A System of Orthopaedic Medicine

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A System of Orthopaedic Medicine

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A System of Orthopaedic Medicine o

with accompanying CD-ROM

Ludwig Ombregt MD (Editor-in-

hief)

Medical Practitioner in Orthopaedic Medicine, Kanegclll, Belgium; inlernation.:li Lecturer in O r th opaedic Medicine

Pierre Bisschop Ph siotherapisl specializing in Orthopaedic Medicine, Kncsselare, Belgium; International Lecturer in Orthopaedic Medicine

Herman J. ter Veer Physiotherapist specializing in Orthopaedic 1edicine and Manual Therapist, Deventcr, The Netherlands; International Lecturer in Orthopaedic Medicine

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CHURCHill LIVINGSTONE

SECOND EDITION ClIURClIILL LIVINGSTONE An imprint of EI.;evier Science Limited

© 1995 WB Saunders Company Limited © 2003, EI�vicr Science Limited. A II right!' re-,erVl.>d. The right!. of Ludwig Ombregl, Pierre Bis�hop ilnd Herman J. ler Veer to be identified as author., of thi., work hao:; been asserted by them in accordance with the Copyright, OCf.,igns and Patents Act 1988. No part of Ih13 publication may be reproduced, stored in a retrieval �ystem, or transmitted in any form or by any means, electronic, mechanical, photocopying, recording or olhen""i�, without either the prior permission of the publi..hers (Permission" Manager, Ebevier Science Limited, Independence Square West, Suite 300, The Curti.. Center, Philadelphia, PA 19106M3399, USA) or a licence per­ mitting restricted oopying in the United Kingdom i..sued by the Copyright Liccn"ing Agency, 90 Tottcnham Court Road, London W IT 4LP. First edition 1995 Second edition 2003 ISBN 0443 073708 British Library Cataloguing in Publication Data

A catalogue record for thi" book is ;lvailable from the Briti')h Library Library of Congress Cataloging in Publication Data

A catalog n,-'cord for this book b available from the Library of Congn:-'S� Note Medical knowledge i'i constantly changing. A" new informal1on become:, available, changes in treatment, proccciurt'S, equipment and the

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become nccC'SScuy. The authors and the publisher::, have taken care to en..ure thai the infonnalion given in thi::, le>.t is accurate and up to date. However, readers are ..trongly advied to confinn that the information, e'ipecial1y with regard to drug u:,age, complies with the latest legislation and standards of practice.

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Contents

Preface to the second edition Preface to the first edition

ix xi

About the CD

xiii

Acknowledgements

xiv

Section one: General principles Ludwig Ombregt, Herman J. ter Veer, Pierre Bisschop

1. 2. 3. 4. 5.

Pain Pressure on nerves Connective tissue Clinical diagnosis of soft tissue lesions Principles of treatment

3 23 33 59 93

Section two: The cervical spine Pierre Bisschop

6. 7. 8. 9. 10. 11. 12. 13.

Applied anatomy of the cervical spine Clinical examination of the cervical spine Clinical spine: interpretation of the clinical examination Mechanical disorders Non-mechanical disorders Headache and vertigo of cervical origin W hiplash-associated disorders Treatment

135 147 165 175 211 223 239 247

Section three: The shoulder Ludwig Ombregt

14. 15. 16. 17. 18. 19.

Applied anatomy of the shoulder Clinical examination of the shoulder Interpretation of the clinical examination Disorders of the inert structures Disorders of the contractile structures Disorders associated with a painful arc

277 291 303 305 349 379

Section four: The shoulder girdle Pierre Bisschop

20. 21. 22. 23. 24.

Applied anatomy of the shoulder girdle Clinical examination of the shoulder girdle Interpretation of the clinical examination of the shoulder girdle Disorders of the inert structures Disorders of the contractile structures

387 395 401 403 411

vi

CONTENTS

Section five: The elbow Pierre Bisschop

25. 26. 27. 28. 29.

Applied anatomy of the elbow Clinical examination of the elbow Interpretation of the clinical examination of the elbow Disorders of the inert structures Disorders of the contractile structures

415 427 435 437 447

Section six: The wrist, thumb and hand Pierre Bisschop

30. 31. 32. 33. 34. 35. 36.

Applied anatomy of the wrist, thumb and hand Clinical examination of the wrist, thumb and hand Interpretation of the clinical examination of the wrist, thumb and hand Disorders of the lower radioulnar joint Disorders of the wrist Disorders of the thumb Disorders of the hand and fingers

473 483 493 495 499 521 533

Section seven: Nerve lesions and entrapment neuropathies of the upper limb Pierre Bisschop

37. Nerve lesions and entrapment neuropathies of the upper limb

543

Section eight: The thoracic spine Ludwig Ombregt

38. 39. 40. 41. 42. 43. 44.

Applied anatomy of the thorax and abdomen Clinical examination of the thoracic spine Interpretation of the clinical examination of the thoracic spine Disorders of the thoracic spine: disc lesions Disorders of the thoracic spine: non-disc lesions Disorders of the thoracic cage and abdomen Ankylosing spondylitis of the thorax

581 593 613 615 635 655 669

Section nine: The temporomandibular joint Pierre Bisschop

45. 46. 47. 48.

Applied anatomy of the temporomandibular joint Clinical examination of the temporomandibular joint Interpretation of the clinical examination of the temporomandibular joint Disorders of the temporomandibular joint

675 679 687 689

Section ten: The lumbar spine Ludwig Ombregt, Herman J. ter Veer

49. 50. 5 1. 52.

Introduction to the lumbar spine Applied anatomy of the lumbar spine Ageing of the lumbar spine The dural concept

699 703 729 743

CONTENTS

53. 54. 55. 56. 57. 58. 59.

The ligamentous concept The stenotic concept Clinical examination of the lumbar spine Lumbar instability Mechanical disorders of the lumbar spine: differential diagnosis Non-mechanical disorders of the lumbar spine Treatment of the lumbar spine

vii

775 787 799 837 847 851 873

Section eleven: The sacroiliac joint and coccyx Ludwig Ombregt, Herman J. ter Veer

60. 61. 62. 63. 64.

Applied anatomy of the sacroiliac joint Clinical examination of the sacroiliac joint Interpretation of the clinical examination of the sacroiliac joint and coccyx Disorders of the sacroiliac joint Anatomy and disorders of the coccyx

941 947 955 957 967

Section twelve: The hip and buttock Herman J. ter Veer, Ludwig Ombregt

65. 66. 67. 68. 69. 70. 71. 72.

Applied anatomy of the hip and buttock Clinical examination of the hip and buttock Interpretation of the clinical examination of the hip and buttock Disorders of the inert structures Disorders of the contractile structures Groin pain Hip disorders in children Summary of hip pain

973 985 997 999 1023 1035 1043 1049

Section thirteen: The knee Ludwig Ombregt, Herman J. ter Veer

73. 74. 75. 76. 77. 78. 79.

Applied anatomy of the knee Clinical examination of the knee Interpretation of the clinical examination of the knee Disorders of the inert structures: capsular and non-capsular patterns Disorders of the inert structures: ligaments Disorders of the contractile structures Differential diagnosis of lesions at the knee

1053 1063 1075 1077 1099 1131 1153

Section fourteen: The lower leg, ankle and foot Ludwig Ombregt

80. 81. 82. 83. 84. 85. 86.

Applied anatomy of the lower leg, ankle and foot Clinical examination of the lower leg, ankle and foot Interpretation of the clinical examination of the lower leg, ankle and foot Disorders of the lower leg Disorders of the ankle and subtalar joints Disorders of the midtarsal joints Disorders of the forefoot and toes

1159 1171 1181 1183 1203 1239 1249

viii

CONTENTS

Section fifteen: Nerve lesions and entrapment neuropathies of the lower limb Ludwig Ombregt

87. Nerve lesions and entrapment neuropathies of the lower limb

1263

Section sixteen: Psychogenic pain Ludwig Ombregt

88. Psychogenic pain

1273

Appendix: Teaching facilities

1281

Index

1283

Preface to the second edition

It is with great pleasure that we present the second

rate diagnoses and to outline safe and effective conser­

edition of A System of Orthopaedic Medicine. We have been

vative treatments.

most gratified with the huge interest shown in the first

For the second edition the text has been changed exten­

edition of our book and the enthusiasm shown by the

sively. Each chapter has been revised completely and the

participants at our courses stimulated us to continue the

references fully updated. New chapters on instability of

work we first undertook more than a decade ago.

the shoulder, the wrist and the lumbar spine, on 51 disor­

The need for such a book seems to be as great now as

ders and on groin pain have been added. In order to help

when the first edition was published. Despite advances

the reader to interpret the outcome of a clinical examina­

in medical technology, basic clinical knowledge and

tion the 'clinical reasoning' sections have been extended.

competence in orthopaedic medicine remain grossly

The new edition contains 55 new photographs and 180

neglected in medical tuition. Clinical medicine is not

new line drawings. Each section also contains a new

popular at our universities - a whole generation of

chapter consisting of an extensive differential diagnosis

general practitioners and physiotherapists has not been

flow-chart that summarises the deductive thought

trained in clinical examination and in clinical reasoning.

sequence that should be followed for the interpretation of

Making a functional diagnosis and offering an easy and

the joint examination.

direct conservative treatment seems to be very difficult these days. Instead, highly sophisticated technical proce­

Lastly, a CD-ROM containing 89 video clips (approx. 30 min) demonstrating the investigations described in the

dures are used to make anatomical diagnoses that very

text has been included.

often lead to expensive and not always harmless surgical solutions. The main goal of A System of Orthopaedic

Ludwig Olllbregt

Medicine remains to help to fill this gap in medical tuition

Pierre Bisschop

and to offer doctors and therapists a hands-on tools , a

Herman ]. ter Veer

system at their fingertips that helps them to make accu-

2003

THIS PAGE INTENTIONALLY LEFT BLANK

Preface to the first edition

This book is based entirely on the Cyriax approach to

ously mislead the examiner resulting in either inappro­

orthopaedic medicine. James Cyriax (1904-1985) the

priate or potentially harmful treatment for the patient.

'father ' of orthopaedic medicine, devoted his whole life

Technology has become in too many cases a substitute

to developing a logical system of clinical examination

for clinical skills and the ability to diagnose and think

designed to elicit accurate diagnoses of locomotor disor­

remains poor.

ders. His system is founded on a few elementary theories:

An accurate clinical diagnosis is the first and most

an injured structure

important obligation for every orthopaedic doctor and

hurts when tension is put on its fibres. A detailed clinical

therapist. Since these skills are not formally taught the

examination using these simple principles outlines clini­

purpose of this book is to provide a systematic approach

referred pnin and selective tension

-

cal patterns that can be interpreted on the basis of the

to clinical examination which can lead to accurate diag­

known facts of applied anatomy and physiology. Logical

nosis. The method described is logical and consists of

conclusions can then be drawn regarding diagnosis,

assessing in turn the function of each moving tissue, the

treatment and spontaneous recovery.

positive and negative responses forming a pattern.

The authors of this book were all trained by Dr Cyriax

These patterns are then translated into clinical syn­

and subsequently taught with him until his death in

dromes. The system relies entirely on basic clinical skills

1985. Ever since, they have continued his work, and as

and requires none of the diagnostic apparatus found

far as possible improved it. The fact that they are all

only in hospitals. For this reason it will be of particular

practitioners, using the system in their daily clinical

value to family doctors, physiotherapists, rheumatolo­

work has helped to add considerable complementary

gists, orthopaediC surgeons and particularly those

clinical experience.

working in sports medicine. Especial emphaSiS is given

Orthopaedic medicine has traditionally been a grossly

to differential diagnosis. Warning signs are highlighted

neglected area of medical education, despite the large

to alert both examiner and therapist to possible pitfalls

number of patients suffering from non-surgical ortho­

and therapeutic dangers.

paedic conditions. Any family practitioner will confirm

Most of the treatments described were devised by

that between a fifth and a quarter of his/her work con­

Cyriax. They are: injections, infiltrations and deep trans­

sists of patients complaining of musculoskeletal pain.

verse friction for muscular, tendinous and ligamentous

This combination of inadequate education and a high

lesions; manipulation for some ligamentous disorders

incidence of disorders leads to a large number of patients

and for reducing displaced fragments of cartilage in the

for whom there is no clear diagnosis nor proper treat­

different joints; traction for some types of lumbar disor­

ment. ChroniCity, neurosis and compensation claims are

ders and capsular stretching for some capsular disorders.

then, in many cases, inevitable consequences.

Although there may be many alternative equally effective

In recent years another trend has had a major impact

treatments practised by others, the authors have confined

on orthopaediC medicine. Outstanding advances such as

themselves to those with which they have considerable

computed axial tomography (CAT), magnetic resonance

personal experience. The techniques described here are

imaging (MRI), arthroscopy and echography have

simple and have through time confirmed their effective­

undoubtedly enhanced the clinician's ability to see

ness. For any treatment to be successful, accurate diagno­

detailed anatomical images and structures. However,

sis must be followed by carefully focused therapy to the

these procedures have brought mixed blessings. Too

affected area. For this reason considerable detail is given

often they are employed unquestioningly before a good

on the correct performance of each therapeutic technique

clinical diagnosis has been established and may con­

supported by numerous clear, explanatory photographs

tribute needlessly to the escalating costs of health care.

and diagrams.

More importantly the 'lesions' these investigations reveal

Finally we wish to stress the importance of close co­

are often not the real cause of the problem and may seri-

operation between physician and (physio) therapiSt. The

xii PREFACE

system of orthopaedic medicine promoted in this book

fessions need to be fully aware of the possibilities, modal­

requires teamwork. Both doctor and therapist examine

ities and potential results.

the patient in the same way, speak the same language and share their assessments and diagnoses. As to treatment,

Ludwig Ombregt

some disorders will respond better to physical treatment

Pierre Bisschop

and others will require a medical approach but both pro-

Herman J. ter Veer Tony Van de Velde 1995

About the CD

The free CD-ROM that accompanies this book includes

Installation and running instructions for the CD can be

video clips of the examination and assessment techniques

found at the back of the book.

described in the text. The techniques demonstrated on the CD are marked in the book by the symbol

8.

Acknowledgements

We would like to recogruze all our friends, colleagues, stu­

his outstanding editorial skills in converting our original

dents and experts, too numerous to mention individually,

text into readable English.

who have given support, encouragement and expertise in

We would also like to thank the following consultants:

the preparation and production of this book. In particular

JP Clarijs, PhD, Professor of Anatomy VUB, University

we would like to thank our colleagues, teachers of the OMI,

of Brussels Belgium; H Vermeersch, MD Professor

Hans Vorselaars, Ton Mink, Stig Fossum, Are Ingemann,

of Plastic Surgery (Head and Neck Surgery) RUG,

Dirk Lammertijn, Jacques Misotten, Jan Pieters, Marc

University of Gent Belgium; M Van der Schueren,

Reyniers, Pierre Stainier, Paul Teulingkx and Piet Van

MD Anaesthesiologist, Kliniek Maria's Voorzienigheid,

Ooteghem. Special thanks go to our late friend Frank Plum,

Kortrijk Belgium, C Dierickx, MD Orthopaedic Surgeon,

who not only encouraged us to start the project but also

Virga Jesse Ziekenhuis, Hasselt Belgium; DR Siewertsz

provided significant help all through the book's gestation.

van Reesema, MD Rheumatologist Stichting Deventer

He was an outstanding adviser and an exceptional linguist

Ziekenhuizen, Deventer, The Netherlands; H. Kinzinger,

providing much expertise and constructive criticism.

MD Orthopaedic Surgeon, Bruges, Belgium.

We are particularly grateful to Professor Dudley, Emeritus Professor of Surgery, University of London for

Special thanks to Mr Stan Van Nieuwenhove for the photographs.

SECTION ONE

General principles

SECTION CONTENTS 1. Pain 3 Definition of pain 3 Perception and modulation of pain Referred pain 6

3

2. Pressure on nerves 23 Anatomy 23 Terrr.inology 26 Pain originating from the peripheral nerve system Behaviour of nervous tissue during pressure 26

Clinical syndromes

26

27

3. Connective tissue

33 Structural composition 33 Connective tissue cells 33 Extracellular matrix (ECM) 34 Structures containing connective tissue 37 Trauma to soft connective tissue 43 Treatment of traumatic soft connective tissue lesions

4. Clinical diagnosis of soft tissue lesions

Introduction 59 Clinical evaluation 63 History 63 Inspection 69 Preliminary examination 70 Functional examination 70 Accessory tests 75 Palpation 77 Diagnostic infiltration or aspiration 80 Technical investigations 80 Interpretation 80 Impairment of active movements 81 Impairment of passive movements 83 Impairment of resisted movements 87 Absence of pain on movement 89 Summary 89 Diagnostic difficulties 89 5. Principles of treatment 93 Introduction 93 Techniques 94 Deep transverse friction 94

Passive movements 102 Active movements 114 Injection and infiltration

115

59

47

THIS PAGE INTENTIONALLY LEFT BLANK

CHAPTER CONTENTS Definition of pain

Pain

3

Perception and modulation of pain 3 Peripheral nociceptive system 4 Afferent nociceptive system 4 Pain modulation systems 5 Referred pain Introduction

6

6

Possible mechanisms 6 Clinical consequences 8 Rules of referred pain 8 Dermatomes 10 Discrepancies between dermatomes and myotomes

15

Referred pain in visceral diseases 16 Referred pain is felt deeply and distally in the dermatome

16

Segmentally referred pain does not cross the midline Dura mater an 'exception' to segmental reference Referred tenderness 18 Factors determining reference of pain 19

17

17

DEFINITION OF PAIN

Pain is the presenting symptom in a lmost every orthopaedic patient. A complaint of pain is always indicative of some variety or degree of dysfunction1 and results from a combination of physical and psychological causes, although sometimes one or the other predomi­ nates. All pain must be regarded as real. Pain entirely devoid of somatic cause is labelled 'psychogenic pain': although no peripheral tissue damage exists, the pain is just as distressing as somatic pain2 (see Section 16 ). The taxonomy commi ttee of the International Association for the Study of Pain defined pain as: 'an unpleasant sensory and emotional experience associ­ ated with actual or potential tissue dam age, or described in terms of such damage' .3 Pain is thus not a 'primary sensation' in the sense that smell, taste, touch, vision and hearing are, but is an 'emotional state', like sorrow, love or hate. The consequence is that it is extremely difficult to explain one's pain to another person. This is reflected in the numerous words that patients use to describe intensity and quality of pain: twinge, ache, distress, discomfort, soreness, cramp, suf­ fering, misery, agony, torment, anguish.4 The fact that pain is always a subjective experience provides the first difficulty in its use in diagnosis. The language used is not always easy to understand, and the examiner usually needs a high level of competence and under­ standing to translate patients' subjective descriptions into more objective and useful statements. However, unlike the other affective states, pain is always felt in some particular part of the body. Having said this, the localization of the pain very often lacks precision, and it is often experienced at some distance from i ts source - 'referred pain' . This constitu tes the second problem in using the symptom of pain as a diagnostic aid.

PERCEPTION AND MODULATION OF PAIN

The intensity of pain does not depend only on the inten­ sity of irritation of the peripheral nociceptive system 3

4 SECTION ONE - GENERAL PRINCIPLES

(receptors and their afferents). Centripetal transmission of peripheral nociceptive stimulation is subject to varying degrees of facilitatory and inhibitory modulation at differ­ ent synapses during its course to the cerebral cortex. An important modulation site, of major concern to the orthopaedic physician, is the gateway synapse in the basal spinal nucleus, but there are also modulation systems in the spinal grey matter, in the thalamus and in the cerebral cortex itself.s

c

PERIPHERAL NOCICEPTIVE SYSTEM Nociceptive receptors are defined as nerve endings that are sensitive to noxious or potentially noxious (mechani­ cal and chemical) stimuli. The perceptual aspect of the nociceptive system consists of unmyelinated free nerve endi ngs, d istributed three d imensionally throughout skin, subcutaneous and adipose tissue, fasciae, apo­ neuroses, ligaments, tendons, muscles, periosteum and bone.6,7 Clinically, three distinct areas of pain perception may be considered: the skin (superficial somatic pain); the locomotor system (deep somatic pain); and the viscera (visceral pain). Of these, only the skin is adapted to local­ ize pain exactly in the region of injury. Deep somatic and visceral pain are often felt in unusual locations (see re ferred pain, p. 6). In normal circumstances, this nociceptive receptor system remains largely inactive. The unmyelinated free nerve endings are depolarized only by the application of mechanical forces sufficient to deform or damage the tissue that contains them or after exposure to sufficient concentrations of irritating chemical substances (lactic acid, serotonin, prostaglandins and histamine ), released from local inflammatory cells and from the peripheral terminals of the primary afferent fibres themselves. 8-1 0 Another important influence on nociceptor sensitivity is the pH of the tissue. High local concentrations of protons are known to occur in infl ammation and the con­ sequent reduction in pH contributes to the sensitization of nociceptors.11,12

AFFERENT NOCICEPTIVE SYSTEM Nerve impulses generated at the nociceptive receptor system are delivered into the spinal cord by small myeli­ nated and unmyelinated nerve fibres (5 .um or less in diameter), that mainly belong to the Ad and C groups of afferent nerve fibres (Fig. 1 . 1 ). Their cell bodies are located in the dorsal root ganglia of the spinal nerves. The very small diameter of the C nerves explains their slow conduction velocity (1 m/ s), and their extreme sensitivity to blockade by local anaesthetic drugs. The myelinated Ad fibres are slightly larger and have a faster conduction velocity (10 m/ S ).13

Figure 1.1 The afferent nociceptive systems. Projection areas: I, perceptual area; II, emotional area; III, memory storage. Three levels of sensory neurone: A, primary sensory neurone; B, dorsal horn cell (gateway synapse); C, thalamic relay.

The nociceptive afferents enter the spinal cord, where they divide into short ascending and descending branches, before they terminate at synapses on various groups of relay neurones in the dorsal horn of the spinal grey matter. Most of the connections are to the neurones in the basal spinal nucleus (at the base of the dorsal horn).14, lS The efferents of these cross the cord obliquely to turn upwards on the contralateral side and form the anterolat­ eral spinal tract, which connects the basal spinal nucleus with the thalamic nuclei and has therefore traditionally been called the 'spinothalamic tract' . Most of the fibres in this tract, however, do not directly ascend to the thalamus without interruption, but instead synapse with neurones in the brainstem recticular system, while others re-enter the spinal grey matter to synapse with internuncial neu­ rones.16 However, the majority of the ascending nocicep­ tive inputs terminate (sometimes after crossing several synapses) in the thalamic nuclear relay sites.171t should be emphasized that not only do the neurones in the thalamic

C H APTER ONE - PAIN 5

centres respond to peripheral noxious stimulation but they can also be activated by mechanoreceptor peripheral stimulation (see Pain modulation systems below). The axons of the thalamic nuclei then ascend to the neurones of the cerebral cortex. Three thalamocortical projections can be defined: those responsible for percep­ tion; those related to the emotional experience; and those responsible for memory.18 The first project to the superior paracentral region of the cerebral cortex and seem to contribute to the so-called 'perceptual component' of pain - the patient's ability to per­ ceive whereabouts (in which segment of his body) the pain is 10calized.1 9 The activation of the second thalamocortical projection system, projections that pass from the medial and ante­ rior thalamic nuclei to the frontal lobes, evokes the emo­ tional disturbances related with pain.2o Thus, a stimulus 'hurts' only when the nociceptive afferent projections arrive at the frontal cortex. A third thalamocortical projection system links some of the medial thalamic nuclei to the cortex of the ipsilat­ eral temporal lobe. Here the recent and long-term memory storage systems of the brain are 10cated.21,22 A fourth projection system exists which relates some thalamic nuclei to subjacent hypothalamic nuclei in the ventral diencephalon. It is very probable that this thalamohypothalamic system provides the means whereby nociceptive afferent activity entering the brain evokes the complex of visceral reflex (cardiovascular and gastrointestinal) effects and hormonal changes that are so often associated with the experience of pain.23 In conclusion, activity of nociceptive receptors distrib­ utes pain into four different projecting systems in the brain, each contributing to a specific component of the global experience 'pain'. However, the projection of pain from a peripheral receptor to the brain is not via a straight-line system. The intensity of pain is not only determined by the intensity of peripheral stimulation but also depends largely on peripheral and central modula­ tion systems at the various synaptic stages in the course of the afferent pathway within the central nervous system. These modulation systems account for the large variation in the intensity of pain experienced. Patients with apparently comparable pathological lesions undergo widely different degrees of suffering; even in an individual patient, the intensity of experience of pain varies widely with the prevailing emotional mood, with concentration on the problem or with suggestions from others.

PAIN MODULATION SYSTEMS There are both peripheral and central pain modulation systems.

Peripheral modulation of pain

One of the most important sites at which a synaptic mod­ ulation operates from both the peripheral and central sources is at the synapses in the basal spinal nucleus. In 1 965, Melzack and Wall,24 basing their theory mainly on the work of Noordenbos,25 published an article entitled: 'Pain mechanism: a new theory' . They called their concept of peripheral pain modulation the gate control theory (Fig. 1 .2), which is based on three premises: Afferent nerves contain two types of fibres: small fibres (P), as described above, and large-diameter afferents (M), which are derived from the various mechanoreceptors in the articular capsule, li gaments and muscle spindles. These fibres produce infonna­ tion about static joint position, pressure changes in the joints, joint movement and stresses that develop in the joint at the extremes of movement. The fibres of mechanoreceptor transmission have a lower stim­ ulation threshold and a faster conduction velocity than the smaller and mostly unmyelinated fibres of the nociceptive system. In the substantia gelatinosa (SG) of the dorsal horn, both afferent systems converge and interrelate, with the overall effect that the large-diameter afferents have an inhibitory effect on the re lay neurones located in the basal spinal nucleus. This inhibition is presynaptic and i s reduced only when there is a massive input from the small nociceptive afferent fibres. The latter thus facilitates central transmission of pain. The interaction between both systems is gate control: impulses travelling along the l arger fibres close the gate, and those in the small fibres open the gate so that impulses to th alamus and cortex can pass through.

•

•

M

�

------------------

DM

I---�I+

� \

----------

TR

p_---L-----J1 Gate control theory (after Melzack and WaI124): P, small nociceptive fibres (pain); M, large mechanoreceptive fibres; TR, transmission cells (relay neurones in the basal spinal nucleus); DM, descending modulation; SG, substantia gelatinosa; +, excitatory effect; -, inhibitory effect. Figure 1.2

6 SECTION ONE - GENERAL PRINCIPLES

•

The activity of the gate is not only modulated by impulses from nociceptive and mechanoreceptor systems but also receives a descending and regulating feedback from the reticular system, the thalamus and the cerebral cortex.

This peripheral modulation of pain has considerable clinical importance. It indicates that centripetal projection into the central nervous system of afferent activity from the nociceptive receptor systems is not passed straight to any 'pain centre' in the brain but receives constant mod­ ulation at its synaptic portal of entry into the neural axis at the level of the basal spinal nucleus. The modulation stems from the concurrent activity of the mechanorecep­ tors located in the same tissues, and from feedback through projection systems descending from the brain­ stem and cerebral cortex. This effect is one of the reasons why movement and selective stimulation of mechano­ receptors can cause inhibition of pain. Central modulation of pain

Awareness of pain is also modulated at the central pro­ jection systems. A modulation system at the reticular formation in the brainstern exerts a continuous inhibitory effect on the projection neurones in the spinal nucleus ganglion via the reticulospinal tract, which i s discharging continuously at varying frequencies throughout life.26 The inhibitory effect on nociceptive afferent transmission is augmented when the attention of the patient is distracted from the site of pain. This is what occurs when another painful site elsewhere in the body is stimulated (counter-irritation), when the patient concentrates on work or other activities or when hypno­ sis is induced.27 The inhibitory effect of this reticular system also increases when the blood concentration of catecholamines is very high, as can be the case in states of great emotional tension.28 Also some drugs (chlor­ promazine, diazepam and morphine) may selectively increase the activity of the reticular neurones that operate this inhibitory system.29 Inhibitory reticular activity is depressed and pain is enhanced when attention is concentrated on the painful site, or following the administration of barbiturates, caffeine or theophylline.3D At the reticular formation.

The cerebral cortex, especially the sectors located in the frontal and paracentral regions, in turn regulates the activity of the reticular formation. Reticular activity is increased, and perception of pain thus inhibi ted during rest and sleep and after the inges­ tion of alcohol. Conversely, depression of reticular activ­ ity is seen during increasing cortical activity, for example with anxiety, uncertainty and fear.

REFERRED PAIN

INTRODUCTION When the skin is pricked with a pin, the patient can exactly pinpoint the injury. This ability to localize the pain is limited to skin and does not apply when the source of the pain is in deep tissue. Deep somatic pain and visceral pain are often felt far from their point of source. In consequence, the examiner needs to know the patterns of pain reference so as not to be misled about where to search for the seat of the trouble. Diagnosis of orthopaedic lesions often rests entirely on history and clinical examination and is therefore almost impossible if the rules and conditions relevant to referred pain are not clearly understood . Those who originally studied pain reference soon noted that although it appeared erroneous and anarchic, some rules of presentation did exist. For instance, pain from specific structures is always referred to the same parts of the body: colic from a ureteral stone to groin and testicle, diaphragmatic disorders typically to the shoul­ der, angina pectoris to one or both arms, and the pain caused by arthritis of a hip very often to the ipsilateral knee. Also pain is, in the main, referred distally and its localization depends in a certain way on the severity of the lesion. In 1 905, Sir Henry Head described referred pain in the abdominal wall caused by a visceral disease.31 Using the dermatological appearances in herpes zoster, he con­ structed schemes of segmental innervation of the skin.32 He also described dermatomic zones that became painful in the event of provocation of a related visceral structure. His theory of pain reference was built on the concept of the segmental organization of the human body and its nociceptive system. Further experiments in this sphere were conducted by Sir Thomas Lewis in 1 936.33 In 1 938 and 1 939, Kellgren published the results of a systematic examination of the phenomena of referred pain, demonstrating segmental radiation and failure to cross the midline.34,35 His experiments were confirmed by others.36-38 Later, the concept of segmental reference of pain was refined39,4D and exact borders of the different derma tomes mapped OUt.41-44

The cerebral cortex.

POSSIBLE MECHANISMS The fact that referred pain is an error in perception was first pointed out by John Hunter in 1835 {ci ted by Cyriax).45 It was obvious that if pain is felt elsewhere than at i ts true site, the nociceptive mechanism is react­ ing inappropriately. However, since there seems to be

C H A PTER ONE - PAIN 7

logical consistency in the way the errors are made (pain from specific lesions is al ways referred to the same areas), there must also be a logical explanation for 'fail­ ures'. (If a machine always makes the same mistake, a structural or functional disorder must exist . ) The basis for the inadequacy must therefore be sought in a mis­ calculation in the pain mechanism. Theoretically, the defect can lie anywhere along the afferent pathway, from the peripheral receptors to the synapses in the spinal cord and the reti cular area and projection zones in the sensory cortex. During the last century, numerous investigators have studied referred pain. Two main hypotheses have been put forward: •

Error at the level of the spinal cord. Most authors have opted for this hypotheSiS. Mackenzie described an 'irritable focus' in the grey matter of the spinal cord as being responsible for the phenomenon.46 Also Livingston47 placed the basis of the error at synapses in the dorsal horns. Wedell et a148,49 and Pomeranz50 accepted a double origin for the sensitive neurone­ afferent fibres of a somatic structure, and those coming from a related visceral structure synapse with the same spinal ganglion. Taylor et al51 and Wells et al52 also made a plea for the spinal explanation of referred pain. Their view is that separate peripheral sensory nerves (deep somatic, skin and visceral) converge on to the same cell in the dorsal horn of the spinal cord (Fig. 1.3).

•

Failure at the sensonj cortex. A number of authors have proposed that the misinterpretation is at the projection area of the sensory cortex rather than at the spinal leveP3,53,54 The concept was clinically elaborated by Cyriax who based his theory on a number of premises:

• • • • •

Referred pain is a pain experience felt elsewhere than at its true site of origin. Skin is an organ adapted to localize the pain accurately. Pain is experienced in the sensory cortex, which is organized dermatome by dermatome. The skin is represented accurately in the sensory cortex. A memory storage system is located in the sensory cortex. This is fed by constant input from the skin. Input from deeper somatic structures is very rare in a normal and healthy individual.

As pointed out previously, pain is experienced at three different locations in the cerebral cortex. Perception - of the site of pain - is located in the superior paracentral cortex. The frontal lobes evoke the emotional disturbances related to pain, and the memory store is in the temporal lobes. The ability to localize pain in the region of injury is limited to skin and does not apply when the source of the pain is in deep tissue. In due course, a certain pain memory is built up in the temporal lobes, and achieves a high degree of anatomical precision. The efficacy of the long-term memory storage system is not simply a func­ tion of the intensity of the painful experience but also relates to the length of time a painful experience lasts or to the frequency with which it is repeated.55,56 Since the frequency of painful stimuli coming from the skin is much higher than the frequency of stimuli coming from deeper structures, it will be obvious that pain memory will centre around painful experiences from the skin . When the same cortical cells receive a painful message arriving from a deep-seated structu re, the memory will interpret it on the basis of past experience; in that the sensory cortex is arranged segmentally, the pain will be ascribed to the correct segment but the system will fail to

..

Superficial somatic pain

Deep somatic pain Sympathetic ganglion

/--- Sympathetic nerve

Figure 1.3 Separate peripheral sensory nerves converge onto the same cell in the dorsal horn of the spinal cord.

8 SECTI ON ONE - GENERAL PRINCIPLES

localize it accurately at the site of the lesion. The brain therefore 'places' it in the tissue it has a reference for - the skin. Pain is thus felt under the surface area connected with the particular cells that belong to the same segment as the tissue from which the nociceptive afferents originate. The pain is felt deep to the skin of the relevant dermatome and not accurately in the skin.

CLINICAL CONSEQUENCES The concept of referred pain is extremely important to the orthopaedic physician, who has to deal daily with the problem. If the principles of erroneous localization by the cortex are clearly understood, the examiner can turn a misleading phenomenon to diagnostic advantage. In the Cyriax concept, referred pain obeys certain rules. The inadequacy in the sensory cortex is structural and there­ fore can easily be accommodated. To a certain degree, referred pain can be compared with the refraction of light when it falls on a water surface. The observer does not see objects under the water surface at their exact localiza­ tion. Howevel� since the error of perception is structural and obeys particu lar physical rules and laws, it is easy to correct what is seen (provided the observer knows the correction formula) and so locate the object accurately. The same applies to referred pain. The examiner must constantly ask if the localization of the pain is also the exact localization of the disorder and, if the answer is negative, what corrections must be made to arrive at the exact localization. Before this discussion of referred pain is continued, it should be stressed that root pain reference does not nec­ essarily mean that a nerve is involved. The false idea that wide radiation of pain is evidence of involvement of nerves is still strongly held by some and is usually the most important obstacle to a logical understanding of referred pain. To approach the problem of referred pain with an open mind, the reader must constantly remember that referred pain is an error of perception. Although the nerve supply to these peripheral structures is distributed on a segmental basis, it does not indicate that referred pain 'runs down' a somatic nerve. For instance, pain at the anterior aspect of the leg does not necessarily mean that a nerve structure (L3, femoral nerve or peripheral branches of the femoral nerve) is involved. Although inflammation of the dural sleeve of the L3 nerve root does of course lead to pain extending in the L3 dermatome, the same pain can be provoked by a lesion in any other tissue belonging to the L3 segment (e.g. hip joint or psoas bursa). There will not be any difference in the nature and extent of the pain. The only distinction between pain as the result of a com­ pressed and inflamed nerve root and pain originating from trau ma to other structures is the appearance of paraesthesia (see Pressure on nerves, Ch. 2).

RULES OF REFERRED PAIN (BOX 1.1) The first rule - reference of pain within the orders of the skin area that belongs to the same segment as the tissue lesion that causes pain - follows directly from the premise that the nociceptive mechanism is organized on a segmental basis. Nociceptors, afferent fibres and sensory cortex are all arranged segmentally. Afferents from skin, deep somatic structures and visceral organs from the same segment relay on the same dorsal neu­ rones and project to the same area in the sensory cortex. Pain reference is therefore confined to, and remains within, the borders of the cutaneous area (or dermatome) that belongs embryologically to the same segment as the tissue from which the pain is arising. To understand the segmental organization of the nociceptive mechanism, it is necessary to reconsider embryogenesis (Fig. 1 .4). Embryogenesis Primitive body. When a fetus is between 4 and 6 weeks old, 42 pairs of somites develop: 4 occipital, 8 cervical, 12 tho­ racic, 4-6 lumbar, 5 sacral and 8-10 coccygeal,57 The first two and the last seven or eight pairs disappear early in development. The ventral aspect of each somite differenti­ ates into the sclerotome which, together with the chorda around the neural tube, forms the origin of the axial skele­ ton. The other part of the somite becomes the myotome, covered by the dermatome. Each pair of somites develops its own segmental innervation which later leads to the development of the spinal ganglion and spinal nerve. In due course, the dermatome differentiates into skin and subcutaneous tissue, the myotome into muscles, tendons, ligaments, capsules and bursae, and the sclero­ tome into bone and fibrous septa. Although the original form of most segments is modified as the limbs are formed, their segmental innervation remains constant throughout life. The projection area in the cerebral cortex also remains segmentally organized.

Limb formation. After the first month of intra-uterine life,

two pairs of buds originate at the lateral sides of the fetus. The proximal papules appear first at the base of the neck, followed by the formation of two distal buds in the caudal Box 1.1 Rules of referred pain -

• The p a in rad i ates segmenta l ly and does not cross the m i d l ine • The pain is usua l ly felt deeply • The pain is referred d ista l ly w ithin the dermatome • The pain does not necessarily cover the a rea of the causative lesion • The pain is felt anywhere in the dermatome but not necessa rily in the whole dermatome

C H A PTER ONE - PAIN 9

10

_--'-"'-11 2

Figure 1.4 Embryogenesis: 1, neural tube; 2, aorta; 3, intestine; 4, myotome; 5, dermatome; 6, primitive spinal ganglion and spinal nerves; 7, myoseptum between the segments; 8, horizontal septum; 9, frontal knob; 1 0, maxillar knob; 11, cranial limb bud; 1 2, caudal limb bud; 13, umbilical cord; I-IV, gill arches.

area. These extensions gradually project from the cylindri­ cal fetal segments from which they originate. As the limbs grow further and further laterally, some dermatomes become totally disconnected from the trunk (Fig. 1 .5). For the upper limb, the dermatomes C5, C6, C7, C8 and T1 leave the trunk completely to form the covering of the arm. T2, although also present at the inner aspect of the upper arm, connects with the trunk again, and borders with C4. In the lower limb, parts of L2, L3 and the whole der­ matomes L4-L5 and Sl withdraw from the trunk to form

the lower limb. S2 is present partly in the limb and partly in the buttock, where it borders with L3. During limb formation, some muscles undergo cen­ tripetal migration and others centrifugal. As a rule, however, dermatomes distally project further than myotomes, and sometimes a muscle becomes completely dissociated from the covering dermatome. An example of dermatome migration is the C5 segment in the upper limb: the myotome does not extend beyond the elbow, but the fifth cervical dermatome descends to the radial styloid. An example of centrifugal dissociation between a

Figure 1.5 Limb formation. As the limbs grow further and further laterally, some dermatomes become anatomically disconnected from the trunk.

10 SECTION ONE - GENERAL PRINCIPLES

muscle and its relevant dermatome is the diaphragm, which has a C4 origin: the C4 dermatome ends at the scapular spine and under the clavicle, and is therefore completely separated from the thoracic localization of the muscle. Another instance of muscle migration is the latis­ simus dorsi muscle (C7-C8) which shifts its origin to the iliac crest. The dermatomes of the seventh and eighth cervical segment, however, do not occupy the trunk, so dissociating the muscle almost completely from its corresponding derma tomes. Because of these muscle migrations, with overlaps and discontinuous areas it is very difficult to draw accu rate maps of the myotomes. However, in the appropriate chapters of this book, we will indicate to which segment each of the structures under discussion belongs.

DERMATOMES The cutaneous area suppl ied by one spinal nerve is a dermatome. The first clinicians to draw dermatomic maps were Head and CampbelJ.58 Their diagrams are the basis for the classical drawings in standard neuro­ logical textbooks. However, they did not take into consideration the significant degree of variability and overlap in derma tonic borders.57,58 Later investigators such as Keegan and Garrett and Fukui et ai59,60 have demonstra ted that derma tomes of adj acent spinal nerves overlap m arkedly. An example of this is pain at the anterior aspect of the thigh, which can be of second or third lumbar origin. The second lumbar dermatome spreads from the groin, down the front of the thigh, to the patella. Pain of third lumbar origin again spreads along the anterior aspect of the thigh and the patella but it can continue down the anterior aspect of the leg, to just above the ankle. Pain at the ante­ rior aspect of the thigh therefore can be of second or third lumbar origin but if it spreads further down below the patella then its origin is third lumbar. Another example of overlap between derma tomes is referred pain in the hand and fingers: C6 pain refers to the dorsal aspect of the hand, the thumb and the index finger, whereas C7 refers also to the dorsum of the hand and the index finger, as well as to the long and ring fingers. In a patient complaining of pain at the back of the forearm or at the dorsum of the hand and the index finger, it is difficult to decide whether the pain is of sixth or seventh cervical origin. We use the charts drawn by Foerster41 in 1933 and cor­ rected by Cyriax in 1982,45 in order to give the broadest possible information about the area to which pain from a particular segment may refer. The extreme importance of accurate localization of pain in orthopaedic medicine requires the physician to use a map of derma tomes that is as close as possible to clinical reality. The figures showing

the derma tomes are based on Foerster,41 Cole et ai,65 Cyriax,45 Conesa,66, Wakasugi,67 and Mitta.68 Cervical and thoracic dermatomes

Cl to C4 occupy the scalp (Cl ), the back of the neck and the temporal area, the upper half of the ear and the upper half of the face (C2), the neck, lower mandibular area and chin (C3), and the lower half of the neck, shoulder area, front of the upper chest and the area above the spina scapulae (C4) (Fig. 1.6). C5 to T2 are projected from the trunk to form the covering of the upper limb (Figs 1.7 and 1.8). C5 covers the deltoid area and the outer aspect of the arm up to the base of the thumb. C6 is the anterolateral aspect of the arm, the thenar eminence, thumb, dorsum of hand and index finger. C7 comprises the back of the arm and hand, together wi th index, long and ring fingers. C8 is the inner aspect of the forearms, the hypothenar area and palm, together with the three ulnar fingers. Tl includes the inner aspect of the forearm as far as the hypothenar eminence. T2 is Y-shaped and overlies the inner aspect of the upper arm and the axilla, where it divides into an ante­ rior and a posterior component. This latter part of the dermatome borders with the inferior aspect of the C4 dermatome. If the upper limb is held outstretched horizontally with the thumb pointing upwards, the original position of the embryological bud is recreated, and one can reconstruct the way the dermatomes project from the trunk. This is a good way to memorize the position of the separate dermatomes in the upper limb (see Fig. 1.9). From T3 to T12, the derma tomes encircle the trunk, more or less following the original segmental construc­ tion of the embryo (Fig. 1.10). T3 constitutes the axilla and a patch on the front of the chest. T4 encircles the trunk at the level of the nipple. T7 reaches the lower costal margin and covers the xiphOid process. TlO is level with the umbilicus, and Tl2 reaches to the groin, and probably also the area between the femoral trochanter and iliac crest. Lumbar and sacral dermatomes

L1 is also more or less circular (Fig. 1.11). It comprises the lumbar region from the second to the fourth lumbar vertebra, and runs along the upper aspect of the buttock and the iliac crest to the lower abdomen and the groin. L2 and L3 are two discontinuous areas, one in the lower lumbar region and upper buttock, and one in the leg (Fig. 1.12). The areas in the buttock largely overlap. Also, in the leg, there is considerable overlap between L2

CHAPTER ONE - PAIN 11

Figure 1.6

C1 to C4 dermatomes.

and L3: L2 involves the whole front of the thigh, from the groin to the patella. L3 also takes in the anterior aspect of the thigh, but spreads further down, as far as the anterior and medial aspects of the ankle. L4, L5 and SI are completely disconnected from the trunk, overlying the surface of the leg and foot (Figs 1 .1 3 and 1 . 14).68 In consequence, the third lumbar dermatome lies adjacent to the upper border of the second sacral dermatome at the lower buttock. L4 occupies the lateral aspect of the thigh, crosses the leg above the ankle, and ends at the medial malleolus, the inner border of the foot and the big toe. L5 consists of the outer aspect of the leg and crosses the ankle above the lateral malleolus, to end on the dorsum of the foot. L5 also comprises the big, second and third toes, and the inner half of the sole. SI includes the calf, the heel, the lateral malleolus and foot, the two outer toes and the whole sole of the foot (Fig. 1 . 15). Sicard and Leca69 demonstrated that the fifth lumbar and first sacral dermatomes also comprise a small vertical band at the posterior aspect of the thigh, which could account for the thigh pain commonly described by patients suffering from L5 or SI sciatica.

S2 is large and comprises the plantar aspect of the heel, the calf, the back of the whole thigh and the lower buttock. In the buttock, it borders with the lumbar part of L3. S3 is a narrow zone at the inner side of the thigh, where it borders with L2 anteriorly and S2 posteriorly (Fig. 1 . 16). The tip ends just proximal to the knee. The upper extent reaches the inguinal ligament where it adjoins the 12th thoracic and first and second lumbar der­ matomes. It follows that the groin is a confluence of der­ rnatomes, and pain, apart from that of local origin, may be referred from a 1 2th thoracic, a first or second lumbar, or a third sacral origin. The groin is also a common site for extrasegmental dural pain reference. S4 comprises the saddle area, anus, perineum, and scrotum and penis or labia and vagina. S5 is the coccyx. As in the upper limb, the original position of the distal embryological bud can be reconstructed by abducting the thigh to 90°, and by lateral rotation until the big toe points upwards. This position demonstrates the way the dermatomes were projected from the trunk and also constitutes a good way of memorizing the position of the various dermatomes in the lower limb (Fig. 1 . 17).

12 SECTION ONE - GENERAL PRINCIPLES

C5

C8

C7

Figure 1.7

C5 to C8 dermatomes.

T2

T1

�_. _---

Figure 1.B

�\0

T1 and T2 dermatomes.

Proximally to distally and then turning proximally again, the following are encountered: L2 at the anterior thigh, L3 at thigh and leg, L4 at the lateral aspect of the leg, anterior aspect of ankle and inner border of foot up to the big toe, L5 at the dorsum of the foot and the three inner toes, Sl at the lateral aspect of the foot, outer malle­ olus and calf, S2 at the posterior aspect of the leg; turning back to the trunk in the gluteal area, the boundary zone

Figure 1.9

Outstretched arm with arrows showing the dermatomes.

14 SECTION ONE - GENERAL PRINCIPLES

L4

Figure 1.13

L5

L4 and L5 dermalomes.

(a )

L4

L5

81

81

(b)

Figure 1.14

L5

81

Dermalomes of Ihe fool, (a) dorsum (b) sole.

82

82

Figure 1.15

81 and 82 dermatomes.

CHAPTER ONE - PAIN 15

84

83

in the perineum, between leg and trunk is comprised of S3 and S4.

DISCREPANCIES BETWEEN DERMATOMES AND MYOTOMES We have mentioned already that, as the outcome of embryological development, dermatomes do not always precisely cover the underlying myotomes. Cyriax described eight areas in the human body where the skin and the structure it covers have completely different embryological derivations (Cyriax45). These are the head, scapular and pectoral region, hand, intrathoracic and intra-abdominal region, buttock and scrotum.

83-85

Head. The skull, head and face are derived from the two remaining occipital somites, originally situated at the back of the neck. During development, a pair of frontal knobs and two mandibular arches form and fold for­ wards to create the skeleton and soft tissues around the buccal cavity. The skin of the head and face, however, are formed from the upper two cervical segments.

The growth of the protuberances that are to become the upper limbs draws some segments out from the cylindrical cervical and thoraric structures. At the same time, the scapula and its muscles, together with latissimus dorsi (C5-C7) move centripetally between the skin of the thorax (Circularly arranged thoraric der­ matomes) and the underlying ribs and intercostal muscles (circularly arranged thoraric sclerotomes and myotomes). Therefore, pain in the scapular area can have both scapular (cervical ) and thoracic pain. Scapular region.

Figure 1.16

83 to 85 dermatomes.

Pectoral region. During the growth of the upper limb bud, the same phenomenon as occurs in the scapular region takes place at the pectoral region. The pectoral muscles, derived from cervical segments (C6-C7) move centripetally between the thoracic dermatomes and their myotomes.

The thenar muscles form part of the eight cer­ vical and first thoracic myotomes, but the skin is formed from the fifth and sixth cervical dermatomes. The interosseus muscles are C8 and TI, but the skin of the dorsum of the hand, except at the ulnar border which is also C8, is derived from the C6 and C7 segments.

The hand.

Figure 1.17

Outstretched and rotated leg, with arrows showing the dermatomes.

Intrathoracic region. It is obvious that there are numer­ ous discrepancies in origin between the thoracic cage and its content. The diaphragm, for instance, is derived from the third and fourth cervical segments and thereafter descends. Hence a lesion of the diaphragm may cause pain felt in the neck and at the upper scapular and pec­ toral region, even though it lies at the lower thoracic level. The heart is derived from C8 to T4. Therefore

16 SECTION ONE - GENERAL PRINCI PLES

myocardial pain may radiate to the chest, the shoulder and the inner aspect of the arm, as far as the ulnar border of the hand. It is presumed that a small part of the myocardium, probably the auricles, has a third cervical origin, which could explain the well-known clinical fact that the pain of angina often radiates to the neck anteri­ orly. The oesophagus is T4-T6 and the lungs have a T2-T5 origin. The abdominal wall has a more or less circular construction, from T7 at the xiphoid process, over TIO at the umbilicus, to LI at the iliac crest, inguinal ligament and groin. In the abdominal wall, the dermatomes exactly overlie the myotomes. Most of the intra-abdominal content also has a mid- and lower thoracic origin. The embryological derivation of the stomach and duodenum (T6-TIO), liver (T7-T9 right), gall bladder (T6-TIO right),7° pancreas (T7-TS) and small intes­ tine (T9-TIO), fit very well with their actual localization in the abdominal cavity, and therefore pain derived from these organs approximates with their surface representa­ tion. Structures of lower thoracic, lumbar or even sacral origin, however, show a more complicated pattern of referred pain. The kidney and ureter, for instance, have a TII-LI derivation and, although they are localized high up in the abdomen, referred pain can reach the inguinal fossa and the groin (TI2-LI ). The colonic flexure is from L2 to L3, which allows the pain not only to radiate to the lower back but also to the front of the thigh. The sigmoid colon and rectum have 53-55 origin. Hence, in diseases of the sigmoid and the rectum, pain can be felt in the iliac fossa, perineum, penis, vulva and inner aspect of the thigh.

