuberculosis

MRI findings ● the findings are of a hip joint effusion ● a well-defined, oval fluid collection, communicating with and extending from the posteroinferior aspect of the hip joint (Fig. 4.34b, c), that displaces the obturator externus muscle and tendon inferiorly and extends medially towards the obturator foramen

The hip bursae

a

b

c

Figure 4.34 Obturator externus bursitis. Coronal proton density-weighted fast spin-echo (FSE) image (a) showing a small fluid-filled protrusion of the capsule (arrow) above the zona orbicularis (arrowhead). Coronal T1-weighted spin-echo (b) and axial T2-weighted FSE fat-suppressed (c) images showing the distended bursa (arrows) arising from the posteroinferior hip capsule and displacing the obturator externus muscle (arrowheads) anteroinferiorly.

b a

c

Figure 4.35 Hip ganglion. Coronal T1-weighted spin-echo (a), short tau inversion recovery (b) and axial T2-weighted fast spin-echo (c) images showing a lobulated septated ganglion cyst (arrows) anterior to the left hip joint.

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The hip joint and pelvic girdle

Hip ganglia80 ● ● ● ●

ganglia related to the hip joint are uncommon pathologically, they may represent an iliopsoas bursa that has lost its communication with the hip joint clinically, ganglia present as painful/painless groin masses, typically in the elderly (~60–70 years) they are usually located anterior to the hip joint and posterolateral to the femoral vessels

MRI findings ● appear as a well-defined, lobulated mass that is hypointense on T1W (Fig. 4.35a) and hyperintense on T2W/STIR images (Fig. 4.35b, c) ● have a thin, hypointense wall and internal septa, which may enhance following gadolinium

THE PAEDIATRIC HIP Proximal focal femoral deficiency81,82 ●

● ● ● ●

●

proximal focal femoral deficiency (PFFD) is a congenital disorder defined as deficiency of the iliofemoral articulation, limb malrotation and leg length discrepancy, with a spectrum from mild femoral shortening with varus deformity to complete absence of both the acetabulum and the proximal femur with only a small distal fragment it is unilateral in ~90 per cent of cases, with an estimated incidence of ~1/52 000 live births PFFD is associated with acetabular dysplasia, which correlates with the degree of femoral head deficiency various classification systems are used to grade the degree of the condition, thereby helping to predict future limb function and the need for surgical intervention82 congenital shortening of the femur is a related disorder comprising shortening and anterolateral bowing of the femur, valgus deformity of the knee, absence of the anterior cruciate ligament, hamstring tightness, ipsilateral fibular hemimelia and foot deformities MRI is useful for pre-operative planning for both conditions

MRI findings ● PFFD: MRI determines the type of PFFD (Fig. 4.36a, b), and predicts the degree of leg length discrepancy, the hip joint integrity and the stability of the femoral segment ● congenital shortening of the femur: MRI demonstrates associated fibular and foot deformity, including the presence of tarsal coalition

b

a Figure 4.36 Proximal focal femoral deficiency. Axial (a) and coronal (b) T2*-weighted gradient-echo images showing a mildly hypoplastic left femur (arrowheads) with a small proximal femoral cartilaginous epiphysis (arrows) representing the mildest form of the disorder.

The paediatric hip

Coxa vara81 ● ● ● ●

●

●

coxa vara is defined as an abnormally small femoral neck–shaft angle (15 mm, but it does not cover the whole of the tibial plateau. Coronal T2*-weighted gradient-echo image (b) showing a meniscus to tibia ratio of 25 per cent. Coronal T2-weighted fast spin-echo fatsuppressed image (c) showing a complete discoid lateral meniscus (arrows) covering the whole of the lateral tibial plateau.

c

a b c

d

e

Figure 5.16 Meniscal flounce. Sagittal T2*-weighted gradient-echo image (a) showing a medial meniscal flounce (arrow). Sagittal proton density-weighted (PDW) fast spin-echo (FSE) image (b) showing buckling of the lateral meniscus (arrow). Ring-shaped lateral meniscus. Coronal PDW FSE image (c) showing a normal peripheral lateral meniscal body (arrow) and the inner margin of the ‘ring’ (arrowhead) in the intercondylar notch. Sagittal PDW FSE images (d,e) showing the normal anterior and posterior thirds of the lateral meniscus (arrows d) and the inner margin of the ‘ring’ (arrows e) in the intercondylar notch.

The menisci

Meniscal malformation41 ● ●

ring-shaped lateral meniscus: a ring-shaped (Fig. 5.16c–e) and flipped lateral meniscus may result in the appearance of a meniscal fragment in the intercondylar notch, simulating a BHT it is a rare congenital anomaly, accounting for four of 164 lateral meniscal variants37

PITFALLS IN THE DIAGNOSIS OF MENISCAL TEARS Increased intrameniscal signal intensity ● ● ● ●

●

the ‘magic-angle’ phenomenon42 results in increased SI in the upsloping inner portion of the posterior third of the meniscus on short TE sequences (Fig. 5.17a) the anterior third of the lateral meniscus:43 speckled areas of high SI can be seen in the central aspect of the anterior third of the lateral meniscus as a normal variant (Fig. 5.17b) edge artefact:22 a horizontal line of increased SI may be seen on the most peripheral sagittal image due to the concave outer margin of the meniscus (Fig. 5.17c) that may be mistaken for a horizontal tear chondrocalcinosis44 results in increased intrameniscal SI on T1W SE, PDW FSE and inversion recovery sequences (Fig. 5.17d, e), thereby reducing the sensitivity, specificity and accuracy of MRI in the diagnosis of meniscal tears haemosiderin–vacuum phenomenon:22 haemosiderin related to previous haemarthrosis and the vacuum phenomenon may result in linear areas of signal void within the joint mimicking a displaced meniscal fragment, appearing most prominently on GE images

a b

c

Figure 5.17 Increased intrameniscal signal intensity (SI). ‘Magic-angle’ effect: Sagittal T2*-weighted (T2*W) gradientecho (GE) image (a) showing increased intrameniscal SI in the central portion of the posterior third of the medial meniscus (arrow). Lateral meniscus: Sagittal proton density-weighted fast spin-echo (FSE) fat-suppressed (FS) image (b) showing normal increased intrameniscal SI in the central portion of the anterior third of the lateral meniscus (arrow). Peripheral rim edge effect: Sagittal T2*W GE image (c) through the periphery of the medial meniscus showing a horizontal line of increased SI due to edge effect. (continued)

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The knee

d

e

Figure 5.17 (continued) Chondrocalcinosis: Coronal T2-weighted FSE FS image (d) and corresponding anteroposterior radiograph (e) showing chondrocalcinosis (arrows) in the menisci.

●

the intra-articular ligaments and tendons: ■ meniscofemoral:45 sagittal MR images may show a pseudotear in the central aspect of the posterior third of the lateral meniscus due to the meniscal insertion of the MFL, which appears as an oblique or a vertical line of increased SI (Fig. 5.18a)

a

b

c d Figure 5.18 Mimics of meniscal tears. Meniscofemoral ligament (MFL): Sagittal T2*-weighted gradient-echo image (a) showing an oblique attachment of the MFL (arrowhead) to the central aspect of the posterior third of the lateral meniscus, simulating a tear (arrow). Transverse intermeniscal ligament: Sagittal proton density-weighted (PDW) fast spin-echo (FSE) images (b, c) showing the insertion of the transverse intermeniscal ligament (arrows) to the anterior third of the lateral meniscus, simulating a tear (arrowhead b). Popliteus tendon: Sagittal PDW FSE fat-suppressed image (d) showing linear high signal intensity (arrow) between the lateral meniscus and the popliteus tendon (arrowhead).

Pathology of the menisci

■ ■ ■

transverse intermeniscal: on sagittal images, the attachment of the transverse ligament to the anterior third of the lateral meniscus may be mistaken for a tear (Fig. 5.18b, c) oblique meniscomeniscal:34 may mimic a displaced tear of the posterior third of the lateral meniscus on coronal images (Fig. 5.12b, c) popliteus tendon: a vertical high SI line is produced by the passage of the popliteus tendon behind the posterior third of the lateral meniscus, mimicking a vertical peripheral tear (Fig. 5.18d)

PATHOLOGY OF THE MENISCI Meniscal subluxation (protrusion, extrusion)46 ●

●

●

● ●

meniscal subluxation is protrusion of the edge of the meniscus beyond the margin of the tibial plateau and is defined arbitrarily as: ■ protrusion of >25 per cent of the width of the meniscus46 or >3 mm of protrusion47 in normal/asymptomatic controls,46 medial meniscal subluxation is identified in 6.5 per cent and 15 per cent of sagittal and coronal MR images, respectively, and lateral meniscal subluxation is identified in 2 per cent and 13 per cent of sagittal and coronal MR images, respectively abnormal meniscal subluxation is reported in 8 per cent of symptomatic knees,47 associated with joint effusion and osteoarthritis (OA)46–48 (Fig. 5.19a); the degree of subluxation is related to the degree of joint space narrowing:48 ■ posterior subluxation of the lateral meniscus is associated with ACL insufficiency46 (Fig. 5.19b) meniscal extrusion is also associated with49 severe meniscal degeneration and meniscal tears, the latter being extensive complex or radial tears or tears involving the meniscal root50 meniscal extrusion is reported in 48 per cent of knees of young athletes,51 associated with joint effusion, meniscal tears and ACL rupture

a

b

Figure 5.19 Meniscal subluxation. Coronal proton density-weighted fast spin-echo fat-suppressed image (a) showing subluxation of the medial meniscus (arrow) in association with medial compartment osteoarthritis (arrowhead). Sagittal T2*-weighted gradient-echo image (b) showing posterior subluxation of the lateral meniscus (arrow) in a patient with a complete anterior cruciate ligament rupture.

Meniscal degeneration2,22 ● ● ●

meniscal degeneration represents mucoid change in the collagen fibres, which occurs with advancing age with increasing intra-substance degeneration, interstitial tears develop that are not clinically relevant meniscal degeneration is identified in approximately 25 per cent of knee MRI studies, appearing as intermediate SI on T1W/PDW sequences and increased SI on T2W FSE FS sequences that is confined to the meniscus (grade 2) (Fig. 5.6b, c) and is typically unchanged on long-term follow-up52

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The knee

MENISCAL TEARS Introduction2,22 ● ● ● ●

●

a meniscal tear may result from progressive degeneration and extension of an interstitial tear to the meniscal surface or as an acute traumatic event clinically, patients present with symptoms of locking, grinding and joint-line tenderness with a positive McMurray’s test on examination meniscal tears occur most commonly in the posterior third of the medial meniscus tears of the anterior third are rare and are over-reported at MRI, with a true-positive rate of 26 per cent reported in the literature:53 ■ increased SI in the anterior third of the meniscus usually does not represent a clinically significant lesion the prevalence of meniscal tears in asymptomatic knees54 is reported as 67 per cent of those in patients with symptomatic meniscal tears on the contralateral side: ■ asymptomatic tears are usually horizontal or oblique (degenerative); asymptomatic radial, complex and displaced tears are rare ■ clinical follow-up of asymptomatic meniscal tears55 has shown an increased incidence of knee pain, stiffness and impaired function during daily activities at a minimum of 2 years compared with individuals with no meniscal tears

MRI of meniscal tears2,22 ● ●

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MRI criteria for meniscal tears may be divided into primary and secondary signs primary signs: ■ increased intrameniscal SI that reaches the articular surface:56 >90 per cent of menisci with increased SI contacting the articular surface on more than one image are torn at arthroscopy (Fig. 5.5e, f), whereas 55 per cent of medial and 30 per cent of lateral menisci with increased SI contacting the articular surface on only one image are torn ■ similarly, unequivocal grade 3 intrameniscal SI reveals tears at arthroscopy in 89 per cent of cases, whereas equivocal grade 2/3 SI is associated with tears in only 10 per cent of cases56 ■ abnormal meniscal morphology: a small or blunted meniscus (Fig. 5.20a, b), in the absence of previous meniscectomy, indicates loss of meniscal tissue and should prompt the search for a displaced fragment secondary signs: ■ an abnormal popliteomeniscal fascicle57 is associated with a tear of the posterior third of the lateral meniscus (Fig. 5.20c), though it does not significantly improve sensitivity ■ posterolateral pericapsular oedema57 is not significantly related to posterior third lateral meniscal tears classification of meniscal tears: meniscal tears are classified into two basic types, vertical and horizontal: ■ vertical tears are typically post-traumatic and are subdivided into radial and longitudinal ■ horizontal (cleavage) tears are typically degenerative ■ complex tears are a combination of more than one morphology ■ MRI can correctly classify tears in ~80 per cent of cases58 the role of MRI in the management of meniscal tears:22 ■ the options for management of meniscal tears include conservative and operative ■ conservative management may be used for stable tears or peripheral tears (within 3 mm of the meniscocapsular junction), which have a high likelihood of spontaneous healing due to the excellent vascularity of the outer (red) zone of the meniscus ■ surgical options include: – meniscal repair: usually undertaken for longitudinal and oblique tears – meniscectomy (partial or complete): for radial, horizontal, complex or unstable tears – the goal is to preserve as much meniscal tissue as possible, since there is a direct correlation between the amount of meniscus resected and the time of onset and severity of OA

Pathology of the menisci

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Figure 5.20 Signs of a meniscal tear. Primary: Sagittal proton density-weighted (PDW) fast spin-echo (FSE) fat-suppressed (a) and coronal PDW FSE (b) images showing blunting (arrows) of the inner margin of the medial meniscus. Secondary: Sagittal T2*-weighted gradient-echo image (c) through the posterior third of the lateral meniscus showing a tear of the inferior popliteomeniscal fascicle (arrow).

Radial tears59,60 ● ●

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radial tears are vertical tears running perpendicular to the long axis of the meniscus (Fig. 5.21a) and account for 14–15 per cent of arthroscopically detected tears they may be small and limited to the free edge of the meniscus or large, running through the whole width of the meniscus; full-thickness radial tears severely compromise meniscal function, leading to premature degenerative change the most common location60 is the posterior third of the medial meniscus (53 per cent), followed by the posterior third of the lateral meniscus (26 per cent) and lateral meniscal body (16 per cent): ■ radial tears of the body or anterior medial meniscus are very rare

MRI findings ● four signs have been described for the diagnosis of a radial tear60 ● the truncated triangle sign is abrupt termination of the normal triangular meniscal contour at the tip of the meniscal inner margin (Fig. 5.21b) ● the cleft sign is a vertical, high SI line passing through the meniscus (Fig. 5.21c, d) ● the marching cleft sign is similar to the cleft sign, but indicates the presence of the vertical tear on consecutive slices, with the position moving either anteriorly or posteriorly on sagittal images or sideways on coronal images ● the ‘ghost meniscus’ sign is a triangular, hyperintense meniscal fragment seen when the image slice passes through the tear (Fig. 5.21e); a normal appearance to the meniscus is seen on adjacent slices: ■ using these four criteria, 89 per cent of arthroscopically diagnosed radial tears were identified retrospectively60 ● the use of fat suppression can increase the sensitivity of detection59

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Figure 5.21 Radial meniscal tear. Axial proton densityweighted (PDW) fast spin-echo (FSE) fat-suppressed (FS) image (a) showing a small radial tear (arrow) of the posterior third of the medial meniscus. Truncated triangle sign: Coronal PDW FSE FS image (b) showing blunting (arrow) of the inner margin of the lateral meniscus. Cleft sign: Sagittal T1-weighted spinecho (c) and coronal T2-weighted FSE FS (d) images in different patients showing a vertical high signal intensity line (arrows) running through the posterior third of the lateral meniscus. ‘Ghost meniscus’ sign: Sagittal T2*-weighted gradient-echo image (e) showing a hyperintense triangle (arrow) where the slice is passing through a full-thickness posterior third medial meniscal radial tear.

Pathology of the menisci

Longitudinal tears2,22 ●

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longitudinal tears run parallel to the long axis of the meniscus at a constant distance from its peripheral margin: ■ if a tear extends significantly through the length of the meniscus, the inner fragment may become displaced into the intercondylar notch, producing a BHT BHTs61–65 may present with locking and account for ~10 per cent of meniscal tears; they are much more common on the medial side

MRI findings ● longitudinal tear: vertically orientated, linear increased SI is seen within the substance of the meniscus (Fig. 5.22)

Figure 5.22 Longitudinal meniscal tear. Sagittal proton density-weighted fast spin-echo image showing a peripheral longitudinal tear of the posterior third of the medial meniscus (arrow).

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BHT: a variety of signs have been described for the displaced fragment: ■ the double-PCL sign results when the meniscal fragment lies anterior and parallel to the PCL, seen on both sagittal and coronal images (Fig. 5.23a, b): – has a reported sensitivity of ~30–53 per cent62 and specificity of 100 per cent65 – the use of coronal STIR61 and 3D volume sequences63 is reported to improve the sensitivity ■ the flipped meniscus sign results when a displaced posterior meniscal fragment flips anteriorly to lie adjacent to the anterior third, making the anterior third of the meniscus appear too large (Fig. 5.23c–e): – has a reported sensitivity of 44 per cent for medial BHT and 27 per cent for lateral BHT, and a specificity of 89.7 per cent65 ■ a fragment in the intercondylar notch sign results when the fragment is displaced into the intercondylar notch adjacent to the tibial spine (Fig. 5.23f): – has reported sensitivity of 69 per cent and specificity of 94 per cent66 BHT: signs related to the residual meniscus include: ■ the absent ‘bow-tie’ sign: a bow-tie sign is present when the body of the meniscus appears as a bow tie in two consecutive 4 mm sagittal images, but is absent if the body appears as a bow tie on only one or no sagittal images:62 – has reported sensitivities and specificities of 71–98 per cent63–65 and a positive predictive value of 76 per cent63 – a false-positive diagnosis may occur with small menisci or with meniscal subluxation

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f e Figure 5.23 ‘Bucket-handle’ tear, displaced fragment. The double posterior cruciate ligament (PCL) sign: Sagittal proton density-weighted (PDW) fast spin-echo (FSE) (a) and coronal PDW FSE FS (b) images showing the displaced meniscal fragment (white arrow a; black arrows b) lying anterior and parallel to the PCL (arrowheads), with a small residual medial meniscal body (white arrow b). The flipped meniscus sign: Sagittal (c), coronal (d) and axial (e) PDW FSE images showing the anterior third of the lateral meniscus appearing too large (arrow c), the posterior third being deficient (arrowheads c, d) with the ‘flipped’ fragment seen on the axial image (arrowheads e). Fragment in the notch sign: Coronal PDW FSE image (f) showing the displaced fragment (arrow) located in the intercondylar notch adjacent to the tibial spine (arrowhead) and the medial meniscal body appearing too small (double arrowhead).

Pathology of the menisci

the disproportionate posterior horn sign results when the central portion of the posterior third appears larger than the peripheral portion of the posterior third of the meniscus67 (Fig. 5.24a–c) and is indicative of a centrally displaced posterior third tear; it is reported in 21–27 per cent of cases64,67 ■ the truncated meniscus sign results when the inner margin of the meniscus appears blunted on coronal images (Fig. 5.24d), and is reported in 64 per cent of cases62 the double ACL sign68 has been reported as a sign of a displaced tear of the lateral meniscus, where the displaced fragment lies posteroinferior to the ACL the quadruple cruciate sign69 has been reported in the rare event of simultaneous BHTs of the medial and lateral menisci, resulting in four structures in the intercondylar notch on coronal images, owing to the two displaced fragments, the ACL and the PCL ■

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Figure 5.24 ‘Bucket-handle’ tear, residual meniscus. The disproportionate posterior horn sign: Sagittal proton densityweighted (PDW) fast spin-echo (FSE) (a) and T2*-weighted gradient-echo (b) images through the posterior third of the lateral meniscus showing a larger central portion (arrow a) than peripheral portion (arrowhead b). Coronal T2-weighted FSE fat-suppressed (FS) image (c) showing the centrally displaced fragment (arrow) located next to the posterior cruciate ligament (arrowhead). The truncated meniscus sign: Coronal PDW FSE FS image (d) showing the blunted inner margin of the medial meniscus (arrow), with the fragment seen in the notch (arrowhead).

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Horizontal cleavage tears2,22 ● ●

horizontal cleavage tears extend through the meniscus in a plane parallel to the tibial plateau, dividing the meniscus into superior and inferior portions they are considered to be degenerative in aetiology and are the commonest type of tear associated with a meniscal cyst

MRI findings ● a horizontal line of increased SI runs through the meniscus, usually extending to the tibial articular surface (Fig. 5.25a–c)

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Figure 5.25 Horizontal cleavage tear. Sagittal T1-weighted spin-echo (a), T2*-weighted gradient-echo (b) and coronal proton density-weighted fast spin-echo fat-suppressed (c) images showing increased linear intrameniscal signal intensity (arrows) extending to the tibial articular surface of the medial meniscus.

an inferior flap tear70 is a type of horizontal tear in which a portion of the medial meniscal body displaces into an adjacent synovial recess (usually the inferior) deep to the MCL (Fig. 5.26a, b) and consequently may be missed at arthroscopy: ■ less commonly, flap tears may occur on the lateral side (Fig. 5.26c, d) ■ the reported sensitivity and specificity of MRI for identifying the recess fragment are 71 per cent and 98 per cent, respectively66

Pathology of the menisci

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Figure 5.26 Flap tear. Medial: Coronal proton density-weighted (PDW) fast spin-echo (FSE) fat-suppressed (FS) (a) and axial T2*-weighted gradient-echo (b) images showing displacement of part of the medial meniscal body (arrows) into the adjacent inferior synovial recess deep to the medial collateral ligament. Lateral: Coronal PDW FSE (c) and axial PDW FSE FS (d) images showing a displaced meniscal fragment (arrows) in the superior lateral joint recess.

Oblique and peripheral tears2,22 ● ●

an oblique tear is also termed a ‘parrot-beak’ tear and shows complex linear increased SI with both vertical and horizontal components (Fig. 5.27a, b); it typically results in a flap of unstable meniscal tissue a peripheral tear is a tear confined to the outer third of the meniscus (the red zone) (Fig. 5.27c) and is more likely to heal with conservative therapy due to the rich peripheral blood supply

Meniscocapsular separation71,72 ●

meniscocapsular separation refers to an injury in which the meniscus separates from the capsule, and may result in meniscal instability: ■ it is more common on the medial side but may also occur along the posterolateral corner, and, because it occurs in the red zone of the meniscus, spontaneous healing may occur ■ on the medial side, tears may occur at the meniscocapsular junction, at the meniscofemoral and meniscotibial (coronary) ligaments, which form part of the deep layer of the MCL, or within the peripheral portion of the meniscus (peripheral tear) ■ on the lateral side, tears may involve the popliteomeniscal fascicles,57,73 resulting in symptomatic lateral compartment knee pain associated with hypermobile lateral menisci

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Figure 5.27 Meniscal tears. Complex tear: Sagittal T1-weighted spinecho (a) and T2*-weighted gradient-echo (b) images showing a combination of horizontal and vertical tears consistent with a complex tear of the posterior third of the medial meniscus. Peripheral: Coronal proton density-weighted fast spin-echo fat-suppressed image (c) showing a tear (arrow) involving the outer third of the medial meniscus.

floating meniscus74 describes a post-traumatic situation in which the meniscus is surrounded by joint fluid, indicative of tearing of the coronary ligaments due to meniscal avulsion from the tibia: ■ clinically, the condition is seen in cases of severe acute knee trauma, including dislocation, and more commonly involves the lateral meniscus ■ meniscal avulsion may be mimicked by the Wrisberg type of discoid meniscus, since this has no attachment to the tibial plateau posteriorly

MRI findings ● meniscocapsular separation: there is meniscal displacement relative to the tibia with fluid between the meniscus and the capsule (Fig. 5.28a, b): ■ a meniscal corner tear, occurring at the outer edge of the meniscus but also involving the superior or inferior meniscal corner (Fig. 5.28c) ■ an irregular meniscal margin and tears of the coronary ligaments (Fig. 5.28d, e) ■ laterally, disruption of the popliteomeniscal fascicles (Fig. 5.29a, b), with lateral meniscal displacement due to meniscal hypermobility (Fig. 5.29c) ■ all of the described features have a poor positive predictive value for the diagnosis of meniscocapsular separation, since72 meniscal displacement relative to the tibia may normally be as much as 10 mm medially or 13 mm laterally, and perimeniscal fluid may also be seen medially, within perimeniscal synovial recesses, within the MCL bursa (which lies between the deep and superficial portions of the MCL), in association with MCL tears and within small meniscal cysts ● floating meniscus:74 the diagnosis is made in the presence of fluid SI of >3 mm thickness in long-axis dimension on sagittal or coronal images, surrounding either the anterior or the posterior third of the meniscus, or fluid between the meniscus and the tibial plateau (Fig. 5.29c, d):

Pathology of the menisci

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Figure 5.28 Meniscocapsular separation. Sagittal T2*-weighted gradient-echo image (a) showing anterior displacement of the posterior third of the medial meniscus relative to the tibia, and fluid (arrow) between the meniscal margin and the posterior capsule. Coronal proton density-weighted (PDW) fast spin-echo (FSE) fatsuppressed (FS) image (b) showing fluid (arrow) separating the body of the medial meniscus from the capsule. Coronal PDW FSE FS image (c) showing a tear of the inferior corner (arrow) of the body of the lateral meniscus. Coronal PDW FSE image (d) showing a tear of the meniscotibial ligament of the medial meniscus (arrow). Coronal PDW FSE FS image (e) showing a tear of the meniscofemoral ligament of the medial meniscus with adjacent bone bruising (arrow).

the meniscotibial ligaments are torn (Fig. 5.29e) but the MFLs are typically intact and the meniscus itself is usually normal apart from the avulsion injury associated cruciate and collateral ligament injuries are common, as are bone contusions (Fig. 5.29f)

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Figure 5.29 Meniscocapsular injury. Popliteomeniscal fascicle rupture: Sagittal proton density-weighted (PDW) fast spinecho (FSE) images (a, b) showing tear (arrow a) and displacement (arrow b) of the superior fascicle. Coronal PDW FSE fatsuppressed (FS) image (c) showing lateral meniscal subluxation (arrow). Floating meniscus: Sagittal (d) and coronal (e) PDW FSE FS images showing fluid (arrows) around the anterior and posterior thirds of the lateral meniscus. Coronal PDW FSE image (f) showing absence of the meniscotibial ligament (arrow) consistent with rupture and the associated acute anterior cruciate ligament rupture (arrowheads).

Pathology of the menisci

Tears of a discoid lateral meniscus37,75–77 ● ● ●

discoid lateral menisci are more prone to tears than normal lateral menisci and may also show intrasubstance degeneration76 (Fig. 5.30a, b) 71–92 per cent of discoid lateral menisci show tears,75,76 which are commonly multiple (Fig. 5.30c); peripheral and horizontal types (Fig. 5.30d) are commonest tear type is related to the type of discoid meniscus;77 complete discoid menisci typically show simple horizontal tears, while the incomplete type shows radial, degenerative and complex tears

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Figure 5.30 Discoid meniscal abnormalities. Degeneration: Sagittal proton density-weighted (PDW) fast spin-echo (FSE) fat-suppressed (FS) (a) and coronal PDW FSE (b) images showing extensive mildly increased intrameniscal signal intensity (arrows). Multiple tear: Sagittal T2-weighted FSE FS image (c) showing both horizontal (arrow) and radial (arrowhead) tears of a lateral discoid meniscus. Degenerative: Sagittal PDW FSE FS image (d) showing a simple horizontal tear (arrow) of the anterior third. Radial: Sagittal T2*-weighted gradient-echo image (e) showing a radial tear (arrow) of the lateral meniscus.

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in a study of 164 lateral meniscal variants (158 discoid),37 six tear patterns were observed, including 33 simple horizontal, 21 combined horizontal, 37 longitudinal, 27 central, 14 complex and 12 radial (Fig. 5.30e) MRI is reported to have a positive predictive value of only 57 per cent for the prospective diagnosis of a torn discoid lateral meniscus75

Clinical utility of MRI for meniscal tears ●

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association with OA:78 ■ meniscal tears are identified in 91 per cent of patients with symptomatic OA and 76 per cent of agematched asymptomatic controls ■ meniscal tears in association with OA have no effect on the degree of pain or functional status MRI criteria for prediction of reparability:79 a longitudinal or oblique high SI line within 3 mm of the meniscocapsular junction (Fig. 5.27c): ■ of irreparability: a high SI line >5 mm from the meniscocapsular junction and/or an abnormal high SI area within the meniscal body (complex tear configuration) (Fig. 5.27a, b) ■ MRI has high accuracy and low sensitivity for the identification of reparable lesions, but is both accurate and sensitive in identifying irreparable lesions ability of MRI to identify unstable meniscal tears:80 an unstable tear is defined as one in which the meniscus or a meniscal fragment can be inappropriately displaced (>3 mm) by a probe at arthroscopy: ■ MRI features indicative of an unstable lesion include: – identification of a displaced fragment: sensitivity 36 per cent, specificity 94 per cent – visibility of the tear on more than three 3 mm thick coronal and two 4 mm thick sagittal images: sensitivity 54 per cent, specificity 94 per cent – more than one orientation plane (complex tear) or more than one pattern (contour irregularity, peripheral separation, tear) (Fig. 5.31a): sensitivity 45 per cent, specificity 94 per cent – intrameniscal high SI on a T2W SE image (indicating joint fluid within the meniscus) (Fig. 5.31b): sensitivity 18 per cent, specificity 100 per cent the sensitivity and specificity for the presence of at least one MRI criterion are 82 per cent regarding the lateral meniscus, abnormality of the popliteomeniscal fascicles (Fig. 5.29a, b) may indicate an unstable lesion47

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Figure 5.31 Unstable tear patterns. Sagittal proton density-weighted fast spin-echo (FSE) image (a) showing a horizontal tear through the posterior third of the medial meniscus, which is also blunted. Sagittal T2-weighted FSE image (b) showing joint fluid (arrow) within a complex meniscal tear.

Meniscal cysts81,82 ●

a meniscal cyst is a cyst arising within (meniscal) or more commonly adjacent to (parameniscal) the meniscus in association with a meniscal tear

Pathology of the menisci

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they are thought to result from an intrameniscal or parameniscal collection of joint fluid, which passes from the joint through a full-thickness meniscal tear; they have a reported incidence of 4 per cent on knee MRI studies and are associated with 7.8 per cent of meniscal tears26 clinically, they most commonly present in men aged 20–40 years, resulting in a focal swelling adjacent to the joint, usually on the lateral side: ■ they are clinically and arthroscopically more commonly evident from the lateral meniscus ■ however, MRI studies indicate that they occur approximately twice as commonly from the medial compartment as from the lateral compartment81

MRI findings ● a well-defined, lobulated lesion is seen within (intrameniscal) or adjacent to (parameniscal) the meniscus, with fluid SI on all pulse sequences (Fig. 5.32a–d) and commonly with internal septation (Fig. 5.32c)

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Figure 5.32 Meniscal cysts. Sagittal T1-weighted spin-echo (a), coronal proton density-weighted (PDW) fast spin-echo (FSE) (b), coronal T2-weighted FSE (c) and sagittal PDW FSE fat-suppressed (FS) (d) images showing fluid signal intensity parameniscal cysts (arrows) associated with medial meniscal tears. Coronal PDW FSE FS image (e) showing a combined intrameniscal (arrow) and parameniscal (arrowhead) cyst arising from the lateral meniscus.

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direct contact with the adjacent meniscal tear is seen in 98 per cent of cases,81 this being the most important diagnostic criterion (Fig. 5.32b, c, e) 90 per cent of tears show a horizontal component rarely, meniscal cysts may result in erosion of the adjacent bone83 patterns of cyst extension:84 ■ medial cysts are most commonly located posteromedially (Fig. 5.33a), penetrating the capsule between layer 1 and the fused layers 2 and 3 (see later) ■ they may then extend anteriorly to lie superficial to the MCL ■ lateral cysts may extend anteriorly to lie deep to the iliotibial band (ITB) (Fig. 5.33b) or posterolaterally to lie deep to the lateral collateral ligament (LCL) cyst extension is also described: ■ anteriorly into Hoffa’s fat pad85 (Fig. 5.33c, d) ■ posterior to the PCL from a posterior third medial meniscal tear (a pericruciate meniscal cyst)86 (Fig. 5.34a–c), which may simulate a PCL ganglion and is differentiated by identifying communication with a posterior third meniscal tear

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Figure 5.33 Meniscal cyst extension. Axial proton density-weighted (PDW) fast spin-echo (FSE) fat-suppressed (FS) image (a) showing posteromedial extension of a medial meniscal cyst (arrows). Coronal T2-weighted FSE FS image (b) showing a lateral meniscal cyst (arrow) lying deep to the iliotibial tract (arrowheads). Sagittal PDW FSE (c) and axial PDW FSE FS (d) images showing extension of an anterior third lateral meniscal cyst (arrows) into Hoffa’s fat pad.

Pathology of the menisci

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Figure 5.34 Pericruciate meniscal cyst. Sagittal T2*-weighted gradient-echo (a, b) and axial proton density-weighted fast spin-echo fat-suppressed (c) images showing extension (arrowhead a) of a posterior third medial meniscal cyst (arrows a) posterior to the posterior cruciate ligament and through the posterior capsule (arrows b, c).

Miscellaneous meniscal pathology ●

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meniscal contusion87 is seen in the setting of acute knee trauma and is associated with ACL injury: ■ MRI findings: contusion appears as a region of poorly defined intrameniscal hyperintensity that reaches the articular surface, with adjacent bone bruising in the posterior aspect of the tibial plateau ■ it may resolve with time meniscal haematoma88 is a very rare phenomenon that is thought to result from trauma-induced bleeding from the perimeniscal capillary plexus: ■ MRI findings: reported cases have shown appearances identical to those of a pericruciate meniscal cyst of the posterior third of the medial meniscus meniscal ossicle89 is a rare intrameniscal bone fragment (ossicle) that is most commonly seen in the posterior third of the medial meniscus and radiographically simulates a loose body: ■ MRI findings: a corticated, marrow-containing structure within the posterior third of the medial meniscus, hyperintense on T1W (Fig. 5.35)

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Figure 5.35 Meniscal ossicle. Sagittal T1-weighted spin-echo image showing a marrow-filled meniscal ossicle (arrow) in the posterior third of the medial meniscus.

THE CRUCIATE LIGAMENTS ANTERIOR CRUCIATE LIGAMENT Normal anatomy2,90–92 ●

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the ACL is an intracapsular/extrasynovial structure that originates from the posteromedial aspect of the lateral femoral condyle, posterior to the intercondylar notch, to insert into the tibia, anterolateral to the anterior tibial spine, between the attachments of the anterior thirds of the menisci it runs inferomedially and parallel to the roof of the intercondylar notch, parallel to Blumensaat’s line, at ~55° to the plane of the tibial plateau the ACL is ~38 mm long and 11 mm wide, and has two functional units: ■ the anteromedial band, which is tight in flexion ■ the posterolateral bundle, which is tight in extension on MRI, it is well visualised in all three planes: ■ the sagittal oblique plane (Fig. 5.36a) optimally demonstrates the length of the ligament, allows differentiation of the two bundles and shows the tibial attachment: – with the knee extended, the ligament appears straight – with the knee flexed, the ligament may appear lax and slightly curved ■ the coronal plane (Fig. 5.36b) shows the ligament within the intercondylar notch, where it runs from superolateral to inferomedial, and allows assessment of both the femoral origin and the tibial insertion ■ the axial plane (Fig. 5.36c) most clearly demonstrates the femoral origin of the ACL: – anteromedial band is hypointense, while the posterolateral bundle is of intermediate SI on T1W and mildly hyperintense on PDW FSE FS/T2W FSE FS/STIR images (Fig. 5.36d), with a fan-like structure and a striated appearance due to regions of fat near its tibial attachment

The cruciate ligaments

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d c Figure 5.36 Normal anatomy of the anterior cruciate ligament (ACL). Sagittal (a), coronal (b) and axial (c) proton densityweighted (PDW) fast spin-echo (FSE) images showing the normal ACL (arrows). The anteromedial band is identified separately from the posterolateral bundle by its hypointense signal intensity. Sagittal PDW FSE fat-suppressed image (d) showing the anteromedial band appearing hypointense (arrowhead) and the posterolateral bundle appearing relatively hyperintense (arrow).

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PATHOLOGY OF THE ANTERIOR CRUCIATE LIGAMENT Complete anterior cruciate ligament rupture2,90–92 ● ● ● ●

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acute ACL rupture typically follows a valgus force on the knee in varying degrees of flexion, with associated external rotation of the tibia or internal rotation of the femur, the so-called ‘pivot shift’ injury it is a relatively common sports injury in skiers and American footballers clinically, examination findings include knee swelling and an anterior drawer or positive Lachman’s test the ACL may be torn in its mid-portion (commonly due to contact sports) (Fig. 5.37a, b) or at its femoral insertion (commonly due to skiing) (Fig. 5.37c, d), or rarely is avulsed from its tibial insertion without (Fig. 5.38a, b) or with a fragment of bone (Fig. 5.38c, d): ■ tibial avulsion accounts for ~5 per cent of cases, usually in the skeletally immature MRI has reported sensitivity of 92–94 per cent and specificity of 95–100 per cent for the diagnosis of complete ACL rupture MRI findings may be divided into primary and secondary signs, of which primary signs are the mainstay of diagnosis: ■ secondary signs do not significantly improve the accuracy of MRI for the diagnosis of ACL rupture93

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Figure 5.37 Acute complete anterior cruciate ligament rupture. Sagittal proton density-weighted (PDW) fast spin-echo (FSE) (a) and PDW FSE fat-suppressed (b) images showing a mid-substance tear (arrows). Sagittal PDW FSE (c) and axial PDW FSE (d) images showing a femoral origin rupture (arrow).

The cruciate ligaments

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c Figure 5.38 Tibial avulsion of the anterior cruciate ligament. Sagittal T1-weighted spin-echo (a) and coronal T2-weighted fast spin-echo (FSE) fat-suppressed (FS) (b) images showing tibial avulsion (arrows) with an intact tibial cortex and femoral origin (arrowheads). Sagittal proton density-weighted (PDW) FSE (c) and PDW FSE FS (d) images showing associated avulsion of the tibial plateau (arrows).

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MRI findings ● primary signs comprise morphological and SI abnormalities; acute tears show a poorly defined, oedematous ligament on T1W, PDW FSE and T2W images (Figs 5.37, 5.38): ■ tears of the femoral insertion are well demonstrated on axial images (Fig. 5.37d) ■ subacute tears (2–4 weeks) have a wavy, horizontal (Fig. 5.39a, b) or retracted appearance: – an abnormal course of the ACL can be identified by Blumensaat’s angle, which is the angle between the roof of the intercondylar notch and the line of the ACL, the apex of which normally points posteriorly (Fig. 5.39c); in ACL rupture, the apex points anteriorly (Fig. 5.39d) ■ chronic tears (6–8 weeks) have a variable appearance, being attenuated (Fig. 5.40a), incompletely visualised or absent (Fig. 5.40b), or the ligament may become fibrosed and attached to the PCL (Fig. 5.40c) ■ synovialisation of the ACL following rupture94 represents a reparative process that can simulate an intact ligament at MRI: – hypointense, comma-like tracts may be seen in the expected course of the ligament

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c d Figure 5.39 Subacute anterior cruciate ligament tear. Sagittal proton density-weighted (PDW) fast spin-echo (FSE) (a) and coronal T2-weighted (T2W) FSE fat-suppressed (FS) (b) images show a horizontal wavy appearance of the ligament (arrowheads a), which appears hyperintense and poorly defined on T2W (arrow b). Blumensaat’s angle: Sagittal T1weighted spin-echo image (c) showing a normal angle with the apex pointing posteriorly. Sagittal PDW FSE FS image (d) showing an abnormal angle with the apex pointing anteriorly.

The cruciate ligaments

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Figure 5.40 Chronic anterior cruciate ligament (ACL) tear. Sagittal T1-weighted (T1W) spin-echo (SE) image (a) showing an attenuated ligament (arrow). Sagittal T1W SE image (b) showing an absent ligament with no ACL tissue seen parallel to the roof of the intercondylar notch (arrowheads). Sagittal proton densityweighted fast spin-echo image (c) showing the abnormal course of the ligament (arrowhead), which appears to be attached to the posterior cruciate ligament (arrow).

Secondary signs of anterior cruciate ligament rupture90–93 ●

secondary signs are related to bone injury in the acute stage and to anterior tibial shift in the chronic stage

MRI findings ● bone injury is seen in the form of bone bruising, classically in the central portion of the lateral femoral condyle (Fig. 5.41a–c) and the posterolateral aspect of the tibial plateau (Fig. 5.41a, b), with reported sensitivity of 50 per cent and specificity of 97 per cent for acute ACL rupture: ■ a similar pattern of bone bruising can be seen in young children with an intact ligament due to relative ligament laxity ■ additional sites of bone injury include the medial margin of the MFC (Fig. 5.42a), the posteromedial tibial plateau (Fig. 5.42b), deepening (>1.5 mm) of the condylopatellar sulcus of the lateral femoral condyle (Fig. 5.42c, d) and an osteochondral fracture of the lateral femoral condyle ■ Segond fracture is an avulsion injury of the lateral tibial plateau

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Figure 5.41 Secondary signs of acute anterior cruciate ligament rupture. Bone bruising: Sagittal T1-weighted spinecho (a), coronal proton density-weighted (PDW) fast spinecho (FSE) fat-suppressed (FS) (b) and axial PDW FSE FS (c) images showing the classical pattern of bone contusion (arrows) in the central lateral femoral condyle and the posterolateral tibial plateau.

a b Figure 5.42 Secondary signs of acute anterior cruciate ligament (ACL) rupture. Additional sites of bone injury: Coronal T2-weighted (T2W) fast spin-echo (FSE) fat-suppressed (FS) image (a) showing bone bruising (arrow) in the medial femoral condyle associated with femoral avulsion of the ACL (arrowhead). Coronal T2W FSE FS image (b) showing bone bruising (arrow) in the posteromedial tibial plateau. (continued)

The cruciate ligaments

c d Figure 5.42 (continued) Sagittal proton density-weighted (PDW) FSE FS (c) and coronal PDW FSE (d) images showing deepening of the condylopatellar recess (arrowheads) of the lateral femoral condyle, associated with mid-substance ACL rupture (arrow d).

●

anterior tibial shift in the form of: ■ the anterior drawer sign: diagnosed when there is 5–7 mm of posterior translation of the lateral femoral condyle with respect to the lateral tibial plateau (Fig. 5.43a) ■ buckled PCL: concavity of the posterior (tibial) portion of the PCL with acute angulation at the apex (Fig. 5.43b) ■ abnormal PCL line: the PCL line is defined on sagittal images as a line drawn along the posterior aspect of the PCL that normally should intersect the posterior femoral cortex within 5 cm of the distal femur (Fig. 5.43c, d)

a

b Figure 5.43 Secondary signs of chronic anterior cruciate ligament rupture. Sagittal T1-weighted (T1W) spin-echo (SE) image (a) through the lateral meniscus showing anterior tibial translation >5 mm (arrow). Sagittal T1W SE image (b) showing a hooked posterior cruciate ligament (PCL) with a concave posterior contour (arrowheads). (continued)

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d

e

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g

Figure 5.43 (continued) The PCL line: Sagittal proton densityweighted (PDW) fast spin-echo (FSE) images (c, d) showing a normal PCL line (c) and an abnormal PCL line (d), in which a line drawn along the vertical part of the PCL does not intersect the posterior femoral cortex (arrowhead d). The PCL index: Sagittal PDW FSE images (e, f) showing a normal (e) and an abnormal (f) PCL index, which is the ratio of the length of a line joining the femoral and tibial attachments of the PCL to the distance between this line and the apex of the ligament. Vertical fibular collateral ligament (FCL) sign: Coronal PDW FSE image (g) showing the FCL (arrows) visualised over its entire length on a single image.

The cruciate ligaments

PCL index:95 if the shortest distance between the femoral and the tibial attachments of the PCL is x and a line drawn perpendicular from x to the apex of the PCL is y, then x/y = PCL index (Fig. 5.43e, f); the mean PCL index for an intact ACL is ~5, while the mean PCL index for complete ACL rupture is ~2.88 ■ posterior displacement of the posterior third of the lateral meniscus relative to the posterior margin of the tibial plateau, which has sensitivity of 57 per cent and specificity of 97–100 per cent (Fig. 5.19b) ■ the vertical fibular collateral ligament (FCL) sign:96 normally, the FCL is not seen in its full course on a coronal image, but with anterior tibial shift it assumes a coronal orientation and may be seen in its entire length on a single coronal slice (Fig. 5.43g) ■ undulation of the patellar tendon associated injuries include97 meniscal tears, which occur in 41–68 per cent of acute ACL injuries and are typically posterior third peripheral tears: ■ articular cartilage injuries are reported in 23 per cent of acute injuries and 54 per cent of chronic injuries ■ posterolateral corner injury is seen particularly with a hyperextension mechanism ■ TCL injury ■ a shearing injury of the infrapatellar fat pad, which must be differentiated from a normal horizontal cleft (see later): – manifests as abnormal fat pad SI together with other signs of acute ACL rupture ■

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Acute anterior cruciate ligament stump entrapment98 ●

stump entrapment following ACL rupture may result in a block to terminal extension of the knee

MRI findings ● two types of abnormality are described: ■ type 1 – a nodular mass located at the anterior aspect of the intercondylar notch (Fig. 5.44a–c), between the lateral femoral condyle and the tibia ■ type 2 – a tongue-like free end with angulation of the stump (Fig. 5.44d)

Partial anterior cruciate ligament rupture12,93,99 ● ● ●

partial ACL tears are more difficult to diagnose than complete ACL rupture and may be stable or unstable they account for 10–35 per cent of ACL injuries diagnosed at MRI and more commonly involve the anteromedial band the addition of coronal oblique12 and assessment of axial97 sequences can improve the diagnostic accuracy of MRI

MRI findings ● ● ● ●

a discrete focus of increased SI and deformity (bowing) is seen within a ligament that has largely intact fibres (Fig. 5.45a, b) bone bruising is less common than with complete tears MRI has reported sensitivity of 40–75 per cent and specificity of 62–89 per cent for the diagnosis of partial ACL rupture98 axial images97 cannot differentiate stable partial tears from intact ligaments, or unstable partial tears from completely ruptured ligaments, but can differentiate stable partial tears from unstable partial tears: ■ stable partial tears appear as an attenuated ligament, while unstable partial tears appear as an isolated ACL bundle, a non-visualised ACL or a cloud-like mass

Mucoid degeneration of the anterior cruciate ligament100,101 ● ● ●

mucoid degeneration of the ACL is an ageing phenomenon, the ligament being functionally intact it may be associated with a ganglion cyst of the ACL, or may represent an intraligamentous ganglion cyst101 it is usually an incidental finding on MRI, reported in ~1 per cent of knee studies101

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d c Figure 5.44 Acute anterior cruciate ligament (ACL) stump entrapment. Type 1 pattern: Sagittal proton density-weighted (PDW) fast spin-echo (FSE) fat-suppressed (FS) (a), coronal PDW FSE (b) and axial PDW FSE FS (c) images showing a nodular mass (arrows) in the anterior aspect of the intercondylar notch. Type 2 pattern: Coronal T2-weighted FSE FS image (d) showing an angulated ACL stump (arrow).

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b

Figure 5.45 Acute partial anterior cruciate ligament (ACL) rupture. Sagittal proton density-weighted (PDW) fast spin-echo (FSE) (a) and coronal PDW FSE fat-suppressed (b) images showing mild deformity of the ACL (arrow a) and focal increased intraligamentous signal intensity (arrow b).

The cruciate ligaments

MRI findings ● the ligament appears ill-defined and expanded but with a normal orientation, showing increased SI on T1W, PDW and T2W sequences (Fig. 5.46a–c)

a b

c

Figure 5.46 Mucoid degeneration of the anterior cruciate ligament. Sagittal proton density-weighted (PDW) fast spinecho (FSE) (a) and coronal (b) and axial (c) PDW FSE fatsuppressed images showing a hyperintense, expanded ligament with intact fibres (arrows).

POSTERIOR CRUCIATE LIGAMENT Normal anatomy2,91,92 ● ● ● ● ● ●

the PCL is an intracapsular/extrasynovial structure that shares the same envelope as the ACL its function is to resist posterior translation; it is twice as strong as the ACL the PCL originates from the posterolateral aspect of the MFC and attaches into the posterior intercondylar fossa of the tibia, approximately 1 cm below the tibial articular surface on sagittal MR images, it is usually a smooth, posteriorly convex structure (Fig. 5.47a), though with the knee in extension it may be slightly buckled (Fig. 5.47b); the apex is termed the genu (Fig. 5.47b) the femoral and tibial attachments are well demonstrated on coronal (Fig. 5.47c, d) and axial (Fig. 5.47e, f) images the ligament is typically uniformly hypointense, though slightly increased SI may be seen on short TE sequences due to the magic-angle effect (Fig. 5.48a–d)

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e Figure 5.47 Normal anatomy of the posterior cruciate ligament (PCL). Sagittal proton density-weighted (PDW) fast spinecho (FSE) images (a, b) showing the smoothly convex appearance of the normal PCL (arrow a), which may appear slightly buckled with the knee extended (arrow b). Coronal PDW FSE images (c, d) showing the femoral (arrow c) and tibial (arrow d) attachments of the normal PCL. Axial PDW FSE images (e, f) showing the femoral (arrow e) and tibial (arrow f) attachments of the normal PCL.

The cruciate ligaments

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d

Figure 5.48 Normal anatomy of the posterior cruciate ligament (PCL). Sagittal T1-weighted spin-echo (a), proton densityweighted (PDW) fast spin-echo (FSE) (b), PDW FSE fat-suppressed (c) and T2*-weighted gradient-echo (d) images showing increased signal intensity in the femoral portion of the PCL due to the ‘magic-angle’ effect (arrows).

PATHOLOGY OF THE POSTERIOR CRUCIATE LIGAMENT Posterior cruciate ligament rupture93,102–104 ● ● ● ● ● ●

PCL rupture is less common than ACL rupture, representing 2–23 per cent of all knee injuries mechanisms of injury include posterior displacement of the tibia with a flexed knee (‘dashboard injury’), hyperextension and rotation combined with valgus or varus force PCL injury is commonly associated with ACL tear and posterolateral corner injury;104 it is isolated in 30 per cent of cases, most commonly when due to a dashboard injury mechanism tear patterns include partial (intra-substance) tear (47 per cent), complete tear (45 per cent) and bony avulsion from the tibial attachment (9 per cent) acute tears occur most commonly in the mid-substance of the ligament healing of the PCL may be demonstrated by MRI as regained continuity of the ligament: ■ this is seen with isolated ligament tears, or those combined with MCL injury, whereas an associated posterolateral corner injury predisposes to failure of PCL healing

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MRI findings ● acute tears (partial or complete) show diffuse ligament thickening with indistinct margins and increased SI on T1W, PDW and T2W sequences (Fig. 5.49a–e) ● with bony avulsion from the tibial plateau, the ligament may appear intact but an avulsed fragment and bone oedema from the posterior tibial plateau are seen (Fig. 5.50a–c) ● complete disruption characterises complete tears and is seen in 66 per cent of cases

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Figure 5.49 Acute posterior cruciate ligament (PCL) rupture. Sagittal proton density-weighted (PDW) fast spin-echo (FSE) (a) and coronal (b) and axial (c) PDW FSE fat-suppressed images showing diffuse thickening and hyperintensity of the ligament, which is also poorly defined (arrows). Acute highgrade partial PCL rupture: Sagittal PDW FSE (d) and PDW FSE FS (e) images showing diffuse thickening and increased signal intensity of the ligament, with a focal region of ligament discontinuity (arrows).

The cruciate ligaments

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Figure 5.50 Acute posterior cruciate ligament avulsion from the tibial plateau. Sagittal proton density-weighted (PDW) fast spin-echo (FSE) (a) and sagittal (b) and coronal (c) PDW FSE fat-suppressed images showing a relatively normal ligament (black arrows) with avulsion of the tibial insertion (white arrows) and subcortical bone oedema.

posterior displacement of the tibia in relation to the femur may be seen chronic tears manifest as a thickened ligament with low SI; chronic PCL deficiency may result in premature patellofemoral OA associated injuries:102 PCL tears are associated with other knee injuries in 66–72 per cent of cases; these include: ■ bone bruising (34 per cent) in the anterior tibia (Fig. 5.51a, b) and anterolateral femoral condyle ■ ligament injury (42 per cent): ACL, MCL and LCL, most commonly the MCL ■ meniscal tears (31–52 per cent) ■ avulsion fracture of the tibial portion of the deep MCL, termed the ‘reverse’ Segond fracture105

Ganglion cysts of the cruciate ligaments106–108 ● ● ● ●

cruciate ganglion cysts are true intra-articular ganglion cysts associated with the cruciate ligaments and account for 75 per cent of reported intra-articular ganglia of the knee107 they are reported in 0.3–2.0 per cent of knee MRI studies101,106 and may be a cause of chronic knee pain, but are not clinically associated with knee instability they may arise within (intraligamentous) or on the surface of the ligament (extraligamentous) ACL ganglia may involve the proximal ligament, the distal ligament or the whole length of the ligament, with a mean diameter of 31 mm (range 20–73 mm)101

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Figure 5.51 Bone bruising associated with posterior cruciate ligament (PCL) tear. Sagittal T1-weighted spin-echo (a) and coronal T2-weighted fast spin-echo fat-suppressed (b) images showing partial avulsion of the PCL from its femoral attachment (arrow a) and anterior tibial bone bruising (arrowheads).

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PCL ganglia typically occur in relation to the posterior aspect of the ligament and are therefore located in the intercondylar notch

MRI findings ● intraligamentous ganglia resemble mucoid degeneration (Fig. 5.52a, b) and are the commonest type involving the ACL (Fig. 5.46) ● extraligamentous ganglia are lobulated or fusiform in shape, simple or complex in architecture, and hypointense on T1W and hyperintense on PDW FSE and T2W images (Fig. 5.53a–d) ● they may show rim enhancement on FS T1W sequences following intravenous contrast, but MR arthrography is of no additional diagnostic value107 ● the differential diagnosis of a cyst in the posterior capsular region includes: ■ a pericruciate cyst arising from a posterior medial meniscal tear (Fig. 5.34) ■ a ganglion cyst arising from the ligament of Humphry109

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Figure 5.52 Intraligamentous ganglion of the posterior cruciate ligament. Sagittal proton density-weighted fast spin-echo (a) and T2*-weighted gradient-echo (b) images showing hyperintensity and swelling of an otherwise intact ligament (arrows).

The cruciate ligaments

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a

d c Figure 5.53 Extraligamentous cruciate ganglia. Anterior cruciate ligament (ACL): Sagittal proton density-weighted (PDW) fast spin-echo (FSE) (a) and T2-weighted FSE fat-suppressed (FS) (b) images showing a small ganglion cyst (arrows) related to the anterior aspect of the tibial attachment of the ACL. Posterior cruciate ligament (PCL): Sagittal PDW FSE FS (c) and coronal PDW FSE (d) images showing a ganglion cyst (arrows) related to the posterior aspect of the PCL and lying within the intercondylar notch.

Intraosseous cysts of the cruciate ligaments101,110 ● ●

cruciate intraosseous cysts are reported in 1–1.5 per cent of knee MRI studies in association with the proximal or distal insertions of the ACL and PCL101 they are typically incidental findings, most commonly arising at the femoral insertion of the ACL (Fig. 5.54a, b) and the tibial insertion of the PCL (Fig. 5.54c–e)

MRI findings ● subcortical cysts at the ligament insertions appear hypointense on T1W and hyperintense on PDW (Fig. 5.54a, c) and T2W/STIR images (Fig. 5.54b, d, e) ● they are rarely associated with marrow oedema (Fig. 5.54e)110

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Figure 5.54 Intraosseous cruciate cysts. Anterior cruciate ligament (ACL): Sagittal proton density-weighted (PDW) fast spin-echo (FSE) (a) and coronal T2*-weighted gradient-echo (b) images showing an intraosseous cyst (arrows) at the site of the femoral insertion of the ACL (arrowhead b). Posterior cruciate ligament (PCL): Sagittal PDW FSE (c), coronal T2-weighted FSE fat-suppressed (FS) (d) and axial PDW FSE FS (e) images showing an intraosseous cyst (arrows) at the site of the tibial insertion of the PCL (arrowhead d), with associated bone marrow oedema (arrowheads e).

THE MEDIAL CAPSULAR STRUCTURES Normal anatomy2,92,111 ● ●

the medial capsular structures are divided into three anatomical layers layer 1: the superficial layer comprises the deep crural fascia: ■ anterosuperiorly, it is continuous with the fascia of the vastus medialis muscle ■ anteriorly, layers 1 and 2 fuse to form the medial patellar retinaculum (Fig. 5.55a)

The medial capsular structures

a b Figure 5.55 Normal anatomy of the medial capsular structures, layer 1. Anterior aspect: Axial proton density-weighted (PDW) fast spin-echo (FSE) image (a) showing the medial patellar retinaculum (arrows). Posterior aspect: Axial PDW FSE image (b) showing layer 1 (the superficial fascia, double arrowheads) investing the sartorius (arrowhead) while the tendons of the gracilis (long arrow), the semitendinosus (short arrow) and the semimembranosus (double arrows) lie deep to the fascia.

centrally, it is separated from the superficial part of the MCL by a variable amount of fatty tissue posteriorly, it is continuous with the sartorius muscle and superficial to the tendons of the semimembranosus, semitendinosus and gracilis (Fig. 5.55b) ■ the tendons of the sartorius, gracilis and semitendinosus join to form the pes anserinus (Fig. 5.56a, b), which inserts into the anteromedial aspect of the proximal tibial metaphysis layer 2: the intermediate layer comprises mainly the superficial part of the MCL (the TCL): ■ the TCL runs vertically along the middle third of the medial part of the knee and functions as a restraint to valgus stress and external rotation2 ■ ■

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Figure 5.56 Normal anatomy of the pes anserinus. Sagittal T2*-weighted gradient-echo images (a, b) showing the tendons of the sartorius (black arrow a) and the semitendinosus (arrowheads) with the gracilis in between, fusing to form the pes anserinus. The semimembranosus (white arrow b) lies anterior to the semitendinosus.

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it arises from the MFC and inserts into the medial tibia, 6–7 cm distal to the joint line (Fig. 5.57a, b) posterior to the TCL is the posterior oblique part of the MCL, which is considered to represent an individual structure termed the posterior oblique ligament (POL) (see later) layer 3: the deep capsular layer: ■ anteriorly, it is continuous with the capsule of the suprapatellar recess ■ centrally, it lies deep to the vertical part of the superficial MCL, forming the deep MCL, a capsular thickening attached to the medial meniscal margin with superior and inferior extensions to form the (coronary) meniscofemoral and meniscotibial ligaments (Fig. 5.7e) ■ posteriorly, it fuses with layer 2 ■ the TCL bursa lies between the superficial and the deep parts of the TCL, but is not identified unless distended with fluid ■ ■

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Figure 5.57 Normal anatomy of the tibial collateral ligament. Coronal proton density-weighted (PDW) fast spin-echo (FSE) fat-suppressed (FS) (a) and axial PDW FSE FS (b) images showing the normal tibial collateral ligament (arrows).

PATHOLOGY OF THE MEDIAL CAPSULAR STRUCTURES Tibial collateral ligament injury93,112,113 ● ● ●

TCL injuries commonly occur in association with other ligament injuries, particularly ACL rupture, and result from valgus stress isolated TCL injuries usually heal spontaneously, resulting in a thickened ligament the overall accuracy of MRI for TCL injury is reported to be 87 per cent,112 though the correlation between clinical grading and MRI grading may not be very good (~65 per cent)

MRI findings ● TCL injury is optimally assessed with a combination of T2W/PDW FSE FS coronal and axial images11 ● abnormalities can be divided into direct signs (related to the ligament) and indirect signs (associated findings) ● direct signs include: ■ grade 1 injury – subcutaneous oedema over the intact TCL (Fig. 5.58a–c) ■ grade 2 injury – increased SI within the TCL on coronal PDW/T2W images (Fig. 5.58d), thickening of the ligament and longitudinal striations within the TCL

Pathology of the medial capsular structures

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e Figure 5.58 Injury to the tibial collateral ligament (TCL). Grade 1: Coronal proton density-weighted (PDW) fast spin-echo (FSE) (a), PDW FSE fat-suppressed (FS) (b) and axial PDW FSE FS (c) images showing oedema (arrows a, b) around an intact TCL (arrow c). Grade 2: Coronal PDW FSE image (d) showing oedema around a thickened but continuous TCL (arrows). Grade 3: Coronal PDW FSE FS image (e) showing oedema around and within a thickened TCL and focal midsubstance ligament discontinuity (arrow). Coronal PDW FSE image (f) showing distal TCL rupture (arrow).

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grade 3 – focal disruption of the TCL (Fig. 5.58e) the ligament may be ruptured at its femoral origin, in its mid-substance or, least commonly, at its tibial insertion (Fig. 5.58f) indirect signs/associated injuries include: ■ ACL rupture, which is always associated with a higher grade of TCL injury than isolated TCL injury112 ■ medial meniscal tears ■ bone bruising,114 which is reported in 45 per cent of cases of isolated TCL injury, occurring either medially due to micro-avulsions from the ligament attachment (Fig. 5.59a) or laterally from the initial valgus impaction (Fig. 5.59b) ■ the healed ligament appears thickened and hypointense on all pulse sequences (Fig. 5.59c, d) ■ intra-articular entrapment of the TCL has been described in severe knee injury115 ■ ■

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Figure 5.59 Injury to the tibial collateral ligament (TCL), associated features. Bone bruising: Coronal short tau inversion recovery image (a) showing mild medial femoral condyle bone oedema (arrows) adjacent to the femoral attachment of the TCL. Sagittal proton densityweighted (PDW) fast spin-echo (FSE) fat-suppressed (FS) image (b) showing lateral tibial plateau bone bruising (arrows). Healed TCL injury: Coronal PDW FSE FS (c) and axial PDW FSE (d) images showing a thickened hypointense ligament (arrows).

Pathology of the medial capsular structures

Pellegrini–Stieda lesion116 ●

the Pellegrini–Stieda lesion is post-traumatic ossification of the femoral insertion of the TCL and/or the adductor magnus insertion

MRI findings ● these depend on the maturity of the ligament ossification ● four types of tendon ossification have been described: ■ beak-like with inferior orientation and femoral attachment (commonest) ■ a drop-like pattern parallel to the femoral condyle ■ an elongated appearance with superior orientation parallel to the femur ■ beak-like with inferior and superior orientation and femoral attachment ● the proximal MCL shows chronic thickening ● bone fragments may appear as areas of signal void if mainly cortical bone, or may have internal fat SI if composed of medullary bone (Fig. 5.60a–d)

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Figure 5.60 Pellegrini–Stieda lesion. Coronal T2-weighted fast spin-echo (FSE) fat-suppressed (FS) (a) image showing marked thickening of the proximal tibial collateral ligament (TCL). Coronal proton density-weighted (PDW) FSE FS (b) and axial PDW FSE (c) images and an anteroposterior radiograph (d) showing thickening of the femoral insertion of the TCL with marrow signal intensity identified on the coronal image (arrow b) corresponding to ligament ossification on the plain film (arrow d).

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Atraumatic tibial collateral ligament oedema117,118 ● ●

grade 1 and grade 2 TCL oedema is present in approximately 90 per cent of cases of medial compartment OA117 (Fig. 5.61) MCL oedema118 has also been noted in 60 per cent of knee MRI studies in the absence of trauma, being significantly associated with the presence of medial meniscal tears, lateral meniscal tears, meniscal extrusion or femoral chondromalacia: ■ patients with MCL oedema were also significantly older than patients without this finding

Figure 5.61 Atraumatic tibial collateral ligament (TCL) oedema. Coronal proton density-weighted fast spin-echo fat-suppressed image showing oedema around the TCL in association with medial compartment osteoarthritis.

THE POSTEROMEDIAL CORNER Normal anatomy119–121 ● ●

the posteromedial corner extends from the posterior margin of the TCL to the medial margin of the PCL the structures of the posteromedial corner include: ■ the posterior third of the medial meniscus and meniscotibial (coronary) ligaments ■ the POL, which arises from the adductor tubercle of the MFC (Fig. 5.62a) and distally has three separate arms: – the tibial arm, which passes inferiorly inserting onto the posteromedial aspect of the tibia and to the posterior third of the medial meniscus – the capsular arm, which is continuous with the posterior capsule and blends with the oblique popliteal ligament (OPL) – the superficial arm, which passes distally to insert onto the tibia together with the fascial tissues of the pes anserinus – the POL is optimally assessed on coronal and axial MR images as a thin, hypointense structure posterior to the TCL (Fig. 5.62a, b) ■ the distal semimembranosus expansions: the semimembranosus muscle arises from the ischial tuberosity and its distal tendon, which may normally contain a small amount of fat (Fig. 5.63a), and splits at approximately the level of the knee joint line into five distinct expansions: – 1 – the anterior (tibial) arm, also termed the ‘pars reflexa’, passes anteriorly deep to the POL and inserts into the tibia deep to the TCL; it is identified on sagittal and coronal MR images (Fig. 5.63b, c)

The posteromedial corner

b a

Figure 5.62 Normal anatomy of the posterior oblique ligament (POL). Coronal proton density-weighted fast spin-echo (FSE) fat-suppressed (FS) image (a) showing the POL (arrows) extending from the adductor tubercle (arrowhead) to the proximal tibia. Axial T2-weighted FSE FS image (b) showing the POL (arrows) extending posteriorly from the tibial collateral ligament (arrowhead).

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Figure 5.63 Normal anatomy of the distal semimembranosus tendon and expansion. Axial proton density-weighted (PDW) fast spin-echo (FSE) image (a) showing a small amount of fat (arrow) within the distal tendon. The anterior limb: Sagittal PDW FSE (b) and coronal PDW FSE fat-suppressed (c) images showing the pars reflexa (arrows), which lies deep to the posterior oblique ligament (arrowheads c). (continued)

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Figure 5.63 (continued) The inferior arm: Sagittal PDW FSE image (d) showing the insertion of the inferior arm (arrow). The capsular arm: Axial PDW FSE image (e) showing the capsular arm (arrow). The oblique popliteal ligament insertion: Axial T1-weighted spin-echo image (f) showing the oblique popliteal ligament (arrow), which is indistinguishable from the posterior capsule (arrowheads).

– 2 – the direct arm is attached to the tibia deep to the pars reflexa and is not seen at MR imaging – 3 – the inferior (popliteal) arm extends more distally than the direct and anterior arms to insert into the tibia just above the tibial attachment of the TCL; it is visualised on sagittal images (Fig. 5.63d) – 4 – the capsular arm is contiguous with the POL and is best seen on axial images (Fig. 5.63e) – 5 – the OPL insertion is an extension of the semimembranosus tendon that blends with the OPL and the posterior capsule (Fig. 5.63f) the OPL extends laterally to fuse with the medial limb of the arcuate ligament and is seen on axial and sagittal images, indistinguishable from the posterior capsule

PATHOLOGY OF THE POSTEROMEDIAL CORNER Introduction120–122 ●

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posteromedial corner injury may result in anteromedial rotatory instability: ■ excessive opening of the medial joint space in abduction at 30° knee flexion ■ simultaneous anteromedial rotatory subluxation of the medial tibial condyle on the central axis of the intact PCL clinically, patients present with posteromedial pain and tenderness in the acute stage pathologically, findings include a spectrum of lesions of the distal semimembranosus complex122

Injuries of the semimembranosus tendon120 ●

semimembranosus tendon injuries include complete tears, myotendinous junction injuries, avulsion injuries, partial tears and insertional tendinosis

Pathology of the posteromedial corner

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complete tendon tears are very rare: ■ MRI findings: tendon disruption and retraction with peri-tendinous haematoma (Fig. 5.64a–c) myotendinous junction injuries typically occur in athletes: ■ MRI findings: oedema/haemorrhage at the myotendinous junction avulsion injuries of the posteromedial corner of the tibial plateau with associated TCL, ACL and medial meniscal tear: ■ MRI findings: a fracture line in the posteromedial tibial plateau, with bone and soft-tissue oedema, and tendon oedema and thickening partial tears of the tendon and POL: ■ MRI findings: abnormal tendon or ligament SI, with fluid in the posteromedial corner of the knee (Fig. 5.64d, e) and lack of visualisation of the anterior limb of the tendon insertion insertional tendinosis, which is associated with chronic repetitive injury and stress of the tibial insertion of the semimembranosus: ■ MRI findings: swelling and oedema of the tendon insertion (Fig. 5.64f, g), with/without irregularity and cystic change within the posterior medial tibia

Acute injury of the posteromedial corner121,122 ●

the structures most commonly involved in posteromedial corner injuries include:122 ■ the POL (99 per cent) (Fig. 5.64d, e), the semimembranosus expansions (70 per cent), the meniscotibial ligament and the MFL (83 per cent)

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Figure 5.64 Pathology of the posteromedial corner. Complete rupture of the semimembranosus tendon: Sagittal (a) and axial (b, c) proton density-weighted (PDW) fast spin-echo (FSE) fatsuppressed (FS) images showing complete discontinuity (arrows a, c) of the tendon at the level of the femoral condyle and swelling/oedema (arrowheads a, b) of the proximal tendon. (continued)

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g

Figure 5.64 (continued) Injury to the posterior oblique ligament (POL): Axial PDW FSE FS image (d) showing excessive fluid in the posteromedial corner around the POL (arrow), consistent with a sprain. Axial PDW FSE FS image (e) showing excessive fluid in the posteromedial corner with a tear of the POL (arrow), and associated bone bruising in the medial femoral condyle (arrowheads). Semimembranosus insertional tendinosis: Sagittal (f) and axial (g) PDW FSE FS images showing swelling and hyperintensity of the anterior (arrow f) and capsular arms (arrowhead g) of the tendon.

MRI findings ● periligamentous oedema, ligament thickening and hyperintensity are seen on T2W images (Fig. 5.65a–d) and partial or complete ligament rupture (Fig. 5.64d, e) ● associated injuries include medial meniscal tears (43 per cent), TCL tears (33 per cent) and ACL rupture (75 per cent), which may be associated with avulsion fracture of the posteromedial tibial plateau or bone bruising at the insertion of the semimembranosus:123 ■ PCL rupture is rare

The lateral capsular structures

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Figure 5.65 Posteromedial corner injury. Sagittal T2*-weighted gradient-echo (a) and coronal T2-weighted fast spin-echo (FSE) fat-suppressed (FS) (b) images showing oedema around the anterior and inferior arms (arrows) of the semimembranosus expansion in a patient with complete anterior cruciate ligament rupture. Sagittal (c) and axial (d) proton density-weighted FSE FS images showing thickening and hyperintensity of the capsular arm (arrows) of the semimembranosus expansion with a posterior third medial meniscal tear (arrowhead c).

THE LATERAL CAPSULAR STRUCTURES Introduction124–126 ●

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the lateral capsule can be divided into three layers:125 ■ layer 1 – the superficial layer comprising the ITB anteriorly and the biceps femoris (BF) tendon posteriorly ■ layer 2 – an incomplete layer comprising the lateral patellar retinaculum anteriorly and the lateral collateral ligament (the FCL) posteriorly ■ layer 3 – the capsular layer, comprising a superficial part containing the fabellofibular ligament, a deep part containing the arcuate ligament complex, and the popliteus tendon, which lies deep to the arcuate ligament the functional anatomy can be divided into anterolateral and posterolateral stabilisers

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THE ANTEROLATERAL STABILISERS Normal anatomy124 ● ●

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the anterolateral stabilisers comprise the capsule (capsular ligament) and the ITB the lateral capsule provides anterior and posterolateral stability and is reinforced by the superior and inferior retinacula and the vastus lateralis muscle: ■ the mid-third capsular ligament30 is a thickening of the joint capsule with attachments to the femoral condyle and the anterolateral tibial plateau (just posterior to Gerdy’s tubercle) (Fig. 5.10) ■ the capsule also has attachments to the lateral meniscus the ITB is an extension of the fascia lata and comprises deep and superficial layers (major tendinous component): ■ the superficial layer inserts onto Gerdy’s tubercle on the anterolateral aspect of the proximal tibia (Fig. 5.66a, b) ■ the deep layer inserts on the intermuscular septum of the distal femur

b a Figure 5.66 Normal anatomy of the iliotibial tract. Coronal proton density-weighted (PDW) fast spin-echo (FSE) (a) and axial PDW FSE FS (b) images showing the distal attachment of the iliotibial tract (arrows a) into Gerdy’s tubercle (arrowheads) on the anterolateral tibia.

PATHOLOGY OF THE ANTEROLATERAL STABILISERS Anterolateral quadrant injury124 ●

anterolateral quadrant injury is caused by a varus force with internal rotation of the tibia resulting in: ■ injury to the posterior fibres of the iliotibial tract ■ avulsion of Gerdy’s tubercle, usually associated with ACL injury (Fig. 5.67)

Iliotibial band friction syndrome127 ● ●

ITB friction syndrome is a cause of lateral knee pain related to intense physical activity, typically occurring in, for example, long-distance runners and cyclists clinically, it presents with tenderness over the lateral femoral condyle, with reproduction of pain during flexion/extension of the knee while pressure is exerted over the condyle

MRI findings ● commonest (75 per cent): poorly defined increased SI is seen on T2W sequences between the ITB, the distal extent of the vastus lateralis and the lateral femoral condyle (Fig. 5.68a–c)

The lateral capsular structures

Figure 5.67 Iliotibial tract avulsion. Coronal T1-weighted spin-echo image showing avulsion of the iliotibial tract from Gerdy’s tubercle (arrowhead) in a patient with complete anterior cruciate ligament rupture.

● ● ●

abnormal SI occasionally extends posterolaterally between the BF and the femoral shaft, distal to the lateral femoral condyle, between the ITB and the LCL, or, rarely, superficial to the ITB typically, in acute/subacute cases the ITB has normal thickness and SI (Fig. 5.68a–c), but it may be thickened in chronic cases (Fig. 5.68d, e) 30 per cent of cases show a well-circumscribed fluid collection between the ITB and the lateral femoral condyle, thought to represent adventitial bursa formation (Fig. 5.68f, g)

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Figure 5.68 Iliotibial band (ITB) friction syndrome: Acute: Coronal (a) and axial (b) proton density-weighted (PDW) fast spin-echo (FSE) fatsuppressed (FS) images showing oedema (arrows) between a normal ITB and the lateral femoral condyle. Axial PDW FSE FS image (c) showing oedema (arrow) between the ITB (arrowhead) and the distal vastus lateralis muscle (double arrowhead). (continued)

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f Figure 5.68 (continued) Chronic: Coronal T2-weighted FSE FS (d) and axial PDW FSE FS (e) images showing oedema (arrows) and thickening (arrowheads) of the ITB. Bursa formation: Coronal (f) and axial (g) PDW FSE FS images showing secondary bursa formation (arrows) between the ITB (arrowheads) and the lateral femoral metaphysis.

Iliotibial band avulsion92 ● ●

avulsion of the ITB, together with the anterior oblique band of the FCL, is considered responsible for avulsion of the lateral tibial rim (Segond fracture), associated with acute ACL rupture the fracture fragment is typically small and the resulting marrow oedema is not significant

THE POSTEROLATERAL STABILISERS Anatomy30,126,128,129 ●

the posterolateral stabilisers (the posterolateral corner) are also termed the ‘arcuate ligament complex’ and comprise: ■ the lateral collateral ligament (the FCL), which originates from the external tuberosity of the lateral femoral condyle, directly anterior to the insertion of the lateral head of gastrocnemius, and inserts as the conjoined tendon together with the BF onto the fibular head: – it is demonstrated on coronal, sagittal and axial images, appearing as a 4–5 mm thick, hypointense band (Fig. 5.69a–c)

The lateral capsular structures

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Figure 5.69 Normal anatomy of the fibular collateral ligament (FCL). Coronal proton density-weighted (PDW) fast spin-echo (FSE) fat-suppressed (FS) (a) and sagittal PDW FSE FS (b) images showing the FCL (arrowheads) extending from the lateral epicondyle (short arrow a) to the fibular head (long arrows). Axial PDW FSE image (c) showing the FCL (arrow) lying adjacent to the femoral condyle.

the BF muscle and tendon: the BF muscle has long and short heads, the long head arising from the ischial tuberosity and the short head arising from the lateral lip of the linea aspera of the distal femur: – the BF tendon descends posterior to the iliotibial tract and inserts as the conjoined tendon with the FCL onto the fibular head (Fig. 5.70a) – it is demonstrated on coronal, sagittal and axial images as a hypointense structure (Fig. 5.70b–d) the mid-third capsular ligament (Fig. 5.10) the popliteus muscle and tendon: the popliteus tendon arises below the FCL in a sulcus on the lateral femoral condyle and passes inferoposteriorly deep to the LCL, descends through the popliteus hiatus deep to the arcuate ligament and joins its muscle, which inserts onto the posteromedial aspect of the proximal tibia: – it is best assessed on a combination of coronal, sagittal and axial images (Fig. 5.71a–e), and may exhibit intermediate SI on short TE images due to the magic-angle effect (Fig. 5.71f) the popliteomeniscal fascicles are extensions from the popliteus tendon to the lateral meniscus, comprising superior and inferior struts that are best assessed on sagittal T2W images (Fig. 5.8d): – the popliteus also has a small muscular attachment to the posterior third of the lateral meniscus (Fig. 5.71g) the popliteofibular ligament, which is considered to be one of the most important stabilisers of the posterolateral corner, extends from the popliteus tendon (just proximal to the musculotendinous junction) to the posteromedial aspect of the fibular styloid (Figs 5.3, 5.71e): – it is identified on 38 per cent of MR studies,125 optimally on coronal oblique images (Fig. 5.3)

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Figure 5.70 Normal anatomy of the biceps femoris. Coronal proton density-weighted (PDW) fast spin-echo (FSE) fatsuppressed (FS) image (a) showing the conjoined tendon (double arrowhead) formed by the biceps femoris (BF) tendon (arrow) and the fibular collateral ligament (arrowhead). Coronal T1-weighted spin-echo (b), axial PDW FSE (c) and sagittal PDW FSE FS (d) images showing the BF tendon (arrowheads) inserting into the fibular head (white arrows b, d). The short head of BF (black arrow b) lies medial to the tendon.

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the arcuate ligament is a Y-shaped thickening of the capsule, reported to be present in 24–87 per cent of knees:125 – the medial limb curves over the popliteus tendon and joins the OPL; it is seen in 25 per cent of MR studies (Fig. 5.71c)125 – the lateral limb extends to the fibular styloid and is identified in 23 per cent of MR studies125 the OPL is a capsular ligament with a lateral attachment to the posterior aspect of the lateral femoral condyle, where it merges with the medial limb of the arcuate ligament, and a medial attachment to the posterior surface of the MFC, where it merges with the tendon of the semimembranosus: – it is indistinguishable from the posterior capsule the fabellofibular ligament is a capsular thickening that extends from the fabella to the styloid process of the fibula: – in the absence of the fabella, the ligament extends to the lateral femoral condyle and is reported to be present in 24–80 per cent of knees,125 though it is identified in only 23 per cent of MRI studies (Fig. 5.72a)125 the lateral gastrocnemius tendon inserts on the supracondylar process of the femur (Fig. 5.72b), just posterior to the FCL, and contains the fabella:130

The lateral capsular structures

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Figure 5.71 Normal anatomy of the popliteus tendon. Axial proton density-weighted (PDW) fast spin-echo (FSE) fatsuppressed (FS) images (a–d) showing the axial course of the popliteus tendon (black arrows) in the posterolateral corner and its relationship to the fibular collateral ligament (arrowheads b–d) and the biceps femoris tendon (double arrowheads b–d). The medial limb of the arcuate ligament (double black arrows c) is seen superficial to the popliteus tendon. Coronal PDW FSE FS image (e) showing the popliteus tendon (arrow) and the popliteofibular ligament (arrowhead). Sagittal T2*-weighted gradient-echo image (f) showing increased signal intensity in the popliteus tendon (arrow) due to the ‘magic-angle’ effect. Sagittal PDW FSE image (g) showing the muscular attachment (arrow) between the popliteus and the posterior lateral meniscus (arrowhead).

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Figure 5.72 The fabella and fabellofibular ligament. Coronal proton density-weighted (PDW) fast spin-echo (FSE) image (a) showing the ligament (black arrow) extending from the fibular head (arrowhead) to the fabella (white arrow). Sagittal T1-weighted spin-echo (b) and axial PDW FSE (c) images showing the lateral gastrocnemius tendon (arrowheads b) inserting into the posterior supracondylar region of the femur. The fabella (arrows) is located at the musculotendinous junction.

– the fabella is a sesamoid bone located in the anterior surface of the lateral head of gastrocnemius tendon, occurring with a reported incidence 11–13 per cent – its anterior surface is covered with smooth hyaline articular cartilage, and it is best assessed on sagittal and axial images (Fig. 5.72b, c) the (sub)popliteus bursa is an extra-articular extension of the synovial membrane of the knee joint that extends from the popliteal hiatus along the proximal part of the popliteus tendon: – the distended bursa appears as fluid around the popliteus tendon and muscle (Fig. 5.73) and may be confused with a tear of the musculotendinous junction

Figure 5.73 The subpopliteus recess. Axial proton densityweighted fast spin-echo fat-suppressed image showing fluid in the subpopliteus recess (arrowheads) deep to the popliteus tendon (arrow).

The lateral capsular structures

PATHOLOGY OF THE POSTEROLATERAL CORNER Posterolateral corner injury91,104,124,126–128,131 ● ●

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posterolateral corner injury is caused by combined varus force and hyperextension of the knee;132 it may be isolated, but is usually associated with PCL and/or ACL injury clinically, it presents with posterolateral rotatory instability, which manifests as posterior subluxation and external rotation of the lateral tibial plateau relative to the femur: ■ it may be clinically undetected due to the associated cruciate ligament injury (ACL in ~60 per cent and PCL in ~20 per cent); missed posterolateral corner injury is a recognised cause of failed cruciate ligament repair various injury patterns can occur, including: ■ FCL tears, which are isolated or combined with other posterolateral corner injuries, may be proximal (Fig. 5.74a, b), mid-substance (Fig. 5.74c, d) or distal (Fig. 5.74e, f), and are graded 1 (oedema) to 3 (complete disruption): – MRI findings:125,131 an irregular contour or focal discontinuity of the ligament, with hyperintensity and surrounding oedema (Fig. 5.74a–f) – avulsion of the conjoined tendon from the fibular head, which is the commonest pattern (Fig. 5.74d, e) – in chronic cases, the tendon may appear diffusely thickened (Fig. 5.74f, g) ■ BF tendon injury has been reported in 79 per cent of cases131 and can take the form of distal avulsion from the fibular head (commonest) (Fig. 5.75a–c) or avulsion fracture of the fibular styloid process

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Figure 5.74 Posterolateral corner injury, fibular collateral ligament (FCL) lesions. Proximal tear: Coronal proton density-weighted (PDW) fast spin-echo (FSE) (a) and PDW FSE fat-suppressed (FS) (b) images showing thickening, hyperintensity and discontinuity (arrows) of the proximal FCL. Mid-substance tear: Coronal T1-weighted spin-echo image (c) showing complete rupture of the FCL (grade 3 injury) with non-visualisation of the ligament, which is replaced by extensive intermediate signal intensity oedema (arrows). (continued)

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e d

g

f Figure 5.74 (continued) Distal tear: Coronal (d) and axial (e) PDW FSE images showing avulsion of the distal FCL (arrowheads) from the fibular head (arrow d). Chronic injury: Coronal PDW FSE (f) and axial T2-weighted FSE FS (g) images showing diffuse thickening of the FCL (arrows).

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■

‘arcuate’ fracture:133–135 avulsion of the fibular head and the styloid at the insertion points of the arcuate complex (arcuate, popliteofibular and fabellofibular ligaments): – MRI findings: an avulsed fragment from the posterosuperior apex of the fibular styloid (Fig. 5.76a, b) with marrow oedema in the fibular head (Fig. 5.76c) – hyperintensity and swelling of the popliteofibular ligament (Fig. 5.76d) and soft-tissue oedema around the medial limb of the arcuate ligament (Fig. 5.76e, f) – associated injuries to the cruciate and collateral ligaments and the medial and lateral menisci and bone bruising in various locations, typically in the anteromedial femoral and tibial condyles popliteus tendon tears136 have been reported in 36 per cent of patients,131 involving the musculotendinous junction in 96 per cent of cases and typically being associated with injuries to the cruciate/collateral ligaments and menisci, with ~8 per cent being isolated: – MRI findings: tears at the musculotendinous junction appear as muscle oedema/haemorrhage extending proximally around the tendon, which may appear normal (grade 1) (Fig. 5.77a, b), partially disrupted (grade 2) (Fig. 5.77c–e) or completely torn (grade 3) (Fig. 5.77f)

The lateral capsular structures

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Figure 5.75 Posterolateral corner injury, biceps femoris tendon lesions. Coronal proton density-weighted (PDW) fast spin-echo (FSE) (a) and axial PDW FSE fat-suppressed (b) images showing a longitudinal tear of the tendon (arrows). Coronal short tau inversion recovery image (c) showing avulsion of the tendon (arrowheads) from its fibular attachment (arrow).

Calcification of the lateral collateral ligament137,138 ● ● ●

calcification of the FCL is a rare entity in which calcification occurs in the proximal portion of the intact ligament clinically, patients present with acute, severe-onset, non-traumatic lateral knee pain pathologically, the condition is likely to be due to hydroxyapatite deposition disease

MRI findings ● thickening of the ligament is seen with focal low SI areas due to calcific deposits ● surrounding inflammatory reaction on T2W or STIR sequences and enhancement following gadolinium ● crystal deposition within the tendon can be confirmed by high-resolution CT138

Fabella syndrome130 ● ●

fabella syndrome is pain arising in the posterolateral corner that is exacerbated by pressure over the fabella it is thought to occur secondary to chondromalacia in younger age groups and OA in older age groups

MRI findings ● these are not described

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Figure 5.76 Posterolateral corner injury, arcuate fracture: Sagittal T1-weighted spin-echo (a) and coronal proton densityweighted (PDW) fast spin-echo (FSE) (b) images showing a subtle avulsion fracture of the fibular styloid (arrows). Axial PDW FSE fat-suppressed (FS) image (c) showing marrow oedema in the fibular head (arrows). Coronal T2*-weighted (T2*W) gradient-echo (GE) image (d) showing oedema and swelling of the popliteofibular ligament (black arrows) and partial detachment from the popliteus tendon (arrowheads) with an intact biceps femoris tendon (long white arrow). Sagittal T2*W GE (e) and axial PDW FSE FS (f) images showing fluid around the thickened medial limb of the arcuate ligament (arrows f).

The lateral capsular structures

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d c

e f Figure 5.77 Popliteus tendon injuries. Grade 1: Sagittal proton density-weighted (PDW) fast spin-echo (FSE) (a) and axial PDW FSE fat-suppressed (FS) (b) images showing oedema at the musculotendinous junction (arrows) and a normal popliteus tendon (arrowhead a). Grade 2: Sagittal T2*-weighted gradient-echo (c), coronal (d) and axial (e) PDW FSE FS images showing oedema at the musculotendinous junction and a thickened irregular hyperintense popliteus tendon (arrows). Grade 3: Sagittal PDW FSE FS image (f) showing complete tendon disruption (arrow).

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THE POSTERIOR CAPSULAR AREA Normal anatomy139,140 ● ● ●

the posterior capsule extends transversely between the medial and lateral femoral condyles, bridging the posterior aspect of the intercondylar fossa it is contributed to on the medial side by the OPL and on the lateral side by the medial limb of the arcuate ligament on its medial aspect, the capsule appears as a thick, band-like structure adjacent to the posterior third of the medial meniscus (Fig. 5.78a, b): ■ the superior medial attachment is to the posterior femoral cortex, a few centimetres above the condylar articular cartilage

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Figure 5.78 Normal anatomy of the posterior capsule. Medial side: Sagittal proton density-weighted (PDW) fast spin-echo (FSE) (a) and T2*-weighted gradient-echo (b) images showing the medial aspect of the posterior capsule (arrows) adjacent to the posterior third of the medial meniscus (arrowheads). Sagittal PDW FSE image (c) showing a fluid-filled joint recess (arrow) between the medial head of gastrocnemius tendon (arrowheads) and the posterior femur. Central: Sagittal PDW FSE image (d) through the intercondylar region showing the posterior capsule (arrowheads) and perforating vessels (arrow). Lateral: PDW FSE image (e) showing a fluid-filled joint recess (arrow) deep to the lateral head of gastrocnemius tendon (arrowheads).

The posterior capsular area

the inferior medial attachment is to the posterior tibial cortex, a few centimetres below the joint line a bursa is present between the capsule and the semimembranosus tendon ■ more laterally, the medial head of gastrocnemius tendon lies posterior to the capsule (Fig. 5.78c) ■ a joint recess is present between the superior attachment of the medial gastrocnemius tendon and the posterior femoral cortex (Fig. 5.78c) in its central aspect, in the intercondylar area, the capsule comprises incomplete fibres with perforations allowing communication between the posterior joint space and the popliteal fossa (Fig. 5.78d): ■ these are penetrated by vessels and nerves (Fig. 5.78d) ■ a joint (PCL) recess, which may contain fluid, is located between the PCL and the posterior capsule (see later) ■ the popliteal vessels are located posterior to the capsule in its lateral aspect, the popliteus hiatus lies between the posterior third of the lateral meniscus and the posterolateral capsule, allowing passage of the popliteus tendon: ■ the subpopliteus recess may extend deep to the capsule and posterior to the proximal tibia ■ the posterolateral knee joint may communicate with the proximal tibiofibular joint (PTFJ) in this region ■ medially, the posterolateral capsule is reinforced by the lateral head of gastrocnemius tendon; a joint recess is also present deep to the lateral head tendon (Fig. 5.78e) ■ ■

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The posterior muscles, vessels and nerves141 ● ●

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the posterior knee muscles include the gastrocnemius, the plantaris and the popliteus the gastrocnemius muscle is the most superficial muscle of the calf, arising via medial and lateral heads from the posterior surface of the femur just proximal to the femoral condyles (Fig. 5.79a, b): ■ the two heads unite to form the main bulk of the muscle, which extends through the calf to terminate as the Achilles tendon ■ function: plantar-flexion of the foot and knee flexion in the non-weight-bearing state the plantaris muscle is a small, strap-like muscle that is absent in 7–10 per cent of the population: ■ it arises from the lateral supracondylar line just above the attachment of the lateral head of gastrocnemius tendon (Fig. 5.79c), and its muscle belly lies deep to the lateral head of gastrocnemius (Fig. 5.79d) ■ the plantaris tendon inserts into the calcaneus or the Achilles tendon the popliteus muscle arises from the posteromedial aspect of the proximal tibial metaphysis and forms part of the floor of the popliteal fossa (Fig. 5.71): ■ its tendon inserts via the popliteus hiatus into the lateral femoral condyle ■ it also has attachments to142 the fibular head via the popliteofibular ligament (seen in 98 per cent of cases) and at least one attachment to the posterior aspect of the lateral meniscus (seen in 95 per cent of cases) ■ function: internal rotation of the tibia on the femur in the non-weight-bearing state and external rotation of the femur on the tibia in the weight-bearing state the accessory popliteus muscle143 is an accessory muscle in the popliteal fossa that has a common origin with the lateral head of gastrocnemius from the posterior femoral condyle: ■ its belly lies between the posterior capsule and the popliteal artery ■ it inserts into the posteromedial aspect of the posterior capsule the popliteal artery is the continuation of the femoral artery at the adductor hiatus, running through the popliteal fossa behind the knee joint and popliteus muscle and deep to the popliteal vein and the tibial nerve (Fig. 5.79e, f): ■ the artery has muscular branches and articular branches to the knee and terminates at the lower border of the popliteus muscle by dividing into the anterior and posterior tibial arteries the tibial nerve is the major branch of the sciatic nerve and runs within the popliteal fossa, initially lateral to, then superficial to and eventually medial to the popliteal artery (Fig. 5.79e, f) the peroneal nerve is the lesser branch of the sciatic nerve; it runs in the lateral aspect of the popliteal fossa to lie posteromedial to the BF muscle, and lateral/superficial to the lateral head of gastrocnemius to run posterior to the fibular head (Fig. 5.79f)

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Figure 5.79 Normal anatomy of the posterior knee muscles. Gastrocnemius: Axial proton density-weighted (PDW) fast spin-echo (FSE) (a) and coronal PDW FSE fat-suppressed (b) images showing the medial (arrows) and lateral (arrowheads) gastrocnemius muscles. Plantaris: Sagittal T1-weighted (T1W) spin-echo (SE) (c) and axial PDW FSE (d) images showing the normal plantaris muscle (arrows) lying deep to the lateral head of gastrocnemius (arrowheads) and superficial to the popliteus (white arrowhead c). Neurovascular anatomy of the popliteal fossa: Sagittal T1W SE (e) and axial PDW FSE (f) images showing the popliteal artery (white arrows), the popliteal vein (black arrows), the tibial nerve (arrowheads) and the common peroneal nerve (small black arrow f) lying posteromedial to the biceps femoris (double arrowhead f).

Pathology of the posterior capsular area

PATHOLOGY OF THE POSTERIOR CAPSULAR AREA Posterior capsular rupture139 ●

posterior capsular rupture may occur following a hyperextension injury and is usually associated with tears of the menisci or cruciate ligaments

MRI findings ● capsular disruption with high SI oedema is seen in the posterior capsular region on T2W images (Fig. 5.80) ● in the chronic stage, the capsule may appear irregular and thickened

Figure 5.80 Posterior capsular rupture. Sagittal T2-weighted fast spin-echo fat-suppressed image in a child with posterior cruciate ligament rupture showing increased signal intensity in the posterior capsular region (arrowheads).

Musculotendinous injuries141 ●

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the gastrocnemius muscle: medial head of gastrocnemius strains may occur at the level of the knee joint and may be associated with tears of the semimembranosus tendon: ■ tears of the lateral head of gastrocnemius occur in association with posterolateral corner injury ■ MRI findings: oedema at the musculotendinous junction, and tendon thickening and disruption (Fig. 5.81a–c) the plantaris muscle: ruptures may occur in association with ACL tears or posterolateral corner injuries: ■ tears of the plantaris or the medial head of gastrocnemius may result in a posterior compartment syndrome ■ MRI findings: increased SI on T2W images in the plantaris muscle or at the musculotendinous junction: – myotendinous rupture, resulting in a mass-like appearance between the popliteus tendon and the lateral head of gastrocnemius – fluid collections between the medial head of gastrocnemius and soleus muscles – associated injuries, as described above the popliteus muscle (see posterolateral corner injuries)

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Figure 5.81 Gastrocnemius tendon injury. Coronal proton density-weighted (PDW) fast spin-echo (FSE) fat-suppressed (FS) image (a) showing injury to the lateral head of gastrocnemius (arrowheads) in association with a posterolateral corner injury. Sagittal (b) and axial (c) PDW FSE FS images showing a grade 1 sprain of the medial head of gastrocnemius tendon (arrows).

FLUID COLLECTIONS, CYSTS AND BURSAE OF THE POSTERIOR CAPSULE The posterior cruciate ligament recess140 ● ●

the PCL recess is a synovial recess that lies between the ACL and PCL and may extend to the medial wall of the posterior intercondylar fossa joint effusion may normally collect within the PCL recess and must be differentiated from cystic structures in this region, including PCL ganglia (Fig. 5.53c, d) and pericruciate meniscal cysts (Fig. 5.34)

MRI findings ● the PCL recess has characteristic features that allow its differentiation from other posterior fluid collections ● it is a round or oval structure lying posterior to the PCL (Fig. 5.82a) and adjacent to the lateral aspect of the MFC (Fig. 5.82b) ● it does not contact the proximal third of the PCL (Fig. 5.82a), and lacks a surrounding capsule ● the recess may be traversed by the ligament of Wrisberg ● sagittal and coronal plane dimensions are ~2¥1 cm and axial plane dimensions are ~1¥1 cm ● the PCL recess communicates with the medial femorotibial compartment (Fig. 5.82c) ● various pathological processes may be encountered within the recess, including loose bodies (Fig. 5.82d)

Pathology of the posterior capsular area

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d Figure 5.82 The posterior cruciate ligament (PCL) recess. Sagittal (a) and coronal (b) proton density-weighted (PDW) fast spin-echo (FSE) images showing joint effusion (arrows) collecting in a recess between the PCL (white arrowheads) and the posterior capsule (double white arrowhead a) and located lateral to the medial femoral condyle (double black arrowhead b). Axial PDW FSE fat-suppressed (FS) image (c) showing communication between the PCL recess (arrow) and the medial femorotibial compartment (arrowhead). Sagittal PDW FSE FS image (d) showing an osteocartilaginous loose body (arrow) within the recess.

Posterior capsular bursae ● ● ●

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various bursae are identified in the posteromedial capsular region the semimembranosus bursa is located below the level of the joint space, and effusion in the bursa may lie deep and superficial to the tendon insertion (Fig. 5.83a) the subgastrocnemius bursa is located between the capsule and the gastrocnemius tendon (Fig. 5.83b), and effusion in the bursa may extend between the proximal semimembranosus tendon and the MFC (Fig. 5.83c): ■ it communicates with the gastrocnemius–semimembranosus bursa (Fig. 5.83d) the gastrocnemius–semimembranosus bursa extends between the tendons of the medial head of gastrocnemius and the semimembranosus (Fig. 5.83e) and when pathologically distended represents a popliteal (Baker’s) cyst (see later) in the posterolateral capsular area, fluid may be seen in the subpopliteus recess (Fig. 5.83e)

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e Figure 5.83 Posterior capsular bursae. The semimembranosus bursa: Sagittal short tau inversion recovery image (a) showing fluid within the semimembranosus bursa (arrows) lying both superficial and deep to the tendon (arrowhead). The subgastrocnemius bursa: Sagittal proton density-weighted (PDW) fast spin-echo (FSE) fat-suppressed (FS) image (b) showing fluid in the subgastrocnemius bursa (arrowheads) between the gastrocnemius tendon (black arrow) and the posteromedial capsule (white arrow). Sagittal T2*-weighted gradient-echo (c) and axial PDW FSE FS (d) images showing extension of the bursal fluid (black arrows) deep to the semimembranosus tendon (arrowheads) and also communication with the gastrocnemius–semimembranosus bursa (long white arrow d). The gastrocnemius–semimembranosus bursa: Axial PDW FSE FS image (e) showing a small effusion (arrow) lying between the medial head of gastrocnemius tendon (white arrowhead) and the semimembranosus tendon (black arrowhead). Fluid is also seen in the subpopliteus recess (double arrowhead).

The extensor mechanism

THE EXTENSOR MECHANISM Introduction ●

the extensor mechanism comprises the quadriceps muscles and tendon, the patellofemoral joint, the patellar tendon, and the associated fat pads, bursae and plicae

THE QUADRICEPS MUSCLES AND TENDON Normal anatomy144,145 ● ● ●

the quadriceps muscles include the rectus femoris, the vastus muscles (medialis, intermedius and lateralis) and the articular muscle the rectus femoris arises from the anterior inferior iliac spine and travels in the anterior aspect of the thigh the vastus medialis arises from the proximal femoral shaft and is located in the anteromedial thigh (Fig. 5.84a):

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d c Figure 5.84 Normal anatomy of the quadriceps muscles. Axial T1-weighted (T1W) spin-echo (SE) image (a) showing the vastus medialis (arrow) and lateralis (arrowhead) and their relationship to the quadriceps tendon (double arrow). Axial proton density-weighted fast spin-echo image (b) showing the vastus medialis obliquus (arrowheads) arising from the adductor magnus tendon (arrow) and inserting into the superomedial aspect of the patella. Sagittal (c) and axial (d) T1W SE images showing the articular muscle (white arrows c; black arrow d) lying deep to the quadriceps tendon (arrowheads) and inserting into the suprapatellar pouch (black arrow c).

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it has a longitudinal component (vastus medialis longus) and an oblique component (vastus medialis obliquus [VMO]) ■ the VMO arises from the tendon of the adductor magnus, inserts into the superomedial aspect of the patella (Fig. 5.84b) and provides a major mediolateral stabilising force on the patella the vastus intermedius arises from the proximal femoral shaft and is located in the anteromedial thigh adjacent to the femur the vastus lateralis arises from the proximal femoral shaft and is located in the anterolateral aspect of the thigh (Fig. 5.84a) the articular muscle146 originates from the distal fifth of the femur and inserts into the suprapatellar bursa (Fig. 5.84c, d): ■ it functions to protect the suprapatellar bursa from entrapment between the patella and the femur during knee movement the quadriceps tendon is formed by a common insertion of the quadriceps muscles into the superior pole of the patella: ■ the average dimensions of the tendon are thickness 6–10 mm and width 28–42 mm ■ it has a laminated appearance on sagittal MR images, with three layers (Fig. 5.85a) in 56 per cent and two layers (Fig. 5.85b) in 30 per cent of cases ■ when trilaminar, the anterior represents the rectus femoris, the middle represents the vastus medialis and lateralis, and the posterior represents the vastus intermedius ■

● ● ●

●

b

a

Figure 5.85 Normal anatomy of the quadriceps tendon. Sagittal proton density-weighted fast spin-echo images (a, b) showing the normal trilaminar (arrows a) and bilaminar (arrow b) appearances of the quadriceps tendon.

PATHOLOGY OF THE QUADRICEPS TENDON Quadriceps tendon rupture144,145 ●

● ●

injury to the quadriceps tendon can result from a direct blow or an indirect injury (more common), occurring: ■ in athletes, due to a rapid deceleration injury ■ in the elderly (typically sixth to seventh decades) due to a fall on a flexed knee, particularly from a flight of stairs predisposing conditions that may result in atraumatic bilateral tendon rupture include gout, diabetes mellitus, hyperparathyroidism, rheumatoid arthritis (RA), systemic lupus erythematosus and renal failure tendon rupture most commonly occurs within 2 cm of the upper pole of the patella and may be partial or complete

The extensor mechanism

● ●

rarer sites include the musculotendinous junction, the muscle belly and the quadriceps tendon (midsubstance) partial ruptures may result in no loss of extensor function and are treated conservatively, while complete tears result in loss of extensor function and are usually treated with early surgery

MRI findings ● partial tears result in focal high SI within the tendon with some intact fibres, resulting in disruption of the typical trilaminar tendon anatomy147 (Fig. 5.86a, b) ● complete tears show no intact fibres (Fig. 5.86c) and the quadriceps tendon may be retracted due to muscular contraction: ■ the patella may be tilted anteriorly and displaced inferiorly (Fig. 5.86d) ● chronic injury (beyond 2–4 weeks) may be associated with atrophy of the tendon and the quadriceps musculature with associated patella baja

a b

d c Figure 5.86 Pathology of the quadriceps tendon. Partial rupture: Sagittal proton density-weighted (PDW) fast spin-echo (FSE) (a) and PDW FSE fat-suppressed (b) images showing focal high signal intensity (arrows) within the deep quadriceps tendon (arrowheads) consistent with a partial tear. Complete tear: Sagittal PDW FSE image (c) showing complete rupture of the quadriceps tendon (arrow) from the superior pole of the patella. Sagittal T2*-weighted gradient-echo image (d) showing a complete rupture (arrow) with inferior displacement and anterior tilt of the patella (arrowhead).

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THE SUPRAPATELLAR FAT PAD Normal anatomy148 ● ●

the suprapatellar fat pad is a triangular fat pad lying deep to the quadriceps tendon and anterior to the suprapatellar bursa, with its base on the superior margin of the patella it is a consistent finding at knee MRI (Fig. 5.87a, b)

a

b

Figure 5.87 Normal anatomy of the suprapatellar fat pad. Sagittal proton density-weighted (PDW) fast spin-echo (FSE) (a) and axial PDW FSE fat-suppressed (b) images of the normal suprapatellar fat pad (arrows b) seen lying between the quadriceps tendon (arrow a) and the suprapatellar pouch (arrowheads a).

PATHOLOGY OF THE SUPRAPATELLAR FAT PAD Suprapatellar fat pad oedema149,150 ● ● ●

quadriceps fat pad oedema: swelling with a mass effect on the suprapatellar bursa/quadriceps tendon is reported in 4.2–12 per cent of knee MR examinations clinically, it is associated with anterior knee pain in ~28 per cent of cases; most patients present with symptoms of meniscal tear (55 per cent) or non-specific knee pain (~14 per cent) rarely reported cases of biopsy have shown vasculitis, and removal of the fat pad has been associated with resolution of symptoms

MRI findings ● there is enlargement of the fat pad with a mass effect on the suprapatellar bursa ● intermediate T1W/PDW and increased T2W/STIR SI indicating oedema (Fig. 5.88a–c), with enhancement following contrast

THE PATELLOFEMORAL JOINT Introduction151 ●

the patellofemoral joint comprises the articulation between the patella and the trochlear groove/adjacent femoral condyles, together with the associated soft-tissue restraints and the medial and lateral patellar retinacula

The extensor mechanism

a b

c

Figure 5.88 Quadriceps fat pad oedema. Sagittal proton density-weighted (PDW) fast spin-echo (FSE) (a), PDW FSE fatsuppressed (FS) (b) and axial PDW FSE FS (c) images showing oedema and swelling of the suprapatellar fat pad (arrowheads).

THE PATELLA Normal anatomy151 ● ● ● ●

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the patella is a sesamoid bone within the extensor tendon (Fig. 5.89a) its articular surface is divided by a vertical ridge into medial and lateral facets, with a small odd facet medially (Fig. 5.89b); the lowest 25 per cent of patella is non-articular the remainder of the patella is covered by hyaline cartilage, which is typically 5–6 mm in thickness (Fig. 5.89b) the relationship between the patellar articular surface and the trochlear groove varies with knee position: ■ in full extension, the patella lies superior to the trochlear groove ■ in 30° flexion, the patella begins to engage with the trochlea ■ at 30–90° flexion, initially the inferior, then the superior patellar cartilage engages with the trochlea ■ beyond 120° flexion, only the odd facet articulates with the femur the stability of the patellofemoral joint relies on passive and active stabilisers: ■ passive stabilisers: the patellar retinacula ■ active stabilisers: the quadriceps muscles patellar type (Wiberg): three types are described, though their clinical relevance is unclear: ■ type 1 – the medial and lateral facets are of approximately equal size (Fig. 5.89c) ■ type 2 – has a smaller medial and a dominant lateral facet (Fig. 5.89d) ■ type 3 – has a dominant lateral facet with a very small medial facet (Fig. 5.89e)

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b

a

d

c

e

Figure 5.89 Normal anatomy of the patella and patellofemoral joint. Sagittal T1-weighted spin-echo image (a) showing the normal patellofemoral joint. Note that the inferior pole of the patella is not covered by articular cartilage (arrow). Axial proton density-weighted (PDW) fast spin-echo (FSE) image (b) showing the lateral (long arrow), medial (short arrow) and odd (arrowhead) facets of the patella. Variation in patellar types: Axial PDW FSE fat-suppressed images through the patellofemoral joint showing a type 1 (c), a type 2 (d) and a type 3 (e) patella. Lateral facet: arrows, medial facet: arrowheads.

Normal variants of the patella151 ●

bipartite patella is a congenital variant that occurs in approximately 2 per cent of individuals and is usually bilateral: ■ it affects the superolateral aspect of the patella and is usually asymptomatic, but may be associated with anterior knee pain ■ MRI findings: the anomaly is best seen on coronal and axial images; the hyaline cartilage overlying the defect is intact (Fig. 5.90a, b): – a symptomatic bipartite patella152 may show evidence of oedema adjacent to the junction of the two bones (Fig. 5.90c, d), and cystic change (Fig. 5.90e) – traumatic separation is a rare complication

The extensor mechanism

b

a

d

c

e

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Figure 5.90 Bipartite patella. Coronal proton density-weighted (PDW) fast spin-echo (FSE) image (a) showing a bipartite patella (arrows). Axial PDW FSE image (b) showing intact cartilage overlying the defect (arrow). Symptomatic bipartite patella: Coronal (c) and axial (d) PDW FSE fat-suppressed images showing oedema within the bipartite fragment (arrows) and fluid (arrowheads c) between the fragment and the patella. Axial T2*-weighted gradient-echo image (e) showing adjacent cyst formation (arrowhead).

dorsal defect is a well-defined focal defect of the subchondral bone located in the superolateral aspect of the patella: ■ it may be associated with anterior knee pain that can respond to surgical treatment ■ MRI findings: a hemispherical defect in the deep cortical surface of the patella with intact overlying cartilage that thickens to fill the defect (Fig. 5.91a–c)

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b a

c

Figure 5.91 Dorsal defect of the patella. Sagittal (a), coronal (b) and axial (c) proton density-weighted fast spin-echo fatsuppressed images showing a cartilage-filled (arrowheads a, c) subchondral defect (arrows) in the superolateral aspect of the patella.

Related anatomy ●

● ●

the medial and lateral patellar retinacula are formed from tendinous fibres of the vastus medialis and the vastus lateralis muscles, respectively: ■ they extend anteriorly from the MCL and the LCL to insert into the medial and lateral aspects of the patella ■ at MRI, they appear as thin, hypointense bands surrounded by fat (Fig. 5.92a) the patellofemoral and patellotibial ligaments are focal condensations of the retinacula the medial patellofemoral ligament is a major medial stabiliser of the knee, arising from the adductor tubercle and inserting into the superolateral margin of the patella: ■ at MRI, it appears as a thickening of the medial patellar retinaculum at the inferior margin of the VMO muscle (Fig. 5.92b)

PATHOLOGY OF THE PATELLA Patella alta and baja153 ● ●

●

patella alta is an abnormally high-riding patella, which may predispose to patellar maltracking and lateral dislocation patella baja is an abnormally low-lying patella and occurs: ■ in neurological conditions, following trauma (quadriceps tendon rupture) and post-harvesting for ACL reconstruction patellar position is most commonly assessed on lateral radiographs using the method of Insall and Salvati, based on the ratio of patellar tendon length (TL) to patellar length (PL): ■ patella alta is diagnosed if TL/PL is >1.2, and patella baja if TL/PL is 1.52 for females and >1.32 for males (Fig. 5.93b) ■ patella baja is defined as TL/PL 8 mm has a reported accuracy of 79 per cent for trochlear dysplasia ● TD is determined by measuring the maximal depths of the medial (a) and lateral (b) femoral condyles, and a line (c) between the deepest point of the trochlea and a line joining the posterior aspect of the condyles (Fig. 5.98b); TD = ([a+b]/2)-c: ■ TD 2 cm (implying lateralisation of the tibial tubercle) is very specific but relatively insensitive for the presence of patellar maltracking qualitative criteria:157 ■ a nipple-like anterior prominence at the superior border of the trochlea, with a reported accuracy of 82 per cent (Fig. 5.99a) ■ a sharp, step-like transition zone, with a reported accuracy of 87 per cent (Fig. 5.99b) cartilage–bone mismatch:160 in trochlear dysplasia, the cartilage and bony contour do not match in the axial plane, the central hyaline cartilage being thicker and resulting in a sulcus angle (mean 186.5°) that is greater than the bony sulcus angle (mean 167.9°) patellar morphology161 is abnormal in patients with trochlear dysplasia compared with normal controls; in trochlear dysplasia, the patella exhibits:

The extensor mechanism

b a

c

e

d

f

Figure 5.99 Trochlear dysplasia, qualitative assessment. Sagittal T1-weighted spin-echo (SE) image (a) showing a nipplelike anterior prominence (arrow). Sagittal T1W SE image (b) showing a sharp step-like transition zone from the distal femur to the trochlea (arrow). Patellar morphology: Axial T2-weighted (T2W) fast spin-echo (FSE) image (c) showing measurement of the transverse dimension. Axial T2W FSE image (d) showing measurement of the medial (arrowhead) and lateral (double arrowhead) facet length. Axial T2W FSE image (e) showing measurement of the cartilaginous Wiberg angle. Axial T2W FSE image (f) showing measurement of the subchondral Wiberg angle. ■ ■ ■

a smaller transverse diameter (mean ~38 mm), representing the maximal transverse patellar diameter on axial images (Fig. 5.99c) a smaller mean medial patellar facet length (~19 mm), representing the medial facet cartilage length on axial images (Fig. 5.99d) a mean cartilaginous Wiberg angle of 130° (the angle between lines drawn parallel to the lateral and the medial facet cartilage on an axial image) (Fig. 5.99e)

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■ ■

a mean subchondral Wiberg angle of 126° (the angle between lines drawn parallel to the lateral and the medial facet cortex on an axial image) (Fig. 5.99f) a type 2 patellar morphology (Wiberg) is more common in trochlear dysplasia

Trochlear chondromalacia162 ● ● ● ●

isolated post-traumatic trochlear chondromalacia has been reported with a prevalence of ~1 per cent (30/2540 MRI studies)162 clinically, trochlear chondromalacia is a cause of anterior knee pain pathologically, the grading system is the same as that for chondromalacia patellae, and lesions may involve the lateral (commonest), the medial or the central aspect of the trochlea associated injuries include meniscal tears (usually medial) and bone bruising, typically affecting the weight-bearing area of the femoral condyle and the femoral trochlea underlying the chondral injury

MRI findings ● ●

altered chondral SI is seen, with hyperintensity on PDW (Fig. 5.100a, b) and T2W FSE FS images, and focal chondral defects of varying depth subchondral oedema (Fig. 5.100c) and cystic change (Fig. 5.100d)

a

c

b

d

Figure 5.100 Trochlear chondromalacia. Sagittal (a) and axial (b) proton density-weighted (PDW) fast spin-echo (FSE) images showing a focal full-thickness chondral defect (arrows). Sagittal PDW FSE fat-suppressed (c) and PDW FSE (d) images showing focal increased chondral signal intensity (arrows) associated with marrow oedema (arrowheads c) and subchondral cystic change (arrowhead d).

The extensor mechanism

PATHOLOGY OF THE PATELLOFEMORAL JOINT Malalignment and maltracking151,156 ● ● ● ● ●

patellofemoral alignment refers to the static relationship between the patella and the trochlea at any given degree of knee flexion patellofemoral tracking refers to the dynamic relationship between the patella and the trochlea during knee motion malalignment and maltracking occur as a result of variation in the bony geometry of the patellofemoral joint and/or variation in the function of the passive and active stabilisers abnormal patellar alignment typically occurs in the first 30–45° of knee flexion malalignment and maltracking may result in chondromalacia, OA and patellar dislocation

MRI findings163 ● anatomical features of the patellofemoral joint that are associated with patellar instability/maltracking include: ■ a shallow trochlear groove (1.2), indicative of patella alta, which has a sensitivity of ~78 per cent ■ a shorter patellar nose (60 per cent of younger patients undergoing arthroscopy, and can occur secondary to meniscal tears and ACL rupture

Miscellaneous knee injuries

at arthroscopy, damaged cartilage may be manifest by softening with/without fissuring/fibrillation, a chondral flap or overt chondral fracture, possibly with a displaced chondral fragment ■ delamination injuries180 represent separation of the articular cartilage from the underlying subchondral bone and occurring as a result of shearing stress concentrated at the junction of the noncalcified and calcified cartilage, resulting in an injury that runs parallel to the articular surface role of MRI in treatment planning:179 management options for chondral injury depend on the location, depth and size of the defect: ■ full-thickness defects are most commonly symptomatic and are the most likely to be treated ■ the larger the lesion, the less the likelihood of a good outcome ■ femoral condyle lesions are most easily treated, while patellar lesions have the poorest prognosis; tibial plateau lesions are also difficult to treat ■ cartilage injuries associated with OA also have a poorer outcome; OA manifests as marginal osteophytes, subchondral cysts and sclerosis ■

●

MRI findings ● ●

●

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the accuracy of MRI in identifying cartilage defects is reported as ~90 per cent, though MRI has only moderate accuracy for grading the depth of cartilage injury on FS T1W 3D spoiled gradient recalled images, cartilage defects are seen as focal areas of reduced SI, with reported sensitivity, specificity and accuracy of 81–93 per cent, 94–97 per cent and 91–97 per cent, respectively, for the detection of cartilage abnormalities on PDW FSE/FS and PDW/T2W FSE images, cartilage defects are seen as linear or irregular focal areas of increased SI of variable size (Fig. 5.121a–c), with 86–94 per cent sensitivity, 94–99 per cent specificity and 81–98 per cent accuracy for the detection of cartilage abnormalities secondary signs of articular cartilage injury include: ■ focal subchondral oedema and cysts: associated with full-thickness cartilage defects (Fig. 5.121d, e), reported in association with 83 per cent of cartilage defects requiring surgical treatment181 ■ subarticular osteophytes: reported in 15 per cent of MR examinations of the knee poorly identified types of cartilage injury include: ■ delamination injuries:180 appear as linear areas of fluid SI on T2W FSE FS images at the junction of the cartilage and the subchondral bone (Fig. 5.122a–d) ■ flap tears (Fig. 5.123a–c), fissures and fibrillation

Osteochondral injuries178,182,183 ●

the term ‘osteochondral injury’ includes bone bruising, osteochondral fracture and OCD

Bone bruising182,184,185 ●

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●

bone bruises are thought to represent areas of post-traumatic haemorrhage, oedema and hyperaemia from trabecular microfracture, which may result from a direct blow, compressive forces or traction forces at sites of soft-tissue avulsion clinical features: bone bruising may be the only finding following knee trauma (10 per cent of cases) and may then account for knee pain: ■ patients with bone bruises and an associated ligament injury show significantly greater functional disability than those without bone bruises in the acute setting, but no such difference is demonstrated at 6-month follow-up186 ■ they are typically painful for ~6 weeks following injury; some patterns of bone bruising are associated with hyaline cartilage damage/loss and predispose to premature OA187 patterns of resolution:188 repeat imaging at ~3 months shows >50 per cent volume reduction of bone bruises in 80 per cent of cases, and rarely shows an increased extent: ■ 70 per cent of bone bruises resolve from the periphery, while the remainder resolve towards the joint surface; the latter are always associated with an osteochondral injury

MRI findings ● bone bruises appear as areas of marrow oedema, with reduced SI on T1W and increased SI on T2W, STIR and FS PDW/T2 W FSE images

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a b

c

d

e

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Figure 5.121 Variable appearance of cartilage defects. Coronal proton density-weighted (PDW) fast spin-echo (FSE) (a) and PDW FSE fat-suppressed (FS) (b) images showing a fullthickness defect (arrows) of the lateral femoral condyle. Axial PDW FSE FS image (c) showing a large defect (arrow) of the medial femoral condyle. Coronal PDW FSE FS images (d, e) showing full-thickness chondral defects of the tibia (arrow) (d) and femur (e) with associated subchondral oedema (arrowhead d) and cyst formation (arrow e).

they are poorly demonstrated on GE imaging bone bruises are typically hemispheric or wedge-shaped with the base against the subchondral plate they usually resolve by 6 weeks post-injury on T1W and T2W FSE, but may persist for up to 6 months on T2W FS or STIR images bone bruises can be classified into two basic types on T1W images: ■ reticular: ill-defined areas of low SI with intervening normal marrow signal adjacent to the subchondral bone plate ■ geographic: diffuse areas of low SI marrow with well-defined margins extending to the subchondral bone plate ■ clinical relevance: reticular lesions heal with no sequelae, whereas geographic lesions are associated with cartilage thinning, chondral defect or cortical impaction in 50 per cent of cases at follow-up MRI

Miscellaneous knee injuries

a b

c

d

Figure 5.122 Chondral delamination injuries. Sagittal (a) and coronal (b) proton density-weighted (PDW) fast spin-echo (FSE) images showing a linear area of increased signal intensity (arrows) parallel to the surface of the medial femoral condyle. Sagittal (c) and axial (d) PDW FSE images showing a delamination injury of the central patellar cartilage (arrows).

Patterns of bone bruising and associated injuries184 ●

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patterns of bone bruising are associated with predictable soft-tissue knee injuries and can be classified into five types: ■ pivot shift injury, dashboard injury, hyperextension injury, clip injury and lateral patellar dislocation pivot shift injury occurs with valgus load on the knee in various degrees of flexion with internal rotation of the femur relative to the tibia: ■ it is associated with ACL rupture, at least one bone bruise being seen in 71–85 per cent of ACL injuries ■ bone bruising pattern (Fig. 5.41): the posterior aspect of the lateral tibial plateau and the central portion of the lateral femoral condyle, near the condylopatellar sulcus ■ the exact location of the lateral femoral condyle bruising depends on the degree of knee flexion, with greater flexion resulting in more posterior bruising ■ bone bruises may also be seen in the medial compartment, the posteromedial lip of the tibial plateau (12 per cent) and the MFC (9 per cent) (Fig. 5.42) ■ associated soft-tissue injuries include posterolateral corner injury, peripheral posterior third lateral or medial meniscal tears, TCL rupture and osteochondral injuries dashboard injury occurs with a direct blow to the anterior proximal tibia with the knee flexed: ■ bone bruising pattern; the anterior aspect of the proximal tibia (Fig. 5.51) and, rarely, the posterior surface of the patella ■ associated soft-tissue injuries include PCL rupture and disruption of the posterior joint capsule

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b

a

c

with severe force, osteochondral injury to the patella may also be seen (Fig. 5.124a, b), as may posterior dislocation of the hip hyperextension injury occurs with a direct force to the proximal anterior tibia with the knee fixed in extension or a forceful kicking motion and associated valgus force: ■ bone bruising pattern: the anterior aspect of the proximal tibial plateau and the anterior aspect of the femoral condyle ■ with associated valgus force the bone bruises are located more medially ■ associated soft-tissue injuries include ACL or PCL rupture, meniscal injury, disruption of the posterior joint capsule, posterolateral corner injury, popliteal neurovascular injury, gastrocnemius injury and, with severe force, dislocation of the knee clip injury occurs with pure valgus stress on the knee while in mild flexion: ■ bone bruising pattern: lateral femoral condyle due to the direct blow and MFC due to avulsive stress at the TCL insertion ■ associated soft-tissue injuries include TCL injury at the femoral insertion lateral patellar dislocation occurs with a direct blow to the medial patella or, more commonly, forced internal femoral rotation on a fixed foot: ■ bone bruising pattern (Fig. 5.105): the anterior aspect of the lateral femoral condyle, the inferomedial aspect of the patella and, rarely, the adductor tubercle of the MFC due to avulsion of the MPFL ■ associated soft-tissue injuries include trauma to the medial supporting structures, medial retinaculum, MPFL and VMO, osteochondral injury to the medial patella and the lateral femoral condyle, and injury to the infrapatellar fat pad ■

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Figure 5.123 Chondral flap tears. Sagittal T2-weighted fast spin-echo (FSE) image (a) showing a flap tear (arrow) of the posterior femoral articular cartilage. Coronal (b) and axial (c) proton density-weighted FSE images showing flap tears of the medial femoral condyle (arrow b) and the patellar cartilage (arrow c).

Miscellaneous knee injuries

a

b

Figure 5.124 Patellar fracture. Coronal (a) and axial (b) proton density-weighted fast spin-echo fat-suppressed images showing an osteochondral fracture (arrows) of the patella.

DIFFERENTIAL DIAGNOSIS OF MARROW OEDEMA AROUND THE KNEE General considerations189 ● ● ●

a

bone marrow oedema has various aetiologies, including ischaemic, mechanical and reactive pain associated with bone marrow oedema is due to raised intraosseous pressure caused by the abnormally high fluid content of the marrow MRI findings: bone marrow oedema is hypointense to marrow fat on T1W images (Fig. 5.125a), hyperintense on FS PDW/T2W and STIR images (Fig. 5.125b) and poorly identified on T2*W GE images (Fig. 5.125c), and enhances following intravenous gadolinium

b

c

Figure 5.125 Characteristics of bone marrow oedema associated with a chondroblastoma (arrows) of the distal femur. Sagittal T1-weighted spin-echo image (a) showing reduced marrow signal intensity (SI), coronal short tau inversion recovery image (b) showing increased SI and coronal T2*-weighted gradient-echo image (c) in which the oedema is not demonstrated.

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Ischaemic bone marrow oedema189 ● ● ● ●

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causes of ischaemic bone marrow oedema include osteonecrosis, bone marrow oedema syndrome, OCD and complex regional pain syndrome osteonecrosis may be idiopathic (spontaneous) or secondary spontaneous osteonecrosis of the knee (SONK) typically occurs in patients >55 years of age, most commonly in women, with isolated involvement of the MFC MRI findings: subchondral bone marrow oedema in the weight-bearing surface of the MFC, with a low SI, subchondral line indicating subchondral fracture (Fig. 5.126a, b): ■ in the later stages, collapse and secondary OA ■ secondary osteonecrosis: risk factors include corticosteroids, and staging is as for osteonecrosis of the hip: – stage 1 – focal subchondral bone marrow oedema – stage 2 – subchondral area of osteonecrosis surrounded by a reactive interface (Fig. 5.126c) (plain films are still normal) – stage 3 – osteochondral fracture (Fig. 5.126d) – stage 4 – development of secondary OA (Fig. 5.126e) bone marrow oedema syndrome is a condition of unknown aetiology that may represent early osteonecrosis or may be the same as transient migratory osteoporosis: ■ plain films are normal, the diagnosis being made by MRI ■ spontaneous healing occurs in 3–12 months; rarely, the condition heals in one location in the knee and develops in another location190 ■ MRI findings: extensive, diffuse bone marrow oedema involving an entire quadrant of the knee joint (Fig. 5.126f, g); the absence of a subchondral line differentiates it from SONK OCD is a manifestation of osteonecrosis in childhood, at a time when the growth plate is still open: ■ bone marrow oedema can be seen in all stages of the disorder (see later) complex regional pain syndrome is also known as algodystrophy, reflex sympathetic dystrophy syndrome and Sudeck’s atrophy: ■ it is usually secondary to trauma/injury of unknown origin and typical symptoms include burning, trophic disturbances and sensorimotor alterations ■ three stages are described: acute, dystrophic and atrophic ■ the diagnosis is made typically by a combination of the clinical features, plain films and scintigraphic findings ■ MRI findings: – acute stage: diffuse bone marrow oedema on both sides of the joint and peri-articular soft-tissue oedema – joint effusion is common

Mechanical bone marrow oedema189 ● ●

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causes of mechanical bone marrow oedema include post-traumatic bone bruising (see above), microfracture, stress-related bone marrow oedema and stress fracture microfracture represents a post-traumatic injury that commonly extends to the cortical surface: ■ MRI findings: a linear area of low SI surrounded by bone marrow oedema (Fig. 5.127a, b), with oedema possibly hiding the fracture line stress-related bone marrow oedema is subchondral oedema secondary to mechanical overload, as occurs with OA: ■ oedema may correlate with pain in OA and is predictive of progressive disease ■ MRI findings: – a wedge-shaped area of subchondral bone marrow oedema with the base of the wedge against the articular surface (Fig. 5.127c), and changes of associated OA stress fracture: insufficiency or fatigue fracture; the imaging features are as for a microfracture but differentiated by the absence of a history of acute trauma: ■ MRI findings: – a linear area of low SI surrounded by bone marrow oedema (Fig. 5.127d, e)

Miscellaneous knee injuries

b

a

c

d

e f

g

Figure 5.126 Ischaemic bone marrow oedema. Spontaneous osteonecrosis of the knee (SONK): Sagittal T1-weighted (T1W) spinecho (SE) (a) and coronal proton density-weighted (PDW) fast spinecho (FSE) fat-suppressed (FS) (b) images showing oedema in the medial femoral condyle (MFC) and a subchondral low signal intensity fracture line (arrows) indicative of SONK. Osteonecrosis: Coronal T1W SE image (c) showing multiple metaphyseal and epiphyseal bone infarcts. Coronal PDW FSE FS image (d) showing development of osteochondral fracture with multiple loose chondral fragments (arrows). Sagittal T1W SE image (e) showing the development of secondary osteoarthritis. Bone marrow oedema syndrome: Sagittal T1W SE (f) and coronal PDW FSE FS (g) images showing extensive oedema in the MFC consistent with transient osteoporosis, the absence of a subchondral line allowing differentiation from SONK.

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a

b

d c

e

Figure 5.127 Mechanical bone marrow oedema. Microfracture: Sagittal T1-weighted spin-echo (a) and axial proton density-weighted (PDW) fast spin-echo (FSE) fat-suppressed (FS) (b) images showing a microfracture (arrow a) of the posterolateral tibial plateau with associated marrow oedema. Stress-related bone marrow oedema: Coronal PDW FSE FS image (c) showing oedema in the medial femoral condyle and the tibial plateau, associated with medial compartment osteoarthritis. Stress fracture: Sagittal PDW FSE (d) and coronal PDW FSE FS (e) images showing marrow oedema associated with a stress fracture of the proximal tibia.

Reactive bone marrow oedema189 ●

bone marrow oedema associated with an underlying primary disorder, including inflammatory arthropathy, infection, tumour or following surgery

Osteochondral fractures181–183 ●

osteochondral fractures are defined as post-traumatic injuries to the articular surface that result in a local cartilage defect or fracture (fracture or impaction of the subchondral bone plate)

Miscellaneous knee injuries

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osteochondral fractures of the distal femur typically result from impaction injuries or shearing injuries: ■ impaction injuries are classically associated with ACL rupture and typically occur at the lateral femoral notch (condylopatellar sulcus), a normal depression in the lateral condylar articular surface that marks the junction of the tibial and patellar articular surfaces of the femur and is normally no greater than 1.2 mm in depth (Fig. 5.128a, b) ■ shearing injuries: in adults, usually result in a cartilage flap tear or defect; in children, usually result in osteochondral fracture, which may progress to OCD osteochondral fractures of the proximal tibia typically occur from impaction injuries, the common locations being: ■ the posterior lateral tibial plateau after ACL rupture or the weight-bearing surface after axial loading injury, usually affecting the lateral tibial plateau: – fractures with >5 mm depression may result in premature OA and are usually treated surgically ■ associated soft-tissue injuries with tibial plateau fractures include191 TCL rupture (55 per cent), lateral meniscal tears (45 per cent), FCL rupture (34 per cent), medial meniscal tears (21 per cent), and ACL (41 per cent) and PCL (28 per cent) rupture ■ MRI findings: – joint effusion or lipohaemarthrosis – cartilage injury manifests as high SI fluid within a cartilage fissure or defect on PDW or T2W images (Fig. 5.128c) – bone injury manifests as a discrete line of subchondral low SI on T1W representing the fracture line, with/without surrounding bone oedema: ◆ the fracture line may appear hypointense if due to impaction injury (Fig. 5.128d) or hyperintense on T2W if it contains fluid (Fig. 5.128e)

Osteochondritis dissecans181–183,192 ● ● ● ● ● ●

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●

OCD is a chronic, post-traumatic lesion affecting convex articular surfaces and resulting in partial or complete separation of a fragment of articular cartilage and subchondral bone around the knee, it can affect the femoral condyle (accounting for ~75 per cent of OCD of all joints), the femoral trochlea193 or the patella (~5 per cent of cases) the incidence of OCD is estimated to be 0.02–0.03 per cent (based on knee radiographs) or 1.2 per cent (based on knee arthroscopy) clinically, it classically presents in adolescence (age 10–15 years), twice as commonly in boys, with vague joint pain and a history of trauma in ~40 per cent of cases bilateral lesions are reported in 15–30 per cent of cases, commonly at different stages of development when involving the femoral condyle, ~70 per cent of cases occur on the medial side, typically involving the lateral margin (Fig. 5.129a): ■ lateral lesions are usually centred on the weight-bearing surface, typically posteriorly, and are associated with the presence of a discoid lateral meniscus194 ■ rarely, lesions occur anteriorly (Fig. 5.129b, c) prognosis is dependent on age at diagnosis and lesion size: ■ juvenile OCD, before fusion of the distal femoral physis, more commonly heals spontaneously ■ adult OCD, after closure of the distal femoral physis, rarely heals without surgical intervention ■ lesions 25 per cent of the meniscus has been resected ■ taking into account the above criteria, the reported accuracy of conventional MRI for recurrent tear is 66–80 per cent meniscal repair: the criteria for a reparable meniscal tear include a tear within the vascularised peripheral third, a longitudinal morphology and length >10 mm or instability: ■ primary repair may be optimally used for traumatic vertical tears >7–10 mm in length in the outer third of the meniscus, though repair of unstable tears in the avascular inner two-thirds may also be successful ■ the meniscal fragments can be fixed using a variety of sutures, bio-absorbable arrows, tacks or darts that span the defect in the meniscal substance ■ healing takes ~4 months; healed or partially healed menisci are usually asymptomatic, whereas failed repairs are usually symptomatic meniscal transplantation with allograft or collagen-based meniscal replacement is usually reserved for symptomatic younger patients who have undergone previous subtotal meniscectomy or who have irreparable tears, with the aim of preventing early onset of OA: ■ meniscal transplantation can be performed arthroscopically via a mini-arthrotomy, with the anterior and posterior meniscal anchors fixed using bone plugs and traction sutures, while the margin of the meniscus is sutured to the joint capsule the role of MRI in the assessment of the post-operative meniscus includes: ■ assessment of stability or recurrent tear of the meniscal remnant ■ identification of a tear in another area of the meniscus ■ identification of non-meniscal causes of recurrent pain, including: – cartilage damage, ligament pathology, intra-articular loose fragments, synovitis and osteonecrosis

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Figure 5.151 Normal post-operative meniscus. Partial circumferential: Sagittal proton density-weighted (PDW) fast spinecho (FSE) (a) and coronal PDW FSE fat-suppressed (FS) (b) images showing the medial meniscus with uniform reduction in size of the meniscal remnant (arrows). Partial segmental: Sagittal PDW FSE image (c) showing resection of part of the posterior third of the lateral meniscus (arrow) with a normal appearance of the anterior third (arrowhead). Meniscectomy for horizontal cleavage tear: Sagittal T1-weighted spin-echo (d), sagittal T2*-weighted gradient-echo (e) and coronal T2-weighted FSE FS (f) images following partial circumferential meniscectomy showing blunting of the inner margin of the remaining meniscus and a residual high signal intensity line extending to the articular surface (arrows).

The post-operative knee

Abnormal post-operative appearances217–221 ●

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features of recurrent tear on conventional MRI include: ■ high SI joint fluid extending into a cleft within the meniscal fragment on T2W images (Fig. 5.152a, b), with a reported accuracy of 80 per cent ■ the presence of a displaced fragment ■ if the initial meniscal resection involved removal of 1 mm may be a useful sign diagnostic accuracy is increased by using direct gadolinium MR arthrography, the indications for which include:221 ■ assessment of meniscal repair or whether there has been >25 per cent meniscal resection (in the absence of OA, chondral injury and osteonecrosis) ■ the diagnostic criteria for a repeat tear include the presence of increased intrameniscal SI (equal to joint fluid) on an FS T2W FSE sequence, which has a reported accuracy of 88–92 per cent ■ the diagnostic criteria for meniscal repair include full-thickness extension of contrast medium across the repair, indicating a re-tear or failure of healing; partial extension of contrast across the repair indicates partial healing MRI following meniscal allografting can provide a variety of information, including the position of the meniscus, the status of the capsular attachment and the presence of meniscal degeneration, fragmentation and tears: ■ however, current literature on low-field MR systems indicates a poor correlation between MRI and clinical findings222

a

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Figure 5.152 Recurrent meniscal tear. Sagittal T2*-weighted gradient-echo (a) and coronal short tau inversion recovery (b) images showing a recurrent tear (arrows) of the posterior third of the medial meniscus.

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THE LIGAMENTS Anterior cruciate ligament reconstruction217–219,223 ●

● ●

techniques for ACL reconstruction include the use of autografts and allografts: ■ autografts include bone–patellar tendon–bone (BPTB) (most commonly used), hamstring (semitendinosus or gracilis) tendon and bone–quadriceps tendon grafts ■ allografts include Achilles tendon, fascia lata, BPTB and hamstring tendon primary repair can be used for avulsion injuries at the femoral or tibial insertion, which are usually seen in children optimal positioning of the graft tunnels is guided by the principles of isometry and the avoidance of graft impingement: ■ isometry allows constant length and tension of the graft through flexion and extension, and is dependent on the position of the femoral tunnel; incorrect tunnel position results in graft elongation and instability ■ avoidance of impingement depends on the position of the tibial tunnel and the size of the intercondylar notch: – impingement most commonly occurs against the roof of the intercondylar notch in terminal extension, against the sidewall of the notch or at the tunnel margins

Normal anterior cruciate ligament graft appearances217–219,223 ● ● ●

MRI technique: use of T2*W GE (Fig. 5.153a) and FS (Fig. 5.153b) images should be avoided due to metal artefact; T2W FSE or STIR sequences should be considered the MRI appearance depends on the type of graft, the fixation technique and the time since repair tunnel position: ■ a correctly positioned femoral tunnel is seen on sagittal images at the intersection of the posterior femoral cortex and the intercondylar roof (Fig. 5.154a) and on coronal images at the posterosuperior corner of the intercondylar notch, at 10–11 o’clock for the right knee (Fig. 5.154b) and 1–2 o’clock for the left knee

b a Figure 5.153 Anterior cruciate ligament reconstruction, metal artefact. Sagittal T2*-weighted gradient-echo (a) and proton density-weighted fast spin-echo fat-suppressed (b) images showing marked artefact at the graft fixation points (arrows).

The post-operative knee

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Figure 5.154 Anterior cruciate ligament reconstruction, tunnel position. Femoral: Sagittal (a) and coronal (b) proton density-weighted (PDW) fast spin-echo (FSE) images showing a normal femoral tunnel position (arrows). Tibial: Sagittal (c) and coronal (d) PDW FSE images showing a normal tibial tunnel position (arrows). Note the relationship to Blumensaat’s line (white line c). Hamstring graft: Sagittal PDW FSE image (e) showing the normal striated appearance of a semitendinosus graft (arrows) 11 months after anterior cruciate ligament reconstruction.

a correctly positioned tibial tunnel is seen on sagittal images posterior to a line drawn along the roof of the intercondylar notch (Blumensaat’s line) (Fig. 5.154c), the centre of the tunnel being one-quarter to one-half of the distance from the anterior to the posterior tibial cortex, and on coronal images centred on the intercondylar eminence (Fig. 5.154d) fluid collections may be normal within the femoral or tibial tunnels for 1 year following hamstring grafting

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graft fixation: metal screws produce a variable amount of artefact (Fig. 5.153), and marrow oedema may persist around the fixation points for up to 12 months post-reconstruction graft type and appearance: ■ BPTB graft is harvested from the central third of the patellar tendon, together with small fragments of bone from the inferior pole of the patella and the tibial tuberosity: – the graft is typically 10 mm wide and 3–4 mm thick; a normally positioned graft runs just posterior and parallel to the roof of the intercondylar notch (Fig. 5.154c) – the SI of the graft depends on graft age; in the first 3–4 months, the graft is avascular and therefore hypointense on T1W and T2W sequences – at 4–8 months, the graft undergoes revascularisation and resynovialisation, appearing as homogeneous low SI or segmental/diffuse intermediate SI on T2W sequences, but never as bright as fluid – by 12–17 months, it appears similar to native ACL, with uniform low SI on all pulse sequences (Figs 5.153, 5.154) ■ hamstring graft is prepared from harvested semitendinosus and gracilis tendons and has an average diameter of 8–9 mm: – the MR appearance is similar to that of a BPTB graft, except that there may be linear areas of increased SI between individual bundles of the graft (Fig. 5.154e)

Post-operative complications of anterior cruciate ligament reconstruction217–219,223,224 ● ●

●

complications following ACL reconstruction may be related to continued or recurrent instability and/or decreased range of motion (loss of extension) recurrent instability may be due to graft disruption or graft stretching: ■ graft disruption: the graft is most at risk during the first few post-operative months, while revascularisation and resynovialisation are occurring: – the most specific sign of graft disruption is complete discontinuity of graft fibres (Fig. 5.155a, b) – during the first 4–8 months post-operatively, the most specific sign of rupture is fluid SI completely traversing the graft on T2W images – MR arthrography is reported to have 100 per cent sensitivity and 89–100 per cent specificity for graft rupture if injected contrast is shown to extend through the defect in the graft fibres225 – fibre continuity in the coronal plane is the most reliable sign of an intact graft – secondary signs of graft failure include anterior tibial shift >7 mm, buckling of the PCL (Fig. 5.155c) and uncovering of the posterior horn of the lateral meniscus ■ graft stretching is diagnosed in the presence of clinical instability by the identification of intact graft fibres: – it is more common with hamstring grafts and manifests as an intact but bowed or buckled graft on sagittal images (Fig. 5.155d) ■ instability may be seen in the presence of an anteriorly placed femoral tunnel (Fig. 5.155e) or a posteriorly placed tibial tunnel (Fig. 5.155f) decreased range of movement (extension) may be due to graft impingement or arthrofibrosis: ■ graft impingement: the commonest cause is anterior placement of the tibial tunnel resulting in contact between the graft and the roof of the intercondylar fossa in full extension, causing fraying, fibrosis and eventual disruption: – MRI demonstrates increased SI within the graft at the site of impingement (Fig. 5.156a), kinking of the graft at the anterior margin of the intercondylar fossa (Fig. 5.156b) and an anteriorly placed tibial tunnel (Fig. 5.156c) – these signs have relatively poor sensitivity and specificity – impingement may be treated by notchplasty, which comprises resection of bone from the roof and lateral side of the intercondylar notch, though recurrent impingement following notchplasty may occur due to fibrocartilaginous overgrowth – SI changes in the graft usually resolve within weeks of successful notchplasty ■ arthrofibrosis is an uncommon complication that typically occurs in the anterior compartment of the knee: – it may be focal or diffuse, and results in anterior knee pain and loss of full extension

The post-operative knee

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f e Figure 5.155 Complications of anterior cruciate ligament (ACL) reconstruction. Graft rupture: Sagittal (a) and coronal proton density-weighted (PDW) fast spin-echo (FSE) (b) images showing discontinuity of the ACL graft (arrows). Sagittal T1-weighted spin-echo image (c) showing a hooked posterior cruciate ligament (arrow) indicative of recurrent instability. Graft instability: Sagittal T2-weighted FSE image (d) showing redundant ACL graft (arrow). Sagittal PDW FSE fatsuppressed (FS) image (e) showing a bowed graft (arrow) associated with an anteriorly positioned femoral tunnel (arrowhead). Sagittal PDW FSE FS image (f) showing a lax graft (arrowhead) associated with a posteriorly placed tibial tunnel (arrow).

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Figure 5.156 Anterior cruciate ligament graft impingement. Sagittal proton density-weighted (PDW) fast spin-echo (FSE) image (a) showing focal increased signal intensity (arrow) within the graft. Sagittal T2*-weighted gradient-echo image (b) showing kinking of the graft (arrow) at the anterior intercondylar notch (arrowhead). Sagittal PDW FSE image (c) showing poor positioning of the tibial tunnel (arrow), which lies anterior to Blumensaat’s (white) line.

– the focal form is termed the ‘cyclops’ lesion, a focal nodule of hyperplastic synovial tissue located between Hoffa’s fat pad and the distal aspect of the ACL graft (Fig. 5.157a–c) – conventional MRI has a reported 85 per cent accuracy for the detection of cyclops lesions, which may be mimicked by a retained native ACL remnant – the diffuse form is typically located throughout Hoffa’s fat pad (Fig. 5.157d) miscellaneous complications include: ■ intra-articular cartilaginous loose bodies ■ recurrent internal derangement resulting in a displaced meniscal tear ■ Hoffa’s disease may occur following ACL reconstruction, possibly as an inflammatory response to debris or due to fat pad injury: – MRI demonstrates an oedematous and hypertrophic fatty mass within the infrapatellar fat pad ■ ganglion formation related to the graft or the tibial tunnel: – graft ganglion cyst formation is related to graft degeneration or partial rupture and is more common with hamstring grafts; it has the typical appearance of a ganglion cyst (lobulated, welldefined and hypointense on T1W and hyperintense on T2W) – a tibial tunnel intraosseous ganglion cyst may enlarge to enter the joint or produce a subcutaneous soft-tissue mass adjacent to the distal opening of the tunnel (Fig. 5.157e,f) – femoral and/or tibial tunnel enlargement may be seen when metallic or absorbable screws are used, and fluid may normally be seen within the tunnels during the first year following hamstring grafting

Donor-site appearances following anterior cruciate ligament reconstruction217–219,223 ●

donor-site complications following ACL reconstruction may be related to the patellar tendon or hamstring harvest sites

The post-operative knee

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Figure 5.157 Complications of anterior cruciate ligament (ACL) reconstruction. ‘Cyclops’ lesion: Sagittal proton densityweighted (PDW) fast spin-echo (FSE) (a), coronal short tau inversion recovery (b) and axial PDW FSE fat-suppressed (FS) (c) images showing a nodular lesion (arrows) anterior to the distal ACL graft (arrowhead a). Diffuse arthrofibrosis: PDW FSE image (d) showing excessive fibrosis (arrows) within Hoffa’s fat pad. Tibial tunnel ganglion. Sagittal PDW FSE FS (e) and axial PDW FSE (f) images showing a lobulated intraosseous ganglion cyst (arrows) extending into the anterior subcutaneous tissues.

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patellar tendon complications include patella baja during the first post-operative year, anterior knee pain, arthrofibrosis, patellar fracture, patellar tendinitis and tendon rupture: ■ the normal tendon initially appears thickened with low SI on T1W and intermediate SI on T2W, and shows a central 5 mm gap at the site of tendon harvesting (Fig. 5.158a) that fills with reparative tissue by 2 years ■ persistent hyperintensity and tendon thickness >10 mm after 12 months are consistent with patellar tendinosis (Fig. 5.158b) hamstring tendon harvest site: fluid may be seen at the site of tendon harvesting for the first 1–2 months: ■ in the following 6–12 months, a ‘neo-ligament’ develops at the site of the respective tendons to within 1–2 cm of the tibial insertions; by 1 year post-harvest (Fig. 5.158c,d), the hamstring muscles may have regained their original bulk ■ complications include persistent muscle atrophy and hamstring weakness at 1 year, and retraction of the semitendinosus muscle belly226

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Figure 5.158 Appearances of the donor site. Axial proton density-weighted (PDW) fast spin-echo (FSE) fat-suppressed (FS) image (a) showing a central defect in the patellar tendon (arrow) at the site of graft harvesting. Sagittal PDW FSE FS image (b) showing diffuse thickening and inhomogeneous hyperintensity of the patellar tendon (arrows) consistent with tendinosis. Hamstring graft: Sagittal PDW FSE (c) and axial PDW FSE FS (d) images showing the semitendinosus neoligament (arrows).