L1 --t--f---WL

L2 L3

82

Intra-abdominal region.

The buttock. The skin of the lower lumbar area and the outer buttock is derived from LI . At the upper buttock, there is considerable overlap with the lumbar patches of the L2 and L3 segments (Fig. LIS). The skin of the lower buttock is derived from 52. The gluteal muscles forming the buttocks are derived from the fourth lu mbar to the first sacral segments. Consequently, the dermatomes descend further distally than the myotomes they cover. Scrotum. The testicles are derived from Tll-TI2 and LI . The epididymis has a TIO origin. The scrotum, however, belongs to the 54 dermatome. A trauma to the testicle therefore may cause not only local pain but also pain spreading along the iliac crest posteriorly and up to the lower thoracic region. Testicular disease frequently pro­ duces pain in one or the other iliac fossa.

REFERRED PAIN IN VISCERAL DISEASES It is important to emphasize that referred pain is not a phenomenon of orthopaedic medicine only. As described

Figure 1.1 B

Overlap of the dermatomes at the back and the buttock.

earlier, many visceral diseases also cause referred pain. For the convenience of practitioners often faced with tho­ racic or abdominal pain, a list of the segmental deriva­ tions of the viscera, based on the work of Cyriax45 (see his p. 30), William and Warwick71, Lindsay et a[72 and Guyton (cited by Van Cranenburgh73 is given in Box 1 .2).

REFERRED PAIN IS FELT DEEPLY AND DISTALLY IN THE DERMATOME An important difference between local pain and referred pain is that in the l atter the pain is felt deeply and

Box 1.2 Referred pain in visceral diseases -

Hea rt ( a uric l es?) Lungs Oesophagus D i a phragm Stomach a nd duode n u m Liver a n d g a l l b l adder S p l een Pancreas Sma l l intestine Appendix

C8-T4 (C3?) T2-TS T4-T6 C3-C4 T6-T10 T7-T9 right T7-T10 left .

Ureter S u pr a ren a l g l a nds

T8 T9-T10 T10-L1 nO-T12 (L1) n1-T12 n1-L1

Kidney

Ovary a nd testis

n1-T12 (L 1)

Epididymis

no

C o lon:

nO-L 1 L2-L3

Rectu m

ascending flexure s i g moid

53-55 53-55

CHAPTER ONE - PAIN 1 7

vaguely. The patient thus does not point to a localized and precise area, but outlines an approximate one and tends to describe it as 'deep' . That pain - with some exceptions - is always referred distally remains a purely empirical clinical observation and has hitherto not been explained on neurophysiolog­ ical grounds. The fact that pain that arises from the proximal part of a segment can be felt distally in the der­ matome but a distal lesion is not referred proximally within this same segment, remains an inconsistency that is hard to rationalize. However, this clinical observation is very important to the clinician confronted with referred pain, for the lesion must never be sought in a structure that is localized distally of the painful area. Pain at the distal aspect of the L3 dermatome (knee and lower limb ) can have a proximal origin (spine, hip), but pain only in the hip or the groin, cannot be caused by a lesion at the knee or the thigh.

SEGMENTALLY REFERRED PAIN DOES NOT CROSS THE MIDLINE The segments in the body are arranged in pairs, each of which has its own segmental innervation and its own projection area in the cerebrum. Hence it is obvious that the cerebral cortex will easily d ifferentiate between a left-side or a right-side pain, and no one will question that a CS pain on the left-side has a left-side origin and vice versa. The fact that pain, stemming from a uni­ lateral structure does not cross the midline becomes important in the interpretation of more or less centrally localized pain, for instance in aches in the neck or back. It is evident that a lesion of a unilateral facet j oint will not cause pain radiating all over the lower back. Only centrally localized structures (vertebral body, longitu di­ nal ligaments, intra- and supraspinal ligaments and dura mater) can theoretically be responsible for a bilat­ erally radiating pain at both sides of the midline. A pain felt centrally or bilaterally must originate from a central structure, or from two bilateral structures (two facet joints or two sacroiliac joints) but it can never be the result of a lesion in a unilateral structure.

DURA MATER AN 'EXCEPTION' TO SEGMENTAL REFERENCE Pain originating from the dura mater has a rather pecu­ liar behaviour. First, in that the dura is a midline struc­ ture, it is innervated from both sides, so that pain refers bilaterally. Second, pain stemming from the dura has a very broad reference and seems to cover several consecu­ tive derma tomes. For instance, pressure of a lumbar disc on the dura at the LS level can cause pain in the back which radiates to the abdomen and groins, down to the

anterior and posterior aspect of both thighs and legs, and upwards to the back of the lower chest. This type of pain reference is inexplicable in terms of segments. We there­ fore call it 'extrasegmental reference' of pain. Because in orthopaedic medicine, the dura is the exclusive source of this type of pain radiation, it is also called dural reference. Pain of this nature can be very difficult to interpret if it is felt in a part or in parts of the possible reference area. As in purely segmental reference, dural reference can be to only a part of the respective derma tomes. Thus, instead of the broad radiation to the whole back, both glutei and both legs, dural pain sometimes only affects a small part, for instance one groin, or one buttock or the whole poste­ rior aspect of the thigh. The differential diagnosis from a more segmental pain, for instance as the result of a nerve root compression, is then difficult. A common clinical finding in a cervical disc protrusion that impacts on the dura is unilateral interscapular pain or pain in the trapezius or in the pectoral area. In the latter instance, suspicion of angina pectoris may then easily arise. Also the removal of an appendix for dural pain of lumbar origin referred extrasegmentally into the iliac fossa and groin is not at all exceptional. A possible explanation for the misleading pain refer­ ence of the dura may lie in its multisegmental origin, which is reflected in the great overlap between the fibres of the consecutive sinuvertebral nerves innervating its anterior aspect. 74-77 More recent researchers describe division of the nerves into ascending and descending branches which ramify variously, to give off longitudi­ nally and transversely orientated branches.?8,79 In a recent study that used the very sensitive acetyl­ cholinesterase method, more ramifications between the nerve branches were demonstrated (Fig. 1 . 1 9).80 Ascending branches up to four segments cranial to the level of entry into the dural nerve plexus and also descending branches extending up to four segments caudally were observed. In addition, many vertical and horizontal i nterconnections between the various ascending and descending branches were seen. The con­ clusion is that dural nerves may spread over eight seg­ ments and that a great overlap exists between adjacent and contralateral dural nerves. These findings may form an anatomical explanation for the clinical observations of Cyriax on the limits of extrasegmental reference of dural pain.81 Upwards, pain originating in the lower cervical part of the dura may spread to the occiput, skull and forehead (Fig. 1 .20). Downwards it can descend to T7 which corresponds with the lower angles of the scapulae. Anteriorly the pain can occupy the whole pectoral area. Extrasegmental pain does not extend beyond the upper half of the arms. A middle thoracic disc lesion can cause dural extraseg­ mental pain that may radiate to the base of the neck, and

18 SECTION ONE - GENERAL PRINCIPLES

Figure 1.20

Limits of dural multisegmental pain of cervical origin.

downwards to the whole abdomen and to the upper lumbar region (Fig. 1 .2 1 ). Dural extrasegmental reference from a low lumbar level may reach the lower thorax posteriorly, the lower abdomen deep to the umbilicus, the groins, the buttocks, and the sacrum and coccyx (Fig. 1 .22). Unlike the cervical dura - which does not radiate far into the arms extrasegmental reference from a lumbar origin may also involve the legs, both the anterior and the posterior aspects, and descend to the ankles.

REFERRED TENDERNESS

Figure 1.19 Montage of photographs showing the nerve plexus of the lumbosacral PLL (L 1 to S4). Dorsal view after complete laminectomy and after removal of the spinal cord and the ventral dura. cut pedicle of a ventral arch; cv, vertebral body; di, intervertebral disc; drg, spinal ganglion; rval, ventral ramus of the spinal branch of the lumbar artery; arrows, sinuvertebral nerves entering the vertebral canal; open arrows, crossing sinuvertebral nerves. Reproduced with permission from Groen GJ. Nerves and nerve plexuses of the human vertebral column. Am J Anal 1 990; 188: 282-296.

There seems to be more to referred pain than just mislo­ cation by the patient. Within or near the area of referred pain, it is often possible to find small trigger points which are exquisitely sensitive. Pressure on one of these imme­ diately produces a deep and radiating tenderness which is i dentified by most patients as the source of their symp­ toms. Classical localizations of these tender spots are:

*,

• •

In cervical dural compression, the upper border of the trapezius, the scapular muscles or the base of the neck. In lower lumbar dural involvement, the sacroiliac region and the upper part of the buttocks.

C HAPTER ONE - PAIN 1 9

Figure 1.21

Limits of dural multi segmental pain of thoracic origin.

If the tender area is palpated without the prior conduct of a proper functional examination of the neck or lumbar spine, the tenderness is regarded as the primary lesion, the more so because the patient insists that it is the appar­ ent origin of the pain. It is no wonder then that 'fibrosi­ tis', 'myofibrositis' or 'myofascial pain' syndromes have long been regarded as primary lesions. The 'fibrositis' concept has been used to explain the cause of lumbago.82 Lewis33 was the first to recognize that trigger points and myalgic spots were not primary lesions and that the painful area, although tender to the touch, did not contain a focus. Cyriax considered that the localized tender area is a secondary effect of pressure on the dura mater.83,84 He derived his theory from the simple clinical observation that the tender spot shifted from place to place over a few seconds after a successful manipulation and that, when a full and painless range of motion had been restored, the tenderness disappeared. However, referred tenderness has also been demon­ strated in muscular and fibrous tissue lesions,85 in visceral lesions such as ischaemic heart attacks86 and in pathologi­ cal viscera. The phenomena are not completely understood

Figure 1.22

Limits of multisegmental pain of lumbar origin.

as yet but it is reasonable to assume that trigger points are caused by summation mechanisms which can be under­ stood in terms of gate-control mechanisms.83 Summation - the excitatory effect of converging inputs - is an important pain mechanism. Pain may be triggered by two sources of nerve impulses: a major one from the lesion; and a minor one from normal skin which add together. If one source is removed, it becomes more difficult for the other to trigger the feeling of pain.87

FACTORS DETERMINING REFERENCE OF PAIN Referred pain is a faulty perception of the origin of a pain. In orthopaedic medicine it is common to see marked differences in the extent of reference between segments, between distinct affected tissues and between different degrees of the same condition. The degree of reference - that is the distance between the localization of the perception and the site of the lesion - depends on four different factors (Box 1.3). Some can be explained on the basis of the known path­ ways, others remain unexplained and resul t purely from clinical observations.

20 SECTION ONE - GENERAL PRINCIP LES

Box 1.3 Factors favouring reference of pain Strength of the sti m u l us : • T h e stronger the sti m u l us, the m o r e reference o f p a i n Position o f the affected tissue: • The more central the lesion, the more reference of p a i n • The more d istal t h e lesion, t h e less reference o f p a i n Depth of the affected structure: • More reference from deep-seated structures • Less reference from s u perfi c i a l structures Nature of the affected tissue:

• Little reference: bone a n d periosteum • More reference: m uscle • M uch refe rence: capsu le, l i g a ment, b u rsa, tendon, d u ra, dural sleeve and peri n e u r i u m

localization of the lesion by the pain it provokes. As a rule, a lesion in the wrist or in the ankle does not give rise to diffuse pain and the patient usually knows quite well where the source is. Lesions in the hand or foot can there­ fore be precisely indicated. Also lesions in the elbow and knee give quite well-defined pain that does not radiate enough to confuse either the patient or the examiner. Lesions that involve the shoulder, the hip, the sacroiliac joints and the spine usually provoke extensive pain refer­ ence. The segments to which the shoulder, hip and sacroiliac joints belong (C5, L3 and 51-52) have the longest dermatomes of the body; as a consequence, pain can be referred a long way distally - calf pain in sacro­ iliac arthritis or knee pain in arthritis of the hip. The depth of the affected structure

The strength of the stimulus

The greater the stimulus, the more extensive the reference of pain. In other words, intense stimulation radiates the pain widely and slight irritation localizes the pain closer to its origin. This phenomenon is used in orthopaedic medicine to estimate the degree of irritation or to evaluate treat­ ment. A classical example is the C5 pain that results from shoulder arthritis. In this disorder there is a typical development of pain which gradually increases. At first, pain is felt only in the deltoid area, close to the shoulder. During the following months it gradually spreads to the arm, first above the elbow but later also to the forearm. At its worst, the pain can even be felt at the distal end of the radius and the base of the thumb. 1£ treatment is suc­ cessful or the condition regresses, the pain gradually leaves the forearm and moves upwards until it is only at the shoulder area. That the area of reference of pain becomes smaller indicates that the strength of the stim­ ulus is decreasing and inflammation improves. Serious sacroiliac arthritis can provoke pain in the whole of the 51 and 52 dermatomes, with pain at the back of the thigh and the leg, down to the heel and the sole. 1£ the condition improves, pain first leaves the heel and the calf. Further regression of the arthritis will probably result in localized pain in only the neighbourhood of the sacroi liac joint with some reference to the buttock. The mechanism of this phenomenon is probably based on the fact tha t the more the peripheral sensory nerve fibres are stimulated, the more is there cerebral cortical activity.88 The position of the affected structure

Pain seems to refer distally only; this being so, the closer to the midline the affected structure lies, the greater the possibility of extensive reference of pain. The further the lesion lies from the midline, the more accurate will be the

As early as 1 939, Kellgren35 and Lewis and Kellgren89 stated that the localizing ability of a structure depended largely on its depth from the surface. This was confirmed later by other studies.38,44 Pain originating from a superficial lesion is usually pinpointed correctly by the patient but deep lesions can cause wide reference. This follows immediately from the way referred pain originates. We have seen that referred pain is an error of perception and that pain memory is based upon the experience gathered by recurrent stimuli through the skin, which is adapted correctly to localize pain. It follows that the deeper structures lie from the skin, the less the chance that they will be stimulated by external factors. When internal (pathological ) factors activate the nociceptors in these deeply situated structures, the memory mechanism is inadequate and places the pain within the affected segment. The nature of the structure

There are many discrepancies in our knowledge of pain referral and further research is required to clarify why some structures give more pain reference than others. For example, pain originating in bone or periosteum, although usually located deeply, hardly radiates at all. This does not mean that bone pain cannot be very severe but it seldom gives extensive reference. This phenome­ non is of great value in clinical diagnosis. Serious but localized pain always points to the possibility of a lesion of the bone. For example, an intense but localized pain in the lumbar spine is typical of a bony lesion, such as frac­ ture, infection or new growth at a vertebra. Also intense, deep, but very localized pain in a limb draws attention to bone disease. Also, severe but localized pain at the shoul­ der, precisely felt at the true site, is always an indication of a bony l esion. Pain stemming from a lesion in a joint capsule, bursa, ligament or tendon is referred in an uncharacteristic way

CHAPTER ONE - PAIN 21

- the degree of pain reference is not determined by the kind of tissue involved. Pain originating in a muscle seems to cause less reference than pain stemming from the tendon or the tenoperiosteal insertion.

Intense pain reference can also result from pressure on the different parts of the peripheral nervous system. Depending on the localization of the compression, the ref­ erence will be segmental or extrasegmental (see earlier).

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f Psychosom Res 1978;22:25. 3. Merskey H. Pain terms: a list with definitions and notes on usage. Recommended by the IASP Subcommittee on Taxonomy.

Paill 1979;6:249. 4. Melzack R, Torgerson WS. A l/aesthesiologIj 1971 ;35:50.

On

the

language

of

pain.

5. Wyke BD. Neurological mechanisms in the experience of pain. Acupul/ct Electrother Res J 1979;4:27. 6. Ralston HI, Miller Ml� Kasahara M. Nerve endings in human fasciae, tendons, ligaments, periosteum and joint synovial membrane. AI/at Rec 1960;136:137. 7. Besson JM, Guilbaud G, Abdelmoumene M, Chaouch A . Physiologie d e la nociception. f Physiol (Paris) 1982;78:7-107. 8. Iggo A. The case for 'pain' receptors, In: Janzen R, Keidel WD, Herz A, Steichele C (eds) Pain: Basic Principles, Pharmacology,

Therapy. Thieme, Stuttgart, 1972:60. 9. Van Hees 10. 11. 12.

13.

I,

Gybels JM. Pain related to single afferent C fibres

from human skin. Brain Res 1 972;48:397. Sarkin LS, Wallace MS. Acute pain mechanisms. Surg Ciin North A/JI 1 999;79(2):213-229. Dray A. Inflam matory mediators of pain. Br J A naesth 1995;75: 125-131 . Reeh PW, Steen KH. Tissue acidosis in. nociception and pain. In: Kunasawa T, Kruger C, Ulisumara K (eds) Progress in Brain Research, vol 13. Elsevier Science, Amsterdam, 1996:143-1 5 1 . Wall PD, McMahon SB. Microneuronography a n d its relation to perceived sensation. Pain 1985;21:209.

14. Nathan PW. The gate-control theory of pain: a critical review. Brain 1976;99:123. 15. Price DD, Dubner R. Neurons that subserve the the sensory­ discriminative aspects of pain. Pain 1977;3:307. 16. Wyke BD. The neurology of low back pain. In: Jayson MIV (ed.) The Lumbar Spille al/d Back Pain, 2nd edn. Pitman Medical, Bath, 1980:265-339. 17. Yaksh TL. Spil/al Afferent Processing. Plenum, New York, 1986. 18. Melzack R, Casey KL. Sensory, motivational and central control determinants of pain: a new conceptual model. In: Kenshalo D (ed.) The Skill Sellses. Thomas, Springfield, 1968:923-993. 19. Hand PJ, Morrison AR. Thalamocortical projections from the ventrobasal complex to somatic sensory area I and I I . Exp Neurol 1970;27:291 . 20. Desijaru T, Purpura D P. Organisation o f specific-nonspecific thalamic internuclear synaptic pathways. Brain Res 1970;21: 169. 21 . Penfield W. The role of the temporal cortex in recall of past experience and interpretation of the present. In: Wolstenholme GEW, O'Connor CM (eds) The Neurological Basis of Behaviour. Churchill, LOl ldon, 1958: 149. 22. Newcombe F. Memory. In: Critchley M, O'Leary JL, Jennett B (eds) Scientific FOllndations of Neurology. Heinemann, London, 1972:205. 23. Black P. Physiological Correlates of ElI1otion. Academic Press, New York, 1970.

24. Melzack R, Wall PD. Pain mechanism: a new theory. Science 1965;150:971-979. 25. Noordenbos W. Pain. Problems Pertaining to the Transmission of Nerve Impulses Which Give Rise to Pain. Elsevier, Amsterdam. 1959. 26. Mayer DJ, Price D. Central nervous system of analgesia. Pain 1976;2:379. 27. Tan S- Y. Cognitive and behavioural methods for pain control: a selective review. Pain 1982;12:201-228. 28. Langen D. Psychosomatic aspects in the treatment of pain. In: Janzen R, Keidel WD, Herz A, Steichele C (eds) Pail7: Basic Principles, Pharmacology, Therapy. Thieme, Stuttgart, 1972: 164. 29. Chapman CR, Feather BW. E ffects of diazepam on human pain tolerance and pain sensitivity. Psychosom Med 1973;35:330. 30. Fields HL, Heruicher MH. Anatomy and physiology of a nociceptive modulatory system. Phil Trans Roy Soc B 1 985;308:361-379. 3 1 . Head H. The afferent nervous system from a new aspect. Braill 1905;28:99. 32. Head H, Campbell AW. The pathology of herpes zoster and its bearing on sensory location. Brain 1900;23:353-523. 33. Lewis T. Pain. MacMillan, New York, 1942. 34. Kellgren JH. Observations of referred pain arising from muscle. Ciin Sci 1938;3:175. 35. Kellgren JH. On the distribution of pain from deep somatic structures. Ciin Sci 1939;4:35. 36. Inman VT, Saunders JB de CM. Referred pain from skeletal structures. J Nerv Men! Dis 1944;99:660. 37. Travell J, Berry C, Bigelow N . Effects of referred somatic pain on structures in the reference zone. Fed Proc 1944;3:49. 38. McCall rw, Park WM, O'Brien JP. Induced pain referred from posterior elements in normal subjects. Spine 1979;4:44 1 . 39. Hansen K , Schliack H . Segmental Innervation. Thieme, Stuttga rt, 1962. 40. Kunert W. Wirbelsaule and innere Medizin. F. Enke, Stuttgart, 1975. 41. Foerster O. Dermatomes in man. Brain 1 933;56 : 1 . 4 2 . Lewis T, Kellgren JH. Observations relating t o referred pain. Visceromotor reflexes and other associated phenomena. Ciin Sci 1939;4:47. 43. Keegan H, Garett FD. The segmental distribution of the cuta­ neous nerves in the limbs of man. Ana! Rec 1948;102:409. 44. Hockaday JM, Whitty CWM. Patterns of referred pain in the

normal subject. Brain 1967;90(3):481-496. 45. Cyriax JH. Textbook of Orthopaedic Medicine, vol. 1, 8th edn. Bailliere Tindall, London, 1982:22, 35. 46. MacKenzie J. Krankheitszeichen und ihre Auslegung 3. Translated by J Miiller, Kabitsch, Wiirzburg, 1 9 1 7. 47. Livingston WK. Pain Mechanisms. Macmillan, New York, 1944. 48. Wedell G, Sinclair DG, Feindel WHo Anatomical basis for alter­ ations in quality of pain sensibility. J Neurophys 1948;11:99. 49. Wedell G. Referred pain in relation to the mechanism of common sensibility. Proc Roy Soc Med 1 957;50:581 . 50. Pomeranz B, Wall PD, Weber WV. Cord cells responding to fine myelinated afferents from viscera, muscle and skin. f Physiol 1968;199:511-532.

22 SECTION ONE - GENERAL P R INC IPLES

5 1 . Taylor DCM, Pierau Fr-K, Mizutain M. Possible bases for referred pain. In: Holden AV, Winslow W (eds) The Neurobiology

of Pain. Manchester University Press, Manchester, 1984: 143. 52. Wells PE, Frampton V, Bowsher D . Pain Managemen t by Physiotherapy, 2nd edn. Butterworth-Heinemann, Oxford, 1 994. 53. Cyriax J H . Massage, Manipulation and Local A n aesthesia. Hami lton, London, 1 94 1 . 54. Ruch T C . Visceral sensation a n d referred pain. I n : Fulton J F (ed . ) Howel/'s Textbook of PhysiologJJ WB Saunders, Philadelphia, 1946.

common bile duct in man and its implication for the theory of referred pain. Br ] Surg 1967;54:599-606. 71 . Williams PL, Warwick R. Gray 's

A'latomy.

Churchill

Livingstone, Edinburgh, 1980. 72. Lindsay KW, Bone I, Callander R. Neurology and Neurosurgery Illustrated, 2nd edn. Churchill Livingstone, Edinburgh, 1 991 . 73. Van Cranenburgh B. Segmentale verschijnselen. Bolm, Scheltema

55. Merskey H, Spear FG. Pain: Psychological and Psychiatric Aspects. Baill iere Tindall and Cassell, London, 1967.

and Holkema, Utrecht, 1985. 74. Pedersen HE, Conrad FJ, Blunck MD, Gartner E. The anatomy of lumbosacral posterior rami and meningeal branches of spinal nerves (sinu-vertebral nerves). J Bone Joint Surg 1956;38A(2): 377-391 .

56. Neurological aspects of the diagnosis and treatment of facial

75. Stillwell DL. The nerve supply of the vertebral column and its

pain. In: Cohen B, Kramer I (eds) Scientific Foundations of Dentistry. Heinemann, London, 1 974: 278.

associated structures in the monkey. Anat Rec 1956;125(2):139-162. 76. Kimmel DL. I nnervation of spinal dura mater, and dura mater of the posterior cranial fossa. Neurology 1961;11:800-809.

57. Patten BM. Human EmbryologJJ McGraw-Hili, New York, 1968. 58. Head H, Campbell AW. The pathology of herpes zoster and its bearing on sensory location. Brain 1900;23:353-523. 59. Keegan JJ, Garrett ED. The segmental distribution of the cuta­ neous nerves in the limbs of man. Anat Rec 1949;101:409. 60. Fukui S, Ohseto K, et al. Distribution of referred pain from the zygapophyseal joints and dorsal rami . Clin ] Pain 1997;13(4):303-307. 6 1 . Schwartz HG. Anastomoses between cervical nerve roots. ] Neurosurg 1956;13:190. 62. Kikuchi S, Hasue M, Nishiyama K, Ito T. Anatomic and clinical studies of radicular symptoms. Spine 1 984;9:23-30.

63. Kadish q, Simons EH. Anomalies of the lumbosacral nerve roots. ! Bone Joint Surg 1984;66B:411-416. 64. Stappaerts K, Van Hees J, Trimpeneers I. Variations in Segmental

Innervation. Instituut voor Lichamelijke Opvoeding, KU Leuven (in press). 65. Cole JP, Lesswing AL, Cole JR. Analysis of lumbosacral der­ matomes in man. Clin Orthop 1968;61:24 1 . 66. Conesa SH, Argote M L . A Visual Aid to the Examination of Nerve Roots. Bailliere Tindall, London, 1976. 67. Wakasugi BDermatomes of the body and the extremeties. Surg Treatment 1982;132:270. 68. Mi tta H. Study on derma tomes by means of selective lumbar spinal nerve block. Spine 1993;18:1 782-1786. 69. Sicard A, Leca A. Place de rachiotomie dans Ie traitement chirurgical des sciatiques. Press Med 1 954;62 : 1 737. 70. Doran FSA. The sites to which pain is referred from the

77. Edghar MA, Nundy S. Innervation of the spinal dura mater. ] Neurol Neurosurg Psychiatr 1966;29:530-534. 78. Jackson He, Winkelmann RK, Bickel WHo Nerve endings in the human lumbar spinal column and related structures. J Bone Joint Surg 1966;48A:1272-1 281 . 79. Edgar MA, Ghadially JA. Innervation o f the lumbar spine. Ciin

Orthop Rei Res 1 976;115:35-41 . 80. Groen GJ, Baljet B, Drukker J. The innervation of the spinal dura mater: anatomy and clinical implications. Acta Neurochir 1988;92:39-46. 8 1 . Cyriax JH. Dural pain. Lancet 1978;1:919-921 . 82. Gowers W. Lumbago. BM] 1904;i:117. 83. Travell JG, Simons DG. Myofascial Pain and Dysfunction. Williams and Wilkins, Baltimore, 1983. 84. Cyriax JH. Fibrositis. BM! 1948;ii:251 . 85. Simons DG. Muscle pain syndromes, part I I . Alii J Phys Med 1976;55:1 5-42. 86. Kennard MA, Haugen FP. The relation of subcutaneous focal sensitivity to referred pain of cardiac origin. Anaesthesiology 1 955;16:297-3 1 1 . 8 7 . Melzack R, Wall P. The Challenge of Pain. Penguin, London, 1991 . 88. Woolsey CN, Marshall WH, Bard P. Observations on cortical somatic sensory medlanism of cat and monkey. ] Neurophysiol 1941;4: 1 . 89. Lewis T, Kellgren JH. Observations relating referred pain, visceromotor reflexes and other associated phenomena. Ciin Sci 1939;4:47.

CHAPTER CONTENTS

23 Roots 24 Nerve plexus and nerve trunk Small peripheral nerve 25

Pressure on nerves

Anatomy

Terminology

25

26

Pain originating from the peripheral nerve system

Nociceptive pain 26 Neuropathic pain 26 Superficial dysaesthetic pain

26

Behaviour of nervous tissue during pressure

Pain 27 Paraesthesia 27 Loss of function 27 27 Small peripheral nerves 28 Nerve trunk/plexus 28 Compression of the nerve root Spinal cord 29

26

26

ANATOMY Peripheral nerves contain both neural and supportive elements. A large multifascicular nerve is composed

Clinical syndromes

of a number of different bundles of nerve fibres or

28

fasciculi (Fig.

2.1).

These are bound together by the

epineurium, a condensation of areolar connective tissue derived from the mesoderm. In humans, the epi­ neurium normally constitutes sectional

area

of

the

30-50%

nerve

of the total cross­

bundle:

it

contains

fibroblasts; collagen (types I and III); variable amounts of fat (possibly to cushion the nerve fibres it surrounds); lymphatic; blood vessels (vasa vasorum); and free nerve endings. In a monofascicular nerve, the epineurium only surrounds the fasciculus and is fused with the perineurium. The perineurium surrounds and protects one fascicle. It has two different layers; an outer collagen-rich connec­ tive one and an inner epithelial layer of contiguous cells.

The perineurium has an important role in maintaining

the osmotic milieu

and fluid pressure within

the

endoneurium and also acts as a barrier against chemical and bacterial invasion.1 The connective tissue of peri- and epineurium possesses blood and lymph vessels - the so-called vasa vasorum.2,3 Also free nociceptive nerve endings which come from the related multifascicular nerve trunks

are

embedded

in

the

perineurium

and

epineurium.4,s Enclosed in the perineurium is the fasciculus - a bundle of nerve fibres bound together and sheltered by the endoneurium. The latter consists of long collagen fibres running with the nerve fibres. The fibrous and cellular components of the endoneurium are bathed in endoneural fluid.6 The nerve fibres are axons - the distal offshoots of nerve cells (Fig.

2.2).

Most axons are surrounded by a

myelin sheath formed from the compressed and concen­ tric Schwann cell membranes. Axons range in size from

0.2 fJ-m (small non-myelinated nociceptive axons) to 20 fJ-m (large and myelinated efferent motor axons) and in length from 1 to 100 cm. They contain most of the cell volume.

23

24 SECTION ONE - GENERAL PRINCIPLES

myelin sheath

Figure 2.1

Axons

Axon, surrounded by myelin sheath.

Figure 2.3 Anatomy of the peripheral nervous system : 1, spinal cord ; 2, nerve root; 3, nerve plexus and nerve trunk; 4, peripheral nerve branches.

----i�'Ma.\:�4.

pressed nerve trunk and a compressed small peripheral nerve.

ROOTS The course of the spinal nerve within the spinal canal, from the emergence of the rootlets at the anterior and

Fat cells

posterior aspect of the spinal cord to the outer border of Figure 2.2

A peripheral nerve is composed of a number of different fasciculi.

the foramen, is called the intraspinal root (Fig.

2.4).7

Being inside the meningeal membranes of the spinal cord, the posterior and anterior roots are devoid of the elaborate epineural and perineural membranes that are From central to peripheral, the nervous system can be clinically divided into four zones (Fig.

2.3):

• The spinal cord. • The spinal nerve, which contains fibres belonging to

characteristic of peripheral nerves. Proximally, the rootlets float freely within the cere­ brospinal fluid which is the main source of their meta­ bolic needs. In this intrathecal part of the intraspinal

one segment. • In the brachial and sacral area, and distal from the

spinal ganglion, the different spinal nerves form a nerve plexus, from which originate the large multi­

4

fascicular nerve trunks.

• Further distally the trunks split into peripheral

nerves, with motor, sensory or combined function. Although the fasciculi, from their exit from the central

nervous system to the distal extremity of the nerve,

exhibit the general morphology summarized above, the structure and behaviour of the connective supportive ele­

ments differ considerably. This may explain the different clinical behaviour of a compressed cord, a compressed

nerve root (within or without its dural sleeve), a com-

2 Figure 2.4 Structure of an intraspinal root: 1, spinal cord; 2, ventral root; 3, dorsal root; 4, dorsal ganglion.

CHAPTER 2 - PRESSURE ON NERVES 25

root, the rootlets are held together by the endoneurium which is more loosely arranged than is typically seen in

the anterior aspect where it receives its innervation from the sinuvertebral nerve belonging to the same

peripheral nerves.8 Further distally, the nerve root

segmentP-14 Pain arising from the dural sheath is seg­

becomes enclosed in the dural sheath - a tubular pro­

mental and obeys the rules of segmental reference of

longation of the dura. In this dural investment the nerves do not lie freely but are bound by the arachnoid membrane (Fig. 2.5).9,10 This area is known as the extrathecal part of the intraspinal nerve root - that length of the root and the dural sleeve between the main dural sac and the exit from the foramen. The extrathecal portion is short in the cervical region but becomes longer with the increasing obliquity of the intraspinal roots in the thoracolumbar and lumbar regions. Distal to the posterior root ganglion, at the level of the foramen, the posterior and anterior roots are fused into one

single

bundle.

Here the

nerve

root

pain (see Ch.

1).

There is no evidence that root pain

arises from involvement of the axons. For example, pressure at the extraspinal nerve root, which misses the nerve root sleeve, as happens in some types of spondylolytic compression, causes not pain but only paraesthesia and neurological deficit. From a clinical point of view, it is important to consider this structural duality: the outer investment is responsi­ ble for segmental pain, whereas the parenchymatous content is responsible for the paraesthesia and the conduction deficits.

becomes

extraspinal. The tissue of the epidural pouch becomes more condensed and blends with the epineurium of the extraspinal nerve root. The segment of the spinal root which is liable to com­ pression, whether by a disc protrusion, an osteophytic outgrowth or a narrow lateral recess, is the extrathecal part of the intraspinal root. To understand the symptom of a compression or inflammation of this part of the peripheral nerve system, it is necessary to recognize the importance of the dural investment - the nerve root sheath. The dural sheath has considerable sensitivity:11

it has many nociceptive nerve endings, especially at

NERVE PLEXUS AND NERVE T RUNK Immediately distal to the foramen, the single fasciculus of the extraspinal root is enclosed in a thin but strong perineurial sheath, external to which is the epineurial areolar connective tissue. Within a few millimetres of its formation, the single fasciculus of the spinal nerve divides into several bundles which form the plexuses. Motor and sensory fibres of one nerve root mix, and more distally there is a redistribution of the fasciculi of various

consecutive nerve roots.IS The brachial plexus is thus formed of the anterior rami of roots C5-T2, and the sacral plexus of the roots L2-55. Distally, the fasciculi continue

88i

+-----+:+-----+: --'""==""-""

in the large nerve trunks of the limbs. The fasciculi of plexus and trunks do not differ significantly from those of the roots or the peripheral nerves. The connective support tissue, however, has some anatomical particularities. Because the monofasci­ cular spinal nerve changes into a multifascicular struc­ ture, there is an increased amount of epineurial tissue, forming a protective packing for the nerve tissue. The perineurium is also reinforced by elastin fibres. The fas­ ciculi have an undulating course, whereas the collagen fibres run more longitudinally. This structure ensures that the nerve fibres are protected from mechanical deformation

(compression and

elongation)

during

normal movements of the limbs.16 Although the epi- and perineurium contain nociceptive nerve endings, these seem to be relatively insensitive.I7

SMALL PERIPHERAL NERVE A small peripheral nerve is the distal termination of a branching nerve trunk. The nerve ending is often mono­ Figure 2.5

Course of spinal nerve: A, intrathecal part of the nerve root; B, extrathecal part of the nerve root; 1, spinal cord; 2, ventral and dorsal rootlets; 3, spinal ganglion; 4, dura mater; 5, arachnoidea.

fascicular. The epineurium is then fused with the peri­ neurium. Peripheral nerves can either have only a motor or a sensory function, or both can be combined. They all

26 SECTION ONE - GENERAL PRINCIPLES

have nociceptive nerve endings in their supporting connective tissue.

from prolonged damage to peripheral nerve tissue, such as avulsion, dissection or amputation.22 The pain is felt in the anaesthetic area, is continuous and burning and is independent of posture or movement, although local

TERMINOLOGY

pressure can increase the pain considerably.23

Lesions of the peripheral nervous system are character­

provoke pain mechanisms without involvement of

Chronic damage or formation of scar tissue seems to

ized by a pathognomonic sensation: paraesthesia ('pins and needles'). Although all tissues in the human body which contain nociceptive structures can be a source of pain, pins and needles will only arise when some part of the peripheral nervous system is at fault. Hence, the medical world is apt to use the term 'neuritis' when pain is accompanied by pins and needles. Strictly, however, the suffix '-itis' implies inflammation. Therefore the

word neuritis should only be used when the peripheral nerve is affected by infectious or toxic irritation - i.e. there is an intrinsic disorder of the nervous parenchyma. Classically, these lesions are classified into mono- and polyneuritis. They are not discussed in this book, except in the shoulder region, where the clinical appearance of three mononeurites and neuralgic amyotrophy of the shoulder girdle is reviewed (see Section 4).

When external pressure is applied to a normal nerve,

peripheral nociception. Also, the formation of a neuroma leads to increased sensitivity and spontaneous pain.24 Research on experimental neuromata has shown that regenerating axons have a spontaneous excitability and an increased sensitivity to mechanical stimuli. An action potential in one axon probably leads to an impulse in a nearby axon. This mechanism of 'cross-talking fibres' accounts for the repetitive train of action potentials in a bundle of regenerating axons.25 A small stimulus thus leads to a self-perpetuating series of action potentials,

and excessive and long-standing pain.26

Another mechanism that may account for neuropathic pain is the loss of inhibitory effects of the large diameter mechanoreceptor afferents in a traumatized nerve. This leads to a relative increase of the activity from the small nociceptive afferents, and thus an opening of the gate at

the' dorsal horn.27 (see Ch.

1).

pins and needles arise although the nerve tissue is ini­ tially not inflamed. If the compression is not severe, the nerve continues to conduct normally. This situation of extrinsic pressure on a normal nerve is not a 'neuritis' and requires a totally different therapeutic approach. In this situation, the terms 'pressure on nerve' or 'entrap­ ment neuropathy' are preferred.

SUPE RFICIAL DYSAESTHETIC PAIN This type of pain is also rare, and is typical of diffuse polyneuritis, for example in diabetes,28 Vitamin B1 deficiency or chemical irritation. Damage to small C fibres leads to sprouting of small offshoots in the regen­ erating axons. This leads to increased excitability, which results in unpleasant painful sensations during normal stroking of the skin (allodynia).29 The patient also com­

PAIN ORIGINATING FROM THE PERIPERAL NERVE SYSTEM

plains of a burning feeling and 'electrical sensations'

NOCICEPTIVE PAIN

is also some analgesia (see Box

when the skin is gently touched (dysaesthesia), and there Peripheral nociceptors in the connective tissue of the

neurogenic pain).

2.1

for an overview of

peripheral nerves are stimulated, and via Ad and C fibres of the nervi nervorum conducted to the spinal cord and thence to the pain projection areas in the cortex.18 There are indications that most of the pain that stems from direct irritation of the peripheral nervous system is of nociceptive origin. 19,20 'Nerve pain' thus behaves identically to other peripheral pain/I

obeys exactly the rules of referred pain and is not to be distinguished from pain of ligamentous, tendinous or

arthrogenic origin (see Ch.

1).

BEHAVIOUR OF NERVOUS TISSUE DURING PRESSURE Entrapment of peripheral nerve tissue is defined as

mechanical compression of the nerve, which includes the reduction of radial dimensions in the neural cells, the neural support elements or any combination of these. Depending on the degree and the duration of compres­ sion, the effects can be subtle or can lead to displace­ ment, deformity and morphological changes in the

NEUROPATHIC PAIN This type of pain, also called' de-afferentation or neuralgic pain' is less common than nociceptive pain and results

compressed tissue (neural tissue or neural support tissue).30 The clinical effects of nerve compression are pain,

paraesthesia and loss of function.

CHAPTER 2

Box 2.1 Neurogenic pain Nociceptive pain: • Common • Irritation of nociceptive structures in the connective support tissues of the nerve • 'Normal' pain sensation, obeys the rules of segmental reference Neuropathic pain:

• Rare • Results from damage to the nerve tissue • Intense pain, sharp, burning

-

PRESSURE ON NERVES 27

felt in the cutaneous area supplied by the nerve tissue involved and distal to the site of the lesion. It is therefore

extremely important to ascertain the precise site of the

symptom, in that this helps to determine the site of compression. Provocation of pins and needles by movements (distant movements or local pressure) or by stroking over the affected skin demonstrates an external origin for the symptoms. In primary afflictions of the peripheral nerve (neuritis), the pins and needles come and go sponta­ neously and movements do not influence them.

Superficial dysaesthetic pain:

• Rare • Polyneuritis: irritation of C fibres • Dysaesthesia, allodynia and anaesthesia in the innervation area of the peripheral nerve

LOSS OF FUNCTION The epineurium and perineurium initially buffer the fasciculi from constrictive effects, but with a greater amount of compression, structural changes of the ele­ ments within the endoneurium follow.34 Recent research

has

demonstrated that

the intraradicular

oedema

PAIN

caused by alteration of the blood-nerve barrier is the

The pain mechanism in entrapment phenomena is

most important factor in the nerve root dysfunction of

usually nociceptive: free nerve endings in the connec­ tive tissue of the nerve or in the dural investment of the nerve root are depolarized by application of mechanical forces or after exposure to irritating chemical sub­ stances, released from inflamed tissues.31 The pain stems from irritation of the support tissue enclosing the

nerve fibres and only exceptionally does it result from pathological processes in the nerve tissue itself (neuro­ pathic and dysaesthetic pain). This has the following clinical consequences.

The pain will depend largely on the density of the nociceptive receptors in the support elements. It follows that the intensity of the pain depends not only on the intensity of compression but also on the localization along the course of the peripheral nerve. Pressure on a

nerve root, for instance, will be more painful than an

equal degree of force applied on a nerve plexus.

Because an external force acts first on the outer sup­ porting structures of the nerve, pain will usually be the first symptom and it sometimes appears before involve­

chronic compression.35,36 Sometimes only the Schwann cells are affected, without damage to the axons. Destruction of the myelin sheath then results in loss of conduction. This type of lesion (lesion of Schwann cells without lesion of the axon fibre) is termed 'neuropraxis'. If the compression has been only temporary, recovery of the Schwann cells will not take more than

2

weeks. This is the type of lesion

responsible for the 'Saturday night palsy' seen after pro­ longed pressure on the radial nerve, or the 'gardener'S palsy' seen after prolonged traction on the peroneal nerve. If considerable compression is maintained for a longer period, atrophy of the nerve tissue occurs and is followed by Wallerian degeneration of the distal part of the axon. Oedema, cellular proliferation and ingrowth of connective tissue also follows.37 If the compression is maintained for long periods, fibrotic degeneration appears at the site of the lesion, which makes recovery most unlikely.38

ment of the parenchyma is present. A chronic but moder­ ate pressure that is insufficient to impair conduction solely influences the outer structures and results in pain only. It is thus possible to have a completely normal examination of the peripheral nervous system, even

though the patient does have nerve compression.32

PA RAESTHESIA Pins and needles are pathognomonic of involvement of the peripheral nervous system in that the sensation cannot be produced in any way other than compression or inflammation of nerve tissue.33 Paraesthesiae are always

CLINICAL SYNDROMES Cyriax39 (see his pp.

37-39)

distinguished four different

syndromes in entrapment phenomena, corresponding to

the site of compression along the peripheral nerve: at the small peripheral sensory nerve, at the nerve trunk/plexus, at the nerve root and at the spinal cord (see Fig.

2.3).

Depending on the localization of compression, the peripheral nervous system behaves differently. These differences are a major help to the clinician trying to ascertain the precise site of the lesion.

28 SECTION ONE - GENERAL PRINCIPLES

ments of the limb or the digits, or stroking over the anal­

SMALL PERIPHERAL NERVES Pressure on a small peripheral sensory nerve results in pain, paraesthesia and numbness. Pain is usually moder­ ate and the main symptom is numbness. Together with some paraesthesia, these symptoms occupy the appropri­ ate area of supply, which is usually well defined with clear-cut borders. The patient can tell precisely where the cutaneous analgesia is felt and where sensation is still normal. The centre of the region is often completely anaesthetic. A typical example is 'meralgia paraesthetica', which results from compression of the lateral cutaneous femoral nerve of the thigh.

gesic area of skin usually brings on or increases the pins

and needles. It is a common experience that the paraes­ thesia in the feet that comes on after relieving pressure on the sciatic nerve increases when the subject walks around or stamps the feet on the ground. Paraesthesia and numbness are usually felt in the distal part of the cutaneous area supplied by the com­

pressed plexus or nerve, no matter at what point in its

course the compression occurs. The lesion lies proximal to the upper edge of the paraesthetic area but not always close to it. Therefore it must not be thought that, if move­ ment of the foot provokes the pins and needles, the lesion lies in the ankle or foot. Clinical examination must

NERVE T RUNK/PLEXUS

include the entire length of the nerve involved.

Minor and intermittent pressure on a nerve trunk or a

the sacral plexus and the nerve trunks of the lower limb.

plexus causes paraesthesia and numbness. Sudden and serious tissue damage may provoke neuropathic pain. Constant pressure on a nerve trunk leading to parenchymatous damage does not usually provoke pain nor paraesthesia but only loss of motor and sensory function. If the pressure is intermittent, a neurological deficit does not appear, even after many years. Paraesthesiae do not appear during the time of compression but only when the pressure on the nerve trunk has been released.

It is common knowledge that pressure on the sciatic nerve while sitting causes only vague analgesia in the

The release phenomenon is typical of compression of The phenomenon is also provoked by compression at the brachial plexus (thoracic outlet syndrome) but

ceases to operate when a nerve trunk distally to the thoracic outlet is compressed. It is a curious clinical fact that pressure on a nerve in the upper limb only pro­ vokes paraesthesia during the moment of compression. Pins and needles in the two ulnar fingers, caused by compression of the ulnar nerve at the elbow, immedi­

ately stop when the compression is released. Similarly,

in carpal tunnel syndrome, the paraesthesiae are felt during the moment of compression.

affected area or no symptoms at all. The shower of pins and needles then only appears when the subject relieves the pressure by standing up. The interval between the

cessation of the pressure and the onset of the tingling depends on the duration of the compression: the longer

the pressure is applied, the longer is the interval between the relief of pressure and onset of symptoms. There is also a relation between the duration of com­ pression and the duration of paraesthesia. Thus, after

15 minutes of 20-60 seconds

pressure, the pins and needles appear after the release and last only

minutes. After release from

15

1

or

2

hours' compression,

paraesthesiae will probably appear only after an inter­ val of some hours, then persist for

1

to

2

hours before

COMP RESSION OF THE NERVE ROOT Pressure on the extra thecal intraspinal nerve root results in a typical set of symptoms (pain and paraesthesia) and signs (motor and sensory deficit) strictly related to the segment involved. Contrary to the pins and needles

brought on by the release of pressure on a nerve trunk,

the paraesthesiae only appear during the period of com­ pression, and cease immediately thereafter.

The sequence of appearance of pain, paraesthesia and deficit and their mutual interrelation have important clinical significance and are often of considerable help in the diagnosis of nerve root compression.

recovering spontaneously. Cyriax39 calls this strange and hitherto unexplained phenomenon the 'release phe­ nomenon' (see his p.

37).

Lundburg and Rydevik have

Pain The nerve root has a dural sheath, which is innervated

demonstrated that fluctuations in membrane permeabil­

by the sinuvertebral nerve.12 The latter is derived from

noticeable when compression on the nerve trunk is

ing from the dural sheath is strictly segmental and

ity of the structures within the endoneurium are more released and oedema appears, than during the compres­ sion of the nerve and its supplying blood vessels.4o This might explain the release phenomenon. Another characteristic of paraesthesia induced by compression at the level of the plexus is that active move-

the corresponding nerve root. Therefore pain originat­ follows the rules of segmental reference of pain. Compression applied to the dural sleeve of the nerve root thus results in pain occupying all or any part of the

dermatome. Pain felt in a particular dermatome in com­ bination with other symptoms of nerve compression,

CHAPTER 2

-

PRESSURE ON NERVES 29

immediately draws attention to an impingement on the nerve root.

Paraesthesia Pins and needles stem from pressure on the parenchyma itself. In root pressure, they accompany the segmental pain, or appear at a later date. Pins and needles indicate that the parenchyma itself is irritated, whereas radicular pain is a symptom of compression of the dural sheath.

In nerve root compressions, paraesthesiae are felt in the distal extremities of the dermatomes, which are areas often not supplied by a particular nerve trunk or nerve. As in compression of a nerve trunk, stroking the skin may provoke or increase the pins and needles but moving the digits does not influence them.

Deficit The absence of the protective packing by epineurial tissue renders the nerve roots more susceptible to direct com­ pression than nerve trunks. Compression disturbs nerve conduction by interfering with the blood supply of the nerve fibres.41 Loss of function of the nerve fibres results in sensory and motor deficit. Paraesthesiae usually dis­ appear with the onset of cutaneous analgesia.

Figure 2.6

Progressive compression of a nerve root.

Progressive compression of a nerve root within its dural sleeve causes a typical sequence of symptoms: pain,

paraesthesia and numbness will follow each other, rather than coincide. This is typically the case in a progressively increasing pressure exerted by an evolving disc lesion: slight compression on the epidural sheath of the nerve root causes pain only (Fig. 2.6a). As the pressure increases,

nerve trunk or peripheral nerve. For instance, the patient may complain of pins and needles in both hands and forearms at both aspects or in both legs from the knees to all the toes.

paraesthesia and muscle fasciculations - symptoms of parenchymatous hyperexcitability - appear42 (Fig. 2.6b). In the final stage, pressure has induced such ischaemic damage to the nerve root that function is completely lost, including the conduction of pain (Fig. 2.6c). The patient

then complains of weakness and numbness but pain and

Box 2.2 Pressure on nerves: summary -

• Peripheral nerve

Numbness> paraesthesia> pain Clearly delineated area

• Nerve trunk

Paraesthesia> numbness> pain Vaguely delineated area

paraesthesia have disappeared.