Posterior cruciate ligament reconstruction217–219,223 ● ●

PCL reconstruction may be performed for bony avulsion injuries and symptomatic knees with grade 3 laxity; most PCL ruptures are treated conservatively bone–patellar–bone and hamstring grafts are most commonly used

The post-operative knee

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the femoral tunnel is located on the lateral aspect of the MFC, at the anterior half of the femoral PCL insertion site (Fig. 5.159a), into which the patellar end of the graft is fixed the tibial tunnel is located 15 mm distal to the articular surface of the tibia (Fig. 5.159b), just below the normal tibial insertion of the native PCL within the first 12 months, the graft appears thickened and relatively hyperintense due to revascularisation: ■ gradually, the graft thickness decreases and the graft returns to low SI on T1W/PDW and T2W images (Fig. 5.159a–c) ■ tibial or femoral tunnel placement is not as crucial as for ACL post-operative complications include arthrofibrosis, which is common after PCL grafts and appears as areas of reduced SI anterior or posterior to the PCL (Fig. 5.159d): ■ graft disruption appears as regions of graft fibre discontinuity and high SI fluid crossing the graft on T2W images

Medial collateral ligament reconstruction217–219,223 ●

MCL reconstruction may be considered for grade 3 injury associated with ACL disruption; isolated MCL injuries are usually treated conservatively

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Figure 5.159 Posterior cruciate ligament (PCL) reconstruction. Normal: Sagittal proton density-weighted fast spin-echo (FSE) (a, b) and coronal T2-weighted FSE fat-suppressed (c) images showing a normal PCL graft (arrows) and the positions of the femoral tunnel (arrowhead a) and the tibial tunnel (arrowhead b). Arthrofibrosis: Sagittal T1-weighted spin-echo image (d) showing fibrosis (arrowhead) anterior to the graft (arrow).

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surgery includes stapling or suturing; the MCL appears thickened and hyperintense initially, eventually reverting to uniform low SI but remaining thickened indefinitely

CARTILAGE Introduction218,227 ●

cartilage repair procedures can be grouped into three main categories: local stimulation techniques, osteochondral autograft transplantation and autologous chondrocyte implantation (ACI)

Local stimulation techniques218,227 ●

local stimulation techniques are now rarely used; they include abrasion arthroplasty, subchondral drilling and microfracture: ■ all of these techniques require the penetration of subchondral bone, with the resulting formation of a fibrin clot that can differentiate and remodel to form fibrocartilage within the chondral defect ■ successful treatment results in complete filling of the lesion with smooth, congruent cartilage that is of similar SI to the native cartilage ■ oedema-like subchondral SI may be seen initially following treatment (Fig. 5.160a,b), but this resolves after several months

a

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Figure 5.160 Microfracture. Sagittal PDW FSE (a) and coronal PDW FSE FS (b) images showing subchondral oedema (arrows) and hyperintense hyaline cartilage (arrowheads).

Osteochondral autograft transplantation (mosaicplasty)218,227 ●

in this technique, osteochondral plugs are harvested from a relatively non-weight-bearing part of the knee joint such as the intercondylar notch or the femoral trochlea and implanted into the chondral defect: ■ various features can be assessed by MRI, including graft incorporation, congruity of the articular surface, appearance of the donor site and post-operative complications ■ graft incorporation: oedema and enhancement at the transplantation site is indicative of graft revascularisation and reparative and inflammatory reactive tissue, and may be seen within 4–6 weeks of transplantation: – this usually subsides at 6–12 months, by which time essentially normal marrow SI should be seen, though mildly increased T2W SI may persist (Fig. 5.161a–c)

The post-operative knee

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Figure 5.161 Autologous osteochondral transplantation. Sagittal proton density-weighted (PDW) fast spin-echo (FSE) fat-suppressed (FS) (a), coronal PDW FSE (b) and T2-weighted FSE FS (c) images showing mosaicplasty of the medial femoral condyle with mature incorporated osteochondral plugs (arrows) but minor irregularity of the resulting articular surface (arrowheads).

congruity of the articular surface: the osteochondral plugs should be flush with the native articular surface, which requires careful surgical technique such that the plugs are placed perpendicular to the articular surface: – incongruity may be due to poor surgical technique, subsequent graft subsidence or graft displacement/rotation SI characteristics of the repair tissue: this may appear as normal hyaline cartilage or show heterogeneous increased SI, indicative of fibrocartilage repair tissue the donor site is seen as cylindrical tubular defects in the subchondral bone and the overlying cartilage, which contains low SI on T1W and high SI on T2W images in the early post-operative period but fills with cancellous bone and fibrocartilage-like material within 6–9 months complications include donor-site pain, condylar fracture, donor-site avascular necrosis, loose bodies, graft incongruence and graft migration/loosening

Autologous chondrocyte implantation218,227,228 ●

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ACI is a two-stage procedure in which chondrocytes are initially harvested via arthroscopy from the femoral trochlear area or intercondylar notch, grown in culture for 4–6 weeks until ~12 000 000 cells are present, and subsequently re-implanted into the debrided defect under a periosteal covering following this, a three-phase period of growth and maturation of the cartilage graft is seen: ■ in the first 6 weeks, the number of cells increases to form a soft, primitive repair tissue

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in the next 20 weeks, formation of type 2 collagen and proteoglycans occurs, with expansion of the extracellular matrix ■ in the final phase (which can last up to 3 years), there is remodelling of the extracellular matrix and integration of the tissue into the underlying bone by 9–18 months, ACI repair tissue should be as firm as native cartilage on arthroscopic probing histological studies have shown hyaline or hyaline-like cartilage in 75–80 per cent of grafts MRI allows assessment of: ■ the status of repair tissue (fibrous or hyaline): in the early post-operative stage, repair tissue shows intermediate SI on PDW and T1W images, and is hyperintense on T2W images with variable enhancement following contrast: – in the mature stage, the ACI should completely fill the defect to the level of the adjacent cartilage, with restoration of the contour of the articular surface and SI characteristics similar to native hyaline cartilage, though it may appear somewhat heterogeneous ■ the interface between the repair tissue and the native articular cartilage may be indiscernible or may appear as a dark line or as a sudden transition of SI (Fig. 5.162a, b): – fissures are commonly identified at the graft–host cartilage junction; if the fissure is not filled with fluid, the graft is usually intact ■ the junction between the repair tissue and the subchondral bone is usually isointense or slightly hypointense to the remainder of the ACI: – a high SI interface suggests poor integration between the repair tissue and the subchondral bone ■ the subchondral bone marrow normally shows oedema for some months following ACI (Fig. 5.162b): – persistence of marrow oedema 1 year post-ACI suggests a problem with the repair – subchondral cyst formation has been reported in 10 per cent of cases (Fig. 5.162c, d), and is associated with a fibrocartilage-like appearance of the graft complications include the following: ■ arthrofibrosis presents with joint stiffness and occurs in ~10 per cent of cases: – MRI findings: hypointense bands of tissue, usually within Hoffa’s fat pad, the suprapatellar pouch and the parapatellar recesses, that may extend to the surface of the ACI ■ hypertrophy of periosteal cover can occur in 26 per cent of cases and is usually asymptomatic: – when symptomatic, it is treated by shaving of the overgrown tissue – MRI findings: protrusion of repair tissue above the level of the adjacent native articular cartilage by >1 mm (Fig. 5.162e, f) – hypertrophied repair tissue may protrude into the intercondylar notch and affect function of the ACL – matrix-based ACI is associated with a reduced incidence of graft hypertrophy ■ underfilling of the defect is usually asymptomatic ■ detachment (delamination) of all or a portion of the repair tissue has a reported incidence of 5–14 per cent and usually occurs within 6–9 months of surgery: – MRI findings: delamination in situ appears as the presence of joint fluid between the repair tissue and the subchondral bone simulating a cartilage flap; displaced delamination appears as a focal cartilage defect that may result in an intra-articular loose body ■ detachment of the periosteal cover may also occur (periosteal delamination) ■

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Post-arthroscopy appearances of Hoffa’s fat pad229 ●

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arthroscopy results in a horizontal, linear scar in the fat pad extending from the arthroscopy portal (Fig. 5.163a), and multiple foci of signal void on GE sequences due to residual, radiographically occult metallic fragments (Fig. 5.163b) scar is most prominent at 6 months post-arthroscopy and typically disappears by 12 months thickening of the medial/lateral retinaculum (Fig. 5.163c) or the patellar tendon (Fig. 5.163d) may be seen depending on the entry site

The post-operative knee

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Figure 5.162 Appearances following autologous chondrocyte implantation. Coronal proton density-weighted (PDW) fast spin-echo (FSE) (a) and PDW FSE fat-suppressed (FS) (b) images showing a hypointense graft (arrows) compared with the native hyaline cartilage with minor subchondral oedema (arrowhead b). Subchondral cyst formation: Coronal PDW FSE (c) and sagittal PDW FSE FS (d) images showing subchondral cyst formation (arrows) with hypointensity of the graft (arrowheads) consistent with fibrocartilage. Graft hypertrophy: Sagittal PDW FSE (e) and coronal PDW FSE FS (f) images showing increased thickness and protrusion of the graft (arrows) beyond the native articular surface.

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d Figure 5.163 Post-arthroscopy changes. Hoffa’s fat pad: Sagittal proton density-weighted (PDW) fast spin-echo (FSE) image (a) showing linear scarring in the fat pad (arrows). Sagittal T2*-weighted gradient-echo image (b) showing hypointense foci due to susceptibility artefact (arrows). Medial retinaculum: Axial PDW FSE image (c) showing thickening of the medial retinaculum (arrow). Patellar tendon: Sagittal PDW FSE image (d) showing thickening of the proximal tendon (arrow) and linear scarring in the fat pad (arrowhead).

REFERENCES 1 2 3

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Stabler A, Glaser C, Reiser M. Musculoskeletal MR: knee. Eur Radiol 2000; 10: 230–41. Carrino JA, Schweitzer ME. Imaging of sports-related knee injuries. Radiol Clin North Am 2002; 40: 181–202. Pereira ER, Ryu KN, Ahn JM, Kayser F, Bielecki D, Resnick D. Evaluation of the anterior cruciate ligament of the knee: comparison between partial flexion true sagittal and extension sagittal oblique positions during MR imaging. Clin Radiol 1998; 53: 574–8. Niitsu M, Ikeda K, Itai Y. Slightly flexed knee position within a standard knee coil: MR delineation of the anterior cruciate ligament. Eur Radiol 1998; 8: 113–15. Lee SY, Matsui M, Yoshida K et al. Magnetic resonance delineation of the anterior cruciate ligament of the knee: flexed knee position within a surface coil. J Clin Imaging 2005; 29: 117–22. Lee JH, Singh TT, Bolton G. Axial fat-saturated FSE imaging of knee: appearance of meniscal tears. Skeletal Radiol 2002; 31: 384–95.

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165 Elias DA, White LM, Fithian DC. Acute lateral patellar dislocation at MR imaging: injury patterns of medial patellar soft-tissue restraints and osteochondral injuries of the inferomedial patella. Radiology 2002; 225: 736–43. 166 Apostolaki E, Cassar-Pullicino V, Tyrrell PN, McCall IW. MRI of the infrapatellar fat pad in occult traumatic patellar dislocation. Clin Radiol 1999; 54: 743–7. 167 Reiff DB, Heenan SD, Heron CW. MRI appearances of the asymptomatic patellar tendon on gradient echo imaging. Skeletal Radiol 1995; 24: 123–6. 168 Mcloughlin RF, Raber EL, Vellet AD, Wiley JP, Bray RC. Patellar tendinitis: MR imaging features, with suggested pathogenesis and proposed classification. Radiology 1995; 197: 843–8. 169 Yu JS, Popp JE, Kaeding CC, Lucas J. Correlation of MR imaging and pathologic findings in athletes undergoing surgery for chronic patellar tendinitis. AJR Am J Roentgenol 1995; 165: 115–18. 170 Garcia-Valtuille R, Abascal F, Cerezal L et al. Anatomy and MR imaging appearances of synovial plicae of the knee. Radiographics 2002; 22: 775–84. 171 Kosarek FJ, Helms CA. The MR appearance of the infrapatellar plica. AJR Am J Roentgenol 1999; 172: 481–4. 172 Cothran RL, Mcguire PM, Helms CA, Major NM, Attarian DE. MR imaging of infrapatellar plica injury. AJR Am J Roentgenol 2003; 180: 1443–7. 173 Helpert C, Davies AM, Evans N, Grimer RJ. Differential diagnosis of tumours and tumour-like lesions of the infra-patellar (Hoffa’s) fat pad: pictorial review with emphasis on MR imaging. Eur Radiol 2004; 14: 2337–46. 174 Chung CB, Skaf A, Roger B, Campos J, Stump X, Resnick D. Patellar tendon–lateral femoral condyle friction syndrome: MR imaging in 42 patients. Skeletal Radiol 2001; 30: 694–7. 175 Vahlensieck M, Linneborn G, Schild H, Schmidt HM. Hoffa’s recess: incidence, morphology and differential diagnosis of the globular-shaped cleft in the infrapatellar fat pad of the knee on MRI and cadaver dissections. Eur Radiol 2002; 12: 90–3. 176 Aydingoz U, Oguz B, Aydingoz O et al. Recesses along the posterior margin of the infrapatellar (Hoffa’s) fat pad: prevalence and morphology on routine MR imaging of the knee. Eur Radiol 2005; 15: 988–94. 177 Ozkur A, Adaletli I, Sirikci A, Kervancioglu R, Bayram M. Hoffa’s recess in the infrapatellar fat pad of the knee on MR imaging. Surg Radiol Anat 2005; 27: 61–3. 178 Bohndorf K. Imaging of acute injuries of the articular surfaces (chondral, osteochondral and subchondral fractures). Skeletal Radiol 1999; 28: 545–60. 179 McCauley T, Recht MP, Disler DG. Clinical imaging of articular cartilage of the knee. Semin Musculoskelet Radiol 2001; 5: 293–304. 180 Kendell SD, Helms CA, Rampton JW, Garrett WE, Higgins LD. MRI appearance of chondral delamination injuries of the knee. AJR Am J Roentgenol 2005; 184: 1486–9. 181 Rubin DA, Harner CD, Costello JM. Treatable chondral injuries in the knee: frequency of associated focal subchondral edema. AJR Am J Roentgenol 2000; 174: 1099–1106. 182 Hinshaw MH, Tuite MJ, De Smet AA. ‘Dem Bones’: osteochondral injuries of the knee. Magn Reson Imaging Clin North Am 2000; 8: 335–48. 183 Loredo R, Sanders TG. Imaging of osteochondral injuries. Clin Sports Med 2001; 2: 249–78. 184 Sanders T, Medynski MA, Feller JF, Lawhorn KW. Bone contusion patterns of the knee at MR imaging: footprint of the mechanism of injury. Radiographics 2000; 20: S135–51. 185 Mandalia V, Fogg AJB, Chari R, Murray J, Beale A, Henson JHL. Bone bruising of the knee. Clin Radiol 2005; 60: 627–36. 186 Vincken PW, Ter Braak BP, van Erkel AR, Coerkamp EG, Mallens WM, Bloem JL. Clinical consequences of bone bruise around the knee. Eur Radiol 2006; 16: 97–107. 187 Boks SS, Vroegindeweij D, Koes BW, Hunink MG, Bierma-Zeinstra SM. Follow-up of occult bone lesions detected at MR imaging: systematic review. Radiology 2006; 238: 853–62. 188 Davies NH, Niall D, King LJ, Lavelle J, Healy JC. Magnetic resonance imaging of bone bruising in the acutely injured knee short-term outcome. Clin Radiol 2004; 59: 439–45. 189 Hofmann S, Kramer J, Anosheh V, Aigner N, Breitenseher M. Painful bone marrow edema of the knee: differential diagnosis and therapeutic concepts. Orthop Clin North Am 2004; 35: 312–33. 190 Moosikasuwan JB, Miller TT, Math K, Schultz E. Shifting bone marrow oedema of the knee. Skeletal Radiol 2004; 33: 380–5. 191 Colletti P, Greenberg H, Terk MR. MR findings in patients with acute tibial plateau fractures. Comput Med Imaging Graph 1996; 20: 389–94.

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192 Crawford DC, Safran MR. Osteochondritis dissecans of the knee. J Am Acad Orthop Surg 2006; 14: 90–100. 193 Boutin RD, Januario JA, Newberg AH, Gundry CR, Newman JS. MR imaging features of osteochondritis dissecans of the femoral sulcus. AJR Am J Roentgenol 2003; 180: 641–5. 194 Deie M, Ochi M, Sumen Y et al. Relationship between osteochondritis dissecans of the lateral femoral condyle and lateral menisci types. J Pediatr Orthop 2006; 26: 79–82. 195 Magee T, Shapiro M. Soft tissue twisting injuries of the knee. Skeletal Radiol 2001; 30: 460–3. 196 McCarthy CL, McNally EG. The MRI appearances of cystic lesions around the knee. Skeletal Radiol 2004; 33: 187–209. 197 De Maeseneer M, Debaere C, Desprechins B, Osteaux M. Popliteal cysts in children: prevalence, appearance and associated findings at MR imaging. Pediatr Radiol 1999; 29: 605–9. 198 Rennie WJ, Saifuddin A. Pes anserine bursitis: incidence in symptomatic knees and clinical presentation. Skeletal Radiol 2005; 34: 395–8. 199 Aydingoz U, Oguz B, Aydingoz O, Comert RB, Akgun I. The deep infrapatellar bursa: prevalence and morphology on routine magnetic resonance imaging of the knee. J Comput Assist Tomogr 2004; 28: 557–61. 200 James SL, Connell DA, Bell J, Saifuddin A. Ganglion cysts at the gastrocnemius origin: a series of ten cases. Skeletal Radiol 2007; 36: 139–43. 201 Williams HJ, Davies AM, Allen G, Evans N, Mangham DC. Imaging features of intraosseous ganglia: a report of 45 cases. Eur Radiol 2004; 14: 1761–9. 202 Okada K, Unoki E, Kubota H et al. Periosteal ganglion: a report of three new cases including MRI findings and a review of the literature. Skeletal Radiol 1996; 25: 153–7. 203 Laor T, Chun GF, Dardzinski BJ, Bean JA, Witte DP. Posterior distal femoral and proximal tibial metaphyseal stripes at MR imaging in children and young adults. Radiology 2002; 224: 669–74. 204 Nawata K, Teshima R, Morio Y, Hagino H. Anomalies of ossification in the posterolateral femoral condyle: assessment by MRI. Pediatr Radiol 1999; 29: 781–4. 205 Bebrski K, Hernandez RJ. Stage-1 osteochondritis dissecans versus normal variants of ossification in the knee in children. Pediatr Radiol 2005; 35: 880–6. 206 Lee K, Siegel MJ, Lau DM, Hildebolt CF, Matava MJ. Anterior cruciate ligament tears: MR imaging-based diagnosis in a pediatric population. Radiology 1999; 213: 697–704. 207 Prince JS, Laor T, Bean JA. MRI of anterior cruciate ligament injuries and associated findings in the pediatric knee: changes with skeletal maturation. AJR Am J Roentgenol 2005; 185: 756–62. 208 Oeppen RS, Connolly SA, Bencardino JT, Jaramillo D. Acute injury of the articular cartilage and subchondral bone: a common but unrecognized lesion in the immature knee. AJR Am J Roentgenol 2004; 182: 111–17. 209 Suh JS, Cho JH, Shin KH et al. MR appearance of distal femoral cortical irregularity (cortical desmoid). J Comput Assist Tomogr 1996; 20: 328–32. 210 Close BJ, Strouse PJ. MR of physeal fractures of the adolescent knee. Pediatr Radiol 2000; 30: 756–62. 211 Chan YL, Griffith JF, Cheng JC. MR imaging of children’s knees. Clin Radiol 2001; 56: 631–46. 212 Bozkurt M, Yilmaz E, Atlihan D, Tekdemir I, Havitcioglu H, Gunal I. The proximal tibiofibular joint: an anatomic study. Clin Orthop 2003; 406: 136–40. 213 Bozkurt M, Yilmaz E, Akseki D, Havitcioglu H, Gunal I. The evaluation of the proximal tibiofibular joint for patients with lateral knee pain. Knee 2004; 11: 307–12. 214 Oztuna V, Yildiz A, Ozer C, Milcan A, Kuyurtar F, Turgut A. Involvement of the proximal tibiofibular joint in osteoarthritis of the knee. Knee 2003; 10: 347–9. 215 Ilahi OA, Younas SA, Labbe MR, Edson SB. Prevalence of ganglion cysts originating from the proximal tibiofibular joint: a magnetic resonance imaging study. Arthroscopy 2003; 19: 150–3. 216 Kim S, Choi J-Y, Huh Y-M et al. Role of magnetic resonance imaging in entrapment and compressive neuropathy: what, where, and how to see the peripheral nerves on the musculoskeletal magnetic resonance image. Part 1. Overview and lower extremity. Eur Radiol 2007; 17: 139–49. 217 McCauley TR. MR imaging evaluation of the postoperative knee. Radiology 2005; 234: 53–61. 218 White LM, Kramer J, Recht MP. MR imaging evaluation of the postoperative knee: ligaments, menisci and articular cartilage. Skeletal Radiol 2005; 34: 431–52. 219 Frick MA, Collins MS, Adkins MC. Postoperative imaging of the knee. Radiol Clin North Am 2006; 44: 367–89. 220 Gopez AG, Kavanagh EC. MR imaging of the postoperative meniscus: repair, resection, and replacement. Semin Musculoskelet Radiol 2006; 10: 229–40.

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221 De Smet AA. MR imaging and MR arthrography for diagnosis of recurrent tears in the postoperative meniscus. Semin Musculoskelet Radiol 2005; 9: 116–24. 222 van Arkel ER, Goei R, de Ploeg I, de Boer HH. Meniscal allografts: evaluation with magnetic resonance imaging and correlation with arthroscopy. Arthroscopy 2000; 16: 517–21. 223 Ilaslan H, Sundaram M, Miniaci A. Imaging evaluation of the postoperative knee ligaments. Eur J Radiol 2005; 54: 178–88. 224 Papakonstantinou O, Chung CB, Chanchairujira K, Resnick DL. Complications of anterior cruciate ligament reconstruction: MR imaging. Eur Radiol 2003; 13: 1106–17. 225 McCauley TR, Elfar A, Moore A et al. MR arthrography of anterior cruciate ligament reconstruction grafts. AJR Am J Roentgenol 2003; 181: 1217–23. 226 Burks RT, Crim J, Fink BP, Boyaln DN, Greis PE. The effects of semitendinosus and gracilis harvest in anterior cruciate ligament reconstruction. Arthroscopy 2005; 21: 1177–85. 227 Trattnig S, Millington SA, Szomolanyi P, Marlovits S. MR imaging of osteochondral grafts and autologous chondrocyte implantation. Eur Radiol 2007; 17: 103–18. 228 James SL, Connell DA, Saifuddin A, Skinner JA, Briggs TWR. MR imaging of autologous chondrocyte implantation of the knee. Eur Radiol 2006; 16: 1022–30. 229 Tang G, Niitsu M, Ikeda K, Endo H, Itai Y. Fibrous scar in the infra-patellar fat pad after arthroscopy: MR imaging. Radiat Med 2000; 18: 1–5.

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6 The ankle and foot

TECHNIQUE Conventional MRI1–7 ●

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● ● ●

routine MRI of the ankle is optimally performed using the three orthogonal planes: ■ coronal, planned from an axial scout and parallel to a line joining the medial and lateral malleoli (Fig. 6.1a) ■ sagittal, running perpendicular to the coronal plane (Fig. 6.1a) ■ axial, covering from above the distal tibiofibular joint to the calcaneal heel pad ■ an axial oblique plane is planned from a sagittal scout showing the peroneal tendons, allowing true axial images through the ankle tendons as they pass around the malleoli (Fig. 6.1b) routine MRI of the foot is performed using: ■ an oblique axial plane, parallel to the long axis of the metatarsal (MT) bones (Fig. 6.1c) ■ an oblique coronal plane, perpendicular to the long axis of the MTs (Fig. 6.1c) ■ a sagittal plane, parallel to the third ray patient’s position may be supine with the ankle in a neutral position or prone with the foot in ~20° plantar flexion, decreasing the ‘magic-angle’ effect on the ankle tendons, accentuating the fat plane between the peroneal tendons and allowing better visualisation of the calcaneofibular ligament (CFL) use of an extremity surface coil enhances spatial resolution technical parameters: field of view (FOV) 12–16 cm, slice thickness 3–4 mm with 0.5–1 mm inter-slice gap, matrix 256¥192–512 sequences: ■ T1-weighted (T1W) spin-echo (SE)/proton density-weighted (PDW) fast spin-echo (FSE) images provide optimal anatomical detail ■ short tau inversion recovery (STIR) or T2-weighted (T2W)/PDW FSE fat-suppressed (FS) images provide optimal assessment of marrow and soft-tissue oedema and joint fluid ■ two-dimensional (2D) or three-dimensional (3D) gradient-echo (GE) sequences may be used for assessment of cartilage

MR arthrography8,9 ● ●

MR arthrography techniques include direct gadolinium, direct saline and indirect the preferred technique is direct gadolinium MR arthrography, which involves intra-articular injection of approximately 10 ml dilute gadolinium solution: ■ the joint is punctured under fluoroscopic control with the needle placed medial to the anterior tibialis tendon (ATT) or medial to the extensor hallucis longus (EHL) tendon: – puncture between the EHL and the extensor digitorum longus (EDL) tendons risks damage to the dorsalis pedis artery

Technique

b

a

c

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Figure 6.1 Planes for conventional MRI of the foot and ankle. Axial T1-weighted (T1W) spin-echo (SE) image (a) through the level of the malleoli showing the planes for coronal and sagittal images of the ankle. Sagittal T1W SE image (b) showing the plane for axial oblique (true axial) imaging of the ankle tendons. Sagittal proton density-weighted fast spin-echo image (c) of the forefoot showing the planes for oblique axial and coronal imaging of the foot.

MR protocol: sagittal, axial and coronal T1W SE FS images in the three orthogonal planes as described above with a sagittal or coronal T2W FSE FS image to assess extra-articular fluid collections and marrow oedema a normal direct ankle MR arthrogram shows: ■ prominent anterior and posterior articular recesses adjacent to the talar dome (Fig. 6.2a) ■ filling of the syndesmotic recess between the distal tibia and fibula (Fig. 6.2b) ■ no contrast should be seen lateral to the ankle joint or posterior to the posterior talofibular ligament (PTFL): – however, in the presence of a capacious anterior recess, contrast may outline the anterior margin of the anterior talofibular ligament (ATFL), simulating a tear (Fig. 6.2c, d) ■ in 25 per cent of cases, contrast fills the flexor hallucis longus (FHL) or flexor digitorum longus (FDL) tendon sheaths and the posterior subtalar joint (Fig. 6.2e) ■ inadvertent instillation of air bubbles may simulate a loose body (Fig. 6.2e), but the bubbles are located in the non-dependent part of the joint indications: ■ ligament injury, especially articular-side partial-thickness tears ■ impingement syndrome ■ osteochondral lesions of the talus (OLTs) ■ articular cartilage lesions ■ intra-articular loose bodies indirect MR arthrography involves intravenous injection of gadolinium followed by 5–10 minutes of light exercise and MRI sequences as for direct gadolinium arthrography potential uses: ■ subtle cartilage defects: defects and subchondral bone show enhancement

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a

b

c d

e

f

Figure 6.2 Direct gadolinium MR arthrography. Sagittal T1-weighted (T1W) spin-echo (SE) fat-suppressed (FS) image (a) showing hyperintense contrast medium (arrows) within the anterior and posterior recesses of the ankle joint. Coronal T1W FS image (b) showing injected contrast filling the syndesmotic recess (arrow). Axial T1W SE FS images (c, d) showing a capacious anterior recess (arrows c) with contrast outlining the anterior aspect of the anterior talofibular ligament (arrowheads d) and showing the posterior talofibular ligament (PTFL) (arrow d). Sagittal T1W SE FS image (e) showing a filling defect (arrow) in the anterior recess due to injected air. Note also contrast medium in the posterior subtalar joint (arrowheads). Indirect MR arthrography: Axial post-contrast T1W SE FS image (f) showing enhancement of the thickened PTFL (arrows) indicating a partial tear.

The distal tibiofibular joint

■ ■ ■

OLTs: enhancement of the fragment–bone interface indicates partial or complete detachment partial ligament tears appear as focal ligament enhancement (Fig. 6.2f) complete ligament tears manifest as contrast extending into the ligament defect

THE DISTAL TIBIOFIBULAR JOINT Normal anatomy9–11 ●

the distal tibiofibular joint is formed by the articulation between the distal tibia and the distal fibula (Fig. 6.3a, b) and is supported by a syndesmotic ligamentous complex comprising: ■ the anteroinferior tibiofibular ligament (AITibFL): extends obliquely upwards and medially from the anterior surface of the fibula to the anterolateral tubercle of the tibia and may comprise two or three bands or may be multifasciculated: – it is the weakest and most commonly torn of the syndesmotic ligaments and is not always identified on MRI

a

b

Figure 6.3 Normal anatomy of the distal tibiofibular joint. Coronal (a) and axial (b) proton density-weighted fast spinecho images showing the distal tibiofibular joint (arrows).

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■

the posteroinferior tibiofibular ligament (PITibFL), which arises from the posterior border of the lateral malleolus and extends upwards and medially to insert into the posterolateral portion of the tibial tubercle: – it is quadrilateral in shape – the AITibFL and PITibFL are demonstrated on axial (Fig. 6.4a) and coronal (Fig. 6.4b) MR images as thin, hypointense structures at the level of the tibial plafond and the talar dome – they appear striated and discontinuous due to the presence of interposed fat and the downwards oblique course of the ligaments from the tibia to the fibula (Fig. 6.4c–e) the interosseous tibiofibular ligament: the lowermost portion of the crural interosseous membrane, comprising short, thick fibres running from the medial aspect of the distal fibular shaft to the lateral surface of the tibia (Fig. 6.4f, g) the transverse tibiofibular ligament: also referred to as the inferior transverse ligament or the deep inferior posterior tibiofibular ligament: – it lies inferior and deep to the PITibFL and extends from the upper part of the distal fibula to the posterior border of the articular surface of the tibia/medial malleolus (Fig. 6.4h)

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b

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e c

d

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Figure 6.4 Normal anatomy of the syndesmotic ligament complex. Axial T1-weighted (T1W) spin-echo (SE) image (a) showing the anteroinferior tibiofibular ligament (AITibFL) (arrow) and the posteroinferior tibiofibular ligament (PITibFL) (arrowheads). Coronal T1W SE image (b) showing the PITibFL (arrows). Axial T2*-weighted images (c, d) showing the striated and discontinuous appearance of the normal AITibFL (arrow c) and PITibFL (arrow d). Axial T1W SE fat-suppressed gadolinium MR arthrogram (e) showing the AITibFL (arrow) and the PITibFL (arrowhead). Coronal (f) and axial (g) proton density-weighted (PDW) fast spin-echo (FSE) images showing the interosseous tibiofibular ligament (arrows). Axial PDW FSE image (h) showing the inferior transverse ligament (arrows).

Pathology of the distal tibiofibular joint

PATHOLOGY OF THE DISTAL TIBIOFIBULAR JOINT Injury8,11 ● ●

the syndesmotic complex is frequently disrupted in association with ankle sprains and distal fibular fractures, injuries to these ligaments accounting for ~10 per cent of ankle sprains the mechanism of injury may be related to pronation and eversion of the foot, combined with internal rotation of the tibia on a fixed foot, and is likely to result in chronic ankle dysfunction

MRI findings ● a ligament sprain may manifest as fluid around an intact ligament (Fig. 6.5a) ● criteria for tear of the AITibFL or the PITibFL include: ■ discontinuity of the ligament (Fig. 6.5b) ■ a ‘wavy’ or curved contour to the ligament or non-visualisation of the ligament ■ accuracies of 97 per cent for the AITibFL and 100 per cent for the PITibFL are reported using both of the above criteria together

b a

d

c Figure 6.5 Syndesmotic complex injury. Axial T2-weighted (T2W) fast spin-echo (FSE) fat-suppressed image (a) showing fluid (arrow) around an intact anteroinferior tibiofibular ligament (AITibFL) consistent with a grade 1 sprain. Axial proton density-weighted FSE image (b) showing thickening of the AITibFL (arrow) and discontinuity from its fibular attachment (arrowhead). Acute AITibFL injury: sagittal short tau inversion recovery image (c) showing oedema (arrows) anterior to the distal fibula. Axial T2W FSE image (d) showing thickening of the AITibFL (arrowhead) and avulsion from its medial attachment (arrow).

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anterolateral ankle oedema/haemorrhage in the acute stage (Fig. 6.5c, d): – however, non-visualisation of the ligament may be due to haemorrhage associated with distal fibular fracture, leading to a false-positive diagnosis of rupture

MR arthrographic findings ● these include thickening, lack of visualisation or irregularity of the ligaments ● MR arthrography may improve the visualisation of syndesmotic ligament tears8

Syndesmotic soft-tissue impingement syndrome12 ● ●

syndesmotic soft-tissue impingement is considered to follow a supination–external rotation injury, resulting in injury to all of the ligaments of the syndesmotic complex chronic syndesmotic ligament inflammation, possibly due to premature mobilisation, is thought to result in formation of scar tissue with subsequent impingement between the distal tibia and the lateral malleolus

MRI findings ● ● ●

thickening and occasional tearing of the various syndesmotic ligaments, most commonly the AITibFL, is observed ligament thickening caused by soft-tissue scarring distinct from the ligaments, showing low signal intensity (SI) on T1W and low/intermediate SI on T2W images however, such scarring is also seen in a large proportion of patients without clinical syndesmotic impingement; the significant differentiating feature between patients with and without impingement is the presence of anterior tibial and talar osteophytes

THE TIBIOTALAR JOINT Introduction ●

the tibiotalar (ankle mortise) joint is formed by the articulation between the distal tibia (plafond and medial malleolus), the distal fibula (lateral malleolus) and the talar dome, supported by the capsule, ligaments and tendons that cross the joint

THE ANKLE MORTISE JOINT Normal anatomy3 ● ●

the margins of the joint are defined by the medial malleolus, the lateral malleolus, the tibial plafond and the talar dome (Fig. 6.6a–c) anatomical variants/pitfalls:13 ■ the pseudo-osteochondral defect of the tibia, which appears as a low SI line on posterior coronal images through the tibial plafond and represents condensation of cortical trabeculae at the normal elevation of the posterior distal tibial articular surface (Fig. 6.6d) ■ the pre-articular fat pad is found within a small fossa along the medial surface of the talar neck (Fig. 6.6e), the outer border being formed by the anterior tibiotalar ligament (ATTL), and may simulate an avulsion fracture on coronal or axial T1W images

The tibiotalar joint

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Figure 6.6 Normal anatomy of ankle mortise joint. Sagittal (a), coronal (b) and axial (c) proton density-weighted (PDW) fast spin-echo (FSE) images showing the articulations (arrows a, c) between the tibial plafond, the medial malleolus (MM) and the lateral malleolus (LM) with the talar dome. Coronal PDW FSE image (d) showing pseudoosteochondral defect of the tibia (arrow). Coronal PDW FSE image (e) showing the pre-articular fat pad (arrow) limited by the anterior tibiotalar ligament (arrowhead).

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PATHOLOGY OF THE ANKLE MORTISE JOINT Anterolateral impingement syndrome14,15 ● ● ●

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anterolateral impingement syndrome is a relatively common cause of chronic lateral ankle pain following minor ankle sprain injuries, possibly occurring following ~3 per cent of ankle sprains it is associated with tears of the ATFL and AITibFL and an accessory fascicle of the AITibFL chronic lateral ankle instability16 results in repetitive synovial inflammation producing a soft-tissue mass of hypertrophied synovial tissue and fibrosis (meniscoid lesion) within the anterolateral recess of the joint the anterolateral recess is an anatomical space bounded posteriorly by the talus and the fibula, and anteriorly and laterally by the joint capsule, the AITibFL, the ATFL and the CFL (Fig. 6.7) clinically, presents with focal anterolateral pain and tenderness exacerbated by dorsiflexion and eversion

Figure 6.7 The anterolateral recess. Axial T2-weighted fast spin-echo image showing a small amount of fluid in the anterolateral recess (arrow) bounded by the anterior talofibular ligament (arrowheads), the talus and the lateral malleolus.

MR findings ● conventional MRI17 demonstrates soft-tissue thickening in the anterolateral gutter that is of low SI on T1W images (Fig. 6.8a) and low/intermediate SI on T2W images (Fig. 6.8b), optimally seen on axial images between the AITibFL and the ATFL: ■ this is not a specific finding, as it is also seen in asymptomatic individuals ● a low SI meniscoid mass within the anterolateral gutter of the ankle joint, optimally visualised on axial and coronal images in the presence of fluid within the lateral gutter (Fig. 6.8c) ● associated features include: ■ a soft-tissue mass within the medial gutter of the tibiotalar joint (50 per cent) ■ abnormality (tear, thickening) of the ATFL (100 per cent) and the CFL (50 per cent) ■ rarely, talar bone bruise, chondral defects, osseous spurs or loose bodies ● the sensitivity and specificity of conventional MRI are 30–100 per cent, and improve in the presence of an ankle effusion ● the optimal demonstration of pathology is with direct MR arthrography8,18 ● indirect MR arthrography has not proven to be of additional value in the diagnosis of anterolateral impingement19

The tibiotalar joint

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c

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Figure 6.8 Anterolateral impingement syndrome. Axial T1-weighted spin-echo (a) and T2-weighted (T2W) fast spin-echo (FSE) (b) images showing irregular thickening of the anterolateral capsule (arrows) with obliteration of the anterolateral recess. Axial T2W FSE fat-suppressed image (c) in the presence of a joint effusion showing a nodular meniscoid lesion (arrow) anterior to the lateral malleolus (arrowhead).

Anterior impingement syndrome14,15 ● ●

anterior impingement syndrome is a relatively common cause of chronic ankle pain, particularly associated with sports requiring repeated dorsiflexion stress on the ankle, such as football pathologically, it is associated with a beak-like, bony prominence from the anterior margin of the tibial plafond and a corresponding osteophyte from the dorsum of the talus, proximal to the talar neck and within the joint capsule; impingement of soft tissues between the two osteophytes in dorsiflexion results in the syndrome

MRI findings ● anterior tibial and dorsal talar osteophytes are seen that may show marrow oedema (Fig. 6.9a, b), with synovitis in the anterior capsular recess of the joint (Fig. 6.9c)

Anteromedial impingement syndrome14,15 ● ●

anteromedial impingement syndrome is an uncommon cause of chronic ankle pain pathologically, it results from formation of a meniscoid lesion of thickened soft tissues anterior to the tibiotalar ligament that may arise in isolation or associated with a partially torn deep deltoid ligament: ■ it may also occur secondary to a thickened ATTL ■ the thickened soft tissue impinges on the anteromedial corner of the talus during dorsiflexion, resulting in formation of an osteophyte and/or a chondral lesion

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Figure 6.9 Anterior impingement syndrome. Sagittal T2-weighted (T2W) fast spin-echo (FSE) fat-suppressed (FS) images (a, b) showing osteophytes arising from the anterior tibial plafond (arrow a) and the dorsum of the talus (arrow b) with associated marrow oedema. Sagittal T2W FSE FS image (c) showing synovitis (arrow) within the anterior recess.

the condition is usually associated with medial collateral ligament (MCL) or lateral collateral ligament (LCL) injury

MRI findings ● conventional MRI may miss the condition unless a joint effusion is present MR arthrographic findings20 ● a medial meniscoid lesion is seen, with irregular thickening of the soft tissues anterior to the tibiotalar ligament and the medial malleolus (Fig. 6.10a, b) ● thickened ATTL and associated talar chondro-osseous injury

Posteromedial impingement syndrome14,15 ● ●

posteromedial impingement syndrome is an uncommon cause of chronic posteromedial ankle pain pathologically, it follows a severe inversion injury with crushing of the deep posterior fibres of the deltoid ligament between the medial wall of the talus and the medial malleolus: ■ posteromedial impingement is associated with lateral ligament disruption, and becomes symptomatic once the lateral ligament injury has been successfully treated ■ inadequate healing of the posterior deltoid ligament results in chronic inflammation and soft-tissue hypertrophy, which is impinged between the medial malleolus and the talus

MRI findings21 ● hyperintensity, enlargement and loss of the normal striated pattern of the posterior deltoid ligament appear as soft-tissue thickening between the medial malleolus and the talar dome (Fig. 6.11a–c)

The tibiotalar joint

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Figure 6.10 Anteromedial impingement syndrome. Axial T2-weighted fast spin-echo (a) and short tau inversion recovery (b) images showing an irregular synovial mass (arrows) in the anteromedial aspect of the joint.

● ● ●

partial encasement of the posterior tibialis tendon (PTT) and the FDL and FHL tendons by the hypertrophied mass (Fig. 6.11d) marrow oedema of the medial talus and the adjacent medial malleolus (Fig. 6.11e) associated features include abnormality of the lateral ligaments (Fig. 6.11d) and posterior/posterolateral synovitis22

Posterior impingement syndrome14,15 ● ● ●

●

posterior impingement syndrome is a group of abnormalities that result from repetitive or acute plantar flexion of the foot and is classically seen in ballet dancers posterior impingement syndrome is also referred to as os trigonum syndrome, talar compression syndrome and posterior block of the ankle pathologically, the posterior process of the talus or os trigonum and adjacent soft tissues become compressed between the posterior tibial margin and the calcaneus; several osseous variants predispose to the condition, including: ■ os trigonum, an accessory ossicle of the lateral process of the talus that persists into adulthood in ~7 per cent of individuals (Fig. 6.12a, b) ■ an elongated lateral process of the talus, termed a ‘Stieda’ process (Fig. 6.12c) ■ a downwards sloping posterior lip of the talus (Fig. 6.12d) ■ pseudarthrosis of the lateral talar tubercle (Fig. 6.12e) ■ a prominent posterior process of the calcaneus ■ loose bodies within the posterior capsular recess (Fig. 6.12f, g) soft-tissue causes of impingement include the posterior intermalleolar ligament: ■ the posterior intermalleolar ligament is a normal variant of the posterior ankle ligament anatomy that extends from the superior margin of the malleolar fossa of the distal fibula to the posterior margin of the medial malleolus ■ it lies between the PITibFL and the inferior transverse ligament above and the PTFL below (Fig. 6.13a–c), is identified in ~82 per cent of cadaveric specimens, and measures ~4 cm in length, 4 mm in width and 3 mm in thickness23 ■ the ligament may have multiple bundles medially that usually combine to form a single cord laterally and occasionally project anteriorly between the tibia and the talus to resemble a meniscus ■ it may become trapped between the tibia and the talus during ankle plantar flexion, resulting in fraying and ‘bucket-handle’ tears causing posterior impingement24 ■ soft-tissue changes associated with posterior impingement include: – synovitis of the FHL tendon sheath – synovitis of the posterior synovial recesses of the tibiotalar and posterior subtalar joints

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Figure 6.11 Posteromedial impingement syndrome. Coronal proton density-weighted (PDW) fast spin-echo (FSE) (a), PDW FSE fatsuppressed (FS) (b) and axial PDW FSE (c) images showing hyperintensity and loss of striation of the deep medial ligament (arrows) medial to the talar dome and anterior to the posterior tibialis tendon (arrowhead c). Coronal oblique PDW FSE image (d) showing partial encasement of the tibialis posterior (short white arrow) and flexor digitorum longus (black arrowhead) tendons by a soft-tissue mass (long white arrow) and associated chronic anterior talofibular ligament injury (black arrows). Coronal T2-weighted FSE FS image (e) showing the mass (black arrow) with associated marrow oedema in the medial malleolus (white arrow) and the talar dome (white arrowhead).

The tibiotalar joint

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Figure 6.12 Osseous variants associated with the posterior impingement syndrome. Sagittal T1-weighted (T1W) spin-echo (SE) (a) and T2-weighted (T2W) fast spin-echo (FSE) fat-suppressed (FS) (b) images showing an oedematous os trigonum (arrows). Axial proton density-weighted FSE FS image (c) showing a ‘Stieda’ process (arrow). Sagittal T1W SE image (d) showing a downwards sloping posterior lip (arrow) of the talus. Axial T1W SE image (e) showing a pseudoarthrosis (arrow) of the lateral process of the talus. (continued)

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g f Figure 6.12 (continued) Sagittal T1W SE (f) and axial T2W FSE (g) images showing an osseous loose body (arrows) in the posterior capsular recess.

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Figure 6.13 Normal anatomy of the posterior intermalleolar ligament. Axial T2-weighted (T2W) fast spin-echo (FSE) image (a) showing the posterior intermalleolar ligament (arrows) extending between the lateral malleolus (LM) and the medial malleolus (MM). Sagittal proton density-weighted FSE fatsuppressed (FS) image (b) showing the posterior intermalleolar ligament (arrow) running between the posterior tibia and the talar dome. Coronal T2W FSE FS image (c) showing the posterior intermalleolar ligament (arrows) running obliquely between the malleoli and superior to the posterior talofibular ligament (arrowheads).

The tibiotalar joint

MRI findings25 ● marrow oedema is seen in the lateral talar tubercle (Fig. 6.14a) and/or the os trigonum (Fig. 6.12b) ● fragmentation of the lateral talar tubercle and/or os trigonum ● synovitis in the posterior soft tissues, including: ■ the FHL tendon sheath (Fig. 6.14b, c) ■ the posterior synovial recesses of the tibiotalar (Fig. 6.14d) and posterior subtalar joints (Fig. 6.14e) ● a thickened posterior intermalleolar ligament (Fig. 6.14f, g)

Cartilage lesions8,26 ● ●

chondral lesions are common in the ankle joint, producing non-specific symptoms MRI grading of cartilage lesions: ■ grade 1 – abnormal intrachondral SI with smooth outline ■ grade 2 – mild surface irregularity with/without focal defect 50 per cent depth but not full thickness grade 4 – full-thickness cartilage loss with denuded subchondral bone MR arthrography has a reported accuracy of ~90 per cent for the detection of cartilage lesions of the tibia, fibula and talus26 ■ ■

●

MRI findings ● higher grade focal defects can be demonstrated on conventional MR images (Fig. 6.15a, b)

Intraosseous ganglion cysts of the ankle joint27 ● ● ●

intraosseous ganglia are relatively uncommon lesions of unknown aetiology, but may be post-traumatic of 75 cases reported in the literature, 55 involved the medial malleolus, nine involved the lateral malleolus and 11 involved the talus clinically, they occur in middle-aged patients (median age 44 years, age range 14–86 years), presenting with mechanical ankle pain and commonly no abnormal physical findings

MRI findings ● subchondral cystic lesions are seen with intermediate SI on T1W and high SI on T2W/STIR (Fig. 6.16a, b) ● may be associated marrow oedema (Fig. 6.16c, d) and joint effusion

The tibiotalar joint

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Figure 6.15 Ankle articular cartilage defect. Sagittal (a) and axial (b) proton density-weighted fast spin-echo images showing a focal grade 4 cartilage defect (arrows) in the anterior tibial plafond.

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Figure 6.16 Intraosseous ganglia of the ankle joint. Coronal T1-weighted (T1W) spin-echo (SE) (a) and sagittal T2-weighted fast spin-echo fat-suppressed (b) images showing a subchondral cyst (arrows) of the medial malleolus. Coronal T1W SE (c) and sagittal short tau inversion recovery (d) images showing a cyst of the talus (arrows) with associated marrow oedema (arrowheads).

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THE LATERAL COLLATERAL LIGAMENT Normal anatomy1,28,29 ● ●

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the LCL complex has three components: the ATFL, the PTFL and the CFL the ATFL extends between the anterior aspect of the lateral malleolus to the talar neck, just anterior to the fibular articular surface: ■ it is optimally demonstrated on axial MR images as a thin, hypointense band running between the lateral malleolus and the talar body (Fig. 6.17a) ■ fluid within the anterolateral recess of the joint highlights the ligament on T2W images (Fig. 6.7) ■ it may normally appear bifasciculated or striated with mildly increased intraligamentous SI on T2W and PDW images30 the PTFL has a broad, fan-shaped origin from the fibular fossa of the distal fibula, attaches to the posterior aspect of the distal tibia, and is the strongest component of the LCL: ■ it is demonstrated on axial and coronal images (Fig. 6.17a, b), appearing striated due to the presence of interspersed fat ■ it may normally exhibit marked heterogeneity and thickening

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Figure 6.17 Anatomy of the lateral collateral ligament complex. Axial T1-weighted (T1W) spin-echo (SE) image (a) showing the anterior talofibular ligament (arrow) and the fanshaped posterior talofibular ligament (PTFL) (double arrows). Coronal T1W SE image (b) showing the PTFL (arrow) and the calcaneofibular ligament (CFL) (arrowhead) lying deep to the peroneal tendons (double arrowhead). Axial oblique proton density-weighted fast spin-echo image (c) showing the CFL (arrows) running deep to the peroneal tendons (arrowheads).

The tibiotalar joint

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the CFL runs between the tip of the lateral malleolus to a small tubercle on the lateral aspect of the calcaneus: ■ it is demonstrated on coronal and axial images (Fig. 6.17b, c), identified as a low SI band deep to the peroneal tendons and often incompletely visualised on axial images due to its oblique orientation ■ visualisation of the CFL may be improved by the use of multi-planar reconstruction from standard 2D turbo spin-echo MR images31 MR arthrography:9 injected contrast medium can outline both the superficial and the deep surfaces of the ATFL and the PTFL (Fig. 6.2c, d) and optimises demonstration of the deep surface of the CFL

PATHOLOGY OF THE LATERAL COLLATERAL LIGAMENT COMPLEX Trauma1,16,28,29 ● ● ●

~85 per cent of ankle sprains involve the lateral ligaments (inversion injuries) and lateral ankle sprains represent 16–21 per cent of all sports-related ankle injuries the ATFL is the weakest ligament and is therefore the first torn, typically followed by the CFL and then the PTFL classification of ankle sprains is based on the number of affected ligaments: ■ first-degree sprain – partial or complete tear of the ATFL ■ second-degree sprain – partial or complete tear of the ATFL and the CFL ■ third-degree sprain – injury to the ATFL, CFL and PTFL

MRI findings changes in morphology of the ligament include discontinuity (Fig. 6.18a), detachment, thickening (Fig. 6.18b, c), and thinning and irregularity (Fig. 6.18d) ● SI heterogeneity with increased SI in and around the ligament on T2W images (Fig. 6.18e) ● associated features include obliteration of fat planes around the ligament (Fig. 6.18f) and extravasation of joint fluid (Fig. 6.18a): ■ CFL tears may be associated with fluid in the peroneal tendon sheath ■ bone bruises32 are reported in ~17 per cent of patients with a lateral ligament injury and most commonly involve the medial talus or occasionally the lateral talus and the calcaneus ● chronic tears show morphological abnormality without the associated soft-tissue and bone SI changes seen with acute injuries (Fig. 6.18g): ■ however, chronic tears may be associated with reduced SI in the surrounding fat due to scarring or synovial proliferation ●

MR arthrographic findings8 ● MR arthrography is more sensitive and accurate than conventional MR for the diagnosis of lateral ligament injury ● non-visualisation of the ligament or extension of contrast medium anterior to the ATFL is indicative of a tear (Fig. 6.19a) ● CFL tear is associated with extension of contrast medium into the peroneal tendon sheath (Fig. 6.19b) ● extension of contrast into the soft tissues posterior to the PTFL indicates a tear

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Figure 6.18 Lateral collateral ligament complex injury, conventional MRI. Axial T2-weighted (T2W) fast spin-echo (FSE) fat-suppressed (FS) image (a) showing discontinuity of the thickened, hyperintense anterior talofibular ligament (ATFL) (arrow) with extravasation of joint fluid (arrowheads) into the soft tissues. Axial T2W FSE FS image (b) and coronal T1-weighted (T1W) spin-echo (SE) image (c) showing thickening, hyperintensity and irregularity of the calcaneofibular ligament (arrows). Axial T1W SE image (d) showing a ‘wavy’ ATFL (arrow). Axial T2W FSE image (e) showing heterogeneous hyperintensity of the posterior talofibular ligament (arrows) with surrounding soft-tissue oedema. Axial T1W SE image (f) showing loss of normal fat planes around the ATFL (arrow). Axial T2W FSE image (g) showing a thickened ATFL (arrows) without any associated soft-tissue changes, consistent with a chronic injury.

The tibiotalar joint

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Figure 6.19 Lateral collateral ligament complex injury, direct gadolinium MR arthrography. Axial T1-weighted (T1W) spinecho (SE) fat-suppressed (FS) image (a) showing absence of the anterior talofibular ligament (black arrow) and extravasation of injected contrast medium (white arrow) from the joint. Sagittal T1W SE FS image (b) showing extension of injected contrast medium (white arrow) around the peroneal tendons (arrowheads) indicating a tear of the calcaneofibular ligament.

THE MEDIAL COLLATERAL LIGAMENT Normal anatomy1,28,29 ● ●

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the MCL complex is also termed the ‘deltoid ligament’ and comprises five components, separated into deep and superficial layers the deep layer comprises: ■ the ATTL, which runs anteriorly from the tip of the medial malleolus to the talar neck, is seen as a thin band on axial images (Fig. 6.20a), but is not always present ■ the posterior tibiotalar ligament is a thick structure that extends between the tip of the medial malleolus to the medial talar surface and comprises multiple fascicles due to the presence of interposed fatty tissue, is demonstrated on both coronal and axial images, and typically has a striated pattern (Fig. 6.20b, c) the superficial layer comprises three ligaments that all arise from the tip of the medial malleolus: ■ the tibiocalcaneal ligament extends to the sustentaculum tali, running deep to the tibialis posterior and FDL tendons, and is optimally visualised on coronal images (Fig. 6.20d) ■ the tibionavicular ligament runs anterior to the navicular and is seen as a thin band on axial images (Fig. 6.20e) ■ the tibiospring ligament extends anterior to the spring ligament MR arthrography does not improve visualisation of the MCLs9

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Figure 6.20 Anatomy of the medial collateral ligament complex. Axial proton density-weighted (PDW) fast spin-echo (FSE) image (a) showing the thin anterior tibiotalar ligament (arrows) running deep to the posterior tibialis tendon (PTT) (double arrowhead) and the flexor digitorum longus (FDL) tendon (arrowhead). Coronal oblique PDW FSE (b) and axial T2-weighted FSE fat-suppressed (c) images showing the striated appearance of the posterior tibiotalar ligament (arrows). Coronal T1-weighted spin-echo image (d) showing the tibiocalcaneal ligament (arrows) running from the medial malleolus (MM) to the sustentaculum tali (ST). Axial PDW FSE image (e) showing the tibionavicular ligament (arrows) running deep to the PTT (double arrowhead) and the FDL tendon (arrowhead).

The tibiotalar joint

PATHOLOGY OF THE MEDIAL COLLATERAL LIGAMENT COMPLEX Trauma1,8 ● ● ●

injury to the deltoid ligament, particularly the tibiotalar component, is associated with inversion injuries (lateral ligament sprains), syndesmotic injuries or a fibular fracture isolated deltoid ligament injuries account for ~5 per cent of all ankle sprains and may follow an eversion, lateral rotation injury mechanism inversion sprains may cause partial tears of the posterior tibiotalar ligament due to crushing between the medial wall of the talus and the medial malleolus, which may progress to posteromedial impingement syndrome

MRI findings ● there is loss of the regular striations normally seen in the deltoid ligament (Fig. 6.21a) ● homogeneous intermediate SI on T1W images and increased SI on T2W images (Fig. 6.21a, b) ● associated features: ■ effusion within the tibialis posterior tendon ● MR arthrography may improve visualisation of partial-thickness tears of the deep aspects of the deltoid ligament8

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Figure 6.21 Medial collateral ligament complex injury. Coronal T1-weighted spin-echo image (a) showing loss of the normal striated pattern of the posterior tibiotalar ligament (arrows). Coronal T2-weighted fast spin-echo fat-suppressed image (b) showing hyperintensity and poor definition of the posterior tibiotalar ligament (arrows) and marrow oedema in the medial malleolus.

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THE FLEXOR TENDONS THE ACHILLES TENDON Normal anatomy5,33,34 ● ● ● ● ● ● ● ●

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the Achilles tendon originates in the mid-calf as the combined tendons of the medial and lateral heads of gastrocnemius and the soleus muscle, and functions to flex the foot as the tendon descends, the fibres rotate laterally by approximately 90° such that the gastrocnemius fibres insert laterally and the soleus fibres insert medially on the superoposterior calcaneus tendon fibres insert into the marrow of the posterosuperior margin of the calcaneus, this insertion being an enthesis the tendon is approximately 10–15 cm long, 5–7 mm thick and 12–16 mm wide it lacks a true tendon sheath but has a paratenon laterally and posteriorly, comprising visceral and parietal layers, the vascular system of which extends both within and outside the tendon the tendon is relatively avascular 2–6 cm proximal to the calcaneal insertion, accounting for the greater prevalence of tears at this site on sagittal MR images, the anterior and posterior margins of the tendon are parallel below the soleus insertion (Fig. 6.22a) on axial MR images: ■ just above the soleus insertion, the anterior margin is typically straight or convex ■ at the soleus insertion, the anterior margin is typically convex and may be focally bulbous (Fig. 6.22b) ■ below the soleus insertion, the anterior margin of the tendon is concave (Fig. 6.22c) ■ small punctate areas of increased SI may be seen in the distal tendon due to interfascicular membranes (Fig. 6.22d) on coronal MR images, the sides of the tendon are straight and the tendon widens distally (Fig. 6.22e) the tendon is typically hypointense on all pulse sequences, though internal longitudinal, linear increased SI on T1W/PDW images may be seen, due to the normal fascicular anatomy of the tendon: ■ such striations should be less prominent or not visible on T2W images increased T1W/PDW intra-tendon SI may also be due to the magic-angle phenomenon, resulting from the normal twisting of fibres within the tendon

Related anatomy34 ● ●

● ●

the plantaris tendon lies medial to the Achilles tendon (Fig. 6.23a) and inserts onto the medial aspect of the superior calcaneal tuberosity or 1 cm anteromedial to the Achilles tendon insertion (Fig. 6.23b) the retrocalcaneal (pre-Achilles) bursa is a true anatomical bursa lying between the distal Achilles tendon and the adjacent calcaneus: ■ it is normally visible on MRI but should measure 5 mm in transverse diameter are likely to be symptomatic ■ in the presence of a smaller neuroma, an alternative cause for forefoot pain should be sought

MRI findings ● a well-defined, spindle-shaped mass is seen between the MT heads (Fig. 6.94a) on the plantar side of the DTML

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e Figure 6.94 Morton’s neuroma. Axial T1-weighted (T1W) spin-echo (SE) image (a) showing a neuroma (arrows) in the second intermetatarsal space. Coronal T1W SE (b) and T2-weighted fast spin-echo (c) images showing a typical Morton’s neuroma (arrows). Coronal post-contrast T1W SE image (d) showing minimal enhancement within the neuroma (arrows). Axial T1W SE (e) and post-contrast T1W SE (f) images showing uniform enhancement of a neuroma (arrows).

● ● ● ● ●

isointense to muscle on T1W images and homogeneously or inhomogeneously hypointense to fat on conventional T2W FSE images (Fig. 6.94b, c) variable SI on STIR with/without minor peripheral oedema they show variable enhancement following gadolinium, ~50 per cent showing little or no enhancement (Fig. 6.94d) and the remainder showing marked enhancement (Fig. 6.94e, f) the diagnostic accuracy of MRI is almost 100 per cent the transverse dimension is typically 3–9 mm, though this is dependent on the scanning position:94 ■ when imaged with the patient prone and the foot plantar-flexed, neuromas are an average of 2 mm wider

The forefoot nerves

THE FOREFOOT TENDONS Normal anatomy ●

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the flexor tendons: in the forefoot, the FDL tendons lie deep to the FDB tendons (Fig. 6.95a): ■ at the level of the proximal interphalangeal joint, the FDB splits to straddle the FDL tendon, the two slips inserting into the base of the middle phalanx (Fig. 6.95b) ■ the FDL tendon continues distally to insert into the base of the distal phalanx (Fig. 6.95c) the extensor tendons: the EDL tendons run in the dorsum of the foot with four tendon slips, each passing to the lateral four digits: ■ at the level of the MTP joints of the second to fourth toes, the EDL tendon is joined on its lateral side by the EDB tendon slip (Fig. 6.95d) ■ the combined extensor tendon runs over the dorsum of the second to fourth toes to join the extensor expansion (Fig. 6.95e)

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e Figure 6.95 Anatomy of the forefoot tendons. Flexor tendons: Coronal proton density-weighted (PDW) fast spin-echo (FSE) image (a) showing the relationship between the flexor digitorum longus (FDL) (arrowheads) and flexor digitorum brevis (FDB) (arrows) tendons. Sagittal PDW FSE image (b) showing the insertion of the FDB tendon (arrow) into the base of the middle phalanx (black arrowhead). The FDL tendon (white arrowhead) now lies superficial to the FDB. Sagittal T1-weighted spin-echo image (c) showing the FDL tendon (arrow) inserting into the base of the distal phalanx (arrowhead). Coronal T2*-weighted (T2*W) gradient-echo (GE) image (d) showing the extensor digitorum longus (arrow) and the extensor digitorum brevis (arrowhead) at the level of the second metatarsal head. Coronal T2*W GE image (e) showing the extensor hood (arrows) at the level of the proximal phalanx.

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at the level of the proximal interphalangeal joint, the extensor expansion divides into three parts: – the central part inserts into the base of the middle phalanx, while the two lateral parts converge to insert into the base of the distal phalanx

PATHOLOGY OF THE FOREFOOT TENDONS Tendon disorders85 ● ●

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tendinosis is characterised pathologically by angiofibroblastic hyperplasia, degeneration and necrosis with little or no associated inflammation tenosynovitis is inflammation of the tendon sheath due to synovial inflammatory disorders, infection or mechanical irritation: ■ mechanical irritation may affect the FHL tendon between the sesamoid bones, where it is subject to repetitive impact, and may also occur under the base of the first MT bone, where the FHL and FDL tendons cross at the knot of Henry stenosing tenosynovitis results from chronic inflammation leading to fibrosis and tendon entrapment

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Figure 6.96 Forefoot tendon pathology. Tenosynovitis: Coronal T1-weighted (T1W) spin-echo (SE) (a) and T2*-weighted gradient-echo (b) images showing fluid within the flexor tendon sheath (arrows) with a normal morphology of the second flexor tendon (arrowheads). Coronal post-contrast T1W SE image (c) showing tendon sheath enhancement (arrow). Partial tendon rupture: Sagittal T2-weighted fast spin-echo (d) and coronal T1W SE (e) images showing partial rupture of the flexor tendon (arrows) and surrounding tendon fluid (arrowheads e).

Miscellaneous paediatric foot and ankle conditions

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tendon rupture occurs in tendons weakened by degeneration or repetitive microtrauma, or associated with systemic disorders such as diabetes mellitus: ■ rupture of a normal tendon is caused by laceration or a sudden traction injury; such ruptures may be partial or complete

MRI findings ● tendinosis: fusiform or diffuse tendon thickening is seen, with mild SI abnormality on T1W/PDW images and increased T2W SI in the presence of mucoid degeneration ● tenosynovitis: normal tendon morphology with increased fluid within the tendon sheath (Fig. 6.96a, b) and tendon sheath enhancement following contrast (Fig. 6.96c) ● stenosing tenosynovitis: thickening of the tendon or tendon sheath due to fibrosis, increased fluid within the tendon sheath and tendon sheath enhancement following contrast ● tendon rupture: partial or complete tendon discontinuity (Fig. 6.96d) with intervening and surrounding oedema and haemorrhage (Fig. 6.96e)

MISCELLANEOUS PAEDIATRIC FOOT AND ANKLE CONDITIONS Normal variants of marrow signal intensity95,96 ●

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patchy bone marrow SI with reduced T1W and increased T2W FSE FS/STIR SI is a normal finding in children’s feet, reported to occur in 63 per cent of symptomatic and 57 per cent of asymptomatic children95 it is most commonly seen in the calcaneus (54 per cent), talus (35 per cent) and navicular (35 per cent) bones, almost invariably at the endosteal surface these changes are typically seen before the age of 16 years, and are believed to represent residual red marrow

MRI findings ● focal or confluent areas of reduced SI on T1W and increased SI on T2W/STIR (Fig. 6.97a–c) are seen, and may be bilateral and symmetrical

Osteochondroses97 ●

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Köhler’s disease is osteochondrosis of the tarsal navicular, which is classically seen in boys aged 3–10 years and is a self-limiting condition, resolving with rest: ■ stress/trauma results in medial foot pain and swelling, which are bilateral in 25 per cent of cases other bones affected include the medial cuneiform in young boys and the posterior calcaneal apophysis (Sever’s disease)

MRI findings ● Köhler’s disease exhibits reduced SI on T1W and increased SI on T2W images in the ossified navicular, with a normal appearance of the surrounding cartilage

Congenital club foot97 ● ● ●

●

congenital club foot (talipes equinovarus) is classified into four types: ■ teratological, syndromic, positional and congenital congenital is the commonest type, with a reported prevalence of 1/1000 live births; it is more common in males and bilateral in 50 per cent of cases pathologically, abnormalities include lateral rotation of the talus, talar and calcaneal equinus, medial rotation of the calcaneus, medial subluxation of the navicular and the cuboid, and soft-tissue contractures MRI may be valuable for pre-operative evaluation since it demonstrates the position of the unossified tarsal bones and the intertarsal joints

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c

Figure 6.97 Normal marrow heterogeneity in children. Sagittal T1-weighted (T1W) spin-echo (SE) (a) and short tau inversion recovery (b) images showing ‘spotty’ areas of altered signal intensity (arrows) due to residual red marrow in the posterior calcaneus. Sagittal T1W SE image (c) showing similar appearances (arrows) in the talus.

MRI findings ● reduction of the talocalcaneal angle is seen in both axial (normally 20–40°) and sagittal (normally 35–50°) planes ● mild dorsal displacement of the navicular

Flat foot and congenital vertical talus97 ● ● ● ●

‘flat foot’ is a term that includes both flexible and rigid flattening of the longitudinal arch of the foot hind-foot deformity includes valgus rotation of the calcaneus on the talus, resulting in vertical rotation of the talus ligamentous laxity contributes to flexible flat foot (planovalgus foot) and may be considered a normal variant rigid flat foot can be acquired or congenital: ■ acquired rigid flat foot may be due to tarsal coalition with associated peroneal spasm, or cerebral palsy ■ congenital rigid flat foot in its most severe form is due to congenital vertical talus, in which case the talus is vertically aligned to the calcaneus, the navicular is dorsally dislocated and the calcaneus is plantar flexed ■ MRI demonstrates the precise orientation of the talus when it is still unossified

Soft-tissue masses of the ankle and foot

SOFT-TISSUE MASSES OF THE ANKLE AND FOOT Introduction93 ● ● ● ●

● ●

soft-tissue masses of the foot and ankle may be non-neoplastic, neoplastic benign or neoplastic malignant ~8 per cent of all benign masses and 5 per cent of all malignant masses (sarcomas) arise in this location non-neoplastic lesions: ganglia and Morton’s neuroma are most commonly seen benign neoplastic lesions: excluding tumours of the skin, the commonest benign lesions are plantar fibromatosis, giant cell tumour of tendon sheath, PVNS, aggressive fibromatosis, lipoma and haemangioma malignant lesions: excluding skin tumours, synovial sarcoma is the commonest the imaging features of these lesions are described in Chapter 8

Ganglia93,98 ●

● ● ● ●

ganglia (ganglion cysts) are tumour-like lesions that arise due to myxoid degeneration of connective tissues and are therefore related to tendons, ligaments, joint capsules and aponeurosis and do not communicate with adjacent joints they are usually detected in young adults and are slightly more common in women pathologically, they are round, oval or lobulated cystic lesions filled with mucinous fluid and surrounded by a fibrous capsule, commonly with internal fibrous septa clinically, many ganglia are asymptomatic, but depending on their location they can result in sinus tarsi syndrome (Fig. 6.65g) or tarsal tunnel syndrome (Fig. 6.72a) in a large study of ankle and foot ganglia,98 ~42 per cent of all clinically suspected soft-tissue masses were ganglia, with reported prevalences of 5.6 per cent and 0.4 per cent for masses around the ankle and foot, respectively: ■ the commonest locations were the sinus tarsi/canal (34 per cent), the Lisfranc joint (23 per cent), the cuneonavicular joint (12 per cent), the tarsal tunnel (12 per cent), the talonavicular joint (9 per cent), the EDL tendon (8 per cent), the distal tibiofibular joint (8 per cent) (Fig. 6.98a, b) and the calcaneocuboid joint (7 per cent)

MRI findings ● well-defined oval, round or multilobulated masses with internal fluid SI characteristics are hypointense to muscle on T1W images (Fig. 6.98c), mildly hyperintense on PDW FSE images (Fig. 6.98d) and markedly hyperintense on T2W FSE (Fig. 6.98e) and T2W FSE FS/STIR images (Fig. 6.98f) ● following contrast, rim and septal enhancement is seen (Fig. 6.98g)

The medial malleolar bursa99 ● ● ●

the medial malleolar bursa is an adventitial bursa that may develop over the medial malleolus in response to abnormal pressure from footwear that closely approximates the ankle in asymptomatic individuals, the soft tissues around the medial malleolus show normal subcutaneous fat in 80 per cent of cases or mild oedematous changes measuring proximal humerus > proximal femur): ■ diaphyseal and epiphyseal extension is common, while primary diaphyseal OS represents 2–11 per cent of cases and primary epiphyseal OS is very rare ■ histologically, the predominant subtype may be osteoblastic, chondroblastic or fibroblastic, but the mixed variety is most common, accounting for the mixed radiographic densities and MRI SIs ■ lytic (osteoclast-rich) OS is a further subtype ■ most lesions are ~8–10 cm in length by the time of presentation and have extended through the cortex to form an extraosseous mass, which may or may not be limited by the periosteum ■ intra-articular extension is most commonly seen with distal femoral lesions, typically in the region of the posterior capsule, the intercondylar notch (related to the anterior cruciate ligament) or into the suprapatellar pouch ■ skip metastases occur in ~8–10 per cent of cases of appendicular OS

MRI findings ● depending on the stage of presentation, tumour tissue may involve part (Fig. 8.37a) or all (Fig. 8.37b) of the transverse extent of the medullary cavity ● the tumour is typically of mixed intermediate SI on T1W images and intermediate/increased SI on T2W/STIR images (Fig. 8.37b, c) ● areas of low SI may be due to predominantly osteoblastic tissue (Fig. 8.37d) or regions of fibrosis, whereas areas of increased SI may represent subacute haemorrhage (Fig. 8.37a) ● extension of tumour across an open growth plate is a relatively common finding (Fig. 8.37e) ● skip lesions appear as foci of similar SI characteristics to the main tumour, separated from the main tumour by a region of normal marrow (Fig. 8.31d) ● extraosseous tumour may be concentric or eccentric and may show spiculated linear low SI on T2W images (Fig. 8.37f) consistent with the vertical (sunburst) periosteal reaction seen on radiographs ● small areas of fluid-level change, typically representing less than one-third of the tumour volume, are relatively common in conventional OS38 (Fig. 8.37g)

Pathology of the bones

a

b c

f d

e Figure 8.37 High-grade central osteosarcoma (OS). Coronal T1-weighted (T1W) spin-echo (SE) image (a) showing an early distal femoral OS (arrows) involving part of the metaphysis and showing focal hyperintensity (arrowhead) due to subacute haemorrhage. Sagittal T1W SE (b) and T2-weighted (T2W) fast spin-echo (FSE) fat-suppressed (FS) (c) images showing a distal femoral metaphyseal OS extending to the growth plate and involving the whole width of the bone. The tumour shows heterogeneous intermediate signal intensity (SI) on both sequences. Axial T1W SE image (d) showing areas of signal void (arrows) consistent with osteoblastic tumour. Sagittal T2W image (e) showing foci of osteoblastic OS (arrows) in the proximal tibial metaphysis, with extension of tumour (arrowhead) across the open growth plate. Axial T2W FSE FS image (f) showing linear hypointense strands (arrowheads) in the extraosseous tumour due to vertical periosteal reaction. (continued)

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h

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k Figure 8.37 (continued) Axial T2W FSE FS image (g) showing small areas of fluid level change (arrows) in the extraosseous tumour. Sagittal post-contrast T1W SE image (h) showing heterogeneous enhancement of solid areas of tumour (arrows) and areas of nonenhancement (arrowhead) due to spontaneous tumour necrosis. Axial T2W FSE FS image (i) showing proximal tibial OS with periosseous oedema (arrows). Axial post-contrast T1W FS image (j) showing enhancement of periosseous oedema (arrows). Granulocyte colony-stimulating factor effect: Coronal T1W SE (k) and short tau inversion recovery (l) images showing a distal femoral osteosarcoma (arrows) with patchy marrow SI abnormality (arrowhead) due to hyperplastic red marrow.

l

Pathology of the bones

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heterogeneous enhancement is seen following contrast (Fig. 8.37h), though routine use of gadolinium is not required peritumoral oedema also enhances following contrast (Fig. 8.37i, j), so conventional post-gadolinium T1W imaging is of no value in differentiating peritumoral oedema from extraosseous tumour however, oedema can be differentiated from extraosseous tumour using dynamic enhancement techniques on post-treatment imaging, following the use of granulocyte colony-stimulating factor (GCSF), extensive areas of marrow hyperplasia may become evident (Fig. 8.37k, l) and should not be mistaken for tumour extension

Telangiectatic osteosarcoma32,39 ● ● ●

telangiectatic OS is an uncommon, aggressive form of central OS accounting for 3.5–11 per cent of cases it affects the same locations as conventional OS and occurs in the same age group pathologically, the tumour is expansile and lytic, comprising multilocular, blood-filled cavities divided and surrounded by thick septa containing malignant cells

MRI findings39 ● the haemorrhagic nature of the lesion results in areas of increased SI on both T1W (Fig. 8.38a) and T2W images ● extensive areas of fluid-level change are characteristic, mimicking ABC (Fig. 8.38b) ● post-contrast MRI may be helpful in differentiating telangiectatic OS from ABC by demonstrating areas of peripheral or nodular septal enhancement due to solid tumour tissue

Small cell osteosarcoma32 ● ●

small cell OS is a rare lesion accounting for ~1 per cent of cases of OS the clinical and imaging features are similar to those of conventional OS, but pathologically the tumour comprises small, round cells similar to Ewing sarcoma

Pseudocystic osteosarcoma40 ●

pseudocystic OS is a rare form of high-grade central OS that radiologically resembles a simple bone cyst (SBC) or an ABC, being purely lytic and expansile with no associated periosteal reaction

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The limbs

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a

Figure 8.38 Telangiectatic osteosarcoma. Coronal T1-weighted spinecho image (a) showing an aggressive tibial diaphyseal lesion with extensive hyperintensity indicating its haemorrhagic nature. Axial T2weighted fast spin-echo fat-suppressed image (b) showing multiple fluid levels.