Release phenomenon: -The pins and needles appear after the compression has ceased -There is a direct relation between

SPINAL CORD

the interval of onset and duration of

Pressure on the anterior aspect of the spinal cord results,

inter alia, in bilateral paraesthesia. Pain is absent if the compression is slowly progressive but dural pain may

compression

• Nerve root

Segmental distribution of symptoms

accompany the paraesthesia if the compression is

Chronological sequence of symptoms Compression phenomenon:

sudden. The main cause of spinal cord compression is

-The pins and needles appear

spinal stenosis at the cervical or thoracic level. When the cord is compressed over the thoracic region, the paraes­ thesiae are felt only in the limbs. In compression at the cervical level, pins and needles will be present in all limbs or in the lower limbs only. The paraesthesiae are usually bilateral and extend beyond the borders of the areas of the cutaneous innervation of any spinal nerve,

Pain> paraesthesia> numbness

during the compression

• Spinal cord

Completely painless (sometimes dural pain) Extrasegmentally and bilaterally distributed paraesthesia Positive neck flexion

30 SECTION ONE - GENERAL PRINCIPLES

The symptoms are not provoked by movements of

distribution of the painless paraesthesiae, positive neck

the limbs nor by stroking the skin. Neck flexion is the

flexion provides the clue to the diagnosis of incipient

only way to bring on the pins and needles (L'Hermitte's

spinal cord compression.

sign). Together with the extrasegmental and bilateral

REFE RENCES 1. Shanta TR, Bourne GH. The perineural epithelium - a new concept. In: Bourne GH (ed) The Structure and FUllctioll of

Nervous Tissue, vol 1. Academic Press, New York, 1968.

2. Sjostrand J, Rydevik B, Lundborg G, McLean WG. Impairment of intraneural microcirculation, blood nerve barrier and axonal transport in experimental nerve ischemia and compression. In: Korr 1M (ed) The Neurobiologic Mechallisms in Manipulative

Therapy.

Plenum Press, New York, 1978.

3. McManis PG, Low PA, Lagerlund TD. Microenvironment of nerve blood flow and ischemia. In: Dyck pJ, Thomas PK, Lambert EH, Bunge R (eds) Peripheral Neuropathy, 3rd edn. Saunders, Philadelphia, 1993:453-473. 4. Hromada J. On the nerve supply of the connective tissue of some peripheral nervous system components. Acta Anat (Basel)

21. Casey KL. Toward a rationale for the treatment of painful neu­ ropathies. In: Dubner R, Gebhart GF, Bond MR (eds) Proceedings

of the Fifth World Congress

011

Pain.

Elsevier, Amsterdam,

1988:165-174. 22. Tasker RR, Tsudat T, Hawrylyshyn P. Clinical neurophysiologi­ cal investigation of de-afferentation pain. Adv Pain Res Ther 1983;5:713-738. 23. Cecht ChI, Van de Brand H), Wajer O. Post-axillary dissection pain due to a lesion of the intercostobrachial nerve. Pain 1989;38:171-176. 24. Wall PO, Gutnick M. Ongoing activity in peripheral nerves: the physiology and pharmacology of impulses originating from a neuroma. Exp NeuroI1974;43:580-593. 25. Burchiel KJ. Effects of electrical and mechanical stimulation on two foci of spontaneous activity which develop in primary

1963;55:343-351. 5. T homas PK, Olsson Y. Microscopic anatomy and function of the connective tissue components of peripheral nerve. In: Dyck PI,

afferent neurons after peripheral axotomy. Pain 1984;18:249-265. 26. Govrin-Lippmann R, Devor M. Ongoing activity in severed

T homas PK, Lambert EH (eds) Peripheral Neuropathy. Saunders, Philadelphia, 1975: 168-189. 6. Low PA. Endoneural fluid pressure and microenvironment of

nerves: source and variation with time. Brain Res 1978;159:406-410. 27. Noordenbos W, Wall PD. Implications of the failure of nerve resection and graft to cure chronic pain produced by nerve lesions.] Neurol Neurosurg Psychiatr 1981;44:1068-1073.

nerve. In: Dyck PI, Thomas PK, Lambert EH, Bunge R (eds) 3rd edn. Saunders, Philadelphia, 1993:599-617.

Peripheral Neuropathy,

7. Hollinstead WHo Anatomy for Surgeolls Limbs. Harper & Row, New York, 1969.

vol

3:

The Back alld the

8. Sunderland S. Traumatized nerves, roots and ganglia: musculo­ skeletal factors and neuropathological consequences. In: Korr 1M (ed) The Neurobiologic Mechanisms Plenum Press, New York, 1978.

in Mallipulative Therapy.

9. Brieg A. Biomechanics of the lumbosacral nerve roots. Acta Radiol (Diagn) 1963;1:1141. 10. Haines DE, Harley He, AI Mefty O. The subdural space, a new look at an outdated concept. Neurosurgery 1993;32:111-120. 11. Lindahl O. Hyperalgesia of the lumbar nerve roots in sciatica.

Acta Orlhop Scand 1966;37:367. 12. Edgar MA, Nundy S. Ilmervation of the spinal dura mater. ] Neurol Neurosurg Psychiatr 1966;29:530-534. 13. Bogduk N. The innervation of the lumbar

spine.

Spille

1983;8:286-293. 14. Murphy RW. Nerve roots and spinal nerves in degenerative disk disease. Clin Orthop Rei Res 1977;129:46-60. 15. Sunderland S. The anatomy of the intervertebral foramen and the mechanisms of compression and stretch of nerve roots. In: Haldeman S (ed.) Modern Developments ill the Principles and Practice ofChiropractice. Appleton-Century-Crofts, New York, 1979. 16. Sunderland S. Nerves and Nerve injuries, 2nd edn. Churchill Livingstone, Edinburgh, 1978. 17. Mumenthaler M, Schliack H. Stuttgart, 1982.

Liisionen peripherer Nerven. Thieme,

18. Raja SN, Meyer RA, Campbell IN. Peripheral mechanisms of somatic pain. Anesthesiology 1988;68:571-590. 19. Asbury AK, Fields HL. Pain due to peripheral nerve damage: a hypothesis.

NeurologIj

1984;34:1587-1592.

20. Janig W, Kotzenburg M. Receptive properties of pial afferents.

Paill

1991;45:77-86.

JR, Asbury Arch NeuroI1967;33:137-141.

28. Brown MI, Marin

AK. Painful diabetic neuropathy.

29. T homas PK. Painful neuropathies. 103-110.

Adv Pain Res Ther

1979;3:

30. Luttges MW, Gerren RA. Compression physiology: nerves and roots. In: Haldeman S (ed.) Modem Developmellts in the Principles and Practice of Chiropractice. Appleton-Century-Crofts, New York, 1979:65-92. 31. Fields HL. The peripheral pain sensory system. In: Fields HL (ed) Pain. McGraw-Hili, New York, 1987:13-40 32. Cyriax JH. Perineuritis. BM] 1942;i:578. 33. Walton IN. Essentials of Neurology, 6th edn. Churchill Livingstone, Edinburgh, 1989. 34. Lundborg G. Structure and function of the intraneural microvessels as related to trauma, edema formation and nerve function. J Bone Joint Surg 1975;57:938. 35. Yoshizawa H, Kobayashi T. Chronic nerve root compression. Spine 1995;20(4):397-407. 36. Matsui T et al. Quantitative analysis of oedema in the dorsal nerve roots induced by acute mechanical compression. Spille 1998;23(18):1931-1936. 37. Aguayo A, Nair CPV, Midgley R. Experimental progressive com­ pression neuropathy in the rabbit. Arch NeuroI1971;24:358. 38. Luttges MW, KelJy PT, Gerren RA. Degenerative changes in mouse sciatic nerves: electrophoretic and electrophysiologic characterizations. Exp NeuroI1976;50:706. 39. Cyriax

JH. Textbook of Orthopaedic Medicine,

vol 1, 8th edn.

Bailliere Tindall, London, 1982:37-39. 40. Lundborg G, Rydevik B. Effects of stretching the tibial nerve of the rabbit.] Bone Joint Surg 1973;558:390. 41. Sunderland S. Avulsion of nerve roots. In: Vinken PI, Bruyen GW (eds) Injuries of the Spille and Spinal Cord (Handbook of Clinical NeurologIj, vol 25). North-Holland, New York, 1976.

CHAPTER 2 - PRESSURE ON NERVES 31

42.

Rasminsky M. Ectopic generation of impulses in pathological nerve fibres. In: Jewett DL, McCarroll HR Jr (eds) Nerve Repair Ilnd Regenemtion - its Clinical Ilnd Experill1ental Basis, CV Mosby, St Louis, 1980: 178-185.

43.

Bissd10p P, De Coninck R, Ombregt L, Van de velde T.

Workbook for the Cyriax Course in Orthopaedic Medicine, Geneml COli cepts. Belgian Scientific Society of Orthopaedic Medicine, De Haan,

Belgium,

1985.

THIS PAGE INTENTIONALLY LEFT BLANK

CHAPTER CONTENTS Structural composition

Connective tissue

33

Connective tissue cells 33 Extracellular matrix (ECM) 34 Non-fibrous ground substance Fibrous elements 34 Vascularization 36 Innervation 36

34

Structures containing connective tissue

37

Trauma to soft connective tissue

43 Intr6duction 43 Inflammation 44 Repair 44 Remodelling 45 Self-perpetuating inflammation 45 Effects of immobilization on healing 46 Effects of mobilization on healing 47

Treatment of traumatic soft connective tissue lesions Muscular lesions 47 Tendinous lesions 50 Ligamentous lesions 52 Capsular lesions 54

STRUCTURAL COMPOSITION

47

Together with muscle, nerve and epithelium, connective tissue is one of the basic components in the human body. It binds structures together, helps in mechanical and chemical protection and also plays a principal role in reparative processes. For this reason it is important to have some basic knowledge of its structure and function in both normal and abnormal conditions. There are two main groups of connective tissue, each with a specific function: • •

ordinary (or general) specialized - cartilage and bone.

COlmective tissue consists primarily of cells and extra­ cellular matrix. The latter is, in turn, composed of fibres and amorphous ground substance. The density and composition of these basic elements differ according to function. For instance, not all types of cell are found in each tissue.

CONNECTIVE TISSUE CELLS Embryologically most arise from the relevant undifferen­ tiated mesenchymal stem cells.1 Fibroblasts are the major­ ity of cells in ordinary connective tissue and are involved in the production of fibrous elements and non-fibrous ground substance. During wound repair they are partic­ ularly active and migrate along strands of fibrin by amoeboid movements to distribute themselves through the healing area to start repair. Fibroblast activity is influenced by various factors such as the partial pressure of oxygen, levels of steroid hormones, nutrition and the mechanical stress present in the tissue. The other cell types characteristic of cOlmective tissue are macrophages, mast cells, plasma cells and pigment cells. Macrophages are large cells with two important roles: phagocytosis; and as director cells in regulation and remodelling. They therefore have a considerable role in the formation of scar.2 Mast cells play a role in the early stages of inflammation.3 Lymphocytes and leukocytes are more variable in nwnber but may increase considerably in pathological conditions. 33

34

SECTION O N E - G E N ERAL PRI NCI PLES

EXTRACELLULAR MATRIX (ECM) Non-fibrous ground substance This is composed of proteoglycans (a family of macromole­ cules) which bind a high proportion of water (60-70% ) and glycoproteins. The latter have a complex shape and are soluble polysaccharide molecules (glycosaminogly­ cans) bound to a central protein core. In cartilage, the proteoglycans are in turn bound to hyaluronan (a long chain of non-sulphated disaccharides) to form a proteo­ glycan aggregate - a bottlebrush three-dimensional structure (Fig. 3.1).4 Glycoprotein secures the link between proteoglycan and hyaluronan and also binds the components of ground substance and cells. The three-dimensional structure of the proteoglycan aggregates and the amount of water bound gives ground substance its high viscosity. A semi-fluid viscous gel is formed within which fibres and fibroblasts are embedded, so facilitating normal sliding movements between connective tissue fibres. In structures subject to high compression forces (e.g. articular cartilage), there is a large amount of proteoglycans but the content is rela­ tively small in tissues such as tendons and ligaments exposed to tension forces. Because of their negative charges, proteoglycans have three effects: •

• •

a large number of water molecules are bound (the degree of hydration of connective tissue is partially dependent on the number of proteoglycans) neighbouring molecules are repelled and the molecules stretch out the arrangement of positively charged collagen fibres is influenced: in load conditions, collagen moves but,

� ,,! I ��\I!

� m

;tl � I

T2

Figure 9.18

None

Continued.

)\

None

None

s: m Ii J: l> z n l>

r-

o VI o ;tl o m ;tl VI .....

\D VI

196 SECTION TWO - THE CERVICAL SPINE

feel. If some movements are painful, these are usually flexion and extension. As long as the pressure on the spinal cord is not considerable, symp toms alone domi­ nate the presentation and there are no root or cord signs. Increased compression leads to the appearance of cord signs: the plantar reflex becomes positive (Babinski's sign), spasticity may occur in upper and / or lower limbs, incoordination of the lower limbs makes it difficult to walk and extensive weakness may be detected when resisted movements are tested. An upper motor neurone lesion has developed. In several cases paraplegia may result. Figure 9.19

Posterocentral disc displacement.

trapezii or to both scapulae, although a slow painless development also occurs. Pain is the result of the pressure exerted on the dura ma ter (Fig. 9.19). If the compression continues and increases in severity, the spinal cord becomes involved and cord symptoms develop: paraesthesia is felt multi­ segmentally, usually distally in the limbs (upper as well as lower extremities). When conduction becomes impaired, cord signs appear - positive p lantar reflex (Babinski's sign), incoordination, spasticity, extensive weakness and sphincter dysfunction - which very soon become irreversible. History. Middle-aged or elderly people may complain of pain, fel t centrally or bilaterally and spreading from the occipu t to both trapezii and scapular areas. The onset is usually with cen tral neck ache, later on spreading up to the occiput and felt when the patient became tired, espe­ cially at the end of the day. Gradually the pain expands, radiating down to the interscapular area and later becom­ ing bilateral. There may come a time when both upper limbs star t to ache. Pain in the arms may alternate: if it is more severe on one side, it is correspondingly less so on the other. By this time the pain has become constant. Then pins and needles may appear in both hands, and some time later in both feet. Neck flexion may bring on or increase the pins and needles. The whole process may go on for several years. In the middle-aged or elderly patients a long painless development may also occur. The patient slowly devel­ ops pins and needles in all four limbs: they are usually felt in both hands and very often radiate into the lower limbs, from the front of both knees to the feet. Gradually the patient's gait may become disturbed. Weakness also appears in both hands. Examination. Articular signs may be quite inconspicu­ ous. Pain is constant but is not very much influenced by articular movements. If the patient is elderly, a full artic­ ular pattern of limitation may be found with a hard end-

Diagnosis. The history is immensely important because it is difficult to make the differentiation between a discal and a non-discal lesion. When the pain is the result of disc trouble, the patient will probably have had attacks of torticollis or of unilateral cervicoscapular pain in the past. Centralization of the pain as age advances, together with a painless full articular pattern on examination, suggests this type of disc lesion. When involvement of the spinal cord is suggested (mul tisegmental paraesthesia, gait disturbance), exami­ nation becomes decisive. A pattern is found that may resemble the full articular pattern in the sense that it is symmetrical, except that extension is usually more limited than expected and flexion may also be positive. Furthermore, flexion influences the pins and needles. The combination of history and functional examination indicates compression of the spinal cord, either by a posterocentral protrusion of disc substance or by a posterocentral osteophyte. It is difficult to distinguish the two clinically. The latter may be the result of longstand­ ing bulging of disc material, which has stretched the posterior longi tudinal ligament and p ulled up the periosteum, towards which new bone has grown. In osteophyte formation the evolution is, of course, very slow. When the posterior longitudinal ligament becomes adherent to the dura mater, neck flexion is a movement to avoid as it overstretches and can damage the spinal cord. Later in the course, the radicular arteries or the anterior spinal vascular channel may become compressed and can result in local degeneration of the spinal cord, leading to paraplegia. Differential diagnosis. When central or bilateral pain is present, great care should be taken to make a differential diagnosis from other lesions that may cause similar symptoms, although these are usual ly associated with a painful limitation of movement: arthrosis, spondylitic arthritis, rheumatoid arthritis, recent fracture, post­ concussional syndrome, disease of bone. In bilateral paraesthesia differential diagnosis must be made from sensory stroke and disseminated sclerosis.

CHAPTER 9 - MEC HANICAL DISORDERS 197

There is a tendency towards sponta. . neous cure but regression of the disc protrusIOn IS s Iow. 63

Natural history.

Posterocentral disc protrusions not compress­ ing the spinal cord can be reduced by ma�pulation, provided rotatory manipulations are aVOIded. !he . manipulation must be performed under suffiClent traction and by an experienced therapist. When symptoms and / or signs of spinal cord com �re �­ sion are present, manipulation is strongly contramdI­ cated and surgery is called for. Treatment.

DEGENERATIVE DISORDERS

Arthrosis of the cervical spine - usually called cervical spondylosis64 or spondylarthrosis - occurs very com­ monly in people over SO. Several studies over the last 60 years have shown that degenerative chan�es in bones and discoligamentous structures take place m 7S-90% of people in this age group.65-70 However, most authors emphasize that there is no consistent correlation between abnormal radiographic appearances and symptoms. 71 -73 From middle age on, degeneration is evident on plain X-rays in more than SO% of asymptomatic people?4,75 . The conclusion that pain originates from degeneratIon of the cervical spine is all too often made by looking at radiographs alone. The importance of arthrotic changes is overestimated because, in most instances, the degenera­ tive condition is, in itself, not painful and leads only to some stiffness. It is the clinician's task to determine the relationship between the degenerative changes and the patient's symp tom.76,77 . . It is important to diagnose cervIcal spondylosIs o n clinical grounds, after a careful examination. This sh ?ws limitation of movement in the capsular proportIOns whereby the movements are merely uncomfortable at the end of range - a clear full but p ai nless articular pattern - with a hard end-feel. When the cervical move­ ments influence the patient's symptoms, the problem lies within the spine but does not necessarily imply that the arthrosis is responsible. Degenerative disorders that cause pain do of course exist, but the hist �ry he �ps to . recognize them: the behaviour of the pam mdIcates whether the condition is arthrotic or not. A disc protru­ sion, for example, may also occur at an arthrotic joint, giving rise to the same symptoms as a disc �isplacement in a normal joint and in that case the dISC has to be treated. A number of less common clinical pictures can be attributed to the effects of arthrosis and give rise to local . root pam . or mye 1opathy.78 pam, •

Headache: this may have multiple causes and is described in Chapter 11.

• •

•

•

•

Vertigo: the cause may lie within the vertebrobasilar system and also within the ear (see p. 232). Pain in the neck: this is usually the resul t of a disco dural interaction at the lower cervical spine and must be described as such (see earlier - Disc disorders). Drop attacks: these are often the result of � n upper . cervical hypermobility, from a rheumatOId condItIOn (see p. 21S). . Radiculopathy: although a radicular syndrome IS by far most commonly caused by a discoradicular inter­ action (see earlier), it may have several other causes, of which one is spondylosis (see p. 199). Myelopathy: this is usually the result of a degenerative condition (see p. 200).

LOCAL PAIN Pain in the neck, either unilateral or bilateral, with or without radiation to the head, occurs in degenerative conditions affecting the upper cervical ligamentous complex or the facet joints. This takes place in ar t�rosis of . the upper two cervical joints, in subacute ar �hntls of u:e atlantoaxial joint, in facet joint arthrosis or m traumatic osteoarthrosis. Arthrosis at the upper two cervical joints, leading to ligamentous contracture with morning headache in the elderly

As age advances increasing pain develops in the C1-C2 dermatomes: it usually starts in the middle of the upper neck, spreads to the occiput, to the vertex (C1) and /or to the temples and forehead (C2). Local pain may be totally absent, so that the patient complains of occipitofrontal headache only?9,80 The main symptom is p ain on waking. This happe �s without fail every morning. After some hours the pam begins to diminish and by midday all symptoms have ceased, to return the next day. Later in the course, the p ai n may last longer into the day. . On examination a full articular pattern IS found. Rotation and lateral flexion are especially limited. They are not very painful but merely uncomfortable. �he end-feel is rather hard, but not bone-to-bone, showmg capsular contracture. , Radiography demonstrates a certain degree of arthrosis, normal for the patient's age. . The differential diagnosis is between traum atIC osteoarthrosis and postconcussional headache. In both, the history is distinctive (see pp. 199 and 204). . . The condition is very easily cured by mampulatIOn: one to four sessions of slow capsular stretching make all symptoms disappear. Age is not a contraindication to manipulation but the older the patient the more gradu-

198 SECTION TWO - THE CERVICAL SPINE

Box 9.12 Morning headache in the elderly

Left

flexion side flexion

• Headache on waking • Full articular pattern • Good response to slow stretching manipulation

Right

side flexion

ally the therapist must work: fewer manoeuvres are done in one session and the interval between the sessions longer (see p. 268 and summary in Box 9.12). Subacute arthritis of the atlantoaxial joint

Subacute arthritis of the atlantoaxial joint is quite rare.81 A man, aged between 25 and 40, develops stiffness and discomfort in the middle of the upper neck and over the following weeks these symptoms gradually increase. On clinical exa mination extension, both side flexions and flexion movements are f ull and painless. Both rota­ tions are equally painful and very limited - only 10-20% is possible. Even in a supine position, the range remains unchanged. The end-feel is soft. This combination of symptoms and signs is clearly a warning sign but further investigations remain negative. There has been no sore throat, no swollen glands or mastoid tenderness, no evidence of ankylosing spondyli­ tis and no fever. Blood examination and radiography are also negative. The diagnosis is not clear and remains tentative. Because only the rotations and no other movements are impaired, the lesion must lie at the joint at which only rotation movement can take place, i.e. between C1 and C2. As the condition recovers when anti-inflammatory therapy is g iven, the cause m ust be non-specific infla mmation.

extension

Figure 9.20

The convergent partial articular pattern in arthrosis at a facet joint (colour indicates pain).

Troisier82 distinguishes a convergent and a divergent pattern of painful movements (Figs 9.20 and 9.21). In the first, there is pain on extension and on lateral flexion and rotation towards the painful side. In the second, the opposite is found: f lexion, lateral flexion and rotation away from the painful side. Such a pattern is compatible with facet joint involvement but does not exclude an ordinary disc displacement. Differentiation between these lesions is sometimes difficult. This condition (summarized in Box 9.13) responds to deep transverse massage at the joint capsule and slow stretching manipulation. Infiltration with a steroid suspension is an alternative.

Arthrosis at a facet joint

Arthrosis at the facet joints occur in all patients from middle age on but rarely provokes symptoms. The only findings on examination are a full but painless articular pattern, indicating generalized spinal arthrosis. Occasionally pain develops as the result of the forma­ tion of adhesions and 'self-perpetuating inflammation', following an overstretching of the arthrotic joint capsule. The lesion usually lies at the levels C3-C4 and C4-C5. The pain has a spontaneous onset, is unilateral mid­ cervical and does not spread. Dural symptoms are absent. Pain is felt when certain positions have to be maintained for a period of time. When the facets are bilaterally affected the pain may be bilateral without pain in the centre of the neck. On exa mination, a partial articular pattern is found: some movements, especially the passive ones, hurt. The end-feel is rather hard. The facts that the pain is quite localized and that it does not radiate indicate the possi­ bility of a facet joint lesion.

Left

flexion

Right

extension

Figure 9.21

The divergent partial articular pattern in arthrosis at a facet joint (colour indicates pain).

CHAPTER 9 - MECHANICAL DISORDERS 199

Box 9.13 Arthrosis of a facet joint --

• Unilateral mid-cervical pain • Partial articular pattern: convergent or divergent? • Treatment: steroid infiltration / deep transverse massage / slow stretching manipulation

It is unusual to find rheumatoid arthritis affecting the cervical facet joints only, without involvement of the other parts of the cervical spine. Two unusual findings draw attention to the possibility of monoarticular arthri­ tis of unknown origin. First the patient, who is between 30 and 50, complains of constant aching in the midcervi­ cal area which is felt to both sides but not in the centre of the neck. Second when the head is moved passively, a soggy end-feel surprises the examiner. Intra-articular injections (one or two) may abolish the pain for several years. Post-traumatic osteoarthrosis

If after a severe injury the patient gradually develops limitation of movements according to the full articular pattern, traumatic osteoarthrosis is likely. On examination, limitation of active and passive movements is found. Because the condition occurs only in patients who are claiming compensation, it is not clear whether the pain is of organic origin. Treatment is difficult.

RADICULAR COMPLAINTS: OSTEOPHYTIC ROOT COMPRESSION A nerve root can become compressed at the point where it leaves the intervertebral foramen. Pressure is exerted either from the anterior aspect by an osteophyte derived from the uncovertebral joint or posteriorly by one origi­ nating from the facet joints, or from both (Fig. 9.22).

These phenomena are very often secondary to degen­ eration of the intervertebral disc. As it loses height, the bony contact between on the one hand the uncovertebral joints and on the other hand the posterior joints increases and osteophytic outgrow results causing diminution of the diameter of the intervertebral foramen.s3 The patient is over 50 years of age and does not com­ plain of much pain. There is none in the neck, merely some stiffness, and the scapular area may or may not hurt a little. Slight root pain may be present for several months and paraesthesia may occur. The patient's complaint is that the arm gradually became weak. On examination, a full but painless articular pattern is found: movements are limited with a hard end-feel, indi­ cating arthrosis. If any movement does hurt, it is usually side flexion towards the affected side, and a twinge may go down the arm. Alternatively, waves of paraesthesia may be felt in the distal part of the relevant dermatome and are clearly the result of the osteophyte being pushed against the nerve root. When resisted movements of the upper limb are performed, gross weakness is found of the muscles belonging to one segment. The most frequent localization is C4-C5. A combination of higher uncinate process, smaller anteroposterior diameter of the interver­ tebral foramen, and a longer course of the nerve root in close proximity to the uncovertebral joint may explain the predilection of nerve root compression at this level.s4 The C5 nerve root thus becomes compressed, identified by the difficulty or sometimes even inability to bring the arm up. In severe cases, the abductor muscles of the shoulder may become wasted. The differential diagnosis is from root compression by a disc protrusion or by a neuroma or metastases and can easily be made on a clinical basis (Table 9.1). The osteo­ phyte grows very slowly and often lies quite far laterally so that it does not exert pressure on the dural investment of the nerve root. Therefore pain, as would occur in a dis­ coradicular interaction, is seldom present. The patient complains mainly of paraesthesia and of a progressive weakness of the upper limb developing over the course of a few months. Nerve root compression by a disc Table

9.1 Differential diagnosis between discal and osteophytic root

compression

Disc History

Examination

Osteophyte

>35 years of age

Elderly: >50 years of age

Shifting pain (scapula > arm)

Arm pain

Typical evolution

No evolution

Intense pain

Slight pain

Pain > weakness

Weakness > pain

Partial articular pattern

Full articular pattern Compression pain

Figure 9.22

Osteophytic nerve root compression.

Subtle weakness

Serious weakness

C7 root

C5 root

200 SECTION TWO - THE CERVICAL SPINE

protrusion is also characterized by a definite chronology: a certain period of bouts of multisegmental pain, referred to the scapular area, is followed by the occurrence of segmental pain, followed by segmental paraesthesia and often moderate neurological deficit of the muscles belonging to the same segment. The condition undergoes spontaneous cure in 2-3 months. A neuroma usually starts in the opposite way: distal paraesthesia, followed by pain, starting distally and spreading in a proximal direc­ tion. Root pain because of a neuroma typically occurs in younger people and root pain from a disc lesion occurs more frequently in middle-aged people. A tumour or metastases leading to root compression usually has a quicker progression than an osteophyte. The diagnosis can be confirmed by radiography of the relevant foramen. Anteroposterior and oblique views show the encroachment. Both views are always taken as a rou tine measure. The uncovertebral osteophytes are best seen on an anterior picture and the posterior os teo­ phytes on an oblique one. When the clinical diagnosis of an osteophytic root palsy h as been made and the X-ray confirms its presence, the diagnosis is clear. Nevertheless, it should be borne in mind that an asymptomatic osteo­ phyte may be seen on radiography. The clinical examina­ tion is decisive. When there is gross muscular weakness or weakness has a tendency to increase, surgical removal of the bony outcrop is indicated. Manipulation is, of course, contra­ indicated. Two infiltrations of triamcinolone suspension around the nerve root - nerve root block - at an interval of 2 weeks may be tried. It alleviates the inflammation at the level of the compressed nerve root, so that the pres­ sure diminishes.8s The discomfort disappears but the anatomical situation has not changed.

COMPRESSION PHENOMENON: THE MUSHROOM PHENOMENON This phenomenon is extensively described in later chapters on the thoracic and lumbar spine (see p. 649 and p. 791) and is summarized in Box 9.14. A cervical mushroom phe­ nomenon is very rare. It occurs in advanced degeneration of the disc, which displaces mainly in the anterior and anterolateral directions. The intervertebral space becomes so narrow that the vertebral bodies lie in apposition. This phenomenon, together with the folding of the posterior longitudinal ligament and the enlargement of the arthrotic facet joints, can cause considerable narrowing of the spinal canal and the lateral recess, which may result in compres­ sion of dura or nerve root during axial loading. An elderly patient declares that there are no symptoms as long as recumbency is maintained: in that position the head can be easily moved in every direction without any problem. However, on standing or sitting for a certain

Box 9.14 The mushroom phenomenon • • • • •

Elderly patient Increasing pain in any position, except lying Diminution of symptoms under traction Full articular pattern Radiographic evidence

amount of time, vague, central and bilateral pain in the neck develops. When the vertical position is maintained, both a vague ache in both arms and paraesthesia in the hands may develop. The symptoms disappear when trac­ tion is applied or the head lifted upwards with the hands. On examination, a full articular pattern is found: pain­ less limitation of movement with a hard end-feel. There are no radicular signs and no cord signs; consequently the diagnosis rests mainly on the history. A radiograph shows severe arthrosis with gross narrowing of the intervertebral space. The patient can be helped either by a weight-relieVing collar or by surgery (arthrodesis).

CERVICAL SPONDYLOTIC MYELOPATHY The term means that the spinal cord has become com­ pressed as the result of diminution of the diameter of the spinal canal, which leaves insufficient space for the cord.86 The condition has only been recognized relatively recently as a clinical entity,S7 although it is the most common cause of spinal cord dysfunction in middle-aged and elderly patients.88 Narrowing of the spinal canal is less frequent in the cervical than the lumbar spine. The anteroposterior diam­ eter of the cervical spinal cord is 10 mm on average and the sagittal diameter of the spinal canal at the level of C4 averages 17.7 mm. So there is a large safety margin and symptoms will only occur when the reduction of the spinal canal has become quite significant.89,9o The role of a narrow cervical spinal canal has been investigated in relation to clinical syndromes. Three groups can be dis­ tinguished on the basis of initial developmental antero­ posterior diameter before the onset of spondylosis .91 •

•

•

Those with diameters between 10 and 13 mm who would only sustain a narrowing of 2-4 mm before developing myelopathy. Those with diameters between 13 and 17 mm would not be at risk of myelopathy but might have symp­ toms because of spondylotic changes. Those with a diameter greater than 17 mm would tolerate spondylosis without symptoms.

Clinical features

In its most severe form the clinical presentation is a spastic gait. Sometimes atrophy, sensory disturbance and

CHAPTER 9 - MECHANICAL DISORDERS 201

spasticity in the hands occur, with impairment of the function of the sphincters. But symptoms of myelopathy may, of course, occur in a wide variety of combinations.92 The variable clinical picture reflects the many complex factors that may affect the spinal cord. Some authors make a distinction between a mechani­ cal and a vascular cause of myelopathy.93,94 The former may be caused by a direct mechanical compression of the spinal cord by osteophytes or a degenerated disc, or by a combination of the two. This is the most common cause in patients over 55 years.95 Ischaemia of the anterior spinal artery or of the cord could result from osteophytic compression directly against the spinal cord. In foraminal osteophytosis the radicular vessels, which contribute to spinal cord perfusion and which accompany the nerve root sleeve, could also become involved. This vascular theory is not however widely accepted. Some believe that a combination of both mechanical and vascular causes has to be considered.96-98 Studies by Ferguson and Caplan delineate four different syndromes.99 •

• •

•

Lateral or radicular: the patient complains mainly of symptoms that are in accordance with the nerve root involved Medial or myelopathic: the patient presents with long tract signs only Combined (also called myeloradiculopathy): the patient experiences lower motor neurone involvement100 (root symptoms) at the level of the lesion - of ten unilateral ­ as well as upper motor neurone signs (cord signs) below, including the lower levels of the upper limbs ­ mostly bilateral; this is the most common presentation Vascular: this seems to be the rarest.

More recently, cervical spondylotic myelopathy has been implicated as a cause of painless weakness in the upper extremities without accompanying symptoms in the lower extremities, thus adding a fifth clinical presen­ tation - the anterior syndrome. This may be the result of a disc protrusion compressing only the anterior horns of the grey matter of the spinal cord.36,lOl-103 It is not illogical to believe that the cause of compres­ sion is multifactorial, involving developmental, degener­ ative and biomechanical factors (Fig. 9.23). •

•

Developmental factors: a congenital narrow spinal canal,1 04,105 short pedicles, low laminer arches could be predetermined.106, 1 07 Arthrotic changes: posterior osteophytosis, fibrosis or ossification of the posterior longitudinal ligament, hypertrophy of the facet joints, hypertrophy of the lig­ amentum flavum and disc degeneration all may lead to cord compression. Another mechanical theory states that the spinal cord is pulled by the tension in the

-::::::I-

_ _ _ _ _ _

-,--

_ _

Iigamentous hypertrophy

posterocentral disc displacement anterolithesis

Figure 9.23

•

Mechanisms of narrowing of the spinal canal (sagittal section).

dentate ligaments, which are tensed by an anterior spondylotic bar.1°8 Biomechanical factors: diminu tion of the diameter of the spinal canal occurs during extension (because of folding of the posterior longitudinal ligament and of the ligamentum flavum)109 and during flexion (the spinal cord is pulled against the osteophytes) Yo Degenerative spondylolisthesis may sometimes cause excessive movement during flexion / extension and so lead to cord compression.lJ1

Deformed unconvertebral

Protruding disc osteophyte or OPLL

Deformed unconvertebral

Yellow ligament Figure 9.24

Mechanisms of narrowing of the spinal cord (coronal section).

202 SECTION TWO - THE CERVICAL SPINE

Teresi et ai 11 2 have shown by MRI that the spinal cord can tolerate quite extensive compression by osteophytes or a disc without any clinical manifestation of myelopa­ thy. Therefore symptoms can depend on different factors: the degree, duration and constancy of the compression. Diagnosis Symptoms. The patient describes a picture of increasing disability over an extended time. A typical complaint is loss of dexterity in the upper extremity, difficulty in writing and abnormal sensations in the hand, which may become clumsy .113 Surprisingly, neck pain is not as common a symptom as one m ight expect. 114,l15 Paraesthesia and / or numbness are often felt in one or both hands and / or feet and indicate a multisegmental distribution; they are made worse by neck flexion. A feeling of weakness soon follows. Patients may also com­ plain of difficulty walking, and of feeling very unsteady on their feet and they often lose their balance. Signs. Examination reveals a gross full articular pattern of limitation of movement with a hard end-feel, suggest­ ing severe arthrosis. Compression of the spinal cord leads to spastic paralysis distal to the level of compression. There is also hyperreflexia, clonus at the patella and ankle and disturbance of coordination and gait, which becomes stooped, broad-based and somewhat jerky.88 This gait is one of the main characteristics of cervical myelopathy (Box 9.15). In a combined compression of nerve root and spinal cord - called 'myeloradiculopathy' - a weak, non-spastic paralysis in a certain segment of the upper limb and a spastic paralysis below that level may be found.1l 6 The weak paralysis is typical of a lesion of the lower motor neurone and the spastic paralysis indicates a lesion of the upper motor neurone. For example in a lesion at the C4 level, with compression of both C5 nerve roots and of the spinal cord at that level, everything above C5 is normal. C5 shows weakness of abduction and external rotation of the shoulder and some weakness of flexion of the elbow. There is no spasticity and the biceps jerk is sluggish or absent. Below C5 there is spasticity, with clonus and hyperreflexia; the triceps jerk is exaggerated and there is a clonus at the patella and ankle.

Box 9 . 15 Motor findings

Lhermitte's sign is present in one-quarter of myelo­ pathic patients:l17 generalized paraesthesia in trunk and / or extremities at the end of a forced flexion or exten­ sion movement of the cervical spine.11 8-1 20 Ono et ai described the finger escape sign and grip and release test as useful in the myelopathic hand syndrome. The finger escape sign is positive when the patient is asked to hold the fingers of the hand in extension and adduction, and the two ulnar fingers fall into flexion and abduction within 30 seconds. In the grip and release test, the patient is asked to repeatedly make a fist and then rapidly release all fingers into extension. A normal patient should be able to perform this movement 20 times in a 10-second period.l2 l In addition, sensory disturbance is very often present. There may be loss of contralateral pain and temperature sensation because of compression of the spinothalamic tract. The neurological level is several segments below the area of compression. I psilateral proprioception and vibration sense may be disturbed as a result of a lesion of the posterior columns. Dermatomal sensation (appreciation of light touch as well as tactile discrimination in pin prick tests) can be affected by a dorsal nerve root compression.122 These sensory findings are summarized in Box 9.16. Later Babinski's sign appears. On the whole, it is a late feature and the detection of clonus or other evidence of hyperreflexia and spasticity of the lower limb, even if the plantar reflex is negative, should direct attention to the possibility of a cord lesion. Other positive reflexes are: Oppenheimer extensor plantar response on stroking the tibia and Hoffman's reflex (reflex finger and thumb flexion with sudden middle finger distal interphalangeal joint extension). Shimizu et ai described the scapulohumeral reflex, which is positive in more than 95% of patients with high cervical cord compression.1 23 This reflex is elicited by tapping the tip of the spine of the scapula, and the test is positive if there is a brisk scapular elevation and abduction of the humerus. The upper skin reflexes (abdominal and cremaster reflex) tend to diminish or disappear. Nurick has classified cervical spondylotic myelopa­ thy largely on the basis of gait abnormality - typically the most common clinical concern of the patient (Table 9.2).1 24,1 25 The Japanese Orthopaedic Association (JOA) has devised a scale to quantitate neurological involvement (Table 9.3). In this, motor functions in the arms and legs are

• Normal above the level of the lesion • Lower motor neurone signs at the level of the lesion

Box 9.16 Sensory find i ngs

(often uni lateral)? • Upper motor neurone signs below the level of the lesion (mostly bilateral) • Abnormal gait

• • • •

.-

Distal to the level of compression Touch often remains normal Possible diminution of contralateral pain and temperature Possible diminution of proprioception and vibratory sense

CHAPTER 9 - MECHANICAL DISORDERS 203

Table 9.2

Nurick's classification of disability i n spondylotic myelopathy

Grade

Symptoms and signs

o

Root symptoms and signs No evidence of cord involvement Signs of cord involvement Normal gait Mild gait impairment Able to be employed

III

Gait abnormality prevents employment

IV

Able to ambulate only with assistance

V

Chair bound or bedridden

each graded from 0 to 4; sensation in each of the arms, the legs and the tnmk are graded from 0 to 2; and bladder func­ tion is graded from 0 to 3. The maximum number of points is 17 (normal).1 26--128 Severity of myelopathy is mainly assessed by long tract signs. 129 Natural history

Compression usually takes place at the anterior aspect of the spinal cord (corticospinal tracts and anterior horn cells), where it causes dysfunction, ischaemia and proTable

gressive degeneration, which in the end elicits the symp­ toms and signs. Involvement of the lateral and posterior funiculi usually follow later in the development.l3O There is relative preservation of the anterior columns.l3l Loss of dexterity is one of the first symptoms. The gait soon becomes disturbed in a way that is characteristic: an unsteady walk, stooped, wide-based and somewhat jerky. The appearance of paraesthesia and / or numbness in both hands and / or both feet confirms that there is spinal cord compression. Neck flexion may augment pins and needles. Weakness and atrophy of the upper extrem­ ities then occur with clumsiness of the hands, which may eventually becomes completely incapable. Finally, absence or impairment of sphincter control may complete the picture (see Box 9. 17). Differential diagnosis

It may be very difficult to differentiate patients with early motor neurone disease or demyelinizing disorders from those who have myelopathy caused by cervical spondyl­ osis and / or stenosis. Thorough neurological examination is therefore necessary. The main possibilities are: •

Multiple sclerosis: the patient also experiences paraes­ thesia, and spasticity; spastic paralysis and clonus are also found.

9.3 Assessment scale for cervical spondylotic myelopathy proposed by the Japanese Orthopaedic Association

I . Motor dysfunclion of the upper extremity

Score

Function

o

Unable to feed oneself

1

Unable to handle chopsticks Able to eat with a spoon

2

I I . Motor dysfunction of the lower extremity

Handle chopsticks with much difficulty

3

Handle chopsticks with slight difficulty

4

None

o

Unable to walk

1

Walk on flat floor with walking aid

2

Up and/or down stairs with handrail

3

Lack of stability and slight widening of stance

4

None

o

Severe sensory loss or pain

I I I . Sensory deficit A. The upper extremity

B. The lower extremity

C. The trunk

IV. Sphincter dysfunction

1

Mild sensory loss

2

None

o

Severe sensory loss or pain

1

Mild sensory loss

2

None

o

Severe sensory loss or pain

1

Mild sensory loss

2

None

o

Unable to void

1

Marked difficulty in micturition (retention, strangury)

2

Difficulty in micturition (increased frequency without increased amount, heSitation)

3

None

204 SECTION TWO - THE CERVICAL SPINE

Box 9.17 Summary of cervical spondylotic myelopathy

Age > 55 years Typical motor findings: Possibly lower motor neurone findings at the level of the lesion Upper motor neurone findings below this level Typical reflex findings: Decrease of upper skin reflexes Increase of lower skin reflexes Hoffman's reflex Shimizu's reflex Sensory changes are confusing because of multiple tract involvement Characteristic gait Sphincter dysfunction

•

• •

Amyotrophic lateral sclerosis: a disorder of the anterior horn cells and of the pyramidal tract (first motor neurone). Usually found betweeen 40 and 60, in one (commonly upper) limb. Advances progressively to the contralateral upper and later the lower limbs. Depending on the localization in the upper or lower motor neurone, spastic or weak paralysis will pre­ dominate. The classic triad is atrophic weakness of the hand and forearm muscles, minor spasticity of the legs, and generalized hyperreflexia, but no presence of sensory changes.? Cerebrovascular disorders that cause spastic hemiplegia. Spinal tumours: space-occupying lesions in the spinal canal, may lead to transverse myelopathy with bladder dysfunction and motor and / or sensory deficit.132 (see Box 9.1 8 for summary ).

Treatment

Once narrowing has occurred, surgery becomes the treatment of choice,133, 134 even in old patients.B5 When myelopathy is caused by aetiological factors that are either unchangeable by nature, such as developmental canal stenosis, or progressive, such as ossification of the posterior longitudinal ligament, surgical treatment should be considered.B6-140 Patients who are treated by surgery seem to have better outcomes.141-1 43 Even gait and equilibrium may improve.144 Prognosis is good when the diagnosis is made early in the course but poor in late diagnosis, when

myelopathy h as become more severe.145 Age and abnormal cervical curvature also seem to predict less neurological improvement.146 Prevention of spinal cord compression is possible by systematically manipulating every posterocentral disc displacement when it occurs. Early reduction pre­ vents the formation of osteophytes within the spinal canal.

CAPSULOLIGAMENTOUS DISORDERS

Capsuloligamentous disorders of the cervical spine are sometimes described under the heading 'postconcus­ sional syndrome'. It is a term used to describe the headache, occipital or upper cervical pain that remains after an accident that resulted in concussion and which m ay also sprain the upper cervical ligaments and, less often, the muscles. Because th e patient is usually confined to bed for a while, early movement, necessary for good healing of the ligaments, does not take place and adhesions have a chance to form. After the brain problem has resolved, the patient is left with occipital and upper cervical pain.

As the patients are very often claiming compensation, the examiner has to take into account the possibility of neurosis or aggravation. Careful history taking and clinical examination should enable the examiner to come to a precise diagnosis. When the patient presents a history with inconsistencies or unlikely combinations of findings and this is followed by an examination during which the signs do not correspond, the patient is probably confabu lating. However, when adhesions in the occipitoatlantoaxial ligaments are responsible, the picture is one of pain at the extremes of extension, both rotations and both lateral flexions. The condition can easily be treated by manipulation. One to three sessions of quick stretch manipulations break the adhesions, after which all symptoms should disappear.

DISORDERS CAUSING PAIN ON RESISTED MOVEMENTS OF THE NECK

MUSCULOTENDINOUS LESIONS Box 9. 18 Diffe rential diagnosis of cervical spondylotic myelopathy

Multiple sclerosis Amyotrophic lateral sclerosis Cerebrovascular disorders Spinal tumours

The presence of a clear contractile tissue pattern is suggestive of a musculotendinous lesion but this is not common in the region of the neck. Only two conditions are rarely encountered, a lesion of the semispinalis or splenius capitis muscle and a lesion of the longus colli muscle - retropharyngeal tendinitis.

CHAPTER 9

Lesions of the semispinalis or splenius capitis muscle

It is understandable that a patient, who has had an acci­ dent severe enough to cause concussion, may also suffer from musculotendinous lesions in the suboccipital muscles. This is infrequent but after recovery from con­ cussion the patient may be left with unilateral or bilateral occipital pain, sometimes radiating to the head. In most instances, a lesion of the occipital muscles does not occur in isolation but in combination with a lesion of the occipitoatlantoaxial ligaments. On examination, resisted movements are positive. In unilateral pain, resisted extension and resisted side flexion towards the painful side are both painful. In bilateral cases, extension and flexion to both sides may be positive. Palpation shows the lesion to lie at the insertion of the semi­ spinalis capitis muscle, rarely at that of the splenius capitis. Treatment consists of two or three sessions of deep transverse massage. In more chronic cases, up to 6 weeks' treatment may be required. Lesion of the longus colli muscle (retropharyngeal tendinitis)

The condition was first described in 1966 in a series of 12 patients of all ages. 147 Biopsy material from one revealed amorphous chalky material. The history and clinical examination are very character­ istic. The patient quite suddenly develops a severe, bilateral pain occupying the whole head and neck and can hardly move the head. Swallowing is very painful and coughing hurts so much that the head is held with both hands. After a few days the pain diminishes and disappears over the course of 10 days. There may be a complaint of fever. On examination a full articular pattern of limitation of movement is found on active testing. Passive movements show a different pattern: when they are done gently, flexion and both side flexions can be performed to full range. Extension and both rotations remain very limited. Resisted rotations and flexion are painful. The lateral r adiograph shows a calcified deposit lying at the anterior aspect of the body of the axis and thickening of the shadow, thrown by the longus colli muscles,148 such that it increases from the usual 3 mm to 10 or 15 mm.

-

MECHANICAL DISORDERS 205

Differential diagnosis must be made with a retropha­ ryngeal abscess, which may present in the posterior tri­ angle of the neck or in the supraclavicular area. Abscesses usually result either from tuberculosis or as a complica­ tion of cervical discography. The condition undergoes spontaneous cure.

SERIOUS DISORDERS Resisted movements of the neck may be painful and / or weak in more serious conditions, because the muscular contraction pulls at an affected structure (i.e. bone) or squeezes a tender structure (i.e. inflamed lymph glands or abscess). This combination of signs has to be consid­ ered a warning sign. The possible conditions are: • • • • • • • •

Vertebral metastases Fracture of the first rib Fracture of the spinous process of C7 or T l Wedge fracture of a vertebral body Glandular fever Retropharyngeal abscess Postconcussional syndrome (see p. 204). Lesion of the sternoclavicular joint (see Ch. 23 ).

DISORDERS CAUSING SYMPTOMS O N ACTIVE ANDIOR RESISTED SHRUGGING OF THE SHOULDERS

Some conditions i n the shoulder girdle may provoke symptoms - pain or paraesthesia - in the pectoroscapu­ lar area which is first examined as part of the neck, and signs - limitation or weakness - on cervical examina­ tion. These lesions are extensively discussed in Section 4 (pp. 385-414). They are: • • • • • • • •

Lesion of the costocoracoid fascia Lesion of the sternoclavicular joint Lesion of the first costotransverse joint Lesion of the conoid / trapezoid ligament Lesion of the subclavian muscle Lesion of the levator scapulae muscle Thoracic outlet syndrome Upper lung disorder (warning sign).

REFERENCES 1 . Horwitz T. Degenerative lesions in the cervical portion of the spine. Arch Intern Med 1940;55:1178. 2. Brain WR, Northfield D, Wilkinson M. The neurological manifestations of cervical spondylosis. Brain 1952;75:13. 3. Kellgren JH, Lawrence JS. Rheumatism ill miners, part II: X-ray study. Br J Indust Med 1952;9:197. 4. Pallis C, Jones A, Spillane J. Cervical spondylosis. Incidence and implications. Brain 1954;77:274.

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CHAPTER CONTENTS

Classification

Non-mechanical disorders

211

Warning signs

212

Osseous disorders

212

Fractures and luxations Bony tumours 213

212

Rheumatoid arthritis and ankylosing spondylitis

Rheumatoid arthritis 216 Ankylosing spondylitis 217 Cricoarytenoid joint involvement Infections

216

Non-mechanical disorders behave differently from mechanical disorders. Although they usually give rise to symptoms felt in the moving parts of the body, they are often not related to activity, movement or posture. This means that the symptoms are not elicited or influenced by movement of the affected part. Symptoms are felt constantly or according to an irregular pattern.

217

217

Intraspinal tumours

217

Extradural tumours 217 Intradural extramedullary tumours Intramedullary tumours 219

218

Neurological conditions with positive signs on neck examination 219 Visceral conditions

WARNING SIGNS

219

Shoulder girdle disorders causing cervicoscapular pain

219

Warning During history and clinical examination, symptoms and signs may come forward which, because of their unusual behav­ iour, put the examiner on his guard. An unusual disorder should immediately be suspected and further complemen­ tary examinations (blood tests, radiography, CT scan, bone scan, MRI) should be sought.

Warning signs disclosed by the history Gradually increasing pain. This can occur in disc lesions but only over a short period of time, after which the pain remains unaltered for a certain period and then diminishes again. If, in contrast, the intensity of the pain increases progressively, a serious lesion is likely. Expanding pain. The pain may start in the centre of the neck, then become bilateral and spread to the scapular area, and finally radiate down one upper limb and then the other. Another possibility is pain developing in one dermatome and then spreading beyond its borders into other dermatomes. Also unusual is an increase of scapu­ lar pain together with an increase of brachial pain. Pain that expands gradually indicates a lesion that expands, e.g. tumour, metastases. Such histories are completely different from shifting pain that starts in the neck, and is later left in the arm thereby remaining monoradicular, which is so typical of a disc problem. Bilateral arm pain. When this occurs at the same level, it shows that both nerve roots are involved, which sug­ gests a non-discal origin. Arm pain in a person younger than 35. Root pain as the result of pressure by an ordinary cervical disc is very 211

212 SECTION TWO - THE CERVICAL SPINE

unusual in this age group, and thus another cause has to be sought. Arm pain lasting longer than 6 months. Root pain caused by a disc usually undergoes spontaneous cure in 3-6 months, depending on the size of the protrusion. If the pain lasts longer it is therefore suspicious. Warning signs disclosed by the functional examination Full articular pattern. Apart from painless limitation seen in elderly patients, which is the result of normal degeneration of the cervical spine, a full articular pattern points to a serious disorder. Muscle spasm on passive movements. Involuntary muscular contraction stops the movement-even when performed extremely gently-with a sudden jerk, thereby protecting the cervical spine against further painful and possibly harmful movement. This phenome­ non never occurs in ordinary disc lesions and is therefore always suspicious. Resisted movements of the neck painful and weak.

Any attempt to contract the muscles against the exam­ iner's resistance is immediately stopped because it is too painful. Normal strength is not apparent and the move­ ments are thus interpreted as being weak. This is always a sign of a serious disorder. Resisted movements may be painful in acute discal conditions but are never weak. Side flexion away from the painful side is the only painful movement. As mentioned earlier this partial

articular pattern is always suspicious and suggests a costoscapuloclavicular lesion or a lesion in the apex of the lung. Scapular elevation limited. Limitation of this move­ ment is extremely rate. When it is found the examiner should perform a more thorough examination of the shoulder girdle and upper thorax. Horner's syndrome. This may result from involvement of the cervical sympathetic ganglia at the base of the neck by a tumour in the thorax or in the superior pulmonary sulcus. There is miosis, blepharoptosis, enophthalmus and ipsilateral decreased sweating (anhydrosis). Hoarse voice. Paralysis of the vocal cords gives rise to a typical hoarseness (releases of much air). The cause may be local lesions or involvement of the recurrent laryngeal nerve by an invasive lesion in the neck or upper thorax. T1 palsy. A palsy of the first thoracic nerve root leads to atrophy and weakness of the intrinsic hand muscles, which is always of non-discal origin. It is often one of the first signs of amyotrophic lateral sclerosis. Excessive loss of power. Root compression as the result of a protruded disc results in a slight muscular paresis. When more extensive paralysis is found, the condition is by definition serioud. Two or three nerve roots involved. Root syndromes as the result of a disc lesion are strictly monoradicular. A disc lesion at two levels is very rare but not impossible.

Involvement of two or more nerve roots, however, sug­ gests a more serious cause. Muscular weakness in the absence of root pain. In a discoradicular interaction, segmental pain-the result of the dural sleeve being compressed-is one of the most important features, followed by paraesthesia and possi­ bly neurological deficit. Wrong time sequence. Root pain starting distally and later moving proximally or distal paraesthesia occuring before the root pain starts again makes a discal problem very unlikely. When the two elements, segmental pain and a strict time sequence, are not present a non-discal cause is suggested.

CLASSIFICATION

Non-discogenic lesions which give rise to symptoms in the neck, trapezius or scapular area or in the upper limb can be classified into the following groups: • • • • • • • •

Osseous Rheumatoid arthritis and ankylosing spondylitis Infectious Intraspinal Neurological Visceral Psychological Other

OSSEOUS DISORDERS FRACTURES AND LUXATIONS

A considerable variety of fractures and dislocations follow trauma between the occiput and the first thoracic vertebra. Most are caused by car accidents with falls and sports accidents next in frequency.1-3 Half of all patients present with neurological problems.4 Early diagnosis is important. The cervical fracture is often combined with another spinal fracture and there­ fore the entire vertebral column must be X-rayed.5 Plain radiographs are the first way in which diagnosis is estab­ lished. Multidirectional CT is particularly advantageous in patients with facet injuries. Computerized tomo­ graphy seems to add most additional information in laminar or posterior column injuries, fractures of the vertebral body or in atlantoaxial subluxations.6 Fractures and dislocations of the atlantoaxial complex Fractures of the axis are common. In 14.0-17.5% of all fractures of the cervical spinal column the lesion lies at the axis.? Most frequent are odontoid fractures. They are

CHAPTER 10

classified as type I - avulsion of the tip of the odontoid process, type II - fracture through the base and type III fracture through the vertebral body.8,9 These are followed in frequency by those of the vertebral body, the pedicle or the lateral mass. Less common is hangman's fracture - a bilateral fracture through the pars interarticularis of the axis. Neurological damage is not frequent in odontoid and hangman's fractures but quite common in the other miscellaneous fractures of the axis.IO Dislocations of the atlas are not uncommon and may lead to serious neurological damage. Fractures of the atlas are rare and seldom cause neurological problems. In order of frequency the following fractures are found: bilateral fracture of the posterior arch, com­ minuted fracture of the ring of the atlas - traumatic spondylolisthesis or Jefferson's fracture, and unilateral fracture of the lateral mass.12 Fractures of the lower cervical spine An accident immediately followed by the occurrence of gross limitation of movement in every direction, especially of extension (full articular pattern) strongly suggests vertebral fracture or dislocation. Apart from possible neurological problems the patient presents with severe central or bilateral neck pain and is unable to move his head as the result of muscle spasm. Properly performed radiological examination is diagnostic. Most fractures in the cervical spine occur below C2. They range from fractures of the articular process to frac­ tures of the vertebral body, lamina, spinous process and pedicle. Frachlres are commonly classified in six groups depending (in order of frequency) on the forces that have acted on the cervical spine: compressive flexion, distrac­ tive flexion, compressive extension, vertical compression, distractive extension and lateral flexion.13 Neurological problems most often occur when the fracture is combined with luxation.14,15 Pathological fractures following a minor injury or a sudden effort give rise to the same clin­ ical picture but the history is much less indicative and may even be misleading. If neurological injury is present, the diagnosis of a probable fracture or dislocation is made more simple. Clay-shoveller's fracture This is a fracture of one or more spinous processes in the lower cervical or upper thoracic spine (mostly C7, some­ times C6 or Tl).16 A traction fracture may occur as the result of strong muscular force from the trapezius transmitted to the spinous processes through the musculature. It happens suddenly. A crack is felt followed by severe pain at the base of the neck and between the shoulders. The same event may occur in motor vehicle accidents where a strong flexion force was applied to the neck, and thus also in whiplash injuriesy,18

-

NON-MECHANICAL DISORDERS 213

If the fracture is the result of a fatigue mechanism, the patient complains of a dull ache at the cervicothoracic junction coming on without clear cause. Neck movements are not really painful but the patient is unable to bring the arms above the horizontal because of pain. The passive shoulder range is full and painless. The radiograph shows avulsion of one or more spinous processes. Spontaneous cure takes 3-6 weeks.

BONY TUMOURS

Primary bone tumours are uncommon. They represent only 0.4% of all tumours and cervical localization accounts for only 4.2% of the primary bone tumours of the spine. This is very much less than in the thoracic or lumbar spine.19 Benign primary tumours occur more often in the first two decades of life, while malignant primary tumours more frequently affect adults. The incidence of malignant tumours increases significantly with age. In the cervical spine, even more than in other parts of the axial skeleton, metastatic lesions are much more frequent than primary tumours. The symptoms may vary and include local heat, ten­ derness, neuralgic pain, root palsy, torticollis-like limita­ tion of neck movements20 and myelopathy, although early in development the symptoms may mimic ordinary soft tissue lesions. Severe pain at night is often a hallmark of neoplasm.21 The presence of one or more inconsistencies during history and / or functional examination is a warning sign and puts the examiner on guard (see Box 10.1). It is again mainly the clinical approach that suggests a serious dis­ order. Radiography - usually the first additional exami­ nation - is not a guarantee, as it appears that more than 30% of the cancellous bone of the vertebral body must be destroyed before a plain X-ray becomes positive.22,23,29 More refined imaging such as CT scan, technetium scan, angiography and MRI confirms the diagnosis. A radiograph and CT scan of the chest or abdomen may be necessary in patients with unknown primary sites. Benign tumours The most common benign neoplasm affecting the cervical spine are, in order of frequency: osteoid osteoma, osteoblastoma, haemangioma, aneurysmal bone cyst, eosinophilic granuloma, giant cell tumour and osteo­ chondroma. They can be found at any level, except Cl, and are most common at C2, C4 and C7Ievels.24-27 osteoma. This is the most frequent benign the cervical spine20 and appears in young in tumour adults, mostly males.28,29 It affects the cervical spine less Osteoid

214 SECTION TWO - THE CERVICAL SPINE

Box 10.1 Warning signs for cervical tumour '

-

History • Central neck pain becoming slowly worse • Elderly person with rapidly increasing pain and/or stiffness of the neck

• Elderly person with neck pain for the first time • Cord symptoms • Dysphagia

Examination • Full articular pattern occurring spontaneously over short period of time

• Gross limitation of rotations • Wrong end-feel: muscle spasm, soggy, empty

• Resisted neck movements painful and weak • Unusual weakness in the arm gross weakness in the absence of severe radicular pain, bilateral weakness, multiradicular weakness,

T1 palsy • Horner's syndrome • Anaemia

frequently than the lumbar spine and is located in the pedicles and vertebral arches.3D The typical symptom is persistent localized pain, especially at night, which can usually be relieved by salicylates. The pain sometimes radiates to the upper limb. Surgical removal is curative. This tumour affects the cervical spine as frequently as it does the thoracic spine. It is more common in the lumbar spine.24 Young adults - males more frequently - are affected and the posterior elements of the vertebra are involved, which may lead to radiculopathy and myelopathy. The neck pain is dull, especially at night and the normal lordosis may be reversed to produce a torticollis­ like picture. Root and cord symptoms may mimic a disc protrusion, except that the patient is too young to have disc protrusion causing root or cord symptoms. Excision usually leads to full recovery.31 Osteoblastoma.

Haemangioma. This occurs most often in women in their fourth decade.32 It is common and usually has an asymptomatic development - one quarter of all cases in the cervical spine. The tumour rarely gives rise to symptoms. Should it do so, localized pain, progressing to cord symptoms are usual. Treatment with low-dose radiation usually suffices.33 Aneurysmal bone cyst. This is seen most frequently in children and young adults, mostly females (under 30 years old).34 25% of spinal aneurysmal bone cysts is

located in the cervical spine.27 It is a destructive tumour and is mostly localized in the neural arch but may also invade the vertebral body. As it expands, it may lead to root pain and even to compression of the spinal cord. Excision and/ or curettage and stabilization with bone grafts is indicated.35 Eosinophilic granuloma. This is a variant of the systemic disorder, histiocytosis-X. The cervical spine can be affected in both children and adults, and the condition has a typical development. The vertebral body collapses, producing sudden pain and sometimes muscle spasm leading to torticollis. A patient with acute torticollis and a sudden onset who presents with pain, limitation and involuntary muscle spasm on careful passive examina­ tion should therefore be radiographed to exclude this disorder, which shows a 'vertebra plana'. The fracture may heal spontaneously. However, when the flattening is significant, neurological symptoms may follow; these are reversible when treatment is started without delay. Open biopsy, followed by immobilization and irradiation may be necessary.36,37 Giant cell tumour. This is more frequent in the sacrum and the lumbar spine but may also affect the cervical spine. It seems to occur in younger patients (between 20 and 40 years old), especially women.38 It leads to destruc­ tion of the vertebral body and can later involve the posterior part of the vertebra. It may cause pain in the neck but can also give rise to radicular symptoms. Excision with bone grafting is the treatment of choice.

This occurs mostly in young adult males. When it affects the spine it is seldom symptomatic, except in the cervical region.39 There is slow progression but neural compression can develop. The results of surgical excision are good.

Osteochondroma.

Malignant tumours The most common malignant neoplasms are: multiple myeloma, chordoma, solitary plasmacytoma, chon­ droma, chondrosarcoma, lymphoma, osteosarcoma, Ewing's sarcoma and metastases. The primary malignant tumours represent 6.3% of all primary bone tumours of the spine and occur mainly from middle age on, much more frequently in men than in women. They are found at all levels, except C1.25 Multiple myeloma. This is the most frequent primary malignant tumour in the spine. It occurs more often in men, usually between 50 and 70 years of age. The patient's main symptom in early cases is pain in the neck. Anaemia and cord symptoms soon follow. The radiograph shows round lytic defects in the bone, without a surrounding sclerotic reaction. Pathological fractures may occur.

CHAPTER 10 - NON-MECHANICAL DISORDERS 215

The treatment of choice is radiation and / or systemic chemotherapy. The outlook is poor. Chordoma. This is an uncommon locally invasive, slow­ growing malignant neoplasm, that arises from the vertebral or suboccipital remnants of the embryonic notochord. In 33-38% it occurs in the upper cervical vertebrae, especially C2, and is found most often in men aged between 50 and 70 years.40,41 Central neck pain becoming slowly worse is a common symptom. After several months, movements become gradually limited, especially rotation, with a soggy end­ feel on passive testing. The tumour often extends anteriorly into the soft tissues and may then result in dysphagia, upper respira­ tory obstruction and Horner's syndrome.42 Posterior extension may be accompanied by neurological compli­ cations, such as epidural spinal cord compression or cervical radiculopathy.43,44 The classical radiological finding is an expanding osteolytic lesion. This life-threatening lesion is best treated surgically by radical resection and, if this fails, repetitive local debulking procedures may be used. The prognosis is bad.

This is a myeloma (plasma cell neoplasm) in a single vertebral body. The patient is over 60 years and complains of slowly progressing neck pain with muscle spasm. The prognosis is much more favourable than in patients with multiple myeloma.45 Collapse of the vertebral body and cord compression may result. The treatment of choice is radiation. Solitary plasmacytoma.

Chondrosarcoma. This tumour usually occurs between 40 and 60 years. It forms cartilaginous tissue in the vertebral body or in the neural arch where it leads to destruction of bone. In most cases a soft tissue mass also develops. lymphoma, osteosarcoma, Ewing's sarcoma. Lymphoma presents either as a skeletal manifestation of a systemic disease or as an isolated tumour. It may involve the epidural space adjacent to the osseous spine. Complete recovery is only possible after total surgical excision. Osteosarcoma and Ewing's sarcoma are extremely uncommon in the spine. These tumours evolve rapidly and osteogenic sarcoma gives early metastases to the lung. Treabnent is biopsy, chemotherapy and / or radiotherapy.

Secondary deposits are the most common malignant tumours of the cervical spine46,47 although this part of the vertebral column is the least affected,48 occurring in 8-20% of patients with known metastatic disease.49 Breast, lung, prostate, colon, kidney and thyroid are the most frequent sites of primaries. Metastases in the spine may pass unnoticed for a considerable time and are sometimes discovered during routine radiography. Metastases.

In symptomatic cases, pain is the earliest and most prominent feature in 90%.50-53 Localized pain that starts spontaneously and becomes gradually worse, especially at night, is the most common picture of spinal metas­ tases. It is axiomatic that a cancer patient who develops neck pain harbours a spinal metastasis until proven otherwise. If a patient presents with neck pain but has a history of a primary tumour, for example breast cancer, even a long time ago, metastases must be taken into con­ sideration. At this time a diagnosis can be made, based on a careful observation of the symptoms and signs presented. Later, nerve root involvement and / or spinal cord compression may supervene and will then facili­ tate diagnosis, because the findings are a useful indica­ tor of the site of compression. The clinical features differ depending on whether the lesion is localized at the upper cervical spine (CI-C3), the lower cervical spine (C4-C7) or the upper thoracic spine (Tl-T3).54

Warning • Spontaneous, localized, progressive nocturnal pain in the neck

• Cancer patient developing neck pain • Neck pain in a patient with a history of a primary tumour

Upper cervical metastases. It may be difficult to detect bony tumours at this level. Some warning signs will probably be found, for example an elderly patient, who for the first time complains of neck pain or who describes rapidly increasing pain and stiffness of the neck coming on in the course of 1 or 2 months. On examination, a pronounced full articular pattern is found: active movements are very limited and, on passive testing, muscle spasm prevents every forced movement. Resisted movements are painful and weak. In the early stage the radiograph shows only arthrosis and osteophytosis but the history and functional exami­ nation show the discrepancy between the actual signs and what is seen on the radiograph. Bone scan and MRI confirm a tentative diagnosis. Lower cervical metastases. Diagnosis here is much easier. Warning signs in the history may suggest severe disease and the examination confirms this. When the movements of the cervical spine are tested, a full articular pattern with gross limitation of movement is again present. The neurological examination of the upper limb also shows that a severe non-discal disorder is present. The possibil­ ities are: gross weakness in the absence of severe radicu­ lar pain, bilateral weakness, multiradicular involvement and palsy of different nerve roots.

216 SECTION TWO - THE CERVICAL SPINE

Upper thoracic metastases. Limitation of movement is difficult to detect and therefore the situation becomes clear clinically only where a bilateral root pain or root palsy occurs. It should be remembered that weakness of the intrinsic muscles of the hand due to a T1 root palsy is never caused by a disc protrusion. Especially if Horner's syndrome is also present, a malignant condition is very probable: either a pulmonary sulcus neoplasm or a neoplasm in the upper thoracic vertebrae. If vertebral metastases are suspected, further investi­ gations are arranged. The vertebral body is usually the initial site of deposition but, as already mentioned, a plain radiograph may remain negative until 30-50% of the cancellous bone in the vertebral body is destroyed. Occasionally the pedicle may be involved, which shows earlier on plain radiographs. 99Technetium bone scan has proved an effective means of surveying the entire skele­ ton for metastatic disease and often demonstrates the site before it is visible on radiographs. CT scan and MRI are invaluable for visualization of paraspinal soft tissue masses and cervical cord impingement.23 Myelography may also be helpful. Treatment is palliative and often consists of irradiation and immobilization. Occasionally stabilization by surgery is indicated. Osseous disorders of the cervical spine are summa­ rized in Box 10.2.

RHEUMATOID ARTHRITIS AND ANKYLOSING SPONDYLITIS RHEUMATOID ARTHRITIS

Rheumatoid arthritis is as frequent in the cervical spine as it is uncommon in other parts of the spine and the atlantoaxial complex especially becomes affected.55 The frequency of involvement of the cervical spine is between 25% and 80%56 and the longer a patient has rheumatoid arthritis the more chance that it reaches the cervical leveJ.57 As in other joints the bony, cartilaginous and ligamentous structures are destroyed and laxity and deformation result. Anterior atlantoaxial subluxation is the most frequent complication - it occurs in 49% of patients58 and repre­ sents 65% of all cervical subluxations59 - and results from laxity of the transverse ligament of the atlas and / or the ligaments of the dens (alar ligaments / apical ligament).6o The subluxation is mostly anterior but may be lateral and occasionally posterior. When, on a flexion / extension radiograph, the distance between the anterior arch of the atlas and the odontoid process of the axis exceeds 3 mm, laxity is probable. More than 10 mm indicates gross instability6J and requires surgical stabilization.62 The spinal cord is seriously threatened at this stage, especially

Box 10.2 Osseous disorders of the cervical spine -

Fractures and luxations Fractures and dislocations of the atlantoaxial complex Fracture of the axis Fractures of the odontoid process Fractures of the vertebral body, pedicle or lateral mass Traumatic spondylolisthesis (Hangman's fracture) Dislocation of the atlas Fractures of the atlas Bilateral fracture of the posterior arch Comminuted fracture of the ring of the atlas (Jefferson's fracture) Unilateral fracture of the lateral mass Fractures and luxations of the lower cervical spine Posttraumatic fractures Pathological fractures Fractures of the lower cervical or upper thoracic spinous processess (clay-shoveller's fracture)

Bony tumours Benign tumours:

Malignant tumours:

• • • • • • •

• • • • •

Osteoid osteoma Osteoblastoma Haemangioma Aneurysmal bone cyst Eosinophilic granuloma

Solitary plasmacytoma Chondrosarcoma Lymphoma, osteosarcoma, Ewing's sarcoma

Giant cell tumour Osteochondroma

Multiple myeloma Chordoma

•

Metastases

during flexion movements. This may in the end lead to spasticity, hyperreflexia (deep tendon reflexes), weak­ ness, sensory loss and urinary problems. More recent reports show a tendency to rely more on the posterior atlantodental interval, the distance between the posterior arch of the atlas and the dens, which should be a minimum 14 mm.63 If the destructive process reaches both the occipito­ atlantal and atlantoaxial joint complexes, the odontoid process of the axis may protrude through the foramen magnum - cranial settling or vertical odontoid subluxa­ tion64,65 which happens in 38% of rheumatoid patients.66 Later in the development, the atlantoaxial instability tends to decrease again,67,68 leaving the patient with only odontoid subluxation. The lower cranial nerves, the cardiorespiratory centre and pyramidal tracts may all become compressed. Mikulowski et al report that 10% of rheumatoid arthritis patients may die of compression of the brainstem which is unrecognized before death.69 It is therefore important to do a radiographiC evalua­ tion of the cervical spine in all patients with rheumatoid arthritis, even when they are asymptomatic. Collins et al found that only 50% of patients with abnormalities on their radiographs had symptoms of their cervical disease.7o The degree of odontoid protrusion can be measured on a lateral radiograph. A line is drawn between the poste­ rior edge of the hard palate and the inferior border of the occiput (the McGregor line). If the tip of the odontoid

CHAPTER 10

process lies more than 4.5 mm above this line, cranial settling is present (Fig. 10.1). If these landmarks are not clear, the Fischgold and Metzger measurement can be used: on an anteroposterior open-mouth tomogram the digastric line is drawn (between the points where the mastoid processes join the base of the skull), and the tip of the dens should lie 1 cm or more below this, to be classed as normal.71 Subaxial subluxation is less frequent (10-20% of patients.) but may arise at several levels,72,73 especially C2-C3 and C3-C4. The laxity then occurs at the zygoapophyseal and uncovertebral joints74 and may result in compression of nerve root and / or vertebral artery, the latter leading to vertebrobasilar insufficiency and its consequent clinical features. Many patients are asymptomatic. There may be a dis­ crepancy between the degree of destruction or instability and the symptoms. Patients may be seen with slight instability and neurological problems only, whereas others may have significant laxity without neurological symptoms?S,76 Neurological dysfunction occurs in 7-34% of patients and may include brainstem, spinal cord and nerve rootS?7 The disorder may cause moderate pain in the neck. Involvement of the upper cervical joints gives rise to pain often felt in the upper neck, radiating bilaterally to the occipital, temporal, auricular and retro-orbital regions. Occasionally the patient may complain of a clunking sensation with flexion movements (Sharp's and Purser's sign)?8 On clinical examination a full articular pattern is found with a soggy or empty end-feel. This characteristic sensa­ tion immediately draws attention to the disorder. A clunking sensation on neck flexion indicates excessive movement between C1 and C2, as happens in atlanto­ axial subluxation. The Sharp-Purser test may help to diagnose the condition; it appears to have a sensitivity of 69% and a specificity of 96% compared with radiological

-

NON-MECHANICAL DISORDERS 217

evidence?9 The patient sits on a chair. The examiner stands to one side and places the index finger on the spinous process of C2. The palm of the other hand lies on the patient's forehead. An attempt is made to slide the head posteriorly and, if a slide between the spinous processes of C1 and C2 is felt, the test is positive. ANKYLOSING SPOND Y LITIS

When, late in its development, the disease reaches the cervical spine, this leads to increasing stiffness and limi­ tation in all directions and, in the end, possibly to ankyl­ osis in flexion. This happens in 75% of patients with a history of more than 16 years.80 The end-feel is hard and may ultimately become bone-to-bone. As long as this bone-hard end-feel is not present the pain can be con­ trolled with slow gradual stretching manoeuvres at regular intervals. Once this bony end-feel has occurred, any forcing of the joints is futile. Complications may occur, such as atlantoaxial instability81 and fractures.82 CRICOARY TENOID JOINT INVOLVEMENT

In long-standing cases of rheumatoid arthritis or of ankylosing spondylitis, involvement of the cricoarytenoid joints is a possibility. Dyspnoea, hoarseness and a feeling that the throat is obstructed may follow. Laryngoscopy is diagnostic.83,84 (Cyriax:8s p. 91.) INFECTIONS

Infectious disease affecting the cervical spine is very uncommon compared to the thoracic and lumbar spines. Tuberculosis in the cervical spine occurs in less than 5% of spinal involvement and infection by pyogenic organ­ isms (i.e. discitis, osteomyelitis) is extremely rare but may lead to severe neurological problems.86,87 Infections of the spinal canal present as epidural, subdural or intra­ medullary abscesses. Parapharyngeal infections may lead to upper cervical ligamentous laxity.88 INTRASPINAL TUMOURS

Cervical intraspinal neoplasms represent about 20% of all spinal tumours and may lie either outside or within the dura. The latter can be extra- or intramedullary. Clinical differentiation is often not easy because these conditions often compromise the same intraspinal structures giving rise to similar symptoms and signs (Table 10.1). EXTRADURAL TUMOURS Figure 10.1 The McGregor line - if the tip of the odontoid process is more than 4.5 mm above the line, cranial settling is present.

These constitute almost one-quarter of all primary spinal tumours. The majority are metastatic89,9o (see Fig. 10.2)

218 SECTION TWO - THE CERVICAL SPINE

Figure 10.2 Location of intraspinal tumours of the cervical spine: 1, extradural tumours (metastases, abscesses); 2, intradural extramedullary tumours (meningiomas, neurofibromas, schwannomas, sarcomas, dermoids, epidermoids, angiomas); 3, intramedullary tumours (astrocytomas, ependymomas).

and invade the vertebral bodies or arches: carcinoma of the bronchus is the most common primary but other sources are the breast, prostate, gastrointestinal tract, thyroid and kidney.91 These tumours must be differentiated from benign and malignant bony tumours of the spine (see p. 212), although any intradural neoplasm may also perforate the dura mater to become extradural. Pyogenic and tuberculous abscesses in the epidural space give rise to similar symptoms and signs. These space-occupying lesions in the spinal canal very commonly lead to radicular symptoms and signs: root pain quickly follows the original local neck pain and motor and sensory deficit supervenes. Very soon in their development, the spinal cord becomes compressed and transverse myelopathy occurs with bladder dys­ function and further progressive sensory and motor deficit (see p. 204).

schwannomas are the most common. Sarcomas, dermoids, epidermoids and angiomas are less frequent. Both meningiomas and neurofibromas are benign and slow growing. They may also occur extradurally, however this is far less common.93 Neurofibromas and schwannomas in the cervical spine are not as frequent as they are in the thoracic spine but are more frequent than in the lumbar spine. Meningiomas, by contrast, are far less common in the cervical than in the thoracic area.94 These tumours show a tendency to present with radic­ ular symptoms very much resembling those caused by a disc protrusion. The root pain is quite constant, slightly influenced by activity and worse at night.95 Of all patients with symptoms consistent with disc herniation, 1% have an intraspinal tumour.96 The ease of differential diagnosis from a cervical disc lesion may vary. In some it is quite easy, while in others it may be extremely difficult. Any of the following features should arouse suspicion: •

• •

•

•

INTRADURAL EXTRAMEDULLARY TUMOURS

These form almost two-thirds of all intradural neo­ plasms,92 of which meningiomas, neurofibromas or

•

Root pain under the age of 35 is very rarely caused by a disc protrusion, so that any patient who is younger than this and complains of radicular pain should be considered very carefully. Root pain that goes on increasing even after some months is certainly not the result of a disc protrusion. Primary posterolateral onset of the symptoms: paraesthesia in the hand first, followed by pain in the forearm and later in the arm is very uncommon in disc lesions but quite normal in root compression by a neurofibroma. Coughing is painful and is felt down the arm: in disc lesions coughing is seldom painful and, when it hurts, it does so in the scapular area. Although radicular symptoms are commonly unilat­ eral, bilateral distribution may occur later in the development: bilateral root pain cannot be caused by a single disc protrusion, and bilateral protrusions, except in elderly people, are very rare. Pins and needles felt all over the body and evoked by neck flexion are characteristic of a neurofibroma

Table 10.1 Differential diagnosis of discoradicular interactions and neurofibroma/schwannoma in the cervical region

Symptoms

Signs

Discoradicular interactions

Neurofibroma/schwannoma

No root pain under 35 years

At any age

Root pain stabilizes after 2 months

Root pain continues to worsen after 6 months

Secondary posterolateral evolution

Primary posterolateral onset

Coughing may hurt in the scapular area

Coughing always hurts down the arm

Unilateral root pain

Unilateral root pain may become bilateral

Paraesthesia felt distally

Paraesthesia is felt all over the body

Articular signs

No articular signs

Slight segmental weakness

Unusual weakness

Symmetrical cord signs

Asymmetrical cord signs

CHAPTER 10 - NON-MECHANICAL DISORDERS 219

(Cyriax:85 p. 88). Again, cord symptoms are mostly unilateral. Warning Signs in the history •

Root pain under the age of 35

•

Root pain increasing for several months

•

Primary posterolateral onset of symptoms

•

Coughing painful in the arm

•

Bilateral root pain

•

Pins and needles felt all over the body

a slow development,lDD which sometimes makes diagno­ sis quite difficult. Pain is typically felt at the level of the lesion and is not radicular. Furthermore, a local band of hyperaesthesia usually occurs. Motor and sensory deficit are more pronounced at the level of the lesion than dis­ tally, and symptoms and signs of cord compression occur quite late. Treatment is laminectomy and leads to good results in ependymomas but astrocytomas are much more difficult to cure. NEUROLOGICAL CONDITIONS WITH POSITIVE SIGNS ON NECK EXAMINATION

Warning Signs arising during functional examination: •

Absence of articular signs

•

Unusual (pronounced) muscle weakness

•

Spinal cord signs

During functional examination, the following signs may indicate the possibility of a non-mechanical lesion: •

•

•

Absence of articular signs: because the lesion is extra-articular, neck movements are negative. It should be noted, however, that this may also happen later in the evolution of a disc protrusion compressing the nerve root. Unusual weakness is strongly suspicious: this means weakness out of proportion to other symptoms and signs, or affecting muscles that are not usually . involved or in muscles derived from more than one segment. Spinal cord signs may occur (spasticity, incoordina­ tion, incontinence, sensory loss) but are rarely symmetrical.

Differential diagnosis should be made with intramedullary and extradural tumours, and non­ neoplastic conditions such as syrinx, spondylotic myelo­ radiculopathy, multiple sclerosis or spinal arteriovenous malformation.97 Radiographs may remain normal for a very long time. CT, myelography and particularly MRI are very useful diagnostic procedures.98 Standard laminectomy is the treatment of choice and the prognosis is good. INTRAMEDULLARY TUMOURS

Astrocytomas and ependymomas are the most common intramedullary tumours. They comprise 30% of all intradural tumours92 but are located in the cervical spine in only 17.5% of all spinal cord tumour cases.99 They have

Some specific neurological conditions can occur to give rise to symptoms that warrant a cervical examination. Positive signs will be found during the neurological examination of the upper limb. Possible conditions are: • • •

•

Mononeuritis of the long thoracic nerve: active elevation of the arm is grossly limited. Mononeuritis of the spinal accessory nerve: active elevation of the arm is slightly limited. Mononeuritis of the suprascapular nerve: resisted abduction and external rotation of the shoulder are weak. Neuralgic amyotrophy: several muscles are weak at random. These conditions are discussed extensively in Chapter 37.

VISCERAL CONDITIONS

Lesions of the lung may give rise to pain felt in the shoul­ der or the upper thoracic area. In particular, pulmonary or visceral lesions interfering with the diaphragm (a C3-C4 structure) cause pain felt at the point of one shoul­ der. Heart diseases may give rise to multisegmental reference of pain, especially in the C3 dermatome, or to segmental reference of pain, felt locally in the upper thorax or down the inner aspect of the upper limb (Tl-T2 dermatomes). Inflammation of the gallbladder may provoke symptoms in the scapular area. Mobility of the shoulder can become impaired as the result of the dense scarring which accompanies healed apical phthisis, limit­ ing the mobility of the costocoracoid fascia. SHOULDER GIRDLE DISORDERS CAUSING CERVICOSCAPULAR PAIN • •

Posterior sternoclavicular syndrome Lesion of the first costotransverse joint

220 SECTION TWO - THE CERVICAL SPINE

Sternoclavicular arthritis (especially when the poste­ rior fibres of the joint are affected) or a lesion of the first costotransverse joint may give rise to pain felt in the trapezius area and so are recognized during cervical examination. The former - posterior sternoclavicular syndrome - presents with pain on shrugging the shoul-

der and on full arm elevation. The latter gives rise to signs on three levels: cervical, shoulder girdle and shoulder. In both cases the complete shoulder girdle examina­ tion must be done and is diagnostic. These conditions are discussed in detail in Chapter 23.

REFERENCES 1. Hadley MN, Browner C, Sonntag VKH. Axis fractures: a com­ prehensive review of management and treatment in 107 cases. Neurosurgery1985;17:281. 2. Weiss MH. Mid- and lower cervical spine injuries. In: Wilkins

RH, Rengachary SS (eds) Neurosurgery, vol 2. McGraw-Hill, New York, 1985:1708. 3. Reiss Sj, Raque GH, Shields CB et a.l Cervical spine fractures with major associated trauma. Neurosurgery1986;18:327. 4. Graham B, Van Peteghem K. Fractures of the spine in ankylos­ ing spondylitis. Diagnosis, treatment and complications. Spine 1989 1 , 4:803. 5. Ducker TB. Comments. Neurosurgery1986;18:330. 6. Clark CR, Igram CM, E l-Khoury GY, Ehara S. Radiographic

evaluation of cervical spine injuries. Spine1988;13(7):742. 7. Clark CR, White AA III, Cooper P. Fractures of the dens: a multi­

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16. White AA III, Panjabi MM. Cl inical Biomechanics of the Spine.

Lippincott, Philadelphia, 1978:166. 17. Wong WB, Panjabi MM, White AA I I I . Mechanisms of injury in

the cervical spine. Basic concepts, biomechanical modeling, experimental evidence, and clinical applications. In: The Cervical Spine Research Society, Clark CR et al. (eds) The Cervical Spine, 3rd edn. Lippincott-Raven, P h i ladelphia, 1998:95. 18. Meyer PR, Heim S. Surgical stabilization of the cervical spine.

In: Meyer PR (ed) Surgery of Spine Trauma, Churchill Livingstone, New York, 1989:414. 19. Weinstein IN. Surgical approach to spine tumours. Orthopedics 1989;12:897-905.

22. Edelstyn GA, G i llespie PG, Grebbel FS. The rad iological

demonstration of skeletal metastases: experimental observa­ tions. c/in Radiol 1967;18:158. 23. Vanzanten TEG, Tevle GJJ, Golding RP, Heidendal GAK. CT and nuclear medicine imaging in vertebral metastases. c/ill Nucl Med1985;14:334. 24. Bohlman HH, Sachs BL, Carter JR, Riley L, Robinson RA.

Primary neoplasms of the cervical spine. Diagnosis and treatment of twenty-three patients. J Bone loint Surg 1986; 68A:483-493.

25. Di Lorenzo N, Delfini R, Ciappetta P, Cantore G, Fortuna A. Primary tumors of the cervical spine: surgical experience with 38 cases. Surg Neuro/1992;38:12-18. 26. Liu H, Liu Z. Surgical treatment of cervical spine tumors. Chill Med J1992;105:564-566. 27. Levine AM, Boriani S, Donati 0, Campanacci M. Benign tumors

of the cervical spine. Spine1992;17:399-406. 28. Pettine KA, Klassen RA. Osteoid osteoma and osteoblastoma of

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Hensinger RN. Osteoid osteoma of the spine.

I

Spinal Disord

1992;5:204-211.

30. Maiuri F, Signorelli C, Lavano A et a.l Osteoid osteomas of the spine. Surg Neuro/1986;25:375. 3 1 . Marsh BW, Bonfiglio M, Brady LP, Enneking WF. Benign osteoblastoma: range of manifestations. J Bone loint Surg 1975;57A(l):1.

32. Healey M, Herz DA, Pearl L. Spinal hemangiomas. Neurosurgery 1983;13:689.

33. Graham H, Yang We. Vertebral hemangioma with compression fracture and paraparesis treated with preoperative emboliza­ tion and vertebral resection. Spine1984;9:97. 34. Stillwell WT, Fielding JW. Aneurysmal bone cyst of the cervico­ dorsal spine. c/in Orthop Rei Res1984;187:144. 35. Hay Me, Paterson 0, Taylor TK. Aneurysmal bone cysts of the spine. J Bone Joint Surg1978;60A(3):406. 36. Fowles JV, Bobechko WP. Solitary eosinophilic granuloma in bone. J Bone Joint Surg1970;52(2):238. 37. Makely JT, Carter JR. Eosinophilic granuloma of bone. c/in 01'thop Rei Res1986;204:37.

38. Dahlin De. Giant-cell tumor of vertebrae above the sacrum. Cancer 1977;39:1350. 39. Malat J, Virapongse C, Levine A. Solitary osteochondroma of the spine. Spine1986;11(6):625. 40. Huvos AG. Bone Tumors: Diagnosis, Treat ment and Prognosis. Saunders, Philadelphia, 1979:373. 41. O'Neill P, Bell BA, Miller JO, Jacobson I, Guthrie W. Fifty years of experience with chordomas in southeast Scotland. Neurosurgery1985;16:166.

20. Levine AM, Boriani S, Donati 0, Campanacci M. Benign

42. Boriam S, Sundaresan N, Weinstein IN. Primary malignant

tumours of the cervical spine. Spine1992;17(10):399-406. M. Primary bone and metastatic tumours of the cervical spine. Spine1998;23(24):2767-2777.

tumors of the cervical spine. In: The Cervical Spine Research Society, Clark CR et a/. (eds) The Cervical Spine, 3rd edn. Lippincott-Raven, Philadelphia, 1998;643-657.

21. Abdu WA, Provencher

CHAPTER 10 - NON-MECHANICAL DISORDERS 221

43. Rich TA, Schiller A, Suit HD, Mank HJ. Clinical and pathologic review of 48 cases of chordoma. Can ce r 1985;56:182. 44. Boriani S, Chevalley E, Weinstein IN et al. Chordoma of the spine above sacrum - treatment and outcome in 2 1 cases. Spine 1996;21: 1569-1571. 45 . McLain RF, Weinstein IN. Solitary plasmocytomas of the spine: a review of 84 cases. J Spin al Dis ord 1989;2(2) :69. 46. Harrington KD. Metastatic disease of the spine. J Bone J oin t Su rg 1986;68A:111O. 47. Onimus M, Schraub S, Bertin D et al. Surgical treatment of vertebral metastases. Spine 1986;11:883. 48. Tubianahulin M . Incidence, prevalence and distribution of bone metastases. Bone 1991;12:9-10. 49. Rao S, Davis RF. Cervical spine metastases. In: The Cervical Spine Research Society, Clark CR et al. (eds) The Ce rvical Spine , 3rd edn. Lippincott-Raven, Philadelphia, 1998:603-619. 50 . Livingston KE, Perrin RG. Neurosurgical management of spinal metastases. J Neu ros u rg 1978;49:839. 5 1 . Perrin RG, McBroom RJ. Anterior versus posterior decompression for symptomatic spinal metastases. Can J Neu rol Sci 1987;14:75. 52 . Levine AM. Operative techniques for treatment of metastatic disease of the spine. Se m Spine Su rg 1990;2:2 10-22 7. 53. Rao S, Badani K. Cervical metastases. J Bone J oin t Su rg 199 4;53A:55 1 1-5556 . 5 4. AtanClsin JP, Badatcheff F, Pidhorz L. Metastatic lesions of the

cervical spine, a retrospective analysis of 20 cases. Spine 199 3;18(10) : 12 79- 128 4. 55 . Grantham SA, Lipson SJ. Rheumatoid arthritis and other non­

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6 4. 65.

infectious inflammatory diseases. In: The Cervical Spine Research Society, Sherk H H et al. (eds) The Ce rvical Spine , 2nd edn. Lippincott, Philadelphia, 1989:564. Rajangam K, Thomas 1M. Frequency of cervical spine involve­ ment in rheumatoid arthritis. J In dian Me d Ass oc 1995 ;93 : 138-139. Oda T, Fujiwara K Yonenobu K Azuma B, Ochi T. Natural course of cervical spine lesions in rheumatoid arthritis. Spine 1995;20:1128-1135. Morizono Y, Sakou T, Kawaida H. Upper cervical involvement in rheumatoid arthritis. Spine 198 7;12: 72 1-725 . Boden SD, Clark CR. Rheumatoid arthritis of the cervical spine. In: The Cervical Spine Research Society, Clark CR et al. (eds) The Ce rvical Spine , 3rd edn. Lippincott-Raven, Philadelphia, 1998:693-703. Stevens Je, Cartlidge NE, Saunders M et al. Atlanto-axial sub­ luxation and cervical myelopathy in rheumatoid arthritis. Q J Me d 1971;40:391. Fielding JW, Cochran G van B, Lawsing JF 3rd, Holh M. Tears of the transverse ligament of the atlas, a clinical and biomechani­ cal study. J Bone J oint Su rg 1974;56A: 1683-1691. Clark CR, Goetz DD, Menezes AH. Arthrodesis of the cervical spine in rheumatoid arthritis. J Bone J oin t Su rg 1989;71A: 381-392. Boden SD, Dodge LD, Bohlman HH, Rechtine GR. Rheumatoid arthritis of the cervical spine. A long-term analysis with predictors of paralysis and recovery. J Bone J oin t Su rg 1993;75A: 1282-1297. Dirheimer Y. The Cran iove rteb ral Re gion in Chron ic Infl ammat ory Rheu mat ic Dis e ases. Springer, Berlin, 1977. Rasker JJ, Cosh JA. Radiological study of cervical spine and hand in patients with rheumatoid arthritis of 15 years' duration; an assessment of the effects of corticosteroid treatment. A n n Rheum at ol Dis 19 78 ;37:529 .

66. Reiter MF, Boden SD. Inflammatory disorders of the cervical spine. Spine 1998;23(24):2 755-2766 . 67. Casey A, Crockard H, Geddes J, Stevens J. Vertical transloca­ tion: The enigma of the disappearing atlantodens interval in

patients with myelopathy and rheumatoid arthritis. Part 1 : Clinical, radiological and neuropathological features. J Neu rosu rg 199 7;87:856-862 .

68. Casey A, Crockard H, Stevens J. Vertical translocation. Part I I : Outcomes after surgical treatment of rheumatoid cervical myelopathy. J Neu ros u rg 1997;87:863-869. 69. Mikulowski P, Wollheim FA, Rotmil P, Olsen I. Sudden death in rheumatoid arthritis with atlanto-axial dislocation. A ct a Me d Scan d 19 75 ;198 :445- 45 1 .

70. Collins DN, Barnes CL, Fitz RL. Cervical spine instability i n rheumatoid patients having total hip o r knee arthroplasty. Cl in Orthop Re i Res 1991;272:127-135. 71. Grantham SA, Lipson SJ. Rheumatoid arthritis in the cervical spine. In: The Cervical Spine Research Society, Sherk HH et at. (eds) The Ce rvical Spine , 2nd edn. Lippincott, Philadelphia, 1989:567. 72. Paimela L, Laasonen L, Kankaanpaa E, Leirisalo-Repo M. Progression of cervical spine changes i n patients with early rheumatoid arthritis. ] Rheu mat oI 199 7;24: 1280- 1284. 73. Yonezawa T, Tsuji H, Matsui H, Hirano N. Subaxial lesions in rheumatoid arthritis. Radiographic factors suggestive of lower cervical myelopathy. Spine 1995 ;20 :208-2 15 . 74. Ball J, Sharp J. Rheumatoid arthritis of the cervical spine. In: Hill AGS (ed) M ode rn Tren ds in Rheu mat ol ogy, vol 2. Butterworth, London, 1971:117. 75. Meijers KAE, van Beusekam GT, Luyendijk W, Duijfjes F. Dislocation of the cervical spine with cord compression in rheumatoid arthritis. J Bone J oin t Su rg 19 74;56B:668 . 76. Shaw DA, Cartlidge NE. Cervical myelopathy in rheumatoid arthritis. A ct a Neu rol Bel g 19 76 ;7 6:2 79 . 77. Clark CR. Degenerative conditions of the spine: d ifferen tial diagnosis and non-surgical treatment. In: Frymoyer JW (ed) The A dult Spine, P rin ciples an d P ract ice , vol 2 . Raven Press, New York, 199 1: 1154. 78. Sharp J, Purser DW. Spontaneous atlanto-axial dislocation in ankylosing spondylitis and rheumatoid arthritis. Alln Rheu mat ol Dis 1961;20:47. 79. Uitvlugt G, Indenbaum S. Clinical assessment of atlanto­ axial instability using the Sharp-Purser test. A rthrit is Rheum 1988;31:918. 80. Wade W, Saltzstein R, Mainman D. Spinal fractures compli­ cating ankylosing spon dylitis. A rch Phys Me d Rehab il 1989;70:39. 81. Ramos e, Gomez A, Guzman JL et at. Frequency of atlantoaxial subluxation and neurologic involvement in patients with anky­ losing spondylitis. ] Rheu mat ol I995 ;22:2 120-2 125 . 82. Olerud D, Frost A, Bring J. Spinal fractures in patients with ankylosing spondylitis. Eu r Spine ] 1996 ;5:5 1-55 . 83. Montgomery WW, Peroue PM, Schall LA. Arthritis of crico­ arytenoid joint. A n n Ot ol Rhin ol L aryn goI 1955 ;64: 1025 . 84. Wojtulewski JA, Sturrock RD, Branfoot Ae, Hart FD. Crycoarytenoid arthritis in ankylosing spondylitis. BM] 1973;ii: 1 45.

85. Cyriax JH. Textb ook of Orthopae dic Me dicine , vol I, Diagn os is of Soft Tissue Les ions , 8th edn. Baill iere Tindall, London, 1982. 86. Forsythe M, Rothman RH. New concepts in the diagnosis and treatment of infections of the cervical spine. Orthop Cl in N orth A m 1978;9:1039. 87. Hsu LCS, Yau ACM. Tuberculosis. In: The Cervical Spine Research Society, Sherk HH et al. (eds) The Ce rvical Spil/e , 2nd edn. Lippincott, Philadelphia, 1989:5 44. 88. Currier BL, Heller JG, Eismont FJ. Cervical spinal infections. In: The Cervical Spine Research Society, Clark CR et al. (eds) The Ce rvical Spine , 3rd edn. Lippincott-Raven, Philadelphia, 1998:659-690.

222 SECTION TWO - THE CERVICAL SPINE

89. Simeone F. Intraspinal neoplasms. In: Rothman R, Simeone F (eds) The Spin e. Saunders, Philadelphia, 1992: 1 515-1528. 90. Sundaresan N, Sachdev VP, Holland JF et al . Surgical treatment of spinal cord compression from epidural metastasis. J CLin On coI 1995;1 3: 2330 -2335 .

9 1 . Fornasier VL, Horne JG. Metastases to the vertebral column. Can cer 1975;36:490. 92. Nittner K. Spinal meningiomas, neurinomas and neuro­ fibromas-hourglass tumors. In: Vinken PJ, Bruyn GW (eds) H an dbook o f Cl ini cal Neuro l og y, vol 20. Elsevier, New York, 1976: 177. 93. Russell DS, Rubinstein U. P atho l og1j o f Tumo ur s o f the Ner vo us S yst em. EA Pall, London, 1977. 94. Simeone FA, Lawner PM. Intraspinal neoplasms. In: Rothman RH, Simeone FA (eds) The Spin e. Saunders, Philadelphia, 1982:1041.

95. Austin GM. The significance and nature of pain in tumors of the spinal cord. S urg Forum 1959;10:782. 96. Epstein JA. Common errors in the diagnosis of herniation of the intervertebral disk. In dust M ed 1 970;39:488. 97. Zeidman SM, Ellenbogen RG, Ducker TB. Intradural tumors. In: The Cervical Spine Research Society, Clark CR et al . (eds) The Cer vi cal Spin e, 3rd edn. Lippincott-Raven, Philadelphia, 1998:587-601. 98. Fine MJ, Kricheff IT, Freed D, Epstein FJ. Spinal cord ependy­ momas: MR imaging features. Radio l og y 1995;197:655-658. 99. Greenwood J Jr. Intramedullary tumors of the spinal cord, a follow-up study aiter total surgical removal. J Neuro surg 1963;20:665. 100. Kinsella LJ, Carney GK, Feldmann E. Lichen simplex chroni­ cus as the initial manifestation of intramedullary neoplasm and syringomyelia. Neuro surg er y 1992;30:418-421.

CHAPTER CONTENTS Headache

Cervicogenic headache Vertigo

Headache and vertigo of cervical origin

223

Non-cervicogenic headache

224

225

227

Anatomy 227 Nystagmus 231 Aetiology and classification of vertigo History 233 Clinical examination 233 Interpretation of the examination Therapy 236

232

235

HEADACHE

Headache is one of the most frequent complaints, even perhaps the commonest of human maladies.1 Some 4-5% of the general population seem to suffer from primary chronic daily headache,2 mean age being 24.5 years (range 7-74 years) with a male:female ratio of 2:1.3 For the public health it is a problem of enormous proportions affecting both the patient and society. It is comparable to back pain in that it affects mostly the active population and thus has socioeconomic consequences, generating high costs for therapy as well as for absence from work.4 Migraine, for example, is extremely frequent, affecting approximately 23 million Americans. An estimated 150 million workdays are lost each year and this costs between 6 and 17 billion dollars.s Headache occurs in both sexes from childhood on, presents in attacks and is felt unilaterally or bilaterally. The causal mechanisms are still not well understood and the patient's description may be so vague that distinction between the common benign forms and more serious syndromes is sometimes difficult. Sensitive structures within the skull can become stimulated by tension, stretching, compression or displacement, all of which can be the consequence of inflammation (e.g. meningitis), increase of pressure (e.g. tumour, haematoma) or decrease in pressure (e.g. lumbar puncture). The same happens when vascular structures dilate or constrict. Very often the problem lies outside the skull, as in tension-type headache of muscular contraction, trigemi­ nal neuralgia, temporal arteritis and conditions affecting the teeth, the temporomandibular joint, the eyes, the sinuses or other structures in this region. Headache may also be psychogenic. Headache is usually classified in three main groups (in order of frequency):6 ,

•

•

Tension-type headache, characterized by mild to moderate dull pain, often brought on by stress and / or depression Migraine, occurring mostly in women, and being of moderate to severe intensity and often accompanied 223

224 SECTION TWO - T H E C E RVICAL SPI N E

•

by nausea, photophobia and/ or phonophobia (see below) Cluster headache, more common in men, with typical multiple recurrent attacks of severe unilateral pain.