MRI findings ● an expansile bone lesion is seen with heterogeneous intermediate SI on T1W and intermediate/high SI on T2W (Fig. 8.39a, b) and no extraosseous tumour mass

Low-grade central osteosarcoma32,41 ● ●

low-grade central OS is a rare lesion accounting for 50 per cent of cases), mainly the femur and the tibia long-bone lesions typically occur eccentrically within the metaphysis, resulting in bone expansion, which can be dramatic; 20 per cent of lesions are diaphyseal intracortical or subperiosteal ABCs66 are also recognised and account for ~15 per cent of ABCs: ■ they most commonly arise from the forearm bones, the femur or the tibia and are typically diaphyseal or metadiaphyseal in location, classically showing erosion of the outer cortex

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involvement of flat bones is commonest in the pelvis, followed by the scapula pathologically, ABC classically comprises multiple blood-filled spaces separated by thin septa: ■ a solid form of ABC is also reported and is termed ‘giant cell reparative granuloma’ (GCRG)67,68

MRI findings ● the typical features are an eccentric, metaphyseal, expansile lesion with a well-defined hypointense rim due to a thin ‘eggshell’ of expanded cortex or periosteum (Fig. 8.68a) ● periosteal reaction in the form of a Codman’s triangle may be seen at the margins of the lesion (Fig. 8.68a)

b

a

d

c

Figure 8.68 Appendicular aneurysmal bone cyst. Coronal short tau inversion recovery image (a) showing an eccentric metaphyseal lesion with a thin hypointense rim (arrows) and a Codman’s triangle (arrowhead). Note also the presence of marrow oedema. Coronal T1-weighted (T1W) spin-echo (SE) image (b) showing heterogeneous signal intensity within the lesion due to haemorrhage. Axial T2-weighted fast spin-echo fat-suppressed (FS) image (c) showing multiple fluid levels and thin hypointense internal septa (arrowheads). Coronal post-contrast T1W SE FS image (d) showing thin septal enhancement (arrowheads). Coronal T1W SE image (e) showing epiphyseal extension (arrow) through a partially closed growth plate.

e

Pathology of the bones

● ●

● ● ● ● ●

the lesion is of heterogeneous intermediate/increased SI on T1W images (Fig. 8.68b) with heterogeneous increased SI on T2W/STIR images (Fig. 8.68a, c) the classical feature is the presence of multiple fluid levels, optimally seen on sagittal or axial T2W images (Fig. 8.68c): ■ most lesions showing more than two-thirds fluid levels are ABCs38 thin, hypointense internal septa are a common feature (Fig. 8.68c), and these may show enhancement following contrast (Fig. 8.68d) adjacent marrow oedema is also a common finding (Fig. 8.68a) epiphyseal extension through a partially closed growth plate may be seen (Fig. 8.68e) similar features are identified in non-long-bone lesions the sensitivity and specificity of MRI for the diagnosis of ABC based on the presence of characteristic features are reported to be 77.8 per cent and 66.7 per cent, respectively65

Giant cell reparative granuloma (solid aneurysmal bone cyst)67,68 ● ●

● ●

GCRG is a rare lesion that is not a true neoplasm, but represents a reactive process, typically occurring in the second to third decades GCRG has a predilection for the maxilla and mandible; the second commonest site of involvement is the small bones of the hands and feet, most commonly the hand phalanges, followed by the metacarpals/MTs, the carpal and tarsal bones and, least commonly, the foot phalanges involvement of the long bones is extremely rare, the femur, ulna and tibia being most commonly involved67 pathologically, the metaphyseal/metadiaphyseal region of tubular bones is usually involved; the lesion produces lytic expansion with an intact cortex and is typically 2–2.5 cm in diameter: ■ mineralisation and trabeculation may be seen within the lesion

MRI findings ● SI characteristics are non-specific, with low/intermediate SI on T1W and T2W images (Fig. 8.69a, b) ● long-bone lesions are described as showing mild hyperintensity compared with muscle on T1W and increased T2W SI with scattered areas of low SI that may represent mineralisation ● cystic areas and fluid levels are very uncommon ● enhancement is seen following contrast (Fig. 8.69c)

Giant cell tumour68 ● ● ● ● ● ● ●

GCT is an aggressive, benign neoplasm accounting for approximately 4–9.5 per cent of primary bone tumours and 18–23 per cent of benign neoplasms 5–10 per cent of GCTs may show primary or secondary malignant change, and benign lesions may rarely metastasise to the lungs multifocal, metachronous GCT occurs in 1 per cent of patients, in which case hyperparathyroidism must be excluded, and GCT can also complicate Paget’s disease of bone approximately 80 per cent of cases occur at 20–50 years of age, only 1–3 per cent occur in children and 9–13 per cent in the over-50s; the male–female ratio is 2:3 84–99 per cent of lesions extend to within 1 cm of subarticular bone or adjacent to a fused apophysis, eccentrically located in 42–93 per cent of cases the distal femur (23–30 per cent), the proximal tibia (20–25 per cent), the distal radius (10–12 per cent) and the proximal humerus (4–8 per cent) are the commonest appendicular sites rarer sites include the proximal femur (4 per cent), the distal tibia (2–5 per cent), the proximal fibula (3–4 per cent), the innominate bone (3 per cent), the hand/wrist (1–5 per cent) and the foot (1–2 per cent)

MRI findings ● GCT is classically a subarticular, eccentric lesion with a well-defined, non-sclerotic margin (Fig. 8.70a) ● poorly defined margins, seen in 10–20 per cent of cases, suggest a more aggressive growth pattern (Fig. 8.70b) ● involvement of subchondral (Fig. 8.70a) or apophyseal (Fig. 8.70c) bone is classical, though lesions arising in the immature skeleton involve the metaphysis adjacent to the growth plate

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The limbs

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b

c

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Figure 8.69 Giant cell reparative granuloma. Sagittal T1-weighted (T1W) spin-echo (SE) image (a) showing an intermediate signal intensity (SI) lesion (arrow) in the anterior calcaneus. Axial T2weighted image (b) showing predominantly low SI (arrow) with a small area of cystic change (arrowhead). Sagittal post-contrast T1W SE image (c) showing diffuse enhancement (arrow).

the tumour usually measures 5–7 cm at presentation cortical expansion is a common feature, with cortical destruction and extraosseous extension in 33–44 per cent of cases (Fig. 8.70b) the tumour is usually of intermediate SI on T1W images (Fig. 8.70a–c) and shows heterogeneous hyperintensity on STIR images (Fig. 8.70d) areas of hyperintensity on T1W indicate the presence of subacute haemorrhage (Fig. 8.70e), whereas areas of low SI indicate chronic haemorrhage (Fig. 8.70f) profound hypointensity on T2W images (Fig. 8.70g), particularly T2*W GE (Fig. 8.70h), in solid areas of the tumour is seen in most cases, due to the deposition of haemosiderin from chronic recurrent haemorrhage solid areas enhance uniformly following contrast (Fig. 8.70i), whereas cystic areas show peripheral and septal enhancement marrow oedema is also relatively common (Fig. 8.70d), while fluid–fluid levels indicate the presence of secondary ABC change (Fig. 8.70j), which is reported in ~14 per cent of cases malignant GCT has no characteristic distinguishing features

VASCULAR LESIONS Haemangioma69,70 ● ●

both solitary and multiple haemangiomas and lymphangiomas occur in bone and may be regarded as congenital vascular malformations however, many present as isolated bone lesions and are therefore included in the differential diagnosis of bone tumour

Pathology of the bones

●

pathologically, haemangiomas are classified histologically as capillary, cavernous, arteriovenous or venous: ■ osseous capillary haemangiomas most commonly affect the vertebral body, whereas osseous cavernous haemangiomas most commonly affect the skull vault ■ involvement of the long bones is uncommon, affecting the medullary canal of the metaphysis and/or epiphysis, usually of the femur, tibia or humerus ■ a characteristic feature of haemangioma is the presence of trabecular thickening, which may be identified on radiographs and CT

e

a

b

c

d

Figure 8.70 Giant cell tumour (GCT). Sagittal T1-weighted (T1W) spin-echo (SE) image (a) showing a distal femoral subarticular lesion with a well-defined non-sclerotic margin (arrows). Coronal T1W SE image (b) of distal radial GCT showing poorly defined margins with the host bone (arrow) and associated extraosseous extension (arrowheads). Coronal T1W SE image (c) showing an apophyseal location in the greater tuberosity (arrow) of the humerus. Coronal short tau inversion recovery image (d) showing a hyperintense matrix (arrow) with associated marrow oedema (arrowheads). Axial T1W SE image (e) of a proximal tibial GCT showing areas of subacute haemorrhage (arrows). (continued)

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The limbs

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h

i

j

Figure 8.70 (continued) Coronal T1W SE image (f) showing areas of low signal intensity due to chronic haemorrhage (arrows). Axial T2weighted (T2W) fast spin-echo (FSE) (g) and T2*-weighted gradientecho (GE) images (h) showing hypointensity in the solid areas of tumour (arrows) that is much more pronounced on the GE sequence (h). Sagittal post-contrast T1W SE image (i) showing uniform enhancement (arrows) in the solid tumour (same case as a). Axial T2W FSE fat-suppressed image (j) showing secondary aneurysmal bone cyst change (arrowhead).

MRI findings ● trabecular thickening is commonly in a vertical orientation along the bone, appearing as multiple, linear, hypointense striations (Fig. 8.71a, b) ● rounded or curvilinear intraosseous vascular channels are also a characteristic feature (Fig. 8.71c–e) ● in the presence of slow-flow lesions, these channels are of intermediate T1W SI and increased T2W SI (Fig. 8.71c–e) ● osseous arteriovenous malformations (AVMs) with high flow have low SI channels on all pulse sequences ● rarely, osseous haemangiomas are confined to the cortex, most commonly in the anterior tibial diaphysis

Pathology of the bones

b

a

c

e

d

Figure 8.71 Osseous haemangioma. Sagittal post-contrast T1-weighted (T1W) spin-echo (SE) (a) and coronal T2-weighted (T2W) fast spin-echo (FSE) fat-suppressed (FS) (b) images showing multiple vertical hypointense trabeculae (arrows) in the proximal tibial epiphysis. Coronal T1W SE (c), short tau inversion recovery (d) and axial proton density-weighted FSE FS (e) images showing multiple round and curvilinear vascular channels (arrows) with intermediate T1W signal intensity (SI) and high T2W SI consistent with slow flow.

Cystic angiomatosis69,70 ● ● ● ● ● ●

cystic angiomatosis is defined as a diffuse, extensive haemangiomatous or lymphangiomatous infiltration of multiple tissues including bone, muscle, viscera and subcutaneous fat it is a condition of the young; 50 per cent present before 20 years of age bone lesions occur in 75 per cent of cases of lymphangiomatosis haemangiomatosis limited to the skeleton has a better prognosis and is seen in 30–40 per cent of cases sites of involvement include the femur, ribs, spine, pelvis, humerus, scapula, other long bones and clavicle the condition may be limited to a single extremity, resulting in gigantism

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The limbs

MRI findings ● the appearances are similar to those seen with solitary haemangioma, but more extensive ● MRI may demonstrate associated soft-tissue extension (Fig. 8.72a, b)

a

b

Figure 8.72 Cystic angiomatosis. Axial T1-weighted spin-echo (a) and T2-weighted fast spin-echo (b) images showing extension of the angiomatous lesion from the vertebral body to the ribs and subsequent extraosseous subpleural disease (arrows).

Massive osteolysis69,70 ● ● ● ● ●

massive osteolysis is also known as Gorham’s disease or vanishing bone disease and is a rare, noninheritable disorder that predominates in children and young adults pathologically, it is characterised by a non-malignant proliferation of vascular or lymphatic structures of bone resulting in progressive bony destruction, often with extension into the surrounding soft tissues it most commonly affects the shoulder region, the mandible and the pelvis progressive resorption of a single bone occurs, but paired bones, several contiguous ribs and segments of the spine may also be affected spontaneous arrest is rarely reported

MRI findings ● the findings are similar to those of other haemangiomatous conditions; destructive lesions of the metaphysis and diaphysis of long bones (Fig. 8.73a–c) and the absence of any major soft-tissue mass are notable features

Malignant vascular tumours71 ● ●

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●

malignant vascular tumours arising in bone include haemangioendothelioma, epithelioid haemangioendothelioma and angiosarcoma haemangioendothelioma is a low-grade malignant endothelial tumour that most commonly presents in the second to third decades and occurs as a multifocal lesion in 25 per cent of cases: ■ the imaging features of individual lesions are non-specific but the presence of multifocal disease, within the same bone or in different bones, is a clue to the diagnosis ■ multifocal lesions may affect a single limb or be randomly scattered throughout the skeleton; appendicular involvement is most common in the lower limb epithelioid haemangioendothelioma is multifocal in ~40 per cent of cases, but has a propensity to be limited to a single anatomical region: ■ individual lesions are lytic with a small extraosseous mass in 40 per cent of cases angiosarcoma is a high-grade vascular neoplasm that may also be unifocal or multifocal: ■ the mean age of presentation is in the third to fourth decades and skeletal involvement is commonest in the long bones (60 per cent of cases), usually the tibia, femur and humerus, and the pelvis

Pathology of the bones

a

b Figure 8.73 Gorham’s disease. Axial T1-weighted spin-echo (a), sagittal T2-weighted (b) and coronal short tau inversion recovery (c) images showing destruction of the fibular metaphysis/diaphysis (arrows) and adjacent tibial metaphysis (arrowheads). Note the absence of any soft-tissue mass.

c

MRI findings ● the imaging features are non-specific, being those of an intermediate to markedly aggressive, lytic destructive process (Fig. 8.74) ● high-flow vascular channels may result in the presence of serpiginous flow voids ● fluid levels are also reported

MALIGNANT ROUND CELL TUMOURS Ewing sarcoma/primitive neuroectodermal tumour72 ● ● ●

Ewing sarcoma and primitive neuroectodermal tumour (PNET) are related entities differentiated by immunohistochemical techniques PNET of the chest wall is termed ‘Askin tumour’ Ewing sarcoma is a rare, highly malignant primary bone neoplasm accounting for ~5 per cent of biopsied primary tumours, and together with OS represents 90 per cent of primary malignant bone tumours in children

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The limbs

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Figure 8.74 Angiosarcoma. Coronal T1-weighted (T1W) spinecho (SE) (a), axial proton density-weighted fast spin-echo (b) and post-contrast T1W SE fat-suppressed (c) images showing a moderately aggressive locally destructive lesion of the femoral neck (arrows a, b).

75 per cent of patients are under the age of 20 years at presentation, mostly 5–15 years (90 per cent 6.0¥1011: ■ any skeletal change results from occasional bone infarction due to increased viscosity of the blood ■ the superimposition of leukaemia and myeloid metaplasia is relatively common and MRI can readily depict conversion of cellular marrow to fatty marrow and vice versa in polycythaemia rubra vera and myeloid metaplasia myelofibrosis: primary myelofibrosis is a slowly progressive marrow disorder of unknown aetiology that affects males and females equally with an age range of 20–80 (median 60 years): ■ it should be diagnosed only after causes of secondary myelofibrosis have been excluded ■ clinically, the disorder presents insidiously with weakness, dyspnoea and weight loss ■ antecedent polycythaemia is common, but obliteration of the marrow by fibrosis or bony sclerosis soon leads to moderate normochromic, normocytic anaemia ■ the natural history is of slow deterioration, with death typically 2–3 years after diagnosis secondary myelofibrosis is the end-stage of the myeloproliferative syndrome and occurs to a greater or lesser degree in leukaemia, lymphoma, Gaucher’s disease, exposure to toxins, carcinomatosis and even infection

MRI findings ● radiographic bone sclerosis manifests at MRI as reduced marrow SI on all pulse sequences, which is also contributed to by marrow fibrosis ● typically, this is diffuse (Fig. 8.87a, b) or occasionally patchy (Fig. 8.87c, d), occurring most often in the axial skeleton, the pelvis and the metaphyses of the femur, humerus and tibia ● sclerosis is due to trabecular and endosteal new bone formation resulting in reduced marrow diameter

Gaucher’s disease89 ●

● ● ● ●

Gaucher’s disease is the commonest lipid storage disorder and is due to the genetic deficiency of an enzyme (glucocerebrosidase) that results in accumulation of the lipid glucocerebroside in the lysosomes of monocytes and macrophages these engorged cells are called Gaucher cells and their accumulation within various organ systems accounts for the symptoms of the disorder many of those affected are Ashkenazi Jews (~1/400–600), but all races are vulnerable three types are recognised: the common type 1, which is non-neuronopathic, and the rare neuronopathic types 2 (acute) and 3 (subacute) clinically, both dull bone pain and acute painful crises occur, the latter characterised by acute episodes of severe skeletal pain, fever, leucocytosis and raised ESR

MRI findings ● lipid storage defects result in large amounts of lipid in the marrow spaces, causing a loss of normal modelling of the long bones in childhood, resulting in an Erlenmeyer flask appearance of their ends ● acute bone crises are due to bone infarcts and manifest as marrow oedema on MRI: ■ they must be differentiated from OM, which also complicates Gaucher’s disease ● osteonecrosis of the femoral and humeral heads is common ● MRI is useful in evaluating the extent of marrow infiltration, which is manifest as homogeneous or inhomogeneous areas of reduced SI on T1W images and increased SI on T2W/STIR images (Fig. 8.88a, b)

Marrow malignancy90 ●

leukaemia: acute lymphocytic leukaemia accounts for 80 per cent, acute myeloblastic leukaemia for 10 per cent and other types for 10 per cent of cases: ■ acute leukaemia is the commonest malignancy of childhood, while chronic leukaemias predominate in adults but sometimes terminate in an acute blastic form ■ adults are most commonly affected by acute lymphocytic leukaemia and chronic myeloid leukaemia ■ chronic lymphatic leukaemia is a disease of the elderly, characterised by enlargement of the spleen and the lymph nodes; skeletal involvement is rare, except as a terminal event

Pathology of the bone marrow

b a

d c Figure 8.87 Myelofibrosis. Coronal T1-weighted (T1W) spin-echo (SE) (a) and axial T2-weighted (T2W) fast spin-echo (FSE) (b) images of the pelvis/sacrum showing generalised reduction of marrow signal intensity. Sagittal T1W SE (c) and T2W FSE (d) images of the humerus showing a nodular pattern of marrow hypointensity.

a

b

Figure 8.88 Gaucher’s disease. Coronal T1-weighted spin-echo image (a) showing heterogeneous reduction of marrow signal intensity (SI). Sagittal T2-weighted fast spin-echo image (b) showing heterogeneous increased marrow SI.

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lymphoma: secondary bone involvement in non-Hodgkin’s lymphoma (NHL) and Hodgkin’s disease usually indicates stage IV disease: ■ ~2 per cent of patients with Hodgkin’s disease present initially with a skeletal lesion, whereas the prevalence of bone involvement at autopsy is almost 75 per cent ■ however, at clinical assessment bone involvement is reported in 15–20 per cent of cases, especially in the more aggressive histological subtypes ■ NHL embraces various follicular and diffuse lymphocytic lymphomas representing monoclonal proliferation of B cells, T cells or histiocytes ■ secondary skeletal involvement occurs in 15–25 per cent

MRI findings ● MRI typically demonstrates diffuse marrow infiltration with reduction of T1W SI in affected areas in both leukaemia and lymphoma (Fig. 8.89a) ● a change from normal to nodular to diffuse low SI can be seen with progression of the disease, together with an increase in the extent of SI abnormality ● MRI can also identify complications of treatment such as osteonecrosis (Fig. 8.89b, c) ● a particular focal lesion occurring in acute myeloblastic leukaemia is granulocytic sarcoma (chloroma), which is usually located in the skull, spine, ribs or sternum of children: ■ this is an expanding geographic tumour caused by a collection of leukaemic cells and reported to occur in 4.7 per cent of patients ■ it has no specific MR features

Mastocytosis91 ● ●

mastocytosis is a disorder of mast cell proliferation within different body tissues that can result in various clinical syndromes, including urticaria pigmentosa, systemic mastocytosis and mast cell leukaemia urticaria pigmentosa accounts for 80–90 per cent of cases and is a self-limiting condition that typically affects children

a

c

b

Figure 8.89 Leukaemia/lymphoma. Coronal T1-weighted (T1W) spin-echo (SE) image (a) of the pelvis in a patient with secondary bone lymphoma showing reduced marrow signal intensity (SI) due to diffuse infiltration of the lumbar spine and pelvic bones. Coronal T1W SE (b) and short tau inversion recovery (c) images in a child with acute leukaemia showing diffuse low marrow SI and acute osteonecrosis of the right femoral head manifest as epiphyseal oedema (arrows) with associated joint effusion.

Pathology of the bone marrow

●

systemic mastocytosis accounts for 50 per cent of patients ■ widespread involvement of the skeleton is present in 80 per cent, the axial skeleton and proximal ends of the limb bones being particularly involved

MRI findings ● ● ● ● ● ●

●

the MRI appearances in MM are variable a normal marrow pattern is seen at presentation in 50–75 per cent of patients with early untreated (stage 1) MM and in 20 per cent of patients with advanced (stage 3) MM a focal pattern comprises localised areas of decreased SI on T1W images (Fig. 8.92a) with corresponding increased SI on T2W/STIR images (Fig. 8.92b) occasionally, focal lesions are relatively hyperintense on T1W and may be identified only on T2W images the diffuse pattern manifests as generalised reduction of marrow SI on T1W images (Fig. 8.92c), marrow hyperintensity on T2W and STIR images (Fig. 8.92d) and diffuse enhancement following contrast a ‘variegated’ pattern is described that comprises multiple tiny foci of reduced SI on T1W (Fig. 8.92e) and hyperintensity on T2W/STIR on a background of normal marrow, a pattern that is almost always seen in early disease these patterns have some prognostic value, in that patients with diffuse marrow abnormality on MRI have a poorer outcome than those with a normal MRI pattern

Bone infarction94 ● ● ● ●

‘bone infarction’ is a term used to describe osteonecrosis occurring in non-epiphyseal sites, where the term ‘avascular necrosis’ or ‘aseptic necrosis’ tends to be used predisposing factors are the same as for avascular necrosis and include corticosteroids, trauma, SCD, metabolic/endocrine disorders, vasculitides, alcoholism and radiotherapy the metaphyses of the femur, tibia and humerus are most commonly involved, in addition to the pelvis cystic bone infarcts:95 cystic degeneration may occur in medullary bone infarcts, which may mimic lytic bone tumours: ■ patients commonly present with mild pain, most commonly involving the humerus or the femur ■ most lesions are described in women, and range from 1.5–12 cm in size

MRI findings the earliest feature is marrow oedema, which is non-specific ● with the development of the infarct, the appearances become typical ● mature infarcts have a geographic/serpiginous outline, with a low SI margin on T1W (Fig. 8.93a) and a hyperintense margin on STIR (Fig. 8.93b) ● the ‘double-line’ sign may be seen on T2W images (Fig. 8.93c) and marginal enhancement can be seen following contrast (Fig. 8.93d) ● the centre of the infarct may show various SI characteristics, as described in the Mitchell classification: ■ class A – high T1W, intermediate T2W consistent with fat (Fig. 8.93a, b) ■ class B – high T1W, high T2W consistent with blood ■ class C – low T1W, high T2W consistent with fluid (Fig. 8.93e, f) ■ class D – low T1W, low T2W consistent with fibrous tissue (Fig. 8.93g, h) ●

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d

e Figure 8.92 Multiple myeloma. Focal lesion: Axial T1-weighted (T1W) spin-echo (SE) (a) and coronal T2-weighted fast spin-echo fat-suppressed (b) images showing focal marrow infiltration of the proximal humerus with associated pathological fracture (arrow b). Diffuse infiltration: Coronal T1W SE (c) and short tau inversion recovery (STIR) (d) images of the pelvis showing diffuse reduction of T1W marrow signal intensity (SI) in the spine and the pelvis with corresponding hyperintensity on STIR. Variegated pattern: Coronal T1W SE image (e) of the pelvis showing multiple tiny foci of reduced marrow SI.

Pathology of the bone marrow

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a b

d

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g

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Figure 8.93 Bone infarction. Coronal T1weighted (T1W) spin-echo (SE) image (a) showing multiple bone infarcts (arrows) with low signal intensity (SI) margins and internal high SI in the femoral lesion. Coronal short tau inversion recovery image (b) showing a tibial metaphyseal infarct (arrow) with peripheral hyperintense margin and central low SI. Axial T2weighted fast spin-echo fat-suppressed (FS) image (c) showing the ‘double-line’ sign (arrow) of a bone infarct. Axial postcontrast T1W SE FS image (d) showing peripheral enhancement (arrow) of an acetabular bone infarct. Sagittal T1W SE (e) and T2*-weighted (T2*W) gradient-echo (GE) (f) images showing a cystic bone infarct (arrows) of the tibia. Sagittal T1W SE (g) and coronal T2*W GE (h) images showing reduced central SI within the infarct (arrows) consistent with fibrosis.

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The limbs

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complications of mature infarcts include sarcomatous transformation, which is suggested by the development of a region of aggressive marrow replacement engulfing the infarct cystic infarcts may be mildly expansile and have reduced T1W SI (Fig. 8.93e), are uniformly hyperintense on T2W (Fig. 8.93f) and show no enhancement following contrast

Radiation osteitis96 ● ●

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soft-tissue and bone tumours may be treated with radiotherapy as a sole method or as an adjunct to surgery and chemotherapy pathologically, irradiation causes damage to osteoblasts, resulting in decreased bone matrix production and unopposed osteoclastic resorption: ■ the threshold for osteoblast injury is thought to be ~30 Gy, with cell death at ~50 Gy ■ there may also be an effect on bone due to radiation-induced vascular injury ■ radiotherapy also affects the haematopoietic elements of the marrow, resulting in myeloid depletion ■ all of the changes are limited to the radiotherapy field the radiographic changes associated with irradiated bone range from osteopenia (at ~1 year post irradiation) to osteonecrosis the changes in bone resulting from radiotherapy are termed ‘radiation osteitis’, while cell death results in radiation osteonecrosis or osteoradionecrosis complications of radiation osteitis include stress and pathological fracture

MRI findings ● acute changes include transient increase in marrow SI on STIR due to marrow oedema, necrosis and haemorrhage and can be seen within 8 days of treatment ● myeloid depletion is associated with replacement of red marrow with fat (yellow marrow), and conversion of red to yellow marrow may be complete as early as 6–8 weeks after radiotherapy ● consequently, irradiated marrow appears hyperintense on T1W/T2W FSE images compared with adjacent uninvolved marrow and hypointense on FS sequences ● radiation osteitis may result in irregular cortical and trabecular thickening ● all of the changes are limited to the radiotherapy field ● reconversion to red marrow is manifest by a progressive reduction in marrow SI on T1W images: ■ reconversion is dose dependent but may be increased with the use of GCSF

Post-radiation sarcoma96,97 ● ●

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● ● ●

‘post-radiation sarcoma’ (PRS) is now the preferred term (as opposed to ‘radiation-induced sarcoma’) for bone sarcoma or soft-tissue sarcoma (STS) that develops following radiotherapy they account for ~1.5 per cent of all bone sarcomas; the criteria for diagnosis of a PRS include the following: ■ a history of radiotherapy, the development of a neoplasm in the radiation field, a latent period of several years (minimum 3–4 years) and histological proof of a sarcoma that differs significantly from that initially treated the commonest treated tumours resulting in the development of PRS are breast carcinoma, lymphoma, head and neck cancers and gynaecological malignancies, which accounts for the greater incidence in women the mean age at presentation is in the sixth decade, with a mean latency period before the development of PRS of ~15 years it is considered that a minimal dose of 30 Gy is required to induce PRS; it is also suggested that the concurrent use of chemotherapy increases the risk the commonest PRS is OS, followed by MFH (together accounting for 90 per cent of cases, 10 per cent being CS) and the commonest sites are the pelvis and the shoulder girdle

Miscellaneous conditions of bone

MRI findings ● typical imaging features include bone destruction, soft-tissue mass, matrix mineralisation and periosteal reaction ● there may also be evidence of radiation change in the underlying bone (radiation osteitis and marrow infarction), such as fatty replacement of normal red marrow ● the tumours have no specific SI characteristics, being of intermediate SI on T1W (Fig. 8.94a, b) and heterogeneous increased SI on T2W/STIR (Fig. 8.94c)

b

a

c

Figure 8.94 Post-radiation sarcoma. Coronal T1-weighted (T1W) spin-echo (SE) image (a) showing an aggressive intramedullary lesion (arrow) with extraosseous extension (arrowhead) and irregular thickening of the femoral cortex (double arrowhead) due to radiation osteitis. Axial T1W SE (b) and short tau inversion recovery (c) images showing extraosseous mass (arrows) and cortical irregularity (arrowheads b).

MISCELLANEOUS CONDITIONS OF BONE Paget’s disease98,99 ● ●

Paget’s disease is a relatively common condition affecting ~3–4 per cent of the population aged over 40 years and up to 10–11 per cent over the age of 80 years pathologically, it is characterised by excessive and abnormal remodelling of bone; three phases of the disease are described, representing a continuum rather than discrete episodes: ■ phase 1 – lytic (incipient active), in which there is predominantly osteolysis ■ phase 2 – mixed (active), with osteoblastic activity superimposed on active osteolysis and eventually predominance of osteoblastic activity ■ phase 3 – blastic (inactive) phase, in which osteoblastic activity subsides

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The limbs

the lytic phase is characterised radiologically by a blade-shaped advancing edge osteoblastic activity results in cortical and trabecular thickening, and eventually bone enlargement and deformity are seen ■ associated bone marrow changes include replacement of normal yellow marrow by fibrovascular tissue in the active phase, with a return to diffuse yellow marrow in the late, inactive phase almost any bone can be involved, though Paget’s disease predominantly affects the axial skeleton; the pelvis (30–75 per cent), the spine (30–75 per cent) and the skull (25–65 per cent) are the commonest sites proximal long bone involvement is also common, with the femur affected in 25–35 per cent of cases other relatively common sites include the shoulder girdle (humerus 31 per cent, scapula 24 per cent, clavicle 11 per cent) long-bone involvement is typically initially subchondral with extension into the diaphysis: ■ primary diaphyseal Paget’s disease is rare and reported to occur in the tibia the disease is monostotic in 10–35 per cent of cases, more commonly when involving the axial skeleton, while polyostotic disease (65–90 per cent of cases) has a predilection for the right side of the body and lower limb involvement clinically, 20 per cent of patients are initially asymptomatic; symptoms of active disease include bone pain, tenderness and increased warmth: ■ later, bone enlargement and deformity are common ■ pain may also be related to pathological/stress fracture and sarcomatous degeneration ■ ■

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MRI findings ● cortical and trabecular thickening (Fig. 8.95a) and cortical hyperintensity due to increased vascularity (Fig. 8.95b) are seen ● marrow SI is variable, being normal in most cases (Fig. 8.95a) ● in the early/active phase, heterogeneous reduced T1W SI with corresponding increased T2W SI may be seen due to fibrovascular tissue in the marrow (Fig. 8.95c, d) ● a flame-shaped, hyperintense leading edge may be seen on T2W FS/STIR images (Fig. 8.95e) ● in the late phase, there may be reduced marrow SI on all pulse sequences, due to marrow sclerosis and fibrosis ● following contrast, cortical and marrow enhancement may be seen with active disease (Fig. 8.95f, g)

Paget’s sarcoma100 ●

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many bone sarcomas arising after the age of 50 years are secondary to Paget’s disease and at least 50 per cent of these are OS; fibrosarcoma or MFH account for 25 per cent and the remainder are anaplastic sarcomas or occasionally GCTs the overall prevalence of malignant change is likely to be under 1 per cent, the incidence increasing to 5–10 per cent in patients with widespread, long-standing Paget’s disease sarcoma can also occur in patients with monostotic disease most patients are over the age of 45 years and the sex ratio of Paget’s sarcoma is similar to that of the primary disease, with men affected twice as often as women the commonest sites are the femur, the pelvis and the humerus; Paget’s sarcoma is rare in the spine and is multifocal in 2.4–17 per cent of cases clinically, development of sarcoma is suggested by a change in the type or severity of bone pain and sometimes by an enlarging mass or a pathological fracture

MRI findings ● imaging demonstrates a large region of bone destruction with an associated large soft-tissue mass, and features of underlying Paget’s disease (Fig. 8.96a, b) ● the presence of osteoblastic matrix results in areas of low SI on all pulse sequences ● MRI is extremely valuable in identifying sarcomatous degeneration, based on the presence of marrow infiltration on a T1W image ● conversely, normal marrow SI on T1W excludes sarcoma with a very high degree of certainty (Fig. 8.96c)

Miscellaneous conditions of bone

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c

d

g

e

f

Figure 8.95 Uncomplicated Paget’s disease. Sagittal T1-weighted (T1W) spin-echo (SE) image (a) showing thickening of the proximal tibial cortex (arrow) and trabecular thickening (arrowhead). Sagittal T2-weighted (T2W) fast spin-echo (FSE) image (b) showing cortical hyperintensity (arrow) of the tibia. Coronal T1W SE (c) and T2W FSE fat-suppressed (FS) (d) images showing patchy marrow signal intensity changes (arrows) due to fibrovascular connective tissue. Coronal short tau inversion recovery image (e) of the femur showing medullary hyperintensity (arrow) and a hyperintense flame-shaped leading edge (arrowhead). Sagittal (f) and axial (g) post-contrast T1W SE FS images showing cortical (arrow f) and medullary (arrows g) enhancement.

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The limbs

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Figure 8.96 Paget’s sarcoma. Coronal T2-weighted fast spin-echo image (a) showing inactive Paget’s disease of the right hemipelvis (arrow) and a large soft-tissue mass (arrowheads) arising from the medial acetabulum. Axial T1-weighted (T1W) spin-echo (SE) image (b) showing malignant infiltration of the posterior acetabulum (arrow) with extraosseous extension of tumour (arrowhead). Pathological fracture: Coronal T1W SE image (c) showing a transverse band of reduced marrow signal intensity (SI) due to pathological fracture (arrows). Normal SI of the proximal and distal humeral marrow (arrowheads) excludes an underlying sarcoma.

Pseudosarcoma in Paget’s disease100 ● ● ● ●

pseudosarcoma refers to a situation in which there is focal proliferation of pagetic periosteal new bone clinically, it presents with pain and swelling, typically affecting bones with long-standing Paget’s disease the femur and the tibia are most commonly involved, with radiographs demonstrating spiculated periosteal new bone formation into the soft tissues the clinical and radiological features are indistinguishable from Paget’s sarcoma and may show destruction of the underlying cortex

MRI findings ● MRI shows the underlying features of chronic Paget’s disease, with a periosteally based soft-tissue mass surrounding the bone with variable T1W and T2W SI depending on the type of tissue contained ● the mass may have intermediate T1W SI with mild T2W hyperintensity or may show the SI features of marrow ● spiculated periosteal reaction may be seen

Musculoskeletal sarcoidosis101 ●

sarcoidosis is an inflammatory disorder of unknown aetiology characterised by the development of noncaseating granulomas in various tissues, with no other evidence of causes of granulomatous disease

Miscellaneous conditions of bone

● ● ● ● ●

the most commonly involved organs are the lungs, lymph nodes, skin and eyes skeletal involvement is reported to occur in 1–13 per cent of cases and may involve bone, joint and soft tissues Löfgren’s syndrome comprises arthralgia, erythema nodosum and bilateral hilar lymphadenopathy granulomatous arthropathy is also reported in 10–35 per cent of cases sarcoid myopathy is reported in 1.4 per cent of patients with sarcoid

MRI findings ● small bone lesions: radiographically detectable lesions typically have a ‘lacy’ lytic appearance: ■ MRI may demonstrate radiographically occult marrow lesions, extraosseous extension of granulomas and periosseous soft-tissue involvement ● large bone lesions: radiologically, lesions may be lytic, sclerotic or occult: ■ MRI may demonstrate poorly defined or well-defined lesions of various sizes and shapes, with reduced T1W SI and variable though usually increased T2W/STIR SI ■ variable contrast enhancement is seen; cortical destruction and extraosseous extension are rare ■ resolution of sarcoid lesions may be seen on follow-up studies ● granulomatous arthropathy: non-specific findings of tenosynovitis, tendinitis, bursitis and synovitis ● nodular sarcoid myopathy: manifests as focal intramuscular masses, often at the musculotendinous junction: ■ the masses may be multiple and bilateral, commonly involving the lower limbs ■ on T2W and post-contrast T1W images, the lesions have a hyperintense periphery and a lower SI centre ● generalised sarcoid myopathy: non-specific findings of proximal muscle atrophy and fatty replacement, similar to polymyositis ● additional features include subcutaneous granulomatous infiltration, skin nodules and soft-tissue masses, with associated lymphadenopathy

Intramedullary osteosclerosis102 ● ● ●

intramedullary osteosclerosis is a rare disorder of unknown aetiology associated with endosteal new bone formation, mainly affecting the tibial shaft in adults, most commonly in women clinically, it presents with chronic leg pain associated with physical activity, thereby mimicking a stress injury radiographs demonstrate cortical and endosteal thickening of the tibial shaft, though other lower limb bones and the humerus may also be affected and the condition may be bilateral

MRI findings ● ●

low medullary SI is seen on all pulse sequences (Fig. 8.97a–c) with a minimal associated increase in medullary and soft-tissue SI on T2W/STIR images (Fig. 8.97c) such areas may show enhancement following contrast (Fig. 8.97d)

Melorheostosis103 ● ● ●

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melorheostosis is a rare sclerosing dysplasia of bone in which, typically, one or several contiguous bones are involved, often following a sclerotomal distribution the lower limbs are more commonly affected than the upper limbs; axial skeletal involvement is rare pathologically, there is cortical and endosteal new bone formation resulting in a ‘flowing candle wax’ appearance on radiographs: ■ soft-tissue masses are also a recognised feature, being reported in 27 per cent of cases ■ these masses are always in continuity with or adjacent to areas of bone involvement and are formed from various combinations of osseous, chondral, fibrolipomatous and vascular elements ■ extension of bone disease into adjacent joints is also recognised, being reported in 35 per cent of cases clinically, it may be asymptomatic or may present with joint contracture or soft-tissue masses, which may be mistaken for sarcoma

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Figure 8.97 Intramedullary osteosclerosis. Coronal (a) and axial (b) T1-weighted (T1W) spin-echo (SE) images showing reduced diaphyseal medullary signal intensity (SI) (arrows a) due to endosteal sclerosis (arrows b). Coronal short tau inversion recovery image (c) showing associated areas of increased medullary SI (black arrowheads) and softtissue oedema (white arrowheads) with endosteal sclerosis (arrow). Axial post-contrast T1W SE fat-suppressed image (d) showing medullary (arrow) and periosteal (arrowheads) enhancement.

MRI findings ● bone lesions appear as well-defined areas of undulating cortical (Fig. 8.98a) and endosteal/medullary (Fig. 8.98b) sclerosis, showing signal void on all pulse sequences (Fig. 8.98c) with no associated reactive changes ● soft-tissue masses have mixed SI on all pulse sequences owing to their varied histological content: ■ areas of signal void due to mineralisation are seen in 70 per cent of cases (Fig. 8.98d) ■ areas of fatty SI are reported in 90 per cent of cases (Fig. 8.98d), while intermediate SI is the predominant pattern in 60 per cent ■ the lesions have poorly defined margins (80 per cent), commonly with involvement of subcutaneous fat (Fig. 8.98d) or deep muscles ■ extension into the knee joint is also well demonstrated (Fig. 8.98e)

Pathology of the soft tissues

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e

Figure 8.98 Melorheostosis. Axial T1-weighted (T1W) spin-echo (SE) image (a) showing undulating cortical hyperostosis (arrows) involving the proximal femur. Sagittal T1W SE (b) and coronal T2*-weighted gradient-echo (c) images showing hypointense endosteal and medullary lesions (arrows). Axial T1W SE image (d) of the elbow showing extraosseous disease with areas of low signal intensity (SI) (arrows) due to mineralisation, fat SI (long arrow) and infiltration of the skin (arrowheads). Sagittal T1W SE image (e) showing extension into the knee joint (arrows) following patellectomy.

PATHOLOGY OF THE SOFT TISSUES MUSCLE TRAUMA Muscle strain9,104 ● ● ● ●

muscle strain is usually secondary to indirect trauma (excessive stretch or tension), usually at the musculotendinous junction in young adults it most commonly affects muscle groups that cross two joints, perform primarily eccentric contraction and contain a predominance of fast twitch (type 2) muscle fibres the commonest muscles injured include the rectus femoris, the hamstrings and the gastrocnemius pathologically, a combination of torn muscle fibres, inflammation, oedema and haemorrhage is seen

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clinically, strain results in acute muscle pain and swelling following a period of strenuous physical activity that typically resolve within 2 weeks muscle strains may be classified into three grades: ■ grade 1 – the commonest (75 per cent of cases) and typically associated with a microscopic injury (5 cm in size the role of MRI in the assessment of a potential soft-tissue mass includes: ■ the demonstration or exclusion of a lesion or pseudomass ■ the precise location (intramuscular, extramuscular, superficial, deep) ■ local staging, related to compartment and adjacent neurovascular structures ■ characterisation of various non-neoplastic, benign neoplastic and some malignant lesions, precluding the need for biopsy

MRI findings ● ●

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●

most intermediate/high-grade STSs have no specific imaging features STSs typically grow in a centrifugal manner until resistance is met, usually in the form of fascial boundaries, after which they follow the path of least resistance, in a longitudinal direction within the compartment: ■ STSs are therefore usually intracompartmental and round or oval in shape STSs are typically isointense to muscle on T1W images (Fig. 8.107a) and heterogeneous on T2W images (in ~90 per cent of cases) with intermediately to mildly increased SI (Fig. 8.107b): ■ a change in SI pattern from homogeneous T1W to heterogeneous T2W is reported in 78–84 per cent of STSs the typical morphology of an STS is a large (>5 cm in 85 per cent of cases), well-defined (owing to formation of a pseudocapsule) mass located deep to the fascia, with lobulated internal architecture separated by ill-defined, fibrous septa (53–75 per cent of cases) (Fig. 8.107c): ■ only 5 per cent of benign soft-tissue tumours exceed 5 cm and ~1 per cent of benign soft-tissue tumours arise deep to the fascia ■ lesion size 5 cm predicts a malignant mass with sensitivity of 74 per cent, specificity of 59 per cent and accuracy of 66 per cent

b

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Figure 8.107 Soft-tissue sarcoma. Coronal T1-weighted (T1W) spinecho (SE) image (a) through the distal arm showing an intramuscular mass (arrows) that is isointense to muscle. Axial T2-weighted (T2W) fast spin-echo (FSE) fat-suppressed (FS) image (b) showing the mass to have mainly intermediate signal intensity (SI) with no surrounding oedema. (continued)

Pathology of the soft tissues

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Figure 8.107 (continued) Coronal short tau inversion recovery image (c) of the thighs showing a lobulated mass in the left adductor compartment with incomplete internal septa (arrowheads). Axial T2W FSE FS image (d) through the popliteal fossa showing areas of fluid T2W SI (arrows) consistent with necrosis. Coronal T2W FSE FS image (e) showing a diffusely hyperintense mass (arrows) consistent with a myxoid lesion. Sagittal T1W SE image (f) showing a mass in the popliteal fossa containing areas of mildly increased SI (arrows) due to haemorrhage and reduced SI (arrowhead) due to necrosis. Axial T1W SE image (g) showing a homogeneously hypointense mass (arrows) consistent with a myxoid lesion. Axial T1W SE image (h) showing a diffuse mildly hyperintense lesion (arrows) compared with muscle.

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using a combination of the following signs, malignancy can be predicted with sensitivity and specificity of 81 per cent: ■ absence of low SI on T2W images, inhomogeneous SI on T1W images and a mean lesion diameter of >33 mm ■ the most sensitive features of malignancy are high T2W SI, inhomogeneous T1W SI and size >33 mm ■ the most specific features of malignancy are the presence of necrosis, bone or neurovascular involvement and a mean lesion diameter of >66 mm the relationship of a subcutaneous tumour to the adjacent fascia may give a clue to its aggressiveness:120 ■ subcutaneous lesions that cross the fascia and exhibit an obtuse angle between the margins of the mass and the fascia are 6–7 times more likely to be malignant than lesions that exhibit an acute angle with the fascia peritumoral oedema is not a striking feature of primary STS, but may be seen with soft-tissue lymphoma or metastasis variations in SI: T2W SI similar to fluid is suggestive of extensive tumour necrosis (Fig. 8.107d), a major myxoid component (Fig. 8.107e) or a cartilaginous lesion: ■ poorly defined areas of mildly increased T1W SI are consistent with the presence of subacute haemorrhage (Fig. 8.107f) ■ areas of reduced T1W SI compared with muscle may be due to necrosis (Fig. 8.107f), while diffuse reduced SI is seen with myxoid tumours (Fig. 8.107g) ■ diffuse mildly increased T1W SI has also been recognised in some sarcomas (Fig. 8.107h) cyst-like lesions:121 certain tumours appear at MRI as cystic lesions, with reduced T1W SI compared with muscle (Fig. 8.107g) and marked hyperintensity on T2W and STIR images (Fig. 8.107e): ■ such lesions may be non-neoplastic (e.g. ganglion, synovial cyst), benign neoplasms (e.g. soft-tissue myxoma) or malignant neoplasms (e.g. myxoid STS) ■ features that are indicative of a malignant lesion are: – larger mean size: benign 4.3 cm vs malignant 7.3 cm – larger greatest dimension: benign 6 cm vs malignant 8 cm – heterogeneity of the lesion on T1W images local staging includes involvement of the adjacent bone (Fig. 8.108a), extracompartmental extension (Fig. 8.108b) and neurovascular bundle encasement (Fig. 8.108c), which are uncommon features that are relatively specific for malignancy but are insensitive: ■ vascular encasement is also seen with fibromatosis, and bone erosion with pigmented villonodular synovitis enhancement is not of value for the routine assessment of STSs but may help in the differentiation of a complex subacute/chronic haematoma from an extensively haemorrhagic sarcoma (Fig. 8.108d–f) dynamic gadolinium-enhanced MRI may be of value in differentiating benign from malignant lesions: ■ on time–intensity plots, benign tumours always show an increase in SI of 30 per cent increase in SI per minute are seen in 84 per cent of malignant tumours, while slopes with a 2 mm) that may show some nodularity (Fig. 8.117c, d) and enhance following contrast (Fig. 8.117e) ● superficial lesions may show thin septa (3 cm at presentation ● occasionally, the dd component constitutes most of the lesion ● the dd component typically shows intermediate SI on T1W images (Fig. 8.118a, b) and intermediate/high SI on T2W images, with failure to suppress on STIR/T2W FSE FS images (Fig. 8.118c) ● enhancement of the high-grade component is seen following contrast

Myxoid liposarcoma125 ● ● ●

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myxoid liposarcoma is the second commonest type of liposarcoma, accounting for 20–50 per cent of all liposarcomas and 10 per cent of all STSs it now encompasses a group of tumours that were previously designated round cell liposarcoma patients typically present in the fourth to fifth decades; myxoid liposarcoma is the commonest type of liposarcoma in children, accounting for 76 per cent of all liposarcomatous tumours in the 11–16-year age range extremity myxoid liposarcomas are typically intermuscular lesions (70–80 per cent of cases), 75–80 per cent affecting the lower limb, particularly the medial thigh or the popliteal fossa the groin, buttock and calf are also affected, while 5 per cent of lesions arise in the upper limb clinically, myxoid liposarcoma presents as a painless mass that may reach 15 cm in size

Pathology of the soft tissues

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Figure 8.118 Dedifferentiated liposarcoma. Sagittal (a) and axial (b) T1-weighted spin-echo images showing a well-differentiated fatty tumour (arrows) with dedifferentiation manifest as a region of intermediate signal intensity (SI) (arrowheads). Axial T2-weighted fast spin-echo fat-suppressed (c) image showing suppression of the fatty component (arrow) and increased SI in the region of dedifferentiation (arrowhead).

MRI findings ● typically, large, well-defined, lobulated intermuscular lesions are seen, with the myxoid stroma resulting in low T1W SI (Fig. 8.119a) and marked T2W/STIR hyperintensity (Fig. 8.119b, c) ● the pathognomonic feature is the presence of fatty tissue within the mass (~50–90 per cent of cases) that constitutes 10 cm at presentation ● most of the lesion shows intermediate T1W SI (Fig. 8.120a) and intermediate/high T2W/STIR SI (Fig. 8.120b) ● haemorrhage and necrosis are common features (Fig. 8.120b) and up to 75 per cent of cases show small focal areas of fat, seen as increased T1W SI (Fig. 8.120a) ● fat and subacute haemorrhage both appear hyperintense on T1W images, but may be differentiated on T2W FSE FS/STIR images, where the fatty component shows low SI and haemorrhage SI remains increased

Mixed-type liposarcoma125 ●

mixed-type liposarcoma accounts for 5–12 per cent of liposarcomas and rarely affects the limbs: ■ MRI demonstrates a combination of the previously mentioned types of liposarcoma

Pathology of the soft tissues

a

b

Figure 8.120 Pleomorphic liposarcoma. Axial T1-weighted spin-echo image (a) showing an intermediate signal intensity (SI) mass (arrows) in the left buttock containing a small area of fat (arrowhead). Coronal short tau inversion recovery image (b) showing the lesion (arrows) to be of heterogeneous increased SI with areas of fluid SI due to necrosis.

FIBROBLASTIC/MYOFIBROBLASTIC TUMOURS Introduction122,126 ●

● ● ●

benign fibroblastic/myofibroblastic tumours include nodular fasciitis, proliferative fasciitis and proliferative myositis, myositis ossificans, myofibroma/myofibromatosis, fibromatosis colli, fibroma of tendon sheath, desmoplastic fibroblastoma, calcifying fibrous tumour, angiofibroma, angiomyofibroblastoma, Gardner fibroma and giant cell angiofibroma intermediate (locally aggressive) fibroblastic/myofibroblastic tumours include superficial fibromatosis (plantar/palmar), desmoid-type fibromatosis and lipofibromatosis intermediate (rarely metastasising) fibroblastic/myofibroblastic tumours include solitary fibrous tumour/haemangiopericytoma, myofibroblastic inflammatory tumour and myofibroblastic sarcoma malignant fibroblastic/myofibroblastic tumours include adult fibrosarcoma, myxofibrosarcoma and lowgrade fibromyxoid sarcoma

Nodular fasciitis126,127 ● ● ● ● ●

●

nodular fasciitis is a benign, soft-tissue tumour of uncertain aetiology and the commonest lesion of fibrous origin it is self-limiting and can occur at any age, though 85 per cent of cases present before the age of 50 years the upper limb (48 per cent) and the trunk (20 per cent) are the commonest sites of involvement, while the lower limb is affected less commonly (15 per cent) the lesion may be subcutaneous (commonest), intramuscular or fascial/intermuscular; rarely, it is intravascular or intradermal clinically, nodular fasciitis presents as a rapidly growing mass that is tender in 50 per cent of cases: ■ neurological symptoms may occur with compression of peripheral nerves, and a history of trauma is noted in 10–15 per cent of cases pathologically, lesions may be classified as myxoid, cellular or fibrous

MRI findings ● lesions are well defined with a round or oval shape and typically ranging in size from 1 to 2.5 cm, rarely reaching 10 cm ● the tumour is slightly hyperintense to muscle on T1W images (Fig. 8.121a) and hyperintense on T2W FSE FS images (Fig. 8.121b) ● T2W FSE images may show reduced SI and enhancement may be uniform or heterogeneous; surrounding oedema is not a typical feature

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b a Figure 8.121 Nodular fasciitis, deep intramuscular type: Coronal T1-weighted spin-echo (a) and axial T2-weighted fast spin-echo fat-suppressed (b) images of the elbow showing a mass lesion (arrows) with no specific signal intensity characteristics.

Elastofibroma dorsi128 ● ● ● ● ● ●

elastofibroma dorsi is a benign, fibroblastic tumour of unknown aetiology with a reported prevalence of ~2 per cent it classically arises deep to the inferior tip of the scapula (99 per cent of cases) and is commonly bilateral (60 per cent) less commonly reported sites include the elbow, shoulder, ischial tuberosity, foot and neck pathologically, it comprises hyalinised collagen with scattered fibroblasts and entrapped islands of mature fatty tissue clinically, elastofibroma dorsi may be asymptomatic (>50 per cent of cases) and found incidentally, may cause mild pain or may manifest as a slowly growing mass the mean age at presentation is 70 years and the lesion is more common in women

MRI findings ● elastofibroma dorsi appears as a poorly defined mass adjacent to the posterolateral rib cage, deep to the serratus anterior, subscapularis, rhomboid and latissimus dorsi muscles ● the lesion comprises multiple hypointense strands arranged parallel to the chest wall and is 5–10 cm in size ● the SI is similar to muscle on both T1W and T2W images, with intermingled areas of fat SI (Fig. 8.122a–c) ● mildly increased SI may be seen on STIR images (Fig. 8.122d) and the degree of enhancement is variable

Myofibroma/myofibromatosis119,129,130 ● ● ●

infantile myofibromatosis is characterised by benign proliferation of fibrous tissue, usually presenting as a slowly growing mass 50 per cent of lesions are present at birth and most occur within the first 2 years of life three types of myofibromatosis are recognised: solitary (myofibroma), multicentric without visceral involvement and multicentric with visceral involvement (a disorder with 75 per cent mortality in the neonatal period): ■ the first two types may undergo spontaneous regression

Pathology of the soft tissues

b

a

d c Figure 8.122 Elastofibroma dorsi. Coronal T1-weighted (T1W) spin-echo (SE) (a) and axial T2-weighted fast spin-echo (b) images showing a hypointense strand-like lesion (arrows) deep to the serratus anterior (arrowhead a) with areas of intermingled fat. Coronal T1W SE image (c) showing bilateral lesions (arrows). Axial short tau inversion recovery image (d) showing mildly increased signal intensity within the lesion (arrows), which is located deep to the serratus anterior (arrowhead).

MRI findings ● variable features are described, including well-defined and ill-defined margins ● lesions are typically hypointense on T1W images (rarely hyperintense) and range from hypo- to hyperintense on T2W images, with variable contrast enhancement ● calcification may be present, while osseous involvement usually affects the metaphyseal regions of the long bones and may be bilateral and symmetrical

Miscellaneous benign lesions122 ●

●

proliferative fasciitis/proliferative myositis are characterised by benign, mass-forming fibrous proliferations that are regarded as variants of nodular fasciitis: ■ MRI findings: a solid, mass-like lesion or a poorly defined mass with associated oedema (Fig. 8.123a–c) fibromatosis colli,119,130 also termed ‘sternocleidomastoid pseudotumour of infancy’, is a benign, fibrous mass associated with torticollis (14–20 per cent of cases) in neonates and infants: ■ it usually presents in the second to fourth weeks of life, typically associated with a history of birth trauma/difficult delivery (90 per cent of cases) ■ MRI findings: enlargement of the lower third of the muscle, with hyperintense or minimally hypointense muscle SI on T2W images

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a

b

c

Figure 8.123 Proliferative myositis. Axial T1-weighted (T1W) spin-echo (SE) image (a) showing diffuse swelling of the left gastrocnemius muscle (arrows). Coronal short tau inversion recovery image (b) showing diffuse muscle oedema (arrows). Axial post-contrast T1W SE image (c) showing diffuse muscle enhancement (arrows).

b

a

c

Figure 8.124 Fibroma of tendon sheath. Coronal T1-weighted spin-echo (a), axial T2-weighted fast spin-echo (b) and sagittal T2*-weighted gradient-echo (c) images of the hand showing a lobular intermediate/low signal intensity mass (arrows) related to the flexor tendons (arrowheads).

Pathology of the soft tissues

●

fibroma of tendon sheath131 is a lesion comprising tightly packed spindle cells surrounded by collagen fibres, with clinical and imaging features similar to GCT of tendon sheath: ■ ~80 per cent of cases involve the upper limb, usually the flexor surfaces of the hand and wrist ■ MRI findings: a well-defined round/oval lesion typically measuring 1–2.5 cm with intermediate to low SI on both T1W (Fig. 8.124a) and T2W (Fig. 8.124b, c)

Deep fibromatosis126,130,132,133 ● ● ● ● ●

●

deep fibromatosis is also termed ‘extra-abdominal desmoid tumour’ or ‘musculoaponeurotic fibromatosis’ and is a lesion of intermediate aggressiveness showing local invasion the peak incidence is at 25–35 years of age and ~70 per cent of cases involve the limbs the shoulder (20 per cent), the chest wall and back (15 per cent), the thigh (12 per cent), the neck (10 per cent) and the knee (7 per cent) are most commonly affected most lesions are solitary but multifocal synchronous lesions are seen in 10–15 per cent of patients, in which case associated metaphyseal dysplasia similar to an Erlenmeyer flask deformity may occur pathologically, fibromatosis exhibits an infiltrative growth pattern and comprises fibroblasts surrounded by a variable amount of collagen, occasionally with areas of myxoid change, haemorrhage and inflammation clinically, patients present with a hard, slowly growing mass that may cause neurological symptoms due to nerve entrapment

MRI findings ● fibromatosis is typically intermuscular, though muscle invasion is common and linear extension along fascial planes is a characteristic feature ● an infiltrative margin is classically seen, though less commonly the margin is well defined ● the SI pattern depends on the histological nature of the lesion; the tumour is typically isointense to muscle on T1W images (Fig. 8.125a, b) and when particularly cellular is also mildly/moderately hyperintense on T2W/STIR images (Fig. 8.125c), showing enhancement following contrast (Fig. 8.125d): ■ relatively hypocellular lesions show intermediate to low SI on T2W/STIR images (Fig. 8.125e) ■ prominent low SI bands of tissue running through the lesion are seen on all pulse sequences due to the presence of dense areas of collagen (Fig. 8.125a–c) ■ areas of fluid T2W SI may also be due to myxoid stroma and/or haemorrhage (Fig. 8.125f) ● pressure erosion of bone/cortical scalloping is seen in 6–37 per cent of cases, and fibromatosis is one of the few benign lesions associated with neurovascular encasement (Fig. 8.125g)

Intermediate (rarely metastasising) fibroblastic tumours122 ●

solitary fibrous tumour/haemangiopericytoma134 was previously classed as a perivascular tumour but shows no histological evidence of pericytes and is more closely related to fibrous tumours: ■ it may have both benign and malignant forms and most commonly involves the lower extremities, the pelvis and the retroperitoneum ■ MRI findings: a non-specific soft-tissue mass with intermediate SI on T1W (Fig. 8.126a) and intermediate/mildly increased SI on T2W (Fig. 8.126b) ■ prominent vascular channels appear as signal voids (Fig. 8.126a, b), while the presence of tumour necrosis suggests malignancy (Fig. 8.126a, b)

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a b

c

e d

f

g

Figure 8.125 Fibromatosis. Cellular lesion: Coronal (a) and axial (b) T1weighted (T1W) spin-echo (SE) images through the proximal calf showing typical features of fibromatosis, an intermediate signal intensity (SI) mass (arrows) with infiltrative margins and central band-like signal voids (arrowhead a) due to collagen deposition. Coronal short tau inversion recovery (STIR) image (c) showing hyperintensity due to the cellular nature of the lesion (arrows), again with low SI collagenous bands (arrowhead). Axial post-contrast T1W SE image (d) showing intense enhancement of the lesion (arrow). Hypocellular lesion: Coronal STIR image (e) through the thigh showing a predominantly hypointense mass (arrows). Axial T2-weighted fast spin-echo image (f) showing cellular fibromatosis of the calf with areas of fluid SI (arrows) due to myxoid degeneration. Neurovascular encasement: Sagittal T1W SE image (g) showing a large lesion (arrows) encasing the popliteal artery (arrowhead).

Pathology of the soft tissues

a

b

Figure 8.126 Haemangiopericytoma. Axial T1-weighted spin-echo (a) and sagittal T2-weighted fast spin-echo fatsuppressed (b) images showing a mass in the anterior soft tissues of the knee with prominent signal voids (arrows) due to vascular channels. Note also the presence of fluid signal intensity (arrowheads b) due to tumour necrosis.

●

●

myofibroblastic inflammatory tumour is a lesion comprising myofibroblastic spindle cells accompanied by an inflammatory infiltrate: ■ it typically affects the soft tissues and viscera of children and young adults and involvement of the musculoskeletal system is unusual myofibroblastic sarcoma is a tumour with fibromatosis-like features but with low metastatic potential: ■ MRI findings: similar to those of fibromatosis or fibrosarcoma

Malignant fibroblastic tumours122 ● ●

●

adult fibrosarcoma has no specific MRI appearances compared with other high-grade STSs myxofibrosarcoma was formerly termed ‘myxoid MFH’: ■ MRI findings: a lesion with typical myxoid features, showing low/intermediate T1W and markedly increased T2W SI low-grade fibromyxoid sarcoma135 is a rare, slow-growing, soft-tissue tumour that affects young and middle-aged adults: ■ most lesions arise from subcutaneous fat, or from the deep soft tissues of the limbs or the chest wall ■ MRI findings: rarely reported; non-specific appearances of a well-defined, lobulated mass with heterogeneous SI and variable enhancement

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FIBROHISTIOCYTIC TUMOURS Introduction122 ● ● ●

benign fibrohistiocytic tumours include GCT of tendon sheath, pigmented villonodular synovitis (see Chapters 3 and 6) and benign fibrous histiocytoma intermediate (rarely metastasising) fibrohistiocytic tumours include plexiform fibrohistiocytic tumour and GCT of soft tissue malignant fibrohistiocytic tumours include pleomorphic MFH, giant cell MFH and inflammatory MFH

Intermediate (rarely metastasising) fibrohistiocytic tumours122 ●

GCT of soft tissue is a rare tumour that is histologically similar to GCT of bone: ■ it occurs in the superficial soft tissues of the upper and lower extremities and may be associated with Paget’s disease ■ MRI findings: an intermediate/low SI T1W and low SI T2W mass (due to haemosiderin deposition) with associated peripheral mineralisation and enhancement following contrast

Pleomorphic malignant fibrous histiocytoma116,122 ● ●

before the WHO reclassification of soft-tissue tumours, MFH was considered one of the commonest STSs in adults, accounting for ~50 per cent of sarcomas involving the limbs in middle-aged and elderly individuals the thigh is the commonest single location

MRI findings ● there are no distinguishing features compared with other high-grade STSs ● internal septation resulting in a lobular architecture is a recognised feature seen on T2W images ● haemorrhage and necrosis are common findings

SMOOTH MUSCLE TUMOURS Introduction122 ● ●

benign smooth muscle tumours include angioleiomyoma and leiomyoma of deep soft tissue malignant smooth muscle tumours include leiomyosarcoma

Angioleiomyoma136 ● ●

angioleiomyoma is a benign tumour arising from vascular smooth muscle (tunica media) and presenting most commonly in the third to fifth decades clinically, it presents as a painful mass in ~60 per cent of cases and may show an increase in size with activity, especially when in the hand

MRI findings ● angioleiomyomas are usually well-defined, small lesions with intermediate SI on T1W images (Fig. 8.127a) and intermediate/increased SI on T2W images (Fig. 8.127b) ● small, curvilinear structures may be evident in the lesion due to tortuous muscular vascular channels (Fig. 8.127b) ● a hypointense rim is seen on T2W images due to a fibrous capsule ● large lesions may be associated with extensive tumour calcification

Leiomyoma of deep soft tissue137 ●

leiomyoma of deep soft tissue is an extremely rare, benign tumour with only a few reported cases, including lesions involving the elbow region, the groin and the popliteal fossa

Pathology of the soft tissues

a

Figure 8.127 Angioleiomyoma. Sagittal T1-weighted spin-echo (a) and axial T2-weighted fast spin-echo (b) images of the foot showing an intermediate signal intensity mass (arrows) containing multiple hyperintense vascular channels (arrowheads b) and a thin hypointense capsule.

● ●

b

of 21 cases in the literature, 10 involved the extremities the age at presentation is wide (3–62 years, mean 25 years)

MRI findings ● lesions show intermediate SI on T1W and intermediate/high SI on T2W with enhancement following contrast ● extensive areas of signal void due to calcification is a characteristic feature

Leiomyosarcoma138 ● ● ●

leiomyosarcoma is a relatively rare, soft-tissue tumour accounting for 5–10 per cent of all STSs it typically presents in adults, but occurrence in younger individuals has been reported in AIDS and after organ transplantation pathologically, leiomyosarcomas are divided into four subtypes, depending on their site of origin (retroperitoneal, deep soft tissue, cutaneous/subcutaneous and vascular)

MRI findings ● the appearances are similar to those of other high-grade STSs, with intermediate T1W SI (Fig. 8.128a), increased T2W SI and heterogeneity due to haemorrhage and necrosis (Fig. 8.128b)

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a

b

c

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Figure 8.128 Leiomyosarcoma. Axial T1-weighted (T1W) spinecho (SE) image (a) showing a large intermediate signal intensity (SI) mass (arrows) in the medial aspect of the thigh. Coronal T2-weighted fast spin-echo fat-suppressed (FS) image (b) showing an intermediate SI lesion (arrows) with extensive areas of necrosis. Note the femoral artery (arrowhead) entering the tumour. Axial post-contrast T1W SE FS image (c) showing enhancement of viable tumour tissue (arrows) and encasement of the femoral artery (arrowhead), possibly indicating a vascular origin of the tumour.

the presence of areas of hyalinisation or metaplastic bone formation may result in foci of low T2W SI, which may suggest the diagnosis tumours of vascular origin may show encasement of the vessel of origin, which may be relatively central within the tumour (Fig. 8.128c)

PERICYTIC (PERIVASCULAR) TUMOURS Introduction122 ● ●

benign pericytic tumours include glomus tumours and myopericytoma malignant pericytic tumours include malignant glomus tumours

Glomus tumours134 ●

●

glomus tumours are benign tumours derived from the neuromyoarterial glomus bodies: ■ they are classically located in the subungual region, the digits and the palms and present with pain and joint tenderness glomangiomatosis139 is a rare condition with multiple glomus tumours, which may not be located in the subungual region (Fig. 8.129a, b)

MRI findings ● glomus tumour presents as a lesion that is typically markedly hyperintense on T2W and shows variable T1W SI depending on its histological cellular pattern (vascular, myxoid or solid)

Pathology of the soft tissues

a

b

Figure 8.129 Glomangiomatosis. Coronal T1-weighted spin-echo (a) and short tau inversion recovery (b) images of the anterior calf showing multiple small glomus tumours (arrows).

SKELETAL MUSCLE TUMOURS Introduction122 ● ●

benign skeletal muscle tumours include rhabdomyoma malignant skeletal muscle tumours include embryonal rhabdomyosarcoma, alveolar rhabdomyosarcoma and pleomorphic rhabdomyosarcoma

Rhabdomyoma122 ● ●

rhabdomyoma is classified as cardiac or extracardiac extracardiac rhabdomyomas are extremely rare and almost all involve the head and neck region

Rhabdomyosarcoma122 ● ●

rhabdomyosarcoma is the commonest STS of childhood, accounting for ~60 per cent of cases and occurring in any soft-tissue site embryonal rhabdomyosarcoma is found in younger patients (2–5 years), while alveolar rhabdomyosarcoma occurs in adolescents (15–19 years) and is the commonest type arising in the trunk and the extremities

MRI findings ● these are as for other high-grade STSs

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VASCULAR TUMOURS Introduction122 ● ● ● ●

benign vascular tumours include haemangiomas/vascular malformations, epithelioid haemangioma, angiomatosis and lymphangioma intermediate (locally aggressive) vascular tumours include kaposiform haemangioendothelioma intermediate (rarely metastasising) vascular tumours include papillary intralymphatic angioendothelioma, haemangioendothelioma and Kaposi sarcoma malignant vascular tumours include epithelioid haemangioendothelioma and angiosarcoma

Haemangioma134,140–142 ● ● ● ● ● ●

haemangiomas are proliferative lesions that usually appear after birth due to pathological angiogenesis, grow rapidly in the first few years of life and subsequently involute over a period of years they are the commonest vascular soft-tissue lesions, constituting 7 per cent of all benign soft-tissue tumours, and are classified as infantile, capillary or cellular most soft-tissue haemangiomas are solitary, ~20 per cent being multiple haemangiomas may be deep (Fig. 8.130a–c) or superficial (Fig. 8.130d, e) and are more common in girls rarely, haemangiomas infiltrate tendon sheaths, in which case the term ‘tenosynovial haemangioma’ is used; such cases are most commonly reported in the hand another rare occurrence is haemangioma arising within a peripheral nerve, when the term ‘intrinsic haemangioma’ of the nerve is used

MRI findings ● haemangiomas typically have a multilobulated appearance resembling a bunch of grapes ● they are isointense (Fig. 8.130a) or mildly hyperintense (Fig. 8.130b, d) to muscle on T1W images and show intense, homogeneous enhancement following contrast (Fig. 8.130c) ● they are heterogeneously hyperintense on STIR/T2W images (Fig. 8.130e) ● the presence of high-flow vessels may result in serpiginous signal voids on SE images (Fig. 8.130b, c) ● small areas of fat may also be seen within and around the lesion (Fig. 8.130a)

Vascular malformations140–142 ● ● ● ● ● ●

●

vascular malformations result from errors of morphogenesis and are classified according to the constituent vessels as arterial, venous (cavernous), lymphatic, capillary or mixed they are present at birth and grow in proportion to the growth of the child, with no tendency to spontaneous regression the prevalence is estimated at 1.5 per cent in the general population venous, lymphatic and capillary malformations are low-flow lesions, while AVMs/arteriovenous fistulae (AVFs) are high-flow lesions these lesions are usually superficial in location but may also be deep, in which case they are usually intramuscular venous (cavernous) malformations are the commonest vascular malformations of the extremities (accounting for 50–66 per cent), usually arising in the flexor muscles of the forearm and the quadriceps muscles: ■ they range from large varicosities to cystic spaces, which may contain phleboliths or thrombus ■ the lesions may be limited to a single tissue or may invade all tissues in the limb, including muscles, tendons, nerves, fat or bone lymphatic malformations comprise chyle-filled macro- or microcysts: ■ most are present at birth and 90 per cent are identified before the age of 2 years

Pathology of the soft tissues

a

b

c

d

e

Figure 8.130 Haemangioma. Intramuscular: Axial T1-weighted (T1W) spin-echo (SE) image (a) showing an isointense lobular mass (arrows) within the calf. Note the presence of fat (arrowheads) within and around the lesion. Coronal T1W SE (b) and post-contrast T1W SE images (c) through the forearm showing a mildly hyperintense mass (arrows b) with intense uniform enhancement (arrows c). Note linear flow voids (arrowheads). Superficial: Axial T1W SE (d) and coronal short tau inversion recovery (e) images showing a superficial haemangioma (arrows) on the lateral side of the lower limb.