These three groups form the so-called 'primary headache disorders' and are opposed to the 'secondary headache disorders', such as temporal arteritis and mass lesions? The former tend to decline with age, while the prevalence of the latter increases.8 Attempts have been made to distinguish a group in which the cause for the headache lies in the cervical spine. In particular the work done by Sjaastad et al has helped to elaborate the criteria that may differentiate 'non-cervicogenic' headache from 'cervicogenic' headache (see below). NON-CERVICOGENIC HEADACHE

The common recurrent headaches are not life threatening but can very much influence the quality of life.9 It is therefore - in order to reach a proper diagnosis - inter­ esting to be able to classify these disorders according to well-delineated criteria. Such criteria were established by the International Headache Society in 1988 and are now widely accepted. Distinction is made mainly between tension-type headache and migraine. Rasmussen et allO support the contention that migraine and tension-type headache are distinct entities. They make up the large majority of cases, with I-week prevalences of 2% and 29%, respectively.ll Except migraine, which can some­ times be treated with techniques described in this book, these primary headache disorders fall outwith the scope of this work and will therefore only be discussed briefly. Tension-type headache is now the term used to describe headaches that have previously been grouped under various ill-defined headings such as 'tension headache', 'stress headache' and 'muscle con­ traction headache'. It is generally accepted to be charac­ terized by mild to moderate pain, felt bilaterally, described as 'pressing' or 'tightening' and not accompa­ nied by major systemic problems or neurological signs. Jensen12 performed a population-based study of 1000 subjects randomly selected from a general population, two clinical studies, and a study of methods of EMG recording. He concluded that tension-type headache more frequent in younger women - had a life-time preva­ lence of 78% in a general adult population. Some 30% were affected more than 2 weeks a year and 3% were labeled as chronic. Diamond13 makes a distinction between an episodic form, which would be a physiologic response to stress, anxiety, depression, emotional conflicts, fatigue or repressed hostility and a chronic form, occurring with depression or persistent anxiety. Tension-type headache.

According to Kunkel both peripheral muscular contrac­ tion and central pain-modulating systems are probably involved.14 Russell et ailS suggest the occurrence of a genetic factor. Jensen and Olesen16 emphasize the poor knowledge of the pathogenesiS and the need for more scientific interest from the medical field which would positively influence the therapeutic approach, that is currently mostly non-specific. They mention pericranial injection of botulinum toxin as the only new strategy. Migraine headache. Migraine is a paroxysmal disorder characterized by recurrent severe attacks of headache which vary in intensity, duration and frequency. Onset is often in adolescence and is characterized by a unilateral throbbing pain in the head which may last between 15 minutes and 1 week but most often lasts for some hours or a day. The pain very often spreads to the whole neck but mobility of the cervical spine remains unchanged. Launer et aI17 found that the prevalence of migraine is higher than previously reported. In women the lifetime prevalence was 33% and the I-year prevalence 25%. In men the lifetime prevalence was 13.3% and the I-year prevalence 7.5%. They state that among patients with migraine in the past year, 63.9% had migraine without aura, 17.9% had migraine with aura and 13.1% had migraine both with and without aura. The diagnosis of migraine can be established when three or more of the following criteria are present:1 8 • • • • •

Unilateral severe headache that may change sides Accompanying anorexia, nausea and vomiting Prodromal focal neurological symptoms ('aura') Family predisposition Response to ergotamine.

Until now the vascular theory has been widely agreed upon. Distinction has been made between two different phases with totally different symptoms. During the pro­ dromal phase, intracranial blood vessels constrict and characteristic visual and/ or sensory disturbances occur. Unilateral tingling in tongue, lips and hands as well as hemiparesis, aphaSia and hemianopSia are less frequent symptoms. In the second phase the blood vessels dilate, which results in acute unilateral headache. There is usually photophobia and the patient prefers to lie down and rest. Loss of appetite, nausea and vomiting supervene, the last sometimes bringing immediate relief. It has been suggested that migraine can be explained by dynamic changes in blood flow, whereby there is an alternation of strong and weak circulation in the small arteries and capillaries. This follows central defects in the hypothalamiC region and results in biochemical changes that are responsible for the appearance of certain mecha­ nisms that trigger an attack. An attack may also be trig-

CHAPT E R 11

gered by different factors, such as excessive effort, certain food and allergic or emotional factors. More recent theories19 tend to explain migraine as a neurovascular disorder. They suggest that the primary dysfunction occurs within the central nervous system which causes changes in blood vessels within pain-pro­ ducing intracranial meningeal structures. This would be responsible for the headache. Aurora et al20 support this theory of migraine having a primary neural basis with secondary vascular changes. By applying advanced imaging and neurophysiological methods during sponta­ neous attacks of migraine they have obtained evidence of spreading neuronal inhibition as the basis of aura. They state that this neurophysiological event is accompanied by hyperoxia of the brain, possibly associated with vasodilatation. They also found evidence that the spread­ ing cortical event can activate the subcortical centres pos­ sibly involved in nociception and associated symptoms of the migraine attack and they conclude that susceptibil­ ity to migraine attacks appears to be related to brain hypereXCitability. Frishberg21 states that a review of the pertinent litera­ ture, expert consensus and a Practice Parameter issued by the American Academy of Neurology all suggest that routine neuroimaging is not necessary in patients with migraine headaches as defined by the International Headache Society (IHS) criteria. He concludes that imaging should be done in patients with: • • • • •

New-onset headaches Headaches with a progressive course Headaches with a significant change in pattern Headaches that never alternate sides Headaches associated with any known secondary cause such as tumour, arteriovenous malformation or other structural lesion.

The classical therapeutiC approach has three major pillars: avoidance of migraine triggers, treatment of the acute attack by medication and regular use of preventive medications of which a wide variety is available, includ­ ing beta-adrenergic blockers, calcium channel blockers or tricyclic antidepressants. Several authors22,23,24 mention a new effective approach, which includes drugs for intranasal administration (sumatriptan, dihydroergota­ mine), and application of the 'triptan' anti-migraine agents (zolmitriptan, naratriptan, rizatriptan, eletriptan). They are serotonergic agonists acting selectively by causing vasoconstriction through 5-HT1B receptors (hydroxytryptamine 1 receptors) in the intracranial arter­ ies and by inhibiting nociceptive transmission through an action at 5-HTlD receptors on peripheral trigeminal sensory nerve terminals in the meninges and central terminals in brainstem sensory nuclei. Other new medication in migraine treatment include substance-P

- H EADAC H E

A N D V E RT I G O OF C E RVICAL O R I G I N 225

antagonists, nitric oxide synthetase inhibitors and calci­ tonin gene-related peptide antagonists. Migraine and orthopaedic medicine. On empirical grounds Cyriax25 found that manipulation of the cervical spine may have a therapeutic effect. The onset can some­ times be aborted by 30 seconds of strong traction, the effect of which cannot be explained but would clearly repay further study. Manipulation has a preventive effect in a minority of patients, especially the middle-aged or elderly. Migraine dating from adolescence, and therefore most unlikely to be triggered off by trouble in the neck, may respond well in middle-age. It is therefore always worthwhile manipulating the cervical spine in patients over 40. When the neck movements are painless, one session usually suffices. Manipulation is performed in four directions: both rotations and both lateral flexions. Painful neck movements may require two or three ses­ sions. The techniques are described on p. 254. The effect of manipulation on migraine was also shown in a study by Tuchin et al26 who reported that some people experience significant improvement in migraines after chiropractic spinal manipulative therapy. Cluster headache. Also called 'Horton's neuralgia', this headache occurs mostly in middle-aged men, with sudden unilateral and sometimes unbearable attacks of pain, at the same hour each day, often starting during the night and lasting 30 minutes to 2 hours. This goes on for 1-3 months; attacks then cease, only to return after several weeks or months. The pain is felt mostly at the same side in the fronto­ temporal and orbital areas. It has a burning and pulsating character and is accompanied by redness and sweating of the affected half of the face. The eye waters and the nose is congested. Sometimes a moderate Horner's syndrome may be present. Cluster headache with aura, either visual or olfactory, is rare.27 The known precipitants are alcohol, histamine and glyceryl trinitrate. But Blau and Engej28 have observed that exercise, a hot bath or elevated environmental tem­ perature provoked cluster headaches within 1 hour in 75 out of 200 patients, perhaps via generalized vasodilata­ tion of hypothalamic activation. The condition responds well to antihistamines or to lithium.29

CERVICOGENIC HEADACHE

Sjaastad and coworkers30-34 have, in consecutive publica­ tions since 1990, established criteria for the diagnosis of headache of cervical origin (Box 11.1), since 1983 known as 'cervicogenic headache'. Other authors support these criteria.35 Pfaffenrath and Kaube36 and Kranzlin and Wiilchli37 found that 14-16% of headache sufferers fulfil

226 S E CT I O N TWO - T H E C E RVICAL S PI N E

Box 11.1 The criteria of Sjaastad et al for diagnosing cervicogenic headache • The headache is mainly unilateral and does not shift • Pain starts in the neck and then spreads to the forehead • There are symptoms and signs of neck involvement, e.g. diminished range of motion • The attack is mechanically precipitated, either by neck movement or by external pressure over the greater occipital nerve of the C2 root • There may be ipsilateral shoulder/arm pain • The pain improves after blockade of the occipital nerves • The following features may also be present: autonomic disturbances, dizziness, phono- and/or photophobia, monocular visual blurring and difficulty in swallowing.

the criteria. Nilsson38 supports the fact that cervicogenic headache is one of the three large headache groups. The pain is mild, usually has an undulating course and may eventually become chronic. There is a marked female preponderance. The neck seems to be involved, either because there has been a trauma, for example whiplash, or because there is limitation of neck move­ ment. There may be accompanying shoulder and/ or arm pain. An attack can be precipitated either as the result of neck movement or of direct pressure, for example on examination.39 Cervicogenic headache may also coexist with migraine without aura.40 In their early publications Sjaastad et al mention the headache as being strictly unilat­ eral. In a recent article they restate this and define unilat­ erality as follows: the headache dominates on one side; when weak, the pain may be only on that side; when severe, it may also be felt on the contralateral side, but to a lesser extent. It never dominates on the contralateral side.41 The fact that neck structures can give rise to headache is generally accepted.42,43 van Suijlekom et al44 have done an in vivo design study which has shown that Sjaastad's criteria for cervi cogenic headache are as reliable as the IHS's criteria for tension-type headache and migraine. Leone et a145,46 believe that further studies are needed to define clinical patterns indicating a neck-headache rela­ tionship and definitively to confirm the validity of cer­ vicogenic headache as a nosological entity. Zwart47 states that cervicogenic headache has been recognized as a pain syndrome by the International Association for the Study of Pain and stresses the importance of quantifying the reduced neck motion by technical means. Bono et al48 con­ sider Sjaastad's criteria as valid in order to make a pre­ liminary identification as a first sequence in an overall clinical and technical examination. The IHS has also established, just as for tension-type headache and migraine, quite similar criteria to diagnose cervicogenic headache (Box 11.2). These criteria have been questioned by some authors49 and supported by others.50

Box 11.2 The 1990 criteria of the International Headache Society for diagnosing cervicogenic headaches1

1.

Pain localized to neck and occipital region. May project to forehead, orbital region, temples, vertex or ears. 2. Pain is precipitated or aggravated by special neck movements or sustained neck posture. 3. At least one of the following occurs:

• Resistance to or limitation of passive neck movements • Changes in neck muscle contour, texture, tone or response to active and passive stretching and contraction • Abnormal tenderness of neck muscles. 4. Radiologic examination reveals at least one of the following: • Movement abnormalities in flexion/extension • Abnormal posture • Fractures, congenital abnormalities, bone tumours, rheumatoid arthritis or other distinct pathology (not spondylosis or osteochondrosis).

Cervicogenic headache and orthopaedic medicine. There are a number of orthopaedic medical conditions that can give rise to headache and that often can be approached very successfully by the use of local treatment (see p. 149). Lesions of the extracranial soft tissues of the loco­ motor system, especially the capsuloligamentous struc­ tures of the occipitoatlantoaxial complex, may give rise to segmental headache. The cervical dura mater is often responsible for the vague, multisegmental occipito­ frontal, temporal or retro-orbital pain (see p. 178). Headache, referred from the cervical dura mater. A disco­ dural interaction at any cervical level or any space­ occupying lesion in the spinal canal may give rise to pain felt in the head. The pain usually radiates from the mid­ neck up to the temple, the forehead and behind one or both eyes but rarely to the bridge of the nose. This 'multisegmentally referred pain' is dural in origin and will disappear when treatment to the neck is accomplished. For further details see pp. 178-179. Matutinal headache in the elderly. As the result of arthro­ sis at the upper cervical joints, ligamentous contracture may develop and can result in 'segmental' pain felt in the upper cervical dermatomes which cover the head. The patient typically complains of occipitofrontal headache felt especially in the morning. Treatment includes capsuloligamentous stretching. For a detailed descrip­ tion see pp. 197-198. Postconcussional headache. The upper cervical capsules and ligaments can also become sprained during trauma, for example an accident that causes concussion of the brain after which a period of immobilization follows. The subsequent build-up of ligamentous adhesions finally results in 'segmental' headache. Several authors recog-

CHAPTER 11

nize the possibility of upper cervical capsuloligamentous conditions causing pain in the head.52,53 The adhesions can be broken manipulatively. A full description can be found on p. 204.

VERTIGO

Vertigo or dizziness is not an uncommon complaint of patients who suffer from disorders that affect the cervical spine. Most often these symptoms are not related to the conditions but just occur at the same time as the cervical disorder. If the dizziness is caused by the functional dis­ turbance in the neck, it may be expected to be as 'treat­ able' as any other symptom originating in that area. It would therefore be very helpful to be able to differentiate 'cervical vertigo' from other possible causes. Vertigo originating as the result of movements of the neck initially suggests a cervical origin. These move­ ments, however, influence not only the proprioceptive system of the cervical spine but also the blood flow through the vertebrobasilar arteries. At the same time, the vestibular apparatus may also be disturbed. All these factors in control of balance are interrelated. ANATOMY

Man is aware of his position in space. The cortex there­ fore receives information from three different systems: optical, vestibular and proprioceptive (superficial and �----t"--

-

H EADAC H E A N D VERT I G O OF CERVICAL ORI G I N 227

deep). Disturbances in one of these areas often result in vertigo. Optical system. Visual stimuli pass via the optical nerve, the optic chiasma and the optic tracts, mainly to the occipital cortex, though some traverse the mesen­ cephalon and interact with eye movement, vestibular activity and the muscles of the cervical spine. Vestibular system. The vestibular system consists of a peripheral part (organ of balance and vestibulocochlear nerve) and a central part (vestibular nuclei and vestibu­ lospinal tract). Peripheral part. The osseous labyrinth lies in the tempo­ ral bone and has three membranous semicircular canals (membranous labyrinth) (Fig. 11.1). Each lies in contact with an ampulla that contains sensory receptors - the cupulae - a gelatinous substance that moves in the endolymph and in which the otoliths float. It also con­ tains the sensory hair cells. Impulses generated by move­ ment of otoliths within the endolymph pass via the vestibulocochlear nerve (vestibular part) to one of the four vestibular nuclei. Central part. This is formed by the four vestibular nuclei in the white substance of the pons cerebri from which several tracts originate (e.g. the vestibulospinal tract). These connections facilitate orientation of the position of the body. There are also many cerebellovestibular connections, responsible for good judgement and adaptation of the

vestibular nuclei

cochlea

medulla oblongata

semicircular canals ductus endolymphaticus

� _ ________���________ � J

membranous labyrinth

Figure 11.1

The vestibular system.

228 SECTI O N TWO - T H E C E RVICAL S PI N E

direction of movements and for control of anti-gravity muscles. Much information comes from the vestibular nuclei to modulate the activity of the oculomotor nuclei and thus the ocular muscles. These stimuli cause nystagmus, the main sign of a vestibular disorder. Proprioceptive system. Superficial, fine tactile sensations are conveyed through the anterior spinothalamic tract. Deep tactile sensations (conscious proprioception is a combination of deep sensation, discrimination sense and vibratory sensation) are transmitted along the fasciculus gracilis and the fasciculus cuneatus. Reflex propriocep­ tion (unconscious proprioception) is conveyed centrally via the ventral and dorsal spinocerebellar tracts and the olivospinal tract.

Blood supply

The vertebrobasilar system is a 'closed' circuit, starting below in the subclavian arteries and ending above in the arterial circle of Willis (Fig. 11.2). The left subclavian artery originates directly from the aortic arch as does the left common carotid artery. The right subclavian artery, as well as the right common carotid artery, are branches of the brachiocephalic trunk. The common carotid artery divides (usually at the level

of the fourth cervical vertebra) into the external and internal carotid arteries. The external carotid artery is of less importance in this context and supplies the outer parts of the head - the face, the temporal area, the occipital region, the skin of the head and the mouth. The internal carotid artery gives off very few branches during its extracranial course but supplies a considerable part of the brain via the anterior cerebral (medial aspect of the hemispheres) and the middle cerebral artery (a continuation of the internal carotid artery, which supplies the entire outer and lateral aspects of the brain), before it anastomoses again with the vertebrobasilar system. The vertebral arteries originate bilaterally from the subclavian arteries, of which they usually form the first and biggest branches. They run parallel on both sides of the spinal column and form the main blood supply for the brainstem, the cervical spinal cord and the cervical spine. They are closely related to this part of the spinal column and the vertebrae are adapted to the presence of the artery in that the transverse processes CI-C6 contain a transverse foramen through which the artery runs (see Ch. 6). A groove for the artery lies above the posterior arch of the atlas, dorsal to the lateral masses. Occasionally, this groove is closed to form an arterial canal.

anterior cerebral artery

anterior cerebral artery

anterior communicating artery

middle cerebral artery

posterior communicating artery

middle cerebral artery

��__

-posterior cerebral artery

-

basilar artery

-------t+--+

internal carotid artery external carotid artery

external carotid artery

If--hl---- vertebral

common carotid artery

artery

common carotid artery

subclavian artery

..f----- subclavian artery

brachiocephalic trunk

�---- aortic arch

Right Figure 11.2

The vertebrobasilar system.

Left

CHAPTER 11

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H EADAC H E AN D V E RT I G O OF C E RVICAL O R I G I N 229

1---V -- 4 1---V - 3

1---V2

Figure 11.4

The course of the vertebral artery in the atlantoaxial area.

V1

The course o f the vertebral artery: V1, extravertebral segment; intervertebral segment; V3, atlantoaxial segment; V4, subforaminal and intracranial segment.

Figure 11.3

V2,

The vertebral artery is divided in four segments54,55 (Fig. 11.3): Extravertebral segment. The artery runs upwards from the subclavian artery to the transverse foramen of the sixth cervical vertebra. It is surrounded anteriorly by the anterior scalenus and longus colli muscles; posteriorly and distally it is adjacent to the first rib and the transverse processes of the first thoracic and the seventh cervical vertebrae. Intervertebral segment. From the sixth to the second ver­ tebrae the vertebral artery passes through a canal formed by the transverse foramina and, between the vertebrae, by ligamentous and muscular structures. The antero­ medial border is formed by the uncovertebral joints (von Luschka's joints). The vertebral artery runs anterior to the nerve roots and spinal nerves, the latter lying in the sulcus for the spinal nerve. An uncoarterioradicular junction is thus formed. This is of clinical importance because arthrotic changes at these levels may have important conse­ quences for the blood flow in these arteries. The contents of the transverse foramina include, in addition to the vertebral artery, two vertebral veins, the periarterial venous plexus of the vertebral artery and the vertebral nerve.

Atlantoaxial segment. Between the axis and atlas the artery curves backwards and outwards (Fig. 11.4) because the transverse foramina of the atlas lie more lat­ erally than those of the other vertebrae. The artery runs dorsally around the lateral mass of the atlas and loops over the posterior arch in the arterial groove. It is sur­ rounded anteriorly by the joint capsules of the atlanto­ occipital joints and posteriorly by the obliquus capitis superior and rectus capitis posterior major muscles. Subforaminal and intracranial segment. The artery curves upwards again and runs cranjally from postero­ lateral to anteromedial to pierce the posterior atlanto­ occipital membrane, the dura mater and the arachnoid mater, and to enter the skull via the foramen magnum. Just below the base of the brain and at the level of the pons, the left and right arteries join to form the basilar artery. The latter trunk then splits into a left and right posterior cerebral artery. From the vertebral and basilar arteries branches originate to supply parts of the brain, especially the cerebellum. A characteristic of the blood supply of the brain is the close connection of the different arteries by means of communicating arteries. Together they form the arterial circle of Willis. From posterior to anterior the circle of Willis contains two posterior cerebral arteries, both origi­ nating from the basilar artery. They are both connected via posterior communicating arteries with their respec­ tive internal carotid artery. From here depart both anterior cerebral arteries, connected by one anterior communicating artery. The circle is thus completed. Blood supply by the vertebral arteries. At the cervical level the vertebral arteries give off cervical branches and cranial branches, the latter anastomosing with the spinal rami. There are extensive anastomoses with the deep cervical artery (originating via the costocervical trunk from the

230 S E CTI O N TWO - T H E C E RVICAL SPI N E

subclavian artery), the thyrocervical trunk and its branch (the ascending cervical artery) and the occipital artery (branch of the external carotid artery). Spinal rami supply the anterior and posterior roots, the epidural blood vessels and the vertebral canal, especially the upper two vertebrae. Articular rami supply the joint capsules of the intervertebral and uncovertebral joints. Muscular rami supply the intrinsic muscles of the cervical spinal column and cutaneous branches supply the skin. Just before both vertebral arteries join to form the basilar artery, they give off, unilaterally or bilaterally, a branch that forms (together with its fellow) the anterior spinal artery, which supplies the anterior aspect of the spinal cord. The posterior spinal arteries also originate from the vertebral arteries and supply the posterior aspect of the spinal cord, where they anastomose extensively with the spinal rami. Intracranially, the branches that form the posterior inferior cerebellar arteries supply the posterolateral part of the medulla oblongata, part of the posterior lobe of the cerebellum, the vermis and the cerebellar nuclei. The basilar artery and its branches form the blood supply for the medulla oblongata, the reticular forma­ tion, the pons, the mesencephalon, parts of the cerebel­ lum (via the anterior inferior cerebellar artery and the superior cerebellar artery), the vestibular system and its nuclear complex (via the labyrinthine artery). The posterior cerebral arteries are part of the circle of Willis via anastomoses with the internal carotid artery. They supply parts of the thalamus and hypothalamus, the occipital lobe, large parts of the temporal lobe, the red nucleus, the substantia nigra, the nuclei of the oculo­ motor nerve (III) and the trochlear nerve (IV). Blood flow

Together the vertebral arteries form a functional unit. In normal circumstances, disturbance of the function of one artery is immediately compensated for by the other, provided it is healthy. Failure adequately to compensate leads to complaints and symptoms, especially vertigo and tinnitus. Provocation tests, directed at the function of the vertebrobasilar system, are designed to test this com­ pensation mechanism (see later). Severely diminished flow in one vertebral artery may well lead to occlusion of the posterior inferior cerebellar artery on that side, resulting in a lateral medullary infarc­ tion - Wallenberg's syndrome (Box 11.3). Blood flow in the vertebral arteries may be influenced by movement, compression, trauma or vascular factors.56 However, the functional adaptability of structures within the spinal canal, and intervertebral and transverse foram­ ina is so high that anatomical changes such as narrowing do not necessarily cause symptoms.

Box 11.3 Characteristics of Wallenberg's syndrome • Dysphagia and ipsilateral palatal weakness (involvement of nucleus ambiguous) • I mpairment of sensation to pain and temperature on the same side of the face (involvement of descending root of the fifth cranial nerve) • Horner's syndrome in the ipsilateral eye (involvement of the descending sympathetic fibres) • Nystagmus (involvement of the vestibular nuclei) • Cerebellar dysfunction in the ipsilateral arm and leg (involvement of the restiform body and cerebellum) • Impairment of sensation to pain and temperature over the opposite half of the body (involvement of the spinothalamic tract)

Movement. Different authors agree that maximal rotation of the cervical spine diminishes blood flow in the con­ tralateral vertebral artery. This effect is greatly increased when rotation is combined with flexion, extension and / or side flexion. Chrost, cited by Gutmann and BiedermalU1,57 has made a survey in terms of percentage of the blood flow in the vertebral arteries in different positions of the head (Table 11.1). Flexion and extension movements have very little influence on the blood flow in the vertebral arteries because the axis of flexion and extension of each segment lies in the same course. Side flexion of the local spine gives rise to moderate diminution of blood flow in the ipsilateral artery. Rotations have greatest influence on the blood flow. 'Redundancy' of length may also help to accommodate movements. For example, the distance between the vertebral artery and the axis of rotation is greatest in the atlantoaxial segment and redundancy is therefore required at this level in the atlantoaxial loop of the artery so that, even if it is extended during full rotation of CIon Table 11.1 Relationship of head position and blood flow Head position

Impact on blood flow

Neutral position

Normal flow

Rotation

Slight decrease in the ipsilateral artery Significant decrease in the contralateral artery

Side flexion

Slight decrease in the ipsilateral arte

ry

No decrease in the contralateral artery Flexion and extension

No decrease

Extension combined

Significant bilateral decrease, most in the

with rotation

contralateral artery

Flexion combined

Significant bilateral decrease

with rotation Flexion combined with

Slight decrease in the contralateral artery

side flexion and

Cessation in the ipsilateral artery

contralateral rotation

CHAPT E R 11

-

H EADAC H E A N D VERTIGO OF C E RV I CAL O R I G I N 231

I

C2, neither the lumen nor flow is reduced. During 30° of rotation there is an influence on the contralateral vertebral artery and during 45° of rotation the artery is almost com­ pletely occluded. On the other hand, there is an atlanto­ occipital loop between Cl and the occiput. This curve does not change during movement and may be considered as a buffer mechanism against strong arterial pulsations. Compressing factors.

,

I

Nature: rhythmic/non·rhythmic Direction: horizontal/vertical rotary/mixed Frequency Amplitude: broad/fine

There are a number of compressing

factors.

Nystagmus

I

1

Physiological: focusing optokinetic vestibular

:

'

I Pathological: congenital acquired spontaneous gaze/gaze deviation

In the extravertebral segment. Exceptionally, compres­ sion may be related to anatomical anomalies (an unusual origin of the artery) or to shortening in the prevertebral musculature.

Figure 11.5

In the intervertebral segment. Osseous growth at the edges of the vertebral bodies (spondylosis) and degener­ ative changes in one or more intervertebral joints (spondylarthrosis) may cause compression.58 The inter­ vertebral disc is of lesser importance here, except in large disc protrusions where the vertebral artery may rarely become threatened.

Nystagmus can be classified according to its nature (rhythmic or not), its direction (horizontal, vertical, rotary or mixed), and its frequency or its amplitude (broad or fine) (Fig. 11.5).

In the atlantoaxial segment. Circulation in the vertebral artery is impaired, on the one hand, by congenital arterial anomalies (hypoplasia of one or both vertebral arteries, aplasia of one artery, anomalies in the circle of Willis) and, on the other hand, anomalies and positional changes in the upper cervical vertebrae, such as basilar impres­ sion, an extraoccipital condyle, assimilation of the atlas (fusion of the atlas with a part of the base of the skull), osseous canal for the vertebral artery at the upper part of the posterior arch of the atlas, odontoid anomalies (aplasia, asymmetry), os odontoideum (articulation between odontoid process and the body of axis) and fusion of CI-C2. These anomalies are rare and are not detected on routine examination. In

the

subforaminal

and

intracranial

segment.

Compression here is very exceptional. Fractures, luxations and contusions (direct or indirect) may also influence blood flow in the vertebrobasilar system.

Traumatic factors.

Vascular factors. Disorders of the vascular wall, haemor­ rhage and embolism, the latter being quite exceptional, have direct influence on blood flow. Disturbances, espe­ cially hyperactivation, in the sympathetic system may lead to vasoconstriction.

NYSTAGMUS

The main sign that characterizes vertigo is the presence of nystagmus, an involuntary repetitive movement of the eyes - the cardinal sign of a vestibular disorder.59

Classification of nystagmus.

Classification

Types.6o

Nystagmus can be physiological or pathological.

Focusing nystagmus occurs when a fixed point is looked at. Optokinetic nystagmus occurs when objects pass by with a certain regularity or when a moving person passes by a number of stationary objects (e.g. sitting in a train). Vestibular nystagmus is seen when the head is quickly turned in one direction. Movement of endolymph within the canals lies in relation to that of the head and contin­ ues momentarily after the head has stopped. The cupula organs in the ampullae of the semicircular canals are moved in the direction of lymph flow and are thus stim­ ulated. Muscles, especially the extraocular muscles, are influenced by this and the position of the eyes changes as the head is turned, in a direction opposite to the rotation. At first the eyes remain behind but are then brought back to their normal position. This eye movement, slow first and opposite to the turning direction, followed by a quick movement in the direction of the rotation is called 'nodding eye movements' or 'nystagmus'. The slow phase is caused by impulses from the labyrinth; the quick phase is the result of corrective mechanisms in the ocular muscles. Physiological nystagmus.

Pathological nystagmus. Nystagmus can be either con­ genital or acquired. In the latter, it occurs spontaneously or as the result of movement (positioning or provoking nystagmus). Spontaneous nystagmus can have a peripheral cause. In this case, a one-sided viewing-direction nystagmus is found: a nystagmus that is latently present becomes worse when the patient is asked to look in one direction.

232 S E CT I O N TWO - T H E C E RVICAL SPI N E

When the problem is central, nystagmus may present in different situations: • •

•

•

Fixation nystagmus occurs when the patient tries to fix a certain point. Two-sided viewing-direction nystagmus (symmetrical nystagmus) is seen when a person looks in one direc­ tion and then in the opposite direction. Exclusive one-sided viewing-direction nystagmus is not latently present but occurs only when looking in one direction. Flagging movements or dysconjugation of movements of the eyes is seen when the examiner makes a pendulum movement with the arm.

Gaze nystagmus or gaze deviation nystagmus always has a central cause. It may be present for as long as the patient gazes and the eye movement may not be horizontal. Clinical importance

One or other type of nystagmus on clinical examination is an absolute contraindication to manipulative treatment and should be investigated by a neurologist.

AETIOLOGY AND CLASSIFICATION OF VERTIGO

It is usual to classify vertigo into two groups, depending on the cause: vestibular and non-vestibular vertigo. Vestibular vertigo is divided into peripheral and central types. Vestibular vertigo

Vertigo is peripheral when the cause of the symptoms lies in the peripheral vestibular system, containing the labyrinth and the vestibular part of the vestibulocochlear nerve. Peripheral vestibular vertigo is characterized by short­ lived heavy turning sensations with a sudden onset. It may be accompanied by hearing disturbances61 (tinnitus, deafness) and sometimes important autonomic nervous system symptoms, such as palpitations, anxiety, nausea, vomiting, sweating and fluctuations in blood pressure. There are some disorders that selectively involve the peripheral vestibular system to cause dizziness without hearing loss, for example benign paroxysmal positional vertigo, vestibular neuritis and bilateral idiopathic vestibulopathy.62 Transitory spontaneous nystagmus, rotating or horizontal, and in the same direction may also be present. It is regular and with a latency period. Most disorders in the peripheral vestibular complex lead to vertigo: Injuries, infections, neoplasms, labyrinthine vascular accident, Meniere's syndrome and vestibular neuronitis. Peripheral.

Central. The lesion lies in the vestibular nuclei or their tracts. Central vertigo may result from injury, multiple sclerosis, tumours, cerebral arteriosclerosis and vertebro­ basilar insufficiency leading to brain stem ischaemia or cerebellar stroke.63 Disturbances of equilibrium accompany the vertigo. Symptoms are persistent, sometimes with acute exacer­ bations. Auditory disturbances are rare and neurovegeta­ tive symptoms are also less pronounced. There is persistent spontaneous nystagmus, which sometimes varies and changes direction. It is irregular and has no latency period.

Non-vestibular vertigo

This type of vertigo may have different causes: ophthal­ mological, psychiatric, orthostatic hypotenSion, visual and auditory disorders, and possibly alteration in the proprioception from the cervical joints. Hyperventilation, circulatory disorders, arterio-sclerosis, brain sclerosis, skull injury and anaemia are other possibilities. A special form of non-vestibular vertigo occurs in dis­ orders which affect the cervical spine. In this form, a distinction can be made between either a vascular or a proprioceptive cause. The former may follow circulatory disorders in the area supplied by the vertebral arteries; the latter results from disturbances in the proprioception of the joints of the upper cervical segments, mainly as the result of arthrosis or a disc protrusion. Important features in the functional examination of a patient complaining of vertigo

In view of the treatment of the neck patient within orthopaedic medicine it is of extreme importance to differentiate between the following types of patients: •

•

•

The patient who shows a contraindication for any type of cervical treatment, when the problem lies within the vertebrobasilar system. The examination is then meant to recognize the possible risk factors. The patient whose vertigo has nothing to do with the neck, when the vestibular system is affected and in whom a normal treatment can be given to the cervical spine. The patient in whom the vertigo is cervicogenic and can be treated as such. This is so when the proprioceptive system is disturbed.

Requests came from several sources for the recognition of risk factors in patients who may need to receive manual and/ or manipulative treatment to the neck. This has led to the development of 'Clinical Standards for Pre­ manipulative Testing of the Cervical Spine'. The first and so far most important and internationally recognized standard is the Australian one,64 from which other stan­ dards have been derived.65-69 There are mutual differ-

CHAPTER 11

ences but from these standards emerges a consensus on some important features: a patient with complaints of vertigo should be put through meticulous history-taking, an orientating otoneurological examination and a number of dizziness provocation tests.

•

HISTORY

The history is extremely important. The moment the patient mentions symptoms that could be something to do with vertigo (dizziness, tinnitus, anxiety, palpitations, excessive perspiration), the examiner should determine whether or not vertigo is truly present. This is achieved by the following sequence of questions. •

• • • • • • •

Are there real turning sensations or just a dizzy feeling ? Turning sensations point towards a vestibular dis­ order, usually in the peripheral part. This also applies to motion sickness, for example car sickness, for which the cause is usually vestibular. How did it start - suddenly or gradually ? This may indicate the type of vertigo present (see below). How long does it last? Does it come in attacks ? How severe are the complain ts ? Is the vertigo influenced by certain positions? Is the vertigo influenced by the position of the head ? How frequently do the attacks occur ?

Questions should also be asked about other symp­ toms, such as deafness, tinnitus, headache, nausea / vom­ iting, neurological symptoms (disturbances of vision or speech, paraesthesia, diminution of consciousness) and infection / fever. Clinical examination is not wholly reliable and much attention should be paid to history. The diagnosis is made on the recognition of certain patterns of symptoms. The importance for the orthopaedic phYSician is that a correct provisional and general diagnosis is made and the patient correctly referred for specialist attention. Based on the history, three types of vertigo can be dis­ tinguished. •

•

Sudden, severe and short: a sudden attack, coming on rapidly, lasts only a short time (from a few seconds to some hours) and disappears quite quickly. The causes can be non-vestibular (benign paroxysmal positioning vertigo, orthostatic vertigo, hyperventilation, cervical vertigo) or vestibular as the result of insufficiency of vertebral and / or basilar arteries. Differential diagno­ sis should be made from Meniere's syndrome, hypo­ glycaemia or syncopation. Sudden, severe and gradually disappearing: a sudden and severe attack is much slower to disappear (over several days to several weeks). It is caused by a peripheral

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H EADAC H E A N D V E RTI G O OF C E RV I CAL O R I G I N 233

vestibular condition, such as vestibular neuritis, labyrinthine injury, labyrinthine vascular accident, (peri)labyrinthitis or herpes zoster oticus. Differential diagnosis is required from multiple sclerosis. Chronic, permanent/long-standing and not severe: not very severe, but continuously present, chronic vertigo with slight exacerbations may go on for months without change. It can be caused by non-vestibular or central vestibular lesions (cerebral atherosclerosis, hypertension, tumour between the pons and cerebellum and skull injury).

CLINICAL EXAMINATION

The information presented here is a summary of some of the clinical tests which enable distinction of a non­ vestibular vertigo from a vestibular one, the latter having either a central or peripheral cause. Orientating examination of equilibrium

The following tests are appropriate for the vestibu)ar system: • • • • •

Neck extension Romberg's test Unterberger's test Babinski-Weill test Barany's test

Neck extension. The patient is asked to look at the ceiling for about 20 seconds or less if he is not able to maintain that position. Romberg's test. Assesses static equilibrium. The patient stands with both feet together, if possible, and performs Jendrassik's grip (reinforcement) (Fig. 11.6). If this seems impossible, he holds his arms outstretched in front of him. When it is possible to hold the position with the eyes open, but not with the eyes closed, the test is considered positive. The patient then usually tends to fall to one side. Further neurological examination is then required. Unterberger's test. The patient stands with the arms for­ wards and must try to 'step' on the spot, lifting the knees. Rotation of 45° per 50 steps is considered normal, more than this is pathological. The examiner should note the direction in which the patient moves (Fig. 11.7). There seems to be disagreement about the value of this test. However, it was demonstrated in a prospective study of 100 patients with unilateral, subsequently histo­ logically proven acoustic neuroma, that Unterberger 's test achieved a higher sensitivity than the Romberg test.7o In a recent prospective, controlled study Kuipers and Oosterhuis concluded that this test does not appear to be useful for detection of abnormalities in the vestibular

234 S E CTI O N TWO - T H E C E RVICAL S PI N E

Eyes open

,

Figure 11.8

Spontaneous nystagmus.

tively. If a lesion is present, the arm deviates towards the affected side. Examination of nystagmus

The examiner observes and analyses the involuntary eye movements. The following should be borne in mind: Figure 11.6

•

Romberg's test with Jendrassik's grip.

0°

•

90°

�--------���.r--------t-

90°

1 80° Figure 11.7 Unterberger's test: the patient walks on the spot. Rotation of more than 45° per 50 steps is pathological.

system or for distinguishing normal individuals from patients?1 A few years earlier Hickey et al came to the same conclusion.72 Babinski-Weill test. The patient is asked, with his eyes closed, to walk five steps forwards, followed by five steps backwards, then forwards again and so on for 30 seconds. The test is positive when the walk is star-shaped. Barany's test. The patient sits. A point is fixed at a minimum distance of 2 m. The patient then closes his eyes and is asked to indicate the point 20 times consecu-

Nystagmus has a slow (pathological) phase and a quick (recovery) phase, and its direction is described by the latter. However, the side of the lesion is better indicated by the former (e.g. a quick recovery phase to the right implies a problem to the left). The patient cannot influence the examination, nor can compensation be achieved.

Nystagmus may occur spontaneously (Fig. 11.8) and a combination of opening and closing the eyes may point towards the type of nystagmus present. The examiner next undertakes tests to recognize positioning or provok­ ing nystagmus (see types of nystagmus above). In orthopaedic medicine two tests are important: the De Kleyn-Nieuwenhuyse and the Dix-Hallpike tests. The patient is in a supine lying position with his head maximally rotated in more or less maximum extension (Fig. 11.9). This provokes diminution or abolition of the blood flow in the con­ tralateral vertebral artery, thereby testing the compensat­ ing mechanism in the ipsilateral vertebral artery and in the basilar artery and its branches. Disturbance of blood flow in the ipsilateral artery may result in the appearance of nystagmus or vertigo. De Kleyn-Nieuwenhuyse test.

The patient sits on the couch with his head turned away. The examiner then brings the patient quickly backwards under guidance. In pathological circumstances nystagmus results, but if it disappears within 30 seconds it is a benign paroxysmal positioning vertigo. Positional nystagmus together with the precip­ itating mechanism and the Dix-Hallpike test seem to be Dix-Hall pike test.

CHAPT E R 11

-

H EADAC H E A N D VERTIGO OF C E RVICAL O R I G I N 235

INTERPRETATION OF THE EXAMINATION

Careful interpretation of the data from the history and of the findings from the clinical examination (see Fig. 11 . 10) must enable the examiner to get an idea of the area where the problem lies: in the vestibular system, the vertebro­ basilar system or the cervical spinal joints. Disturbance in the vestibular system

Disturbance of the vestibular system is movement induced. The rapid execution of different neck move­ ments may cause dizziness and probably also nausea ('motion sickness'). The examiner must keep in mind that vestibular vertigo, because of its blood supply via the basilar artery, may also be the result of acute ischaemia of the vestibular tissues. Disturbance of the vertebrobasilar system Figure 11.9

Test of de Kleyn and Nieuwenhuyse.

the best predictors of benign paroxysmal positioning vertigo.73 Provocation tests for dizziness

The patient, either sitting or lying, is subjected to differ­ ent neck movements: they are performed rapidly and repeatedly at first and then sustained in the end range for at least 10 seconds. The neck movements are purely physiological but may be combined. • • • • • • • •

Flexion Extension Side flexion Rotation Flexion, combined with rotation Extension, combined with rotation If manipulation is considered, the patient's head is also put in the different manipulation positions Movements of the trunk while the patient's head is held motionless.

Technical investigations

The most valuable otological examination methods are electronystagmography and audiometry. Electronystag­ mography seems to be useful when the cause is thought to be central or is uncertain. It is not significantly helpful in the diagnosis of peripheral lesions except as confirmation. 74 Of the clinical neurophysiological methods, brainstem auditory evoked potentials are more useful than electro­ encephalography. Computed tomography and magnetic resonance imaging should be used when a central nervous system disorder is suspected.75

The most important symptoms that are experienced by patients suffering from vertebrobasilar insufficiency are described by Coman59 as the 5 Os: dizziness, dysarthria, dysphagia, diplopia, drop attacks. Other symptoms, such as weakness, numbness, gait disturbance and visual abnormalities are also possible?6 The sustained neck positions provoke dizziness and / or nystagmus. Disturbance of propriocepsis of the cervical spine

Elements that point towards a vestibular disorder (i.e. turning sensations, motion sickness) are absent. The patient does not mention one of the 5 0 symptoms. There is no nystagmus. The neck movements are positive in that they indicate a cervical disorder: pain, stiffness, pos­ sibly diminished range of motion, articular pattern. The movements may or may not provoke dizziness. There may be balance disturbance?7 Benign positional paroxysmal vertigo is common in the elderly and even more common in patients with migraine.78 Multivariate analysis demonstrated that the presence of a turning sensation and the absence of a light­ headed sensation predicted its presence?9 Some authors describe upper cervical joint dysfunc­ tion as a possible cause of vertigo.8o Others doubt the existence of cervical vertigo as an independent entity and strongly emphasize the need to exclude neurological, vestibular and psychosomatic disorders first.81,82 Posturographic assessment of human posture dynamics could be a possible future tool for use in diagnosing cervical vertigo.83 Oostendorp et al69 describe a turning / stop turning test (without head and neck movements) that could act as a differentiating element between vestibulogenous dizzi­ ness and cervicogenic dizziness.

236 S E CTION TWO - T H E C E RVICAL SPI N E

Turning/stop turning test. The patient sits on a revolving stool with closed eyes. The examiner turns the patient ten times with constant speed in one direction. He then stops the movement and waits until an eventual dizziness has disappeared. The same is then performed in the other direction. The test is positive when the patient recognizes the symptoms, i.e. turning sensations. When this test is positive the problem is rather vestibu­ logenous. If the cervical provocation tests are also posi­ tive there is clearly a cervicogenous component as well. When the test is negative and the provocation tests posi­ tive, the dizziness is of cervical origin.

THERA PY

A patient with vestibular vertigo should be referred for specialist examination and treatment. Acute vertigo as the result of dysfunction of the labyrinth or of a serious

central nervous system process demands prompt inter­ vention to avoid long-term disability. Chronic vertigo may need surgery or rehabilitative measures, for example physiotherapeutic adaptation exercises, for lasting relief.84 Non-vestibular proprioceptive vertiginous complaints can have a discal origin. In these cases, manipulation with maximum traction and no articular movement (straight pull, traction with leverage) usually gives good results, especially in the elderly. This should of course only be performed by an experienced operator. For the technique, see pp. 260 and 267). If there is any doubt, other conditions must first be excluded by specialized examination. The same techniques have the surprising result of also curing tinnitus. Kessinger mentions good results on cervical manipulation for vertigo, tinnitus and diminished hearing.ss Physical therapy also seems to be an effective treat­ ment for benign positional paroxysmal vertigo . 86,s7

Non·vestibular Sudden/short Vestibular

History

Sudden/slow

�----------�

'--'

Peripheral vestibular

Non-vestibular Chronic Central vestibular

r-E;;-;;mt;;;;;;--�-..J ;; Equilibrium

Tests: Neck extension Romberg Unterberger Babinsky-Weill Barany

Examination Observation Nystagmus Tests: De Kleyn-Nieuwenhuyse Dix-Hallpike

Flexion

I---.! Extension

Provocation tests '---------'

Figure 11.10

History and examination of vertigo.

Side flexion Rotation Flexion, combined with rotation Extension, combined with rotation Manipulation positions Movements of the trunk

Vestibular

CHAPT E R 11

-

H EADAC H E A N D VERTIGO OF C E RV I CAL O R I G I N 237

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CHAPTER CONTENTS Definition Incidence

240

Classification Pathology

Whiplash-associated disorders

239

240

241

Several lesions 241 Other lesions 241

Medicolegal consequences Psychological problems Diagnosis

Natural history Chronicity

242

tissue neck injury, cervical strain, cervical sprain - to

242

describe the lesion and the consequences that occurred after the typical car accident: a rear-end motor vehicle

243

collision.

243

Therapeutic approach

Previous accounts used different terms - whiplash injury, hyperextension injury, acceleration injury, soft

242

Clinical picture

241

When a vehicle is struck from the rear, the occupan ts 243

rarely have warning and do not brace the muscles to prevent head movement. As a result, the body is pro­ pelled forwards and the neck hyperextends well beyond the normal range of allowable movement (Fig. 12.1). This violent motion is followed by a less rapid recoil into flexion that can often result in a head injury if the head impinges on the windscreen. Although rear-end impacts are much more common with hyperextension-hyperflexion injuries as a result, other types of car accident may also cause whiplash-type injuries and, in any trauma, complex head and neck movements may occur leading to different lesions that resemble whiplash.

DEFINITION Medical literature, in an attempt to find a proper definition, has so far described 'whiplash injury' in the light of the mechanism of the accident, the type of lesion that is caused or the clinical appearance after the injury. In 19951 the Quebec Task Force (QTF) proposed the following definition:

Whiplash is an acceleration-deceleration mechanism of energy transfer to the neck. It may result from rear-end or side-impact motor vehicle collisions but can also occur during diving or other mishaps. The impact may result in bony or 50ft-tissue injuries (whiplash injury), which in turn may lead to a variety of clinical manifestations (whiplash­ associated disorders).

The term 'whiplash-associated disorders' (WAD) indi­ cates the clinical features that result from an accident in which the two elements - acceleration, followed by decel­ eration - are responsible for the traumatic forces that act on the cervical spine and related structures. 239

240 SECTION TWO - THE CERVICAL SPINE

(a)

Figure 12.1

(b)

Whiplash injury: (a) hyperextension on impact, followed by (b) recoil into flexion.

INCIDENCE

Box 12.1 Clinical (Quebec) classification of whiplash­ associated disorders

As the result of increased mobility and the increase in

Grade

Clinical presentation

number of cars all over the world, motor vehicle acci­

o

No complaint about the neck

dents have become very frequent with, as a result, an

No physical sign(s)

enormous increase in whiplash-type trauma. It is one of

Neck complaint of pain, stiffness or tenderness only

the most common mechanisms of injury to the cervical

No physical sign(s)

spine. The incidence is not precisely known. A figure of 1 per

II

Neck complaint AND

1000 people per year has been suggested.2 The QTF mentions figures on whiplash injuries in Canada. In 1987 in the province of Quebec there were

Musculoskeletal sign(s) III

AND Neurological sign(s)

approximately 131 whiplash injuries per 100 000 vehi­ cles per year - 70 injuries per 100 000 inhabitants. This

Neck complaint

IV

cost the Canadian government CAN $19 000 000 of

Neck complaint AND Fracture or dislocation

which 70% was income compensation. The female:male ratio is about 1.5:1 and the main age group 20-24 years. Other studies in Canada mention 5000 whiplash cases a year in the province of Quebec, accounting for 20% of

In both classifications there is no suggestion made

all insurance claims after motor vehicle accidents.3,4 In the United States 11 300 000 car accidents were

about the lesion present or about the type of tissue

reported for the year 1991, of which 2 690 000 were rear­ end collisions and caused 85% of all whiplash injuries.s

occur after acceleration-deceleration injury.

CLASSIFICATION The QTF, persuaded that proper diagnosis is difficult to achieve, has proposed two classifications: one accord­ ing to the severity of the symptoms and signs (grades) (Box 12.1) and one according to the time elapsed since the accident (stades) (Box 12.2).

damage. They reflect only the clinical appearances that

Box 12.2 Classification according to the time elapsed since the accident Stade I

II

4 days

IV

III

21 days

45 days

6 months

V

CHAPTER 12

-

WHIPLASH-ASSOCIATED DISORDERS 241

the acute phase and it took a few weeks for the radicular

PATHOLOGY

symptoms to appear. In postmortem studies Taylor et ai

Depending on the movement of the head during the

damaged structure.IS-17 J6nsson et ai l S Also confirmed the

accident, several lesions may occur, ranking from severe to moderate and slight. Hyperextension is the most common mechanism, followed by hyperflexion and

describe the intervertebral disc as the most frequently large number of disc lesions after whiplash and during surgery were able to confirm the MRl findings. Posterocentral protrusions lead to central, bilateral or

lateral flexion.6

unilateral pain in a multisegmental distribution: pain in

SEVERE LESIONS

nation a symmetrical (mimicking a full articular pattern)

Hyperextension and distraction of the neck may rupture

cases the picture may be torticollis-like. For a detailed

the neck, trapezius and upper scapular area. On exami­

the anterior longitudinal ligament as well as some discs. A ruptured disc can lead to a backward displacement of the above-lying vertebra - the upper facets then slide down on the lower - with damage to the spinal cord as a result? Spinal cord injuries after motor vehicle accidents occur most often in young car drivers - the age group

15-24 years.S,9 Pure hyperextension may also cause compression of the spinClI cord in those cases in which retrolisthesis or spinal stenosis already existed. In other instances, com­ pression fractures of the posterior elements may occur. Hyperflexion injury may lead to fractures of the verte­ bral body - most fractures of the atlas10 and of the axis11 are the result of motor vehicle accidents - and I or to dis­ ruption of posterior ligaments and occasionally facet joint luxation. Less frequently, lesions of arteries, veins, neural struc­ tures, oesophagus and retropharyngeal tissues may occur.

or asymmetrical pattern of limitation is found. In acute description of disc pathology, see page 192.