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The limbs

macrocystic lesions were previously termed ‘lymphangiomas’ or ‘cystic hygromas’ and may result from obstruction of major lymphatic channels during development ■ the commonest site is the posterior triangle of the neck or the axilla; the limbs are less often involved ■ microcystic lesions are usually cutaneous and infiltrating AVMs/AVFs comprise ~10 per cent of extremity vascular malformations: ■ AVFs are formed by direct communication between arteries and veins, whereas AVMs comprise feeding arteries and draining veins connected by multiple dysplastic vessels ■ AVMs typically present in puberty as a result of infection, thrombosis or trauma ■ massive skeletal overgrowth and limb hypertrophy are relatively common various syndromes are associated with vascular malformations; ■ Maffucci’s syndrome comprises multiple (en)chondromas and soft-tissue cavernous haemangiomas ■ Osler–Weber–Rendu syndrome (hereditary heamorrhagic telangiectasia) is a systemic fibrovascular dysplasia of all vessels and comprises telangiectasias, AVMs and aneurysms, possibly with associated osseous lesions ■ Klippel–Trenaunay–Weber syndrome comprises cutaneous haemangioma, bone and soft-tissue hypertrophy and varicose veins, usually unilateral and affecting the lower limbs; arteriovenous fistulae may also be present ■ Proteus syndrome is a rare vascular anomaly associated with verrucous naevi, lipoma/lipomatosis, macrocephaly, asymmetric limbs with partial gigantism of the hands and feet, and cerebriform plantar thickening, with abundant fat within the malformation at MRI ■ Kasabach–Merritt syndrome is a rare complication of large haemangiomas in which there is thrombocytopenia and purpura ■

●

●

MRI findings ● MRI can define the extent of vascular malformations (classified as focal, multifocal or diffuse) and distinguish between low-flow and high-flow lesions: ■ this distinction helps to guide treatment towards percutaneous embolisation for low-flow lesions and transarterial embolisation for high-flow lesions ● venous (cavernous) malformations are typically well-defined, lobular lesions that are isointense on T1W images (Fig. 8.131a), hyperintense on T2W/STIR images (Fig. 8.131b), commonly with low SI internal septation/striations (Fig. 8.131b), and enhance diffusely following contrast: ■ phleboliths and thrombi appear as low SI central dots (Fig. 8.131c), and fluid–fluid levels may be seen on T2W images (Fig. 8.131d) ● lymphatic malformations: macrocystic lesions are hyperintense on T2W images and show septal enhancement following contrast; fluid–fluid levels may be seen: ■ microcystic lesions tend to show diffuse enhancement and cannot be distinguished from venous malformations ● AVMs/AVFs appear as prominent serpentine vessels with areas of signal void due to rapid blood flow (Fig. 8.131e): ■ adjacent dilated, tortuous feeding arteries and draining veins may be seen, the latter demonstrated to advantage by enhanced MR angiography (Fig. 8.131f) ● in the differentiation of haemangiomas/vascular malformations from malignant soft-tissue masses, the finding of the combination of lobulation, septation and central low SI dots was exclusive to haemangiomas and not seen in sarcomas140

CHONDRO-OSSEOUS TUMOURS Introduction122 ● ●

benign chondro-osseous tumours include soft-tissue chondroma malignant chondro-osseous tumours include mesenchymal CS and extraskelatal OS

Benign soft-tissue chondroma143 ●

soft-tissue chondroma is a rare, benign lesion comprising hyaline cartilage and accounting for ~1.5 per cent of benign soft-tissue tumours

Pathology of the soft tissues

a

b

c

d

e Figure 8.131 Vascular malformation. Venous malformation: Axial T1-weighted (T1W) spin-echo (SE) (a) and coronal short tau inversion recovery (b) images showing a low-flow venous malformation (arrows) lying deep to the iliotibial band (white arrowheads b). Note also the thin internal hypointense septa (black arrowheads b). Axial T2weighted (T2W) fast spin-echo (FSE) image (c) showing small low signal intensity areas (arrowheads) due to intravascular thrombi or phleboliths. Axial T2W FSE image (d) showing multiple fluid levels (arrowheads). Arteriovenous malformation (AVM): Axial post-contrast T1W SE image (e) of the forearm showing a deep enhancing mass (arrows) with multiple flow voids due to high-flow vessels (arrowheads). Coronal MR angiogram (f) showing the AVM (arrows) with multiple associated draining vessels (arrowheads).

f

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●

they most commonly present in the 30–60-year age range and are typically located in the hands or feet, usually near a joint

MRI findings ● soft-tissue chondromas are typically 0.5–3 cm in size ● the SI characteristics are as for intramedullary chondromas, with intermediate SI on T1W (Fig. 8.132a) and hyperintensity on T2W (Fig. 8.132b) ● chondral-type calcification appears as foci of punctate or curvilinear signal voids, which if extensive result in a predominantly low T2W SI

a

b

Figure 8.132 Soft-tissue chondroma. Coronal T1-weighted spin-echo image (a) showing an intermediate signal intensity mass (arrow) adjacent to the first metatarsal head. Coronal T2-weighted fast spin-echo fat-suppressed image (b) showing marked hyperintensity of the mass (arrow) with focal signal void due to calcification (arrowhead).

Extraskeletal mesenchymal chondrosarcoma51 ●

approximately 30–75 per cent of cases of mesenchymal CS occur in the soft tissues, typically affecting adults aged 15–35 years, with the thigh the commonest musculoskeletal region involved

MRI findings ● typically, intermediate SI is seen on T1W and T2W images with heterogeneous, prominent enhancement following contrast ● areas of necrosis may be evident, while focal signal voids due to areas of matrix mineralisation are relatively common ● serpentine signal voids may also be seen due to tumour vessels

Extraskeletal osteosarcoma144 ● ●

extraskeletal OS is a rare lesion accounting for 10 cm, absence of calcification, presence of cystic areas and haemorrhage, and the presence of the ‘triple-signal’ pattern

a

b

d

c

e

Figure 8.137 Synovial sarcoma. Cystic synovial sarcoma: Sagittal short tau inversion recovery (STIR) image (a) showing a multiloculated cystic mass (arrows) with a thin well-defined capsule (arrowheads). Sagittal proton density-weighted fast spin-echo image (b) showing a fluid level (arrowheads). Non-aggressive appearances: Axial T1-weighted (T1W) spin-echo (SE) image (c) showing a homogeneous mildly hyperintense mass (arrows) within the vastus medialis. Axial post-contrast T1W SE fat-suppressed image (d) showing uniform enhancement of the lesion (arrows). Sagittal STIR image (e) showing marked hyperintensity (arrows).

Pathology of the soft tissues

Epithelioid sarcoma151 ● ● ●

epithelioid sarcoma is a rare, soft-tissue tumour that typically affects adolescents and young adults aged 10–35 years ~60 per cent of cases involve the distal upper limb, particularly the hands and forearms, the distal and proximal lower limbs being affected in 15 per cent and 12 per cent of cases, respectively pathologically, the lesion may be subcutaneous, presenting as a solitary or multilobulated, irregular mass: ■ deep-seated lesions are typically larger and firmly attached to tendons, tendon sheaths and fascia, with a tendency to spread along neurovascular bundles, resulting in vascular invasion and metastasis ■ lesions arising in the proximal extremities have a poorer prognosis

MRI findings the tumour is 2.5–19 cm in size; most are poorly defined with infiltrative margins, arising in an intramuscular location (Fig. 8.138) or in the subcutaneous tissues, in which case they have a ‘flattened’ appearance ● the tumour is usually homogeneous and isointense to muscle on T1W images (Fig. 8.138a), but may show areas of increased or decreased SI due to haemorrhage or necrosis ● the T2W SI is very variable, from hypointense to fat (Fig. 8.138b) to hyperintense to fat, and with variable enhancement (Fig. 8.138c) ● additional features: peritumoral muscle oedema may be seen in 50 per cent of cases, reactive cortical thickening without medullary invasion of the adjacent bones, regional lymphadenopathy in 50 per cent of cases and, rarely, calcification ●

a

c

b

Figure 8.138 Epithelioid sarcoma. Axial T1-weighted (T1W) spin-echo (SE) image (a) through the distal forearm showing a poorly defined intramuscular lesion (arrows). Axial T2-weighted fast spin-echo image (b) showing a heterogeneous intermediate signal intensity mass (arrows) surrounding the adjacent tendons (arrowheads). Axial post-contrast T1W SE image (c) showing uniform enhancement (arrows). The tumour is surrounding the adjacent extensor tendons (arrowheads).

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Alveolar soft-part sarcoma152 ● ●

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alveolar soft-part sarcoma (ASPS) is a rare tumour, accounting for 0.5–1% of all soft-tissue sarcomas and usually affecting young adults clinically, the lesion is slow growing and, therefore, commonly asymptomatic, apart from the presence of a mass: ■ alternatively, since the tumour is highly vascular, it may present as a pulsatile mass with an audible bruit, mimicking an AVM most lesions involve the thigh or lower leg, although the head and neck area may be involved in children metastases are relatively common at presentation

MRI findings ● ASPS is typically heterogeneously hyperintense on both T1W (Fig. 8.139a) and T2W/STIR (Fig. 8.139b) images, with all cases showing either homogeneous (40%) (Fig. 8.139c) or heterogeneous (60%) enhancement following contrast ● central or peripheral round/serpentine flow voids are seen in ~70% of cases, indicative of the vascular nature of the lesion (Fig. 8.139a)

Clear cell sarcoma of soft tissue153 ● ●

clear cell sarcoma of soft tissue is a rare tumour that is also termed ‘malignant melanoma of soft parts’ due to its melanocytic differentiation it most commonly affects young to middle-aged adults

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Figure 8.139 Alveolar soft-part sarcoma. Coronal T1-weighted (T1W) spin-echo (SE) image (a) showing a mildly hyperintense lesion (arrows) in the right calf, with multiple serpentine signal voids (arrowheads) due to peripheral neovascularity. Axial fat-suppressed (FS) T2-weighted fast spin-echo image (b) shows moderate hyperintensity (arrows). Coronal post-contrast FS T1W SE image (c) showing uniform enhancement of the lesion (arrows).

Pathology of the soft tissues

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pathologically, the tumour arises in the deep soft tissues of the limbs, adjacent to tendons, aponeuroses and fascial structures: ■ it is well-defined, lacking perilesional oedema, bone erosion, necrosis and satellite nodules and therefore appearing as a ‘benign’ lesion most arise in the lower limbs (most commonly the foot and the thigh) or less commonly the upper limb

MRI findings ● clear cell sarcoma of soft tissue is usually a well-defined, oval/fusiform or round lesion, occasionally lobulated and least commonly spider-like in shape, of size 1.7–10 cm ● most lesions are homogeneous and hyperintense to muscle (~50 per cent) on T1W images (Fig. 8.140) due to the paramagnetic effect of the melanin contained within them ● the remainder are isointense or hypointense to muscle on T1W images ● most are hyperintense on T2W images or less commonly of intermediate SI or hypointense ● marked enhancement following contrast is typical

Figure 8.140 Clear cell sarcoma of soft tissue. Coronal T1-weighted spin-echo image showing a lobulated mildly hyperintense mass (arrows) in the antecubital fossa.

Extraskeletal myxoid chondrosarcoma51 ● ● ●

extraskeletal CS accounts for ~2 per cent of all STSs, extraskeletal myxoid CS being the commonest subtype the mean age at presentation is 50 years, with a reported age range of 4–92 years the thigh is the commonest location, with most lying deep to the fascia, though 25–33 per cent are located superficially

MRI findings ● owing to its myxoid nature, the tumour is typically hypointense to muscle on T1W images (Fig. 8.141a) and markedly hyperintense on T2W/STIR images (Fig. 8.141b) ● a lobulated growth pattern is typical ● following contrast, the characteristic septal/peripheral enhancement pattern of chondral tumours is seen (Fig. 8.141c)

Soft-tissue lymphoma154,155 ●

lymphoma involving skeletal muscle is rare, reported in 1.4 per cent of all cases of lymphoma, and can occur as a result of haematogenous spread from systemic involvement, from extraosseous spread of bone lymphoma or, least commonly, as a primary muscle lesion

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Figure 8.141 Extraskeletal myxoid chondrosarcoma. Axial T1-weighted (T1W) spin-echo (SE) (a), coronal short tau inversion recovery (STIR) (b) and axial post-contrast T1W SE (c) images of the groin showing the typical lobulated appearance of a chondral tumour (arrows) with marked hyperintensity on STIR and a predominantly septal/peripheral enhancement pattern.

~0.3 per cent of cases of Hodgkin’s lymphoma and 1.5 per cent of NHL arise as primary muscle disease muscle lymphoma may also represent a musculoskeletal complication of AIDS, in which case it must be differentiated from pyomyositis and polymyositis since the extension of bone lymphoma to adjacent soft tissues is a common occurrence, the diagnosis of primary muscle lymphoma requires certain criteria, including: ■ a large soft-tissue mass with normal or minimal bone marrow involvement ■ the absence of systemic or nodal disease at the initial presentation the commonest sites are the thigh, the calf and the upper limb

MRI findings ● typically, the lesion involves a long length of the extremity, a growth pattern that is unusual for STS (Fig. 8.142a) ● the tumour mass is usually diffuse and not limited by anatomical compartments (Fig. 8.142b), with poorly defined, infiltrative margins (Fig. 8.142c) ● extension through the deep fascia with resulting involvement of subcutaneous fat (Fig. 8.142d), often in a reticular pattern, and the skin (Fig. 8.142e) is also recognised ● the tumour is isointense (Fig. 8.142f) or minimally hyperintense (Fig. 8.142g) to muscle on T1W images and hyperintense to muscle on T2W images (Fig. 8.142b, c, e) ● as with other round cell tumours, lymphoma may exhibit homogeneous intermediate to low SI on T2W images (Fig. 8.142d) owing to the densely cellular nature of the lesion ● diffuse (Fig. 8.142h) or irregular (Fig. 8.142a) enhancement following contrast is typical ● relatively minor adjacent bone marrow SI abnormalities are not uncommon (Fig. 8.142i) ● associated peritumoral oedema is a feature that helps to distinguish lymphoma from other primary STSs (Fig. 8.142d)

Pathology of the soft tissues

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Figure 8.142 Soft-tissue lymphoma. Coronal post-contrast T1weighted (T1W) spin-echo (SE) image (a) showing extensive longitudinal involvement of the calf (arrows). Axial T2-weighted (T2W) fast spin-echo (FSE) image (b) showing involvement of the anterior, lateral and deep posterior compartments (arrows) of the calf. Axial T2W FSE image (c) showing poorly defined infiltrative margins to the lesion (arrows). Coronal T2W FSE fat-suppressed (FS) image (d) showing extension of the hypointense calf mass (double arrows) into the subcutaneous tissues (arrow) with associated subcutaneous oedema (arrowheads). Coronal T2W FSE FS image (e) through the arm showing extension of lymphoma (arrow) to the subcutaneous tissues with infiltration of the skin (arrowheads). Axial T1W SE image (f) showing the lesion (arrows) to be isointense to muscle. (continued)

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Figure 8.142 (continued) Axial T1W SE image (g) through the forearm showing a mildly hyperintense mass (arrows) in the flexor compartment. Axial post-contrast T1W SE image (h) showing diffuse enhancement of the mass (arrows, same case as in f). Coronal short tau inversion recovery image (i) showing marrow oedema of the ulna (arrow) associated with forearm muscle lymphoma (arrowheads).

Non-communicating intramuscular ganglion156 ● ● ●

ganglia are relatively common soft-tissue masses comprising thick-walled, cystic spaces containing myxoid tissue they are thought to represent a degenerative phenomenon, most commonly associated with joints, tendons and ligaments primary intramuscular ganglia with no joint communication are rare and most commonly identified in the quadriceps muscles

MRI findings ● the lesion is typically elongated and well-defined with a lobulated outline ● as with other ganglia, they are relative hypointense on T1W (Fig. 8.143a) and show marked hyperintensity on T2W/STIR (Fig. 8.143b, c) ● a thin, hypointense wall and hypointense internal septa are characteristic, both showing enhancement following contrast

MISCELLANEOUS LESIONS OF THE SKIN/SUBCUTANEOUS TISSUES Subcutaneous granuloma annulare157 ● ● ●

granuloma annulare is an uncommon, benign skin condition that may be classified as localised, generalised, perforating or subcutaneous the latter is termed ‘subcutaneous granuloma annulare’ and may present as a soft-tissue tumour subcutaneous granuloma annulare most commonly affects otherwise healthy young children (typical age range 2–5 years), manifesting as a non-mobile, painless mass

Pathology of the soft tissues

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Figure 8.143 Intramuscular ganglion. Coronal T1-weighted spin-echo (a) and short tau inversion recovery (b) images showing an elongated lesion (arrows) pointing towards the suprapatellar pouch (arrowheads) but with no joint communication. Axial T2-weighted fast spin-echo image (c) showing the homogeneous hyperintense mass (arrows) within the vastus lateralis.

●

~65 per cent occur in a pre-tibial location; less commonly, they occur in a pre-patellar location, in the upper limb or in the buttock

MRI findings ● the lesion has ill-defined margins and is surrounded by abnormal, oedema-like SI that can extend into the surrounding subcutaneous tissues for several centimetres; extension up to but never deep to the adjacent deep fascia is typical ● on T1W images, the lesion is isointense or slightly hyperintense to adjacent skeletal muscle (Fig. 8.144a) and on T2W/STIR images heterogeneous increased SI is seen (Fig. 8.144b) ● following contrast, enhancement may be homogeneous or heterogeneous; enhancement of the oedemalike SI is typical (Fig. 8.144c)

Dermatofibrosarcoma protuberans158 ● ● ●

dermatofibrosarcoma protuberans is an uncommon, spindle cell tumour that typically arises in the dermis as a multinodular mass that spreads into the subcutaneous tissue and muscle it occurs most commonly between the second and fifth decades and is slightly more common in males it most commonly occurs in the trunk (~50 per cent of cases) and the limbs, followed by the head and neck, and lesions are 1–25 cm in size

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Figure 8.144 Subcutaneous granuloma annulare. Sagittal T1-weighted (T1W) spin-echo (SE) image (a) showing a subcutaneous mass (arrow) that is isointense to muscle and extends to the extensor tendons (arrowhead). Sagittal short tau inversion recovery image (b) showing increased signal intensity in the lesion (arrows). Note the absence of extension deep to the tendon (arrowhead). Axial post-contrast T1W SE fat-suppressed image (c) showing enhancement of the lesion and associated oedema-like tissue (arrows). The extensor tendons (arrowheads) are not involved.

MRI findings ● the tumour usually appears as a well-defined (rarely irregular), multilobular, superficial mass that may extend deep to the skin, with a mean depth of 17 mm (range 8–60 mm) ● occasionally, the lesion is purely deep with no identified superficial component ● the tumour is usually isointense to skeletal muscle on T1W images and less commonly is hypo- or hyperintense (Fig. 8.145a) ● on T2W images, the lesion is hyperintense or of intermediate SI, and it is always hyperintense on T2W FSE FS/STIR images (Fig. 8.145b) ● contrast enhancement is uniform or heterogeneous

Epidermoid cyst159 ● ●

epidermoid cyst is a common benign, soft-tissue tumour that arises in the skin and is thought to occur because of deep migration of epidermal tissue in most cases, the diagnosis is clinically evident, but occasionally the cysts increase to such a size that they mimic STSs

Pathology of the soft tissues

b Figure 8.145 Dermatofibrosarcoma protuberans. Coronal T1-weighted spin-echo image (a) showing a mildly hyperintense lobulated subcutaneous mass involving the skin (arrows). Axial T2-weighted fast spin-echo fat-suppressed image (b) showing the hyperintense nature of the lesion (arrows).

a

MRI findings ● the MRI signal characteristics depend on the chemical composition and physical state (fluid vs solid) of the cyst contents and are therefore highly variable ● epidermoid cysts are located in the subcutaneous tissues and involve the overlying skin; they are surrounded by a thick, well-circumscribed capsule and are 2–10 cm in size (mean 5.2 cm) ● the lesion is slightly hyperintense (Fig. 8.146a) or isointense to skeletal muscle on T1W images and hyperintense on T2W and STIR images (Fig. 8.146b, c) ● heterogeneity is seen on T2W due to the presence of debris ● either no enhancement or rim enhancement is seen following contrast: ■ irregular/nodular enhancement of part of the tumour margin may indicate malignant change

b a

c Figure 8.146 Epidermoid cyst. Axial T1-weighted spin-echo image (a) showing a mildly hyperintense subcutaneous mass (arrow) attached to the skin. Axial T2-weighted fast spin-echo fat-suppressed image (b) showing heterogeneous increased signal intensity with a thin hypointense capsule (arrowheads). Coronal short tau inversion recovery image (c) showing marked hyperintensity in the lesion (arrow).

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Fat necrosis160 ● ● ● ●

fat necrosis occasionally presents as a soft-tissue mass, usually overlying bony protuberances it may present as a subcutaneous lesion or may complicate fatty tumours such as lipoma clinically, patients may be asymptomatic or may present with pain, skin induration, bruising, skin retraction, or skin thickening aetiological factors in the development of fat necrosis include trauma, collagen vascular diseases, myeloproliferative disorders and pancreatic disorders, which may result in disseminated lesions

MRI findings ● subcutaneous fat necrosis appears as a globular lesion with central fat SI, surrounding irregular hypointensity on T1W images (Fig. 8.147a) and increased SI on STIR/T2W FSE FS images (Fig. 8.147b): ■ enhancement of the low SI margin may be seen (Fig. 8.147c)

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Figure 8.147 Fat necrosis. Subcutaneous: Axial T1-weighted (T1W) spin-echo (SE) (a) and short tau inversion recovery (STIR) (b) images through the arm showing a globular fatty mass (arrows) with a scarlike margin (arrowheads). Axial post-contrast T1W SE fat-suppressed image (c) showing peripheral enhancement of the lesion (arrows). Complicating lipoma: Coronal T1W SE (d) and STIR (e) images showing a deep lipoma adjacent to the ischium containing linear areas of reduced T1W and increased STIR signal intensity (arrows) due to fat necrosis, as well as metaplastic ossification (arrowhead d).

Pathology of the soft tissues

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fat necrosis complicating lipoma appears as cloud-like, hypointense stranding in the fatty component of the lesion (Fig. 8.147d, e)

POST-OPERATIVE IMAGING OF SOFT-TISSUE TUMOURS Local recurrence161 ● ●

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~ 50 per cent of patients treated for STS may have a local recurrence features that increase the risk of local recurrence include: ■ poorly defined lesions such as fibromatosis, due to inadequate surgical tumour margins ■ histologically high-grade tumours ■ tumours located deep to the fascia, due to difficulty in achieving wide margins post-operative MRI assessment of possible local recurrence requires a knowledge of the pre-operative tumour SI characteristics, since tumour recurrence typically has the same SI features (Fig. 8.148a–d) from a technical viewpoint, the proximal and distal ends of the patient’s scar should be marked with skin capsules: ■ the diagnosis of local recurrence or seroma can usually be made without the need for contrast administration ■ contrast may be of value in the differentiation of recurrent tumour from haematoma, for the assessment of recurrent fibromatosis and for the differentiation of rare post-radiotherapy inflammatory pseudotumours from local recurrence

MRI findings local recurrence is characterised by the presence of a distinct, nodular, soft-tissue mass, typically with intermediate T1W SI, heterogeneous increased T2W SI (Fig. 8.148e, f) and enhancement following contrast ● recurrence of myxoid sarcomas may mimic a post-operative cyst, since these appear hypointense on T1W images and hyperintense on T2W images, similar to the original lesions ●

Post-operative changes161 ●

post-operative appearances following sarcoma surgery are affected by (neo)adjuvant treatments including: ■ chemotherapy: neoadjuvant chemotherapy may be administered for some STSs such as synovial sarcoma and extraskeletal Ewing sarcoma ■ radiotherapy: this may be given before or more commonly after tumour resection ■ myocutaneous flaps: these comprise muscle and overlying skin and may be required after extensive tissue resection following sarcoma surgery: – they may be required in up to two-thirds of extremity sarcoma resections and are of various types – rotational flaps are rotated into position to cover the soft-tissue defect while preserving the native neurovascular supply via a pedicle – free flaps are detached completely and placed over the soft-tissue defect, with re-anastomosis of the vascular pedicle using microsurgical techniques

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f e Figure 8.148 Local recurrence. Axial T1-weighted (T1W) spin-echo (SE) (a) and coronal T2-weighted (T2W) fast spin-echo (FSE) (b) images showing a myxofibrosarcoma (arrows) of the right thigh. Coronal T1W SE (c) and axial T2W FSE fatsuppressed (FS) (d) images showing a local recurrence (arrows) with similar signal intensity (SI) characteristics. Coronal T1W SE (e) and axial proton density-weighted FSE FS (f) images showing a lobular local recurrence (arrows) of high-grade soft-tissue sarcoma in the posterolateral aspect of the left thigh.

Pathology of the soft tissues

MRI findings ● chemotherapy: significant increase in tumour size may occur due to chemotherapy-induced intratumoral haemorrhage: ■ response to chemotherapy may be indicated by a marked reduction in tumour volume ● radiotherapy: results in oedema-like SI within the soft tissues that is maximal at 12–18 months posttreatment and typically resolves by 2–3 years in 50 per cent of cases: ■ oedema in the subcutaneous tissues appears as a trabecular or lattice-like pattern of reduced T1W SI and increased T2W FS/STIR SI with associated skin thickening (Fig. 8.149a) ■ oedema in muscle results in a more diffuse pattern of increased T2W SI (Fig. 8.149b, c) with minimal enhancement and maintenance of muscle shape and texture, though the muscle may eventually atrophy ■ SI changes are more marked and persistent in the intermuscular septa than in the adjacent soft tissues ■ rarely, an inflammatory pseudotumour develops following radiotherapy (reported incidence ~1 per cent) and can be differentiated from recurrent tumour by its dynamic enhancement characteristics: – pseudotumour enhances at 4–7 minutes post-contrast injection, whereas recurrent tumour enhances 1–3 minutes after contrast ● myocutaneous flaps: flaps exhibit time-dependent changes in their MR appearances (size, SI characteristics and enhancement patterns): ■ all flaps atrophy with time, showing decreased muscle mass and increased fat content ■ initially, all flaps appear relatively hyperintense on T2W images (Fig. 8.149d–f), returning to normal muscle SI at 5–21 months after surgery in one-third of cases ■ initial enhancement is seen in ~75 per cent of cases, returning to normal muscle enhancement at 18 months in about one-third of cases ■ radiotherapy increases the T2W SI and contrast enhancement of flaps

Post-operative seroma162 ●

post-operative seroma, also known as hygroma, is a well-defined fluid collection at the site of tumour resection, most commonly associated with sarcoma surgery (~90 per cent) and usually seen in the buttock or the lower limb (90 per cent)

MRI findings ● seromas are well-defined lesions with a thin, hypointense pseudocapsule on T2W images (Fig. 8.150a) ● 74 per cent show homogeneous low SI on T1W images (Fig. 8.150b) with rim enhancement following contrast (Fig. 8.150c), while 26 per cent show hyperintensity (Fig. 8.150d) ● on T2W images, 79 per cent are homogeneous and hyperintense (Fig. 8.150a) ● T2W heterogeneity due to septation (Fig. 8.150e), fluid–fluid levels (Fig. 8.150f) or debris is seen in 21 per cent of cases ● a feathery pattern may be seen arising from the inner margin of the seroma or from the septation ● most seromas are round or oval in cross-section (Fig. 8.150a, c, e); they are less commonly angular, extending between muscle planes (Fig. 8.150g), or linear/flame-shaped (Fig. 8.150h) ● with time, 66 per cent of seromas decrease in size, while ~20 per cent increase

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e Figure 8.149 Post-operative features. Radiotherapy change: Coronal short tau inversion recovery (STIR) image (a) showing a lattice-like area of increased signal intensity in the subcutaneous fat (arrows) with associated skin thickening and hyperintensity (arrowhead). Coronal STIR (b) and axial proton density-weighted fast spin-echo (FSE) fat-suppressed (FS) (c) images showing poorly defined oedema of the adductor muscle (arrows). Gastrocnemius myocutaneous flap: Coronal T1weighted spin-echo image (d) showing a medial gastrocnemius flap (arrows). Sagittal STIR (e) and axial T2-weighted FSE FS (f) images showing hyperintensity in the flap (arrows) compared with normal skeletal muscle.

Pathology of the soft tissues

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Figure 8.150 Post-operative seroma. Axial T2-weighted (T2W) fast spin-echo (FSE) fat-suppressed (FS) image (a) showing a uniformly hyperintense oval mass (arrow) in the posterior thigh with a thin hypointense pseudocapsule. Axial T1-weighted (T1W) spin-echo (SE) image (b) showing uniform hypointensity in the lesion (arrow). Axial post-contrast T1W SE image (c) showing rim enhancement (arrow). Axial T1W SE image (d) showing a mildly hyperintense seroma (arrows) in the medial thigh. Coronal short tau inversion recovery (STIR) image (e) showing heterogeneity within the lesion due to debris (arrowheads). Sagittal STIR image (f) showing a fluid level (arrowheads). (continued)

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Figure 8.150 (continued) Axial T2W FSE FS image (g) showing a wedge-shaped seroma (arrow). Coronal STIR image (h) showing a flame-shaped seroma (arrow).

MISCELLANEOUS DISORDERS OF SKELETAL MUSCLE Polymyositis/dermatomyositis109,163 ● ● ●

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polymyositis and dermatomyositis are diseases of unknown aetiology that predominantly affect females at any age polymyositis usually presents in the fourth decade, whereas dermatomyositis has a bimodal age presentation, with peaks in childhood and the fifth decade the diagnosis is based on the presence of three of the following four features: proximal and symmetrical muscle weakness with/without myalgia, increased serum creatinine kinase levels, multifocal myopathic pattern on electromyography, and fibre necrosis/regeneration and mononuclear cell infiltrates without perifascicular atrophy on muscle biopsy dermatomyositis is characterised by the addition of a permanent or transient exanthem of the face, the chest or the extensor surfaces of the extremities clinically, these diseases are typically chronic and progressive with variable patterns of muscle involvement MRI is of value in the early diagnosis, staging of extent and guiding of muscle biopsy, as well as in the demonstration of response to treatment similar clinical and MRI features may be seen in inclusion body myositis, which is thought to be due to paramyxovirus infection

MRI findings ● the primary abnormality is muscle oedema, with the muscles appearing hyperintense on T2W/STIR images (Fig. 8.151a–c) but essentially normal on T1W images ● oedema may be focal or diffuse, but is typically symmetrical and most marked in the proximal muscles ● the most commonly involved muscles include the vasti, glutei, adductors, hamstrings, tibialis anterior, gastrocnemius and soleus ● relative sparing of the rectus femoris and the biceps femoris has been reported in dermatomyositis ● associated features include oedema, which may be seen in a myofascial distribution, around involved groups of muscles: ■ skin changes include thickening of subcutaneous tissues with an abnormal reticular pattern ■ fatty infiltration is indicative of chronic disease that is unresponsive to treatment and may be followed by muscle atrophy ■ soft-tissue calcification is rare and may appear as foci of signal void

Pathology of the soft tissues

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Figure 8.151 Dermatomyositis. Axial T2*-weighted (T2*W) gradient-echo (GE) image (a) showing diffuse symmetrical oedema of the quadriceps (arrows) and adductor (arrowheads) muscles. Axial T2*W GE image (b) showing additional patchy oedema of the hamstrings (arrows). Coronal short tau inversion recovery image (c) showing diffuse oedema of the quadriceps (arrows) and adductor (arrowheads) muscles.

Focal myositis164 ● ● ● ●

focal myositis is a very rare, benign, inflammatory pseudotumour of unknown aetiology and is selflimiting it most commonly affects the muscles of the thigh (50 per cent) or calf (25 per cent) and multiple muscle involvement may be seen the age range for reported cases is 10–67 years clinically, it presents as a rapidly growing, painful, soft-tissue mass that may mimic a sarcoma, with spontaneous regression occurring over months to years: ■ unilateral hypertrophy of the calf due to focal inflammatory myositis of the gastrocnemius secondary to denervation from chronic S1 radiculopathy has been described165

MRI findings ● focal myositis: an ovoid/fusiform, intramuscular mass measuring 2–10 cm and associated with diffuse muscle oedema is seen: ■ lesions are typically isointense on T1W images (Fig. 8.152a) and hyperintense on T2W/STIR images (Fig. 8.152b, c), with enhancement following contrast ■ alternatively, diffuse muscle swelling with hyperintensity on T2W/STIR images may be seen (Fig. 8.152d, e) ● gastrocnemius hypertrophy: diffuse muscle enlargement with increased T1W SI due to fatty replacement and increased STIR SI due to oedema (Fig. 8.152f, g)

Muscle necrosis and diabetic muscle infarction166,167 ● ●

diabetic muscle infarction is a rare, spontaneous, aseptic complication of diabetes mellitus that presents with the acute onset of painful swelling of the affected muscle and occasionally a palpable mass the condition is more common in women (>60 per cent), with a mean age at presentation of ~42 years, and may occur in both type 1 (more commonly) and type 2 diabetes

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Figure 8.152 Focal myositis. Mass-like: Axial T1-weighted (T1W) spin-echo (SE) image (a) showing a poorly defined isointense mass (arrows) within the adductor magnus muscle. Axial T2-weighted (T2W) fast spin-echo (FSE) (b) and coronal short tau inversion recovery (c) images showing the mass (arrows) to be hyperintense to muscle with associated oedema (arrowheads). Diffuse: Axial T1W SE image (d) showing enlargement of the right tensor fascia lata muscle (arrow) compared with the normal muscle (arrowhead) on the left. Coronal T2W FSE image (e) showing mildly increased muscle signal intensity on the right (arrow) compared with the normal left tensor fascia lata (arrowhead). Gastrocnemius hypertrophy: Coronal T1W SE image (f) showing fatty infiltration of the medial and lateral heads of gastrocnemius (arrows). Axial T2W FSE image (g) showing muscle swelling (arrows) and hyperintensity due to oedema.

Pathology of the soft tissues

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●

the mean time from onset of diabetes to the first episode of diabetic muscle infarction is ~14 years and most patients have multiple complications of diabetes, including peripheral vascular disease and nephropathy the commonest sites of involvement are the thigh (especially the quadriceps) in ~80 per cent of cases and the calf in ~20 per cent; the condition is bilateral in ~8 per cent

MRI findings ● the primary finding is muscle inflammation with isointensity or reduced SI on T1W images and hyperintensity on T2W and STIR images (Fig. 8.153a) ● foci of T1W hyperintensity due to haemorrhage may be seen (Fig. 8.153b) ● areas of muscle inflammation enhance following contrast, and rim enhancement around areas of necrotic muscle is also seen ● additional features include diffuse muscle enlargement with loss of muscle margins and fluid in the perimuscular soft tissues (Fig. 8.153c)

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Figure 8.153 Diabetic muscle infarction. Coronal short tau inversion recovery image (a) of the thigh showing poorly defined oedema (arrows) in the quadriceps muscles. Coronal T1-weighted (T1W) spin-echo (SE) image (b) showing areas of hyperintense muscle haemorrhage (arrows). Axial T2-weighted (T2W) fast spin-echo (FSE) fat-suppressed image (c) showing diffuse muscle swelling (arrows) and perimuscular/perifascial oedema (arrowheads). Calcific myonecrosis. Sagittal T1W SE (d) and axial T2W FSE (e) images showing an irregular mass (arrows) in the anterior compartment of the calf, with increased T1W signal intensity (SI), predominantly reduced T2W SI and a low SI rim (arrowheads) due to calcification of the wall.

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Calcific myonecrosis168,169 ● ● ● ●

calcific myonecrosis is a rare late complication of lower limb trauma, almost all reported cases affecting the calf predisposing conditions include compartment syndrome, peroneal nerve injury and severe lower limb trauma clinically, patients present with a slowly enlarging, painless mass; the mean age at presentation is 51 years and the mean time from injury to presentation is 37 years radiographs demonstrate a well-defined fusiform mass with peripheral calcification

MRI findings ● the mass may be limited to a single anatomical compartment or may involve the whole calf ● a thick, nodular, hypointense rim is seen on all pulse sequences due to peripheral calcification (Fig. 8.153d, e) ● on T1W images, the contents of the mass may be isointense, hyperintense or hypointense to skeletal muscle ● the contents of the lesion are mainly intermediate SI on T2W images with only small areas of fluid SI, and no enhancement is seen following contrast

Muscle denervation163 ●

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neuropathy results in muscle denervation, which may be occult on MRI performed within the first few weeks (acute denervation) but manifests as increased muscle SI (oedema-like pattern) on STIR/T2W FSE FS images between 1 month and 1 year (subacute stage) rarely, acute denervation manifests within 2–4 days with restoration of nerve function, subacute denervation changes may return to normal the chronic stage of muscle denervation results in atrophy and fatty replacement, which is irreversible, while muscle hypertrophy is a rare occurrence following denervation MRI has been used to aid the diagnosis of neurogenic foot drop by demonstrating the pattern of muscle denervation in the calf:170 ■ peroneal nerve pattern: involvement of the tibialis anterior and extensor digitorum muscles, if the deep ramus is affected: – the peroneus longus muscle if the superficial ramus is affected and a combination of the above if both branches are affected (Fig. 8.154a, b) ■ L5 radiculopathy pattern: tibialis posterior and popliteus, in addition to the tibialis anterior, extensor digitorum and peroneus longus ■ unspecific pattern: a mixed pattern including some of the above muscles together with portions of the gastrocnemius or soleus muscle

MRI findings subacute denervation appears as diffuse muscle oedema with increased muscle SI on T2W FSE FS/STIR images (Fig. 8.154c) and a normal appearance on T1W images (Fig. 8.154d) ● chronic denervation appears as muscle atrophy and fatty infiltration resulting in increased muscle SI on T1W (Fig. 8.154e, f) and T2W FSE images with reduced muscle SI on FS sequences ●

Rhabdomyolysis163 ● ● ●

rhabdomyolysis is a severe form of skeletal muscle injury characterised by the loss of integrity of muscle cell membranes aetiological factors include trauma (including severe exercise), ischaemia, burns and toxins, intravenous heparin therapy and autoimmune inflammation the disorder may result in renal failure (from myoglobinuria), tetany and compartment syndrome

MRI findings ● initially, there is oedema throughout the affected muscles, the severity of the SI changes correlating with severity of the injury ● mild cases may resolve, while severe cases may progress to myonecrosis

Pathology of the soft tissues

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Figure 8.154 Muscle denervation. Subacute: Axial T2-weighted (T2W) fast spin-echo (FSE) (a) and short tau inversion recovery (b) images through the calf showing diffuse oedema involving the tibialis anterior (arrows), the extensor digitorum (black arrowheads) and the peroneus longus (double arrowheads) consistent with peroneal nerve compression. Axial T2W FSE fat-suppressed (c) and T1-weighted (T1W) spin-echo (SE) (d) images showing mild denervation oedema of both heads of gastrocnemius (arrows c), which appear normal on the T1W image (arrows). Chronic: Coronal (e) and axial (f) T1W SE images showing advanced fatty atrophy of the anterior compartment calf muscles (arrows) due to a peroneal nerve lesion.

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THE PERIPHERAL NERVES Introduction171 ●

● ●

anatomy of the peripheral nerves: individual nerve fibres comprise conducting axons, insulating Schwann cells and a supporting connective tissue matrix: ■ each nerve fibre is embedded within connective tissue termed the ‘endoneurium’, which is surrounded by the perineurium ■ the perineurium divides nerves into individual fascicles, which is the smallest component of peripheral nerves that can be visualised at MRI ■ the nerve fascicles are embedded within the interfascicular epineurium, which is enclosed by the epineurium to constitute the peripheral nerve peripheral nerves are 1–20 mm in diameter and contain 1–100 fascicles; the size of the nerve determines whether it is visualised at MRI nerves that are routinely seen on high-quality clinical MR examinations include those of the brachial and lumbosacral plexuses, the ulnar and median nerves in the arm/forearm/wrist, the radial nerve at the arm/forearm, the sciatic nerve in the buttock/thigh and the common peroneal/tibial nerves in the popliteal fossa and proximal calf

a

c

b

d

Figure 8.155 The sciatic nerve. Normal: Axial proton density-weighted (PDW) fast spin-echo (FSE) image (a) showing the fascicular pattern of the nerve (arrows) in the proximal thigh, with individual fascicles surrounded by fat. Axial T2weighted (T2W) FSE images (b, c) showing the normal low signal intensity sciatic nerve (arrow b) in the distal thigh and mildly hyperintense sciatic nerve (arrow c) in the proximal thigh. Axial PDW FSE fat-suppressed (FS) image (d) showing the isointense sciatic nerve (arrow) in the distal thigh. (continued)

Pathology of the peripheral nerves

f

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g

Figure 8.155 (continued) Pathological: Axial T1-weighted spin-echo image (e) showing enlargement of the sciatic nerve (arrow) in the mid-thigh with loss of the fascicular pattern. Coronal short tau inversion recovery (f) and axial T2W FSE FS (g) images showing swelling and hyperintensity of the left sciatic nerve (arrows) following radiotherapy, compared with the normal right sciatic nerve (arrowhead g).

MRI findings ● normal peripheral nerves appear on axial imaging as multiple small dots representing the individual fascicles, which are slightly hypointense to muscle on T1W/PDW images (Fig. 8.155a), isointense (Fig. 8.155b) or mildly hyperintense (Fig. 8.155c) to muscle on T2W and PDW FSE FS/T2W FSE FS images (Fig. 8.155d) and are surrounded by fat SI due to the perineurial and epineurial fat components (Fig. 8.155a): ■ prominent nerve fascicles appear slightly hyperintense compared with the perineurium and the epineurium due to endoneurial fluid ● pathology of the peripheral nerves can result in changes in the fascicular architecture and nerve SI: ■ enlargement of a nerve, particularly focal enlargement, is considered abnormal ■ an altered fascicular pattern, such as inability to resolve individual fascicles in large nerves (e.g. the sciatic) (Fig. 8.155e), or a non-uniform fascicular pattern (e.g. clumping of the fascicles, irregular size of individual fascicles) is also considered pathological ■ hyperintensity of the nerve on T2W images, most reliably assessed on T2W FSE FS/STIR (Fig. 8.155f, g), is also abnormal

PATHOLOGY OF THE PERIPHERAL NERVES NERVE COMPRESSION SYNDROMES Radial nerve ● ● ●

the radial nerve is the major continuation of the posterior cord of the BP, and may be compressed in the upper arm at the mid-humeral diaphyseal level while running in the spiral groove clinically, patients present with weakness of the triceps, the brachioradialis and the extensor and supinator muscles of the hand and wrist the radial nerve may also be damaged following a humeral diaphyseal fracture

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Anterior interosseous nerve syndrome172,173 ●

●

●

the anterior interosseous nerve is the largest branch of the median nerve, arising 2–8 cm distal to the medial epicondyle and extending within the pronator teres to eventually run anterior to the interosseous membrane (Fig. 8.9c): ■ it is a purely motor nerve that supplies the flexor pollicis longus, the radial belly of the flexor digitorum profundus and the pronator quadratus anterior interosseous nerve syndrome, also known as Kiloh–Nevin syndrome, manifests clinically as pain and weakness of the flexor pollicis longus, the flexor profundus of the index finger and the pronator quadratus, without sensory deficit, and may simulate flexor tendon rupture sites of compression of the anterior interosseous nerve include a fibrous band deep to the ulnar head of pronator teres, the tendinous origin of the flexor digitorum superficialis muscle, and anomalous vessels, fibrous bands and accessory muscles ■ the nerve may also be injured by direct trauma/laceration or fracture ■ some cases appear to be spontaneous, resolving with conservative treatment, and are thought to be secondary to neuritis of the anterior interosseous nerve

MRI findings denervation oedema/atrophy of the radial half of the flexor digitorum profundus, the flexor pollicis longus and the pronator quadratus is seen in various combinations (Fig. 8.156a, b) with demonstration of intact flexor digitorum profundus and flexor pollicis longus tendons

●

a

b

Figure 8.156 Anterior interosseous nerve syndrome. Axial proton density-weighted (PDW) fast spin-echo (FSE) image (a) through the mid-forearm showing denervation oedema of the flexor pollicis longus (arrows). Axial PDW FSE image (b) through the distal forearm showing denervation oedema of the pronator quadratus (arrows).

Common peroneal nerve171 ●

●

●

the common peroneal nerve is a branch of the sciatic nerve arising in the proximal popliteal fossa, running posterior to the biceps femoris muscle and then wrapping around the fibular neck: ■ deep to the peroneus longus tendon, it enters the peroneal tunnel, where it divides into superficial and deep branches clinically, compression of the common peroneal nerve in the peroneal tunnel results in pain along its sensory dermatome, which may mimic a tibial stress fracture/shin splints or compartment syndrome: ■ nerve compression is characterised clinically by exacerbation of symptoms by inversion and/or plantar flexion of the foot ■ eventually, foot drop may develop due to denervation of the foot extensors causes include repetitive inversion/pronation of the foot, prolonged squatting and repetitive flexion/extension of the knee: ■ fracture and haemorrhage around the fibular neck, tight casting around the knee, proximal tibiofibular joint or intraneural ganglia and lateral meniscal cysts

Pathology of the peripheral nerves

MRI findings ● denervation/atrophy of the muscles supplied by the deep peroneal nerve is seen (Fig. 8.154a, b) ● the underlying cause, such as a ganglion cyst

NEUROGENIC TUMOURS Introduction122 ● ●

benign neurogenic tumours include schwannoma (neurilemoma), neurofibroma and perineurioma malignant neurogenic tumours include malignant peripheral nerve sheath tumour (MPNST)

Schwannoma174,175 ● ●

●

schwannoma most commonly affects patients aged 20–30 years and accounts for ~5 per cent of all benign soft-tissue tumours commonly involved sites include the spinal and sympathetic nerve roots of the head and neck, and the nerves of the flexor compartments of the upper and lower limbs (particularly the ulnar and peroneal nerves) schwannomas are usually solitary, small (50 per cent of lesions are solitary schwannomas ■ the incidence of MPNST is not related to the presence of NF1, ~11 per cent being related to previous radiotherapy the commonest benign non-neurogenic primary BP tumours are fibromatosis (~33 per cent of cases) and lipoma: ■ fibromatosis typically infiltrates the plexus following involvement of the serratus anterior and scalenus anterior muscles malignant primary BP tumours include PRS, synovial sarcoma and lymphoma, which can involve the plexus in two ways: ■ first, compression of the plexus by enlarged lymph nodes, cervical and supraclavicular nodes involving the upper plexus (C5–6) and mediastinal/axillary nodes involving the lower plexus (C7–T1): – the BP is involved in 5–15 per cent of patients with Hodgkin’s lymphoma – perineural spread of lymphoma may result in epidural and intradural extension ■ second, neurolymphomatosis, a rare manifestation of lymphoma that primarily involves the peripheral nerves and results in diffuse thickening of the plexus regarding surgical management, the following issues are of importance: ■ differentiation between neurofibroma and schwannoma ■ the proximal intraneural/intraspinal/intradural extension of MPNST, which may render the lesion incurable by surgery ■ the relationship of any lesion to the ipsilateral vertebral artery

Pathology of the peripheral nerves

a b

c

d

e

Figure 8.164 Acute adult brachial plexus (BP) injury. Pseudomeningocele: Axial T2*-weighted (T2*W) gradient-echo (GE) image (a) showing acute pseudomeningocele formation (arrow) following left BP injury. Note also the intradural avulsion of the nerve root (black arrowhead) and the absence of the left dorsal root ganglion compared with the normal right side (white arrowhead). Sagittal T1-weighted spin-echo (b) and axial T2*W GE (c) images showing a chronic left pseudomeningocele (arrows). Coronal T2weighted (T2W) fast spin-echo (FSE) fat-suppressed image (d) showing bilateral pseudomeningocele formation (arrows). Root avulsion: Axial scout image (e) showing the oblique plane for imaging root avulsion. Coronal oblique T2W FSE image (f) showing avulsion of the C7 root (arrow) with intact adjacent roots (arrowheads).

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Figure 8.165 Acute adult brachial plexus (BP) injury, secondary changes. Cord/intraspinal changes: Sagittal T2-weighted (T2W) fast spin-echo (FSE) image (a) showing traumatic central cord oedema (arrow) and sagittal T1-weighted (T1W) spin-echo (SE) image (b) showing intramedullary haemorrhage (arrows), both indicative of intradural root avulsion. Axial T1W SE image (c) showing intradural haematoma (arrow). Axial T2*-weighted gradient-echo image (d) showing extradural haematoma (arrow). Extraspinal changes: Coronal T1W SE (e), T2W FSE fat-suppressed (f) and sagittal T2W FSE (g) images showing oedema and scarring (arrows) around the BP.

Pathology of the peripheral nerves

MRI findings ● the MR appearances of the various lesions are identical to those seen with non-BP tumours (as described previously) ● the diagnosis of a tumour arising from the plexus, as opposed to other tumours arising in the neck, depends on various factors: ■ a tumour involving the roots or trunks lies in the plane between the anterior and middle scalene muscles (Fig. 8.166a, b) ■ since neurofibromas and schwannomas tend to be oval, with their long axis oriented to the nerve of origin, lesions arising from the upper roots lie in an oblique plane from superomedial to inferolateral (Fig. 8.166b), whereas lesions arising from the inferior roots lie in a horizontal plane ■ tumours arising from the retroclavicular and infraclavicular plexus run in an oblique direction from superomedial to inferolateral (Fig. 8.166c, d) ■ proximal intraspinal extension may result in well-defined neural foraminal enlargement and scalloping of the posterolateral vertebral body (Fig. 8.166e–g)

a

b

c

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Figure 8.166 Primary brachial plexus (BP) tumours. Schwannoma arising from the trunks of the right BP: Axial T1weighted (T1W) spin-echo (SE) image (a) showing an oval lesion (black arrow) lying between the anterior (white arrow) and middle (arrowhead) scalene muscles. Coronal T2-weighted (T2W) fast spin-echo (FSE) image (b) showing the oblique orientation of the plexus tumour (arrow). Schwannoma arising from the retroclavicular and infraclavicular BP: Coronal (c) and sagittal (d) T1W SE images showing an oval lesion (arrows) lying in an oblique plane and displacing the subclavian artery (arrowheads) inferiorly and anteriorly. (continued)

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Figure 8.166 (continued) Malignant peripheral nerve sheath tumour of the right BP: Coronal T1W SE image (e) showing an irregular lobulated lesion (arrows) arising from the inferior roots of the right BP with proximal extension into the spinal canal (arrowhead). Sagittal T2W FSE image (f) showing the mass (arrows) lying posterior to the subclavian artery (arrowhead) and the anterior scalene muscle (double arrowhead). Axial post-contrast T1W SE image (g) showing diffuse enhancement of the mass (arrows) with proximal intraneural extension resulting in enlargement of the neural foramen and posterior scalloping of the vertebral body (arrowhead).

g

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Figure 8.167 The brachial plexus (BP) in neurofibromatosis type 1: Sagittal T1-weighted (T1W) spin-echo (SE) (a) and axial T2*-weighted gradient-echo (b) images showing diffuse swelling of the cervical nerve roots (arrows) with mild foraminal enlargement (arrowheads b). Plexiform neurofibroma: Coronal T1W SE image (c) showing diffuse involvement of the whole of the right BP (arrows). Coronal short tau inversion recovery image (d) showing lobulated enlargement of the retroclavicular and infraclavicular BP (arrows) and terminal branches (arrowhead).

Pathology of the peripheral nerves

■ ■

in the setting of NF1, neurofibromas may be multiple and result in diffuse involvement of the BP (Fig. 8.167a, b) or may present as plexiform lesions (Fig. 8.167c, d) non-neurogenic tumours of the BP have the same imaging characteristics as those in other locations in the body (Fig. 8.168a–c)

b

a

c

Figure 8.168 Fibromatosis of the brachial plexus. Coronal proton density-weighted fast spin-echo (FSE) (a), T2*-weighted gradient-echo (b) and axial T2-weighted FSE fat-suppressed (c) images showing an irregular infiltrative mass (arrows) filling the axilla and obscuring the retroclavicular plexus.

Metastatic involvement of the brachial plexus189,190,196 ●

●

Pancoast tumour is a primary lung carcinoma arising in the superior pulmonary sulcus that may invade the BP (usually the lower trunk) and the subclavian vessels: ■ it results in Pancoast’s syndrome: shoulder pain, pain in the C8–T1 distribution, muscle atrophy in the hand, Horner’s syndrome (20 per cent of cases) metastatic involvement: supraclavicular or axillary lymphadenopathy from carcinoma of the breast may secondarily involve the BP (usually the medial cord), resulting in neurovascular compromise: ■ true haematogenous metastases to the BP are rare

MRI findings ● Pancoast tumour: an apical lung mass is seen, commonly with adjacent bone destruction and involvement of the inferior roots of the BP ● metastatic lymph node involvement: intermediate SI T1W and heterogeneous intermediate/increased SI T2W mass in the supraclavicular fossa or axilla ● melanoma metastases may appear relatively hyperintense on T1W (Fig. 8.169a–c)

Radiation fibrosis of the brachial plexus189,190,196 ● ●

radiotherapy is the commonest cause of inflammatory lesions of the BP, which most often occur following treatment to the axillary lymph nodes for breast carcinoma neurological symptoms manifest 5–30 months post-treatment, peaking at 10–20 months, and are dose related

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Figure 8.169 Metastatic involvement of the bracial plexus. Axial T1-weighted spin-echo (a), sagittal T2-weighted fast spin-echo (b) and short tau inversion recovery (c) images showing a melanoma metastasis (arrows) involving the infraclavicular plexus (arrowheads).

clinically, three patterns of radiation fibrosis are described: ■ delayed progressive radiation fibrosis is most likely to occur in patients who have received >60 Gy and results in fibrosis of the plexus with associated wallerian degeneration: – symptoms include paraesthesia, hyperaesthesia, pain and weakness, usually involving the upper trunk distribution, with weakness of the arm flexors and shoulder abduction – the reported incidence is 5–9 per cent and symptoms usually occur within the first year posttreatment ■ reversible (transient) plexopathy occurs at a median of 4.5 months post-treatment, with paraesthesia as the main symptom and complete resolution in all cases ■ acute ischaemic plexopathy is a very rare occurrence in which there is acute plexus ischaemia due to radiation-induced subclavian artery occlusion

MRI findings radiation fibrosis results in diffuse thickening and enhancement of the BP without a focal mass, with low SI on both T1W and T2W images

●

COMPRESSION NEUROPATHY Thoracic outlet syndrome172,190,197 ●

thoracic outlet syndrome (TOS) is a compressive neuropathy/vasculopathy of the BP and/or the subclavian artery/vein; three typical syndromes are described according to the location of the BP entrapment: ■ anterior scalene syndrome results from compression in the interscalene triangle (Fig. 8.163a–c)

Pathology of the peripheral nerves

costoclavicular syndrome results from compression between the clavicle and the first rib (the costoclavicular space) ■ retropectoralis minor syndrome results from compression deep to the pectoralis minor muscle as it attaches to the coracoid process (the subcoracoid tunnel) clinically, presentation depends on whether the compression involves only the vessels (vascular TOS), only the nerves (neurological TOS) or a combination of both (combined/neurovascular TOS): ■ neurological TOS is also referred to as cervical rib (and band) syndrome, and is almost always unilateral, occurring most commonly in women: – it presents as a chronic, lower trunk (C8–T1) plexopathy with wasting of the hand muscles and sensory disturbance along the medial arm/forearm with occasional extension into the hand and the medial fingers – symptoms are exacerbated by hyperabduction and external rotation of the arm – the commonest cause is a congenital fibrous band that extends from the first thoracic rib to a cervical rib/elongated C7 transverse process ■

●

MRI findings ●

distortion/displacement of the plexus by a cervical rib/band (Fig. 8.170a) has reported sensitivity and specificity of 79 per cent and 87.5 per cent, respectively, at conventional MRI in patients with clinical symptoms of TOS:190 ■ the affected plexus roots may appear slightly oedematous (Fig. 8.170b)

b a

c

d

Figure 8.170 Thoracic outlet syndrome. Neurologic: Sagittal T1-weighted (T1W) spin-echo (SE) image (a) showing a cervical rib (arrow). Coronal short tau inversion recovery image (b) showing mild hyperintensity of the left brachial plexus trunks (arrows) and the tip of the cervical rib (arrowhead). Vascular: Sagittal T1W SE images with the arm by the side (c) and the arm elevated (d) showing reduction of the costoclavicular space between the clavicle (white arrows) and the first rib (white arrowheads). The subclavian vein (black arrows) and artery (black arrowheads) are normal with the arms by the side, but are compressed with the arms elevated. (continued)

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h

Figure 8.170 (continued) Sagittal T1W SE image (e) showing measurement of the subclavius muscle (double-headed arrow). Sagittal T1W SE image (f) showing measurement of the retropectoralis minor space (double-headed arrow) deep to the pectoralis minor muscle (arrowhead) and containing the traversing axillary vessels and nerves (arrows). Coronal MR angiogram with the arms by the side (g) showing patent subclavian arteries (arrows) and with the arms elevated (h) showing occlusion of the right subclavian artery (arrow).

●

● ● ●

changes in the size and morphology of the thoracic outlet occur with arm hyperabduction and external rotation in both healthy volunteers and patients with TOS:197,198 ■ in TOS, there is a significant reduction of costoclavicular distance as measured on sagittal images (Fig. 8.170c, d), a significant increase in the width of the subclavius muscle bilaterally as measured on sagittal images (Fig. 8.170e), and a significant increase in retropectoralis minor space as measured on sagittal images (Fig. 8.170f) ■ compression of the subclavian vein is commonly seen in both volunteers and patients following arm elevation (Fig. 8.170c, d) ■ however, arterial (72 per cent) and neural (7 per cent) compression are seen only in TOS patients reduction of the costoclavicular space is also commonly seen in TOS with the arm in 90° abduction and the patient imaged in an open scanner199 vascular TOS can be demonstrated using MR angiography with the arms in adduction and abduction, the latter position showing stenosis or occlusion of the subclavian artery (Fig. 8.170g, h)200 compression of the BP and subclavian artery can also be caused by a hypertrophied scalenus anterior muscle, with/without hypertrophy of the scalenus medius (scalenus anticus syndrome)190

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Link TM, Haeussler MD, Poppek S et al. Malignant fibrous histiocytoma of bone: conventional X-ray and MR imaging features. Skeletal Radiol 1998; 27: 552–8. Parman LM, Murphey MD. Alphabet soup: cystic lesions of bone. Semin Musculoskelet Radiol 2000; 4: 89–101. Margau R, Babyn P, Cole W et al. MR imaging of simple bone cysts in children: not so simple. Pediatr Radiol 2000; 30: 551–7. Mahnken AH, Nolte-Ernsting CC, Wildberger JE et al. Aneurysmal bone cyst: value of MR imaging and conventional radiography. Eur Radiol 2003; 13: 1118–24. Maiya S, Davies M, Evans N, Grimer J. Surface aneurysmal bone cysts: a pictorial review. Eur Radiol 2002; 12: 99–108. Ilaslan H, Sundaram M, Unni KK. Solid variant of aneurysmal bone cysts in long tubular bones: giant cell reparative granuloma. AJR Am J Roentgenol 2003; 180: 1681–7. Murphy MD, Nomikos GC, Flemming DJ et al. Imaging of giant cell tumor and giant cell reparative granuloma of bone: radiologic–pathologic correlation. Radiographics 2001; 21: 1283–1309. Choi JJ, Murphey MD. Angiomatous skeletal lesions. Semin Musculoskelet Radiol 2000; 4: 103–12. Wenger DE, Wold LE. Benign vascular lesions of bone: radiologic and pathologic features. Skeletal Radiol 2000; 29: 63–74. Wenger DE, Wold LE. Malignant vascular lesions of bone: radiologic and pathologic features. Skeletal Radiol 2000; 29: 619–31. Kransdorf M, Smith SE. Lesions of unknown histogenesis: Langerhans cell histiocytosis and Ewing sarcoma. Semin Musculoskelet Radiol 2000; 4: 1123–6. Shapeero LG, Vanel D, Sundaram M et al. Periosteal Ewing sarcoma. Radiology 1994; 191: 825–31. Saifuddin A, Whelan J, Pringle JA, Cannon SR. Malignant round cell tumours of bone: atypical clinical and imaging features. Skeletal Radiol 2000; 29: 646–51. Mulligan M. Myeloma and lymphoma. Semin Musculoskelet Radiol 2000; 4: 127–35. Heyning FH, Kroon HM, Hogendoorn PC, Taminiau AH, van der Woude HJ. MR imaging characteristics in primary lymphoma of bone with emphasis on non-aggressive appearance. Skeletal Radiol 2007; 36: 937–44. Kirsch J, Haslan H, Bauer TW, Sundaram M. The incidence of imaging findings, and the distribution of skeletal lymphoma in a consecutive patient population seen over 5 years. Skeletal Radiol 2006; 35: 590–4. Campbell RS, Grainger AJ, Mangham DC, Beggs I, Teh J, Davies AM. Intraosseous lipoma: report of 35 new cases and a review of the literature. Skeletal Radiol 2003; 32: 209–22. Murphey MD, Carroll JF, Flemming DJ, Pope TL, Gannon FH, Kransdorf MJ. Benign musculoskeletal lipomatous lesions. Radiographics 2004; 24: 1433–66. Kransdorf MD, Murphey MD, Sweet DE. Liposclerosing myxofibrous tumour: a radiologic pathologic distinct fibro-osseous lesion of bone with a marked predilection for the intertrochanteric region of the femur. Radiology 1999; 212: 693–8. Azouz EM, Saigal G, Rodriguez MM, Podda A. Langerhans’ cell histiocytosis: pathology, imaging and treatment of skeletal involvement. Pediatr Radiol 2005; 35: 103–15. Van Der Woude HJ, Hazelbag HM, Bloem JL, Taminiau AH, Hogendoorn PC. MRI of adamantinoma of long bones in correlation with histopathology. AJR Am J Roentgenol 2004; 183: 1737–44. Choi JA, Lee KH, Jun WS et al. Osseous metastasis from renal cell carcinoma: ‘flow-void’ sign at MR imaging. Radiology 2003; 228: 629–34. Hwang S, Panicek DM. Magnetic resonance imaging of bone marrow in oncology, Part 1. Skeletal Radiol 2007; 36: 913–20. Tunaci M, Tunaci A, Engin G et al. Imaging features of thalassaemia. Eur Radiol 1999; 9: 1804–9. Ejindu VC, Hine AL, Mashayekhi M, Shorvon PJ, Misra RR. Musculoskeletal manifestations of sickle cell disease. Radiographics 2007; 27: 1005–21. Umans H, Haramati N, Flusser G. The diagnostic role of gadolinium enhanced MRI in distinguishing between acute medullary bone infarct and osteomyelitis. Magn Reson Imaging 2000; 18: 255–62. Guermazi A, De Kerviler E, Cazals-Hatem D, Zagdanski AM, Frija J. Imaging findings in patients with myelofibrosis. Eur Radiol 1999; 9: 1366–75. McHugh K, Olsen EOE, Vellodi A. Gaucher disease in children: radiology of non-central nervous system manifestations. Clin Radiol 2004; 59: 117–23. Vande Berg BC, Lecouvet FE, Michaux L, Ferrant A, Maldague B, Malghem J. Magnetic resonance imaging of the bone marrow in hematological malignancies. Eur Radiol 1998; 8: 1335–44.

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99 100 101 102 103 104 105 106 107 108 109 110 111 112 113 114 115 116 117 118 119 120

Roca M, Mota J, Giraldo P, Garcia Erce JA. Systemic mastocytosis: MRI of bone marrow involvement. Eur Radiol 1999; 9: 1094–7. Lecouvet FE, Vande Berg BC, Malghem J, Maldague BE. Magnetic resonance and computed tomography imaging in multiple myeloma. Semin Musculoskelet Radiol 2001; 5: 43–55. Angtuaco EJ, Fassas AB, Walker R, Sethi R, Barlogie B. Multiple myeloma: clinical review and diagnostic imaging. Radiology 2004; 231: 11–23. Saini A, Saifuddin A. MRI of osteonecrosis. Clin Radiol 2004; 59: 1079–93. Hermann G, Singson R, Bromley M, Klein MJ, Springfield D, Abdelwahab IF. Cystic degeneration of medullary bone infarction evaluated with magnetic resonance imaging correlated with pathologic examination. Can Assoc Radiol J 2004; 55: 321–5. Williams HJ, Davies AM. The effect of X-rays on bone: a pictorial review. Eur Radiol 2006; 16: 619–63. Sheppard DG, Libshitz HI. Post-radiation sarcomas: a review of the clinical and imaging features in 63 cases. Clin Radiol 2001; 56: 22–9. Smith SE, Murphey MD, Motamedi K, Mulligan ME, Resnick CS, Gannon FH. Radiologic spectrum of Paget disease of bone and its complications with pathological correlation. Radiographics 2002; 22: 1191–216. Whitten CR, Saifuddin A. MRI of Paget’s disease of bone. Clin Radiol 2003; 58: 763–9. Lopez C, Thomas DV, Davies AM. Neoplastic transformation and tumour-like lesions in Paget’s disease of bone: a pictorial review. Eur Radiol 2003; 13 Suppl 4: L151–63. Moore SL, Teirstein AE, Golimbu C. MRI of sarcoidosis patients with musculoskeletal symptoms. AJR Am J Roentgenol 2005; 185: 154–9. Chanchairujira K, Chung CB, Lai YM, Haghighi P, Resnick D. Intramedullary osteosclerosis: imaging features in nine patients. Radiology 2001; 220: 225–30. Judkiewicz AM, Murphey MD, Resnick CS, Newburg AH, Temple HH, Smith WS. Advanced imaging of melorheostosis with emphasis on MRI. Skeletal Radiol 2001; 30: 447–53. Elsayes KM, Lammie M, Shariff A, Totty WG, Habib IF, Rubin DA. Value of magnetic resonance imaging in muscle trauma. Curr Probl Diagn Radiol 2006; 35: 206–12. Yu JS, Habib PA. Common injuries related to weightlifting: MR imaging perspective. Semin Musculoskelet Radiol 2005; 9: 289–301. Koulouris G, Connell DA. Hamstring muscle complex: an imaging review. Radiographics 2005; 25: 571–86. Parikh J, Hyare H, Saifuddin A. The imaging features of post-traumatic myositis ossificans, with emphasis on MRI. Clin Radiol 2002; 57: 1058–66. Ledermann HP, Schweitzer ME, Morrison WB. Pelvic heterotopic ossification: MR imaging characteristics. Radiology 2002; 222: 189–95. Garcia J. MRI in inflammatory myopathies. Skeletal Radiol 2000; 29: 425–38. Struk DW, Munk PL, Lee MJ, Ho SG, Worsley DF. Imaging of soft tissue infections. Radiol Clin North Am 2001; 39: 277–303. Soler R, Rodriguez E, Aguilera C, Fernandez R. Magnetic resonance imaging of pyomyositis in 43 cases. Eur J Radiol 2000; 35: 59–64. Kim JY, Park HA, Choi KH, Park SH, Lee HY. MRI of tuberculous pyomyositis. J Comput Assist Tomogr 1999; 23: 454–7. Arslan A, Pierre-Jerome C, Borthne A. Necrotizing fasciitis: unreliable MRI findings in the preoperative diagnosis. Eur J Radiol 2000; 36: 139–43. Moulton SJ, Kransdorf MJ, Ginsberg WW, Abril A, Persellin S. Eosinophilic fasciitis: spectrum of MRI findings. AJR Am J Roentgenol 2005; 184: 975–8. Comert RB, Avdingoz U, Ucaner A, Arikan M. Water-lily sign on MR imaging of primary intramuscular hydatidosis of sartorius muscle. Skeletal Radiol 2003; 32: 420–3. Weatherall P. Imaging of muscle tumors. Semin Musculoskelet Radiol 2000; 4: 435–58. Kransdorf MJ, Murphey MD. Radiologic evaluation of soft-tissue masses: a current perspective. AJR Am J Roentgenol 2000; 175: 575–87. De Schepper AM, De Beuckeleer L, Vandevenne J, Somville J. Magnetic resonance imaging of soft tissue tumors. Eur Radiol 2000; 10: 213–23. Laor T. MR imaging of soft tissue tumors and tumor-like lesions. Pediatr Radiol 2004; 34: 24–37. Galant J, Marti-Bonmati L, Soler R et al. Grading of subcutaneous soft tissue tumours by means of their relationship with the superficial fascia on MR imaging. Skeletal Radiol 1998; 27: 657–63.

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121 Harish S, Lee JC, Ahmad M, Saifuddin A. Soft tissue masses with ‘cyst-like’ appearance on MR imaging: distinction of benign and malignant lesions. Eur Radiol 2006; 16: 2652–60. 122 Vilanova JC, Woertler K, Narváez JA et al. Soft-tissue tumours update: MR imaging features according to the WHO classification. Eur Radiol 2007; 17: 125–38. 123 Bancroft LW, Kransdorf MJ, Peterson JJ, O’Connor MI. Benign fatty tumors: classification, clinical course, imaging appearance, and treatment. Skeletal Radiol 2006; 35: 719–33. 124 Ritchie DA, Aniq H, Davies AM, Mangham DC, Helliwell TR. Hibernoma-correlation of histopathology and magnetic-resonance-imaging features in 10 cases. Skeletal Radiol 2006; 35: 579–89. 125 Murphey MD, Arcara LK, Fanburg-Smith J. Imaging of musculoskeletal liposarcoma with radiologic– pathologic corelation. Radiographics 2005; 25: 1371–95. 126 Dinauer PA, Brixey CJ, Moncur JT, Fanburg-Smith JC, Murphey MD, Pathologic and MR imaging features of benign fibrous soft-tissue tumors in adults. Radiographics 2007; 27: 173–87. 127 Leung LY, Shu SJ, Chan AC, Chan MK, Chan CH. Nodular fasciitis: MRI appearance and literature review. Skeletal Radiol 2002; 31: 9–13. 128 Malghem J, Baudrez V, Lecouvet F, Lebon C, Maldague B, Van de Berg B. Imaging study findings in elastofibroma dorsi. Joint Bone Spine 2004; 71: 536–41. 129 Koujok K, Ruiz RE, Hernandez RJ. Myofibromatosis: imaging characteristics. Paediatr Radiol 2005; 35: 374–80. 130 Robbin MR, Murphey MD, Temple T, Kransdorf MJ, Choi JJ. Imaging of musculoskeletal fibromatosis. Radiographics 2001; 21: 585–600. 131 Fox MG, Kransdorf MJ, Bancroft LW, Peterson JJ, Flemming DJ. MR imaging of fibroma of the tendon sheath. AJR Am J Roentgenol 2003; 180: 1449–53. 132 Tanaka H, Harasawa A, Furui S. Usefulness of MR imaging in assessment of tumour extent of aggressive fibromatosis. Radiat Med 2005; 23: 111–15. 133 Lee JC, Thomas JM, Phillips S, Fisher C, Moskovic E. Aggressive fibromatosis: MRI features with pathologic correlation. AJR Am J Roentgenol 2006; 186: 247–54. 134 Vilanova JC, Barcelo J, Smirniotopoulos J et al. Hemangioma from head to toe: MR imaging with pathologic correlation. Radiographics 2004; 24: 367–85. 135 Koh SH, Choe HS, Lee IJ, Park HR, Bae SH. Low-grade fibromyxoid sarcoma: ultrasound and magnetic resonance findings in two cases. Skeletal Radiol 2005; 34: 550–4. 136 Ramesh P, Annapureddy SR, Khan F, Sutaria PD. Angioleiomyoma: a clinical, pathological and radiological review. Int J Clin Pract 2004; 58: 587–91. 137 Misumi S, Irie T, Fukuda K, Tada S, Hosomura Y. A case of deep soft tissue leiomyoma: CT and MRI findings. Radiat Med 2000; 18: 253–6. 138 Pilavaki M, Drevelegas A, Nenopoulos H et al. Foci of decreased signal on T2-weighted MR images in leiomyosarcoma of soft tissue: correlation between MR and histological findings. Eur J Radiol 2004; 51: 279–85. 139 Park EA, Hong SH, Choi JY, Lee MW, Kang HS. Glomangiomatosis: magnetic resonance imaging findings in three cases. Skeletal Radiol 2005; 34: 108–11. 140 Teo EL, Strouse PJ, Hernandez RJ. MR imaging differentiation of soft-tissue hemangiomas from malignant soft-tissue masses. AJR Am J Roentgenol 2000; 174: 1623–8. 141 Vilanova JC, Barcelo J, Villalon M. MR and MR angiography characterization of soft tissue vascular malformations. Curr Probl Diagn Radiol 2004; 33: 161–70. 142 Fayad L, Hazirolan T, Bleumke D, Mitchell S. Vascular malformations in the extremities: emphasis on MR imaging features that guide treatment options. Skeletal Radiol 2006; 35: 127–37. 143 Hondar WHT, Chen W, Lee O, Chang CY. Imaging and pathological correlation of soft-tissue chondroma: a serial five-case study and literature review. Clin Imaging 2006; 30: 32–6. 144 Kajihara M, Sugawara Y, Hirata M et al. Extraskeletal osteosarcoma in the thigh: a case report. Radiat Med 2005; 23: 142–6. 145 Murphey MD, Mcrae GA, Fanburg-Smith JC, Temple HT, Levine AM, Aboulafia AJ. Imaging of soft tissue myxoma with emphasis on CT and MR and comparison of radiologic and pathologic findings. Radiology 2002; 225: 215–24. 146 Luna A, Martinez S, Bossen E. Magnetic resonance imaging of intramuscular myxoma with histological comparison and a review of the literature. Skeletal Radiol 2005; 34: 19–28. 147 Blacksin MF, Siegel JR, Benevenia J, Aisner SC. Synovial sarcoma: frequency of non-aggressive MR characteristics. J Comput Assist Tomogr 1997; 21: 785–9.