Facet joint problems Whiplash may also lead to problems at the level of the zygapophyseal joint capsules.19 Lord et al undertook a placebo-controlled prevalence study after whiplash and found chronic cervical facet joint pain common.20 The pain is felt unilaterally and is usually rather localized. A convergent or divergent motion pattern may occur, although any asymmetrical pattern is com­ patible. (Facet joint pathology is discussed on p. 198.)

Ligamentous lesions Ligaments can become overstretched, leading to minor lesions12 or may become adherent as the result of post­ traumatic immobilization. They present with vague stretching pain felt at the end of range of those move­ ments that stretch the ligament (see p. 204)

OTHER LESIONS

Muscular lesions

The less severe lesions are much more frequent and may

clinical studies,21,22 on echography,23 in experiments in

involve the intervertebral discs, the zygapophyseal joints, the cervical ligaments and muscles. These lesions may occur in isolation but are more often combined and therefore sometimes difficult to recognize. The common complaint is neck pain.

Muscular lesions, mostly anteriorly, are described in animals24,2s and in postmortem studies.26 Muscles, particularly their occipital insertions, can be strained during the injury. The subsequent pain will be quite localized and can be elicited during either contraction or stretching - the contractile tissue pattern (see p. 204).

Discodural and discoradicular interactions Recent retrospective studies have shown that the occur­ rence of disc lesions after whiplash injury are quite importantI2,13 and one prospective study indicates the value of clinical diagnosis.14 Most disc lesions are end­ plate avulsions and ruptures of the anterior annulus fibrosus. As the result of the hyperextension element during the trauma the disc may have fissured. The subsequent flexion or hyperflexion element causes displacement of disc material in a posterior direction. Davis et al describe a number of posterolateral disc lesions with radicular symptoms as the result of a hyperextension whiplash trauma.12 These herniations seemed to develop only after

MEDICOLEGAL CONSEQUENCES As WAD automatically involve compensation claims, they have considerable consequences. If a significant number of patients remain with some disability - and this number still seems to increase - the costs of diagno­ sis, treatment and indemnity become progressively higher. The different parties involved in the approach to WAD are: • The patient seeking for help and for a refund of

money. For most patients the two elements do not

242 SECTION TWO - THE CERVICAL SPINE

influence each other but for a number of people the

forming the necessary technical investigations: radiogra­

compensation claim is essential. This may result in

phy, CT scan, scintigraphy and / or MRI.

absence from work, illness behaviour, social disability, malingering and fraud. • The doctors looking for a diagnosis. Physicians treating

technique to use should be based on clinical grounds.

the patient wish to reach a diagnosis and to confirm it

Radiographs in patients with soft tissue injuries are often

by technical investigations. They also - because of the often complex syndrome - use an extensive pattern of

negative: no fractures or luxations are found. The finding most commonly obtained is loss of the normal cervical

treatment techniques. Doctors who work for the insur­

curvature on a lateral view.29 CT scanning and MRI are

ance company are sometimes biased and tend to over­

not very helpful in recent cases but may become impor­

diagnose the condition as 'psychogenic' or 'simulation'. • The insurance companies trying to minimize their

tant when the condition persists, although their use is still controversial. Scintigraphy may be useful to screen

payments. As the result of the lack of consensus about

for occult fractures. 3D

diagnosis and treatment of WAD, the insurance compa­

The reader is referred to the section on non-discogenic disorders (p. 211) for further information about the diag­

rues see their compensation payments and indemnities

•

Technical investigations in posttraumatic neck patients are mandatory but the decision about which imaging

rise considerably. They exert pressure on governments in order to keep these expenses under control.

nosis of non-mechanical conditions.

The lawyers protecting either the insurance company

examination must be initially suggestive of some of the

In most cases the condition is not severe and clinical

or the patient. Discussions about the confirmation of

above mentioned conditions although the picture may

the lesions and the consequences for patients' profes­

sometimes be'vague and difficult to interpret.

sional activities lead to an increase in litigation. It is clear that eligibility for compensation for pain and suffering furthers the perseverance of symptoms and a tendency to chrOnicity. Where this compensation can be eliminated a decrease of the incidence and an improved prognosis is seen.27

Diagnostic difficulties Most patients present a genuine clinical pattern. The symptoms and signs are clear and not too difficult to interpret. Some patients describe a more diffuse picture, probably because there is a combination of lesions. The examiner should then concentrate on the features that are understood and compatible with a known syndrome.

PSYCHOLOGICAL PROBLEMS Most whiplash-associated disorders start as an ordinary trauma followed by pure physical disturbance. When subsequent treatment is unable to rehabilitate the patient after a short period of time, secondary emotional and psychological changes may occur. They make the patient more aware of neck pain and subsequently aggravate and perpetuate the pain, or even turn a simple neckache into chronic pain and disability.28

Most difficult are the patients who exaggerate or sim­ ulate their symptoms. They pretend to have problems in the hope to better persuade the examiner or to inculcate belief in their story. The examiner should look for inherent unlikelihoods and positive inconsiscencies in history and functional examination which will enable a positive diagnosis of 'psychogenic pain' or 'malingering' to be made.

Symptoms Immediately after the accident the patient is stunned and confused and complains mainly of any head problem

DIAGNOSIS CLINICAL PICTURE

present. A feeling of discomfort in the neck, often associ­ ated with some degree of nausea, may develop. Although not usually reported, up to 60% of the patients have evi­

Making a diagnosis in patients who underwent a

dence of concussion with momentary loss of conscious­ ness. Examination in the emergency department of a

whiplash-type injury is no different from other patient

hospital may not reveal any positive signs and discharge

groups. It requires proper history taking, inspection and

follows. In the following hours and days a cluster of

careful functional examination, including a neurological

symptoms may then develop: soreness, tenderness and

evaluation.

swelling in the anterior neck region, stiffness and restric­

Severe lesions should be recognized and the patient

tion of movement at the neck, headache, visual and audi­

immediately treated as necessary. Most of these condi­

tory disturbances, dizziness, concentration and memory

tions are classified as grade IV and fall outside the scope

disturbances, pain in the upper thorax, scapular area,

of this book. They will probably be recogrtized clinically

shoulder and arms, and numbness or paraesthesia in the

when warning signs are present but certainly by per-

upper limbs accompanied by a feeling of heaviness and

CHAPTER 12 - WHIPLASH-ASSOCIATED DISORDERS 243

weakness. Most symptoms gradually disappear but the

found that 30% of patients still complained, even 4-7 years

majority of patients are left with pain in the neck, radiat­

after the accident.34 Another study showed that increasing

ing to the scapular area or to the shoulder region.

age and the severity of the initial neck pain were predictors

The examiner should enquire about the mechanism

of lasting symptoms after 6 months.35 Objective neurolog­

and the velocity of the trauma that will enable a judge­

ical signs and degenerative changes on radiographs or

ment on the severity of the injury and to make a progno­

MRl (spondylosis, diminution of the diameter of the spinal

sis.31 Other important information relates to the delay

canal) may be associated with poor prognosis.

between the accident and the onset of symptoms, which

In 30-40% the condition needs up to 1 year to recover,

often is 2-3 days.32 Many patients have associated low

aching diminishing quite considerably in the first 2

back pain33 and this is noted and assessed later. Important information can be obtained by asking the

months. The pain usually disappears but, when nothing is done, movements may remain restricted.

patient to describe exactly the localization of the symp­ toms: central or bilateral symptoms suggest a condition lying at the midline, whereas unilateral symptoms may stem either from a central or a unilateral condition. The examiner also concentrates on inherent likelihood for a certain lesion, for example multisegmental pain in disc lesions, segmental pain in facet lesions, local pain in muscular lesions. When a patient continuously presents inconsistencies or an improbable combination of symp­ toms and this is later confirmed during the functional examination, the examiner should be on guard.

Signs Inspection of the position of the patient's neck may indi­ cate an acute condition, for example when a torticollis­ like picture is found or when muscle spasm is present. When the head is fixed in flexion with central or bilat­ eral pain a posterocentral disc displacement is clearly present. Articular signs - pain on movement with or without limitation - suggest involvement of the intervertebral joint or the facet joints, certainly when movement is shown to be restricted. Discodural or discoradicular interactions are considered when the articular signs are accompanied by dural or radicular signs (see p. 178). When there is no dural or nerve root involvement, the possibility of a condition of the facet joint exists; the pain is purely unilateral, i.e. when either a convergent or divergent pattern is found. Limitation of movement inculpates the joints. End-range pain is typical for ligamentous or muscular conditions, the latter also giving rise to positive resisted movements (see p. 205).

CHRONICITY Not all patients will develop chronic symptoms after whiplash injury. In most instances it is a benign, self­ limiting condition. All patients destined to recover will do so in the first 2-3 months after trauma. Those who do not may claim symptoms for another few years. Recent studies have indicated that between 14 and 42% of patients develop chronic symptoms and that about 10% have permanent trouble,36-42 although patients may improve even after many years.43 A predisposing factor for chronicity could be pre-existing spondylosis.44 The study of the QTF clearly demonstrates that the most common whiplash injury - without bony or cord lesions­ is essentially a benign and self-limiting condition. A small number of patients are refractory and responsible for the enormous costs incurred by the injury: about 50% of all costs are spent on an eighth of the total number of victims. Of 1 000 000 whiplash injuries per year in the USA, the majority of the patients become asymptomatic after a limited number of weeks or months. According to certain statistics, 20-40% continue to have invalidating symp­ toms for several years. In those countries where the entity of 'chronic pain' resulting from rear-end collisions is not known and conse­ quently there is no fear of long-term disability leading to indemnity and litigation, symptoms after whiplash injury are self-limiting, exist only over a short period of time and there is no evolution towards the chronic stage.45

Because combined lesions are not at all uncommon, the clinical picture may become difficult and therefore hard to interpret. It should be looked at in the light of the

THERAPEUTIC APPROACH

anatomical reality and compared to the known clinical pictures occurring in the cervical spine (see Ch. 8).

There is still some discussion about how to approach patients with lasting symptoms from WAD. It is difficult to find objective signs and physicians are therefore

NATURAL HISTORY

divided into two groups: those who believe the patients and those who think in terms of psychogenic pain,

The natural history of whiplash-associated disorders is

personality and chronicity because of concerns about

difficult to predict. An extensive study in Switzerland

financial compensation.

244 SECTION TWO - THE CERVICAL SPINE

There is some consensus about the possibility of

performed immediately because it is unwise to leave the

making the patient develop an active and positive atti­

displacement in that posterocentral protrusions draw

tude towards the problem. In those patients who do not

out osteophytes fairly quickly; this may lead to a situa­

present intensive neck pain immediately following the

tion in which extension or one rotation becomes perma­

accident, who do not show clinical signs of cord or root

nently blocked. Because a posterocentral protrusion is

compression and in whom the routine radiographs show

present, great care must be taken in the choice of the

no bony abnormalities, all further extensive and expen­

techniques and operation: rotation movements are

sive examinations should. be avoided.

avoided and the therapist must be experienced. In acute

The patients should be encouraged to remain active

cases with gross deviation, manipulation is performed

and functional. In the acute phase analgesics and anti­

every day. Traction in the direction of the deviation, fol­

inflammatories should be administered but only tem­

lowed by pure traction manipulations without articular

porarily. A collar should not be used for more than a few

movement, leads quickly to full recovery. The more

days and should be replaced by early mobilization of the cervical spine. The patient should be taught how to do

moderate and long-standing cases require more treat­

active movements and prolonged physiotherapy must

weeks. The techniques for posterocentral protrusions

be avoided in order not to push the patient into a passive

are used: straight pull, lateral flexion, anteroposterior

disabled attitude.

gliding and traction with leverage (see pp. 262-263).

ments, performed once or twice a week over a few

Such an approach is also recommended by the QTF in

Facet joint lesions can be treated either with steroid

order to avoid prolonged disability.46 It is advocated that

infiltration or with deep transverse massage; in more

early return to work is one of the best measures to avoid

chronic cases slow stretching is used (see pp. 269-270).

chronicity. Immobilizing measures such as bed rest and

Ligamentous lesions can best be treated with deep

collars are best avoided.

transverse massage, unless there are adhesions which can

Specific treatment

deep transverse friction or infiltration with local anaes­

In those cases where the diagnosis is clear the condition

thetic. If a combination of ligament and muscle damage

must be treated properly at the side of the lesion.

exists, the muscle should be treated first.

be manipulatively broken. Muscular lesions respond to

When a discal pattern is found and thus a disco dural

Proper treatment and re-examination on a regular

or discoradicular interaction is present, manipulation is

basis are the guarantees of a maximal therapeutic result.

REFERENCES 1. Scientific Monograph of the Quebec Task Force on Whiplash­ Associated Disorders. Spine 1995:20(85):22S. 2. Barnsley L, Lord S, Bogduk N. Whiplash injuries. Pain 1994;58:283-307. 3. Girard N. Statistiques descriptives sur la nature des blessures. Quebec: Regie de l'assurance automobile du Quebec, Direction des services medicaux et de la readaptation, Avril. Internal Document, 1989. 4. Giroux M. Les blessures 11 la colonne cervicale: importance du probleme. Le Medecin du Quebec 1991;5ept:22-26. 5. Van Goethem JWM, Biltjes IGGM, van den Hauwe L, Parizel PM, De Schepper AMA. Whiplash injuries: is there a role for imaging? Eur J RadioI1995;22:8-14. 6. Hohl M. Soft-tissue neck injuries. In: The Cervical Spine Research Society, Sherk HH et al (eds) The Cervical Spine, 2nd edn. Lippincott, Philadelphia, 1989:436-441. 7. Kinoshita H. Pathology of hyperextension injuries of the cervi­ cal spine. Paraplegia 1994;32:367-374. 8. Northrup BE. Evaluation and early treatment of acute injuries to the spine and spinal cord. In: The Cervical Spine Research Society, Clark CR et al. (eds) The Cervical Spine, 3rd edn. Lippincott-Raven, Philadelphia, 1998:541-549. 9. Myers BS, McElhaney JH. Cervical Spine Injury Mechanisms. Biomechanics and Prevention. Springer, New York, 1993:311-361. 10. Kurz LT. Fractures of the first cervical vertebra. In: The Cervical Spine Research Society, Clark CR et al. (eds) The Cervical Spine,

3rd edn. Lippincott-Raven, Philadelphia, 1998:409-413. 11. Clark CR, White AA III. Fractures of the dens: a multicenter study. J Bone Joint Surg 1985;67A:1340-1348. 12. Davis S, Teresi L, Bradley W, Ziemba M, Bloze E. Cervical spine hyperextension injuries: MR findings. RadiologJJ 1991;180: 245-251. 13. Hamer AJ, Gargan MF, Bannister GC, Nelson RJ. Whiplash injury and surgically treated cervical disc disease. Injury 1993;24:549-550. 14. Pettersson K, Hildingsson C, Toolanen G, Fagerlund M, Bj6rnebrink J. Disc pathology after whiplash injury. A prospec­ tive magnetic resonance imaging and clinical investigation. Spine 1997;22(3):283-287. 15. Taylor JR, Finch PM. Neck sprain. J Ausl Fam Physician 1993;22:1623-1629. 16. Taylor JR, Twomey LT. Acute injuries to cervical joints: an autopsy study of neck sprain. Spine 1993;18(9):1115-1122. 17. Taylor JR, Twoney LT. Disc injuries in cervical trauma. Lallcet 1991;338:1340-1343. 18. J6nsson H Jr, Cesarini K, Sahlstedt B, Rauschning W. Findings and outcome in whiplash-type neck distorsions. Spine 1994;19: 2733-2743. 19. Ketroser DB. Whiplash, chronic neck pain, and zygapophyseal joint disorders. A selective review. Minn Med J 2000;83(2):51-54. 20. Lord SM, Barnsley L, Wallis BJ, Bogduk N. Chronic cervical zygapophysial joint pain after whiplash. A placebo-controlled prevalence study. Spine 1996;21(15):1737-1745.

CHAPTER 12 - WHIPLASH-ASSOCIATED DISORDERS 245

21. Frankel V H. 1976 Pathomechanics of whiplash injuries to the

35. Radanov BF, di Stefano G, Schnidrig A, Ballinari P. Role of

neck. In: Morley TP (ed) Current Controversies in Neurosurgery. Saunders, PhjJadelphia, 1996:39-50. 22. Jeffreys E. Soft tissue injuries of the cervical spine. In: Disorders of the Cervical Spine. Butterworth, London, 1980:81-89. 23. Martino F, Ettore GC, Cafaro E et al. L'ecographia musculo­ tendinea nei traumi distorvi acuti del colla. Radiol Med Torino

psychosocial stress in recovery from common whiplash. Lancet

1992;83:211-215.

24. Macnab r. Whiplash injuries of the neck. Manitoba Med Rev 1966;46:172-174. 25. La Rocca H. Acceleration injuries of the neck. Clin Neurosurg 1978;25:209-217. 26. J6nsson H Jr, Bring G, Rauschning W, Sahlstedt B. Hidden

cervical spine injuries in traffic accident victims with skull fractures.] Spinal Discord 1991;4:251-263. 27. Cassidy JD, Carroll LJ, Cote P et al. Effect of eliminating compensation for pain and suffering on the outcome of insur­ ance claims for whiplash injury. NE]M 2000;342(16):1179-1186. 28. Waddell G. The Back Pain Revolution. Churchill Livingstone, Edinburgh, 1998:173-186. 29. Daifner RH. Evaluation of cervical injuries. Sem Roentgenol 1992;27:239-253. 30. Kitchel SH. Soft-tissue neck injuries. In: The Cervical Spine

Research Society, Clark CR et al. (eds) The Cervical Spine, 3rd edn. Lippincott-Raven, Philadelphia, 1998:351-355. 31. Gebhard JS, Donaldson DH, Brown CWO Soft tissue injuries of the cervical spine. Orthop Rev 1994;suppl1:9-17. 32. Jolliffe VM. Soft tissue injury of the cervical spine: consider the nature of the accident. BM] 1993;307:439-440. 33. Taylor JR, Finch PM. Neck sprain. Aust Fam Physician 1993;22:1623-1625. 34. Dvorak J, Valach L, Schmidt S. Cervical spine injuries in

Switzerland.] Manual Med 1989;4:7-16.

1991;338:712-715. 36. Hodgson SP, Grundy M. Whiplash injuries: their long-term

prognosis and its relationship to compensation. Neuro-Orthop 1989;7:88-91. 37. Hildingsson C, Toolanen G. Outcome after soft-tissue injury of

the cervical spine. A prospective study of 93 car-accident victims. Acta Orti1op Scand 1990;61:357-359. 38. Pettersson K, Karrholm J, Toolanen G, Hildingsson C. Decreased width of the spinal canal in patients with chronic symptoms after whiplash injury. Spine 1995;20(15): 1664-1667. 39. Barnsley L, Lord S, Bogduk N. Clinical review. Whiplash injury. Pain 1994;58:283-307. 40. Maimaris C, Barnes MR, Allen MJ. 'Whiplash injuries' of the

neck: a retrospective study. Injun) 1988;19:393-396. 41. Gargan MF, Bannister Gc. Long-term prognosis of soft-tissue

injuries of the neck. ] Bone Joint Surg 1990;72B:901-903.

42. Olsson I, Bunketorp 0, Carlsson G et at. An in-depth study of

neck injuries in rear end collisions. In: Proceedings of the International !RCOBI Conference on the Biomechanics of Impacts, Bron-Lyon, France, Sept 12-14. 1990:269-280. 43. Olivegren H, Jerkvall N, Hagstrom Y, Carlsson J. The long-term prognosis of whiplash-associated disorders (WAD). Eur Spine J 1999;8(5):366-370.

44. Bonuccelli U, Paverse N, Lucetti C et al. Late whiplash syn­

drome: a clinical and magnetic resonance imaging study. Functional NeuroI1999;14(4):219-225. 45. Obelieniene D, Schrader H, Bovim G, Miseviciene I, Sand T.

Pain after whiplash: a prospective controlled inception cohort study. J Neurol Neurosurg Psychiatry 1999;66(3):279-283. 46. Scientific Monograph of the Quebec Task Force on Whiplash­ Associated Disorders. Spine 1995;20(85):36S.

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CHAPTER CONTENTS Treatment of discodural and discoradicular interactions Manipulation 247 Traction 264 Injection at a nerve root 266 Epidural injection 266 Collars 267 Prophylaxis 267 Awaiting spontaneous recovery 267 Surgery 267 Treatment of the other, non-discogenic lesions Manipulation/capsular stretching 268 Deep transverse friction 269 Injection/infiltration 270 Collar 271 Surgery 271

267

247

Treatment

A number of therapeutic measures exist to treat the various mechanical conditions that occur in the cervical spine. Discodural and discoradicular interactions, the most common disorders, are approached by either manipula­ tion or traction. Prophylactic measures may then help to avoid recurrence. In non-reducible instances it is best to wait for spontaneous cure although nerve root block and, more rarely, epidural injection or surgery may prove necessary. In some non-discogenic disorders, manipulation, deep transverse massage, infiltration and partial immobiliza­ tion may prove possible conservative therapeutic approaches. Surgery is another possibility. In all circumstances, great care should be taken to make the correct diagnosis and to consider indications and contraindications.

The purpose of treatment in these disorders is to break the vicious circle of the involvement of both the disc and the sensitive structure that it compresses. This can be achieved by concentrating treatment on one of the involved structures. Because the disc displacement not only affects the dura mater or the nerve root but also dis­ turbs the function of the intervertebral joint, it is logical first to try to influence the disc. The question then arises: Can the disc fragment be reduced or not? Reducible discs can be managed by manipulation or continuous traction. The choice of treatment depends on the nature of the dis­ placement: either annular or, less frequently, nuclear. In those instances where for some reason reduction has become impossible, measures are taken to abolish the pain during the period of spontaneous recovery. Surgery is called for when the pain becomes intolerable or when a posterocentral protrusion menaces the spinal cord. MANIPULATION

CONTROVERSY Manipulation of the cervical spine has become very con­ troversial and its popularity depends on the school of 247

248 SECTION TWO - T H E CE RVICAL S PI N E

thought of the practitioner. Popularity tends to increase amongst patients because they are happy with the 'spectacular results' in the hands of those outside the field of classical medicine. In more orthodox medicine, manip­ ulation as a treatment for spinal conditions is hardly ever used. At the other end of the spectrum are chiropractors whose main treatment is chiefly manipulative. Osteopathy, McKenzie techniques and manual therapy are somewhat in between these extremes. Cyriax placed his method somewhere in the middle, using manipulation in some well-defined instances - about half of all mechan­ ical spinal conditions - and avoiding it in all the rest. In the light of numerous reports of complications after manipulation of the cervical spine (see below), different schools have published in their own class of journal and manipulation is either defended or rejected as a useful therapeutic measure. Treatment is, of course, chosen as a function of diagnosis. Because different schools speak professionally different languages and sometimes have totally different and divergent approaches to the many spinal disorders, they pursue clinical practice in different ways and come to different diagnoses. They then adapt their treatment to what they think is the cause of symp­ toms and may therefore manipulate for different reasons. Osteopaths and manual therapists use manipulative techniques to restore range in vertebral segments where they have found loss of mobility; chiropractors try to readjust the spine to get rid of perceived malalignment between vertebrae; in Cyriax's orthopaedic medicine and less frequently in the McKenzie approach, manipulation is used to abolish an internal derangement caused by a disc displacement. About 200 cases of more or less serious complications after manipulative treatment of the neck have been reported.1,2 Many authors therefore have become very cautious in accepting the suitability of this modality.3-12 The main arguments against manipulation are the possi­ ble hazards to the vertebrobasilar system or the spinal cord that are usually irreversible. Therapists who are familiar with manipulative techniques continue to use them because they consider the risks as minimal and the results satisfactory. Today, of course, such conclusions have to be the subject of comparative scientific studies which look for objective evidence.

DANGERS OF MANIPULATION Every act in medicine carries a risk: complications may occur during or after a surgical operation; any injection may result in an anaphylactic reaction; patients may die from internal bleeding after anticoagulant therapy or after the use of anti-inflammatory agents; invasive inves­ tigations - for example cardiac - may cause complica­ tions. Although such risks exist, in most instances no one

will stop using the techniques: the advantages outweigh the disadvantages. In manipulation risks are present but minimal by com­ parison with the number of treatments carried out daily all over the world by all types of practitioners who range from trained medical personnel to lay people: doctors, physiotherapists, manual therapists, osteopaths, chiro­ practors and bone setters. The accidents that are reported13-1S represent only one in millions of manipulations. The most common minor complications, such as increase in pain in the head or neck, vagal reactions and nausea, are only temporary and are therefore not reported. Those that are described are the more serious: dizziness, visual disturbances, syncope, ataxia, fainting, Barre-Lieou syndrome, Wallenberg syn­ drome, 'locked-in' syndrome, cardiac arrest, spastic quadriplegia and unexplained sudden death but the risk of such serious complication is extremely low - between 1 in 500 000 and 1 in 3 000 000 cervical manipulations.16--31 The majority of authors believe that some accidents go unreported but one by contrast has suggested there is over-reporting.32 The risks must also be put in context. Several authors have made a comparison between the occurrence of injury following manipulation and the complications of other treatments for cervical disorders. The incidence of a serious complication such as a gastrointestinal event after the use of non-steroidal anti-inflammatory drugs is 1 in 1000 whereas serious complications after manipulation occur only once in 1 000 000 to 2 000 000.33 After surgical procedures to the cervical spine, 1.6% of complications occur. These figures confirm those put forward earlier17 and can be used to argue that risks from other causes such as drug therapy can be between 100 and 400 times greater than after cervical manipulation. Most accidents seem to occur in the hands of chiro­ practors and only a very small fraction have taken place in the practice of medical doctors or physiothera­ pists.2,28,34-39 The difference probably arises from the fact that manipulation is the main therapeutic technique of chiropractors and thus is far more often used than in phYSiotherapeutics. Risk then cannot be an argument against manipulative practice if suitable instances are chosen and techniques are used that reduce the hazard to the spinal cord and vertebral arteries. Of course any patient who gets a serious complication is one too many and therefore every possible measure should be taken to minimize risks (see Precautions, p. 249). Many tests have been described to detect vertebrobasi­ lar insufficiency.40-44 They are based on the assessment of the compensating ability of the ipsilateral vertebral artery after reduction of the lumen and therefore blood flow of the contralateral vessel in the testing positions.4S-47

CHAPTER 1 3

A PA-protocol for pre-manipulative testing of the cervical spine Section I

Sub j ective examination

Questio n i ng rega rding the presence of d i zzi ness a n d other symptoms suggestive o f V B I , i nclud i n g l i ght headed­ ness, strange sensations i n the head, dysarthria, d i p lopia, d rop attacks, blackouts, d istu rbances of vision, t i n n itus.

Section II II a.

Physical examination Basis pre-manipulative scanning of patients without dizziness; Standard routine tests . sitt i ng an d/or s u p i n e lying susta i n ed extension susta i ned rotat i o ns susta i ned rotations with extension sim u l ated m a n i p u l ative position

II b.

Additional tests for patients with dizziness testing position/move ment which provokes d izzi ness test i n g q u ick neck movements which provoke d i zzi ness rotation tests in standing position to d ifferen­ tiate between neck and inner ear

II c.

Summary mani pu lation is contra-ind icated when any VBI tests are positive mani pulation is contra-i ndicated when d izzi ness is provoked w h i lst adopting a treatment position, d u r i n g a treatment tec h n i q ue or fo l l owi n g a treatment tec h n i q ue m a n i pu lation is a l l owed when V B I tests are negative and no contra-ind ications have been el icited

Section III Informed consent Verbal consent must be given by the patient to the fo l l owi n g wording: 'I wish to m a n i p u l ate your joint using a q u ick movement i n the position i n which I a m h o l d i ng your neck. You may hear a c l ick and this is normal. Neck m a n i pu lation can be dangerous but this is extremely uncommon. I have carried out the reco m mended preca utionary tests and in my opinion there is l ittle risk in your case. Are you agreeable for me to go a head?'

-

TREAT M E NT 249

that this is not significant.63-65 In addition, a test that is positive today is not necessarily positive tomorrow66 and complications may occur even in those who have not shown any previous symptoms of vertebrobasilar insufficiency.67 ,68 It can even be argued that examination procedures and mobilization techniques can be as dangerous as therapeutiC manipulation, especially when done at the end of range.69 The doctor or physiotherapist who intends to manipulate should always be aware that even tests during examination have a risk and that there will always be a factor of unpredictability even when all premanipulative tests are negative and even if the patient responded positively to earlier manipulations. Fear of damage to the vertebral artery must be judged relative to many other activities of daily living which are as dangerously aggressive for the artery as any therapeu­ tic technique.70-76 Stretching and momentary occlusion of the artery occur in normal daily activities or sports and are asymptomatic. This is only possible because the major flow to the brain comes not only from the vertebrals but also from the carotid systems which are much less influenced by head movements.41 Review of the literature, especially of the many case histories that have been described, leads some to con­ clude that a number of serious complications could have been prevented had the practitioner recognized warning signs which should have excluded manipulation.77-8o A review81 mentions faulty diagnosis, insufficient clinical knowledge or examination, inaccuracy as a result of routine, overconfidence, bad technique and therapeutic obstinacy as the main causes of complications. Manipulation is indeed potentially dangerous. It is therefore important, on the one hand, that the indication is sound and the patient is suitable and, on the other hand, that the right technique is chosen. Most failures are the result of incorrect diagnosis rather than faulty technique.

Section IV Recording Physiotherapists should a lways accurately record the d izzi­ ness tests undertaken and the patient response to each test.

Mainly as an outcome of the work of Grant48,49 the Australian Physiotherapy Association has formalized a protocol for premanipulative testing. 50 It is widely accepted as of great value during preparation for manipulative techniques.3 9,51,52 Several authors also confirm that the level of risk may be further reduced by prudent premanipulative practice.53, 54 However, prema­ nipulative testing should not be considered as the ultimate safety precaution: several reports warn of its relative insensitivity.55-58 One test - rotation/ extension has even been subject to contradictory reports: most stress a reduction in blood flow5 9-62 while others indicate

DANGERS OF NOT MANIPULATING As important to consider as the dangers of manipulation are the dangers of not doing so for subjects who need it. Many discodural interactions, especially those causing unilateral or bilateral cervicoscapular pain, have no ten­ dency to spontaneous cure. Unless manipulative reduc­ tion is achieved, the patient is left in pain that continues intermittently and that could have been relieved by a few sessions of treatment. Delay is also harmful because there may come a point when a protrusion, originally suitable for manipulation, becomes irreducible or dangerous. A disc displacement that is left untreated, particularly a posterocentral one, exerts constant pressure against the posterior longitudinal ligament. It may slowly become larger or give rise to an osteophyte in the spinal canal as

250 T H E CE RVICAL S PI N E

Box

1 3. 1

Protocol for premanipulative testing -

Before m a n i p u lation, check the following items: • Have I taken a proper h istory and done a thorough sta n d a rd ized funct i o n a l exa m i nation? • Have I correctly i nterpreted the exa m i nation? • Have I been a b l e to positively d i agnose a d isco d u ra l o r d iscora d i c u l a r i nteraction? • Have I checked o n a l l poss i b l e warn i n g signs? • Have I checked o n all poss i b l e contra i n d ications? • Have I fou n d a clear i n d ication? • Have I a chance of success? • Have I done prema n i p u lative testing? • Have I reca l led Cyriax's advice? • Am I master of the m a n i pu lative tech n i q ue? • Do I know the m a n i p u lative proced u re? • Do I know the m a n i p u lation strategy?

a consequence of ligamentous traction. When the bulge enlarges it may eventually compress the spinal cord as well as the anterior spinal artery. The symptoms and signs elicited may finally become irreversible. For all these reasons it is unwise to leave an early minor disc displacement unreduced.

EVIDENCE - RESULTS Everyone who undertakes manipulation sees good and sometimes spectacular results in daily practice. Prospective randomized trials and a meta-analysis resulted in a strong trend favouring the manipulative group.82-8 5 Very few other studies have been done. However it is time that studies are pursued to judge on the effects of manipulation of the spine particularly in view of the reports of its danger.8 6 A good study would start with a representative selection from the population of patients - those with real indications rather than those with non-specific neck or back complaints. If such a group is followed in a proper way, the results will be more likely to correspond with the empirical findings that have been made by so many 'manipulators.'

Proper history taking followed by a thorough standardized functional examination

The diagnosis of discodural or discoradicular interaction is made on clinical grounds and therefore a detailed history is necessary and takes time. The complaints are recorded chronologically from the first appearance of symptoms up to the present. All possible symptoms are noted and a record is made of their behaviour and relationship to activity, movement and / or posture. Functional examination is always complete and no tests are omitted. Movements are examined for pain and range and muscle strength is ascertained. Neurological features are tested in detail. Proper interpretation of the examination (clinical reasoning)

The results of the examination, both positive and nega­ tive, are then interpreted in the light of anatomical reality (see p. 165). Interrelationship is sought with the historical findings, looking for example at the behaviour of pain referred versus local, onset, development and the pres­ ence and pattern of paraesthesia. Examination features are related to possible articular, root or cord origin. Articular signs may have features of limitation of movement or pre­ cipitation of pain. Root involvement may be obvious from motor or sensory deficit or disturbances of reflexes. Evidence of cord involvement may be interpreted from particular patterns of neurological presentation. Diagnosis: discodural or discoradicular interaction

These interactions are diagnosed when the whole clinical picture is compatible with that of disc displacement symptoms and signs are found that incriminate one or several of the following structures: •

•

PRECAUTIONS (see Box 13.1) In orthopaedic medicine the utmost precautions are taken to avoid any possible complication: diagnosis is made on clinical grounds and if necessary confirmed with technical investigation. Warning signs and contra­ indications are heeded and only a clear indication for manipulation is accepted. Prognosis is determined and if provisionally positive manipulation is begun with strict methods. The manipulator will only proceed when sure of personal skill. During each manipulative session, con­ stant reassessment is made and whether or not to con­ tinue is totally dependent on the response obtained so far.

•

•

The dura mater and/or dural nerve root investment.

Multisegmental pain and tenderness show the dura mater to be affected whereas root pain is purely segmental. Coughing may be considered as a dural symptom when pain is experienced in the scapular area. The intervertebral joint. An asymmetrical pattern of pain and/ or limitation ('partial articular pattern') indicates internal derangement in the intervertebral joint. Other features are pain on movement and/ or posture, twinges and, in more acute examples, deviation of the head. The nerve root parenchyma. Segmental (dermatomal) paraesthesia may accompany the root pain. Neurological deficit (motor, sensory and reflexes) is often present. The spinal cord. Multisegmental paraestheSia in the hands and / or feet is provoked by neck flexion; other signs of motor and / or sensory tract involvement may also be found.

CHAPT E R 13 - TREAT M E NT 251

Exclusion of warning signs

During all history taking and functional examination the examiner must remain alert and constantly aware not to overlook possible warning signs (for details see p. 211 and Box 13.2). The presence of one of these features is an absolute bar to any active treatment and the patient is referred for specialized investigations. Exclusion of contraindications

It is more important to know when not to manipulate than it is to be unsure of when manipulation should be done. Great caution should be observed in detecting potential contraindications during history taking and functional examination. Manipulation has attained a bad reputation chiefly because contraindications are not taken seriously. Absolute contraindications Some circumstances are clearly absolute contraindica­ tions: compression of the spinal cord, basilar ischaemia, drop attacks, rheumatoid arthritis, anticoagulant therapy, ankylosing spondylitis and an adherent dura mater. Compression of the cord. The moment there is clinical evidence of an upper motor neurone lesion, manipulation must be abandoned. Symptoms are: paraesthesia in the hands and/ or the feet influenced by neck flexion. Signs are: positive plantar reflex, spasticity and incoordination.

A patient who complains of vertigo or dizziness, especially on neck movements or on changing posture, should receive special consideration. Unless the manipulator is very experienced and techniques are used under strong traction and with a minimum of articular Basilar ischaemia.

Box

1 3.2

Warning signs in cervical disorders .�-

History • • • • •

G ra d u a l i ncreasing pa i n Expa n d i n g pa i n B i lateral arm pa i n

Arm pain i n a patient u nder 35 Arm p a i n for more than 6 months

Examination • • • •

F u l l articular pattern M u sc le spasm Resisted neck movements painful and weak Side flexion away from the painful side is the o n l y p a i n f u l movement • Sca p u l a r el evation l i mited • Horner's syndrome

• • • • • •

Hoarse voice T1 palsy Excessive loss of power Two or three nerve roots involved M u scle weakness without root pain Wrong t i me seq uence

movement (straight pull and traction with leverage), manipulation is contraindicated. Drop attacks. Drop attacks, whatever their possible cause, form an absolute bar to manipulation. The exam­ iner is not only alerted by the history but also can be warned by the end-feel during clinical examination or any attempt at manipulative treatment. Rheumatoid arthritis. This condition can lead to liga­ mentous laxity at the upper cervical joints, which creates an absolute contraindication to manipulation. The typical soggy end-feel puts the examiner on guard.87,88

It is unwise to manipulate a patient who is on anticoagulant therapy because of the danger of an intraspinal haematoma. Only if the therapy can b� stopped for the duration of treatment is manipu­ lation possible.

Anticoagulant therapy.

Ankylosing spondylitis. In the inflammatory stage of ankylosing spondylitis or in the unlikely event of a patient with this disorder developing a disc lesion, manipulation is not at all safe, especially in the cervical spine, where luxations, fractures and cord compression have been described.

The dura mater may become adherent to the cervical or thoracic vertebrae. This becomes apparent during an attempt to manipulate, even in patients who otherwise seem suitable. When traction is applied, the patient has paraesthesia in the hands. Traction must be released immediately and manipulation abandoned.

Adherent dura mater.

Relative contraindications Other conditions - posterocentral discodural interaction, acute torticollis in young patients, gross deformity, brachial pain during an attempt to manipulate - form a contraindication to certain techniques. Rotation techniques are contraindicated. The larger the protrusion seems to be, the more the manipulator resorts to techniques without articular movement. Techniques are used under consid­ erable traction, the effects of which help to reduce the fragment of disc (see p. 263). Posterocentral disc protrusions.

Muscular guarding renders manipulation under traction in the direction limited by spasm impossible. Because the con­ dition is the result of nuclear prolapse, the very restricted rotation and lateral flexion initially present are increased by gently sustained pressure. Restoration of movement is thus achieved (see p. 262).

Acute torticollis in patients under 30 years.

Gross deformity. Important deviations of the cervical spine, either in side flexion or in flexion, make manipula­ tion under traction impossible. Before the usual tech-

252 T H E CERVICAL S P I N E

niques can be used, the manipulator must bring the patient's head back to the neutral position. This happens after repeated tractions (whether or not with manipula­ tive thrust) in the line of the deformity (see p. 261). The slightest increase in root pain during initial traction shows that the technique chosen is not suitable, because it clearly pushes the protrusion further against the nerve root. The same applies when traction causes twinges down the upper limb or when it sets up previously absent discomfort in the arm. Manipulation

causing

brachial

pain.

Circumstances in which manipulation is futile It is inappropriate to manipulate when a disc protrusion is not present, when the root pain has lasted for a long time or when neurological deficit has supervened. Protrusion absent at the time of presentation. It is possible that the patient gives a history indicative of disc trouble but that protrusion is not currently present, in which case clinical examination is negative. Manipulation during such a symptom-free period is futile. The patient should wait until the condition relapses or, in the presence of an unstable fragment, measures should be taken to prevent recurrences. It is also inappropriate to use manipulation, as chiro­ practors often do, as a prophylactic measure. This approach cannot prevent the disc from shifting again at any time. Root pain lasting longer than 2 months. Experience has shown that root pain that exists for more than 2 months seldom responds to manipulation. The worst period is over and spontaneous recovery is to be expected within 1 or 2 months. However, in the exceptional circumstances where discogenic root pain lasts longer than 6 months, the apparently delayed mechanism of spontaneous cure can be re-started by manipulation. Root pain with neurological deficit. The presence of a neurological deficit shows that the discoradicular interaction is too intense. The disc fragment can therefore not be replaced but the vain endeavour to do so is not dangerous. An occasional case with very minimal deficit may in fact respond.

The patient develops cervicoscapular pain, followed by root pain and paraes­ thesia the next day. The protrusion moves very quickly from a posterocentral position to a fully posterolateral one and this course cannot be stopped. Neurological deficit may be expected very quickly. Root pain with swift progression.

Root pain with primary posterolateral development.

When root pain is caused by a unilateral disc protrusion it does not respond to manipulative reduction, because, as in the lumbar spine, the displacement is nuclear.

Unfavourable neck signs. When some neck movements elicit or influence the root pain, the chance that manipu­ lation will work is very small. Nuclear disc prolapse. These cases are characterized by an elastic recoil, felt during a manipulative attempt and by the discrepancy between active and passive rotation during clinical examination. Acute cases have to be reduced by gradual forcing in the restricted directions. Chronic circumstances need continuous traction. Contraindications to cervical manipulation for disc lesions are summarized in Box 13.3.

Recognition of a clear indication

It is not sufficient to have excluded warning signs and contraindications. It is as important to make sure that a clear indication is present, either a posterocentral or posterolateral disc protrusion causing a discodural or discoradicular interaction (see Box 13.4). Posterocentral discodural interaction with unilateral cer­ vicoscapular pain Acute torticollis with side flexion deformity. Acute torti­ collis forms a good indication for manipulation and the patient may be helped within a few sessions. Although this condition has a course to spontaneous cure, treat­ ment helps from the outset to diminish the pain. A distinction is made between the torticollis in the young (under 30 years old), which is usually of the nuclear type, and that in those beyond the age of 30 who suffer a cartilaginous displacement (see p. 181).

Box 1 3.3 Cervical manipulation for disc lesions: contraindications Absolute • • • • • • •

Compression of the spinal cord Basilar ischaemia Drop attacks Rheum atoid arthritis Anticoa g u l a n t therapy Ankylosing spondylitis Adherent d u ra mater

Relative • • • •

Posterocentral d isc protrusion Acute torticol l is in you n g patients G ross deformity M a n ip u lation increases root pain

Futile • • • • • • •

No protrusion Root pain lasting too long Root pain with n e u rolog ical deficit Root pain with swift prog ression Root pain with primary poste rolateral development U nfavou rable neck signs N uclear d isc protrusion

CHAPTE R 1 3

Box 1 3 .4 Cervical manipulation for disc lesions: indications

.�

• Posteroce ntral discod u ra l i n teraction with u n i lateral cervicosca p u l a r p a i n • Posterocentral d i scod u ra l i n teraction with central neck pain or bi lateral cervicosca p u l a r pa i n • Posterocentral d iscorad i c u l a r i nteraction with b i l ateral root pain • Posterolateral d iscoradicular i n teraction with u n i lateral root pain, with out neu rological defi cit

Unilateral cervicoscapular pain. Symptoms of this nature are almost always the consequence of an annular dis­ placement. They can be treated with manipulation at any time and, no matter how long the protrusion had existed, the response is usually good. Full recovery is to be expected after one to three sessions. Protrusions at the mid-cervical spine (C2-C3 and C3-C4) with pain felt at one side of the upper neck tend to be more difficult to reduce.

Posterocentral discodural interaction with central neck pain or bilateral cervicoscapular pain Central or bilateral neckache with or without radiation to the trapezii or scapular areas, but without symptoms of spinal cord compression, can be manipulated provided the techniques are adapted to the specific situation. The manipulator has to realize that a posterocentral displace­ ment may threaten the spinal cord and therefore great care is needed. Acute torticollis with flexion deformity. This situation is more delicate because the protrusion is large and can impinge against and threaten the spinal cord. This is a clear contraindication to the techniques usually used in the treatment of unilateral disc displacement (see below), i.e. rotation. Special techniques that avoid too much articular movement are used. Chronic neckache. Central or bilateral pain can be treated with manipulation, provided the rotatory tech­ niques are avoided.

Posterocentral discoradicular interaction with bilateral root pain If root pain is thought to be the result of a disc protrusion, no time limit is set - unlike unilateral cases - for the manipulation to succeed. Slight bilateral root pain pre­ ceded by paraesthesia in both hands tends to respond well, although the discal cause is not always certain. Posterolateral discoradicular interaction with unilateral root pain. without neurological deficit The success of manipulative treatment in such circum­ stances depends on the stage at which the patient is seen.

-

TREAT M E NT 253

Reduction by manipulation is possible only in the first 2 months of the development of the picture as measured from the moment that the root pain appeared rather than from the onset of the original scapular discomfort. The signs found during clinical examination are impor­ tant prognostically. If neck movements elicit or influence the pain in the scapular area rather than pain down the arm ('favourable' neck signs), this shows that the protru­ sion still lies in contact with the dura mater and suggests that reduction may still be possible. When movements of the cervical spine increase the root pain, this is 'unfavourable' and diminishes the chance of success. Once neurological deficit has appeared (muscular weakness, sensory loss and sluggish or absent reflexes) no further benefit can be expected from manipulative treatment, except in the following two situations: • When severe scapular pain has remained after the root pain

•

began: usually the scapular pain and the articular signs disappear or considerably diminish when brachial pain occurs. In the rare event that some movements remain limited and cause severe pain in the scapular area, especially at night, one manipulative session may abolish the scapular pain and restore a full painless range of movement. The root pain remains unaltered and continues its spontaneous course (see p. 191). When root pain lasts for a considerable period: most root pain progresses to full recovery in the course of 3-4 months - except C8 pain which may take up to 6 months to recover. Occasionally a patient may be seen with root pain that has lasted longer than 6 months, even up to 1 or 2 years and investigation has not shown a neuroma or other similar lesion. Manipulation will not immediately influence the root pain; however, a few days after manipulation the pain starts to diminish and after a second treatment 2 weeks later all symptoms may disappear. This peculiar clini­ cal phenomenon could be explained by the concept that root pain is the result of a discoradicular interac­ tion whereby a fragment of disc has displaced and compresses the dural sleeve of the nerve root, as a result of which the latter becomes inflamed and swollen. Manipulation shifts the disc back but it takes some time for the inflammation to abate and thus for the pain to diminish.89,90

Prognosis: criteria of reducibility - presence of favourable or unfavourable signs

Before manipulation is decided upon, the chances of success should be assessed by considering the following questions. How large is the protrusion? Gross deviation indicates that a large fragment of disc is displaced. Reduction may take more sessions of manipulation.

254 THE CE RVICAL S P I N E

The more pronounced the articular signs, the larger the protrusion. However, this does not mean that reduction would be more difficult, as in, for example, acute torti­ collis. Neurological deficit indicates that the protrusion is larger than the opening through which it escaped and that reduction is impossible.

Box

Criteria of reducibility --

Protrusion is reducible in: U n i l atera l pa i n in the neck a nd/or sca p u l a r area without root pain or n e u rolog ical defi cit (one or two sessions are needed) U n i lateral cervicosca p u l a r pain with root pa i n but without n e u rolog ical deficit and with 'favou rable' neck signs (mostly reducible)

Is the protrusion central, unilateral or bilateral? A uni­ lateral protrusion usually responds well to the ordinary manoeuvres, i.e. rotation and side flexion movements under traction. A central or bilateral protrusion is more difficult and forms a contraindication to rotational manipulation. Other manoeuvres are possible, except in severe cases, in which strong traction is applied without any movement. A central protrusion with spinal cord compression is potentially dangerous and any sign - positive plantar reflex, spasticity, incoordination, gross weakness - must therefore be considered as an absolute bar to manipula­ tion (see p. 251).

B i l atera l pain in the cervicosca p u l a r area with 'favou rable' neck signs and i rrad iation down the arms p l u s paraesthesia i n h a n ds a nd/or feet

(50%

cha nce of

successfu l m a n i p u l ation in one to four sessions) U n i lateral sca p u l a r p a i n with root pain and slight paraesthesia exist i n g for less than 1 month and with good neck signs (sometimes red uc i b le)

Protrusion is irreducible in: U n ilateral pain i n the sca p u l a r a rea, with root pain, but n o neu rological deficit, a n d w i t h 'unfavou ra ble' n e c k signs B i latera l p a i n in sca pulae and a rms a n d pa raesthesia i n h a n ds an d/or feet with 'favou ra ble' neck s i g ns and without n e u rolog i cal deficit (50% are irreducible)

U n i lateral root pa i n fol l owed b y sca p u l a r pain

Is the pain influenced by articular movements? When movements affect scapular pain, this is considered as 'favourable' and manipulation has a fair chance of success. Circumstances in which neck movements augment the root pain have to be regarded as 'unfavourable' and the result of manipulation is not very favourable (see p. 258).

U n i l atera l sca p u l a r pa i n with root pain and s l i g ht paraes­ thesia with 'favou rable' neck signs and ex ist i n g for longer than 1 month- but less than 6 months U n i lateral sca p u l a r pa i n that goes on after the d isa ppearance of root pain, with only one movement being painful U n i lateral sca p u l a r pain and root pain with ma rked n e u rological defi cit and 'unfavourable' neck s i g ns Q u i c k evolution from sca p u l a r pain to root pain with paraesthesia a n d 'favou rable' neck signs E lastic recoil a n d limitation of active rotation

How long has the protrusion been present? Scapular pain or bilateral root pain can be manipulated at any time, unilateral root pain within the first 2 months but not later.

Para esthesia i n hands an d/or feet with cord signs

The answer to these four questions reveals a number of possibilities (Cyriax:91 p. 105; also see Box 13.5).

Unilateral scapular pain and root pain for >6 months with reasonable neck signs and in which any neurological deficit is recovering:

Decision to manipulate: patient's consent, type of patient, premanipulative testing

The decision to manipulate should be taken after all previous safety measures have been considered. Some authors propose asking for a patient's consent, eventually even written. This is not standard procedure in medicine. It is clear that patients should be informed about what treatment will be started but only up to a certain point. Patients can have problems in being objec­ tive and if they are informed about possible dangers, they will have difficulties in accepting the treatment or relax­ ing during the manipulative manoeuvres. Cote et a158 even state that from an ethical point of view, the conse­ quences of unnecessarily alarming patients about the risk of a potential stroke are unsupported and unacceptable. The manipulator must of course take into account the patient's personality. It is clear that certain patients are not suitable for manipulation because they cannot cope with aggressive treatment. Others, for some reasons, do not want to become better: those patients are not manipulated.

1 3.5

May be m a n i p u lated to restart the mechanism of spontaneous recovery: two or t h ree sessions at 2-week intervals suffice

Grant39,51,52 suggests including in the premanipulative testing those positions that will be adopted during the manipulations procedure. The positions that could be adopted are: • • •

Slight longitudinal traction Full rotation under slight traction Full side flexion under slight traction

The position is held for at least 30 seconds and unusual reactions noted, such as dizziness, nystagmus or vagal reactions. The manipulator should realize that even negative premanipulative tests do not exclude the possibility of unwanted complications (see also pp. 233-236).

CHAPT E R 1 3

We still consider Cyriax's advice the best precaution against possible accidents (J.H. Cyriax, personal com­ munication, 1976): J.H. Cyriax: If you do not know whether m a n ip u l ation w i l l work or n ot, try. If you do not know whether manip u l ation is safe or n ot, d o not try.

MANIPULATION TECHNIQUE General remarks

Position of the patient. The patient lies face upwards on the couch with the occiput just beyond the upper edge. This enables the manipulator to hold the patient's neck either in slight extension or in neutral position during the manipulative manoeuvres. The physiological lordosis is maintained and positively influences the direction in which the discal fragment moves. Dentures must not be removed, to avoid lillcomfortable overclosure of the mouth. The patient must try to relax during the entire manoeuvre because any muscular tension may result in after-pain. Holding on to the edges of the couch (with the intention to resist the traction) is not allowed, because this makes the muscles of neck and shoulders contract so complicating manipulation.

LW iii

Position of the assistant. An assistant is needed for fixation. Positions are chosen whereby the patient's body does not move when traction is applied to his head. There are a number of possibilities (Fig. 13.1). Fixation at the patient's feet. This is the most common method of fixation. The assistant stands at the patient's feet, takes hold of the ankles and bends forwards to bring his shoulders over the patient's feet. When the assistant's arms are then adducted the feet are firmly fixed between the assistant's body and upper arms. Fixation at the patient's shoulder. This is needed during a side-flexion manipulation. The assistant stands at the patient's side, opposite to the direction in which the head will be moved and passes one arm between the patient's arm and body until the hand lies under the shoulder; the other hand lies on top of the shoulder. The fingers are clasped. The assistant's foot is placed against the leg of the couch and the assistant leans well backwards to resist the traction. Fixation at the patient's side. This fixation method is used during the lateral gliding technique. The assistant stands at the side of the patient, who is asked to move towards him. With one hand he grasps the patient's opposite upper arm and with the other hand takes the lower arm. The patient's body is then pulled firmly

Figure 1 3.1

Positions of the assistant for fixation.

-

TREAT M E NT 255

256 T H E CERVICAL SPINE

against that of the assistant, who will thus be able to resist the movements executed at the patient's head. Position of the manipulator. All techniques, except the lateral gliding manoeuvre, are performed under traction. The maximum traction that is tolerable for the patient . and allows him to relax is used. This traction is of vital importance because of the following beneficial effects: • •

•

• •

Traction induces a subatmospheric pressure in the joint which results in a suction effect - a centripetal force. Compression on the pain-sensitive structures exerted by the protruded disc diminishes with, as a result, diminution or even disappearance of the pain. As an additional advantage, the patient will have no prob­ lems in relaxing muscles. As the muscles are well relaxed the vertebrae can be distracted by a few millimetres so that the loose fragment has room to move. The facet joints are disengaged, which again makes movement easier. The posterior longitudinal ligament is taut and helps to exert a centripetal force on the disc.

All factors are thus present to push the disc away from the spinal cord and the anterior spinal artery, which in this way are protected. In order to obtain this traction the manipulator, after having taken hold of the patient's head, puts his feet against the legs of the couch. One leg is internally and the other externally rotated so that purchase is taken with the outer midtarsal area of one foot and the inner midtarsal area of the other. This position enables backwards leaning and the use of body weight for traction. Traction is built up gradually, which enables the oper­ ator to take up the slack when the vertebrae separate. When both feet are put against the couch and the manip­ ulator moves away from the patient's head, by extending the knees and arms, maximal traction is obtained. This is not often necessary. The amount of traction depends on the type of patient. It is evident that traction will be much less in, for example, a woman of 45 kg than in a man of 95 kg. The traction is adapted to the patient's constitution and also to the ability of the patient to relax. Some patients are inclined to tense their musculature as soon as the head is pulled, others just relax under strong traction because it brings pain relief. The manipulator's experi­ ence is crucial in determining the amount of traction. In order to become accustomed to how to apply trac­ tion, novices are advised in the beginning to put one foot further backwards. The traction force will be less. The foot is then gradually brought forwards until it reaches the couch (Fig. 13.2). The more the foot is put forwards, the more traction is applied. An advantage of using traction is that the operator's body, rather than the hands, executes the traction element as well as the movement during taking up of the slack.

(a)

(b)

------ �-

-----

(c) Figure 1 3.2 Degrees of traction during manipulation: (a) slight traction, (b) moderate traction, (c) full traction.

The result is that both elements are much better con­ trolled than if they were performed by the hands only. Preparative massage to splenius and semispinalis capitas muscles at their midcervical extent. Deep transverse massage to these muscles can be used in those patients who have difficulties in relaxing during manipulation. Massage will help to inhibit voluntary contraction. The couch should have an opening near its head, through which the patient can breathe while face down. If this is not available, the patient's head is supported on a pillow.

C H A PTER 13

Figure 1 3.3

-

TREATM ENT 257

Preparative massage to the splenius and semispinalis.

The patient lies prone and the therapist stands level with the patient's head at the contralateral side. The fingers are placed on the affected area while the thumb supplies counterpressure at the ipsilateral side of the neck (Fig. 13.3). Massage is imparted for 10 minutes by alternately flexing and extending the wrist, thus moving the fingers over the muscles. Manipulation follows immediately. Techniques

Circumduction during traction. The patient lies supine on the couch, an assistant holding the feet. After having decided in what direction to turn the head, the manipulator hooks one hand under the patient's chin. For rotation to the right the right hand is used, and the left hand for left rotation. The little finger is held in extension to avoid pressure on the trachea. The other hand grasps the occiput between thumb and fingers and supports the head. When the patient's head is grasped, pinching the chin or the occiput must be avoided. This could be very uncomfortable for the patient and cause difficulties in relaxation. The manipu­ lator now puts his feet against the legs of the couch, pointing them in the same direction as the rotation movement to be performed, and leans backwards. Moderate traction is exerted and during this some slow rotary movements are executed without approaching the full range. This gives some idea of the state of the patient's neck. The latter now realizes what is to happen; confidence is established and the patient can relax. During the manoeuvre some 'cracks' may be felt. After a few movements traction is released.

�IIII Practitioner's checklist • Use to make patient accustomed with tec h n iq ues u nder traction • Use to get a better relaxation • Not a real m a n i p u lation but a preparative m o bilization • Moderate traction • N o im p u lse

Figure 1 3.4

Straight pull.

Straight pull. The patient and assistant adopt the same position as for the circumduction during traction. The manipulator hooks one hand under the patient's mandible and the other under the occiput, puts his feet against the couch and leans well backwards. The elbows are straight­ ened as much as possible (Fig. 13.4). After having taken up the slack and having assessed the end-feel the therapist sharply pulls his shoulders backwards. This movement results in a quick manipula­ tive thrust in line with the spine, during which a click may be felt. Traction is now gradually released.

"IIII Practitioner's checklist • • • • •

Avoid neck flexion Use a comforta ble g r i p Lean well backwards E q u a l traction by both h a n ds Manipulative i m pulse is performed only on a relaxed patient

Rotation during traction. The patient and assistant are in the same position as described for the previous two manoeuvres. The manipulator takes hold of the patient's head, places his feet against the couch and leans back­ wards to take up the slack (Fig. 13.5a). For a rotation to the right, the right hand is at the patient's chin and the feet point in the same direction. The head is now slowly rotated to the right. This is not done by a hand movement but is the result of the manipulator side flexing his trunk. The head is turned to half range on the first occasion, then two-thirds and finally to the end of range. The degree of rotation depends on the response obtained from the patient, which is reassessed after each manoeuvre. At full range the end-feel should be assessed and when this is right the impulse is given: a quick movement over a very small amplitude ( 1-2° only). In contrast to the previous trunk movement, this final thrust is performed by the

258 T H E CERVICAL SPIN E

hands only. The head is then brought back to the neutral position and traction is released. The further the head is rotated, the more chance there is that one or more clicks will be felt. They are relevant when the movement seems to have improved afterwards. When click is not felt, nothing has happened. The end­ feel at the end of the manipulative thrust tells the manip­ ulator if further forcing is indicated.

�"� Practitioner's checklist • • • •

-

D i rection of rotation dete rmi nes position of hands Feet p o i nt i n the d i rection of rotation Equal traction d u ring the entire m a n oeuvre At the end of range, assess end-feel before m a n i p u l ation

Full rotation during t raction. When repetition of the pre­ vious manipulation ceases to afford benefit, this technique may follow. The traction force will be somewhat less but it will be easier to achieve full rotation (Fig. 13.5b). The patient and assistant maintain the same position. For a rightwards rotation the manipulator puts the right hand on the patient's left cheek; the arm is held in prona­ tion, the thenar eminence lies on the maxilla and the fingers are hooked under the chin. The other hand grasps the occiput in the same way as previously described in the technique, circumduction during traction. After having put his feet against the couch, the operator leans back­ wards, thus applying traction, and turns the patient's head to full range. When the end-feel is good, a quick manipulative thrust will be performed. The head is turned back to neutral and traction is relaxed.

fI"� Practioner's checklist • • • •

-

Thenar e m i nence on maxil la; avo i d c h i n movement P u re rotation, n o lateral flex i o n component Assess en d-feel before m a n i p u l ation Equal traction d u ring the entire m a n oeuvre

Side flexion during traction . The patient lies supine on the couch. The assistant stands level with the patient's shoulder at the painful side to apply counter-traction (Fig. 13.6) (see p. 255). The manipulator puts one hand under the patient's occiput. The second metacarpophalangeal joint is applied against the posterior aspect of a facet joint at the midcer­ vical area. The thumb is kept in extension to avoid pres­ sure on the external carotid artery and the third, fourth and fifth fingers support the head. The other hand is hooked under the mandible in such a way that the forearm comes to lie anteriorly to the ear. The head will thus be prevented from rotating too much during side flexion (see Fig. 13.6b). The lateral aspect of the ipsilateral

( a)

(b) Figure 1 3.5

(a) Rotation during traction. (b) Full rotation during traction.

foot is now put against the nearer leg of the couch. The other leg is extended out and backwards. Traction in line with the spine is now achieved and this will be facilitated by bending the knee. After having taken up the slack the manipulator now swivels the body, thus bringing the patient's neck into side flexion with the help of the forearm. Simultaneously, counterpressure is applied by the other hand. When the movement comes to an end, the end-feel is assessed and the manipulation performed with a quick adduction movement of the contralateral shoulder. A click is felt after which the head is brought back to the neutral posi­ tion and traction released.

fI"� Practitioner's checklist • • • •

Traction in l i ne with the s p i n e Avoid rotation Cou nterpressure d u ri n g lateral fl exion movement Assess end-feel before m a n i pu lation

C HAPTER 1 3

-

TREAT M E NT 259

The manipulator stands at one side of the patient's head, facing it. One hand supports the head under the occiput and the other is put at the patient's chin with the following grip: the web between thumb and index finger is applied to the chin so that thumb and index finger lie on either side. The forearm is kept vertical. The flexed third, fourth and fifth fingers hook under the chin in order to enable traction. The manipulator now places his feet against the legs of the couch and leans sideways, using body weight for traction. After having taken up the slack, the head is gently glided anteriorly with the use of the hands (Fig. 13.7a). It is then glided posteriorly as far as it would go with a manipulative thrust, the result of a sudden flexion of both knees (Fig. 13.7b).

tIVII Practitioner's checklist • • • • •

(a)

Stand at one side of the patient's head The patient's head must be wel l over the edge of the couch Traction is obta i n e d by l ea n i n g sideways Gentle a nterior g l ide, fo l l owed by sudden poste rior g l ide Avoi d flexion-extension movement

lateral gliding. The patient lies supine on the couch. The assistant stands at the patient's side and firmly fixes the patient's body (see p. 255). The manipulator stands at the patient's head, feet apart. With the forearms supinated, the hands support the head and, with the thumbs kept horizontal along the cheeks, the thenar eminences are placed anteriorly to the ears on either side. Movement is now carried out without traction. By bringing the body weight over to one leg and then back to the other at the same time taking the patient's head with the movement, the neck is moved sideways (Fig. 13.8). The position of the hands should enable the manipulator to hold the patient's head continuously in line with the body. Side-flexion movements should be avoided and the movement is purely horizontal.

tIVII Practitioner's checklist • • • • •

(b) Figure 1 3.6 (a) Side flexion during traction. (b) Position of the hands for the side flexion technique.

Anteroposterior glide during traction. The patient lies supine on the couch, the head well over the edge, the shoulder level with it. An assistant holds the feet.

Avo i d compression of the ears No traction Avo i d side-flex i o n movements Avo i d flexion P u re hori zonta l g l i d i n g

Traction with leverage. The patient lies supine on the couch with the occiput exactly level with the upper edge; an assistant holds the feet firmly so that the body does not move at all during the manipulative thrust. The manipulator puts one hand, protected by a layer of sponge rubber 2-3 cm thick, under the patient's occiput. The patient's mandible is grasped with the other hand, holding the neck in slight flexion.

260 T H E CERVICAL SPINE

(a) Anteroposterior glide during traction: (a) starting position; (b) ending position. Figure 1 3.7

Figure 1 3.8

Lateral glide.

Before manipulating, great care is taken in positioning the patient's head in relation to the edge of the couch. An endeavour is made to move the head gently into more extension so as to assess how far such movement can be made. If extension can take place to a considerable

(b)

degree, this is because the patient is too high on the couch; if movement does not take place at all, this indi­ cates that the patient is too low. It should be possible to place the patient's head in the neutral position where it comes to a stop. The manipulator then puts the feet against the couch and leans far backwards until the whole or part of the body weight is sustained by the hand under the chin. Traction is not applied via the hand under the occiput, which only steadies and is squeezed between head and couch to provide a fulcrum. The knees are now sud­ denly flexed, thus pulling the patient's neck with a jerk (Fig. 13.9). This results in a sudden increase of traction in the anterior spinal column from the foramen magnum downwards.

tillII Practitioner's checklist • Avoid flexion • Careful posit i o n i n g • D u r i n g m a n i pu l ation: n o movement, o n l y traction

C H A PTER 1 3 - TREAT M ENT 261

•

session overcorrection is produced - the unilateral pain then changes sides - this manoeuvre is performed. Pure traction techniques - straight pull and traction with leverage - are especially designed for the treatment of posterocentral disc protrusions. Articular movement is thus avoided.

Gentle start

Each time a new technique is chosen the manipulator starts gently. The intensity of a technique is only increased when the patient has responded satisfactorily to the previous technique. Assessment of progress

Figure 1 3.9

Traction with leverage.

MANIPU LATION PROCEDURE Choice of technique

to the muscles of the neck enhances relaxation and so is useful when a patient does not feel sufficiently relaxed (see p. 256). Circumduction and straight pull can be used as the first manoeuvres, to accustom the patient to the traction element. Rotation manipulation is used for unilateral disc protrusions but is avoided in central displacements. Rotation is first performed in the most comfortable direction and afterwards, if still necessary, in the least comfortable direction. It is executed to half range first, then to three-quarters and only then to full range. When the other direction is chosen, a similar gentle start is again recommended. Full rotation during traction is only used when rotation caused improvement and only in the direction in which the result was obtained. Side flexion is mostly performed in the direction away from the painful side and very rarely towards the painful side - when, after a few sessions and after having tried the other techniques repeatedly, a full result is not yet obtained. When taking up the slack produces or increases arm pain, the manoeuvre is abandoned. Anteroposterior gliding is indicated in unilateral disc displacements when the range of extension does not improve with rotation and / or lateral flexion techniques. In central protrusions it can be used in combination with straight pull and lateral flexion. Lateral gliding helps to get rid of possible post­ manipulative soreness. When during a manipulation

• A preparative massage

•

•

•

•

•

•

After the use of each technique the patient is asked to sit and the result assessed. A decision is then taken whether to continue in the same way or to change. Experience, the result of each particular manoeuvre, the end-feel during exertion, the patient's age and estimation of tolerance all affect the types of manoeuvre employed. A change in the symptoms or signs is interpreted as improvement when (a) intensity of pain has diminished; (b) range has increased; (c) fewer movements are painful; and (d) pain has centralized, for example scapular pain instead of arm pain, trapezius pain instead of scapular pain, central pain instead of unilateral pain, or shortening of pain. If one manoeuvre has helped, it should be repeated until symptoms and signs no longer alter. Then another is tried. If the manoeuvre does not give any positive result, it can be tried a second time with slightly more intensi ty. If improvement still does not occur the manoeuvre is aban­ doned and either another technique chosen or the same technique used in another direction. For example, if rota­ tion to the right does not give the expected result, either a lateral flexion technique can be tried or rotation to the left. If a manoeuvre makes the patient worse it is not con­ tinued. The manipulator must then make up his mind whether the worsening is the result of a wrong technique or of poor relaxation by the patient and whether the con­ dition is in fact suitable for manipulation. If the technique is not appropriate, another can be chosen, perhaps with less movement and more traction. When two consecutive trials still increase the symptoms, manipulation is stopped. The patient is re-examined on the next occasion and the decision taken whether to continue. Such a deci­ sion is not always easy and therefore much attention should be given to what the patient reports during and after each manoeuvre, and in the hours that followed the treatment. The moment there is the slightest doubt, manipulation is not done.

262 T H E CERVICAL SPIN E

MANIPULATION STRATEGY Repetition of techniques

Acute conditions are best treated on a daily basis, more chronic cases are manipulated two to three times a week. Manipulation is a short-term treatment which means that, if no result is obtained after a few sessions, another approach is chosen. Young patients can easily stand several (six to eight) techniques in a session. Elderly patients receive the same treatment but only one to three techniques per session and the interval between the treatments is longer - one to three times a week. When the results after each manoeuvre are only slight or minimal, manipulation is continued until the greatest possible result is obtained. When a significant improve­ ment is suddenly noted, the session is stopped and the result reassessed on the next occasion. The therapist should try to follow the sequence of manoeuvres as recommended in the following section but should develop enough flexibility and creativity to work according to the results obtained in each individual case. Course of a manipulative session

Posterocentral disc protrusion with unilateral cervico­ scapular pain. Two types of cases fall into this group. In nuclear­ type torticollis the following procedure is applied. The manoeuvres are performed in a strict order, whereby manipulation in directions limited by the condition is avoided. .On the first day:

Acute torticollis with side flexion deformity.

1. Traction manipulation (straight pull) in the direction of the deviation: the head is gradually brought back to the neutral position. No other technique is used before the patient is able to maintain the head in the neutral position when seated upright. 2. Rotation manipulation under traction is then performed in the less restricted direction until this movement has become painless. 3. Lateral flexion manipulation under traction and towards the painless side should then restore a full painless range in that direction. 4. Progressive rotation, without traction, in the restricted direction: the head is gradually pushed to the point where pain begins and then immobilized in that posi­ tion until the pain has disappeared, after which further movement is undertaken. This is continued until a full range is achieved. The time taken for the pain to disap­ pear at each stage may vary from a few minutes to 5 minutes or more, which means that up to 20 minutes may be necessary to restore the range of rotation.

5. Progressive lateral flexion, without traction, in the restricted direction: the same slow procedure is fol­ lowed until full side flexion is obtained. This move­ ment usually improves more quickly than rotation; 5-10 minutes are required. 6. When the patient is reassessed after the whole proce­ dure is finished, what has been achieved provides a basis for prognosis. When, after the first treatment, full painless range in all directions is attained, this indicates that by the next day the patient will be much improved or even cured. 7. The patient is then advised to repeat these progressive manoeuvres every 2-3 hours and certainly before going to bed because there is a tendency to relapse. Instruction should also be given on what precautions to take to keep recurrence minimal: sleeping in the supine position is preferred. A very thin pillow should be used but support under the neck should be pro­ vided (e.g. a rolled towel with a diameter of 5-10 cm). Alternatively, if the patient sleeps on the side, a thick pillow should assure that the cervical spine lies in line with the thoracic spine. Sleeping prone should be avoided. The patient is seen on a second day and, if consider­ ably better, treatment then consists of the manipulations as for an ordinary unilateral disc protrusion (see below). When, on the contrary, a considerable relapse has taken place, the whole procedure is repeated. Full relief is usually obtained in two to three sessions (Fig. 13.10). Annular-type torticollis in patients over 30 can be manipulated in the ordinary way (see below). Unilateral cervicoscapular pain. These cases are almost always annular in nature and therefore respond very well to manipulative treatment. The following sequence is recommended:

Correction of head deviation

Rotation/side flexion manipulation in the most comfortable direction

Progressive sustained rotation/side flexion in the least comfortable direction

Postural advice

Figure 1 3 . 1 0

Procedure in unilateral acute torticollis.

C H A PTER 13

1. Straight pull or circumduction under traction to make the patient familiar with strong traction techniques. 2. Rotation under traction to less than full range in the less restricted or less painful direction. 3. Rotation under traction to full range in the same direction. 4. Rotation under traction to less than full range in the most restricted or most painful direction. S. Rotation under traction to full range in the same direction. 6. Lateral flexion under traction towards the painless side. 7. Lateral glide (see Fig. 13.11). Posterocentral disc protrusion with central or bilateral cervicoscapular pain. This includes three types of case. The same proce­ dure is used as for torticollis with deviation in lateral flexion, except that the traction in line with the deviation starts in flexion (enough time must be taken to bring the patient's head gradually back to the neutral position) and rotations are avoided. Side flexion manipulations under traction can be performed in both directions, after which the patient is put on his side and the limited extension very gradually forced to full range.

Acute torticollis with flexion deformity.

Chronic neckache.

be taken.

A direct or an indirect approach can

DIRECT APPROACH:

1. Straight pull: strong traction manipulation in line with the spine. 2. Traction with leverage. 3. Lateral glide.

-

TREATM ENT 263

INDIRECT APPROACH:

1. Straight pull. 2. Lateral flexion under traction which can be done bilaterally. 3. Anteroposterior glide. 4. Lateral glide. The decision to use one approach or another depends on the severity of the clinical picture present. In very mild cases it is easy to switch from one approach to the other. The more pronounced the articular signs are and the more extension is limited, the more the manipulator will be inclined to choose the direct approach, following the principle of 'maximal traction with a minimum of articu­ lar movement'. Signs of spinal cord involvement form an absolute bar to manipulation. Bilateral root pain. The same procedure (see Fig. 13.12) is used as in bilateral chronic neckache.

Posterolateral disc protrusion with unilateral root pain, without neurological deficit. The normal techniques are used: 1. Straight pull. 2. Rotation under traction in the less restricted or painful direction, first to less than full range and then to full range. 3. Rotation under traction in the most restricted or painful direction, first to less than full range and then to full range. 4. Lateral flexion under traction towards the painless side. S. Lateral glide. Before the impulses are given the manipulator must make sure that taking up the slack does not influence the pain down the arm. If this does take place, the technique

Direct way

Figure 1 3 . 1 1

Procedure in unilateral cervicoscapular or root pain.

Figure 1 3 . 1 2

Indirect way

Procedure in central or bilateral cervicoscapular pain.

264 T H E CE RVICAL SPINE

is abandoned and another manoeuvre is chosen. When two different techniques make the arm pain worse, the condition is not suitable for manipulation.

TRACTION

ADJ UVANT TRACTION Traction is a very important element of the manipulation procedures because of its beneficial effects on the pro­ truded fragment of disc (p. 255).

TRACTION AS A TREATMENT Patients who have received many treatments by head suspension are often seen. Some have not benefited at all and others may have improved but only after 10 or more sessions - a result which could have been achieved much more quickly with ordinary manipulations because most disc protrusions at the cervical spine are of the annular type. Traction alone is usually not necessary and thus not so often used in orthopaedic medicine. However, it has a small number of well-defined indications. It is most often given at the physiotherapist's room, but can - in some specific situations - be performed in bed, either long­ standing or continuous. Therefore traction is only indi­ cated in some specific circumstances: head suspension in nuclear protrusions or, in cases of discal instability, a few hours' traction for severe root pain and traction in bed for the more severe cases. Head suspension

Indications. There are four main indications for head suspension: early nuclear protrusion, minor postero­ central disc protrusion, to maintain reduction in unstable protrusions and as an alternative to manipulation. Early nuclear disc prolapse. Differential diagnosis with an annular-type protrusion is not always easy which means that it may happen that a patient is manipulated probably without success. During the manipulation, at the end of passive movement, an elastic rebound is felt, after which the full range that was reached during the manipulation cannot be obtained actively. These dis­ placements do not respond well to manipulation but recent prolapses respond quite well to daily traction in three to six treatments. Long-standing cases do not benefit very much from this treatment. Sustained traction in bed may be consid­ ered before deciding to go to surgical removal. Minor posterocentral discodural interactions. Traction can also be considered. Some manipulations are con-

traindicated (see p. 251) and traction is therefore a good alternative. Even if the lesion is of the annular type it may respond to traction, provided the patient is not too old and the articular signs are minor. Four to eight daily ses­ sions usually lead to a good result. To stabilize a recurrent disc. Two different situations may occur. First, when the patient always relapses the day after a manipulation session, traction is substituted. After four to six sessions the disc should have stabilized. If not, daily suspension at home is prescribed: 10 minutes' traction every morning may prevent the disc from protruding during the day. Second, when the patient responds well to manipula­ tion but continuously relapses a few weeks after the treat­ ment, the manipulation treatment can be re-started but is then followed by a week to 10 days' daily traction. This procedure has a stabilizing effect; recurrence will be delayed. Instead of manipulation. This may be considered as an alternative in those patients who, for some reason, cannot be manipulated; 10-15 treatments may then be necessary.

Contraindications. These include the following. Paraesthesia induced by traction. When traction pro­ vokes paraesthesia felt in hands and / or feet, it must be stopped at once because this indicates involvement of the spinal cord. It has been suggested that the cause is an adherent dura mater (Cyriax:91 p. 105). Brachial pain caused or increased by traction. When trac­ tion to the cervical spine elicits or increases root pain, the protrusion is clearly pulled in the wrong direction further against the nerve root.

Although not contraindicated, traction is not the treatment of choice. This disc displace­ ment can so easily be reduced by manipulation in a few sessions that it is unwise to use traction, which will indeed eventually reduce it but which will take much more time (see Box 13.6 for a summary of indications for and contraindications to head suspension). Annular disc protrusion.

Box 1 3 .6 Head suspension: indications and contraindications Indications Early n uclear d isc protrus ion M i nor posterocentral d isc protrusion To manta i n red uction in u nstable protrusion Instead of m a n i p u lation

Contraindications Paraesthesia i n d u ced by traction B ra c h i a l pain caused/increased by traction An n u l a r d isc protrusion

C H A PTER 1 3 - TREATM ENT 265

Technique. Traction can be applied with the patient sitting or lying supine (Figs 13.13 and 13.14). A leather collar is strapped under the patient's chin and occiput in such a way that the anterior portion clears the trachea while supporting the mandible. The collar is attached to a spreader and hangs by a cord passing over a pulley to the centre of the spreader. The therapist must make sure that the patient's ears are not squeezed. Traction is applied in the neutral position or with the head held in very slight flexion. The physiotherapist stands by the patient and pulls gradually on the cord until the required force - usually between 8 and 15 kg - is obtained. The traction is contin­ uous and the force maintained for 15-20 minutes. long-standing traction. This approach is a weak alterna­ tive for nerve root block (see p. 265) but can be used for patients with very severe radicular pain that prevents sleep who for some reason cannot get the injection. A pulley is attached to the upper end of the bed. The patient wears a collar that is attached to a weight of 710 kg by a cord going over the pulley. The pain down the arm will disappear after traction for a few minutes and the patient falls asleep. This position can be maintained for as many hours as are convenient. When the traction is released the pain returns, but at least the patient has rested, which makes pain tolerance more possible. Continuous traction in bed

This is used only when everything else has been tried and failed. It is an alternative to immediate surgery. It has of course to be done in hospital because the patient requires full nursing care 24 hours a day. The traction (4-5 kg) is kept on for the first 24 hours and then gradually dimin­ ished and released. The pain is expected to subside slowly and to have diminished after 7-12 days92 and the patient may then leave hospital.

Figure 1 3 . 1 3

Traction performed sitting (head suspension).

Figure 1 3. 1 4

Traction performed lying down.

Indications. There are three main indications for contin­ uous traction. Very severe root pain without neurological deficit.

Those cases that do not respond to manipulation, head suspension or nerve block can be helped by traction in recumbency in the hope of quick diminution of the pain, which may otherwise take 3-4 months to abate. Nuclear disc prolapse. Rarely, a young adult may be seen with a gross nuclear displacement: quite severe scapular pain is present with gross limitation of rotation in one direction. All the other movements of the neck are normal. Manipulation does not work. During attempted manipulation the typical elastic recoil is felt - the head can be turned passively to full range but the active range remains very restricted. If head suspension fails, traction in bed is the onJy alternative.

Early posterocentral disc protrusion. Manipulation or head suspension are indicated and should lead to good results. When these measures do not help, traction in bed is substituted.

266 T H E CERV I CAL SPI N E

INJECTION A T A NERVE ROOT

Indications. Any radicular pain caused by a discoradicu­ lar interaction with or without neurological deficit may benefit from this injection. In a prospective study with independent clinical review it was demonstrated93 that in a series of 68 patients with monoradiculopathy 84% responded well to nerve block, whereas 16% required epidural injection. 76% of the patients recovered fully and 24% were clearly better with an average of 2.5 injec­ tions and thus avoided surgery. The conclusion was injec­ tions were efficacious over and above the natural course of the disorder and that the prognosis is even better for cervical root pain than for lumbosacral radiculopathies. •

• •

Root pain without neurological deficit in the first 2 months: as an alternative to manipulation or when there is inadequate response. Root pain without neurological deficit lasting longer than 2 months. Recent root pain with neurological deficit too severe to await spontaneous cure.

Tec hnique. A 2 ml syringe filled with 20 mg of triamcin­ olone acetonide is fitted to a 4 em needle. The lateral edge of the corresponding transverse process is identified, just behind the posterior edge of the stern­ ocleidomastoid muscle. The needle is inserted between the palpating finger and the midline and aims at the identified transverse process (Fig. 13.15). It is inserted until it meets bone. Half a millilitre is injected there, and the needle is then moved laterally and slightly cranially lmtil it slips over the edge and the rest of the injection is made here. During the injection the patient may feel the radicular pain, which disappears after a few minutes. One to six injections at weekly intervals may be neces­ sary, depending on the severity of the symptoms.

EPIDURAL INJ E CTION

Radicular pain lasting longer than a year without any tendency to spontaneous recovery and not responding to manipulation (see p. 253) can be treated with epidural injection. It is given in theatre conditions, and 10 ml of either a steroid solution or a mixture of local anaesthetic and steroid is injected at the C7-T1 interspace.94,95 This approach has again become popular. There are a number of studies supporting the benefit of epidural injection in the lumbar spine but only a few discuss cervical epidurals and show their safety and effective­ ness.96-98 In a retrospective study 64% of patients with root pain of cervical origin reported clear pain relief and a return to normal activity.99 One injection seems to be

Figure 1 3 . 1 5

Injection at a nerve root.

enough in most instances and no serious complications have been reported.100--102 Some patients may need up to four injections (Cyriax:92 p. 114). A review of 100 patients who received epidural steroids concluded that patients with radiculopathy responded better than those with neck pain.103

CHAPTER 1 3

COLLARS

Collars are prescribed far too frequently. Partial or total immobilization of the neck may not be considered as a treatment for neck pain but may be useful for preven­ tion or as a psychological support. The collar has a high patient satisfaction because it feels comfortable and gives the patient a sense of security. 104 A collar should not be prescribed before the disc has been reduced. It does not bring about reduction but merely adds further discomfort to that already caused by the protrusion. It also has no influence on the normal spontaneous evolution of radicular pain. Immobilizing collars are intended to avoid excessive movement that could exacerbate the pain. Soft collars seem to have little effect on controlling neck move­ mentl05-107 and the hard collars (for example the Philadelphia collar, the NecLoc collar and the Miami J collar), although more rigid, also do not attain the neces­ sary effect.108-111 Weight-relieving collars (for example the Four Poster brace) diminish the weight of the head on the spine and can therefore be used in compression phenom­ ena, such as cord compression, lateral recess stenosis or intractable neck pain.

PROPHYLAXI S

The best approach to a patient with a disc displacement is to try to reduce the displacement. When reduction suc­ ceeds, all symptoms disappear. Because a disc is a carti­ laginous structure it cannot heal, which means that it may displace again at any time. When recurrences are fre­ quent the disc is unstable and after further reduction, measures must be taken to prevent a new protrusion. Postures that involve keeping the neck in flexion or fixed for a certain period of time should be avoided or, if possible, altered. During the night a pillow should be used that enables the patient to hold the neck in the physiological lordosis when lying supine, or in the neutral position when lying on the side. When necessary, wearing a collar during the day (and if possible also at night) for several weeks or daily suspen­ sion at home may help to stabilize the reduced fragment.

AWAI TING SPONTANEOUS RECOVE RY

TREATM E N T 267

diminish, but it may take 7-10 days for the pain to disap­ pear completely. Unilateral, central or bilateral neckache or cervico­ scapular pain have no tendency to spontaneous recov­ ery, nor has bilateral arm pain with or without paraesthesia in the hands. Unilateral radicular pain recovers spontaneously in the course of several months, reckoned from the onset of radicular pain not of scapular discomfort. When muscu­ lar paresis is not present, recovery may take 3-4 months. When a palsy is present, the pain disappears more speed­ ily, usually in 2-3 months. Muscular power is restored within 3-6 months after the symptoms have ceased. The only exception is a C8 root palsy, which may take up to 6 months to disappear and may occasionally leave a patient with a permanently weak thumb. Time and patience should be taken to explain the mechanism of spontaneous recovery to the patient and to give a good prognosis. A continued interest should be taken, with regular review until symptoms have largely subsided so as to discourage the patient from going else­ where for futile and expensive treatments.

SURG ERY

Surgical intervention for neck pain, in the absence of neurological deficit, has no better prognosis than the natural history of the process.ll2 Indications • • •

Intractable root pain Posterocentral disc protrusion pressing on the spinal cord and giving rise to cord signs Posterolateral disc protrusions at more than one level.

Technique

Description of the surgical techniques falls outside the scope of this book. Since 1952 there has been a tendency to abandon the posterior in favour of the anterior approach. Refinements to the techniques described by Robinson-Smith (1955) and Gloward (1958 ) have been made and are now performed with success. Microsurgery has also become very popular. 113,114

-1 ,L

. �

--

�

Acute torticollis undergoes spontaneous cure in 1-2 weeks. The pain is constant, quite severe and the head may be fixed in deviation, usually side flexion and occa­ sionally flexion. After a few days the symptoms begin to

-

.

':. -

. .J�l I

r.t•:..,. .! I

• " .t't: �

The treatment techniques discussed here are: manipula­ tion and capsular stretching, deep transverse friction, injection infiltration, application of a collar and surgery.

268 T H E C E RVICAL SPI N E

MANI PULATION/CAPSULAR S TRETCH ING

INDICATIONS FOR MANIPULATION UNDER TRACTION Migraine

It is sometimes possible to instantly abort an attack of migraine with 30 seconds of strong traction on the neck. Although it is not clear what mechanism is responsible, Cyriax thought that stretching the carotid artery might be responsible.91 In middle-aged or elderly people, and especially in those who have migraine from adolescence, manipula­ tion can be preventative. When neck movements do not cause pain one session - one manoeuvre in the four direc­ tions - may suffice. Painful movements indicate that two to three treatments may be necessary before all discom­ fort ceases. This is a purely empirical finding which Cyriax identified when patients, treated for an ordinary disc lesion, reported afterwards that subsequent to manipulation their attacks of migraine diminished or even disappeared. Postural vertigo

Patients who suffer from postural vertigo can be helped by manipulation under considerable traction with a minimum of articular movement: straight pull and trac­ tion with leverage. This should only be performed by an experienced manipulator.

unchanged but the discomfort is largely abolished after two to four sessions, eventually in combination with deep transverse friction (see p. 269) or with facet injection (see p. 270) . Ankylosing spondylitis. The painful stiffness of the neck can be temporarily offset by slow stretching in all direc­ tions. The manoeuvre can be repeated as often as seems necessary - not during a flare up of the condition - and such mobilizations are effective as long as bone-to-bone end-feel has not been reached. Postconcussional syndrome. When diffuse capsular adhesions have formed about the occipitoatlantoaxial joints they can easily be ruptured by quick stretch manip­ ul ation in the direction that has been found to be painful at its extreme. Two to three treatments may be required. Matutinal headache in the elderly. The symptoms can be lastingly abolished by one to two sessions of slow stretch­ ing. There is no upper age limit to this approach. In very old patients only one movement is forced at a time which means that the patient may have to attend several times before full recovery is obtained. See Box 13.7 for a summary of indications for manipu­ lation / capsular stretching for non-disc lesions.

TYPES OF MANIPULATION Some techniques used for reduction of disc displace­ ments under traction can be employed to treat a number of non-discal conditions (Box 13.8).

Tinnitus

TECHNIQUES

When an aural cause has not been discovered, tinnitus can sometimes be abolished by manipulating the cervical spine. The same techniques are used as for postural vertigo.

Straight pull

INDICATIONS FOR MANIPULATION WITHOUT

See pp. 257-258.

TRACTION Capsuloligamentous disorders

Generalized arthrosis. Early arthrosis of the upper cervi­ cal joints with a moderate full articular pattern and an end-feel indicating that stretching is possible, responds well to a few sessions of quick stretching in rotation and side flexion to both sides. More advanced cases show gross symmetrical limita­ tion with a hard end-feel and are preferably treated with gradual slow stretching again in all four directions. Up to four sessions may be necessary. Facet arth rosis . Manipulation of the facet joint by gradual capsular stretching leads to reasonable results. The range of movement will probably remain

See previous section on disc lesions, p. 257. Rotation and side flexion under traction.

Traction with leverage

See pp. 259. Box 1 3 .7 Cervical manipulation/capsular stretching for non-disc lesions: indications M i g ra i n e Postural vert i g o Ti n n itus Ca ps u l o l igamentous d isorders • Generali zed arthrosis

• • • •

Facet arth rosis Ankylos i n g spondylitis Postco ncussio n a l syndrome Matutinal headache in the eld erly

C H APTER 1 3 - TREAT M E NT 269

Box 1 3 .8 Summary of types of manipulation for non­ disc lesions -

Under traction Straight p u l l : attack of m i g raine Rotations/s ide flexions: migra i n e Traction with leverage: postural vert i g o/tin n itus

Without traction Q u i ck stretch: early arth rosis d iffuse capsular ad hesions after tra u m a S l ow stretch : advanced a rthrosis a n kylosing spondyl itis a rthrosis at a facet j o i nt matutinal headache in the elderly

Forced rotation

The patient lies supine on the couch. The manipulator stands at the patient's head. If the neck is to be rotated to the right or left, the right or left thenar eminence is placed against the patient's left or right maxilla at the temporomandibular joint and the fingers are hooked around the chin. The other hand grasps the occiput and the head is held in slight exten­ sion. The head is turned to the end of range and move­ ment is then forced by a simultaneous action of both hands in opposite directions. Quick stretch results from a manipulative thrust over a very small amplitude and with high velocity. Ligamen­ tous adhesions may be felt (and heard) to break. This manoeuvre is done once and a painless range follows. Slow stretch is obtained by maintaining a steady push at the extreme of range for as long as the patient can tolerate, usually between 30 and 40 seconds. Pressure is then very slowly released and the head gradually brought back to the neutral position (Fig. 13.16). The movement is then repeated once or twice, depending on the patient's age.

Figure 1 3 . 1 6

Forced rotation.

During slow stretch sustained procedure keeps the head side flexed at the extreme of range (Fig. 1 3.17). Because this force has to be maintained for some time, this technique is quite tiring for the operator and there­ fore extra pressure can be applied with the knee against the elbow. The foot is therefore placed on a stool.

DEEP TRANSVERSE F R I C TION

Deep transverse friction can be given to the occipital muscular insertions and to the capsules of the facet joints.

POSTTRAUMATIC MUSCULAR LESIONS Posttraumatic lesions at the occipital insertion of the semispinalis capitis and, rarely, the splenius capitis

Forced side flexion

The patient lies supine on the couch and the manipula­ tor stands at the patient's head. When side flexion is to be to the right the head is supported under the occiput with the fingers of the left hand and the thenar emi­ nence lies against the side of the head above the ear. The metacarpophalangeal joint of the index finger of the right hand is placed against the transverse process of the sixth cervical vertebra and the thumb is kept extended to avoid the patient's trachea. This hand serves as a fulcrum and helps to keep the movement localized to the cervical spine only. The quick stretch manoeuvre is a short manipulative thrust, the result of a simultaneous scissors fashion movement of both hands in opposite directions.

Figure 13.17

Forced side fiexion.

270 T H E C E RV I CAL SPI N E

muscle give rise t o occipital pain on resisted extension and resisted side flexion towards the affected side. These features can be treated with deep transverse massage performed two to three times a week. Chronic cases may need up to 20 sessions for recovery. Technique

The patient lies prone on a couch with an opening near the head through which he can breathe. The physiother­ apist sits at the painless side, level with the patient's neck. The head is steadied with one hand and the other imparts the massage. This is done with the index finger, reinforced by the middle finger, and counterpressure is taken with the thumb at the painless side. Tenderness is sought in the attachment of the semispinalis capitis between the superior and inferior nuchal lines. If the lesion lies in the splenius capitis, tenderness is found more laterally at the mastoid process. The working forearm is held in slight supination which enables the therapist to exert upwards pressure against the occipital bone, at the exact point of the lesion. The thumb is used as a fulcrum and massage imparted by a to-and-fro movement over the tender area (Fig. 13. 1 8 ).

FACET ARTHROSIS Early arthrosis, usually localized at the C2-C3 or C3-C4 interapophyseal joint, can be treated with deep trans­ verse friction. If the result is poor, either capsular stretch­ ing or infiltration of a steroid suspension is substituted. Technique1 1S

(Technique described by o. Troisier and D. Elroy.)

Figure 1 3 . 1 8 Deep transverse friction to the occipital insertions of semispinalis or splenius capitis muscles.

The patient sits at the couch with the elbows resting on it and the chin supported by cupped hands. The phYSiotherapist, standing by the patient's painful side, palpates the area where the lesion is expected to lie. If the most tender spot corresponds to the facet joint considered responsible for the pain, massage is applied there. The articulation is found quite laterally, just behind the posterior border of the sternocleidomastoid muscle. Massage is done with the flexed thumb and counterpressure with the fingers. The direction is oblique, so that, parallel to the joint line, the thumb passes downwards as it is drawn backwards by inter­ nally rotating and abducting the shoulder and flexing the wrist (Fig. 13. 19). After 5 minutes' treatment, movements are tested again. When the correct spot has been reached, there should be some improvement in which case the massage is continued for another 5-10 minutes. Lack of improve­ ment indicates that the chosen level is not exact and reassessment is done. The patient is treated two to three times a week and 3-6 weeks of treatment may be required.

I NJECTION/I NF I LTRATION

Early and more advanced arthrosis of an interapophyseal joint may respond to intra-articular steroid injection. Unilateral localized pain at the mid-neck which does not respond to manipulation must be considered to originate from a facet joint and is most frequent at the C2-C3 and C3-C4 levels. Intra-articular steroid is called for when ankylosing spondylitis or rheumatoid arthritis has affected the cervical spine and one or two particular facet joints only are painful.

Figure 1 3 . 1 9

Deep transverse massage (Troisier and Elroy technique).

CHAPTER 1 3

- TREAT M E N T

271

TECHNIQUE The patient sits at the couch with the elbows resting on it and the chin supported by cupped hands. The operator stands behind the patient and palpates for the tender facet joint which lies 2-2.5 cm from the midline. A 1 ml tuberculin syringe is filled with 10 mg of triamcinolone acetonide suspension and fitted with a thin needle 3 cm long. The needle is inserted until it strikes the lamina and is then moved until it traverses a tough ligamentous structure, the capsule, before it abuts against cartilage. This feeling assures the operator that he has reached the joint. A few drops are then infiltrated at several adjacent points, some intra capsular, some intraarticular. If the needle is thrust in too close to the midline it is possible to traverse the inter laminar space and enter the spinal canal. One to two infiltrations will render the patient pain-free for a considerable period (Fig. 13.20). When a nerve root becomes compressed by an osteo­ phytic outcrop and symptoms occur which are severe enough to concern the patient, an infiltration with triam­ cinolone acetonide around the nerve root is tried. The technique for this is described on pp. 265-266.

Figure 1 3.20

COLLAR

SURG E RY

Patients who suffer from instability due to rheumatoid arthritis of the cervical joints or in whom acroparaesthe­ sia does not respond to manipulative treatment are best provided with an immobilizing collar. A weight-relieving collar, diminishing the compres­ sion strain, proves effective in patients who suffer from lateral recess stenosis (see p. 266).

Surgery is not within the scope of this book. In our opinion surgical decompression is certainly called for in patients with vertebrobasilar ischaemia caused by pres­ sure on the vertebral artery. Those with instability prob­ lems can be helped with arthrodesis; other indications are tumours and osteophytic outcrops lying either in the vertebral canal or the intervertebral foramen.

Infiltration of a facet joint capsule.

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SECTION THREE

The shoulder

SECTION CONTENTS 14. Applied anatomy of the shoulder Bones 278 Joints and intracapsular ligaments Extracapsular ligaments 281 Bursae 282 Shoulder movements 283

277

Haemarthrosis 316 Crystal synovitis 316 Septic arthritis 316 Primary tumours 317 Metastases 317 Asceptic necrosis 317 Osteoarthrosis 317 Neuropathic destructive arthropathy Non-capsular pattern 319

279

Muscles and tendons 283 Rotator cuff 287 Nerves and blood vessels 288

318

Limitation of active elevation

15. Clinical examination of the shoulder Referred pain 292 History 292

Inspection 294 Functional examination Palpation 300 Accessory tests 300 Technical investigations

319 324 Limitation of passive lateral rotation Limitation of passive medial rotation 326 Full range of movement 326 Excessive range of movement: instability of the shoulder 335

291

294 18. 300

16. Interpretation of the clinical examination 305 Limited range of movement: capsular pattern 305 Introduction 305 Staging 306 Conditions 306 Traumatic arthritis 307 Immobilizational arthritis 312 Monoarticular 'steroid-sensitive' arthritis Shoulder-hand syndrome 315 Rheumatoid-type arthritis 315

303

17. Disorders of the inert structures

313

Disorders of the contractile structures Introduction 349 Rotator cuff 350 Resisted abduction 353 Resisted abduction 360 Resisted lateral rotation 364 Resisted medial rotation 368 Resisted elbow flexion 371 Resisted elbow extension 374 Resisted flexion of the arm 374

349

19. Disorders associated with a painful arc 379 Disorders of the inert structures 380 Disorders of the contractile structures 380

Disorders mimicking painful arc

382

THIS PAGE INTENTIONALLY LEFT BLANK

CHAPTER CONTENTS

Bones

Applied anatomy of the shoulder

277

Introduction

278

Scapula 278 Humerus 279 Clavicle

279

Joints and intracapsular ligaments Glenohumeral joint 279 Subacromial space 280 Acromioclavicular joint 280 Sternoclavicular joint 281

279

Scapulothoracic gliding mechanism

281

Extracapsular ligaments

281 Coracoclavicular ligaments 281 Costocoracoid fascia 282 Coracoacromial ligament

Bursae

282

Subacromial-subdeltoid bursa Shoulder movements

283

Muscles and tendons

283

Adduction Abduction

284 285

Medial rotation Lateral rotation

285 286

Flexion of the elbow

286 286

Extension of the elbow Flexion 287

282

281

INTRODUCTION1 The main function of the joints of the shoulder girdle (Fig. 14.1) is to move the arm and hand into almost any position in relation to the body. As a consequence the shoulder joint is highly mobile, where stability takes second place to mobility, as is evident from the shape of the osseous structures: a large humeral head lying on an almost flat scapular surface. Stability is provided mainly by ligaments, tendons and muscles; the bones and capsule are of secondary importance. The function of the shoulder girdle requires an optimal and integrated motion of several joints. In fact five 'joints' of importance to 'shoulder' function can be distinguished: The glenohumeral joint (1). The acromioclavicular joint (2). • The sternoclavicular joint (3). • The subacromial joint or subacromial gliding mechanism (4): the space between the coracoacromial roof and the humeral head, including both tubercles. This is the location of the deep portion of the subdeltoid bursa. •

Rotator cuff

287

•

Nerves and blood vessels 288 Suprascapular nerve 288 Axillary nerve 288 Subclavian artery and vein

288

Figure 14.1

A global view of all five joints of the shoulder girdle (see text). 277

278 SECTION THREE - THE SHOULDER

•

The scapulothoracic gliding mechanism (5): this func­ tional joint is formed by the anterior aspect of the scapula gliding on the posterior thoracic wall.

Optimal mobility also requires an intact neurological and muscular system. It is not our intention to give a complete anatomical review, which can be obtained from anatomy texts. Only those structures which are of specific clinical importance will be focused on.

The ventral surface of the scapula is flat and covered with the attachment of the subscapularis muscle, except for the medial border and inferior angle where the serra­ tus anterior muscle is inserted.

BONES Osseous structures of interest are the scapula, humerus and clavicle. Neither the vertebral column nor the thoracic cage are discussed here (see chapters on the anatomy of the cervical and thoracic spine).

SCAPULA The scapula is a thin sheet of bone that functions mainly as a site of muscle attachment (Figs 14.2 and 14.3). Its medial border is parallel to the spine, the lateral and superior borders are oblique. It has a superior, a lateral and an inferior angle. The inferior angle corresponds to the interspinal level between the spinous processes of T7 and T8. The scapula contains four processes: the acromion, the coracoid, the spine and the articular process (the glenoid). The dorsum of the scapula is convex. It is divided by its spine into two fossae: the supraspinal and infraspinal fossa, containing the corresponding muscles. The scapu­ lar spine runs from the junction of the upper and middle third of the medial border, where it is rather flat, and corresponds to the level of the third thoracic spinous process. Laterally it becomes more prominent and meets the acromion at a right angle posteriorly. This angle is easily palpable and is one of the main bony landmarks at the shoulder. The acromion turns further anteriorly and covers part of the humeral head. The coracoid process is found at the anterior aspect of the scapula. The tip points outwards and is easily pal­ pated in the lateral part of the subclavian fossa. Further down, on the anterior aspect of the scapula, is a large con­ cavity which contains the subscapularis muscle. At the lateral angle, just beyond the neck of the scapula, is the glenoid fossa. This has a rather shallow surface, which is directed anterolaterally and slightly cranially tilted. It is approximately one-quarter the size of the humeral head and this, plus its shallow concavity, makes the joint both very mobile and vulnerable to (sub)luxations.