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148 Valenzuela RF, Kim EE, Seo JG, Patel S, Yasko AW. A revisit for MRI analaysis for synovial sarcoma. Clin Imaging 2000; 24: 231–5. 149 Nakanishi H, Araki N, Sawai Y. Cystic synovial sarcomas: imaging features with clinical and histopathological correlation. Skeletal Radiol 2003; 32: 701–7. 150 Tateishi U, Hasegawa T, Beppu Y, Satake M, Moriyama N. Synovial sarcoma of the soft tissues: prognostic significance of imaging features. J Comput Assist Tomogr 2004; 28: 140–8. 151 Hanna SL, Kaste S, Jenkins JJ et al. Epithelioid sarcoma: clinical, MR imaging and pathological findings. Skeletal Radiol 2002; 31: 400–12. 152 Suh JS, Cho J, Lee SH et al. Alveolar soft part sarcoma: MR and angiographic findings. Skeletal Radiol 2000; 29: 680–9. 153 De Beuckeleer LH, De Schepper AM, Vandevenne JE et al. MR imaging of clear cell sarcoma (malignant melanoma of the soft parts): a multicenter correlative MRI–pathology study of 21 cases and literature review. Skeletal Radiol 2000; 29: 187–95. 154 Beggs I. Primary muscle lymphoma. Clin Radiol 1997; 52: 203–12. 155 Ruzek KA, Wenger DE. The multiple faces of lymphoma of the musculoskeletal system. Skeletal Radiol 2004; 33: 1–8. 156 Beggs I, Saifuddin A, Limb D. Non-communicating intramuscular ganglia. Eur Radiol 1998; 8: 1657–61. 157 Chung S, Frush DP, Prose NS, Shea CR, Laor T, Bisset GS. Subcutaneous granuloma annulare: MR imaging features in six children and literature review. Radiology 1999; 210: 845–9. 158 Torreggiani WC, Al-Ismail K, Munk PL, Nicolaou S, O’Connell JX, Knowling MA. Dermatofibrosarcoma protruberans: MR imaging features. AJR Am J Roentgenol 2002; 178: 989–93. 159 Shibata T, Hatori M, Satoh T, Ehara S, Kokubun S. Magnetic resonance imaging features of epidermoid cyst in the extremities. Arch Orthop Trauma Surg 2003; 123: 239–41. 160 Chan LP, Gee R, Keogh C, Munk PL. Imaging features of fat necrosis. AJR Am J Roentgenol 2003; 181: 955–9. 161 Kransdorf MJ, Murphey MD. Soft tissue tumors: post-treatment imaging. Radiol Clin North Am 2006; 44: 463–72. 162 Davies AM, Hall AD, Strouhal PD, Evans N, Grimer RJ. The MR imaging appearances and natural history of seromas following excision of soft tissue tumours. Eur Radiol 2004; 14: 1196–202. 163 May DA, Disler D, Jones EA, Balkissoon AA, Manaster BJ. Abnormal signal intensity in skeletal muscle at MR imaging: patterns, pearls and pitfalls. Radiographics 2000; 20: S295–315. 164 Llauger J, Bague S, Palmer J, Matias-Guiu X, San Roman L, Doncel A. Focal myositis of the thigh: unusual MR pattern. Skeletal Radiol 2002; 31: 307–10. 165 Gobbele R, Schoen SW, Schroder JM, Vorwerk D, Schwarz M. S-1 radiculopathy as a possible predisposing factor in focal myositis with unilatyeral hypertrophy of the calf muscles. J Neurol Sci 1999; 170: 64–8. 166 Trujillo-Santos AJ. Diabetic muscle infarction. Diabetes Care 2003; 26: 211–15. 167 Kattapuram TM, Suri R, Rosol MS, Rosenberg AE, Kattapuram SV. Idiopathic and diabetic skeletal muscle necrosis: evaluation by magnetic resonance imaging. Skeletal Radiol 2005; 34: 203–9. 168 Dhillon M, Davies AM, Benham J, Evans N, Mangham DC, Grimer RJ. Calcific myonecrosis: a report of ten new cases with an emphasis on MR imaging. Eur Radiol 2004; 14: 1974–9. 169 O’Dwyer HM, Al-Nakshabandi NA, Al-Muzhami K, Ryan A, O’Connell JX, Munk PL. Calcific myonecrosis: keys to recognition and management. AJR Am J Roentgenol 2006; 187: W67–76. 170 Bendszus M, Wessig C, Reiners K, Bartsch AJ, Solymosi L, Koltzenberg M. MR imaging in the differential diagnosis of neurogenic foot drop. AJNR Am J Neuroradiol 2003; 24: 1283–9. 171 Kim S, Choi J-Y, Huh Y-M et al. Role of magnetic resonance imaging in entrapment and compressive neuropathy: what, where, and how to see the peripheral nerves on the musculoskeletal magnetic resonance image. Part 1. Overview and lower extremity. Eur Radiol 2007; 17: 139–49. 172 Kim S, Choi J-Y, Huh Y-M et al. Role of magnetic resonance imaging in entrapment and compressive neuropathy: what, where, and how to see the peripheral nerves on the musculoskeletal magnetic resonance image. Part 2. Upper extremity. Eur Radiol 2007; 17: 509–22. 173 Grainger AJ, Campbell RSD, Stothard J. Anterior interosseous nerve syndrome: appearances at MR imaging in three cases. Radiology 1998; 208: 381–4. 174 Murphey MD, Smith WS, Smith SE, Kransdorf MJ, Temple HT. Imaging of musculoskeletal neurogenic tumours: radiologic–pathologic correlation. Radiographics 1999; 19: 1253–80.

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175 Pilavaki M, Chourmouzi D, Kiziridou A, Skordalaki A, Zarampoukas T, Drevelengas A. Imaging of peripheral nerve sheath tumours with pathologic correlation: pictorial review. Eur J Radiol 2004; 52: 229–39. 176 Maccollin M, Chiocca EA, Evans DG et al. Diagnostic criteria for schwannomatosis. Neurology 2005; 64: 1838–45. 177 Isobe K, Shimizu T, Akahane T, Kato H. Imaging of ancient schwannoma. AJR Am J Roentgenol 2004; 183: 331–6. 178 Jee WH, Oh SN, Mccauley T et al. Extraaxial neurofibromas versus neurilemmomas: discrimination with MRI. AJR Am J Roentgenol 2004; 183: 629–33. 179 Yamamoto T, Maruyama S, Mizuno K. Schwannomatosis of the sciatic nerve. Skeletal Radiol 2001; 30: 109–13. 180 Huang GS, Huang CW, Lee HS et al. On the AJR viewbox. Diffuse neurofibroma of the arm: MR characteristics. AJR Am J Roentgenol 2005; 184: 1711–12. 181 Hourani R, Rizk T, Kung S, Boudghene F. Elephantiasis neuromatosa in neurofibromatis type I. MRI findings with review of the literature. J Neuroradiol 2006; 33: 62–6. 182 Hornick JL, Fletcher CD. Soft tissue perineurioma: clinicopathologic analysis of 81 cases including those with atypical histologic features. Am J Surg Pathol 2005; 29: 845–58. 183 Van Herendael BH, Heyman SRG, Vanheonacker FM et al. The value of magnetic resonance imaging in the differentiation between malignant peripheral nerve sheath tumors and non-neurogenic soft-tissue tumors. Skeletal Radiol 2006; 35: 745–53. 184 Uetani M, Hashmi R, Hayashi K, Nagatani Y, Narabayashi Y, Imamaura K. Peripheral nerve intraneural ganglion cyst: MR findings in three cases. J Comput Assist Tomogr 1998; 22: 629–32. 185 Spinner RJ, Amrami KK, Rock MG. The use of MR arthrography to document an occult joint communication in a recurrent peroneal intraneural ganglion. Skeletal Radiol 2006; 35: 172–9. 186 Golan JD, Jacques L. Non-neoplastic peripheral nerve tumors. Neurosurg Clin North Am 2004; 15: 223–30. 187 Moore KR, Tsuruda JS, Dailey AT. The value of MR neurography for evaluating extraspinal neuropathic leg pain. AJNR Am J Neuroradiol 2001; 22: 786–94. 188 Perez-Lopez C, Gutierrez M, Isla A. Inflammatory pseudotumour of the median nerve. J Neurosurg 2001; 95: 124–8. 189 Todd M, Shah GV, Mukherji SK. MR imaging of brachial plexus. Top Magn Reson Imaging 2004; 15: 113–25. 190 Bowen BC, Pattany PM, Saraf-Lavi E, Maravilla KR. The brachial plexus: normal anatomy, pathology and MR imaging. Neuroimag Clin North Am 2004; 14: 59–85. 191 Tavakkolizadeh A, Saifuddin A, Birch R. Imaging of adult brachial plexus traction injuries. J Hand Surg [Br] 2001; 26-B: 183–91. 192 Rankine JJ. Adult traumatic brachial plexus injury. Clin Radiol 2004; 59: 767–74. 193 Doi K, Otsuka K, Okamoto Y, Fujii H, Hattori Y, Baliarsing AS. Cervical nerve root avulsion in brachial plexus injuries: magnetic resonance imaging classification and comparison with myelography and computerized tomography myelography. J Neurosurg (Spine) 2002; 96: 277–84. 194 Hayashi N, Masumoto T, Abe O, Aoki S, Ohmoto K, Tajiri Y. Accuracy of abnormal paraspinal muscle findings on contrast-enhanced MR images as indirect signs of unilateral cervical root-avulsion injury. Radiology 2002; 223: 397–402. 195 Saifuddin A. Imaging tumours of the brachial plexus. Skeletal Radiol 2003; 32: 375–87. 196 Wittenberg KH, Adkins MC. MR imaging of nontraumatic brachial plexopathies: frequency and spectrum of findings. Radiographics 2000; 20: 1023–32. 197 Demondion X, Herbinet P, Van Sint Jan S, Boutry N, Chantelot C, Cotten A. Imaging assessment of thoracic outlet syndrome. Radiographics 2006; 26: 1735–50. 198 Demondion X, Bacqueville E, Paul C, Duquesnoy B, Hachulla E, Cotten A. Thoracic outlet: assessment with MR imaging in asymptomatic and symptomatic populations. Radiology 2003; 227: 461–8. 199 Smedby O, Rostad H, Klaastad O, Lilleas F, Tillung T, Fosse E. Functional imaging of the thoracic outlet syndrome in an open MR scanner. Eur Radiol 2000; 10: 597–600. 200 Charon JP, Milne W, Sheppard DG, Houston JG. Evaluation of MR angiographic technique in the assessment of thoracic outlet syndrome. Clin Radiol 2004; 59: 588–95.

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9 The spine

TECHNIQUE Conventional MRI1,2 ●

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in the routine assessment of degenerative disc disease: ■ sagittal T1-weighted (T1W) spin-echo (SE) and T2-weighted (T2W) fast spin-echo (FSE) images are used for assessment of disc degeneration, prolapse, dural sac compression and reactive marrow changes ■ in the cervical region, T2*-weighted (T2*W) gradient-echo (GE) images are the preferred axial sequence3 ■ in the lumbar region, T2W FSE images with/without additional T1W SE images are most commonly used ■ axial slices may be planned from a sagittal scout and limited to each disc level (Fig. 9.1a) or may be planned as a block to cover pedicle to pedicle (Fig. 9.1b): – the latter technique has the advantage of demonstrating the complete course of the nerve root from the dura to the extraforaminal region ■ the use of coronal/coronal oblique imaging planes (Fig. 9.1c, d) has been described for the assessment of extraforaminal stenosis in the lumbar region in patients with lumbosacral transitional anomalies4 ■ the sagittal oblique plane has also been described for the assessment of cervical foraminal stenosis5 in the assessment of marrow disease:6 ■ the addition of a sagittal short tau inversion recovery (STIR) or fat-suppressed (FS) T2W FSE image is valuable since marrow infiltration/oedema may be subtle on T1W images and missed on T2W FSE images (Fig. 9.1e–g) ■ the STIR sequence has reported positive predictive value and negative predictive value for the detection of vertebral bone marrow abnormalities of 99.3 per cent and 95.9 per cent, respectively7 the role of contrast medium: ■ in the presence of a normal STIR sequence, the addition of a contrast-enhanced T1W SE sequence adds no new information, whereas in the presence of an abnormal STIR image the addition of contrast-enhanced T1W images may be of use7

Additional sequences ●

fast T1W fluid-attenuated inversion recovery (FLAIR) sequence:8 ■ compared with conventional T1W turbo SE imaging, the FLAIR sequence improves cerebrospinal fluid (CSF) nulling and therefore improves the contrast between the disc margins and the CSF and between the conus medullaris and the CSF, while still demonstrating reactive marrow changes

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c

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d

Figure 9.1 Imaging techniques. Sagittal T2-weighted (T2W) fast spin-echo (FSE) image (a) showing the technique of taking axial images limited to the disc space. Sagittal T1-weighted (T1W) spin-echo (SE) image (b) showing the technique of planning axial images from pedicle to pedicle. Sagittal T2W FSE images showing the planes for coronal (c) and coronal oblique (d) imaging of the lumbar spine. (continued)

Technique

e

g

f

Figure 9.1 (continued) Use of fat suppression for assessment of marrow disease: Sagittal T1W SE (e), T2W FSE (f) and T2W FSE fat-suppressed (FS) (g) images in a patient with multiple myeloma. All sequences demonstrate pathological collapse of T11 (arrows), though marrow signal intensity is unaltered on T2W FSE (f). The T2W FSE FS image (g) demonstrates additional small lesions (arrowheads). ●

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diffusion-weighted imaging6,9 is a functional imaging technique that is sensitive to the microscopic motion of water protons: ■ applications in spinal imaging include differentiation of benign from pathological collapse; osteoporotic fractures appear hypointense compared with normal marrow, whereas pathological fractures appear hyperintense chemical shift imaging,10 also termed ‘in-phase and out-of-phase’ or ‘opposed-phased’ imaging, may be of value in differentiating normal marrow and benign lesions from malignant marrow infiltration, as normal marrow/benign marrow lesions exhibit a much greater reduction of marrow signal intensity (SI) on out-of-phase imaging compared with in-phase imaging

MR myelography11–13 ● ● ●

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MR myelography is a heavily T2W MR sequence in which the SI is produced mainly from water with minimisation of signal from adjacent solid non-water structures, such as the discs and vertebral bodies various MRI techniques are available, which produce a myelogram-like image that can be viewed in anteroposterior (AP), oblique and lateral imaging planes (Fig. 9.2a, b) recently reported techniques include: ■ a single-slice technique using a single-shot turbo SE sequence11 ■ a heavily T2W half-Fourier single-shot fast SE-type sequence12 ■ multi-shot turbo-SE T2W sequences13 MR myelography can demonstrate various intra- and extradural pathologies, including:11 ■ normal variants such as conjoined nerve roots ■ congenital anomalies such as a tethered cord or syrinx ■ post-traumatic conditions such as pseudomeningocele (Fig. 9.2c) ■ post-treatment complications such as arachnoiditis ■ pathological conditions including intraspinal tumours, dural arteriovenous malformations and extradural compression from vertebral tumours: – extradural filling defects due to disc prolapse or from spinal stenosis (Fig. 9.2d)

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b

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d Figure 9.2 MR myelography. Anteroposterior (AP) projections of a lumbar MR myelogram (a, b) showing the conus medullaris (arrow a), the roots of the cauda equina (arrowhead b) and the nerve root sheaths (arrows b). AP projection of a cervical MR myelogram (c) showing bilateral post-traumatic pseudomeningoceles (arrows). AP projection of lumbar MR myelogram (d) showing degenerative scoliosis and multi-level central canal stenosis (arrows).

Technique

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clinical utility: for the assessment of cauda equina and nerve root compression due to disc prolapse or spinal stenosis, routine use of MR myelography has not been found to be essential for establishing a diagnosis compared with conventional sagittal and axial MRI:12 ■ for the assessment of vertebral end-plates (VEPs) and intervertebral discs (IVDs), MR myelography can demonstrate disc degeneration and may be more sensitive than conventional MRI for showing disc and end-plate oedema13

Positional MRI/upright weight-bearing MRI14–16 ●

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conventional spinal MRI is performed in the supine position without axial load, and also with hip/knee flexion, reducing lumbar lordosis: ■ these factors result in optimisation of spinal canal dimensions, potentially missing dynamic spinal canal stenosis or nerve root compression ■ cadaver and myelographic studies have indicated that there can be clinically significant changes in spinal canal/foraminal dimensions and nerve root compression with axial loading, flexion/extension and lateral rotation upright, weight-bearing MRI requires a vertical open-configuration MR system which allows sitting/standing images of the whole spine to be obtained in the sagittal and axial planes and also with flexion, extension and lateral rotation both the cervical15,16 and the lumbar14,15 regions can be assessed weight-bearing MRI of the lumbar spine results in reduction of both central canal dimensions and foraminal dimensions in healthy individuals that is maximal in the weight-bearing, extended position: ■ these changes are mainly related to an increase in posterior disc bulging and in the thickness of the ligamentum flavum (LF), due to buckling during spinal extension changes identified on vertical weight-bearing spinal MRI include: ■ reduced spinal height, termed ‘spinal column telescoping’ due to loss of disc height at degenerate disc levels (Fig. 9.3a, b) ■ decrease in central canal (Fig. 9.3c, d), lateral recess and foraminal dimensions (Fig. 9.3e, f) that are most marked with spinal hyperextension ■ increase in size of posterior disc protrusions (Fig. 9.3g, h) and dynamic spondylolisthesis (Fig. 9.3c, d)

Axial loaded MRI of the lumbar spine ●

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axial loaded MRI of the lumbar spine14,17 allows simulated upright MRI in the supine position within a conventional closed-configuration MR system: ■ the use of an MR-compatible compression device (Dynawell; DynaWell Int. AB, Billdal, Sweden) that produces axial load between the shoulders and the feet simulates axial loading ■ the technique involves standard MR imaging of the lumbar spine with sagittal and axial T1W and T2W FSE sequences, which are repeated following compression to 50 per cent body-weight for 5 minutes with the addition of lumbar extension using a small pad placed under the lumbar spine ■ this technique results in increased lumbar lordosis (Fig. 9.4a, b) and reduction of dural cross-sectional area owing to a combination of increased disc bulging, flaval thickening and change in morphology of the posterior epidural fat pad (Fig. 9.4c, d) ■ axial loaded MRI of the lumbar spine has been shown to demonstrate occult central spinal (Fig. 9.4e, f) and lateral recess stenosis (Fig. 9.4g, h), the development of lumbar high-intensity zones (HIZs) not identified on standard MRI18 and occult dynamic degenerative spondylolisthesis19 ■ however, demonstration of a disc prolapse not seen on conventional MRI is very unlikely ■ it also has a demonstrable effect on clinical decision-making in patients with lumbar radiculopathy20 cervical spine:21 loading of the cervical spine results in increased cervical lordosis and narrowing of the central canal

MR discography22 ●

gadolinium may be used as a discographic contrast agent since it is radio-opaque; subsequent MR imaging provides an MR discogram

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Figure 9.3 Upright/positional MRI. Sagittal T2-weighted (T2W) fast spin-echo (FSE) images in the supine (a) and erect (b) positions showing reduction of disc height at L4–5 and L5–S1 (arrows) in the erect position. Sagittal T2W FSE images in the erect flexed (c) and extended (d) positions showing reduced central canal dimensions at L3–4 (arrowheads) and dynamic degenerative spondylolisthesis at L4–5 (arrows). (continued)

Technique

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Figure 9.3 (continued) Sagittal T2W FSE images in the erect flexed (e) and extended (f) positions showing reduction of L4–5 foraminal dimensions in extension (arrows) with subsequent L4 root compression. T2W FSE images in the supine (g) and erect (h) positions showing accentuation of L5–S1 disc prolapse (arrows) in the erect position (h).

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advantages include its use in patients with allergy to iodinated contrast agents and the reduction of radiation exposure compared with CT discography following conventional disc injection under fluoroscopic control, sagittal (Fig. 9.5a) and axial (Fig. 9.5b, c) T1W SE images are obtained the technique has been shown to be equivalent to CT discography for the demonstration of disc normality, disc degeneration, annular fissure, disc herniation and contrast leakage

The post-operative spine23 ●

reduction of hardware artefacts:24 ■ increasing use of metallic implants in spinal surgery may pose problems for post-operative imaging, which was particularly the case when stainless steel was used for the manufacture of implants ■ currently, titanium is the most commonly used metal for spinal implants and has a much reduced magnetic susceptibility effect compared with steel

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Figure 9.4 Axial loaded MRI. Sagittal T2-weighted (T2W) fast spin-echo (FSE) images in the supine (a) and supine loaded (b) condition showing an increase in lumbar lordosis with axial loading (b). Axial T2W FSE images in the supine (c) and supine loaded (d) positions showing a reduction in dural cross-sectional area (arrows) on axial loading (d) and change in morphology of the posterior epidural fat pad (arrowheads). Sagittal T2W FSE images in the supine (e) and supine loaded (f) positions showing the development of central canal stenosis at L3–4 and L4–5 (arrows) on axial loading (f). Axial T2W FSE images in the supine (g) and supine loaded (h) positions showing the development of bilateral L5 root compression due to dynamic lateral recess stenosis (arrows) mainly as the result of increased flaval thickening (arrowheads).

Technique

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a Figure 9.5 MR discography. Sagittal (a) and axial (b, c) T1weighted spin-echo images showing hypointense contrast within the L4–5 and L5–S1 discs (arrows), the former showing normal morphology (arrow b) and the latter showing nuclear c degeneration (arrow c).

■ ■

MRI does not result in clinically significant hardware migration or heating reduction of implant-induced MR artefact is multifactorial and dependent on factors such as: – field strength: the degree of implant-related artefact increases with increasing field strength – the type of sequence selected: turbo/fast SE sequences result in less artefact than conventional SE sequences, while marked magnetic susceptibility artefact is associated with GE sequences, owing to the absence of a 180° refocusing pulse – echo time (TE): shorter TE sequences (T1W SE/proton density-weighted [PDW]) are associated with less artefact than long TE sequences (T2W/STIR) – number of pixels in the frequency-encoding direction (Nx) and field of view (FOV): artefact is dependent on the FOV to Nx ratio (FOV/Nx) and decreasing this ratio decreases artefact – artefact along the slice select direction is reduced with thicker sections – orientation of the frequency-encoding gradient: artefact is greatest along the direction of the frequency-encoding axis – orientation of the implant to the main magnetic field (Bo): artefact is greatest if the implant is orientated parallel to Bo

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THE CRANIOCERVICAL JUNCTION NORMAL ANATOMY The bones and joints25–28 ●

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the craniocervical junction refers to the occiput, the atlas (C1), the axis (C2), the respective joints between these bones and the supporting ligaments: ■ these bony and ligamentous structures provide protection for the cervicomedullary junction, the upper cervical spinal cord and the upper cranial nerves the atlanto-occipital joints are synovial joints (Fig. 9.6a, b) formed by the articulation between the occipital condyles, which project from the inferior aspect of the occiput at the anterolateral margin of the foramen magnum, and the concave superior articular surfaces of the lateral masses of the atlas: ■ these joints are shallower in children, accounting for the greater incidence of atlanto-occipital injuries in the paediatric population ■ asymmetry between the left and right joints may be seen in ~60 per cent of asymptomatic individuals29 ■ the atlanto-occipital joint axis angle is formed by lines drawn parallel to the joints, which typically intersect at the centre of the odontoid process when the condyles are symmetrical (Fig. 9.6c): – the mean angle is 125° with a range of 124–127°, the angle becoming more obtuse in the presence of occipital condylar hypoplasia the atlas is a bony ring formed by three primary ossification sites, the anterior arch and two neural arches; the latter fuse with the anterior arch by 7 years of age and they fuse to each other posteriorly to form the posterior arch by 3 years of age: ■ failure of anterior or posterior fusion may occur, resulting in normal variants that may mimic fractures

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Figure 9.6 Normal anatomy of the atlanto-occipital joints. Sagittal (a) and coronal (b) proton density-weighted (PDW) fast spin-echo (FSE) images showing the joints (white arrows) formed by articulation between the occipital condyle (arrowheads) and the lateral mass of C1 (black arrows). Coronal PDW FSE image (c) showing the atlanto-occipital joint axis angle.

The craniocervical junction

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the fully formed atlas comprises two lateral masses (Fig. 9.6a, b) attached by anterior and posterior arches the anterior tubercle (Fig. 9.7a, b) located in the midline on the anterior arch, serves as an attachment site for the anterior longitudinal ligament (ALL) and longus colli muscles the posterior tubercle (Fig. 9.7a, c) serves as an attachment site for the ligamentum nuchae the vertebral artery passes over a groove in the superior aspect of the posterior arch before entering the foramen magnum (Fig. 9.7c)

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Figure 9.7 Normal anatomy of the atlas (C1). Sagittal proton density-weighted (PDW) fast spin-echo (FSE) image (a) showing the anterior (arrow) and posterior (arrowhead) tubercles. Axial PDW FSE image (b) showing the anterior tubercle (arrow) and the anterior arch (arrowheads). Axial PDW FSE image (c) showing the posterior tubercle (arrow), the posterior arch (arrowheads) and the vertebral artery (double arrowhead) as it enters the spinal canal.

the axis is formed from four primary ossification centres, one for each neural arch, one for the body and one for the odontoid process: ■ a secondary ossification centre forms at the tip of the odontoid (os terminale) at 3–6 years of age and fuses to the dens by 12 years ■ the odontoid fuses to the body by 3–6 years of age; the line of fusion may be seen on sagittal MRI as the subdental synchondrosis (Fig. 9.8a) and should not be mistaken for a fracture ■ the two neural arches fuse posteriorly by 2–3 years of age and with the body by 3–6 years ■ the fully formed axis comprises the odontoid process (dens) (Fig. 9.8a–c), the body (Fig. 9.8a, d), the lateral masses (Fig. 9.8d) for articulation with the axis superiorly (Fig. 9.8b) and C3 inferiorly, the pedicles and a commonly bifid, large spinous process (Fig. 9.8e): – the dens normally lies centrally between the lateral masses of C1, but is deviated to the left or right side in ~12–14 per cent of asymptomatic individuals29 the atlanto-axial joints30 comprise four synovial articulations: ■ two lateral joints: formed between the lateral masses of C1 and C2 and surrounded by a synoviumlined fibrous capsule (Fig. 9.9a, b) ■ two median joints: an anterior articulation between the dens and the anterior arch of the atlas (Fig. 9.9c, d), which has a synovium-lined fibrous capsule, and a posterior joint between the dens and the transverse atlantal ligament (Fig. 9.9c, d)

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Figure 9.8 Normal anatomy of the axis (C2). Sagittal T1-weighted spin-echo image (a) showing a transverse hypointense line (arrow) representing the persistent synchondrosis. Coronal (b) and axial (c) proton density-weighted (PDW) fast spin-echo (FSE) images showing the odontoid peg (white arrows b, c), the lateral masses (black arrows b) and the atlanto-axial joints (arrowheads b). Axial PDW FSE image (d) showing the body (arrow) and the lateral masses (arrowheads). Axial PDW FSE image (e) showing the laminae (arrows) and the bifid spinous process (arrowhead).

asymmetry of the C1–2 facets29 may be seen in ~50 per cent of asymptomatic individuals and a small amount of fluid may be seen in the joint in ~50 per cent of cases following intravenous contrast administration,30 enhancement can be seen in the lateral joints in 100 per cent and around the dens (median joints) in ~50 per cent of asymptomatic individuals: – the enhancement may be punctuate, confluent or band-like in children, pseudo-spread of the lateral masses of the atlas on those of the axis by up to 6 mm may be seen on coronal MR images to the age of 7 years, mimicking a Jefferson fracture28 in children, overriding of the anterior arch of the atlas on the odontoid can be seen in extension in up to 20 per cent of cases

The craniocervical junction

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c Figure 9.9 Normal anatomy of the atlanto-axial joints. Sagittal (a) and coronal (b) proton density-weighted (PDW) fast spin-echo (FSE) images showing the lateral joints (arrows). Sagittal (c) and axial (d) PDW FSE images showing the anterior (arrows) and posterior (arrowheads) median joints.

The craniocervical junction ligaments26,27 ● ● ●

the craniocervical junction ligaments can be subdivided into intrinsic and extrinsic the extrinsic ligaments include the ligamentum nuchae, which extends from the external occipital protuberance to the posterior aspect of the atlas and the cervical spinous processes the intrinsic ligaments are located within the spinal canal and provide most of the ligamentous stability, forming three layers anterior to the dura: ■ from dorsal to ventral, they include the tectorial membrane, the cruciate ligament and the odontoid ligaments ■ the tectorial membrane is the cephalad extension of the posterior longitudinal ligament (PLL) and connects the posterior body of the axis to the posterior cortex of the clivus, just above the anterior margin of the foramen magnum (the basion): – it is seen as a thin, hypointense line on sagittal (Fig. 9.10a) and axial (Fig. 9.10b) MR images and is inseparable from the anterior dura ■ the cruciate ligament is located between the tectorial membrane and the odontoid process and comprises various structures: – the transverse atlantal ligament is the strongest component, connecting the posterior odontoid to the inner margin of the anterior arch of the atlas/lateral masses, and is well demonstrated on a combination of axial (Fig. 9.10c) and coronal (Fig. 9.10d) MR images:31 – superior and inferior vertical bands extend from the transverse ligament to the foramen magnum and the body of the axis, respectively, but cannot be differentiated at MRI from the tectorial membrane31

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Figure 9.10 Normal anatomy of the craniocervical ligaments. Sagittal proton density-weighted (PDW) fast spin-echo (FSE) (a) and axial T2*-weighted (T2*W) gradient-echo (GE) (b) images showing the tectorial membrane (arrows) inserting into the clivus (double arrowhead a) as an extension of the posterior longitudinal ligament (arrowheads a). Axial T2*W GE (c) and coronal PDW FSE (d) images showing the transverse atlantal ligament (arrows) running behind the dens to the lateral masses of the atlas (arrowheads). Coronal PDW FSE image (e) showing the alar ligaments (arrows) extending from the dens to the occipital condyles (arrowheads). Sagittal T2-weighted FSE image (f) showing the apical ligament (arrow). Sagittal PDW FSE image (g) showing the posterior atlanto-occipital membrane (white arrow) extending between the posterior arch of the atlas (black arrow) and the opisthion (arrowhead).

The craniocervical junction

the odontoid ligaments comprise alar and apical ligaments; the paired alar ligaments connect the lateral aspect of the odontoid process to the medial border of the occipital condyles (Fig. 9.10e), while the relatively weak apical ligament runs between the tip of the odontoid and the basion (Fig. 9.10f): – the alar ligaments are demonstrated in ~80–100 per cent of MR images, being visualised in all three orthogonal planes29,31 – asymmetry in size is present in almost 90 per cent of cases; the ligament is commonly poorly defined and of heterogeneous SI29 – changes in the morphology of the alar ligaments occur with head rotation; elevation and wrapping of the contralateral ligament around the dens occurs, associated with slight upward movement of C1–2 on that side32 the posterior atlanto-occipital membrane31 connects the posterior margin of the foramen magnum (the opisthion) to the superior aspect of the posterior atlantal arch: ■ it appears as a well-defined, thin, hypointense structure that is generally inseparable from the posterior dura (Fig. 9.10g) the anterior atlanto-occipital membrane connects the superior border of the anterior atlantal arch to the basion, but is poorly identified at MRI31 ■

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Craniometry of the craniocervical junction25,26,28,33 ●

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various lines and measurements can be applied to the craniocervical junction to aid understanding of the normal and abnormal relationships between the various osseous structures as seen on mid-sagittal MR images McRae’s line runs from the basion to the opisthion (Fig. 9.11a); the tip of the odontoid process always lies inferior to this line in normal individuals the Wackenheim clivus baseline, also referred to as the basilar line, is drawn parallel to the posterior clivus and extrapolated distally into the spinal canal (Fig. 9.11b), where it should touch the tip of the odontoid process the craniovertebral or clivus-canal angle is formed by the intersection of the basilar line with a line drawn along the posterior cortex of the axis and the odontoid process (Fig. 9.11b): ■ the normal range is 150° in flexion to 180° in extension; ventral spinal cord compression is likely to occur when the angle is 50 years) ■

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MRI findings ● the fracture is manifest as discontinuity of the cortical signal void (Fig. 9.18a–c) with associated traumatic marrow oedema (Fig. 9.18d) and pre-vertebral oedema/haemorrhage (Fig. 9.18d) ● displacement of the fractured dens may also be seen (Fig. 9.18c, d), posterior displacement potentially resulting in upper cervical cord compression

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Figure 9.18 Odontoid fractures. Type 2: Sagittal T1-weighted (T1W) spin-echo (SE) image (a) showing a transverse fracture (arrow) through the base of the dens. Type 3: Sagittal T2-weighted (T2W) fast spin-echo (FSE) image (b) showing a fracture (arrow) extending into the body of the axis. Sagittal T1W SE image (c) showing an anteriorly displaced fracture (arrow). Sagittal T2W FSE fat-suppressed image (d) showing pre-vertebral oedema (arrows) and an anteriorly displaced dens (arrowhead).

Pathology of the craniocervical junction

Hangman’s fracture of the axis27,38 ●

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hangman’s fracture is traumatic spondylolisthesis of the axis, most commonly occurring secondary to an RTA or a fall, and accounting for ~15 per cent of all cervical spine fractures and 23 per cent of axis fractures the fracture results from hyperextension with axial loading, and neurological injury is uncommon due to the auto-decompression of the spinal canal from separation of the fracture fragments pathologically, the hyperextension/axial load mechanism results in bilateral vertical fractures of the pars interarticularis: ■ with more severe injury patterns, rebound flexion or flexion/distraction results in disruption of the C2–3 disc and the PLL, with possible stripping of the ALL fracture classification is based on the degree of translation and angulation between C2 and C3: ■ type 1 injuries – bilateral pars fractures with 3 mm translation and marked angulation, due to rupture of the C2–3 disc and PLL, with associated stripping of the ALL (Fig. 9.19c, d) type 3 injuries – a combination of pars fracture with associated dislocation of the C2–3 facet joints; a very unstable injury with the highest incidence of neurological deficit

MRI findings ● type 1 injuries may be identified only on mid-sagittal images by the posterior displacement of the C2 spinolaminar line (Fig. 9.19a) ● the fracture line may be demonstrated on axial images by the break of the cortical signal void best appreciated on T1W/PDW FSE images (Fig. 9.19b) or by the presence of fluid within the fracture line on T2W images ● type 2 injuries exhibit extension of the plane of injury through the C2–3 disc on sagittal images with anterior displacement of the C2 body and increased sagittal canal dimensions (Fig. 9.19c, d) ● pre-vertebral oedema and haemorrhage manifests as increased T2W SI (Fig. 9.19a, d)

INFECTION Pyogenic osteomyelitis of the craniocervical junction39 ● ● ●

pyogenic osteomyelitis at the craniocervical junction is very rare, most reported cases representing Staphylococcus aureus infection involving the C2 vertebra39 rare cases of septic arthritis of the atlanto-axial joint have also been reported40 inflammatory disorders of the upper neck may result in secondary transverse atlantal ligament insufficiency, possibly due to hyperaemia and decalcification of the anterior arch of the atlas, a condition termed ‘Grisel syndrome’:41 ■ the condition is usually seen in children who present with atlanto-axial instability following an upper respiratory tract infection; it is also seen, rarely, in adults

MRI findings as for vertebral osteomyelitis elsewhere, with bone destruction, enhancing marrow oedema and epidural abscess/phlegmon (Fig. 9.20a–d) ● destruction of the transverse atlantal ligament may result in atlanto-axial subluxation and cord compression ●

Craniocervical tuberculosis42 ● ● ● ●

cervical tuberculosis (TB) accounts for ~10 per cent of all cases of spinal TB, but is very rarely isolated to the C0–2 region (~1 per cent of cases) it may be a relatively common cause of craniocervical junction instability and cervicomedullary compression in developing countries clinically, patients present with suboccipital pain and marked neck stiffness, possibly with neurological compromise, including quadriparesis pathologically, three stages of craniovertebral junction TB have been described: ■ stage 1 – includes cases with intact ligaments, minimal bone destruction and no signs of instability ■ stage 2 – includes cases of atlanto-axial subluxation, but still with minimal bone destruction ■ stage 3 – includes cases with advanced bone destruction and complete obliteration of the anterior arch of C1, often with associated occipitocervical instability

MRI findings marrow oedema and bone destruction involving the clivus, the occipital condyles, the atlas and the axis may be seen (Fig. 9.21a–c) ● soft-tissue masses in the paravertebral, pre-vertebral (Fig. 9.21a, b, d, e) and epidural space are common, being present in >80 per cent of cases ● cord compression may be due to a combination of epidural mass and atlanto-axial instability ●

Pathology of the craniocervical junction

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Figure 9.20 Osteomyelitis of the dens. Sagittal T1-weighted (T1W) spin-echo (SE) (a) and T2-weighted fast spin-echo (b) images showing oedema of the dens (arrows) and destruction of the odontoid process (arrowheads). Post-contrast sagittal (c) and axial (d) T1W SE fat-suppressed images showing marrow enhancement (arrow c), destruction of the body (arrows d) and cord compression (arrowhead c).

ARTHROPATHY Rheumatoid arthritis34,43–45 ● ●

~50 per cent of patients with rheumatoid arthritis (RA) have cervical spine involvement, most commonly affecting the atlanto-axial joint pathologically, this manifests as destruction of the atlanto-axial joint as a result of pannus formation, with involvement of the transverse atlantal, alar and apical ligaments resulting in spinal instability: ■ atlanto-axial (horizontal) instability is the commonest, occurring in up to 49 per cent of cases and representing anterior subluxation of C1 in relation to C2, defined as a distance of >3 mm between the posterior cortex of the anterior arch of the atlas and the anterior cortex of the dens (Fig. 9.22a) ■ vertical instability relates to cranial migration of the dens, occurring in 38 per cent of cases, and is also termed ‘cranial settling’ or ‘atlanto-axial impaction’ (Fig. 9.22b)

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Figure 9.21 Tuberculosis of the dens. Sagittal T1-weighted (T1W) spin-echo (SE) (a), T2-weighted fast spin-echo (b) and axial T2*-weighted gradient-echo (c, d) images showing bone destruction (arrowheads a, b), erosion of the odontoid (arrow c) and soft-tissue phlegmon (arrows a, b, d). Post-contrast axial T1W SE image (e) showing enhancement of the inflammatory mass (arrows).

the two conditions may occur together and result in life-threatening brain stem/spinal cord compression (Fig. 9.22c) indications for MRI in patients with cervical RA include: ■ symptomatic patients: in whom cervical myelopathy is suspected, those with cranial nerve disease, symptoms of cervicomedullary compression or vertebrobasilar insufficiency ■ asymptomatic patients: in whom radiographs show vertical subluxation, an anterior atlanto-axial distance >9 mm, a posterior atlanto-odontoid interval (the distance between the posterior cortex of the dens and the posterior arch of C1) 50 per cent of that of the canal (double-headed arrow). Sagittal T2W FSE image (b) showing an extrusion (arrow) connected to the parent disc by a high signal intensity pedicle (arrowhead). Sagittal T1-weighted (T1W) spin-echo (SE) image (c) showing discontinuity of the hypointense disc margin (arrow) indicating posterior annular rupture. Sequestration: Sagittal T2W FSE image (d) showing a cranially migrated disc fragment (arrow) that is hyperintense relative to the disc of origin (arrowhead). Post-contrast T1W SE image (e) showing peripheral enhancement of a left paracentral sequestrated disc fragment (arrows). Axial T1W SE image (f) showing swelling of the right S1 root (arrow) distal to a sequestrated disc herniation (not shown).

Degenerative disorders of the subaxial spine

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Figure 9.69 Lumbar disc herniation, end-plate changes. Sagittal T2-weighted fast spin-echo image (a) showing a posterior corner end-plate defect (arrow). Sagittal T1-weighted spin-echo image (b) showing an L5–S1 disc prolapse (arrowhead) with an avulsion of the posterior ring apophysis (arrow).

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Figure 9.70 Adolescent disc prolapse. Sagittal T1-weighted spin-echo (a) and axial T2-weighted fast spin-echo (b) images showing a large central nuclear prolapse (arrows).

Discal cyst120 ●

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a discal cyst is a very rare intraspinal cyst of unknown aetiology that communicates with the IVD and has a clinical presentation that is indistinguishable from a disc herniation, namely a unilateral nerve root lesion discal cysts tend to occur in a slightly younger age group (mean age ~32 years) than disc hernias and are more commonly encountered at the upper and mid-lumbar lumbar disc levels (L2–3 to L4–5) communication with the underlying disc can be confirmed by discography

MRI findings ● discal cysts appear as well-defined, oval or round mass lesions in the lateral recess with fluid SI characteristics, appearing hypointense on T1W images (Fig. 9.71a) and markedly hyperintense on T2W images (Fig. 9.71b) ● rim enhancement of the cyst wall may be evident following contrast ● the adjacent disc typically shows minimal degenerative changes (Fig. 9.71c)

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Figure 9.71 Discal cyst. Axial T1-weighted spin-echo (a) and T2-weighted (T2W) fast spin-echo (FSE) (b) images showing a cyst (arrows) in the right lateral recess. Sagittal T2W FSE image (c) shows mild degenerative disc disease (arrowhead) associated with the cyst (arrow).

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Schmorl’s nodes53,83,121 ● ● ●

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a Schmorl’s node is a vertical herniation of the NP through the cartilaginous end-plate into the vertebral body MRI studies have reported an incidence of 57 per cent in teenagers and 5 per cent in the sixth decade of life, most cases occurring between T7 and L2 early-onset Schmorl’s nodes develop during growth and are likely to be secondary to weakness of the discovertebral junction at the site of the notochordal remnant; they commonly occur at multiple levels and are considered to be clinically irrelevant late-onset Schmorl’s nodes are usually isolated and are a recognised cause of back pain, which can be reproduced by discography: ■ symptomatic Schmorl’s nodes tend to be larger than asymptomatic lesions and are more likely to be surrounded by reactive marrow oedema122 ■ rarely, Schmorl’s nodes may tunnel through the posterior vertebral body cortex and result in nerve root compression123

MRI findings ● early-onset lesions appear as small indentations of the end-plate located slightly posteriorly at the site of the notochord and are best appreciated on sagittal T1W images (Fig. 9.72a): ■ they are surrounded by a thin, hypointense rim and are associated with normal surrounding marrow ● late-onset lesions appear on sagittal T1W (Fig. 9.72b) and T2W (Fig. 9.72c) images as an irregular extension of disc material through the end-plate into the vertebral body, the disc of origin usually being degenerate: ■ a zone of sclerosis is commonly seen around the herniated material, appearing as reduced marrow SI on T1W and T2W images (Fig. 9.72d) ■ marrow SI changes similar to type 1 (Fig. 9.72e, f) and type 2 Modic changes may also be seen, type 1 changes showing enhancement on post-contrast studies, which may also show vascularised tissue (Fig. 9.72g) within the Schmorl’s nodes122 ● diffuse vertebral body oedema (Fig. 9.72h) has also been reported in association with Schmorl’s nodes and should not be mistaken for infection or neoplastic marrow inflitration124 ● tunnelling Schmorl’s nodes extend in a sagittal plane through the posterior vertebral body cortex (Fig. 9.72i, j)

Degenerative disorders of the subaxial spine

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g h Figure 9.72 Schmorl’s nodes. Early-onset lesions: Sagittal T1-weighted (T1W) spin-echo (SE) image (a) showing small end-plate defects (arrows) without associated marrow changes. Late-onset lesions: Sagittal T1W SE (b) and T2-weighted (T2W) fast spin-echo (FSE) (c) images showing poorly defined intraosseous disc herniation (arrows). Axial T2W FSE image (d) showing a sclerotic margin (arrows) to the lesion (arrowhead). Acute lesions: Sagittal T1W SE (e) and axial T2W FSE (f) images showing an intraosseous disc herniation (arrows) with associated type 1 marrow changes (arrowheads). Postcontrast coronal T1W SE image (g) showing enhancing granulation tissue (arrow) within a Schmorl’s node. Sagittal short tau inversion recovery image (h) showing a small intraosseous disc herniation resulting in diffuse marrow oedema (arrow). (continued)

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j i Figure 9.72 (continued) Tunnelling Schmorl’s node: Sagittal T1W SE (i) and axial T2W FSE (j) images showing a chronic Schmorl’s node (arrows) extending through the posterior cortex of L5.

Cystic Schmorl’s nodes125 ● ●

cystic Schmorl’s nodes are a rare variant of Schmorl’s nodes of unknown aetiology that appear as large, intraosseous cysts and must be differentiated from other cystic lesions of the vertebral body reported cases typically present in relatively young individuals (mean age 20 years) with a history of low back pain

MRI findings ● the lesions are well-defined showing hypointensity on T1W (Fig. 9.73a) and marked hyperintensity on T2W (Fig. 9.73b, c), with a low SI rim that enhances following contrast (Fig. 9.73d) ● the lesions are connected to a degenerate IVD and occupy one-half to the whole of the vertebral body height, measuring 18–25 mm

Fatty Schmorl’s nodes126 ● ● ●

fatty Schmorl’s nodes are a rare variant of Schmorl’s nodes that appear as large, lytic lesions adjacent to the end-plate all reported cases have affected the lower lumbar vertebrae and were identified incidentally or during imaging for chronic low back pain, usually in patients in the fourth to sixth decades the cause of the fatty lesions is unknown

MRI findings ● a well demarcated lesion is seen involving most of the height of the vertebral body and attached to the adjacent end-plate, showing fatty SI on all pulse sequences (Fig. 9.74a–c)

Anterior limbus vertebra53,127 ● ● ●

anterior limbus vertebra occurs in childhood and results from anterior herniation of the NP between the ring apophysis and the vertebral body it is most commonly identified in the upper lumbar region and is a cause of adolescent low back pain it may also be first identified in adults undergoing lumbar spine imaging, but is not considered to be a cause of adult low back pain

Degenerative disorders of the subaxial spine

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c Figure 9.73 Cystic Schmorl’s node. Sagittal T1-weighted (T1W) spinecho (SE) (a), (SE) T2-weighted (T2W) fast spin-echo (FSE) (b) and axial T2W FSE (c) images showing a cyst (arrows) in the L2 vertebra associated with a Schmorl’s node (arrowheads). Post-contrast sagittal T1W SE image SE (d) showing rim enhancement of the lesion (arrows).

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MRI findings ● acute lesions exhibit anterior herniation of the disc between the ring apophysis and the vertebral body (Fig. 9.75a, b), with reduction of anterior disc height and mild focal kyphosis: ■ the posterior aspect of the disc and end-plate appear intact, helping to differentiate the condition from discitis ■ type 1 reactive marrow SI changes may be evident ● chronic lesions exhibit separation of the ossified anterior ring apophysis from the vertebral body by intervening degenerate disc material (Fig. 9.75c, d), possibly with associated type 2 fatty marrow changes

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Figure 9.74 Fatty Schmorl’s node. Sagittal T1-weighted spin-echo (a), axial T2-weighted fast spin-echo (b) and sagittal short tau inversion recovery (c) images showing extensive fatty lesions (arrows) associated with small intraosseous disc herniations (arrowheads).

THE FACET JOINT AND THE NEURAL ARCH Facet osteoarthritis128–130 ●

● ●

facet OA usually occurs as a consequence of degenerative disc disease, with reduction of disc height resulting in altered mechanical stresses across the joint and subsequent capsular synovitis and cartilage loss, progressing to osteophyte formation and facet hypertrophy in ~20 per cent of cases, facet OA precedes degenerative disc disease clinically, the facet joints are considered to be a source of low neck and back pain, the so-called ‘facet joint syndrome’: ■ low back pain characteristics that may suggest origin from the facet joints include age >65 years and pain that is not worsened by coughing, hyperextension, forward flexion, rising from flexion or extension–rotation but which is significantly relieved by recumbancy129

MRI findings ● facet OA is manifest by imaging findings that are similar to those seen in other synovial joints, namely cartilage loss (Fig. 9.76a), synovial hypertrophy (Fig. 9.76b) and effusion (Fig. 9.76c), subchondral sclerosis (Fig. 9.76a, d), erosion (Fig. 9.76e) and cyst formation, osteophytosis (Fig. 9.76f) and hypertrophy of the articular processes (Fig. 9.76g, h) ● facet OA has been graded as follows:130 ■ grade 0 – normal facet joint space (2–4 mm width) ■ grade 1 – narrowing of the facet joint (13 mm, a measurement of 10–13 mm representing borderline/relative spinal stenosis ■ normal cervical cord measurements depend on the level, the mean measurements (AP ¥ transverse) based on MRI being 9¥12 mm at C2, 9¥14 mm at C4 and 7¥11 mm at C7 ■ with severe, prolonged central stenosis, the cord may undergo compressive myelomalacia

MRI findings ● degenerative disc disease is seen with disc bulging/osteophytes (Fig. 9.87a, b) and loss or reversal of normal cervical lordosis (Fig. 9.87c) ● effacement of the CSF space around the spinal cord with cord compression (Fig. 9.87d) ● compressive myelopathy appears in the early stage as poorly defined T2W hyperintensity at the site of cord compression (Fig. 9.87b), corresponding to oedema and microvascular venous stasis, with possible contrast enhancement due to breakdown of the blood–brain barrier: ■ in a more advanced stage, intramedullary areas of low T1W SI and high T2W SI are demonstrated, due to cystic necrosis and gliosis in the central grey matter, which produce the ‘snake-eye’ appearance on axial T2W images (Fig. 9.87e, f) ■ eventually, progressive cystic necrosis may result in syrinx formation159 and cord atrophy (Fig. 9.87g) ● qualitative assessment of cervical spinal stenosis and cord deformation may be useful for predicting outcome following decompression, but may be limited by poor inter-observer agreement160 ● MRI may show some correlation with the outcome following surgical decompression: ■ prognosis is best in patients with no cord SI change or only increased T2W SI, while the combination of low T1W SI and high T2W SI is associated with a poor outcome161 ■ the prognosis is also better if the cord abnormality is limited to a single level (Fig. 9.87b) rather than multi-level (Fig. 9.87h)162 ■ the snake-eye appearance163 has been correlated with poor outcome following decompression ■ expansive cord oedema164,165 is reported following cervical decompression/laminoplasty in ~6 per cent of cases, and may be associated with distal, diffuse paresis of the upper limb with no deterioration of lower limb function

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Figure 9.87 Cervical spondylotic myelopathy. Sagittal T1-weighted (T1W) spin-echo (SE) (a) and T2-weighted (T2W) fast spin-echo (FSE) (b) images showing mild multi-level cord compression (arrows a) due to a combination of disc bulge and osteophyte with associated cord oedema at C4–5 (arrow b). (continued)

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g Figure 9.87 (continued) Sagittal T1W SE image (c) showing advanced multi-level cervical spondylosis with reversal of the cervical lordosis. Axial T2*-weighted (T2*W) gradient-echo (GE) image (d) showing a diffuse disc bulge (arrows) resulting in effacement of the ventral cerebrospinal fluid space and mild cord compression. Sagittal (e) and axial (f) T2W FSE images showing advanced single-level cord compression (arrow e) with cord signal intensity (SI) change (arrowhead e) and the ‘snake-eye’ appearance (arrows f). Axial T2*W GE image (g) showing advanced cord atrophy (arrows). Sagittal T2W FSE image (h) showing multi-level cord SI change (arrows).

Degenerative disorders of the subaxial spine

Lumbar central canal stenosis59,166,167 ● ● ●

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spinal stenosis is by definition a narrowing of the spinal canal, which is a common finding in the ageing and degenerate spine, but which may also be asymptomatic classification is based on aetiology and location congenital spinal stenosis may be a manifestation of conditions such as achondroplasia, or may occur in otherwise normal individuals who have relatively large vertebral bodies and short, round pedicles (Fig. 9.88a–c) (developmental/idiopathic stenosis), with symptoms occurring early following the development of disc bulging (typically in the 30–45-year age range): ■ such patients may have a trefoil configuration to the spinal canal, with a short sagittal diameter and deep lateral recesses acquired spinal stenosis is most commonly degenerative in nature, occurring as a result of a combination of diffuse disc bulging, facet joint bony and capsular hypertrophy and thickening/buckling of the LF, which compress the cauda equina: ■ miscellaneous causes of acquired spinal stenosis include Paget’s disease anatomically, stenosis may involve the central canal (causing cauda equina compression), the lateral (subarticular) recess, the IVF or the extraforaminal region (resulting in nerve root claudication, most commonly at the L4–5 level): ■ lateral stenosis may involve the DRG pathological processes that may contribute to stenosis include degenerative spondylolisthesis (usually at L4–5) and retrolisthesis (usually at L5–S1) clinically, the condition typically occurs in individuals aged 65–70 years; women are more commonly symptomatic than men:

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Figure 9.88 Congenital lumbar spinal stenosis. Sagittal T1-weighted spin-echo image (a) showing a narrowed anteroposterior canal dimension (arrows). Sagittal (b) and axial (c) T2-weighted fast spin-echo images showing marked shortening of the pedicle (arrows).

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■ ■ ■ ■

patients present with low back pain and neurogenic claudication, which represents various combinations of leg pain, weakness and difficulty in walking that may or may not be associated with a neurological deficit leg symptoms may be asymmetrical, vary from paraesthesia and cramps to severe pain, and may involve the buttocks with extension into the legs symptoms classically increase with walking and spinal extension, and are relieved by spinal flexion neurological deficits are typically minor, and bladder/bowel symptoms are rare nerve root symptoms are due to a combination of compression, vascular compromise and inflammation

MRI findings ● these may be divided into the causative factors and their effects on the thecal sac/cauda equina ● causative factors: ■ IVD degeneration, manifest by loss of T2W nuclear SI, reduction of disc height and diffuse disc bulging (Fig. 9.89a, b), resulting in anterior compression on the thecal sac ■ facet joint degeneration, manifest by capsular hypertrophy and osteophyte formation (Fig. 9.89c), resulting in posterolateral compression on the thecal sac ■ LF thickening and inward buckling due to loss of disc height (Fig. 9.89c), resulting in posterolateral thecal sac compression ■ posterior epidural fat pad may change in morphology, becoming elongated rather than triangular and assuming a flattened or convex ventral margin (Fig. 9.89d), which may contribute to posterior thecal sac compression ● effects on the thecal sac/cauda equina: ■ quantitative signs: reduction of thecal sac cross-sectional area to 10 years): ■ currently, it is subdivided into early onset (5 years) based on the fact that serious cardiopulmonary compromise may occur with presentation before 5 years of age due to underdevelopment of the lungs189 clinically, the typical presentation is a right thoracic curve in an adolescent female with no associated symptoms of spinal pain or lower limb neurological deficit, in which case routine spinal MRI is unlikely to identify a spinal cord/hindbrain anomaly:191 ■ indications for whole-spine MRI include192 early age of onset, unusual curve pattern, absence of thoracic apical lordosis and the presence of any neurological symptoms or signs, but not the presence of spinal pain ■ unilateral absence of the superficial abdominal reflexes, though a relatively uncommon sign, is an important indicator of intraspinal abnormality193

MRI findings ● several morphological findings are common in idiopathic scoliosis and should not be mistaken for pathology, including:194 ■ vertebral deformity: progressive vertebral wedging (Fig. 9.106a), thinning of the pedicles on the concavity of the curve (Fig. 9.106b) and intravertebral axial rotation,194 all of which are maximal at the apex of the curve ■ absence or reversal of the normal cervical lordosis (Fig. 9.106c) ■ tethering of the spinal cord such that it always lies in the concavity of the curve (Fig. 9.106d, e) ■ wedging of the IVD and displacement of the NP to the convex side of the curve (Fig. 9.106a, f) ● abnormalities of the neuraxis195 include Chiari I malformation (Fig. 9.107a, b) and syrinx (Fig. 9.107c–e), which may occur in combination or in isolation and are reported in ~20 per cent of cases in which MRI is indicated

Congenital scoliosis188,195,196 ● ● ●

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congenital scoliosis is caused by an abnormality of one or several vertebral elements and is therefore also referred to as ‘osteogenic scoliosis’ classification is based on a combination of the location and the type of the vertebral abnormality, the latter due to failure of formation, failure of segmentation or mixed failure of formation may be incomplete or complete: ■ incomplete: results in a wedge vertebra, with reduced height of one side but with two pedicles ■ complete: failure of formation of half of the vertebral body results in a hemivertebra, which may be fully segmented (has a disc both above and below), partially segmented (is fused to one adjacent vertebra and has one adjacent disc) or unsegemented (is fused to both adjacent vertebrae) failure of segmentation results in the presence of bony bars between adjacent vertebrae, which may be bilateral producing a block vertebra, or unilateral producing a bony bar that acts as a tether to growth on the concave side of the curve mixed abnormalities are not uncommon and include combinations such as a unilateral bar and a contralateral hemivertebra: ■ multiple vertebral abnormalities may be associated with absence or fusion of ribs, which may contribute to the deformity

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Figure 9.106 Normal findings in idiopathic scoliosis. Coronal T2-weighted (T2W) fast spin-echo (FSE) image (a) showing mild vertebral wedging on the concavity of the curve apex (doubleheaded arrows) and displacement of the nucleus pulposus to the convexity of the curve (arrows). Axial T1-weighted spin-echo image (b) showing thinning of the pedicle (arrow) on the concavity of the curve compared with the normal contralateral pedicle (arrowhead). Sagittal T2W FSE image (c) showing reversal of the normal cervical lordosis (arrows). Coronal (d) and axial (e) T2W FSE images showing displacement of the spinal cord (arrows) to the concave side of the curve. Axial T2W FSE image (f) showing displacement of the nucleus pulposus (arrow).

Subaxial spinal deformity

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Figure 9.107 Neuraxis abnormalities in idiopathic scoliosis. Chiari I malformation: Sagittal T1-weighted (T1W) spin-echo (SE) (a) and axial T2-weighted (T2W) fast spin-echo (FSE) (b) images showing herniation of the cerebellar tonsils (arrows) through the foramen magnum. Syrinx: Coronal T1W SE (c), axial T1W SE (d) and sagittal T2W FSE (e) images showing a large syrinx (arrows) extending from C2 into the thoracic region and associated with cord expansion.

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■ neural arch abnormalities may also be present, including spina bifida or fusion of laminae development of scoliosis depends on the ability of the abnormality to produce unbalanced growth; the most benign anomaly is a block vertebra and the most severe is a unilateral bar with a contralateral, fully segmented hemivertebra associated spinal neuraxis and non-spinal anomalies are relatively common in the setting of congenital scoliosis, the latter including cardiac, renal and gastrointestinal defects (e.g. VATER syndrome):

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neuraxis anomalies197,198 have been reported in 24–31 per cent of patients with hemivertebra, with no significant difference between an isolated hemivertebra and a complex hemivertebra pattern of deformity reported abnormalities include diastematomyelia, syrinx, tethered cord, arachnoid cysts, Chiari I malformation and a lipoma of the filum terminale

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Figure 9.108 Congenital scoliosis, failure of formation. Coronal T2-weighted (T2W) fast spin-echo (FSE) image (a) showing a complex anomaly with a wedge vertebra (arrow) and multiple contralateral hemivertebrae (arrowheads). Coronal T1-weighted (T1W) spin-echo (SE) image (b) showing a fully segmented hemivertebra (arrow) with discs on either side (arrowheads). Coronal T2W FSE image (c) showing a partially segmented hemivertebra (arrow) with a disc (arrowhead) on the superior side only. Coronal T1W SE image (d) showing an unsegmented hemivertebra (arrow) with no disc material between it and the adjacent vertebrae. Sagittal T2W FSE images (e, f) showing multi-level laminar fusion (arrows e) and a thoracic syrinx (arrow f).

Subaxial spinal deformity

MRI findings ● failure of formation: wedge vertebra and hemivertebra are optimally demonstrated on coronal images (Fig. 9.108a): ■ fully segmented (Fig. 9.108b), partially segmented (Fig. 9.108c) and unsegemented hemivertebrae (Fig. 9.108d) can be demonstrated ■ associated features include laminar fusions (Fig. 9.108e) and syringomyelia (Fig. 9.108f)

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Figure 9.109 Congenital scoliosis, failure of segmentation. Block vertebra: Sagittal T2-weighted (T2W) fast spin-echo (FSE) image (a) showing segmentation failure between L1 and L2 (arrows) with associated spinous process fusion (arrowheads). Unilateral bar: Coronal (b) and sagittal (c) T2W FSE images showing multi-level vertebral fusion (arrows) in the concavity of the curve with involvement of the laminae (arrowheads c). Coronal T2W FSE image (d) showing unilateral pedicle fusion in the concavity of the curve (arrows) with normal pedicles on the convexity (arrowheads). Mixed abnormality: Coronal T2W FSE image (e) showing combined block vertebra (arrow) and hemivertebrae (arrowheads).

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failure of segmentation: block vertebra demonstrates failure of formation of the IVD resulting in fusion of the adjacent vertebral bodies and neural arches (Fig. 9.109a), while unilateral failure of fusion shows disc material on one side of the vertebral body and continuous bone on the concavity of the curve (Fig. 9.109b–d) mixed abnormalities: combined hemivertebrae and block vertebrae (Fig. 9.109e)

Developmental scoliosis188 ●

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developmental scoliosis results from an abnormality of the intrinsic bony architecture of the spine or is due to ectodermal/mesenchymal dysplasias, the commonest of which is neurofibromatosis type 1 (NF1), which accounts for 2–3 per cent of all patients with significant scoliosis199–201 spinal deformity is classified as non-dystrophic or dystrophic based on the absence or presence of skeletal dysplasia: ■ the associated vertebral anomalies include vertebral rotation (~50 per cent), posterior (~30 per cent) (Fig. 9.110a), lateral (13 per cent) (Fig. 9.110b) and anterior (Fig. 9.110c) vertebral scalloping, vertebral wedging (36 per cent), spindling of the transverse processes (~30 per cent) (Fig. 9.110d), increased interpediculate distance (~30 per cent) and enlargement of the intervertebral foraminae (25 per cent) (Fig. 9.110e) ■ rib pencilling occurs in ~60 per cent of cases and may be identified on coronal spinal MR images ■ the associated kyphosis may result in cord stretching and neurological deficit including paraplegia clinically, non-dystrophic curves can be managed similarly to idiopathic scoliosis, whereas dystrophic curves, which typically take the form of short-segment, high-thoracic kyphoscoliosis, progress rapidly and require early anterior and posterior fusion

MRI findings ● vertebral scalloping is seen, which may or may not be associated with dural ectasia or adjacent abnormal soft tissue201 (Fig. 9.110a–e) ● dural abnormalities include dural ectasia (Fig. 9.110a, c, d) and lateral thoracic meningocele formation (Fig. 9.110b, f)

Subaxial spinal deformity

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c Figure 9.110 Spinal deformity in neurofibromatosis type 1. Sagittal T2-weighted (T2W) fast spin-echo (FSE) image (a) showing posterior scalloping (arrows) associated with dural ectasia. Coronal T2W FSE image (b) showing lateral scalloping (arrowhead) and a lateral thoracic meningocele (arrow). Sagittal T1-weighted (T1W) spin-echo (SE) image (c) showing anterior scalloping (arrowheads) associated with abnormal pre-vertebral soft tissue (arrows). Axial T2W FSE image (d) showing spindling of the transverse process and pedicle (arrows) and posterior vertebral scalloping (arrowhead). (continued)

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g i Figure 9.110 (continued) Sagittal T2W FSE image (e) showing enlargement of the intervertebral foramen (arrows). Axial T2W FSE image (f) showing a lateral thoracic meningocele (arrows). Coronal T1W SE (g), axial T2W FSE (h) and postcontrast coronal T1W SE (i) images showing a plexiform neurofibroma (arrows) related to the convexity of the curve.

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whole-spine MRI200 may identify mild dystrophic features in ~40 per cent of radiographically nondystrophic curves, which is an important finding since it may predict rapid progression of the deformity paraspinal tumours may also be identified on MRI;200 these are solitary neurofibromas or plexiform neurofibromas: ■ they are more commonly seen in relation to dystrophic curves (43 per cent) than non-dystrophic curves (27 per cent), are typically not related to the curve and, when so, are commonly on the convexity of the curve (Fig. 9.110g–i)

Subaxial spinal deformity

KYPHOSIS Introduction202,203 ●

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kyphosis is an abnormally increased sagittal plane Cobb angle, which varies depending on the region of the spine involved: ■ the overall normal thoracic curvature in the sagittal plane is 20–40°, whereas in the upper thoracic region (T1–5) the normal Cobb angle is ~12° and in the thoracolumbar region (T10–L2) it is ~7° kyphosis has various causes, which may differ in the paediatric and adult age groups causes of paediatric kyphosis (excluding trauma and infection)202 include conditions such as Scheuermann’s disease, NF1 (see above), congenital kyphosis and kyphosis associated with various syndromes such as Marfan’s syndrome: ■ adult kyphosis203 may be a continuation of deformity in childhood, or may develop due to conditions such as vertebral collapse from tumour or infection, trauma or osteoporosis, or following multi-level laminectomy

Scheuermann’s disease202 ● ●

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Scheuermann’s disease is a condition of unknown aetiology that may affect the thoracic, thoracolumbar or lumbar regions thoracic disease has a prevalence of 0.4–8 per cent and is diagnosed by a Cobb angle of >40° associated with anterior wedging of at least 5° in more than three consecutive vertebrae that also exhibit end-plate irregularities: ■ the apex of the kyphus is usually between T7 and T9 and 20–30 per cent of patients also have scoliosis ■ these patients also have an increased incidence of spondylolysis thoracolumbar disease typically has an apex at T10 to T12 with a Cobb angle of ~20° and is associated with considerable pain and cosmetic deformity lumbar disease manifests as multiple Schmorl’s nodes, end-plate irregularities and reduced disc height, and typically presents with pain

MRI findings ● sagittal images show abnormal spinal alignment (Fig. 9.111a–c) with anterior vertebral wedging, end-plate irregularity and degenerative changes in the disc, with low T2W SI, reduced disc height and Schmorl’s nodes ● the spinal cord is draped over the kyphus but is not compressed

Congenital kyphosis202 ● ●

congenital kyphosis, as in congenital scoliosis, may result from failure of formation or failure of segmentation pure kyphosis accounts for ~6 per cent of congenital spinal deformity while kyphoscoliosis accounts for ~13 per cent, the remainder being pure congenital scoliosis (see above)

MRI findings ● sagittal images demonstrate the abnormal, usually acute kyphosis with the underlying vertebral anomaly (Fig. 9.112a, b)

Marfan’s syndrome202 ● ● ●

patients may be divided into those with the syndrome and those with a Marfan’s (marfanoid) habitus Marfan’s syndrome has a prevalence of ~1:10 000 and 10 per cent have thoracic or thoracolumbar kyphosis, which usually manifests in late infancy or childhood and is most prominent in the sitting position a reversal of normal sagittal alignment, namely thoracic lordosis and lumbar kyphosis, is unique to this condition, and Marfan’s syndrome is also a recognised cause of posterior vertebral scalloping and dural ectasia

MRI findings ● abnormal sagittal alignment is seen with associated dural ectasia and posterior vertebral scalloping (Fig. 9.113a, b)

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Figure 9.111 Scheuermann’s disease. Sagittal T1-weighted spin-echo (a) and T2-weighted fast spin-echo (b, c) images showing mid-thoracic kyphosis, anterior vertebral wedging (arrowheads a, b), end-plate irregularity (arrows a, b) and Schmorl’s node formation (arrow c).

Subaxial spinal deformity

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a Figure 9.112 Congenital kyphosis. Sagittal T1-weighted spin-echo image (a) showing acute kyphosis due to a failure of formation at T12 (arrow). Sagittal T2-weighted fast spin-echo image (b) showing kyphosis due to a failure of segmentation between T9 and T12 (arrows).

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Figure 9.113 Marfan’s syndrome. Sagittal (a) and axial (b) T2-weighted fast spin-echo images show loss of normal lumbar lordosis, posterior vertebral scalloping (arrows a) and dural ectasia (arrow b).

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SPINAL DYSRAPHISM Introduction188,204,205 ●

‘spinal dysraphism’ is a term that encompasses a wide variety of complex congenital anomalies of the neuraxis, the basic defect being a failure of midline fusion of the mesenchymal, bony or neural structures: ■ osseous anomalies include near total absence of the neural arch, butterfly vertebra, hemivertebra, and cleft and block vertebra (Fig. 9.114a–c)

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Figure 9.114 Vertebral anomalies associated with spinal dysraphism. Coronal T1-weighted (T1W) spin-echo (SE) (a) and sagittal T2-weighted fast spin-echo (b) images showing a sagittally cleft vertebra (arrows). Coronal T1W SE image (c) showing a butterfly vertebra (arrows) and bilateral hemivertebrae (arrowheads).

Subaxial spinal deformity

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clinically, infants may present with a variably sized back mass, or cutaneous manifestations such as a hairy patch, a naevus, skin pigmentation abnormalities, a sacral dimple, haemangioma or a sinus tract: ■ children with occult dysraphism can present during the adolescent growth spurt with lower limb neurological deficits and bladder and bowel dysfunction that may be a manifestation of mechanical tethering and stretching of the spinal cord and is referred to as tethered cord syndrome205 spinal dysraphism may be divided into three categories: ■ 1 – dysraphism with a non-skin-covered back mass (spina bifida aperta): meningomyelocele and myelocele ■ 2 – dysraphism with a skin-covered back mass (spina bifida cystica): lipomyelomeningocele, myelocystocele and posterior meningocele ■ 3 – occult dysraphism (spina bifida occulta): diastematomyelia, dorsal dermal sinus, spinal lipoma, tight filum terminale, anterior sacral meningocele, lateral thoracic meningocele, split notochord syndrome, caudal regression syndrome and syringohydromyelia

Spina bifida aperta204 ● ● ●

a meningomyelocele comprises a sac of exposed, dorsally cleft neural tissue that herniates through a large defect in the dura, bone and skin, with tethering of the spinal cord at this level the defect is slightly more common in girls and is usually located in the lumbosacral region, less commonly involving the thoracolumbar junction or the thoracic region associated features include Chiari II malformation, diastematomyelia, spinal arachnoid cyst and syringohydromyelia

MRI findings ● sagittal and axial T1W images optimally demonstrate the intraspinal and extraspinal abnormalities ● a large cystic mass with CSF SI characteristics is seen extending from the spinal canal through a neural arch defect and the subcutaneous tissues, with tethering of the spinal cord to the cyst

Spina bifida cystica204 ●

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a lipomyelomeningocele comprises a skin-covered back mass composed of neural tissue, CSF and meninges, with an associated lipoma that extends from the subcutaneous fat into the spinal canal and causes tethering of the spinal cord: ■ associated osseous abnormalities include neural arch defects, segmentation anomalies and sacral agenesis ■ Chiari I malformation may also be seen ■ MRI findings: lipomyelomeningocele – a low-lying cord tethered by a large, fatty mass (Fig. 9.115a, b) that extends into the distal spinal canal through a large neural arch defect (Fig. 9.115c), with associated vertebral anomalies (Fig. 9.115a, b) a myelocystocele comprises cystic dilation of the lower end central canal of the spinal cord, which is enclosed in a skin-covered back mass, associated with a low-lying tethered cord but no extension of fat into the sac or cord: ■ MRI findings: myelocystocele – a low-lying cord terminating in a cystic subcutaneous mass that may appear hyperintense to CSF on T1W images owing to a high protein content posterior meningocele comprises a herniated sac of CSF containing meninges that protrudes from the back and is covered with skin: ■ MRI findings: posterior meningocele – the spinal cord and conus are in a normal position, with the meningocele appearing as a cystic subcutaneous mass passing through a small neural arch defect, usually in the lumbosacral region

Spina bifida occulta188,204,205 ●

diastematomyelia,206 also termed ‘split spinal cord malformation (SSCM) syndrome’, is one of the commonest forms of occult spinal dysraphism and represents a partial or complete sagittal cleft of the spinal cord, usually located in the lumbar or thoracic region:

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Figure 9.115 Lipomyelomeningocele. Sagittal T1-weighted (T1W) spin-echo (SE) image (a) showing a fatty mass (arrows) in the lumbosacral canal and block vertebrae at L4–5 (arrowheads). Sagittal T2-weighted fast spin-echo image (b) showing a low-lying spinal cord (white arrows) tethered by a fatty mass (arrowhead) that is continuous with a large subcutaneous lipoma (black arrows). Axial T1W SE image (c) showing a wide neural arch defect (arrows) at L5.

in ~50–60 per cent of cases, there is a fibrous or osteocartilaginous bar extending from the posterior vertebral body to the neural arch, creating a separate dural sac for each hemicord, the two hemicords usually uniting below the bar (type 1 SSCM); in ~40–50 per cent of cases, there is a single dural sac around the two hemicords (type 2 SSCM), occasionally with an intradural fibrous band/spur ■ occasionally, the two hemicords persist, each having a separate conus and filum terminale ■ the bar is usually located between L2 and L4 and rarely is in the cervical, thoracic or sacral regions ■ in type 1 SSCM, the bar may be midline, dividing the canal into two equal halves with symmetrical hemicords, or it may slant to one side, resulting in unequal division and asymmetrical hemicords ■ each hemicord gives rise to a single ipsilateral ventral and dorsal root; in rare cases, true cord duplication occurs, a condition termed ‘diplomyelia’ ■ associated abnormalities include syringohydromyelia, filum terminale or intradural lipoma and vertebral abnormalities such as hemivertebra, block vertebra, butterfly vertebra and extensive spina bifida with laminar fusion ■ MRI findings: the split cord and fibrous/bony bar are optimally demonstrated on a combination of axial and coronal T1W and T2W images, but can also be seen in the sagittal plane (Fig. 9.116a–f); associated cord and vertebral abnormalities are also clearly demonstrated dorsal dermal sinus comprises an epithelium-lined tube that extends inwards from the skin surface; if it arises above the sacrococcygeal region, it may terminate in the spinal canal or the conus and the distal spinal cord in the form of an epidermoid or dermoid cyst: ■ MRI findings: the sinus appears as a thin, hypointense line optimally seen on sagittal and axial T1W images; its cystic termination is hyperintense on T2W images and of variable T1W SI depending on its contents intradural lipoma comprises a localised collection of fat within the dural space that is connected to but does not infiltrate the spinal cord: ■ if the lipoma is located in the lumbosacral region, the cord is tethered and low lying (Fig. 9.117a–c) ■ associated lesions include diastematomyelia and spina bifida ■ MRI findings: the lipoma appears uniformly hyperintense on T1W and T2W images (Fig. 9.117d–f) ■

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Figure 9.116 Diastematomyelia. Type 1 split spinal cord malformation (SSCM): Sagittal (a), coronal (b) and axial (c) T1-weighted spin-echo images showing a complete bony bar (arrows a, c) and a split spinal cord (arrows b, arrowheads c) that is tethered at the lumbosacral junction (arrowhead a). Note also the abnormal vertebral morphology. Type 2 SSCM: Sagittal (d), coronal (e) and axial (f) T2-weighted fast spin-echo images showing an intradural fibrous band (arrows) associated with a split and tethered spinal cord (arrowheads) that unites distal to the band.

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Figure 9.117 Intradural lipoma. Sagittal T1-weighted (T1W) spin-echo (SE) (a), T2-weighted (T2W) fast spin-echo (FSE) (b) and axial T1W SE (c) images showing a lumbosacral lipoma (arrows) tethering the cord and associated with congenital thoracic kyphosis (arrowheads a, b). Sagittal T1W SE (d), T2W FSE (e) and axial T1W SE (f) images showing an intradural lipoma (arrows) connected to the spinal cord, which terminates at a normal level.

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tight filum terminale comprises a thickened filum terminale (owing to lipomatous or fibrous tissue) measuring >2 mm to which the spinal cord is tethered: ■ MRI findings: the thickened filum should be measured on axial T1W images at the L5–S1 level and appears hyperintense if fatty or hypointense if fibrous; the conus is at a normal level or low lying (below L2 in 86 per cent of cases) anterior sacral meningocele is the herniation of a meningocele through an anterior sacral defect into the posterior pelvic cavity: ■ alternatively, the meningocele may remain within the sacrum resulting in expansion of the sacral canal ■ MRI findings: a pre-sacral cystic mass (Fig. 9.118a, b) and associated osseous abnormalities (Fig. 9.118c) caudal regression syndrome comprises a spectrum of abnormalities involving the genitourinary system with absence of the lower spine: ■ MRI findings: the conus is proximally located and bulbous, and there may be stenosis of the distal spinal canal with various vertebral anomalies and variable absence of the lumbosacral spine (Fig. 9.119a, b) syringohydromyelia: hydromyelia is an ependymal cell-lined dilation of the central spinal canal, whereas syringomyelia represents dissection of CSF through the cord substance: ■ the two conditions cannot be differentiated with MRI, so the term ‘syringohydromyelia’ is used to include both entities ■ MRI findings: a focal, multisegmental or diffuse cavity within the spinal canal with the SI characteristics of CSF (Fig. 9.107c–e) that may result in fusiform cord expansion

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Figure 9.118 Anterior sacral meningocele. Sagittal T1-weighted (T1W) spin-echo (SE) (a) and axial T2-weighted fast spinecho (b) images showing a large cystic mass (arrows) extending through a defect in the sacrum (arrowheads b) and an associated posterior thoracic hemivertebra (arrowhead a). Sagittal T1W SE image (c) showing multiple congenital wedge vertebrae (arrows).

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Figure 9.119 Caudal regression syndrome. Coronal T1-weighted spin-echo (a) and sagittal T2-weighted fast spin-echo (b) images showing a bulbous termination of the cord (black arrows) at the T7–8 disc level and absence of the spine below T11 (white arrow b).

MISCELLANEOUS CONGENITAL SPINAL DISORDERS Achondroplasia26 ● ●

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achondroplasia is the commonest form of dwarfism associated with spinal involvement; it is an autosomal dominant condition but with high rates of genetic mutation and sporadic cases are common pathologically, the condition arises due to defective endochondral bone formation with normal membranous ossification, which in the axial skeleton results in characteristic skull-base and spinal column deformity subaxial spinal involvement comprises severe spinal canal stenosis and kyphoscoliosis: ■ stenosis is probably due to premature fusion of the neurocentral synchondrosis, resulting in reduced AP (Fig. 9.120a) and transverse (Fig. 9.120b) bony canal dimensions and small intervertebral foramina (Fig. 9.120c), the sagittal stenosis involving the entire length of the spine, while the transverse stenosis tends to be limited to the lumbar region ■ scoliosis/kyphosis occurs in ~30 per cent of patients, with vertebral wedging typically resulting in thoracolumbar junction kyphoscoliosis (Fig. 9.120d, e) pseudoachondroplasia produces thoracolumbar kyphosis with excessive lumbar lordosis and occasionally atlanto-axial instability

MRI findings ● vertebral morphological abnormalities include short (Fig. 9.120a), flat vertebral bodies, short, thick pedicles and posterior vertebral scalloping (Fig. 9.120f) ● vertebral wedging with thoracolumbar kyphoscoliosis (Fig. 9.120d, e) ● congenital disc hypertrophy (Fig. 9.120g) and bulging, resulting in exacerbation of cauda equina compression, worsened by the onset of degenerative disc disease (Fig. 9.120h) ● multi-level spinal stenosis may be seen; therefore, imaging of the whole spine is required

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Figure 9.120 Achondroplasia. Sagittal T2-weighted (T2W) fast spin-echo (FSE) image (a) showing reduced vertebral body anteroposterior dimension (arrows) and spinal stenosis. Axial T2W FSE image (b) showing reduced transverse canal dimension. Sagittal T2W FSE image (c) showing reduced foraminal dimensions (arrows). Sagittal T2W FSE images (d, e) showing thoracolumbar kyphosis due to severe vertebral wedging (arrows). Sagittal T2W FSE image (f) showing posterior vertebral scalloping (arrows). Sagittal T2W FSE image (g) showing congenital disc hypertrophy (arrows). Sagittal T2W FSE image (h) showing multi-level spinal stenosis (arrowheads) that is contributed to by disc degeneration (arrows).

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Klippel–Feil syndrome26 ● ●

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Klippel–Feil syndrome refers to any condition associated with congenital fusion of the cervical vertebrae, which may be localised, multisegmental or diffuse clinically, the classic triad comprises low posterior hairline, a short, webbed neck and limitation of neck movement, though this is seen in 2 mm from adjacent levels (Fig. 9.124g)

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Figure 9.124 Spinal anatomy relevant to trauma. Anterior column: Sagittal T2-weighted (T2W) fast spin-echo (FSE) image (a) showing the anterior longitudinal ligament (arrow), the anterior end-plate (arrowhead) and the anterior vertebral body (double-headed arrow). Middle column: Sagittal T2W FSE image (b) showing the posterior longitudinal ligament (arrow), the posterior end-plate (arrowhead) and the posterior vertebral body (double-headed arrow). Posterior column: Sagittal T2W FSE image (c) showing the ligamentum flavum (arrowheads), the interspinous ligaments (white arrows) and the supraspinous ligament (black arrows). Sagittal T1-weighted (T1W) spin-echo (SE) image (d) showing normal vertebral body alignment. Sagittal T1W SE image (e) showing normal spinolaminar line alignment. Sagittal T1W SE image (f) showing normal facet joint alignment (arrows). Sagittal T1W SE image (g) showing normal spinous process alignment (arrows).

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Normal variants that simulate trauma ●

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pseudosubluxation:28 in children, the C2–3 vertebrae, and to a lesser extent the C3–4 vertebrae, may show normal physiological displacement: ■ C2–3 pseudosubluxation has been reported on lateral flexion–extension radiographs in 46 per cent of children 20 per cent of the posterior vertebral body height vascular channels: prominent venous channels within the vertebral body may be mistaken for fluidcontaining fracture lines (Fig. 9.125b, c)

Mechanisms and classification of spinal injuries207 ● ● ●

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there are four major mechanisms that result in spinal trauma: hyperflexion, hyperextension, rotation and shear; axial loading is a potential additional component to all of these except extension each mechanism produces a relatively characteristic pattern of bone and soft-tissue injury, irrespective of the location within the subaxial spine hyperflexion injuries typically occur around a fulcrum centred at the posterior third of the disc space, producing anterior compression and posterior distraction and resulting in four distinct subtypes: ■ simple wedge compression fractures, burst fractures, flexion–distraction injuries and flexion–dislocations hyperextension injuries are most common in the cervical region and can be of variable severity, the most extreme being the hyperextension sprain: ■ extension injuries in the thoracic and lumbar regions are rare rotational injuries typically occur at the thoracolumbar junction due to a combination of torsion and axial load, and are the most severe vertebral body injuries

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Figure 9.125 Mimics of spinal trauma. Sagittal T2-weighted (T2W) fast spin-echo (FSE) image (a) showing mild anterior C2 subluxation and angulation (arrow) but a normal C1–3 spinolaminar line. Axial T1-weighted spin-echo (b) and T2W FSE fat-suppressed (c) images showing prominent vascular channels (arrows).

shear injuries are produced by horizontal or oblique forces usually without axial loading resulting in lateral horizontal or oblique distraction/dislocation: ■ they most commonly occur at the thoracolumbar junction and are associated with a high incidence of cord damage

MRI FEATURES OF SPINAL TRAUMA Bone injury207,208 ● ●

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bony injury may be manifest on MRI as fractures, abnormality of vertebral body morphology and abnormality of vertebral body marrow SI fractures of the cortex appear as breaks in the cortical signal void of the vertebra (Fig. 9.126a) or neural arch (Fig. 9.126b); fractures through the vertebral body may appear as linear areas of increased T2W SI due to haemorrhage/oedema within the fracture line, or if impacted as hypointense lines surrounded by oedema (Fig. 9.126a) morphological changes are usually seen with compression injuries and include anterior wedging (Fig. 9.126c), end-plate disruptions (Fig. 9.126a) and disruption of the posterior vertebral body line (Fig. 9.126c) abnormalities of marrow SI are due to associated marrow haemorrhage and oedema in the acute setting (Fig. 9.126c); the presence of oedema-like SI in the absence of morphological change of the vertebra indicates a vertebral bone bruise209 (Fig. 9.126c) imaging of the whole spine with at least a sagittal T2W FSE FS/STIR image (Fig. 9.126d) is essential to exclude/demonstrate non-contiguous spinal fractures210

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c Figure 9.126 Vertebral fractures. Sagittal T2-weighted (T2W) fast spinecho (FSE) fat-suppressed (FS) image (a) showing disruption of the inferior end-plate (arrow) and an intraosseous impaction fracture (arrowhead). Axial T1-weighted spin-echo image (b) showing a fracture of the spinous process (arrow). Sagittal T2W FSE FS image (c) showing abnormal vertebral morphology (arrows) due to a burst fracture and bone bruising (arrowheads) in adjacent vertebrae. Sagittal T2W FSE FS image (d) showing multi-level upper thoracic bone bruises and wedge compression fractures (arrows).

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whole-spine MRI, in the setting of acute spinal trauma, has demonstrated a second level of vertebral injury in 77 per cent of cases, most being bone bruises a secondary, non-contiguous vertebral fracture (wedge compression or burst) was demonstrated in 34 per cent of patients

Disc injury207,208 ● ●

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disc injury may manifest as abnormality of disc SI, disc morphology, disc prolapse or annular rupture abnormal disc SI: injured IVDs may show evidence of oedema and/or haemorrhage, appearing markedly hyperintense on T2W images (Fig. 9.127a) and hyperintense on T1W images in the subacute stage due to methaemoglobin (Fig. 9.127b) abnormal morphology: disc height may be reduced, as is commonly seen with flexion–compression injuries (Fig. 9.127c), or may be increased anteriorly, as occurs with hyperextension injuries (Fig. 9.127d)

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e d f Figure 9.127 Disc injury. Sagittal T2-weighted (T2W) fast spin-echo (FSE) fat-suppressed (FS) (a) and T1-weighted (T1W) spin-echo (SE) (b) images showing hyperintensity in the discs (arrows) due to subacute haemorrhage. Sagittal T2W FSE FS image (c) showing reduction of T12–L1 disc height (arrow). Sagittal T2W FSE image (d) showing increased anterior C5–6 disc height (arrow) and horizontal increased signal intensity (arrowhead) due to disc avulsion from the end-plate. Sagittal T1W SE image (e) showing acute disc prolapse (arrow) associated with C3–4 bifacet dislocation. Sagittal T2W FSE FS image (f) showing traumatic intraosseous disc prolapse (arrow).

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disc prolapse: acute extradural disc prolapse most commonly occurs in the setting of cervical facet subluxation/dislocation (Fig. 9.127e), while intraosseous disc prolapse is seen with flexion–compression injuries (Fig. 9.127f) annular rupture: acute traumatic annular rupture is seen in cervical hyperflexion or hyperextension injuries (Fig. 9.127d) and thoracolumbar shearing injuries, manifesting as discontinuity of the normal signal void of the disc annulus with adjacent oedema on T2W images

Ligament injury208 ● ● ●

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ligament injury manifests as discontinuity of the black stripe of the spinal ligaments (Fig. 9.128a, b) with oedema on T2W FSE FS/STIR images avulsion of the ligament attachment to the vertebral body during hyperextension injuries in the cervical spine (combined osseo-ligamentous injury) is also recognised (Fig. 9.128c) the use of FS T2W images for assessment of injury to the PLC (Fig. 9.128d) has been highlighted, since on conventional T1W (Fig. 9.128e) and T2W FSE sequences the interspinous space is normally hyperintense owing to fat on either side of the thin interspinous ligament, which may obscure subtle oedema/haemorrhage MRI has been shown to have very high diagnostic accuracy in the assessment of PLC injuries, reported as 90.5 per cent for the supraspinous ligament and 94.3 per cent for the interspinous ligament; T1W images are most specific for the former211 however, the use of T1W sagittal images in isolation may not be reliable in assessment of the cervical spinal ligaments, since absence of the black stripe at disc level is relatively frequently seen (Fig. 9.128a), particularly in the setting of degenerative disc disease212

Acute spinal cord injury208,213 ● ●

acute spinal cord injury (SCI) may be primary or secondary to cord compression clinically, acute SCI may be incomplete or complete on the basis of the extent of loss of motor or sensory function: ■ a complete cord injury involves loss of both functions in the lower sacral segments, while there are various acute cord syndromes occurring that result in incomplete SCI ■ acute traumatic central cord syndrome (ATCCS)214 typically occurs following mid- or lower cervical hyperextension injury, usually in the setting of cervical spondylosis, and is characterised by motor deficit that is maximal in the upper limbs (particularly the hands), bladder dysfunction (usually retention) and variable sensory disturbance below the injury level ■ anterior cord syndrome due to disruption of the anterior spinal artery typically affects the upper thoracic cord and is characterised by significant motor loss but absent or insignificant sensory loss ■ Brown–Séquard syndrome results from hemisection of the cord and is characterised by ipsilateral weakness and loss of proprioception and vibration sense, with contralateral loss of pain and temperature sensation ■ cauda equina syndrome results from injury to the cauda equina and comprises difficulty in walking and deficient perineal sensation

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Figure 9.128 Ligament injury. Sagittal T1-weighted (T1W) spin-echo (SE) image (a) showing discontinuity of the anterior longitudinal ligament (ALL) (short arrow) and the posterior longitudinal ligament (long arrow) due to rupture, with poor definition of the ALL (arrowheads) due to degenerative disc disease. Sagittal T1W SE image (b) showing discontinuity of the supraspinous ligament (arrow) due to rupture. Sagittal T1W SE image (c) showing avulsion of the inferior anterior corner of C3 (arrow) by an intact ALL. Sagittal T2-weighted fast spin-echo fat-suppressed (d) and T1W SE (e) images showing hyperintensity in the interspinous space (arrows d) and fluid-filled discontinuity of the supraspinous ligament (arrowhead d) that are not appreciated on the T1W SE image (arrow e).

spinal cord injury without radiographic abnormality (SCIWORA)28,215 is defined as SCI without any radiographic or CT evidence of spinal trauma: ■ the condition is particularly seen in children due to the marked difference in elasticity between the spinal column and the spinal cord; traction injuries result in cord trauma and radiologically occult ligamentous rupture but no bony injury

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pathologically, acute cord injuries include cord transection, intramedullary haemorrhage, contusion and oedema: ■ intramedullary haemorrhage is usually associated with a clinically complete or irreversible SCI, whereas cord oedema may be associated with a minimal deficit and a good prognosis

MRI findings ● these include changes related to the cord (haemorrhage, oedema, compression, transection) and changes responsible for the cord injury (compression from acute disc herniation, retropulsed bone fragments and epidural haematoma) ● internal cord SI changes have been classified into three types: ■ type 1 – pure intramedullary haematoma, manifest as a focal area of reduced T2W SI (optimally seen on T2*W GE images) without surrounding oedema; very rare ■ type 2 – pure cord oedema without haemorrhage, appearing as a diffusely swollen cord with increased T2W SI (Fig. 9.129a–c)

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Figure 9.129 Acute spinal cord injury. Type 2: Sagittal T1-weighted spin-echo (a), T2-weighted (T2W) fast spin-echo (FSE) (b) and axial T2*-weighted gradient-echo (c) images showing diffuse cord swelling (arrows a) and increased T2W signal intensity (SI) (arrows b, c) due to cord oedema. Type 3: Sagittal T2W FSE image (d) showing a tiny focus of central hypointensity (arrow) due to intramedullary haemorrhage and surrounding flame-shaped cord oedema (arrowheads). (continued)

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Figure 9.129 (continued). Acute traumatic central cord syndrome: Sagittal T2W FSE image (e) showing increased central T2W SI (arrows) following hyperextension injury. Transection: Sagittal T2W FSE fat-suppressed image (f) showing complete cord discontinuity (arrow) following C4–5 fracture–dislocation. Spinal cord injury without radiographic abnormality: Sagittal T2W FSE images (g, h) showing lower cervical cord transection (arrow g) and conus contusion (arrows h) with no evidence of spinal trauma/dislocation.

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type 3 – a combination of haemorrhage and oedema, manifest on T2W images as a small, central area of hypointensity surrounded by a flame-shaped area of hyperintense oedema (Fig. 9.129d); the commonest pattern ■ non-haemorrhagic contusion has also been described, appearing as focal reduced T1W SI and increased T2W SI ATCCS211 appears as central cord oedema without haemorrhage, typically located at the C3–4 (~80 per cent of cases) to C5–6 level (Fig. 9.129e) cord transection is uncommon, occurring in ~2 per cent of spinal trauma cases, and appears as total discontinuity of the cord (Fig. 9.129f) spinal cord changes seen in SCIWORA include215 haemorrhagic and non-haemorrhagic contusion, cord infarction and cord transection (Fig. 9.129g, h) prognostic value of MRI: the presence of intramedullary haemorrhage is a poor prognostic indicator, while the presence of cord oedema only is associated with a good outcome: ■ other poor prognostic indicators include a greater length of cord abnormality, the presence of cord compression and cord transection ■

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Chronic spinal cord injury213,216 ●

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spinal trauma may result in the development of new symptoms and signs several weeks to years later due to various conditions, the most important of which is post-traumatic syringomyelia (PTS), since it may be amenable to surgical intervention PTS is estimated to occur in 3–4 per cent of cases and may be present within 8 weeks of injury; it is due to cystic degeneration of the injured spinal cord at/near the site of trauma: ■ clinically, the symptoms are non-specific, most commonly ascending neurological deficit; it can be treated with shunting post-traumatic myelomalacia is reported in 0.3–3.2 per cent of chronic SCI patients (but ~50 per cent of patients imaged >20 years after injury) and may occur from 2 months to 20 years after trauma, possibly as a precursor to PTS: ■ clinically, its presentation is as for PTS; ~75 per cent of patients have a complete SCI spinal cord atrophy usually occurs several years following trauma and is seen in ~15–20 per cent of cases of SCI, though it has been reported in ~60 per cent of patients imaged >20 years following injury: ■ ~75 per cent of cases are associated with a complete SCI spinal cord cyst has a prevalence of 9 per cent in patients imaged >20 years after injury and represents a fluid collection that is limited to the level of the injury, most commonly in the cervical region: ■ cysts may expand the cord but rarely require intervention; they are associated with complete SCI in 3 cm in craniocaudal dimension is associated with a poor prognosis ■ abscess can also form within the vertebral body and disc, showing a fluid SI centre and a peripheral penumbra sign (Fig. 9.146f–h) ● MRI can also demonstrate healing, which manifests as fatty transformation of the vertebral marrow with absence of enhancement (though contrast enhancement can be seen for some months following healing), and areas of reduced SI due to subchondral fibrosis and osteosclerosis ● the overall sensitivity and specificity of MRI for the diagnosis of pyogenic spondylodiscitis are reported as 96 per cent and 94 per cent, respectively ● the sensitivity of MRI for the various MRI findings of pyogenic spondylodiscitis has also been reported236 for paraspinal or epidural inflammation (~98 per cent), disc enhancement (~95 per cent), fluid SI of the disc on T2W (~93 per cent), erosion/destruction of at least one VEP (~84 per cent) and effacement of the intranuclear cleft on T2W images (~83 per cent): ■ features with low sensitivity include reduction of disc height (~52 per cent) and disc hypointensity on T1W images (~30 per cent) ● features that aid in the differentiation of neuropathic spinal arthropathy and spondylodiscitis have also been investigated;237 neuropathic arthropathy is suggested by the presence of vacuum disc, facet involvement, spondylolisthesis, debris, diffuse SI changes within the vertebral body and rim enhancement of the disc: ■ features that do not aid in the differentiation include end-plate erosion and sclerosis, osteophytes, paraspinal soft-tissue masses and reduction of disc height

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f Figure 9.145 Early pyogenic vertebral osteomyelitis. Axial T1-weighted (T1W) spin-echo (SE) (a), T2-weighted (T2W) fast spin-echo (FSE) (b) and post-contrast T1W SE (c) images showing a focus of infection in an anterolateral subchondral location (arrows) with extension into the left psoas muscle. Sagittal T1W SE (d), T2W FSE fat-suppressed (e) and postcontrast T1W SE (f) images showing the anterior focus of infection (arrows d, e) and diffuse marrow oedema (arrowheads d, e) in the infected vertebra that enhances following contrast (arrow f) with less pronounced oedema in the adjacent vertebra.

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Figure 9.146 Late pyogenic vertebral osteomyelitis. Sagittal T1-weighted (T1W) spin-echo (SE) (a) and T2-weighted (T2W) fast spin-echo (FSE) fat-suppressed (b) images showing end-plate destruction (arrows), heterogeneous T2W hyperintensity of the disc and a small epidural extension (arrowheads). Post-contrast T1W SE image (c) showing peripheral end-plate enhancement (arrows). Phlegmon: Axial T1W SE (d) and post-contrast axial T1W SE (e) images showing uniformly enhancing extraosseous tissue (arrows) in the left paravertebral space. (continued)

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Figure 9.146 (continued) Disc abscess: Sagittal T1W SE (f), T2W FSE (g) and post-contrast T1W SE (h) images showing a rim-enhancing fluid collection spanning the L2–3 disc with surrounding marrow oedema.

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epidural abscess238 is usually secondary to discitis, but may be primary, appearing as an irregularly enhancing epidural mass (Fig. 9.147a–c) that may be associated with marked and extensive dural enhancement (Fig. 9.147c)

Tuberculous discitis/spondylitis233,234,239 ●

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tuberculous spondylitis accounts for 50 per cent of cases of skeletal TB, which may be increasing in prevalence due to the presence of drug-resistant strains of Mycobacterium and an increase in the number of immunocompromised patients pathologically, spread is most commonly via the haematogenous route from a primary focus in the lung or the genitourinary tract, with the development of granulomas and cold abscesses, which may show extensive distant spread along tissue planes and may eventually calcify (Fig. 9.148a, b): ■ the thoracolumbar junction and the lumbar spine are most commonly affected, with the sacrum and cervical regions less commonly involved ■ the anterior subchondral region of the vertebral body is initially involved; subligamentous spread and involvement of the disc space and adjacent vertebra are common, as is contiguous extension along several vertebral segments (Fig. 9.148c, d) ■ erosion of the anterior vertebral body with relative preservation of the disc is typical, though disc involvement is eventually seen in ~75 per cent of cases ■ subligamentous spread may also occur deep to the PLL, with possible associated cord compression ■ secondary extension to the neural arch is seen in >40 per cent of cases (Fig. 9.148e, f), while isolated posterior element lesions are reported in ~3 per cent of cases240 (Fig. 9.148g): – isolated lesions most commonly involve the laminae (~73 per cent), the pedicles (~61 per cent), the spinous processes and the articular processes (~57 per cent), often bilateral and associated with a soft-tissue mass non-contiguous lesions can also occur (Fig. 9.148h), indicating a need for whole-spine imaging: ■ multifocal, non-contiguous disease has been reported in ~70 per cent of cases241

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Figure 9.147 Primary epidural abscess. Sagittal (a) and axial (b) T2-weighted fast spin-echo image showing a heterogeneous hyperintense collection (arrows) in the left side of the epidural space. Post-contrast sagittal T1-weighted spin-echo image (c) showing irregular enhancement of the abscess (arrow) with extensive dural enhancement (arrowheads).

isolated vertebral body TB242 (see below) is also reported and may mimic neoplastic vertebral involvement various patterns of spinal TB have been proposed, including paradiscal, anterior and central: ■ paradiscal pattern is seen in >50 per cent of adults and represents metaphyseal involvement with erosion of the end-plate (Fig. 9.149a–c) and herniation of the disc into the end-plate (Fig. 9.149d), resulting in significant loss of disc height ■ anterior pattern: stripping of the periosteum, avascular necrosis and vertebral collapse (Fig. 9.149e) ■ central pattern: involvement of the whole of the vertebral body (Fig. 9.149f, g) vertebral collapse is seen in 73 per cent of cases and may result in kyphosis, particularly in the thoracic region, with associated neurological deficit paraspinal (78 per cent) and epidural (68 per cent) abscesses are common, the latter being a major cause of neurological compromise: ■ depending on the site of spinal involvement, paraspinal abscesses may occur in the retropharyngeal space, the mediastinum or the psoas muscles, in which case they can track to the groin arachnoiditis, meningitis and spinal cord infection may also be seen spinal TB in children243 shows similar pathological features to that in adults, with kyphosis reported in 79 per cent, contiguous involvement of two or more vertebrae in 85 per cent, an epidural or paraspinal phlegmon/abscess in 98 per cent and subligamentous spread in 64 per cent atypical Mycobacterial infections244 have no distinguishing imaging features

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Figure 9.148 Tuberculous spondylodiscitis. Axial T2-weighted (T2W) fast spin-echo (FSE) image (a) and corresponding CT image (b) showing a calcified paravertebral abscess (arrows). Sagittal T1-weighted (T1W) spinecho (SE) (c) and coronal T2W FSE (d) images showing contiguous extension across three vertebral levels (arrows) with an associated left psoas abscess (arrowhead d). Sagittal (e) and axial (f) T1W SE images showing extension of disease into the neural arches (arrows). (continued)

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Figure 9.148 (continued) Axial T2W FSE image (g) showing isolated neural arch involvement (arrows). Sagittal short tau inversion recovery image (h) showing multi-level non-contiguous vertebral involvement (arrows).

h

Infective disorders of the subaxial spine

a

b

c

f d e

g

Figure 9.149 Tuberculous spondylodiscitis, patterns of spinal involvement. Paradiscal: Sagittal T1-weighted (T1W) spin-echo (SE) (a), T2-weighted (T2W) fast spin-echo (FSE) (b) and post-contrast T1W SE fat-suppressed (FS) (c) images showing end-plate erosion (arrows a, b), disc enhancement (arrow c) and marrow oedema. Sagittal post-contrast T1W SE image (d) showing herniation of the disc into the end-plate (arrow). Anterior: Sagittal T1W SE image (e) showing prevertebral extension with stripping of the anterior longitudinal ligament (arrows) and hypointensity of the L2–4 vertebral bodies due to osteonecrosis. Central: Sagittal T1W SE (f) and T2W FSE FS (g) images showing diffuse vertebral involvement (white arrows) with pre-vertebral (arrowheads) and epidural (black arrows) extension but relative sparing of the discs.

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Figure 9.150 Tuberculous spondylodiscitis. Sagittal T2-weighted (T2W) fast spin-echo (FSE) image (a) showing vertebra plana of T3 (arrow) with associated soft-tissue abscess and cord compression. Axial T2W FSE image (b) showing anterior subligamentous spread (arrows). Sagittal T2W FSE image (c) showing posterior subligamentous spread (arrows). Coronal (d) and axial (e) T2W FSE images showing a large left psoas abscess (arrows). Sagittal T2W FSE image (f) showing C3–4 involvement with a large epidural abscess (arrows) causing cord compression. Sagittal post-contrast T1weighted spin-echo image (g) showing L4 vertebral infection (arrow) with an enhancing granuloma (arrowhead) in the conus.

Infective disorders of the subaxial spine

MRI findings ● marrow oedema is seen with reduced SI on T1W and increased SI on T2W FS/STIR images, and a variable degree of vertebral collapse, which may result in vertebra plana (Fig. 9.150a) ● end-plate and disc destruction as seen with pyogenic spondylitis (Fig. 9.149a–c) ● anterior (Fig. 9.150b) and posterior (Fig. 9.150c) subligamentous spread ● large, tracking paraspinal (Fig. 9.150d, e) and epidural abscesses; the latter may cause cord compression (Fig. 9.150f) ● meningeal and cord involvement manifest as meningeal and cord enhancement (Fig. 9.150g): ■ increased T1W SI of the CSF indicates CSF involvement, while arachnoiditis is manifest by clumping of caudal nerve roots

Brucella spondylodiscitis245 ● ● ● ●

Brucella infection occurs as an occupational disease in developed countries or from the consumption of non-pasteurised milk or milk products from infected animals clinically, patients present with various musculoskeletal symptoms including peripheral arthritis, sacroiliitis and spondylodiscitis osteoarticular involvement occurs in 20–60 per cent of cases; the spine is affected in 8–13 per cent, usually in older age groups the lumbar region is commonly involved, the thoracic and sacral spine less so

MRI findings ● the commonest pattern is disc involvement with spondylitis of the adjacent vertebral bodies ● loss of disc height is common ● additional features include paravertebral soft-tissue inflammation; paravertebral abscess formation is rare (~14 per cent of cases): ■ exuberant osteophyte formation is seen in ~50 per cent of cases ● vertebral collapse and epidural inflammation/abscess are not reported

Miscellaneous spinal infections234 ●

● ●

Salmonella infection may occur in patients with sickle cell disease or in elderly men with genitourinary tract infections: ■ Salmonella infection complicating sickle cell disease is more commonly seen in the relatively avascular central area of the VEP, rather than the anterolateral aspect Proteus spondylitis may be seen in elderly men secondary to genitourinary tract infections and has no distinguishing radiological features Actinomyces infection tends to have an indolent clinical course similar to that of TB; spinal infection is uncommon but occurs as a result of direct spread from the adjacent lung or ribs: ■ radiologically, there is a combination of lytic and sclerotic vertebral destruction, with extension to the neural arch but sparing of the disc ■ soft-tissue abscess and sinus tracts may develop

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● ● ● ● ● ●

●

nocardiosis: this infection resembles TB and actinomycosis hydatid disease produces similar changes to actinomycosis with vertebral involvement, lack of vertebral collapse and sparing of the disc Candida infections are seen in immunocompromised patients: ■ MRI features are non-specific with increased T2W disc and/or vertebral SI Aspergillus infections are seen in immunocompromised patients: ■ MRI demonstrates features of spondylodiscitis; paravertebral abscess formation is relatively common Cryptococcus infection rarely involves the spine, with no specific imaging features blastomycosis is endemic in the Americas and Africa: ■ spinal involvement occurs secondary to haematogenous spread from the lungs, resulting in marked vertebral destruction and sclerosis; direct extension into the rib cage with skip lesions is common coccidioidomycosis: the findings are similar to blastomycosis, with the addition of paravertebral and epidural involvement

Vertebral osteomyelitis without disc involvement246 ●

● ●

pyogenic vertebral osteomyelitis without involvement of the IVD is a rare finding, accounting for 2–3 cm are seen, and are termed ‘giant bone islands’ ● osteomas are multiple (in the same or adjacent vertebra) in 20 per cent of cases

b a Figure 9.152 Vertebral osteoma. Sagittal T1-weighted spin-echo (a) and T2-weighted fast spin-echo (b) images showig a small area of signal void (arrows) with a spiculated margin.

Osteoid osteoma250–253,254 ● ●

●

●

osteoid osteoma is located in the spine in 8–10 per cent of cases, usually presenting in the 5–25-year age range 59 per cent involve the lumbar region, 27 per cent the cervical and 12 per cent the thoracic, with ~80 per cent located in the lamina, the articular facet or the pars: ■ ~10–15 per cent involve the transverse or spinous process and 2500 rad clinically, most osteochondromas are asymptomatic or present as hard mass lesions; only 1–2.5 per cent of cases occurring in MHE result in spinal cord compression:

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solitary cases most commonly present at ~30 years of age, while in MHE presentation is usually in childhood ■ solitary lesions most commonly arise in the cervical spine (~56 per cent, usually at the C1–2 level)), followed by the thoracic (38 per cent) and lumbar (6 per cent) levels pathologically, most are sessile lesions arising from the neural arch or occasionally the vertebral body ■

●

MRI findings ● the lesion is surrounded by a thin rim of hypointense cortical bone, the centre of the lesion with marrow SI (Fig. 9.156a) and continuous with the marrow cavity at the site of origin (Fig. 9.156b) ● the thin cartilage cap is seen as a layer of high T2W SI (Fig. 9.156c); the presence of a thick (>1 cm) cartilage cap in an adult raises the suspicion of secondary chondrosarcomatous degeneration

Chondroblastoma260 ● ●

spinal chondroblastoma represents 1.4 per cent of all chondroblastomas, with most (~55 per cent) arising in the thoracic region clinically, most patients are male, with a mean age at presentation of ~30 years: ■ symptoms include localised spinal pain and neurological deficit due to the relatively frequent occurrence of spinal cord compression

b

c a Figure 9.156 Vertebral osteochondroma. Sagittal (a) and axial (b) T1-weighted spin-echo images showing an ossified lesion (arrows) arising from the right lamina (arrowheads b). Coronal T2-weighted fast spin-echo image (c) showing a hyperintense cartilage cap (arrows).

Primary spinal tumours

●

pathologically, the lesion typically causes vertebral expansion, commonly with involvement of both the vertebral body and the neural arch

MRI findings ● vertebral chondroblastoma presents as an expanded lesion involving both the vertebral body and the neural arch, with bone destruction and an associated soft-tissue extension in most cases ● spinal cord compression is present in >50 per cent of cases ● the lesion shows intermediate T1W SI and T2W hyperintensity; reactive marrow/soft-tissue oedema and fluid levels have not been reported

Chondrosarcoma250,251,253,261,262 ●

●

●

chondrosarcoma is the second commonest primary malignant bone tumour of the spine, representing 7–12 per cent of primary malignant vertebral tumours: ■ conversely, 3–12 per cent of chondrosarcomas arise in this location clinically, spinal chondrosarcoma has a wide age of presentation, with a mean reported age of 37 years: ■ symptoms include local pain and neurological deficit due to root or cord/cauda equina compression and most arise in the thoracic spine (~60 per cent of cases) pathologically, spinal chondrosarcoma may represent a central lesion or may arise in an underlying osteochondroma, presenting as a large, calcifying, cartilaginous mass extending from the vertebral body or the neural arch: ■ most are histologically low grade and ~60 per cent arise in the lumbar region ■ rarely, histological subtypes such as clear cell or mesenchymal chondrosarcoma may involve the spine

MRI findings ● central vertebral chondrosarcoma tends to involve the neural arch (40 per cent), the neural arch and the vertebral body (45 per cent) (Fig. 9.157a–d) and rarely the vertebral body in isolation (15 per cent): ■ as with chondrosarcomas elsewhere, the lesion shows low to intermediate T1W SI (Fig. 9.157a, c) and high T2W SI (Fig. 9.157b) and exhibits septal and rim enhancement following contrast (Fig. 9.157d) ■ foci of punctate signal void may be present due to matrix mineralisation (Fig. 9.157a–c) ■ cortical destruction and extraosseous extension is common, with extension across the disc into an adjacent vertebra reported in 35 per cent of cases ● peripheral spinal chondrosarcoma appears as a T2W hyperintense, lobulated paraspinal mass attached to the spine via its bony stalk, with a low SI peripheral rim and hypointense internal septa ● mesenchymal chondrosarcoma shows a more aggressive growth pattern, with intermediate SI on both T1W (Fig. 9.157e) and T2W (Fig. 9.157f) images and diffuse enhancement of solid tumour following contrast

HAEMATOPOIETIC TUMOURS Plasmacytoma250,263 ● ● ● ●

solitary plasmacytoma is a solitary focus of malignant plasma cell proliferation without generalised marrow infiltration spinal plasmacytoma most commonly involves the lower thoracic spine (T7–12), followed by the lumbar spine and then the cervical spine clinically, patients usually present after the age of 60 years with pain and signs of neural compression in 75 per cent of cases pathologically, the lesion is located in the vertebral body but commonly extends into the pedicle: ■ scalloping of the cortex may result in apparent vertical trabeculation, and sclerosis of the end-plate is also a feature ■ end-plate erosion and partial vertebral collapse may occur and the tumour can extend into the disc space

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a

d

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f

Figure 9.157 Vertebral chondrosarcoma. Sagittal T1-weighted (T1W) spin-echo (SE) (a) and T2-weighted (T2W) fast spinecho (FSE) (b) images showing a lesion involving both the vertebral body (arrows) and the spinous process with extension into the posterior epidural space (arrowheads) resulting in cord compression. Axial T1W SE (c) and post-contrast T1W SE (d) images showing a lesion involving the vertebral body (arrowhead c) and the right transverse process (arrows c) with septal (arrowhead d) and peripheral (arrow d) enhancement. Mesenchymal chondrosarcoma: Sagittal T1W SE (e) and T2W FSE (f) images showing a lesion involving both the vertebral body (arrows) and the spinous process (arrowheads) with associated conus compression.

Primary spinal tumours

MRI findings ● the tumour appears isointense or hypointense to muscle on T1W images (Fig. 9.158a) and shows heterogeneous hyperintensity on T2W images (Fig. 9.158b) ● curvilinear low SI areas within the tumour (Fig. 9.158c) and irregularity of the endosteal cortex (Fig. 9.158d) are characteristic features that may help to differentiate the tumour from a solitary metastasis

a

c

b

d

e

Figure 9.158 Vertebral plasmacytoma. Sagittal T1-weighted (T1W) spin-echo (SE) image (a) showing pathological vertebral collapse (arrow). A second radiologically occult lesion is also demonstrated (arrowhead). Sagittal T2-weighted (T2W) fast spin-echo (FSE) fat-suppressed image (b) showing vertebral collapse due to a mildly hyperintense lesion (arrow). Axial T1W SE images (c, d) showing curvilinear low signal intensity areas (arrow c) and endosteal irregularity (arrowheads d). Extension of tumour into the pedicle is also demonstrated (arrow d). Sagittal T2W FSE image (e) showing tumour extension across the disc space (arrow).

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extension into the neural arch is common (Fig. 9.158d), with circumferential involvement and vertebral collapse combining to produce spinal cord/cauda equina compression (Fig. 9.158b) the tumour may extend across the disc space (Fig. 9.158e) and MRI may show radiographically occult lesions (Fig. 9.158a), indicating a diagnosis of multiple myeloma rather than plasmacytoma: ■ all patients should therefore undergo imaging of the whole spine

Multiple myeloma250,252,253,264 ● ● ●

●

multiple myeloma is a monoclonal proliferation of malignant plasma cells within bone marrow and involves the spine in ~66 per cent of cases the disease typically presents over the age of 50 years, and after metastatic disease is the commonest malignant lesion of the spine pathologically, three patterns of marrow involvement are described at MRI: ■ the marrow may appear normal at presentation in 50–75 per cent of cases of stage 1 myeloma and in 20 per cent of cases of stage 3 disease ■ a focal pattern with well-demarcated margins ■ a diffuse pattern of marrow involvement, which is indicative of a higher tumour burden compression fractures are seen in up to 80 per cent of myeloma patients, due to a combination of lytic lesions and generalised osteoporosis, with associated cord/cauda equina compression in 20 per cent of cases: ■ of all compression fractures in myeloma, ~66 per cent have a benign appearance while ~33 per cent appear pathological ■ benign compression fractures are most commonly seen at the thoracolumbar junction

MRI findings ● the marrow SI may appear normal, simulating richly cellular marrow, in which case contrast-enhanced T1W images may show intense marrow enhancement with subtle, diffuse myelomatous infiltration ● focal/multifocal involvement results in regions of reduced T1W SI (Fig. 9.159a) and increased T2W/STIR SI (Fig. 9.159b) that enhance intensely following contrast: ■ occasionally, lesions are relatively hyperintense on T1W and are missed, being evident only on T2W/STIR

a b

Figure 9.159 Vertebral multiple myeloma. Sagittal T1-weighted (T1W) spin-echo (SE) image (a) showing advanced pathological collapse of T12 (arrow) with focal marrow involvement in L1 (arrowhead). Sagittal T2-weighted fast spin-echo fat-suppressed image (b) showing multifocal hyperintense lesions (arrows) throughout the thoracic spine. (continued)

Primary spinal tumours

c

d

e

f

g Figure 9.159 (continued) Axial T1W SE image (c) showing involvement of both the vertebral body (arrowhead) and the neural arch (arrow). Sagittal T1W SE image (d) showing a combined pattern of diffuse (arrow) and focal (arrowheads) marrow involvement. Coronal T1W SE image (e) showing the variegated pattern of marrow disease. Sagittal (f) and axial (g) T1W SE images showing pathological vertebral collapse (arrow f) with cord compression (arrowhead g) and extraosseous extension (arrow g).

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● ●

■ involvement of the vertebral body and the neural arch is typical (Fig. 9.159c) diffuse marrow infiltration results in a generalised reduction of T1W SI, such that the IVDs appear isointense or hyperintense to the vertebral body, with generalised increased marrow SI on T2W/STIR images: ■ a combination of diffuse and multifocal vertebral involvement may also be seen (Fig. 9.159d) the variegated pattern, also termed the ‘pepper and salt’ pattern, is characterised by multiple tiny foci of reduced T1W (Fig. 9.159e) and increased T2W SI that enhance following contrast: ■ this pattern is almost exclusively seen in early disease vertebral collapse with cord compression is common (Fig. 9.159f), the latter also being due to extraosseous soft-tissue extension (Fig. 9.159g) the benign form of vertebral compression fracture may also exhibit the vertebral vacuum phenomenon

Lymphoma250,265,266 ● ●

lymphoma: both non-Hodgkin’s lymphoma and Hodgkin’s disease may affect the spine as paravertebral disease, vertebral involvement or epidural infiltration, in an isolated manner or in any combination pathologically, vertebral involvement is more commonly due to haematogenous spread than to direct invasion from adjacent nodal disease, and results in a sclerotic, mixed sclerotic and lytic, or purely lytic pattern of destruction: ■ invasion by local lymph node masses may result in anterior vertebral scalloping ■ epidural mass with foraminal extension with/without bone involvement is another mode of presentation

MRI findings ● patterns of marrow involvement are similar to those reported with multiple myeloma and may be diffuse and uniform (Fig. 9.160a), diffuse and heterogeneous or multifocal (Fig. 9.160b) ● typically, both the vertebral body and the neural arch are infiltrated (Fig. 9.160c, d) ● the SI characteristics are non-specific, being intermediate on T1W images (Fig. 9.160a–c) and increased on T2W FSE FS/STIR images (Fig. 9.160d), though sclerotic forms of lymphoma show reduced marrow SI on all sequences ● paravertebral (Fig. 9.160e) and epidural extension (Fig. 9.160f, g) are commonly seen, but associated cortical destruction is less common than with metastatic disease and may be a useful differentiating feature (Fig. 9.160e)

a

b

Figure 9.160 Vertebral lymphoma. Sagittal T1-weighted (T1W) spin-echo (SE) images (a, b) showing diffuse (arrows, arrowheads a) and multifocal (arrows b) marrow infiltration patterns. (continued)

Primary spinal tumours

d

c

e

f

g

Figure 9.160 (continued) Sagittal T1W SE (c) and axial T2-weighted (T2W) fast spin-echo (FSE) fat-suppressed (d) images showing combined vertebral body and neural arch involvement (arrows). Axial T2W FSE image (e) showing paravertebral extension (arrow) through an intact cortex (arrowhead). Sagittal T2W FSE (f) and axial T1W SE (g) images showing pathological collapse (arrow f) and combined epidural (arrowhead g) and paravertebral (arrows g) extension.

ROUND CELL TUMOURS Ewing sarcoma250,253,267 ●

Ewing sarcoma is the commonest primary malignant bone tumour of the spine in children; 3.5–10 per cent of all cases of Ewing sarcoma arise in this location, though metastatic spinal involvement is far more common: ■ regarding spinal location, ~3 per cent occur in the cervical region, 10 per cent in the thoracic region, 25 per cent in the lumbar spine and the remainder in the sacrum

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clinically, presentation is usually at age 10–30 years, with signs of spinal cord or nerve root compression in ~60 per cent of cases at the time of diagnosis pathologically, the tumour most commonly produces lytic vertebral collapse, though vertebral sclerosis related to osteonecrosis may also occur and may originally present as a sclerotic pedicle: ■ the tumour usually arises in the neural arch but commonly extends to the vertebral body, also producing a large paravertebral/extradural mass, while isolated vertebral body and neural arch involvement are rare ■ multi-level vertebral involvement is reported in 10 per cent of cases267

MRI findings ● the signal characteristics are non-specific, with intermediate T1W SI (Fig. 9.161a) and intermediate to high T2W SI (Fig. 9.161b), though vertebral sclerosis results in areas of reduced marrow SI (Fig. 9.161c) ● in most cases, a large, paravertebral, soft-tissue mass (Fig. 9.161d) with epidural and foraminal extension is commonly present (Fig. 9.161e–g) ● rarely, Ewing sarcoma presents with marked vertebral collapse (Fig. 9.161h), occasionally resulting in vertebra plana

b

a

c

d

Figure 9.161 Vertebral Ewing sarcoma. Coronal T1-weighted (T1W) spin-echo (SE) (a) and sagittal T2-weighted (T2W) fast spin-echo (FSE) (b) images showing non-specific marrow infiltration of the L2 vertebra (arrows). Axial T1W SE image (c) showing low marrow signal intensity (arrows) due to marrow sclerosis. Axial T1W image SE (d) showing destruction of the right pedicle with associated paravertebral (arrows) and epidural (arrowhead) extension. (continued)

Primary spinal tumours

f

e

h

g Figure 9.161 (continued) Sagittal T1W SE (e), axial T2W FSE (f) and post-contrast sagittal T1W SE (g) images showing extensive enhancing epidural (arrows) and paravertebral (arrowheads) disease. Sagittal T1W SE image (h) showing C4 vertebral collapse.

VASCULAR TUMOURS Haemangioma251–253 ● ● ●

vertebral haemangiomas are identified in 10–12 per cent of spines at post-mortem, most located in the vertebral body with extension into the neural arch being relatively rare ~50 per cent are located in the thoracic region, with the remainder equally divided between the cervical and the lumbar vertebrae multi-level involvement is recognised (Fig. 9.162a), while sacral haemangiomas are rare

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clinically, most haemangiomas are asymptomatic, being discovered incidentally on imaging studies: ■ occasionally, pain occurs due to pathological fracture ■ rarely, compressive myelopathy occurs during the third trimester of pregnancy and resolves postpartum pathologically, they comprise thin-walled, endothelium-lined blood vessels within a stroma composed of varying amounts of fat, fibrous tissue, smooth muscle and bone: ■ erosion of the primary trabeculae leads to hypertrophy of secondary trabeculae, resulting in the classical vertical striation seen radiographically, and the dense, multiple ‘polka dots’ seen on CT

MRI findings ● trabecular thickening is identified as multiple dots of signal void on axial images (Fig. 9.162b) and linear, hypointense areas on sagittal images (Fig. 9.162c) ● classical haemangiomas are hyperintense on T1W (Fig. 9.162d) and T2W (Fig. 9.162e) images due to their high fat content; the T2W hyperintensity is contributed to by slow flow within the vessels ● on STIR and T2W FS images, the SI may be low or high depending on the relative composition of fatty and vascular tissue ● enhancement is seen following contrast, particularly on T1W FS images ● very vascular haemangiomas with little fat show intermediate T1W SI (Fig. 9.162f) but remain hyperintense on T2W (Fig. 9.162g)

b

c

a Figure 9.162 Vertebral haemangioma. Sagittal T2-weighted (T2W) fast spin-echo (FSE) image (a) showing multi-level vertebral involvement (arrows). Axial T1-weighted (T1W) spin-echo (SE) (b) and T2W FSE (c) images showing hypointense ‘dots’ (arrowheads b) and vertical lines (arrow c) due to thickened trabeculae. (continued)

Primary spinal tumours

d

e f

Figure 9.162 (continued) Sagittal T1W SE (d) and T2W FSE (e) images showing a hyperintense thoracic haemangioma (arrows). Vascular haemangioma: Sagittal T1W SE image (f) showing an intermediate signal intensity lesion in L1 (arrow). Axial T2W FSE image (g) showing a hyperintense lesion extending into the pedicles (arrows).

g

Aggressive haemangioma251,253,268 ● ● ●

aggressive haemangioma refers to the rare occurrence of enlargement of the vertebra by haemangiomatous tissue, which may result in neurological symptoms from spinal cord compression this is most commonly seen in the thoracic spine (~90 per cent of cases), 75 per cent of cases occurring between T3 and T9 pathologically, the trabecular thickening seen with conventional haemangiomas is not usually seen and extension to the neural arch is far more common

MRI findings ● the typical fatty SI of conventional haemangiomas is frequently not appreciated on T1W (Fig. 9.163a), while the lesion is markedly hyperintense on T2W (Fig. 9.163b) ● however, the lesion may appear hyperintense on T1W images in ~50 per cent of cases (Fig. 9.163c) and signal voids may be present in 20–30 per cent of cases (Fig. 9.163a, b) ● extraosseous extension is also commonly seen (Fig. 9.163d), as is enhancement following contrast (Fig. 9.163e) ● vertebral height is usually maintained, and the cortex adjacent to the extraosseous mass is also usually intact

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d

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Figure 9.163 Aggressive vertebral haemangioma. Sagittal T1-weighted (T1W) spin-echo (SE) (a) and T2-weighted (T2W) fast spin-echo (FSE) (b) images showing a lesion expanding L3 (arrows) with internal flow void (arrowheads). Sagittal T1W SE (c) and axial T2W FSE (d) images showing a markedly hyperintense lesion (arrow c) with posterior extraosseous extension (arrows d). Post-contrast axial T1W SE image (e) showing intense tumour enhancement.

Gorham’s disease269,270 ● ●

●

Gorham’s disease, also known as massive osteolysis or disappearing bone disease, is a rare condition resulting in spontaneous resorption of bone associated with angiomatosis of blood or lymphatic vessels clinically, it is most commonly seen in young adults, but can occur at any age, presenting with the insidious onset of dull pain: ■ spinal involvement is rare and potentially fatal due to associated severe neurological deficits pathologically, the disease is commonly polyostotic, involving multiple contiguous bones without the presence of skip lesions: ■ dislocation of the spine may occur

MRI findings ● the lesions are typically hyperintense on T2W/STIR images and isointense or hyperintense on T1W images (Fig. 9.164a–c)

Primary spinal tumours

a

c

b

Figure 9.164 Gorham’s disease of the spine. Sagittal T1-weighted (T1W) spin-echo (SE) (a) and short tau inversion recovery (STIR) (b) images showing contiguous involvement of three vertebrae with increased T1W SE signal intensity (arrows a) and marked hyperintensity on STIR (arrows b). Axial T1W SE image (c) showing focal hypointensity (arrow).

TUMOURS OF NOTOCHORD ORIGIN Giant vertebral notochordal rest271 ● ●

notochordal rests most commonly occur as microscopic foci of residual notochordal tissue that may be identified within the vertebral bodies rarely, macroscopic foci of benign notochordal tissue, which is histologically distinct from chordoma, may occur and result in local symptoms of back pain

MRI findings ● reported lesions appear as well-defined, intravertebral masses located adjacent to the end-plate, with intermediate T1W SI and increased T2W SI (Fig. 9.165a–c), similar to that of the NP, and no vertebral destruction ● diffuse vertebral involvement is also reported ● a clue to the diagnosis is the presence of normal radiographs in all previously reported cases and the absence of bone destruction on CT, which may show mild vertebral sclerosis or trabecular thickening

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a

Figure 9.165 Giant vertebral notochordal rest. Sagittal T1-weighted spin-echo (a), T2-weighted (T2W) fast spin-echo (FSE) (b) and axial T2W FSE (c) images showing a lobulated lesion (arrows) within L4 with the signal intensity characteristics of the nucleus pulposus.

Vertebral chordoma250,251,272,273 ●

●

●

chordoma is the commonest primary bone tumour of the sacrum (see later), but can also occur in the mobile spine, most commonly in the lumbar region (7–8 per cent, most ofen L2 or L3) followed by the cervical region (5 per cent, particularly C2) and the thoracic region (~2 per cent) clinically, vertebral chordoma is more common in males and typically presents in the seventh decade with a combination of neck/back pain and neurological deficit depending on the presence of nerve root or spinal cord compression pathologically, chordoma is a slow-growing, malignant tumour arising from remnants of the notochord, and is therefore typically centred on sites of notochordal rests, arising centrally and towards the posterior aspect of the vertebral body, or less commonly anteriorly: ■ sparing of the neural arch is a potentially distinctive feature, while purely extraosseous spinal chordoma mimicking a neurogenic tumour has also been reported

MRI findings the myxoid stroma results in a lesion that is typically isointense or slightly hyperintense to muscle on T1W images (Fig. 9.166a) and hyperintense on T2W images (Fig. 9.166b), with variable enhancement following contrast (Fig. 9.166c) ● internal, hypointense, fibrous septa may be visible on T2W images ● increased T1W SI may be seen due to the presence of haemorrhage, while T2W images may show internal, hypointense septation and lobulation ● extraosseous soft-tissue tumour is common and can extend over several vertebral levels resulting in spinal cord (Fig. 9.166d) or cauda equina (Fig. 9.166e) compression, foraminal enlargement (Fig. 9.166f) and a pre-vertebral mass ● vertebral collapse is also a feature (Fig. 9.166e), as is extension into the disc space and an adjacent vertebral body (Fig. 9.166e) ●

Primary spinal tumours

b

a

d

c

f

e

Figure 9.166 Vertebral chordoma. Sagittal T1-weighted (T1W) spinecho (SE) (a) and axial T2-weighted (T2W) fast spin-echo (FSE) (b) images showing a lesion (arrows) arising in the posterior aspect of L4 with epidural extension. Post-contrast sagittal T1W SE image (c) showing variable enhancement (arrow). Sagittal T2W FSE image (d) showing a large tumour arising from C3 (white arrow) involving the adjacent vertebrae and causing cord compression (black arrows). Sagittal T2W FSE image (e) showing L5 vertebral collapse with a small pre-vertebral mass (white arrow), extension of tumour to L4 (arrowhead) and epidural extension (black arrows) resulting in cauda equina compression. Axial short tau inversion recovery image (f) showing extension through the intervertebral foramen with a large paravertebral mass (arrows).

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MISCELLANEOUS TUMOURS Simple bone cyst274 ● ●

simple bone cyst is a rare occurrence in the spine, with fewer than 20 cases reported in the literature the cervical and lumbar regions are most commonly affected, most involving the vertebral body or spinous process, though the pedicle may be rarely involved

MRI findings ● the lesion is well defined and has fluid SI on all pulse sequences (Fig. 9.167a–c), showing either no or rim enhancement (Fig. 9.167d) following contrast ● surrounding reactive marrow and soft-tissue changes are not a feature

b

a

c

d

Figure 9.167 Vertebral simple bone cyst. Sagittal T1-weighted (T1W) spin-echo (SE) (a) and coronal short tau inversion recovery (b) images showing a homogeneous fluid signal intensity lesion (arrows) in the right lateral mass of C1. Axial T1W SE (c) and post-contrast T1W SE (d) images showing rim enhancement of the lesion (arrows).

Aneurysmal bone cyst250,251,253 ● ●

●

ABC involves the spine in ~12–30 per cent of cases, most commonly in the lumbar region, followed by the cervical and the thoracic clinically, 80 per cent of patients present at age 5–20 years with a palpable mass, local back pain, root pain and variable neurological deficit, including paraplegia due to spinal cord compression: ■ spinal deformity (structural scoliosis and/or kyphosis) occurs in ~10 per cent of cases (Fig. 9.168a) pathologically, the tumour typically comprises multiple blood-filled spaces, but it may be predominantly solid (solid ABC) in 5–7.5 per cent of cases:

Primary spinal tumours

b

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e Figure 9.168 Vertebral aneurysmal bone cyst (ABC). Post-contrast coronal T1-weighted (T1W) spin-echo (SE) image (a) showing unilateral collapse in an upper thoracic lesion resulting in mild structural scoliosis (arrow). Sagittal (b) and axial (c) T1W SE images showing an intermediate signal intensity lesion in the posterior aspect of L3 (arrows) with expansion into the left neural arch (double arrows c). Axial T2-weighted (T2W) fast spin-echo (FSE) image (d) showing multiple fluid levels (arrowheads) within the tumour. Post-contrast axial T1W SE image (e) showing septal enhancement (arrowheads). (continued)

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Figure 9.168 (continued) Sagittal T1W SE (f), axial T2W FSE fat-suppressed (FS) (g) and post-contrast sagittal T1W SE FS (h) images showing a solid region (arrows f, g) that enhances (arrows h) combined with a cystic area containing fluid levels (arrowhead g). Sagittal T1W SE image (i) showing a thoracic ABC involving the spinous process causing cord compression (arrow).

i

■ ■ ■

most (65–99 per cent) are considered to be primary lesions, most often arising in the neural arch but commonly extending into the vertebral body (75 per cent of cases) in 70 per cent of cases, the lesion is limited to one side of the midline; extension to the adjacent vertebra is also recognised lesions located predominantly in the spinous or transverse processes tend to show a greater degree of expansion than those in the pedicle/vertebral body

MRI findings ● the lesion is lytic and expansile, with intermediate T1W SI (Fig. 9.168b, c) and increased T2W SI, commonly with extensive fluid-level change (Fig. 9.168d) ● a hypointense rim and hypointense internal septa are characteristic, and can enhance following contrast (Fig. 9.168e) ● the presence of an enhancing solid component raises the possibility of secondary ABC change (Fig. 9.168f–h) ● extension into the vertebral body may result in partial vertebral collapse (Fig. 9.168a, b), while expansion of the neural arch can cause spinal cord compression (Fig. 9.168i) ● a large soft-tissue mass may also occur

Giant cell tumour250–253 ●

giant cell tumour (GCT) involves the spine in 7 per cent of cases, of which ~90 per cent arise in the sacrum (see later), and accounts for 8.5–15 per cent of osseous spinal tumours excluding myeloma

Primary spinal tumours

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clinically, patients present in the third to fourth decades; the tumour occurs more commonly in women: ■ symptoms include back pain, with radicular symptoms in 33 per cent of cases ■ a dramatic increase in the size of the lesion may be seen during pregnancy pathologically, unlike most benign spinal tumours, GCT preferentially involves the vertebral body; extension into the neural arch is common, while extension to an adjacent vertebra is rare: ■ the thoracic spine is most commonly involved, followed by the cervical and the lumbar

MRI findings ●

the tumour shows intermediate to low SI on T1W images (Fig. 9.169a) and low SI in the solid component on T2W images in 63–96 per cent of cases (Fig. 9.169b); the low SI is due to a combination of fibrosis and haemosiderin from recurrent haemorrhage

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c Figure 9.169 Vertebral giant cell tumour. Sagittal T1-weighted (T1W) spin-echo (SE) image (a) showing pathological collapse of L5 (arrows) due to an intermediate signal intensity (SI) lesion containing areas of low SI. Axial T2-weighted (T2W) fast spin-echo (FSE) image (b) shows profoundly reduced SI (arrows) with areas of cystic degeneration (arrowheads). Post-contrast sagittal T1W SE image (c) showing uniform enhancement of solid areas of the tumour (arrows). Sagittal (d) and axial (e) T2W FSE images showing a large extraosseous extension (arrows) with associated cord compression (arrowheads).

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cystic areas (Fig. 9.169b) and secondary ABC change may also be apparent, and the lesion is limited by a peripheral, hypointense pseudocapsule enhancement of the solid areas is seen following contrast (Fig. 9.169c) vertebral collapse, possibly with cord compression (Fig. 9.169d) and soft-tissue extension (Fig. 9.169e), may also be seen

Fibrous dysplasia250,275,276 ● ●

● ●

vertebral involvement is uncommon in fibrous dysplasia, but when it occurs it is usually associated with polyostotic disease; there are only a few case reports of monostotic spinal fibrous dysplasia274 in polyostotic fibrous dysplasia, the prevalence of spinal involvement is reported as 63 per cent based on scintigraphy, with the lumbar and thoracic regions most commonly involved: ■ a 40 per cent incidence of scoliosis is reported in polyostotic disease in monostotic fibrous dysplasia, all reported cases have involved the lumbar spine, usually the upper and mid-lumbar regions, with involvement most commonly of both the vertebral body and the neural arch both forms present with two types of radiographic appearance: a lytic lesion with preservation of the vertebral cortex or a ‘blown-out’ lesion with a preserved, thin cortical shell: ■ intralesional ossification and ground glass matrix may also be seen, these features optimally demonstrated by CT

MRI findings ● the lesion demonstrates intermediate SI on T1W (Fig. 9.170a) and variable T2W SI (Fig. 9.170b), dependent on the amount of intralesional ossification and cystic degeneration ● involvement of an adjacent vertebra or rib (Fig. 9.170c) may aid in the diagnosis

Metastasis250,277 ●

metastases are the commonest vertebral tumours, involving mainly the thoracic and lumbar spine and accounting for 40–70 per cent of all bone metastases

c

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Figure 9.170 Vertebral fibrous dysplasia. Sagittal T1-weighted (T1W) spin-echo (SE) (a) and T2-weighted fast spin-echo (b) images showing collapse of T3 (arrows). Axial T1W SE image (c) showing involvement of the adjacent rib (arrows).

Primary spinal tumours

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clinically, the commonest complaint is pain secondary to pathological fracture, which may be the presenting feature of cancer in 10 per cent of cases pathologically, vertebral metastases occur in 10 per cent of patients with malignant tumours, in adults arising from the breast (22 per cent), lung (15 per cent), prostate (10 per cent), lymphoma or sarcoma (~10 per cent each), kidney (7 per cent) or gastrointestinal tract (5 per cent); in ~10 per cent of cases, the site of origin is unknown: ■ the commonest primary sites of lytic metastases (70 per cent of cases) are the breast and the bronchus, of sclerotic metastases (9 per cent) the breast and the prostate, and of mixed lesions (21 per cent) the breast ■ intertrabecular metastases278 are characterised by metastatic tumour deposits that result in little trabecular destruction and are therefore occult at radiography, being optimally demonstrated by MRI: – they have a reported incidence of ~37 per cent of cases

MRI findings ●

lytic metastases are typically of intermediate SI on T1W images (Fig. 9.171a), mildly hyperintense on T2W FSE images (Fig. 9.171b) and hyperintense on T2W FSE FS/STIR images (Fig. 9.171c), showing heterogeneous enhancement following contrast (Fig. 9.171d, e)

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Figure 9.171 Vertebral metastasis. Sagittal T1-weighted (T1W) spin-echo (SE) (a) and T2-weighted (T2W) fast spin-echo (b) images showing an intermediate T1W (arrows a) and mildly hyperintense T2W (arrows b) metastasis involving C3 and C4. Sagittal short tau inversion recovery image (c) showing a hyperintense lesion associated with pathological collapse (white arrow) resulting in distal thoracic cord compression (black arrow). Axial T1W SE (d) and post-contrast axial T1W SE (e) images showing bilobed epidural extension of tumour (arrows d) due to the posterior longitudinal ligament (arrowhead d) with heterogeneous enhancement (arrows e).

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d Figure 9.172 Vertebral metastasis. Sclerotic: Axial T1-weighted (T1W) spin-echo (SE) (a) and sagittal T2-weighted (T2W) fast spin-echo (FSE) (b) images showing reduced marrow signal intensity (arrows). Sagittal T2W FSE fat-suppressed (FS) image (c) showing a small hypointense lesion (arrow) surrounded by a rim of hyperintensity (arrowheads) resulting in the ‘target sign’. Mixed: Sagittal T1W SE image (d) showing a mixture of sclerotic (arrows) and lytic (arrowhead) lesions. Flow voids: Sagittal T2W FSE FS image (e) showing multiple tiny flow voids within a collapsed T12 vertebra from renal cell metastasis. Cord compression: Sagittal T1W image (f) showing distal thoracic cord compression (arrowhead) due to epidural extension of tumour (arrows).

Primary spinal tumours

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sclerotic metastases exhibit heterogeneous, reduced marrow SI on T1W (Fig. 9.172a) and T2W (Fig. 9.172b) and may be identified only on FS sequences by a halo of surrounding marrow oedema (Fig. 9.172c) mixed lesions show a combination of markedly reduced and intermediate T1W SI (Fig. 9.172d) flow voids279 have been described as a feature of renal carcinoma metastases (Fig. 9.172e) extraosseous extension is typically focal, as opposed to the more circumferential extraosseous tissue seen with vertebral infection extension into the spinal canal typically has a bilobed appearance (‘curtain sign’) due to the presence of the PLL (Fig. 9.171d) spinal cord compression occurs secondary to pathological fracture from posteriorly dislocated bone impinging on the cord (Fig. 9.171c), epidural extension of tumour (Fig. 9.172f) or a combination of both

Pathological vertebral collapse280,281 ● ●

pathological vertebral collapse is most commonly secondary to metastatic disease, primary bone tumours or vertebral involvement with myeloma, lymphoma or leukaemia such fractures must be differentiated from benign vertebral compression fractures (see later)

MRI findings ● T1W images show complete replacement of the vertebral body marrow by reduced SI due to marrow infiltration, with corresponding intermediate or increased T2W SI ● the SI abnormality may be homogeneous or heterogeneous, with enhancement following contrast: ■ rarely, a small amount of residual normal fatty marrow is seen ● the ‘fluid sign’282 is rarely seen in pathological collapse, being reported in only 6 per cent of cases ● the presence of additional spinal metastases increases the likelihood of pathological compression fracture ● morphological features include: ■ a convex bulge of the whole of the posterior vertebral body cortex, seen in 74 per cent of cases ■ involvement of the pedicles (85 per cent of cases) or posterior elements (59 per cent) ■ an epidural (74 per cent of cases), encasing epidural or focal paraspinal mass (41 per cent) ● MRI has overall sensitivity, specificity and accuracy of 100 per cent, 93 per cent and 95 per cent, respectively, for the diagnosis of metastatic compression fractures

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MISCELLANEOUS CONDITIONS OF THE VERTEBRAE Benign compression fracture280–282 ●

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benign vertebral compression fractures (BVCFs) are most commonly associated with underlying osteoporosis, but may also be seen with trauma, eosinophilic granuloma, Paget’s disease and vertebral haemangioma clinically BVCF presents with acute-onset back pain, commonly in an age group that suffers from malignant disease, and therefore the imaging differentiation between BVCF and pathological collapse is important

MRI findings ● the MRI features depend on the time elapsed since the fracture ● acute BVCF (50 per cent of cases and may be the end result of intradiscal invasion of Paget’s disease, or due to the reported association of Paget’s disease with DISH and ankylosing spondylitis (AS) ■ MRI findings: sagittal T1W and T2W images show continuity of pagetic bone across the disc space (Fig. 9.176a, b)

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Figure 9.176 Vertebral Paget’s disease, complications. Pagetic vertebral ankylosis: Sagittal T1-weighted (T1W) spin-echo (SE) (a) and T2-weighted fast spin-echo (b) images showing ankylosis across the disc space (black arrows), intradiscal invasion of pagetic bone (arrowheads) and anterior bridging osteophytes (white arrows). Pagetic spinal stenosis: Sagittal (c) and axial (d) T1W SE images showing expansion of the L3 vertebra (arrows) and associated central canal stenosis (arrowheads).

Miscellaneous conditions of the vertebrae

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pathological fracture is the commonest complication of Paget’s disease, usually involving the lumbar spine and rarely the sacrum, coccyx or dens: ■ retropulsion of bone into the spinal canal may contribute to pagetic spinal stenosis neurological compromise in Paget’s disease is multifactorial and may be due to compressive myelopathy secondary to bony overgrowth, ossification of epidural fat, platybasia and sarcomatous degeneration (see below): ■ pagetic spinal stenosis is defined as compression of the spinal cord, cauda equina or spinal nerves by expanded pagetic bone and most commonly occurs at a single level in the lumbar region, resulting in combinations of central canal, lateral recess and foraminal stenosis ■ non-compressive spinal cord dysfunction is a recognised finding and is thought to be due to a vascular steal phenomenon ■ MRI findings: expansion of the vertebral body, the neural arch and the facet joints resulting in spinal stenosis and cauda equina or nerve root compression (Fig. 9.176c, d) sarcomatous degeneration is a rare complication of Paget’s disease, with a reported prevalence of 0.7 per cent: ■ it is particularly rare in the spine, accounting for ~4 per cent of all Paget’s sarcomas, osteosarcoma being the commonest malignancy ■ MRI findings: as with other Paget’s sarcomas, there is typically a large, soft-tissue mass on the background of the typical features of vertebral Paget’s disease; the demonstration of normal fatty marrow SI at MRI excludes malignant transformation

Eosinophilic granuloma250,252,253 ● ● ●

●

eosinophilic granuloma is the localised form of Langerhans’ cell histiocytosis the spine is affected in 7.8–15 per cent of cases of solitary eosinophilic granuloma, typically presenting in children under the age of 10 years, but occasionally in young adults clinically, patients present with a combination of pain, muscle spasm and kyphosis: ■ rarely, cord compression occurs due to pathological collapse or extradural spread of disease ■ the thoracic spine is most commonly involved (55 per cent), followed by the lumbar (24 per cent) and cervical (21 per cent) regions; a single vertebra is affected in ~50 per cent of cases ■ cord compression is rarely reported pathologically, the vertebral body is usually involved, pathological collapse being common, though the characteristic vertebra plana is present in only ~30 per cent of cases: ■ preservation of the neural arch, end-plate and disc is typical, but a small paravertebral mass may be seen ■ isolated involvement of the neural arch rarely occurs

MRI findings ● ● ● ● ●

the SI characteristics are non-specific (Fig. 9.177a, b) vertebral collapse is typical (Fig. 9.177a, b), usually starting in the anterior aspect of the vertebral body and resulting in a wedge-shaped vertebra occasionally, a small, paravertebral mass is present (Fig. 9.177c) that probably represents soft-tissue oedema and haemorrhage with healing, there is partial resolution of vertebral body height and conversion of oedema-like marrow SI to fatty replacement of the marrow (Fig. 9.177d, e) MRI may be used to identify the actively involved vertebra, which shows oedema-like SI changes, in cases when multi-level vertebral collapse is seen on radiographs (Fig. 9.177d, e)285

Osteonecrosis286 ●

osteonecrosis (avascular necrosis) of the vertebral body is an uncommon condition that is thought to occur from ischaemic non-union of benign compression fractures: ■ it most usually manifests on radiographs and CT as an intravertebral vacuum cleft phenomenon; when occurring after minor trauma, is referred to as Kümmell’s disease ■ clinically, patients are typically over 60 years of age at presentation and the condition is more frequently seen in women

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Figure 9.177 Vertebral Langerhans’ cell histiocytosis. Sagittal T1-weighted (T1W) spin-echo (SE) (a) and T2-weighted (T2W) fast spin-echo (FSE) (b) images showing wedge collapse of T11 (arrows) with non-specific signal intensity changes. Axial T1W SE image (c) showing a small paravertebral mass (arrows). Sagittal T1W SE (d) and T2W FSE (e) images showing an active lesion at T5 (arrows) and a healed lesion at T2 (arrowheads).

Miscellaneous conditions of the vertebrae

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■ a single vertebral body is involved in most cases vertebral body osteonecrosis without vertebral collapse is a very rare condition with no known predisposing causes;287 reported cases occur in adults who present with non-specific spinal pain

MRI findings ● Kümmell’s disease: the vacuum cleft appears as linear, intravertebral low SI on T1W and T2W images and as signal void on T2*W GE images: ■ fluid may also be seen within the cleft, appearing as focal or linear areas of T2W hyperintensity (Fig. 9.174a, b) ■ vacuum or fluid is seen in ~40 per cent of cases, while 20 per cent show both fluid and gas ■ intravertebral vacuum cleft is associated with a greater degree of vertebral collapse, may also be associated with gas in the adjacent disc (intradiscal vacuum) and is more commonly associated with benign collapse of adjacent vertebrae ● osteonecrosis without collapse287 appears as a well-defined rectangular area of vertebral marrow abnormality that shows reduced T1W SI, increased T2W SI and lack of enhancement following contrast: ■ marrow oedema is not a feature and the disc space is normal ■ follow-up studies show a stable appearance with no progression to vertebral collapse ■ clues to the diagnosis include mild marrow sclerosis on CT and lack of increased uptake on scintigraphy

Sarcoidosis288,289 ● ● ● ● ●

sarcoidosis is a multisystem disorder of unknown cause that involves the skeletal system in 1–13 per cent of cases involvement of the axial skeleton is extremely rare, with only a few reported cases clinically, most patients with osseous sarcoid have evidence of pulmonary and/or skin disease spinal involvement presents with non-specific spinal pain, most commonly in the lumbar and thoracic regions; multi-level involvement is common radiological features include a mixture of lytic and sclerotic lesions

MRI findings ● SI abnormalities may be nodular or diffuse, showing homogeneous reduced T1W SI, isointense T2W SI and increased STIR SI, with enhancement following contrast; these areas are due to granulomatous infiltration of the marrow ● sclerotic foci show low SI on all pulse sequences ● lesions predominantly involve the vertebral bodies with occasional extension into the neural arch or extraosseous extension into the epidural/paravertebral space ● granulomatous discitis is a rare feature and may be indistinguishable from pyogenic discitis ● associated features include paraspinal masses, which may be due to lymphadenopathy, and paravertebral ossification ● the appearances are similar to those of metastases or myeloma ● following successful therapy, the marrow may revert to normal

Pigmented villonodular synovitis290 ● ● ● ● ●

pigmented villonodular synovitis is a proliferative process of the synovium of unknown aetiology and may be diffuse or focal (nodular), affecting the synovium of joints, bursae and tendon sheaths spinal involvement is rare, with lesions typically arising from the synovium of the facet joints clinically, the mean age at diagnosis is 28 years (range 7–44 years) with females affected slightly more commonly than males presentation is with pain and/or neurological symptoms, or occasionally a painless paraspinal mass ~50 per cent of cases affect the cervical spine, with the remainder distributed equally in the thoracic and lumbar regions

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MRI findings ● the average size of the lesion is ~3¥2¥2 cm; >90 per cent affect the facet joint and have an associated paraspinal mass ● involvement of the pedicles and neural foramina occurs in ~70 per cent of cases with extension to the vertebral body in ~30 per cent ● the mass is typically well defined and of intermediate T1W SI and intermediate to low T2W SI, and occasionally shows focal areas of fluid SI ● diffuse enhancement is seen following contrast ● marrow oedema is not a feature but adjacent soft-tissue oedema is seen in 40 per cent of cases

Synovial osteochondromatosis291 ● ●

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primary vertebral synovial osteochondromatosis is an extremely rare lesion, with fewer than 10 cases reported in the English-language literature clinically, the commonest presentation is with pain (~90 per cent of cases) and neurological deficit (~60 per cent): ■ the commonest location is the cervical region, followed by the thoracic and lumbar pathologically, the lesion usually arises from the facet joint, and less commonly from the costotransverse joint

MRI findings ● synovial osteochondromatosis appears as a lobulated mass centred on the facet joint with hypointense T1W SI and hyperintense T2W SI, typical of cartilage ● focal, tiny areas of signal void may be present due to matrix mineralisation, and heterogeneous enhancement is seen following contrast ● bone erosion and extension into the paravertebral space and spinal canal may be seen, the latter potentially resulting in cord compression

INFLAMMATORY DISORDERS OF THE SUBAXIAL SPINE Rheumatoid arthritis43,44 ● ●

the subaxial spine may be involved by RA pathologically, this is manifest as erosive arthropathy of the facet and neurocentral joints, with resulting anterior vertebral displacement: ■ subaxial instability occurs in 10–20 per cent of cases ■ multi-level involvement produces a ‘stepladder’ deformity of the cervical spine, which is reported in 31 per cent of RA patients ■ extension of pannus from the neurocentral joint into the disc may also result in disc destruction

MRI findings ● in the acute stage, active arthritis is manifest as synovitis with joint effusion and subchondral T2W marrow hyperintensity, which enhances following contrast ● pannus extension into the IVD may result in disc enhancement ● in the chronic stage, a stepladder deformity is demonstrated: ■ erosion of the spinous processes, particularly that of C7 is also seen ● subaxial spinal stenosis292 secondary to hypervascular, active pannus is a recognised cause of cervical cord compression, being reported in ~75 per cent of cases: ■ it frequently occurs both anterior and posterior to the spinal cord, resulting in a segmental, cuff-like extension of enhancing soft tissue around the thecal sac ■ enhancement in the facet joints, paraspinal soft tissues and ligamentum nuchae is also reported

Inflammatory disorders of the subaxial spine

Ankylosing spondylitis293–296 ● ●

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AS is an idiopathic inflammatory arthritis that predominantly affects the axial skeleton, with a reported prevalence of 0.2–1.6 per cent in the USA clinically, the disease most commonly affects young men (male–female ratio 3:1) aged 20–40 years, and there is a strong association with HLA-B27 (present in~96 per cent of patients): ■ presenting symptoms include low back pain, typically in the deep gluteal region, early-morning stiffness relieved by activity and persistence of symptoms for at least 3 months ■ the late stages of the disease are characterised by spinal stiffness due to ligament and disc ossification and joint ankylosis ■ non-spinal manifestations include peripheral arthropathy pathologically, initial changes are a result of inflammatory synovitis involving the synovial joints (facet, neurocentral, costovertebral and costotransverse) and/or inflammatory enthesopathy at sites of ligamentous attachments (disc annulus, spinal ligaments): ■ the repair process leads to abnormal soft-tissue ossification, reduction of joint space and eventually endochondral ossification across joints spinal involvement is most commonly seen at the thoracolumbar junction with a progressive ascending distribution, but the lumbar and cervical spine are also involved later the spine may be involved in various ways, with a combination of inflammatory and destructive lesions affecting the vertebral bodies, the discovertebral unit, the apophyseal joints and the spinal ligaments: ■ spondylitis/vertebral osteitis is an inflammatory enthesopathy at the attachment of the longitudinal ligament and the annulus to the vertebral body, most commonly involving the anterosuperior and anteroinferior corners of the vertebra and eventually resulting in the radiographic ‘shiny corner’ sign, which represents the healed lesion: – anterior lesions are termed ‘anterior spondylitis’, are also known as the ‘Romanus lesion’ and most commonly occur at the T10–L2 level (Fig. 9.178a–c) – less commonly, the posterosuperior and posteroinferior margins of the vertebra are involved, this being termed ‘posterior spondylitis’ (Fig. 9.178d); combined involvement of the anterior and posterior regions is termed ‘marginal spondylitis’ ■ syndesmophytes are bony outgrowths from the anterior vertebral margins (Fig. 9.179c) and are seen in ~15 per cent of vertebrae in affected individuals: – they may eventually result in bony bridging across the disc space, resulting in the radiographic appearance of the ‘bamboo spine’ ■ spondylodiscitis is a destructive discovertebral lesion involving the IVDs and adjacent VEPs with a reported incidence of 2.7–28 per cent and is termed the ‘Andersson lesion’: – two types of discovertebral lesion are described: inflammatory and non-inflammatory – the inflammatory type usually occurs within the first 9 years of the onset of AS and is characterised by herniation of disc material through the end-plate, possibly secondary to the presence of a subchondral, granulomatous inflammatory process; it may be asymptomatic or may present with focal, mechanical-type back pain (Fig. 9.180a, b) – the non-inflammatory type usually occurs 12 years or more following the onset of the disease and represents a pseudarthrosis developing following a stress fracture through the IVD (transdiscal) or the vertebral body (transvertebral), with an associated fracture of the posterior column (Fig. 9.180c–e), rendering the spine unstable ■ disc calcification usually affects the thoracic and lumbar discs and increases in incidence with disease duration, occurring as a result of endochondral ossification extending from the cartilaginous endplate to eventually involve the whole disc (Fig. 9.181) ■ facet, costovertebral and costotransverse joint involvement occurs as a result of synovitis and eventually leads to joint ankylosis ■ spinal ligaments: involvement of the interspinous and supraspinous ligaments is common in the form of enthesopathy, which may also affect the adjacent spinous process marrow

MRI findings the Romanus lesion: in the active stage, anterior spondylitis manifests as areas of oedema-like SI change (reduced T1W and increased T2W/STIR) in the anterosuperior and anteroinferior corners of the involved vertebral bodies that enhance following contrast (Fig. 9.178a–c):

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Figure 9.178 Ankylosing spondylitis. Romanus lesion: Sagittal T1-weighted (T1W) spin-echo (SE) (a), T2-weighted (T2W) fast spin-echo (FSE) (b) and post-contrast sagittal T1W SE fat-suppressed (c) images showing oedema-like signal intensity (SI) changes (arrows a, b) in the anterosuperior corner of the vertebral body with enhancement following contrast (arrow c). Posterior spondylitis: Sagittal T2W FSE image (d) showing oedema-like SI changes (arrows) in the posterosuperior and posteroinferior corners of L4. Sagittal T2W FSE image (e) showing diffuse vertebral body oedema (arrow). Chronic stage: Sagittal T1W SE (f) and T2W FSE (g) images showing fatty marrow SI change (arrows) in the anteroinferior corner of L3.

Inflammatory disorders of the subaxial spine

these changes are radiographically occult and are usually associated with normal SI in the adjacent discs ■ similar changes may be seen posteriorly in posterior spondylitis (Fig. 9.178d) and more diffuse marrow oedema may also be demonstrated (Fig. 9.178e) ■ later, the SI pattern changes to one of fatty degeneration with increased SI on both T1W and T2W (Fig. 9.178f, g) and no enhancement, this corresponding to the presence of radiographic changes and the development of marginal syndesmophytes ‘squaring’ of the vertebral body is another feature of healing that occurs as a result of the laying down of new bone on the anterior aspect of the vertebral body (Fig. 9.179a, b) syndesmophytes are not particularly well demonstrated at MRI; they occur at the anterolateral vertebral margin and manifest by thickening of the longitudinal ligaments, which show variable SI depending on disease activity: ■ they may eventually result in ankylosis across the anterior disc space (Fig. 9.179c) inflammatory spondylodiscitis: increased T2W disc SI with disc herniation and adjacent marrow oedema, the herniated disc surrounded by a hypointense rim due to sclerosis (Fig. 9.180a, b): ■ the marrow oedema commonly has a hemispherical configuration ■

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Figure 9.179 Ankylosing spondylitis, osseous changes. Sagittal T1-weighted (T1W) spin-echo (SE) (a) and axial T2-weighted fast spin-echo (b) images showing ‘squaring’ of the L5 vertebra due to anterior periosteal new bone deposition (arrows). Sagittal T1W SE image (c) showing a syndesmophyte (arrow) arising from the superior margin of L5.

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Figure 9.180 Ankylosing spondylitis, discovertebral changes. Inflammatory: Sagittal short tau inversion recovery (a) and post-contrast T1-weighted (T1W) spin-echo (SE) fat-suppressed (b) images showing disc herniation into the adjacent vertebral bodies with a hypointense rim (arrows) and surrounding enhancing oedema (arrowheads). Pseudarthrosis: Sagittal T1W SE (c) and T2-weighted (T2W) fast spin-echo (FSE) (d) images showing irregular widening of the disc (arrows) and heterogeneous low marrow signal intensity (SI) (arrowheads). Para-sagittal T2W FSE image (e) showing heterogeneous marrow SI (arrowheads) and a non-union through the fused posterior column (arrow).

Inflammatory disorders of the subaxial spine

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Figure 9.181 Ankylosing spondylitis, disc calcification. Sagittal T1-weighted (T1W) spin-echo (SE) (a) and T2-weighted (T2W) fast spin-echo (FSE) (b) images showing end-plate (arrows) and diffuse type (arrowheads) disc calcification. Sagittal T1W SE (c) and T2W FSE fat-suppressed (FS) (d) images showing annular calcification (arrows). Sagittal T1W SE (e) and T2W FSE FS (f) images showing complete ossification of the disc and the annulus (arrows).

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the absence of a paravertebral mass and epidural involvement helps to differentiate this lesion from pyogenic spondylodiscitis pseudarthrosis: widening of the disc space with reduction of adjacent marrow SI on T1W (Fig. 9.180c) and heterogeneous T2W SI (Fig. 9.180d, e) due to a combination of oedema and fibrous tissue, with the pseudarthrosis extending to the posterior elements disc calcification most commonly manifests as increased disc SI on T1W images, with variable T2W SI, and may involve the cartilaginous end-plate (Fig. 9.181a, b), the AF (Fig. 9.181c, d) or the NP, or most commonly is diffuse (Fig. 9.181a, b), eventually resulting in ossification through the disc space (Fig. 9.181e, f) joint involvement initially manifests as subarticular marrow oedema, articular erosion (Fig. 9.182a, b) with loss of joint space, effusion and eventually marrow sclerosis and joint ankylosis, the last indicated by the presence of solid medullary bone extending across the obliterated joint space and capsular ossification (Fig. 9.182c–e) interspinous/supraspinous ligament involvement is seen as ligament thickening and increased SI on STIR and contrast-enhanced images: ■ oedema in the adjacent spinous processes may also be evident ■

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Figure 9.182 Ankylosing spondylitis, facet joint disease. Axial T1-weighted (T1W) spin-echo (SE) (a) and T2-weighted (T2W) fast spin-echo (FSE) (b) images showing costovertebral joint erosion (arrowheads) and subarticular oedema (arrows). Axial T1W SE (c) and sagittal T2W FSE (d) images showing ankylosis of the facet joints (arrows) and capsule (arrowhead c). Axial T1W SE image (e) showing ankylosis of the costovertebral (arrowhead) and costotransverse (arrow) joints.

Inflammatory disorders of the subaxial spine

Fractures in ankylosing spondylitis293,297 ● ●

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spinal fractures occur more commonly in AS because of the combination of osteopenia and spinal rigidity, the risk increasing with duration of disease and the extent of spinal involvement clinically, a spinal fracture should be suspected in the presence of new back pain in a patient with an ankylosed spine, especially if there is a history of trauma, which may be minor and is most commonly a fall: ■ associated neurological deficit may be present in ~65 per cent of cases297 three patterns of fracture are recognised: ■ 1 – stress fractures leading to pseudarthrosis that represent the non-inflammatory discovertebral lesion (see above) ■ 2 – compression fractures secondary to osteoporosis that usually result in a stable kyphosis ■ 3 – transversely orientated shear fractures, which are acute traumatic lesions that usually traverse the disc space or vertebral body and extend to involve the posterior column: – they most commonly occur in the lower cervical region (C6–7) or at the cervicothoracic or thoracolumbar junction – spinal instability nay result in neurological compromise – multi-level fractures may occur simultaneously additional traumatic lesions that may result in neurological deficit include acute epidural haematomas and ventral dislocation of an ossified LF

MRI findings ● acute fracture lines have reduced T1W SI and increased T2W SI due to fluid and often extend into the posterior elements (Fig. 9.183a, b), with variable enhancement following contrast: ■ reduced T2W SI may also be seen in the fracture due to formation of fibrous tissue ● ALL disruption may be identified (Fig. 9.183c), as may traumatic spondylolisthesis (Fig. 9.183c) or retrolisthesis, with displacement at the fracture site potentially resulting in cord compression ● epidural haematomas appear as long, tapered, extradural masses with variable SI depending on their age

Cauda equina syndrome in ankylosing spondylitis293 ● ●

●

cauda equina syndrome is a rare but well-recognised complication of long-standing AS clinically, it typically presents with the insidious onset of neurological deficit in late, often inactive disease: ■ symptoms include sensory deficits in the L5 and sacral dermatomes, sphincter disturbances, variable lower limb weakness and occasionally leg and perineal pain pathologically, it is thought to occur secondary to facet joint inflammation, resulting in mild arachnoiditis, dural adhesions and eventually diverticula formation with dural ectasia and scalloping of the neural arches

MRI findings ● multiple, bilateral and multi-level dural diverticulae are seen that are isointense to CSF on all pulse sequences (Fig. 9.184a, b) ● enlargement of the spinal canal with scalloping of the posterior elements (Fig. 9.184c, d) ● displacement (Fig. 9.184e) or clumping of nerve roots, displacement of the lower spinal cord and dilation of the lumbosacral nerve root sleeves may also be seen

Psoriatic arthropathy and Reiter’s syndrome294,298 ● ● ●

in psoriatic arthropathy, isolated spinal involvement is seen in ~5 per cent of patients; the spine is more commonly involved in association with sacroiliitis spinal involvement in association with peripheral joints disease is seen in 20–40 per cent of cases pathologically, psoriatic spondylitis affecting the thoracic and lumbar regions is characterised by the presence of paravertebral ossification, coarse asymmetrical bony bridging and relative sparing of the apophyseal joints: ■ paravertebral ossification appears as poorly defined areas of bone formation or thin, curvilinear, dense lines, paralleling the lateral vertebral margin and the IVDs

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Figure 9.183 Ankylosing spondylitis, fracture. Sagittal T1-weighted spin-echo (a) and T2-weighted (T2W) fast spin-echo (FSE) (b) images showing a fluid-filled fracture through the superior aspect of L1 (arrows) with extension through the ossified posterior column (arrowheads). Sagittal T2W FSE fat-suppressed image (c) showing fracture through the anterior longitudinal ligament (arrow) with traumatic spondylolisthesis.

bony bridging may occur from the margins of the vertebrae (in ~25 per cent of cases) as in AS, or more centrally from the vertebral body in the cervical spine, erosions may be seen anywhere along the vertebral margins and also involve the apophyseal joints: ■ additional features include ALL calcification and atlanto-axial subluxation in Reiter’s syndrome, similar paravertebral ossifications can be seen, though the cervical spine is typically spared ■

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●

Gout299 ● ● ●

gouty spinal involvement can manifest as erosions of the neural arch, facets and vertebral bodies, while disc involvement can mimic spondylodiscitis spinal stenosis can occur secondary to infiltration of the neural arch300 or secondary to the presence of tophi in the spinal canal gouty tophi in the IVD301 have also been described

Inflammatory disorders of the subaxial spine

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Figure 9.184 Ankylosing spondylitis, cauda equina syndrome. Sagittal T1-weighted (T1W) spin-echo (SE) (a) and T2-weighted (T2W) fast spin-echo (FSE) (b) images showing posterior dural diverticula (arrows) at the mid-lumbar level. Axial T1W SE (c) and T2W FSE (d) images showing enlargement of the spinal canal with scalloping of the posterior elements (arrows). Axial T2W FSE image (e) showing displacement of nerve roots (arrowhead) into the diverticulae.

MRI findings ● gouty tophi in the spine have the same SI characteristics as those elsewhere in the body, appearing hypointense on T1W and of variable T2W SI ● appearances mimicking an epidural abscess or disc space infection may also be seen

Calcium pyrophosphate deposition disease47 ● ●

CPDD may occur in the IVDs, the joint capsules, the synovium, the articular cartilage, bursae and ligaments CPPD disease of the thoracic and lumbar discs may occur in the annulus or the nucleus with advancing degenerative change and is of uncertain clinical significance

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ligament involvement may result in spinal cord compression from enlargement of the LF in the cervical or thoracic regions (see above) pseudogout of the facet joint,302 resulting in acute low back pain and manifesting on MRI as a joint effusion, has also been reported

Hydroxyapatite deposition disease303 ● ●

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spinal involvement in hydroxyapatite deposition disease results from tendon and ligament calcification clinically, the longus colli muscle is most commonly affected in the cervical spine (at the C2 level) of middle-aged patients, resulting in neck pain, stiffness and dysphagia: ■ spontaneous resolution and relief of symptoms typically occur hydroxyapatite deposition disease may also involve the longitudinal ligaments, the IVDs and the apophyseal joints

Amyloid spondyloarthropathy304 ● ●

amyloid spondyloarthropathy occurs in renal failure patients, who are typically on dialysis pathologically, the cervical region (most commonly C4–6) is involved in 85 per cent of cases, with the lumbar in 10 per cent and the thoracic in 5 per cent

MRI findings ● spondyloarthropathy is characterised by end-plate erosion, disc space narrowing and absence of osteophytes, mimicking spondylodiscitis ● erosions tend to involve the anteroinferior and anterosuperior margins of the vertebral body and the facet joints ● abnormal paraspinal soft-tissue masses with low T1W and T2W SI may also be seen ● following contrast, vertebral body and disc enhancement may occur

SAPHO syndrome305,306 ● ● ● ●

SAPHO syndrome (synovitis, acne, pustulosis, hyperostosis and osteitis) is an inflammatory condition of unknown aetiology the spine is the second commonest site of skeletal involvement, being affected in 33 per cent of cases spinal involvement manifests as synovitis of the costovertebral joints and SIJs and osteitis of the vertebral bodies; the thoracic spine is most commonly involved, followed by the lumbar and cervical regions pathologically, the anterior corner of the vertebral body is typically involved by erosion, with adjacent sclerosis and hyperostosis, which may extend to the adjacent rib: ■ osteophyte and syndesmophyte formation and paravertebral ligamentous ossification are also seen ■ narrowing of the disc space with end-plate erosion mimics spondylodiscitis, while vertebral collapse, which may result in cord compression, may be mistaken for neoplastic involvement ■ sclerosing arthritis of the costovertebral joint, which may progress to ankylosis, is also recognised

MRI findings ● anterior vertebral corner erosion is seen with adjacent marrow change comprising a mixture of sclerosis and oedema-like SI (Fig. 9.185a, b), which enhances following contrast (Fig. 9.185c) ● erosion may extend to the anterior vertebral cortex and the end-plate, particularly the inferior (Fig. 9.185b) ● involvement of several contiguous (Fig. 9.185d, e) or non-contiguous vertebrae (Fig. 9.185f) is common ● paravertebral soft-tissue swelling occurs at the level of the involved vertebra (Fig. 9.185g) and may be predominantly fatty in nature ● the disc is usually normal (Fig. 9.185d, e), but may show enhancement ● late features: healed cases are associated with increased T1W marrow SI due to fatty replacement (Fig. 9.186a) ● other late features include osteophytosis and the formation of syndesmophytes, which may progress to vertebral ankylosis (Fig. 9.186b), and vertebral collapse with kyphosis (Fig. 9.186c) and possible cord compression

Inflammatory disorders of the subaxial spine

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a

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Figure 9.185 SAPHO syndrome. Sagittal T1-weighted (T1W) spin-echo (SE) (a) and T2-weighted (T2W) fast spin-echo (FSE) (b) images showing anterior vertebral erosion (large arrow a), oedema-like signal intensity (small arrows) and marrow sclerosis (arrowheads). Post-contrast sagittal T1W SE image (c) showing focal marrow enhancement (arrow). Sagittal T1W SE (d) and T2W FSE (e) images showing contiguous multi-level disease (arrows). Sagittal T1W SE image (f) showing non-contiguous multi-level disease (arrows). Axial T1W SE image (g) showing paravertebral swelling (arrows).

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marrow SI changes in the neural arch (Fig. 9.186d) may extend from the vertebral bodies or be associated with costovertebral arthropathy (Fig. 9.186e)

Diffuse idiopathic skeletal hyperostosis307 ● ●

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DISH, also known as Forestier’s disease, is a systemic, bone-forming disorder of unknown aetiology with primary spinal manifestations and various extraspinal features clinically, it may present with mid- or lower spine stiffness and chronic mild pain, though most cases are asymptomatic and identified incidentally on imaging studies: ■ cervical involvement may produce dysphagia, and thoracic myelopathy has also been reported ■ the prevalence is ~15 per cent in women and 25 per cent in men after the age of 50 years rising to almost 30 per cent after 80 years ■ spinal fracture is recognised, often as a result of cervical hyperextension injury, which is associated with a high prevalence of neurological deficit pathologically, the diagnostic criteria include flowing ossification along the anterolateral borders of at least four contiguous spinal segments, absence of degenerative changes and absence of sclerosis/ankylosis of the facet joints/SI joints, which helps to distinguish the condition from AS: ■ fewer than four segments may be involved and the lower thoracic region (T7–11) is most commonly affected

MRI findings ● large, ‘flowing’ osteophytes are seen arising from the anterolateral vertebral body margins, which are commonly continuous across the disc space (Fig. 9.187a) ● axial images show the osteophytes extending horizontally from the vertebral body margins (Fig. 9.187b), more commonly on the right side of the thoracic region and symmetrical in the cervical and lumbar regions ● associated features include thick ligamentous calcification, hyperostosis of the costovertebral joints and relative absence of spinal degenerative changes ● in the cervical region, secondary ankylosis of the uncovertebral and apophyseal joints may occur, as may OPLL, LF hypertrophy and mild cervical kyphosis, the combination of these occasionally resulting in cervical myelopathy ● in the lumbar region, the upper lumbar levels are typically affected, with interspinous ligament calcification and associated degenerative changes in the lower lumbar spine (L4–S1) ● fracture is demonstrated as a horizontal break through the anterior flowing osteophytes (Fig. 9.187c, d), possibly with associated cord injury

Spinal neuropathic arthropathy237,308 ●

spinal neuropathic arthropathy, also known as Charcot’s joint of the spine, is a destructive disorder of the IVD and the adjacent vertebral bodies that may occur in isolation or in 6–21 per cent of patients presenting with neuropathic peripheral arthropathy

Inflammatory disorders of the subaxial spine

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Figure 9.186 SAPHO syndrome. Sagittal T1-weighted (T1W) spinecho (SE) image (a) showing fatty replacement of the marrow (arrows) indicating healing. Sagittal T1W SE image (b) showing anterior syndesmophytes (arrow) and vertebral ankylosis (arrowhead). Sagittal T2-weighted fast spin-echo image (c) showing vertebral collapse (arrow) resulting in kyphosis. Postcontrast sagittal T1W SE fat-suppressed (FS) image (d) showing enhancing oedema (arrow) extending from the vertebral body into the neural arch. Post-contrast axial T1W SE FS image (e) showing active costovertebral arthropathy (arrow).

clinically, patients most commonly present with progressive thoracolumbar kyphosis, occasionally associated with back pain, change in neurological status (especially increased lower limb spasticity) and a cracking sensation during movement: ■ patients typically present many years after the initial neurological disorder ■ the thoracolumbar junction region is most commonly affected; cervical, thoracic and sacral involvement are extremely rare predisposing causes include hemiplegia, syringomyelia, peripheral neuropathy, severe degenerative spinal diseases, congenital insensitivity to pain, infections or tumours of the spinal cord, and diabetes mellitus:

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Figure 9.187 Diffuse idiopathic skeletal hyperostosis. Sagittal T2-weighted (T2W) fast spin-echo (FSE) image showing continuous bone growth across several thoracic disc levels (arrows). Axial T1-weighted (T1W) spin-echo (SE) image (b) showing the anterolateral location of osteophytes (arrows). Fracture: Sagittal T1W SE (c) and T2W FSE (d) images showing a break (arrowheads) in the continuous anterior osteophytes (arrows).

tabes dorsalis is now a rare cause the development of neuropathy may be exacerbated by multi-level laminectomy pathologically, it results from a loss of joint protection mechanisms secondary to various conditions that affect the deep sensation pathways, leading to rapid degenerative spinal dislocation with involvement of the vertebral body, the IVD and the facet joint ■ ■

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MRI findings ● the destructive vertebral lesion (Fig. 9.188a, b) affects two or three segments in continuity, associated with kyphosis and spondylolisthesis

The lumbosacral junction

enhancing, oedema-like SI changes may be seen in the vertebral bodies, adjacent to the disc (Fig. 9.188b) or diffusely throughout the vertebra reduction of disc height occurs (Fig. 9.188a, b) with fluid SI within the disc (Fig. 9.188c), which may show rim enhancement following contrast occasionally, hypertrophic changes are seen (Fig. 9.188a, b) with invasion of the soft tissues; associated infection is rare involvement of the facet joint (Fig. 9.188c) is one of the best discriminators between neuropathic arthropathy and spondylodiscitis

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b

a

c

Figure 9.188 The neuropathic spine. Sagittal T1-weighted spin-echo (a) and T2-weighted (T2W) fast spin-echo (FSE) (b) images showing irregular reduction of disc height, anterior hypertrophic new bone (white arrows) and mild vertebral body oedema (arrowhead b) in a patient treated with laminectomy (black arrows) for thoracic syrinx. Sagittal T2W FSE image (c) showing fluid within the disc space (arrow) and the adjacent facet joint (arrowhead).

THE LUMBOSACRAL JUNCTION Normal anatomy ●

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the IL:309 the lumbosacral junction is characterised by the presence of the IL, which connects the transverse process of L5 to the ilium, providing additional stability by restraining motion at L5–S1, particularly in flexion and lateral bending the IL comprises two main bands, the anterior (ventral) and the posterior (dorsal), while a separate sacroiliac part of the IL (the SIPIL) is also recognised:310 ■ the anterior IL arises from the anterolateral aspect of the L5 transverse process and terminates via a broad insertion into the iliac tuberosity on the anterosuperior aspect of the posterior iliac crest, and also into the anterior fascia of the quadratus lumborum: – the anterior band measures 8–22 mm in length

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the posterior IL arises from the posteroinferior tip of the L5 transverse process, extending to the posteromedial aspect of the posterior ilium, the posterior fascia of the quadratus lumborum and occasionally the dorsal sacroiliac ligament: – the posterior band measures 3–17 mm in length ■ the SIPIL310 arises from the craniomedial aspect of the sacral ala, immediately below the L5 transverse process, and inserts into the anteromedial part of the iliac tuberosity of the posterior ilium, together with the anterior band the IL has been classified into two groups: ■ group A – ~70 per cent of cases in which the anterior and posterior bands clearly run separately ■ group B – ~30 per cent in which they run together as a single band the IL is clearly depicted on axial (Fig. 9.189a) and coronal (Fig. 9.189b) MRI studies as a single or double hypointense band of variable thickness, extending between the L5 transverse process and the posterior iliac crest ■

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a

b

Figure 9.189 The iliolumbar ligament (IL). Axial T1-weighted spin-echo (a) and coronal T2-weighted fast spin-echo (b) images showing the IL (black arrows) extending from the L5 transverse process (arrowheads) to the posterior ilium (double arrowheads) and also the sacroiliac part of the IL (long arrow b).

Lumbosacral transitional vertebra311 ●

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in lumbosacral transitional vertebra (LSTV), the last lumbar vertebra shows elongation of its transverse process, with varying degrees of fusion to the first sacral segment; the reported prevalence is 4–21 per cent LSTV has been classified into four types based on the plain radiographic appearance (Castellvi) classification: ■ type I – a unilateral (Ia) or bilateral (Ib) dysplastic transverse process that measures >19 mm in height but does not attach to the sacrum (Fig. 9.190a) ■ type II – a unilateral (IIa) or bilateral (IIb) enlarged transverse process that forms a pseudarthrosis with the sacral ala (Fig. 9.190b) ■ type III – a unilateral (IIIa) or bilateral (IIIb) enlarged transverse process that forms a complete ankylosis with the sacral ala ■ type IV – mixed, with a type IIa articulation on one side and a type IIIa articulation on the other side the presence of LSTV can be identified on sagittal MR images based on the morphology of the LSTV and the lumbosacral disc: ■ the LSTV appears ‘squared’ (Fig. 9.190c) ■ the lumbosacral disc has two different appearances on sagittal T2W FSE images: – type 1 – smaller than the normal disc at the adjacent mobile segment, maintains its SI, lacks an intranuclear cleft and shows no evidence of fusion between the anterior vertebral body end-plates (Fig. 9.190d); associated with type II LSTV

The lumbosacral junction

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a

d c

f e Figure 9.190 Lumbosacral transitional vertebra (LSTV). Coronal T2-weighted (T2W) fast spin-echo (FSE) images (a, b) showing a type I (arrow a) and a type II (arrow b) LSTV with no fusion (arrowhead a) and pseudarthrosis (arrowhead b) between the enlarged transverse process and the sacral ala. Sagittal T1-weighted (T1W) spin-echo (SE) image (c) showing ‘squaring’ of the LSTV (arrows). Sagittal T2W FSE image (d) showing a type 1 transitional disc (arrow) with no fusion of the adjacent end-plates (arrowhead). Axial T1W SE images (e, f) showing an enlarged left L5 transverse process (arrows) attached to the left sacral ala (black arrowhead f) via a pseudarthrosis (white arrowhead f).

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– type 2 – a rudimentary disc appearing smaller than the type 1 disc, with normal SI and no intranuclear cleft, but with associated fusion of the anterior end-plates; associated with type III or type IV LSTV ■ on axial images, the enlarged transverse process is demonstrated (Fig. 9.190e) and the pseudarthrosis appears as a transverse, oblique, hypointense line between the transverse process and the sacral ala (Fig. 9.190f) numbering of LSTV:312–314 various methods have been proposed to decide whether LSTV represents a ‘sacralised’ L5 or a ‘lumbarised’ S1: ■ the use of a whole-spine localiser has been suggested, allowing counting from C2 caudally312 ■ the position of the right renal artery313 has also been used since it commonly lies adjacent to the L1–2 disc level, though this technique cannot be used in ~25 per cent of cases because the artery is not identified or because it lies between two disc levels

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the origin of the IL ligament:314 in the presence of normal lumbar segmentation, the IL ligament always arises from the L5 vertebra, making it an anatomical marker of the L5 level: – in the presence of LSTV, if the IL ligament is identified above the LSTV, the LSTV is labelled S1, whereas if the IL ligament is not identified, the LSTV is labelled L5 and a rudimentary IL ligament that resembles the SIPIL is demonstrated – when there is a unilateral transverse process enlargement (type IIa or IIIa), the IL ligament is seen to arise from the contralateral transverse process and the LSTV is labelled L5

PATHOLOGY OF THE LUMBOSACRAL JUNCTION Bertolotti’s syndrome311 ●

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Bertolotti’s syndrome315 is an association between low back pain and the presence of LSTV and is said to affect 4–8 per cent of the population: ■ the cause of the low back pain is unclear, but it may be related to the increased prevalence of disc degeneration at the level immediately above the LSTV, an association that has been identified in several studies:316,317 – in association with this is the very infrequent finding of degeneration within the transitional disc, which can occur only in the presence of a pseudarthrosis ■ alternative causes of pain include the pseudarthrosis itself, based on the abolition of pain following image guided-injection into the false joint, and pain arising from the facet joint contralateral to a unilateral pseudarthrosis318 Bertolotti’s syndrome has been reported with a prevalence of 11.4 per cent in patients under 30 years of age

MRI findings ● axial images demonstrate unilateral or bilateral transverse process enlargement (Fig. 9.191a) with degeneration of the disc at the level above (Fig. 9.191b)

a Figure 9.191 Bertolotti’s syndrome. Axial T1-weighted spin-echo image (a) showing enlargement of the right transverse process (arrow) indicating a lumbosacral transitional vertebra (LSTV). Sagittal T2-weighted fast spin-echo image (b) showing degeneration (arrowhead) at the level above the LSTV (arrow).

b

Nerve root compression319,320 ● ●

nerve root compression in association with LSTV can be due to various causes the incidence of spinal stenosis or lumbar disc herniation at the level immediately above an LSTV, even in the absence of spondylolisthesis, is significantly greater than in the absence of an LSTV319

Pathology of the lumbosacral junction

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in the presence of a type II–IV LSTV, the enlarged transverse process forms an osseous tunnel with the sacral ala through which the nerve root has to pass (Fig. 9.192a–d): ■ osteophyte formation in relation to the pseudarthrosis may result in stenosis and compression of the exiting root320

MRI findings ● axial images show stenosis of the osseous tunnel, with loss of fat around the exiting nerve root (Fig. 9.192e)

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Figure 9.192 Lumbosacral transitional vertebra. Consecutive axial T1-weighted (T1W) spin-echo (SE) images (a–d) showing an enlarged right transverse process (white arrows) forming an osseous tunnel for the exiting nerve root (black arrows). Axial T1W SE image (e) showing stenosis of the osseous tunnel associated with a left-sided pseudarthrosis (arrowheads) resulting in compression of the exiting root (white arrows) compared with the normal right L5 root (black arrow).

Traumatic lumbosacral dislocation321 ●

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traumatic lumbosacral dislocation, or traumatic lumbosacral spondylolisthesis, is a rare lesion caused by dislocation of the L5–S1 facet joints, and may be partial (subluxation), complete (dislocation), unilateral or bilateral clinically, it typically occurs in patients who have suffered severe polytrauma and may therefore go unrecognised, presenting late with advanced spondylolisthesis: ■ associated pulmonary, abdominal, vascular and brain injuries may occur pathologically, the condition is due to flexion–distraction with/without additional lateral or rotational forces and has been classified into three basic types:

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type I – pure facet dislocation without fracture, may be unilateral (IA), bilateral with lateral displacement (IB) or bilateral with anterior displacement (IC) type II – unilateral facet fracture–dislocation with contralateral pure facet dislocation, commonly resulting in asymmetrical L5 spondylolisthesis type III – bilateral facet fracture–dislocation with spondylolisthesis (IIIA) or rotational displacement (IIIB) and disc injury

MRI findings ● midline sagittal images demonstrate variable lumbosacral spondylolisthesis, with potential disc and PLC rupture (Fig. 9.193a) ● para-sagittal and axial (Fig. 9.193b) images demonstrate the associated subluxation or dislocation of the facet joints and abdominal wall injury (Fig. 9.193c) ● articular process fractures are optimally demonstrated with high-resolution CT and multi-planar reconstruction

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Figure 9.193 Traumatic lumbosacral dislocation. Sagittal T2-weighted (T2W) fast spin-echo (FSE) image (a) showing rupture of the L5–S1 disc and the posterior ligamentous complex (arrowhead). Axial T2W FSE image (b) showing dislocation of the right L5–S1 facet joint (arrow). Axial T2W FSE image (c) showing extensive damage to the posterolateral soft tissues of the abdominal wall (arrows).

THE SACRUM AND SACROILIAC JOINTS Normal anatomy322 ●

the sacrum comprises five rudimentary vertebral bodies that are fused together to form a single, wedgeshaped bone that articulates superiorly with L5, inferiorly with the coccyx and laterally with the iliac blades through the SIJs (Fig. 9.194a–c): ■ the sacral promontory is formed by a forwards bulge of the anterosuperior margin of S1 (Fig. 9.194a) ■ the spinous processes fuse posteriorly to form the median sacral crest (Fig. 9.194d), which extends downwards to the sacral hiatus (Fig. 9.194a), a defect in the posterior wall of the sacrum at the S5 level

The sacrum and sacroiliac joints

the sacral canal continues caudally from the lumbar spinal canal and contains the meninges (which typically terminate at ~S2) (Fig. 9.194e), the sacral and coccygeal nerve roots, the filum terminale and the fibro-fatty tissue of the epidural space, which terminates at the sacral hiatus ■ the sacral foramina are four paired openings in the anterior and posterior sacrum for transmission of the S1–4 ventral and dorsal nerve roots, respectively (Fig. 9.194f, g) ■ the lateral masses are located between the sacral foramina and the SIJs, the lateral mass of S1 being termed the ‘sacral ala’ (Fig. 9.194h), which are parts of the sacrum that are relatively devoid of bony trabeculae the SIJs are formed by the articulation between the lateral masses of the sacrum and the posteromedial aspects of the iliac blades, and have a ligamentous and a synovial portion (Fig. 9.195a, b): ■ the ligamentous part corresponds to the posterosuperior one-half to two-thirds of the joint ■ the synovial part corresponds to the anteroinferior one-third to one-half of the joint and is lined by a 3–5 mm thick hyaline cartilage on the sacral side and a ~1 mm thick fibrocartilage on the iliac side ■

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Figure 9.194 Anatomy of the sacrum. Sagittal T1-weighted (T1W) spin-echo (SE) image (a) showing the sacrum (white arrows), the sacral promontory (black arrowhead), the sacral hiatus (white arrowhead) and the coccyx (double arrows). Oblique coronal T1W SE image (b) showing the sacral articulations with L5 (arrow) and the iliac blades via the sacroiliac joints (arrowheads). Axial T1W SE image (c) showing the sacral body (arrows). Axial T1W SE image (d) showing the sacral laminae (arrowheads) and the fused spinous process forming the median sacral ridge (black arrow). Sagittal T2-weighted fast spin-echo fat-suppressed image (e) showing the termination of the meninges (arrow) at the S2 level. (continued)

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f Figure 9.194 (continued) Sagittal (f) and axial (g) T1W SE images showing the ventral (arrows) and dorsal (arrowheads) sacral foraminae. Oblique coronal T1W SE image (h) showing the sacral alae (arrows).

the irregular, interdigitating surfaces of the joints (Fig. 9.195c) aid in joint stability, which is mainly provided by the sacral ligaments the sacral ligaments: three pairs of ligaments provide stability to the sacrum: the sacroiliac, the sacrotuberous and the sacrospinous: ■ the sacroiliac ligaments include the ventral (Fig. 9.195d), the dorsal (Fig. 9.195e) and the interosseous (Fig. 9.195f, g); the first two surround the anterior and posterior portions of the SIJ and the last forms the ligamentous portion of the joint ■ the sacrotuberous ligament extends from the sacrum, the posterior iliac spine and the coccyx to the ischial tuberosity ■ the sacrospinous ligament extends from the lower sacrum and the coccyx to the ischial spine detailed histological study of the SIJs323 has indicated that the synovial aspect of the joint may show numerous anatomical variants that could simulate sacroiliitis, including: ■ osseous clefts, cartilage and subchondral defects (Fig. 9.195h) and enhancing vascular connective tissue within the subchondral marrow ■ these features are optimally demonstrated on a combination of axial and coronal oblique MR sequences the coccyx is a small, triangular bone comprising four fused vertebrae that extends from the lower aspect of the sacrum (Fig. 9.194a) ■

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a

b Figure 9.195 Anatomy of the sacroiliac joint (SIJ). Coronal (a) and axial (b) T1-weighted (T1W) spin-echo (SE) images showing the ligamentous (arrows) and cartilaginous (arrowheads) portions of the SIJ. (continued)

The sacrum and sacroiliac joints

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g h Figure 9.195 (continued) Coronal T1W SE image (c) showing the interdigitating surfaces of the joint (arrows). Axial T1W SE images (d, e) showing the ventral (arrow d) and dorsal (arrow e) sacroiliac ligaments. Oblique coronal (f) and axial (g) T1W SE images showing the interosseous sacroiliac ligaments (arrows) appearing as a linear meshwork of hypointense structures within the ligamentous portion of the joint. Oblique coronal T1W SE image (h) showing intermediate signal intensity subchondral defects (arrows) on either side of the joint.

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PATHOLOGY OF THE SACRUM AND SACROILIAC JOINTS CONGENITAL LESIONS Sacral agenesis322 ●

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sacral agenesis is also termed ‘caudal regression syndrome’ (see spinal dysraphism), represents abnormal sacral development of variable degree and may be classified into four types: ■ type 1 – unilateral agenesis confined to the sacrum or the coccyx ■ type 2 – partial but bilateral, symmetrical distal sacral agenesis, the iliac blades articulating with S1 ■ type 3 – total agenesis of the sacrum, the iliac bones articulating with the lowest part of the lumbar spine ■ type 4 – total agenesis of the sacrum, the iliac bones fusing posteriorly in the midline clinically, the condition is very rare, occurring in 0.005–0.01 per cent of the population, though it occurs with higher frequency in mothers with diabetes (0.1–0.2 per cent of cases)

TRAUMA Sacral fractures322,324 ● ●

sacral fractures may be easily missed on radiography, commonly because of the association with a more severe pelvic fracture–dislocation classification: sacral fractures may be classified according to the location of the fracture within the sacrum: ■ zone 1 – lateral to the sacral foramina and not usually associated with any neurological deficits ■ zone 2 – involve one or more of the neural foramina, potentially resulting in unilateral sacral radiculopathy: – they may extend into zone 1 ■ zone 3 – involve the central sacral canal, with/without involvement of the other two zones: – significant bilateral neurological deficits are common, often with bladder/bowel incontinence – transverse zone 3 fractures account for 5–10 per cent of sacral fractures and may be isolated injuries due to a severe direct blow or may occur in association with thoracolumbar burst fractures

MRI findings ● transverse zone 3 fractures may be identified while imaging lumbar burst fractures, and appear as a cortical break with anterior angulation of the distal fragment, associated with traumatic marrow oedema (Fig. 9.196a–c)

Sacral stress fracture325,326 ● ●

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stress fractures of the sacrum can be classified as insufficiency325 or fatigue326 depending on whether they occur in normal or abnormal bone insufficiency fractures325 typically affect older individuals with osteoporosis, or who have undergone radiotherapy for pelvic malignancy, but have also been reported in association with RA, fibrous dysplasia, Paget’s disease, osteopetrosis, osteomalacia, osteogenesis imperfecta and hyperparathyroidism: ■ they are commonly bilateral, occurring in the sacral alae, parallel to the SIJs and occasionally involving the sacral body ■ extremely rarely, the fracture runs in a sagittal plane through the midline of the sacral body (Fig. 9.197a) ■ associated stress fractures of the iliac blades, pubic bones and acetabulae may be seen fatigue fractures326 are relatively rare and are secondary to overuse, occurring in physically active, young individuals, including long-distance runners and military recruits, and in association with pregnancy clinically, they typically present with unilateral or bilateral buttock/low back pain and both are more commonly seen in women:

Pathology of the sacrum and sacroiliac joints

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Figure 9.196 Sacral fracture. Sagittal T1-weighted (T1W) spinecho (SE) (a), short tau inversion recovery (b) and oblique coronal T1W SE (c) images showing a transverse fracture (arrows) through the S2 segment.

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Figure 9.197 Sacral stress fracture. Axial T1-weighted (T1W) spin-echo (SE) image (a) showing a sagittal midline sacral stress fracture (arrow) following partial sacrectomy and radiotherapy. Acute fatigue fracture: Axial T1W SE (b) and T2weighted (T2W) fast spin-echo (FSE) (c) images showing oedema (white arrows) in the right sacral ala and a hypointense oblique fracture line (arrowheads). Note the relationship of the fracture to the right L5 nerve root (black arrow c). Acute insufficiency fracture: Coronal short tau inversion recovery image (d) showing bilateral band-like vertical oedema (arrows) within the sacral alae and a horizontal band of oedema (arrowheads) in the sacral body. (continued)

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Figure 9.197 (continued) Coronal T1W SE image (e) showing a band of oedema (arrows) within the left sacral ala and an irregular hypointense fracture line (arrowheads). Sagittal T1W SE image (f) showing the horizontal component of the fracture (arrow). The ‘fluid sign’: Sagittal (g) and axial (h) T2W FSE images showing hyperintense fluid (arrows) within the fracture. Chronic: Oblique coronal T1W SE image (i) showing fatty replacement of the marrow (arrows) in the right sacral ala and a persistent fracture line (arrowhead).

sciatica327 due to irritation of the L5 root as it passes anterior to the sacral ala (Fig. 9.197b, c) is a rare presentation and occurs at the stage of active periostitis, resolving with healing of the fracture cauda equina syndrome328 secondary to sacral stress fractures has also been described

MRI findings ● insufficiency fracture appears as a vertical, band-like area of marrow oedema running parallel to the SIJ (Fig. 9.197d, e), occasionally with a joining horizontal fracture line through the sacral body (Fig. 9.197d, f): ■ the fracture line may be demonstrated within the region of oedema (Fig. 9.197e, f) ■ the fluid sign:329 fluid has been described within sacral insufficiency fractures and may indicate nonunion (Fig. 9.197g, h) ● fatigue fracture: in the acute stage, oedema is demonstrated in the upper sacrum medial to the SIJ, within which there is an oblique, vertical, hypointense fracture line (Fig. 9.197b, c): ■ the lesion is bilateral in ~16 per cent of cases ■ in the chronic stage, the oedematous changes may resolve completely or convert to fatty marrow (Fig. 9.197i) ■ a variant pattern of sacral stress injury has been described in which there was resolution of marrow oedema on T2W images330

Pathology of the sacrum and sacroiliac joints

INFLAMMATION Inflammatory sacroiliitis293–296,331 ●

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inflammatory sacroiliitis occurs with the seronegative spondyloarthropathies, comprising AS, psoriatic arthropathy, Reiter’s syndrome, inflammatory bowel disease-related arthritis and unclassified spondyloarthropathy: ■ inflammatory sacroiliitis is considered a ubiquitous finding in AS and is a requirement for the diagnosis based on the New York Criteria, radiographic evidence of sacroiliitis developing within 9 years in >80 per cent of cases clinically, patients present with deep, chronic buttock and low back pain pain that is typically worse on waking and eases with activity pathologically, changes initially occur on the iliac side of the joint; the findings are occasionally unilateral early in the disease (10 per cent of cases) but are eventually bilateral: ■ both the synovial and the ligamentous parts of the joint are involved, the synovitis resulting in joint space widening and erosions, leading to capsular ossification, joint ankylosis and ossification of the interosseous ligaments in the superior aspect of the joint ■ in psoriatic arthropathy, bilateral, symmetrical sacroiliitis is seen in ~50 per cent of cases of severe disease; the erosions are larger than those seen in AS and proliferative new bone formation is characteristic, though joint ankylosis is relatively uncommon ■ in Reiter’s syndrome, 40–60 per cent of chronic cases have SIJ involvement, which is usually bilateral MRI is more sensitive than radiography in the early detection of sacroiliitis, allowing direct evaluation of the articular cartilage and differentiation between acute and chronic disease

MRI findings ● peri-articular bone marrow changes: three types of marrow SI changes can be seen: ■ type 1 lesions – reduced T1W SI (Fig. 9.198a) and increased T2W/STIR SI (Fig. 9.198b, c) with enhancement following contrast ■ type 2 – irregular low SI on all pulse sequences (Fig. 9.198d, e), corresponding to medullary sclerosis seen on radiographs and CT ■ type 3 lesions – a thin zone of fatty SI is seen on all pulse sequences on the iliac side of the joint, thought to correspond to ongoing inflammation ● articular cartilage initially shows heterogeneity of SI, with focal or linear areas of hyperintensity on T2W images and enhancement following contrast: ■ dynamic post-contrast scanning shows rapid enhancement of the joint space, the degree and rate of enhancement correlating with the severity of inflammation ■ enhancement of the joint capsule and the synovial membrane is also seen, as is enhancement at the entheses, the sites of attachment of the interosseous ligaments between the ilium and the upper sacrum ■ absence of enhancement in the peri-articular soft tissues (muscle and fat) helps to differentiate the inflammation of spondyloarthropathy from septic sacroiliitis ● erosions appear as focal areas of increased SI on both T1W and T2W images within the normally low SI iliac and sacral cortices extending into the subchondral bone (Fig. 9.198e); they are most prominent on the iliac side of the joint, anteriorly and inferiorly: ■ erosions 80 per cent of cases present before the age of 20 years pathologically, the lesion usually arises in the sacral ala with secondary extension into the sacral body

Pathology of the sacrum and sacroiliac joints

MRI findings ● the lesion is often expansile (Fig. 9.206a, b), and the classical finding of multiple fluid levels is suggestive of the diagnosis (Fig. 9.206c, d) ● reactive marrow oedema may also be seen (Fig. 9.206b)

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Figure 9.206 Sacral aneurysmal bone cyst. Sagittal T1-weighted spinecho (a) and coronal short tau inversion recovery (b) images showing an expansile lesion (arrows) arising in the right sacral ala with adjacent reactive marrow oedema (arrowhead b). Sagittal T2-weighted (T2W) fast spin-echo (FSE) fat-suppressed (c) and axial T2W FSE (d) images showing multiple fluid levels (arrowheads).

Osteoid osteoma and osteoblastoma322,337 ● ●

osteoid osteoma and osteoblastoma are rarely located in the sacrum, with only 2 per cent of spinal osteoid osteomas and 17 per cent of spinal osteoblastomas found in this location clinically, both occur in young adults with local, low back/buttock pain with/without sciatica

MRI findings ● osteoid osteoma: the appearances are similar to those elsewhere in the spinal column, with a low/intermediate SI nidus and florid reactive marrow and soft-tissue oedema (Fig. 9.207a–c) ● osteoblastoma shows a more aggressive growth pattern and has been reported to cross the SIJ340

Osteochondroma337 ●

1–4 per cent of solitary osteochondromas and 7–9 per cent of MHE occur in the spine, rarely involving the sacrum

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Figure 9.207 Sacral osteoid osteoma. Coronal T1-weighted spin-echo (a), short tau inversion recovery (b) and axial T2-weighted fast spin-echo (c) images showing a small hypointense nidus (arrows) with a combination of reactive marrow sclerosis and oedema (arrowheads).

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clinically, depending on their site in relation to the sacrum, they may present as a bony, hard mass or with signs of sacral root compression

MRI findings ● the lesion arises in continuity with the medullary cavity of the sacrum and its SI characteristics depend on the degree of mineralisation of the cartilage; predominantly low SI is seen in the presence of heavy calcification (Fig. 9.208a, b) ● following contrast, the typical pattern or peripheral/septal enhancement may be evident (Fig. 9.208c)

MALIGNANT TUMOURS Sacrococcygeal chordoma322,337,341 ● ● ● ●

chordoma is the commonest primary malignant sacral tumour and arises from notochordal rests, mostly in a midline or paramedian location in relation to the spine chordoma accounts for 2–4 per cent of primary malignant bone tumours, with 50–60 per cent located in the sacrococcygeal region clinically, they present in the fourth to seventh decades and there is a 2:1 male–female ratio pathologically, ~40 per cent are located purely in the sacrum (Fig. 9.209a), 3 per cent in the coccyx (Fig. 9.209b) and the remainder in the sacrococcygeal region (Fig. 9.209c); almost 50 per cent involve the S1 segment: ■ the lesion is usually large and destructive at presentation, with a prominent pre-sacral mass (100 per cent) that may displace, but typically does not invade, the posterior rectal wall (Fig. 9.209a, b) ■ posterior extraosseous extension is reported in 77 per cent of cases (Fig. 9.209d); lateral extension to involve the SIJs (23 per cent), the sciatic notch (Fig. 9.209e, f) and both the anterior and the posterior muscles (piriformis, gluteus maximus, erector spinae) is recognised (Fig. 9.209g) ■ matrix calcification may be seen at radiographic and CT examination ■ rarely, dedifferentiated342 and sarcomatoid343 components are identified histologically, dedifferentiation being more likely following previous treatment with radiotherapy

Pathology of the sacrum and sacroiliac joints

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Figure 9.208 Sacral osteochondroma. Sagittal T1-weighted (T1W) spin-echo (SE) (a) and coronal T2-weighted fast spin-echo (b) images showing a heavily mineralised chondral tumour (arrows) arising from the posterolateral aspect of S1 (arrowhead a) and displacing the adjacent thecal sac and nerve roots (arrowheads b). Post-contrast axial T1W SE image (c) showing typical chondral enhancement (arrows).

MRI findings ● the tumour measures 3–22 cm at presentation, forming a well-defined, encapsulated, multilobulated mass located centrally in 90 per cent of cases and eccentrically in 10 per cent ● the lesion has low/intermediate T1W SI (Fig. 9.209a–c) and heterogeneous hyperintensity on T2W/STIR images (Fig. 9.209d, f) owing to its prominent myxoid stroma ● focal regions of further increased SI may be evident due to haemorrhage (Fig. 9.209h, i), and variable enhancement is seen following contrast; nodular, peripheral and septal enhancement patterns are recognised ● a thin, hypointense rim (Fig. 9.209d, g) and multiple internal septa are typical features on T2W images (Fig. 9.209d), and further areas of low SI may be due to the presence of haemosiderin ● rarely, bony metastases are seen in the adjacent pelvic bones (Fig. 9.209j)

Malignant round cell tumours322,337,344 ● ●

primary lymphoma of bone is considered the third commonest primary malignant sacral tumour and occurs in the second to fifth decades Ewing sarcoma/PNET are histologically similar small round cell tumours that infrequently arise in the spine, though the sacrum is the commonest spinal location: ■ clinically, patients present aged 5–30 years in ~90 per cent of cases

MRI findings these are non-specific, with an aggressive tumour infiltrating the sacrum and extending into both the presacral space and the spinal canal ● there are no particular SI characteristics (Fig. 9.210a–c) ●

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Figure 9.209 Sacrococcygeal chordoma. Sagittal T1-weighted (T1W) spin-echo (SE) images (a, b, c) showing tumours arising from the sacral (arrows a), coccygeal (arrows b) and sacrococcygeal (arrows c) regions with associated displacement of the rectal wall (arrowheads a, b). Axial T2-weighted (T2W) fast spin-echo (FSE) image (d) showing a lobulated heterogeneous hyperintense mass with a thin hypointense capsule (arrowheads), hypointense internal septa (arrows) and a large posterior soft-tissue extension (double arrowheads). Coronal T1W SE (e) and short tau inversion recovery (f) images showing lateral extension through the sciatic notch (arrows) and to the sacroiliac joints (arrowheads f). Axial T2W FSE image (g) showing a thin hypointense rim (arrowheads) and nodular infiltration of the right gluteus maximus muscle (arrow). (continued)

Pathology of the sacrum and sacroiliac joints

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Figure 9.209 (continued). Axial T1W SE (h) and sagittal T2W FSE (i) images showing areas of increased signal intensity (arrows) due to haemorrhage. Axial T2W FSE fat-suppressed image (j) showing a hyperintense lobulated tumour (arrows) with bony metastases (arrowheads) to the right pubic bone and the left posterior acetabulum.

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c Figure 9.210 Sacral Ewing sarcoma. Axial T1-weighted (T1W) spin-echo (SE) (a), sagittal T2-weighted fast spin-echo fatsuppressed (b) and post-contrast axial T1W SE (c) images showing an aggressive mass arising from the sacrum (arrows b) with both anterior (arrows a) and posterior (arrowheads b) extraosseous extension and almost uniform enhancement following contrast (arrows c).

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Chondrosarcoma337 ● ●

chondrosarcoma affects the spine in 3–12 per cent of cases and sacral involvement is rare, usually occurring in the 30–60-year age range and more commonly in men pathologically, they are usually low grade

MRI findings ● these are as for low-grade chondrosarcoma at other locations, showing a lobulated growth pattern, low/intermediate T1W SI (Fig. 9.211a), increased T2W/STIR SI (Fig. 9.211b) and peripheral/septal enhancement following contrast (Fig. 9.211c)

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Figure 9.211 Sacral chondrosarcoma. Coronal T1-weighted (T1W) spin-echo (SE) (a) and sagittal T2-weighted fast spin-echo (b) images showing a lesion (arrows) arising in the left sacral ala. Postcontrast coronal T1W SE image (c) showing typical peripheral (arrows) and septal (arrowhead) enhancement.

Osteosarcoma337 ● ●

osteosarcoma is the fifth commonest primary malignant sacral neoplasm, accounting for only 4 per cent of malignant primary sacral tumours pathologically, many sacral osteosarcomas arise in pre-existing Paget’s disease, in which case they appear lytic in ~50 per cent of cases

MRI findings ● the tumour shows aggressive infiltration of the sacrum, with lytic areas showing intermediate T1W SI (Fig. 9.212a), hyperintensity on T2W FSE/STIR (Fig. 9.212b) and enhancement following contrast (Fig. 9.212c); any heavily ossified areas maintain low SI on all pulse sequences (Fig. 9.212b, c)

Metastases and myeloma322,337 ●

metastases are the commonest sacral tumours, with lung, breast, kidney and prostate the most common primary sites: ■ contiguous spread from local malignancy such as rectal, uterine, prostate or bladder may also occur

Pathology of the sacrum and sacroiliac joints

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Figure 9.212 Sacral osteosarcoma. Oblique coronal T1-weighted (T1W) spin-echo (SE) (a) and axial T2-weighted fast spin-echo fat-suppressed (FS) (b) images showing a poorly defined infiltrative sacral tumour (arrows a) with markedly reduced signal intensity (SI) in the ossified component (arrows b). Postcontrast oblique coronal T1W SE FS image (c) showing enhancement of the lytic component (arrows) while the ossified component maintains a low SI (arrowheads).

plasmacytoma and myeloma may involve the sacrum; myeloma is the second commonest primary malignant sacral tumour, arising typically in the sixth to seventh decades and with a 2:1 male predominance

MRI findings ● these are non-specific, showing a variably sized, aggressive, destructive mass, with/without extraosseous extension and compression of the distal thecal sac and sacral roots ● lytic lesions show intermediate T1W SI and heterogeneous intermediate to high T2W/STIR SI ● sclerotic metastases show reduced SI on all pulse sequences

Sacroiliac joint invasion by bone tumours345 ● ● ●

SIJ invasion by sacral/iliac tumours is well recognised, the SIJ being the commonest joint to be involved by tumour invasion identification of this phenomenon is critical to the surgical staging of malignant pelvic tumours pathologically, invasion of the SIJ can occur with aggressive benign tumours such as GCT or with malignant tumours, and involves the ligamentous portion of the joint in isolation or the whole of the joint

MRI findings ● articular spread may be diagnosed when continuous tumour tissue is demonstrated to cross all or part of the SIJ, optimally demonstrated on coronal (Fig. 9.213a) and axial (Fig. 9.213b) images

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Figure 9.213 Sacroiliac joint (SIJ) invasion by tumour. Coronal T1-weighted spin-echo image (a) showing extension of a large iliac tumour (arrows) across the synovial portion of the right SIJ (arrowhead). Axial T2-weighted fast spin-echo image (b) showing a large iliac osteosarcoma (arrows) extending into the ligamentous portion of the SIJ (arrowheads).

THE POST-OPERATIVE SPINE Introduction23,346,347 ●

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surgical procedures for relief of symptoms caused by degenerative disc disease include various combinations of nerve root or cauda equina decompression (discectomy/laminectomy) for prolapsed intervertebral disc (PID) or spinal stenosis and spinal fusion (instrumented or non-instrumented) for discogenic low back pain failed back surgery syndrome (FBSS) is a clinical situation in which there is a failure of resolution of symptoms, or the production of new symptoms (low back pain and/or radiculopathy) following any surgical procedure for degenerative disc disease FBSS has many possible causes depending on the nature of the surgery that has been performed, knowledge of which is therefore required for an adequate assessment of the post-operative status following discectomy for PID, possible causes of FBSS include operation at the wrong level, epidural scarring, recurrent/residual disc hernia, haematoma, post-operative discitis, arachnoiditis, pseudomeningocele, foreign body and development of lateral recess or foraminal stenosis following spinal fusion, possible causes of FBSS include misplaced/displaced instrumentation, non-union (pseudarthrosis) and adjacent segment degenerative disease

LUMBAR DISCECTOMY Normal appearances following discectomy346,347 ●

surgical approach depends on the size and the location of the PID: ■ a small paracentral PID may be adequately accessed via resection of part of the LF, a procedure termed ‘fenestration’, which is seen on MRI as focal absence of part of the LF in the presence of an intact neural arch (Fig. 9.214a) ■ larger central or paracentral PID may require partial resection of the inferior aspect of the lamina (laminotomy) or unilateral/bilateral laminectomy, which is optimally identified on axial (Fig. 9.214b) and sagittal (Fig. 9.214c) images, while intraforaminal PID may require partial resection of the medial part of the facet joint ■ following laminectomy, it is normal to see bulging of the thecal sac into the laminectomy defect (Fig. 9.214d, e) ■ tiny metallic artefacts may be seen at the disc margin (Fig. 9.214f)

The post-operative spine

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e Figure 9.214 Normal post-discectomy appearances. Fenestration: Axial T2-weighted (T2W) fast spin-echo (FSE) image (a) showing partial resection of the right S1 ligamentum flavum (arrow). Laminectomy: Axial T1-weighted spin-echo (b) and sagittal T2W FSE (c) images showing resection of the S1 (arrow b) and L5 (arrow c) lamina and ligamentum flavum. Sagittal (d) and axial (e) T2W FSE images showing bulging of the thecal sac (arrows) into the laminectomy defect. Sagittal T2W FSE image (f) showing metallic artefact (arrow) at the L5–S1 disc margin.

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Early post-discectomy appearances23,346,347 ●

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the early post-discectomy period has been arbitrarily defined at the first post-operative 6 months, and many changes related to the disc/end-plates, the epidural space/thecal sac/nerve roots and the laminectomy space/posterior soft tissues may be apparent that should not be considered pathological the IVD: focal increased T2W SI within the disc (Fig. 9.215a) in the form of a high SI band extending from the nucleus to the site of annular disruption is a common finding and may persist for up to 2 months:

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Figure 9.215 Normal post-discectomy appearances. Axial T2-weighted (T2W) fast spin-echo (FSE) image (a) showing increased signal intensity (arrow a) at the site of annular incision. Sagittal T2W FSE image (b) showing disruption of the intranuclear cleft (arrow) with metallic artefact (arrowhead) in the disc space. Post-contrast axial T1-weighted (T1W) spin-echo (SE) image (c) showing annular enhancement (arrow c). Sagittal T2W FSE image (d) showing marked loss of disc height (arrow) and oedema in the end-plates (arrowheads). Axial T1W SE image (e) showing a small residual disc prolapse (arrow).

The post-operative spine

contrast enhancement within the disc is reported in ~67 per cent of cases for up to 6 weeks postdiscectomy and the intranuclear cleft may disappear (Fig. 9.215b) with focal enhancement of the posterior AF (Fig. 9.215c) ■ loss of disc height may occur depending on the thoroughness of the discectomy (Fig. 9.215d), and this may contribute to delayed lateral recess or foraminal stenosis ■ residual/recurrent disc herniation has been reported in 24 per cent of patients within 6 weeks following successful discectomy; 16 per cent show a mild/moderate mass effect on the dural sac and 5 per cent show severe thecal sac compression, these changes still being identified at 6 months (Fig. 9.215e) the end-plate: reactive type 1 end-plate changes are occasionally identified following discectomy, with enhancement reported in 19 per cent of asymptomatic individuals at 6–18 months post-discectomy (Fig. 9.215d) the epidural space: an enhancing, anterior epidural mass may be seen at the site of discectomy in ~80 per cent of cases (Fig. 9.216a–c), resulting in poor definition of the posterior disc margin and the thecal sac: ■

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Figure 9.216 Normal post-discectomy appearances. Sagittal T1-weighted (T1W) spin-echo (SE) (a), T2-weighted (T2W) fast spin-echo (FSE) (b) and axial T2W FSE (c) images showing a large anterior epidural mass (arrows) 3 days after L5–S1 discectomy. Axial T1W SE (d) and post-contrast T1W SE (e) images showing enhancement of the swollen left S1 nerve root (arrows).

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the mass is considered to represent epidural oedema or possible haematoma, and the incidence of such epidural soft tissue decreases to ~50 per cent after 2 months the thecal sac: cauda equina adhesions may be seen in the first 6 weeks but gradually resolve: ■ shrinkage of the thecal sac may be observed, but this typically returns to normal by 3 weeks the nerve roots: intrathecal nerve root enhancement has been reported in 20–62 per cent of asymptomatic individuals 3–6 weeks following discectomy, but in only 2 per cent at 6 months: ■ nerve root enhancement 6–8 months post-discectomy should be considered pathological, and correlates with ongoing leg pain (Fig. 9.216d, e) the laminectomy space may be filled with intermediate SI soft tissue (Fig. 9.217a), which enhances (Fig. 9.217b) and may be continuous with anterolateral enhancing epidural soft tissue and posterior intermuscular soft tissue along the surgical track: ■ enhancement of the facet joint (Fig. 9.217c) is reported to occur in 63–88 per cent of cases within the first 6 weeks, representing a response to surgical dissection posterior soft tissues: oedema and swelling of the posterior muscles (Fig. 9.217d) on the side of surgical dissection is always present and small fluid collections may be seen on T2W images: ■ a track of enhancing tissue is seen to extend posteriorly from the laminectomy space in all early postoperative cases but in only 18 per cent of cases at 6 months post-discectomy ■ a large fluid collection, particularly in the setting of postural headache, should raise the suspicion of a CSF leak, while a fluid collection with a thick, irregular, enhancing wall is suggestive of an abscess ■

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d c Figure 9.217 Normal post-discectomy appearances. Sagittal T1-weighted (T1W) spin-echo (SE) (a) and post-contrast axial T1W SE fat-suppressed (b) images showing soft tissue within the laminectomy space (arrow a) extending from the thecal sac (white arrowhead a) to the subcutaneous tissues (black arrowhead a) with enhancement (arrows b) following contrast. Post-contrast axial T1W SE image (c) showing enhancement of the left L5–S1 facet joint (arrow). Sagittal T2-weighted fast spin-echo image (d) showing swelling and oedema of the posterior paraspinal muscles (arrows).

The post-operative spine

COMPLICATIONS OF LUMBAR DISCECTOMY Epidural fibrosis23,346,347 ● ●

epidural fibrosis (scar) is a well-recognised complication of discectomy, though the relationship of scar tissue to symptoms is somewhat controversial the incidence of epidural fibrosis as a cause of recurrent symptoms has been estimated at 8–14 per cent: ■ it has been suggested that diffuse scar is more likely to be related to recurrent symptoms than small areas of focal scarring

MRI findings ● an intermediate T1W SI mass is seen effacing the epidural fat in the anterior/anterolateral epidural space and typically conforming to the outline of the thecal sac (Fig. 9.218a) ● the T2W SI of epidural scar depends on the age of the scar tissue; relatively new scar shows intermediate/high SI (Fig. 9.218b) while scar tissue appears hypointense after 2 years (Fig. 9.218c) ● the scar tissue shows uniform enhancement on early post-contrast T1W images (Fig. 9.218d), which may also demonstrate the tethered nerve root (Fig. 9.218e) ● occasionally, scar tissue shows a mass effect on the thecal sac that may still be present after 6 months

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Figure 9.218 Post-discectomy epidural fibrosis. Axial T1-weighted (T1W) spin-echo (SE) image (a) showing intermediate signal intensity (SI) scar tissue (arrows) replacing the anterior and left lateral recess epidural fat. Axial T2weighted fast spin-echo images (b, c) showing intermediate SI epidural scar (arrows b) and chronic hypointense scar (arrow c). Post-contrast axial T1W SE image (d) showing scar enhancement (arrows). Post-contrast axial T1W SE image (e) showing enhancing epidural scar (arrows) tethering the right S1 nerve root (arrowhead).

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Recurrent/residual disc herniation23,346,347 ● ●

recurrent PID has been defined as a PID occurring at the same level, ipsilateral or contralateral, with a pain-free period of at least 6 months; it has a reported incidence of 5–11 per cent residual PID may result from incomplete/inadequate discectomy, or rarely from operation at the wrong level, which is particularly likely to occur in the presence of an LSTV

MRI findings ● an anterior/anterolateral, polypoid, epidural mass (Fig. 9.219a) is seen indenting the thecal sac that may be identified as continuous with the disc space on sagittal T2W images (Fig. 9.219b), has intermediate SI on T1W images (Fig. 9.219a) and shows rim enhancement on early (