Posterior view of the scapula: 1, coracoid process; 2, acromion; 3, glenoid; 4, infraspinal fossa; 5, scapular spine; 6, supraspinal fossa.

Figure 14.2

2

Figure 1 4.3 Anterior view of the scapula: 1, acromion; 2, coracoid process; 3, glenoid fossa; 4, anterior surface.

CHAPTER 14

-

APPLIED ANATOMY 279

:n�----- 2

:-#------ 4

.-;:Cl--- 3

Figure 14.4 Superior view of humerus: 1, humeral head; 2, minor tuberosity·' 3, major tuberosity; 4, bicipital sulcus.

HUMERUS The articular surface of the humeral head points in a medial, posterior and slightly caudal direction and is sep­ arated from the major and minor tuberosities by its anatomical neck. When the arm is hanging down the side with its ante­ rior aspect facing the body, the greater tuberosity lies lat­ erally, the lesser tuberosity anteriorly. They are separated from each other by the bicipital sulcus (Fig. 14.4).

CLAVICLE The clavicle joins the sternum to the acromion. At its medial end it has a forward convexity whereas its lateral end is rather more concave. The joint capsules of both the sternoclavicular and the acromioclavicular joints are reinforced by several liga­ ments. The clavicle has many muscular and ligamentous attachments. The insertion of the coracoclavicular liga­ me�t is ?f practical importance. It is found laterally on the mfenor aspect of the clavicle, and just medial to it is the origin of the subclavius muscle. he clavicle gives support to the shoulder girdle by actmg as a strut between scapula and sternum. Due to its S-shape, the outer end describes a much larger rotation during arm elevation than its inner end. Therefore lesions of the acromioclavicular joint ligaments are more frequent than are lesions of the sternoclavicular joint ligaments.

�

JOINTS AND INTRACAPSULAR LIGAMENTS

GLEN OHUMERAL JOIN T The glenohumeral joint (Fig. 14.5) is a ball-and-socket between humeral head and glenoid fossa. There is a

Figure 14.5 Shoulder (glenohumeral) jOint: 1, labrum; 2, glenoid cartilage; 3, shoulder capsule.

remarkable geometrical relationship between glenoid and head which is responsible for the considerable mobil­ ity of the joint but is also an important predisposing factor to glenohumeral instability. First, the large spheri­ cal head of the humerus articulates against the small shallow glenoid fossa of the scapula (only 25-30% of the humeral head is covered by the glenoid surface). Second, the bony surfaces of the joint are largely incongruent (flat glenoid and round humerus). However, the congruence is greatly restored by the difference in cartilage thickness: glenoid cartilage is found to be the thickest at the periph­ ery and thinnest centrally, whereas humeral articular cartilage is thickest centrally and thinnest peripherally. This leads to a uniform contact between humeral head and glenoid surface throughout shoulder motion. The labrum is a fibrous structure that forms a ring around the periphery of the glenoid. It acts as an anchor point for the capsuloligamentous structures and for the long head of the biceps. It further contributes to stability of the joint by increasing the depth of the glenoid socket, enlarging the surface area and acting as a load-bearing structure for the humeral head. The synovial membrane of the joint capsule is mainly attached to the labrum, covering its inner surface, and at the anatomical neck of the humerus. It forms a sleeve around the intra-articular and inter-tubercular part of the long tendon of the biceps. The fibrous portion of the capsule is very lax and has several recesses, depending on the position of the arm. At its caudal end it forms the axillary recess, which allows normal elevation of the arm. Very often adhesions form here. The joint capsule is large, loose and redundant: the capacity of the glenohumeral joint capsule is larger than that of the humeral head to allow full and free range of motion of the shoulder. At the anterior portion of the capsule three local rein­ forcements are present: the superior, medial and inferior glenohumeral ligaments (Fig. 14.6). These contribute, together with the subscapularis, supraspinatus, infra-

280 SECTION THREE - THE SHOULDER

2

Figure 14.6 medial

The glenohumeral joint capsule and ligaments: superior (1),

(2) and inferior (3) glenohumeral ligaments.

Figure 14.7

The subacromial space and subdeltoid bursa: 1, acromion; deltoid muscle; 4, subdeltoid bursa; 5, clavicle; humerus; 7, scapula.

2, supraspinatus muscle; 3,

spinatus and teres minor muscles, to the stability of the joint. The supraspinatus, infraspinatus, teres minor and sub­ scapularis tendons reinforce the superior, posterior and anterior capsule. By virtue of the blending of their tendons with the glenohumeral capsule and ligaments, selective contraction of the cuff muscles can adjust the tension in these structures, producing 'dynamic' ligaments.

6,

der. Normally there is no communication between the bursa and the glenohumeral joint space but it may be established by rupture of the rotator cuff.

ACROMIOCLAVICULAR JOINT SUBACROMIAL SPACE The suprahumeral gliding mechanism consists of the coracoacromial arch (see below) on one side and the proximal part of the humerus, covered by the rotator cuff and the biceps tendon on the other. Both parts are sepa­ rated by the subacromial bursa that acts as a joint space (Fig. 14.7). Investigators point to the importance of contact and load transfer between the rotator cuff and the coracoacromial arch in the function of the normal shoul-

�--

.

"" . '...... :: . " ... ;:"...:. ... ,

�... .

. ..

Figure 14.8

..

The acromioclavicular joint (Fig. 14.8) is the only articu­ lation between the clavicle and the scapula. It contains a disc which usually has a large perforation in its centre. The capsule is thicker on its superior, anterior and poste­ rior surfaces than on the inferior surface. The anteropos­ terior stability of the acromioclavicular joint is controlled by the acromioclavicular ligaments and the vertical stability is controlled by coracoclavicular ligaments (conoid and trapezoid).

:}�.' ...

- �-,---------'.' 4"....;:

Acromioclavicular joint:

. . .... •. .

S, superior; I, inferior; L, lateral; M, medial.

CHAPTER 14

STERN OCLAVICULAR JOIN T The only osseous connection between the skeleton of the trunk and the upper limb is formed by the clavicle. Its medial end lies in contact with the superolateral angle of the sternal manubrium and with the medial part of the cartilage of the first rib, to form the sternoclavicular joint (Fig. 14.9). In both the vertical and anteroposterior dimensions, the clavicular portion is larger than the opposing manubrium and extends superiorly and poste­ riorly relative to the sternum. The prominence of the clav­ icle enables its palpation. The sternoclavicular joint is mobile along all axes and almost every movement of the scapula and the arm is associated with some movement at this joint. The capsule of the joint is thin at its inferior aspect but is reinforced anteriorly by the anterior sternoclavicular ligament, posteriorly by the posterior sternoclavicular ligament and cranially by the interclavicular ligament. The latter courses further above the sternum, to which it is firmly attached. Just lateral to the inferior part of the capsule is the costoclavicular ligament This connects the medial end of the clavicle to the cartilage of the first rib. An intra-articular meniscus, firmly attached at its circumference to the joint capsule, to the clavicle and to the cartilage of the first rib, divides the joint into two separate cavities. Behind the left joint is the common carotid artery, behind the right joint the innominate (brachiocephalic) vein. Both structures must be kept in mind when infiltrat­ ing on ei ther side.

SCAPULOTHORACIC GLIDIN G MECHANISM The serratus anterior muscle and the subscapularis are interposed between the scapula and the posterior thorax. The scapula is normally able to rotate, glide and tilt on the thorax. This mobility is an absolute necessity for normal function of the shoulder joint. Disorders

-

APPLIED ANATOMY 281

2

Figure 14.10

The extracapsular ligaments: 1, coracoacromialligament;

2, trapezoid ligament; 3, conoid ligament.

of one of those structures, as in irregularity of the posterior thoracic wall, can result in pain on movements of the arm or scapula.

EXTRACAPSULAR LIGAMENTS (Fig. 14.10)

CORACOACROMIAL LIGAMENT The coracoacromial ligament originates from the lateral aspect of the coracoid process and runs laterally and upwards to the tip of the acromion. It forms, together with the acromion and outer end of the clavicle, the coracoacromial roof. The coracoacromial arch provides a strong ceiling for the shoulder joint, along which the cuff tendons must glide during all shoulder movements. Passage of the proximal humerus and its cuff tendons under this roof is facilitated by the gliding surfaces of the subacromial bursa. Because there is normally no gap between the cuff and the roof, the slightest amount of superior translation may compress the cuff tendons and / or the bursa between the humeral head and the arch (Figs 14.10 and 14.13). Changes in the coracoacromial arch have been described in association with cuff disorders along with variations of acromial shape. Classically three types of acromion morphology are described: flat, curved and hooked. There seems to be a relationship between the presence of a hooked acromion and the prevalence of cuff lesions although a hooked acromion and a cuff defect can both be merely the consequences of age.

CORACOCLAVICULAR LIGAMENTS

Figure 14.9

Sternoclavicular joint.

The trapezoid ligament originates superiorly on the cora­ coid process and inserts at the inierior-lateral aspect of the clavicle.

282 SECTION THREE - THE SHOULDER

3

Figure 14.11

The costocoracoid fascia:

4

1, pectoralis major muscle;

2, clavipectoral fascia; 3, subclavius muscle; 4, pectoralis minor muscle; 5, costocoracoid fascia; 6, cephalic vein.

The triangular conoid ligament lies medial to the trape­ zoid ligament. Its origin. is at the medial aspect of the superior surface of the coracoid process and it inserts at the conoid tubercle at the inferior clavicular aspect. Both ligaments join together and form a half of a cone. They attach the scapula to the inferior outer side of the clavicle. Their structure enables the clavicle to rotate around its long axis on elevation of the arm. In this posi­ tion the clavicular insertion of both ligaments points more or less anteriorly.

Figure 1 4.12

Anterior view of the bursae of the shoulder:

1, subdeltoid bursa;

2, deltoid muscle; 3, subscapularis muscle; 4, subcoracoid bursa.

3

COSTOCORACOID FASCIA Deep-to the pectoralis major muscle lies a group of asso­ ciated muscles and fascia: the clavipectoral fascia, the subclavius and pectoralis minor muscles (Fig. 14.11). The costocoracoid fascia is that part of the clavipec­ toral fascia which is situated superomedial to the pec­ toralis minor muscle. A spontaneous loss of its normal elasticity may end in a contracture of this structure, causing limitation of elevation of the arm.

BURSAE The bursae are shown in Figures 14.12 and 14.13.

SUBACROMIAL-SUBDELTOID BURSA It is important to realize that there is only one bursa here. However, for clinical reasons two portions may be distin­ guished: a deep, subacromial part and a more superficial one. The former cannot be palpated, the latter is within a finger's reach.

Figure 1 4.13 Lateral view of the subdeltoid bursa of the shoulder: 1, subdeltoid bursa; 2, teres major muscle; 3, subscapularis muscle; 4, supraspinatus muscle; 5, infraspinatus muscle; 6, teres minor muscle; 7, long head of biceps.

A good idea of the anatomical localization of this bursa is obtained if the palm of the contralateral hand is put on top of the shoulder. The metacarpophalangeal joints must lie contiguous with the lateral acromial rim. The area covered by the palm overlies the deep subacromial portion of the bursa, the area covered by the fingers, and delineates the superficial (subdeltoid) part of it. The subacromial-subdeltoid bursa is normally only a potential 'space': two serosal surfaces in contact with each other, one on the surface of the cuff, the other on the undersurface of the coracoacromial arch (subacromial part) and the undersurface of the deltoid muscle (subdel-

CHAPTER 14

toid part). It normally produces a small amount of fluid which acts as a lubricant. The bursa permits the two layers to glide in relation to each other and can so, to a certain extent, be considered as the synovial portion of the 'subacromial joint', an extension of the glenohumeral joint. Inflamed, the bursa becomes compromised by oedema and adhesions and may cause considerable pain and functional disturbance.

SUBCORACOID BURSA Another clinically important bursa is the subscapularis bursa, which develops between the upper portion of the subscapularis tendon, the neck of the scapula and the base of the coracoid process. The bursa is covered by the pectoralis major muscle. Bursitis here can give rise to an isolated limitation of passive lateral rotation. Since this movement stretches the muscle, it will painfully pinch the inflamed subcoracoid bursa, provoking a spasm of the pectoralis major.

SHOULDER MOVEMENTS The glenohumeral joint is the most mobile joint of the human body. It can move around three different axes, all transversing the head of the humerus (Fig. 14.14): this is a horizontal axis coursing from the left to the right shoulder. Anterior and pos­ terior directed movements around it are flexion and extension. • b-b' - Sagittal axis: this horizontal axis lies in antero­ posterior sense through the head of the humerus. Movement of the arm around this axis is named • a-a' - Transverse axis:

-

APPLIED ANATOMY 283

adduction (the arm moves towards the body) and abduction (away from the body). • c-c' - Vertical axis: with the right arm hanging in neutral position (radial side pointing anteriorly and elbow bent to 90°) on outward movement of the arm around a vertical axis, bringing the palm of the hand anteriorly, is lateral rotation. The movement in the opposite direction is medial rotation. If the arm is first abducted to 90°, movement around the vertical axis, which brings the arm anteriorly and posteriorly, is named horizontal adduction and horizontal extension. When the patient actively elevates the arm, the initial movement takes place at the glenohumeral joint. Later the scapula rotates synchronously. Clinically this is easily checked by palpating the inferior scapular angle during elevation. Wallace2 states that both movements take place in a ratio of about 2:1; that means for every 2° of move­ ment at the glenohumeral joint there exists 1° of scapular rotation. These simultaneous movements are known as the scapulothoracic or scapulohumeral rhythm. Mobility of the glenohumeral joint is usually tested in three directions: abduction, medial rotation and lateral rotation. Abduction is movement in a frontal plane between a mobile humerus and a stabilized scapula. Medial and lateral rotation are assessed with the arm hanging in the neutral position. The term elevation indicates the move­ ment of the shoulder complex (glenohumeral joints and shoulder girdle) in a frontal plane. Normally the arm can move through an angle of approximately 0° to 180° in ele­ vation; the normal range for the glenohumeral joint is about 90° of abduction and the same for medial and lateral rotation. The most important function of the shoulder - arm elevation - has been extensively studied, in particular the relationship and contribution of the glenohumeral and scapulothoracic joints and the 'scapulothoracic' rhythm has been determined. During full elevation of 180° only 90° takes place at the glenohumeral joint. The remaining half is the consequence of scapular rotation, clavicular movement and, finally, adduction of the humerus which is only possible when the scapula has been fully rotated.

MUSCLES AND TENDONS

Figure 14.14

The axes of the shoulder.

The clinically important contractile structures of the shoulder joint are those whose tendons form the rotator cuff: the supraspinatus, infraspinatus, subscapularis and, of less importance, the teres minor. The adductors are those muscles which act below the sagittal axis, and the abductors those acting above

284 SECTION THREE - THE SHOULDER

(Fig. 14.15). Medial rotators act in front of the vertical axis, lateral ones behind it. The origins and insertions of the muscles are shown in Figure 14.16.

ADDUCTION

3

Figure 14.15 Muscle functions: 1, adductors; 4, lateral rotators,

12

2,

abductors;

3, medial rotators;

Adduction of the arm is performed by four different muscles: teres minor and major, the pectoralis major and latissimus dorsi (Fig. 14.18). The first is also a lateral rotator, while the latter three are medial rotators. The teres minor arises at the lower outer rim of the scapula, just above the origin of the teres major muscles and inserts on the major tubercle, just distal to the inser­ tion of the infraspinatus muscle. The teres major runs from the lower scapular angle towards the anterior aspect of the humerus, where it inserts on the minor tubercular crest, together with the latissimus dorsi muscle. The triangular space at the posterior aspect of the shoulder between both teres muscles is divided by the long head of the triceps muscle into a quadrilateral space laterally and a triangular space medially.

9

12

7

Figure 14.16 Muscle origins and insertions: 1, supraspinatus; 2, deltoid; 3, infraspinatus; 4, teres minor; 5, teres major; 6, pectoralis major; 7, latissimus dorsi; 8, subscapularis; 9, pectoralis minor; 10, coracobrachialis; 11, short head of biceps; 12, trapezius; 13, triceps brachii; 14, brachialis; 15, serratus anterior; 16, levator scapulae; 17, rhomboid,

CHAPTER 14

The latissimus dorsi muscle originates partly from the spinous processes of the lower dorsal vertebrae, partly from the lumbar vertebrae, partly from the iliac crest and sometimes from the lower ribs. It runs outwards and upwards in the direction of the lesser tubercular crest, where it inserts just lateral to the insertion of the teres major muscle. The pectoralis major muscle originates from the medial end of the clavicle, the sternum, the cartilage of the second to the sixth rib and the uppermost part of the rectus abdominis muscle. The upper fibres have a slightly downward course; the lower fibres run in a craniolateral direction. It inserts on the crest of the greater tuberosity. Table 14.1 summarizes the adductors. Table 14.1 The adductors

APPLIED ANATOMY 285

pletely ruptured the patient can no longer lift the arm actively and must make a swinging movement of the whole body in order to start the movement. Once the arm has moved through 30° the deltoid muscle takes over and carries out further abduction. The deltoid has three different parts: the clavicular, the acromial and the scapular spinal. In addition to the muscle's overall effect in abduction, its different parts each have other functions of their own. The clavicular component helps horizontal adduction of the arm, and the scapular spinal component assists horizontal exten­ sion movement. With the arm in neutral position, the former helps flexion, the latter extension. Table 14.2 summarizes the abductors. Table 14.2 The abductors

Nerve

Muscle

-

Spinal nerve root

Muscle

Nerve

Spinal nerve root

Pectoralis major

Pectoral

C5-C8

Deltoid

Axillary

C5 (C6)

Latissimus dorsi

Thoracodorsal

C7 (C6, C8)

Supraspinatus

Suprascapular

C5 (C6)

Teres major

Subscapular

C5-C8

Teres miner

Axillary

C5 (C6)

MEDIAL ROTATION ABDUCTION The supraspinatus muscle together with the deltoid is mainly responsible for this movement. Clinical differenti­ ation of the two structures i.s made by testing resisted movement of horizontal adduction and horizontal exten­ sion, which are secondary functions of the deltoid muscle. The supraspinatus, which originates in the supraspinal fossa, passes laterally, underneath the cora­ coacromial roof and inserts at the greater tubercle of the humerus (Fig. 14.17). The tendon and the tenoperiosteal junction are about 1 cm in width. On palpation it feels like a rather flat cord with a ty pical tendinous consis­ tency. The muscle plays a particularly important role in the initiation of abduction. When this tendon is com-

Three medial rotators have been discussed already: teres major, latissimus dorsi muscle and pectoralis major (Fig. 14.18). All are also adductors. The fourth medial rotator is the subscapularis (Fig. 14.19). Its origin lies in the subscapular fossa and the insertion in the minor tuberosity and towards the proximal extent of the minor tubercular crest. The tenoperiosteal insertion has a width of about 3 cm, is very thin and cannot be distinguished on palpation. Location of the insertion depends entirely on bony landmarks, i.e. the minor humeral tubercle. On abduction of the arm, the upper fibres pass underneath the acromial roof. Therefore a momentary

2

Figure 14.17

Figure 14.18 Supraspinatus muscle from above and anterior.

major;

Muscles used in medial rotation: 1, subscapularis;

3, latissimus dorsi; 4, teres major.

2, pectoralis

286 SECTION THREE - THE SHOULDER

Figure 14.19

Subscapularis, 1; and supraspinatus muscle,

2. Figure 14.20

impingement of a lesion in this location can happen and produce a painful arc. Horizontal adduction brings the lower half of the sub­ scapularis insertion in contact with the coracoid process, and a lesion in this portion provokes pain on this move­ ment. Table 14.3 summarizes the medial rotators. Table 14.3 The medial rotators Muscle

Nerve

Spinal nerve root

Subscapularis

Subscapular

C5-C8

Pectoralis major

Pectoral

C5-C8

Latissimus dorsi

T horacodorsal

C7 (C6, C8)

Teres major

Subscapular

C5-C8

LATERAL ROTATION This movement is performed mainly by the infraspina­ tus, teres minor being only a weak lateral rotator. The infraspinatus originates in the infraspinal fossa and passes laterally underneath the acromion. It inserts on the greater tuberosity over about 2 cm. The upper fibres are in very close relationship with the insertion of the supraspinatus (Fig. 14.20). On palpation the insertion is flatter and has a harder consistency than the insertion of the supraspinatus tendon. The lateral rotators are summarized in Table 14.4.

infraspinatus;

Supraspinatus, 1 and muscles used in lateral rotation:

2,

3 teres minor.

FLEXION OF THE ELBOW Although this movement is performed by other struc­ tures as well, it is the tendon of the long head of the biceps that is the most important here (Table 14.5). Arriving from the supraglenoid tubercle it is directed downward towards the bicipital groove, where it lies underneath a transverse ligament. Part of it is intra-artic­ ular, where it is surrounded by a synovial membrane. On contraction of the biceps the tendon itself does not move. It plays an important role in the stabilization of the humeral head in the glenoid fossa during powerful flexion of the elbow and supination of the forearm. The tendon of the short head of the biceps, originating from the coracoid process, seldom causes any problem. The other flexor muscles are described in the chapter on the Applied Anatomy of the Elbow. Table 14.5 The flexors of the elbow Muscle

Nerve

Spinal nerve root

Biceps brachii

Musculocutaneous

C5, C6

EXTENSION OF THE ELBOW Extension of the elbow is performed by the triceps brachii (Table 14.6). The long head originates from the lower margin of the glenoid. Triceps lesions at the shoulder are

Table 14.4 The lateral rotators Muscle

Nerve

Spinal nerve root

Infraspinatus

Suprascapular

C5 (C6)

Teres minor

Axillary

C5 (C6)

Table 14.6 The extensors of the elbow Muscle

Nerve

Spinal nerve root

Triceps brachii

Radial

C7 (C6, C8)

CHAPTER 14

extremely rare. Because the humeral head is pulled up towards the coracoacromial roof on resisted extension of the elbow, it can provoke an impingement of a lesion sited between the head of the humerus and the coraco­ acromial arc. Therefore, if resisted extension of the elbow provokes pain at the shoulder, it is usually considered as analogous to a painful arc.

-

APPLIED ANATOMY 287

Subscapularis

FLEXION

Infraspinatus The pectoralis major, biceps brachii, subscapularis and deltoid muscles, which are as flexors, have already been discussed. The only other structure that can provoke pain on resisted flexion of the arm is the coracobrachialis. Its origin is at the coracoid process, together with the short head of the biceps, and it inserts at the medial aspect of the midportion of the upper arm, below the minor tuber­ cular crest. The flexors are summarized in Table 14.7. Table 14.7 The flexors of the shoulder Muscle

Nerve

Spinal nerve root

Coracobrachialis

Musculocutaneous

C5, C6

Pectoralis major

Pectoral

C5-C8

Deltoid (anterior portion)

Axillary

C5 (C6)

Subscapularis

Subscapular

C5-C8

Biceps brachii

Musculocutaneous

C5, C6

The anatomy of other muscles which are mainly asso­ ciated with movements of the scapula - such as the sub­ clavius, levator scapulae and others - are discussed in the chapter on the Applied Anatomy of the Thoracic Spine.

ROTATOR CUFF Although the rotator cuff muscles have been discussed individually, some remarks about the cuff as a whole are in order. The rotator cuff is a complex of four muscles that arise from the scapula and attach to the tuberosities of the humerus. Although the muscles are separate superficially, in their deeper region they merge with each other, with the capsule underneath and with the tendon of the long head of the biceps. Their intimate relationship with each other and with the capsule, together with their unique localization, provide the rotator muscles with some particular functions. •

First: the rotator cuff muscles 'rotate' the humerus with respect to the scapula - a function that has been discussed earlier. However, the insertion of these tendons as a continuous cuff around the humeral

Figure 14.21

Concavity compression.

head permits the cuff muscles to provide an infinite variety of movements to rotate the humerus. • Second: by contracting together, the rotator cuff muscles and the biceps compress the humeral head into the glenoid fossa, locking it into position and providing a secure scapulohumeral link for upper extremity function - known as 'concavity compression' (Fig. 14.21). • Third: they provide muscle balance. In the shoulder, no fixed axis exists and, in a specified position, acti­ vation of one muscle will create a set of different rota­ tional movements. In order to produce movement in one direction, the other movements initiated by the contracting muscle must be neutralized by other muscles. The rotator cuff muscles are critical elements of this shoulder muscle balance equation: by contract­ ing selectively, they resist displacing forces resulting from contraction of the principal shoulder movers (deltoid, pectoralis major, latissimus dorsi). • Fourth: they have an important role in capsular stability of the joint. By virtue of the blending of their tendons with the glenohumeral capsule and liga­ ments, selective contraction of the cuff muscles can adjust the tension in these structures, so producing 'dynamic' ligaments (see Fig. 14.22).

-+\-----Coracoid ����::::;:!!!IP.�o;:_---- Subscapularis Biceps ---

*",�-:H--- Supraspinatus ����iiil����""'--- lnfrasPinatus �Jf:i!���--- Spina (resected) Figure 14.22

The rotator cuff.

288 SECTION THREE - THE SHOULDER

2

NERVES AND BLOOD VESSELS

SUPRASCAPULAR N ERVE This nerve is derived from the brachial plexus. It contains motor fibres of the C5 (C6) root and passes in the scapu­ lar incisura, under the transverse scapular ligament (Fig. 14.23), whereas the suprascapular artery lies above the transverse ligament. It innervates the supraspinatus and infraspinatus muscles.

7

AXILLARY NERVE The axillary nerve (Fig. 14.23 and 14.24) contains both motor and sensory fibres from C5 (C6). Originating on the brachial plexus anteriorly, it passes dorsally via the lateral axillary foramen. Its close contact with the humeral neck often results in injury in the event of a dislocation.

Figure 14.24 The anterior scapulohumeral region; 1, subclavian artery; 2, suprascapular artery and nerve; 3, axillary nerve; 4, radial nerve; 5, subscapularis nerve; 6, pectoralis minor muscle; 7, subscapularis muscle; 8, teres major muscle; 9, latissimus dorsi muscle; 10, anterior circumflex humeral artery; 11, thoracodorsal nerve and artery.

cut edge

3

It gives a branch to the teres minor muscle and ends in the deltoid muscle. The terminal branch is the lateral superior brachial cutaneous nerve, which innervates the upper and outer aspect of the skin over the deltoid.

SUBCLAVIAN ARTERY AND VEIN

Figure 14.23

The posterior scapulohumeral region: 1, suprascapular nerve; axillary nerve; 3, supraspinatus muscle; 4, infraspinatus muscle; 5, deltoid muscle; 6, teres minor muscle.

2,

The subclavian blood vessels are of particular importance since their compression can give rise to the subclavian steal syndrome or may play a role in the thoracic outlet syndrome. The vessels lie between the first rib and the clavicle, medially to the brachial plexus, and are sepa­ rated by the scalenus anterior muscle.

REFERENCES 1.

Kapandji 1. Bewegingsleer, vol I, De Bovenste Extremiteit. Bohn, Scheltema & Holkema, Utrecht/ Antwerp, 1986.

2.

Wallace W. The dynamic study of shoulder movement. In: Bayley I, Kessel L (eds) Shoulder Surgery. Springer, Berlin, 1982:139-143.

BIBLIOGRAPHY Aids to the Examination of the Peripheral Nervous System. Bailliere

Burns W, Whipple T. Anatomic relationships in the shoulder impingement

syndrome.

Clin

Orthop

Rei

Res

1933;294:

96-102. Claessens H, De pijnlijke Schoulder. Stafleu's Scientific Editing Company, Leiden, 1967.

Clarys

J,

Cabri

J,

Vanderstappen D. Functione/e Allatomie, vol 3.

V UB-uitgaven, 1989.

Tindall, London. 1986.

Codman E. Normal motions of the shoulder joint. In: The Shoulder. Thomas Todd, Boston, 1934:52. Cooper 0, Arnoczky S, O'Brien S, Warren R, CiCarlo E, Allen A. Anatomy, histology, and vascularity of the glenoid labrum. J Bone Joint Surg 1992;74A(1):46-52.

CHAPTER 14 - APPLIED ANATOMY 289

Cooper D, O'Brien S, Warren R. Supporting layers of the gleno­ humeral joint. Clill Orthop Rei Res 1993;289:144-144.

Fautrez J. Leidraad bij de studie van de stelselmatige ontleedkunde van de mens, vols I and II. Editor Desoer, L, 1967.

Guyot J. Atlas of Human Limb joints, 2nd ed. Springer, Berlin, 1990. Hoppenfeld S. Physical Examination of the Spine and Extremities. Appleton-Century-Crofts, Norwalk, Connecticut, 1976. Kaltsas D. Comparative study of the properties of the shoulder joint capsule with those of other joint capsules. Clin Orthop Rei Res 1983;173:20-26. Keating

J,

McMinn R, Hutchings R. Atlas of Human Anatomy. Mosby, London, 1993. Mink A, Ter Veer H, Vorselars H. Extremiteiten: Functieonderzoek en Manuele

Therapie.

Bohn,

Schelteme

Holkema

Utrecht/

of Medical

Illustrations,

Antwerpen, 1990. Netter

F.

The

Ciba

Collection

vol 8,

Musculoskeletal System, Part I. Ciba-Geigy Corporation, Summit,

New Jersey, 1987. Nobuhara, K. Contracture of the shoulder. Clin Orthop Rei Res 1990;254:105-110.

Waterworth P, Shaw-Dunn J, Crossan J. The relative

strengths of the rotator cuff muscles. j Bone joint Surg 1993;758(1):137-140.

Reilly

J, Nicholas J. The chronically inflamed bursa. Clin Sports Med

1987;6(2):345-370. Saha A. The classic mechanism of shoulder movements and a plea

1986;120(8):

for the recognition of 'zero position' of the glenohumeral joint.

Kumar V, Satku K, Balasubramanium P. The role of the long head of

Sarrafian S. Gross and functional anatomy of the shoulder. C1in

Kingma M. Schouderpijn. Ned Tijdschr

Geneeskd

325-337. biceps brachii in the stabilization of the head of the humerus. Clill Orthop Rei Res 1989;244:172-175.

Lipmann K. Clinical Disorders of the Shoulder, 2nd edn. Churchill Livingstone, London. 1986. Matsen F, Fu F, Hawkins R. {eds} The Shoulder: A Balance of Mobility alld Stability. September 1992, Vail, Colorado.

C1in Orthop Rei Res 1983;173:3-10. Orthop Rei Res 1983;173:11-19.

Sobotta J, Becher H. Atlas der Anatomie des Menschel1, vols 1 and 3. Urban & Schwarzenberg, Munich, 1967. V leeming A, Stoeckart R, Klein H, Volkers A. Misunderstandings concerning bursae of the shoulder. Ned Tijdschr Geneeskd 1987;131(41):1807-1809.

THIS PAGE INTENTIONALLY LEFT BLANK

Clinical examination of the shoulder

CHAPTER CONTENTS

292 Pain referred to the shoulder 292 Pain referred from the shoulder 292

Referred pain

History

292

Inspection

294

294 Preliminary examination 294 Basic functional examination of the shoulder

Functional examination

Palpation

300

Accessory tests

300

Technical investigations

300

295

Pain in the shoulder is, after low back pain, the most fre­ quent complaint of orthopaedic patients. Despite the fre­ quency of shoulder lesions - and the consequent pain and disability - much confusion still exists as to aetiology, terminology and treatment, l in contrast to the sta tement made by Cyriax:2,3 The shoulder is the most rewarding joint in the whole body. As a rule, one can always come to a clear diagnosis, and, if treated in the proper way, most shoulder lesions seem to be curable. Moreover, it is the most suitable joint for the general practi­ tioner, since almost no technical aids are required. A good history and full clinical examination, together with a detailed knowledge of the anatomy, suffices to solve the majority of the shoulder problems. Complicated cases that are difficult to diagnose exactly are encountered. If clinical findings are difficult to inter­ pret, the following general points should be of help. First, it should be realized that double lesions do exist, clouding the diagnosis. For example, it is not uncommon to find supraspinatus tendinitis together with infraspina­ tus tendinitis or in association with subdeltoid bursitis. In these doubtful cases, a diagnostic infiltration of a local anaesthetic can be most helpful in isolating the second lesion. On other occasions, patients present with a painful limitation of passive movement together with pain on resisted movements, and the question arises as to whether the problem is in an inert or in a contractile structure. If there is capsular limitation on examination, the joint should be treated first. If resisted movements remain painful after the joint has been managed appro­ priately, then the tendons should be treated. This approach is the best one, because resisted movements very often become negative after arthritis has disap­ peared. The only explanation for the phenomenon is the close relationship between the capsule of the shoulder and the surrounding tendons.4 It can easily be under­ stood how tension on the contractile structures may influence the pain originating in arthritis. Therefore pain on resisted movement(s) in association with an articular pattern should not be interpreted as being caused by a simple tendinitis. Of course, a severe tendinitis can limit 291

292 SECTION THREE - THE SHOULDER

active movement, because of the pain. But passive movements are of full range with a normal end-feel, even though there might be severe pain at the end of movement. An arthritis is an arthritis, a tendinitis is a tendinitis and both have to be treated as such. It is a common mis­ belief that as long as steroid is injected somewhere in the shoulder area it will spread and cure the lesion no matter where the lesion lies or where it was injected.s In fact if there is one region in the body which ought to be diag­ nosed and treated very specifically it is the shoulder. It is necessary to replace a vague diagnosis such as 'rotator cuff disease' or frozen shoulder by a precise one indicat­ ing exactly what is wrong. 6-8 REFERRED PAIN PAIN REFERRED TO THE SHOULDER

Pain referred to the shoulder, and possibly further down the arm, can be caused by nerve root compression, mainly as the consequence of a posterolateral cervical disc protrusion. A good history is important: the pain has usually started in the neck, probably interscapularly, and has shifted laterally into the ann and hand. Very often the pain is worst at night and is accompanied by pins and needles and numbness. Most frequently the C7 nerve root is compressed, causing pain at the posterior aspect of the whole arm to the second, third and fourth fingers. Other nerve roots can also be involved in a cervical disc lesion but this is far less frequent. Referral to the appro­ priate dermatome is usual. In a posterocentral cervical disc lesion with compres­ sion of the dura mater, the pain does not spread beyond the deltoid area. Therefore arm pain is not present. A rare disorder causing pain down the arm is a cervi­ cal neuroma. The condition starts with pain in the arm, which progressively spreads proximally as the tumour increases in size. Other possible causes for referred pain at the shoulder are visceral disorders. The diaphragm is largely devel­ oped from the third and fourth cervical segment, the heart from the eight cervical to the fourth thoracic. Therefore both can give rise to pain in the shoulder and arm. Irritation of the diaphragm and of the phrenic nerve, for example by blood or air under the diaphragm, is another well-known source of acute shoulder pain. A pulmonary neoplasm at the base of the lung with involvement of the diaphragm can provoke pain in the shoulder area. The same may also happen in a tumour of the superior sulcus (Pancoast's tumour). The majority of those patients complain of shoulder pain and are often mistakenly thought to be suffering from a musculoskele­ tal lesion.9

PAIN REFERRED FROM THE SHOULDER

Most structures around the shoulder are derived from the C5 segment. There is one important exception, namely the acromioclavicular joint, which is of C4 origin (Fig. 15.1). In acromioclavicular joint problems the pain is felt at the tip of the shoulder, with little spread. Exceptionally, when the lesion lies at the inferior acromioclavicular ligament, the pain can spread into the upper arm. In a lesion of one of the other shoulder structures, such as in all types of tendinitis, arthritis and subdeltoid bursitis, the pain is felt not so much at the tip of the shoulder but starts in the deltoid region and may spread further down the radial aspect of the arm to the base of the thumb (C5 dermatome; Fig. 15.2). How far down the arm the pain is referred depends on the severity of the lesion: the more severe the inflammation, the further the pain will spread. In glenohumeral arthritis, the degree of pain reference is of particular interest in following the healing process: as the patient improves the inflamma­ tion decreases and the pain spreads less far.

HISTORY

The first question to be elucidated by the history is whether the pain in the arm is genuinely from a shoulder lesion or whether it is the consequence of a more proxi­ mal lesion, arising perhaps from the cervical spine. If the answer to this is not clear from the history, a preliminary examination, including tests of the cervical spine, shoul­ der and elbow, is necessary. In an arthritis of the shoulder, the history will be important to establish the stage (see p. 306). In other disorders it is of less significance. The answers to a number of questions (summarized in Box 15.1) will be needed. What is your age? Age can be relevant in several

•

disorders. It can be helpful in defining the exact type of arthritis. Traumatic arthritis will only be met after 40 years of age, arthritis from immobilization after

Box 1 5.1 Summary of history taking • • • • •

Age? Where is the pain? Does it radiate? Pain at rest or only at use? Can you lie on that side at night? How did the pain come on: spontaneously/overuse/injury?

• For how l ong have you had the pain? • Are other joints affected? • General condition? Any operations?

CHAPTER 15

-

CLINICAL EXAMINATION 293

D

anterior

posterior Figure 15.2

•

D

•

anterior

posterior Figure 15.1

•

The CS dermatome.

the age of 60. Subdeltoid bursitis might be present between 15 and 65 years of age. Tendinitis can occur at any adult age. What is the pain and does it radiate? Pain starting in the deltoid area and spreading towards the wrist, along the radial aspect of the arm, is caused by a lesion that originates in C5. Such pain may be felt in the whole dermatome or only in part of it. The majority of the shoulder structures belong to the C5 segment. The acromioclavicular joint, a C4 structure, is the main exception. A patient who indicates the tip of the shoulder only as the site of pain suggests strongly that there is a lesion of the acromioclavicu­ lar joint. Whether the pain is caused by arthritis, bursitis or simple tendinitis will make no difference

•

The C4 dermatome.

to where or how far distally the pain is felt. The distal spread of referred pain depends only on the degree of inflammation. It is routine to ask if the pain remains above the elbow or radiates below it a matter of particular importance in arthritis. Is there any pain in the arm at rest? This gives information about the severity of the lesion: if sponta­ neous pain is present, a greater degree of inflamma­ tion is present than if pain is felt only on movement. Again, the answer to this question is one of the criteria for judging the stage of arthritis. Can you lie on the affected side at night? Pain when lying on the shoulder indicates more severe inflammation than just pain on exercise. Bursitis, tendinitis or arthritis may make it impossible for the patient to lie on the affected side at night. Consequently, this question is not of much help in defining the exact nature of the structure at fault. t!owever, it is rather important in following the resolution of the disorder: as the condition improves, the pain at night diminishes and finally disappears. Did the pain come on spontaneously or was there any particular reason for it, such as overactivity or an injury?

•

It is clear that overactivity may provoke tendinitis. In a ruptured tendon, however, one should not necessarily expect recent overuse. Overactivity can also cause arthritis in an already osteoarthrotic joint; this is as true for the acromioclavicular joint as it is for the glenohumeral joint. In haemophilia, haemarthrosis usually comes on spontaneously; it is more common at the knee but may occur at the shoulder as well. For how long have you had the pain? If the pain has already been present for some months, an acute subdeltoid bursitis can be excluded because the full course of this condition is 6 weeks. In addition, onset

294 SECTION THREE - THE SHOULDER

•

is abrupt over a few days, sometimes only hours, as in an attack of gouty arthritis. Arm pain because of root compression by a cervical disc protrusion wears off in about 4 months. Long-standing pain can be the outcome of a chronic subdeltoid bursitis or a simple tendinitis. Both can last for years. Mono-articular steroid-sensitive arthritis can take up to 2 years to disappear spontaneously. Are any other joints affected? A more generalized inflammatory disorder is expected if other joints have been previously involved or are attacked at the same time. Indeed, the shoulder joint can be the seat of rheumatoid arthritis, lupus erythematosus and ankylosing spondylitis.

• How is your general condition? Have you had any opera­

tions? Recent unexplained loss of weight can be the first sign of a carcinoma. A primary tumour at the shoulder or metastases, can be a local source of shoulder pain. A Pancoast's tumour of the lung often provokes pain in the shoulder area. Frequently, the pain is initially and mistakenly regarded as arising from the locomotor system.

INSPECTION

The inspection starts with checking what position the head is held in and whether both shoulders are level. It is important to check for redness, swelling, muscular wasting or any deformity such as scapular winging. Effusion of greater than 10-15 ml arising from the gleno­ humeral joint is normally visible on inspection at the anterior centre of the humeral head. Local swelling may also be found in acute, haemorrhagic or chronic subdel­ toid bursitis and in acromioclavicular joint cysts,lO as well as in tumours.

practice to perform a preliminary examination of the upper quadrant in the following situations: • • • • • • •

There is or was neck pain There is or was trapezius pain The pain is only at the top of the shoulder and / or at the clavipectoral area The pain is in the arm but remains quite localized The pain in the arm is influenced by movements of the neck Coughing, sneezing or taking a deep breath increases the pain There is paraesthesiae.

The preliminary examination of the upper quadrant com­ prises the following tests (Box 15.2): 1. Six active movements for the cervical spine - range of movement and / or painfulness; quick survey of the cervical spine 2. Active elevation of the shoulder girdle - range of movement and / or painfulness; quick survey of all the structures of the shoulder girdle

Box 15.2 Preliminary examination --

Neck Active movements

1. Flexion 2. Extension 3. Side flexion to the left 4. Side flexion to the right 5. Rotation to the left 6. Rotation to the right R esisted movements 7. Rotation to the left (Cl) 8. Rotation to the right (Cl)

Scapula 9. Active elevation of both scapulae

10. R esisted elevation of both (C2-C4) scapulae Shoulder

FUNCTIONAL EXAMINATION

The shoulder is an easy joint to examine. The intention is to obtain maximum information from a minimum number of tests. A recent study has shown the high relia­ bility of the examination scheme presented.ll

11. Active elevation of both arms 12. R esisted abduction (C5)

Elbow Passive movements 13. Flexion 14. Extension R esisted movements 15. Flexion (C5, C6) 16. Extension

PRELIMINARY EXAMINATION

In most cases of shoulder-arm pain the history will reveal whether the pain originates from the shoul­ der itself or is of cervical origin. Sometimes however the examiner is not quite sure and will then use a quick survey of all structures between C1 and T2 to exclude other sources of pain in the upper quadrant. It is good

(G)

Wrist 17. R esisted flexion

(G)

18. R esisted extension (C6)

Thumb 19. R esisted extension (C8)

Finger 20. Resisted adduction of the little finger (Tl)

CHAPTER 15 - CLINICAL EXAMINATION 295

3. Resisted rotations of the cervical spine and resisted elevation of the scapulae; quick survey of the nerve roots C1-C2-C3-C4 4. Active elevation of both arms - range and pain; quick survey for shoulder and shoulder girdle 5. Resisted movements of the upper limb - strength and pain; is both a quick test for perpheral lesions at the elbow-arm-wrist and a neurological examination for roots C5-C6-C7-C8-Tl and for the periphral nerves of the upper limb 6. Passive examination of the elbow; quick test for the elbow joint.

movements does not exclude a disorder in an inert structure nor pain on passive movements one in a con­ tractile structure. These results may sometimes lead to diagnostic difficulties (see Ch. 4). Accessory tests may be called for. They will only be performed if, after the basic functional examination, the diagnosis still remains unclear. After the basic examina­ tion is complete, at least a differential diagnosis should be in mind. To arrive at the final diagnosis, one or more accessory tests may be useful.

Any influence on the pain or any weakness will guide the examiner approximately towards the affected area, which is then examined thoroughly. If the examination reveals the lesion to lie in the shoul­ der, the examiner will try to define in which particular structure the lesion is situated by carrying out a detailed shoulder examination which comprises the 12 basic test (summarized in Box 15.3, p. 000)

Active elevation. The patient is asked to raise both arms sideways above the head, as far as possible (Fig. 15.3a). The range of movement and the influences, if any, on pain are noted. The onset of this movement is done by the supraspina­ tus muscle. 12 At about 35° the pars intermedius of the deltoid muscle takes over. Because the scapula rotates during elevation of the arm, other structures such as the trapezius and serratus anterior muscle are also involved. Therefore this test may draw attention to disorders of both the shoulder and shoulder girdle. Active elevation can be disturbed in disorders of both contractile and inert structures. For example, arthritis of the glenohumeral joint or ankylosis of the acromioclavicular joints limits this movement but limitation is also encountered in total rupture of the supraspinatus. This test also gives a good idea of the patient's will­ ingness to cooperate and so can be of importance in iden­ tifying a patient who has no genuine lesion but is feigning illness.

BASIC FUNCTIONAL EXAMINATION OF THE SHOULDER

Clinical examination should not begin by palpation for local tenderness. This widespread habit is a common cause of misdiagnosis, because pain arising from a shoul­ der structure is seldom felt at the site of the lesion. The basic shoulder examination consists of 12 tests. It is important always to perform every basic test, and never to stop even if the diagnosis appears clear after a limited number of tests. Stopping too soon can easily lead to an incomplete diagnosis. It should also be realized that in mixed patterns of pain on both passive and resisted movement(s), pain on resisted Box 15.3 Summary of basic functional examination of the shoulder -

Elevation 1. Active elevation of both arms 2. Passive el evation 3. Painful arc

Glenohumeral joint 4. Passive scapulohumeral abduction

5. Passive lateral rotation 6. Passive medial rotation

Resisted movements 7. Adduction 8. Abduction 9. Lateral rotation

10. Medial rotation 11. Flexion of the elbow 12. Extension of the elbow

Elevation of the arm o

Passive elevation. The examiner takes the patient's arm just proximal to the elbow, brings it upwards from the side and pushes it as far as it will go towards the head. At the same time counterpressure is applied over the contralateral shoulder, preventing the patient from side-flexing to the other side (Fig. 15.3b). Pain, range of motion and end-feel are noted. Because this movement comes to a halt when the axillary portion of the capsule is stretched, the normal end-feel is elastic. o

Painful arc. The patient raises the arm, actively, in a frontal plane and concentrates on pain likely to occur at mid-range, being asked to indicate where pain starts and where it stops on further elevation (Fig. 15.3c). A painful arc is defined as the symptom appearing somewhere around the halfway mark, with the arm near the horizontal and disappearing before the end of the movement (Fig. 15.4). This description holds even if pain is again present at the end-point. Some patients have an ascending arc, others a descending one: both are regarded as a real painful arc and no diagnostic

296 SECTION THREE - THE SHOULDER

(a) Figure 15.3

(b)

(c)

Elevation of the arm: (a) active elevation; (b) passive elevation; (c) painful arc.

A painful arc is more likely to occur during active ele­ vation rather than during passive movement because the contraction of the abductor muscles pulls humerus and acromion closer to each other. It always implies a lesion in the subacromial area or its neighbourhood. Because of their localization between acromion and greater or lesser humeral tuberosity, the affected structures can be painfully pinched. Three tests for the glenohumeral joint

Figure 15.4

Painful arc.

distinction is made between them. Sometimes an arc becomes visible to the examiner, i.e. when the patient avoids the painful movement by bringing the arm towards the front of the body during elevation.

Passive scapulohumeral abduction. The lower angle of the scapula is immobilized by the thumb and index. With the other hand, the examiner takes the patient's arm just above the elbow and lifts it up until the scapula starts to move (Fig. 15.5a). It is important that the patient does not assist this movement actively, because then the scapula immediately starts to rotate, so making the movement a compound one involving several joints. The normal range of scapulohumeral abduction is about 90°. Performed in the way described, only move­ ment between humerus and scapula takes place. If the movement is impaired, the glenohumeral or the subacro­ mial joint is at fault.

The examiner takes the patient's arm above the wrist, flexes the elbow to a right angle and pulls the arm with gentle pressure into Passive lateral rotation.

CHAPTER 15

-

CLINICAL EXAMINATION 297

full lateral rotation, meanwhile avoiding extension by holding the patient's elbow against the side of the abdomen. The trunk is immobilized by bringing the other hand around the patient's contralateral shoulder (Fig. 15.5b). This movement comes to a stop by stretching the ante­ rior portion of the capsule. Therefore the end-feel is elastic. The normal range is about 90°. Since individual differences exist, both sides should always be compared.

Besides the anterior portion of the joint capsule, other structures such as the subcoracoid bursa, the acromio­ clavicular joint and the subscapularis tendon are tested as well. Limitation of the movement is mainly found if something is wrong with the scapulohumeral joint itself; in this event, a harder end-feel is usually present. A simple tendinitis of the subscapularis does not cause lim­ itation of the movement but may render it very painful.

(a)

(b)

(c)

Figure 15.5 Three tests for the glenohumeral joint: (a) passive scapulohumeral abduction; (b) passive lateral rotation; (c) passive medial rotation.

298 SECTION THREE - THE SHOULDER

Passive medial rotation. With one hand still just above the patient's wrist and flexing the patient's elbow to 90°, the arm is brought into full medial rotation, without extension. The examiner's other hand is placed dorsally between the scapulae (Fig. 15.5c). The normal amplitude is about 90°. As before, this movement should be compared on both sides. Occasionally a painful arc can be present on medial rotation. This has the same diagnostic value as a painful arc on elevation and bears the practical consequence that to test for a real limitation of movement the examiner must persist to get beyond the painful arc. o

Resisted movements Resisted adduction. The patient is asked to pull the right arm towards the body as hard as possible. The examiner puts one hand around the elbow, the other one at the patient's ipsilateral side (Fig. 15.6a). o

Resisted abduction. The test is performed with the arm hanging down, a few degrees of abduction being permitted. The examiner asks the patient to push his or her arm to the side, meanwhile giving counter­ pressure at the elbow. The examiner's other hand stabi­ lizes the patient at the contralateral side (Fig. 15.6b). o

o

Resisted lateral rotation. The patient is asked to bend the elbow to a right angle and to push the

Resisted medial rotation. This is tested in the same position as resisted lateral rotation, but the patient's arm is held at the inner part of the wrist and the forearm is pulled towards the body (Fig. 15.7b). o

Resisted elbow flexion. With the elbow still bent at a right angle and the forearm supinated the forearm is pulled up. Counterpressure is applied to the distal part of the forearm just above the wrist. The other hand is placed on the patient's ipsilateral shoulder (Fig. 15.8a). o

Resisted elbow extension. In the same position as for flexion, the patient attempts to extend the elbow. To be able to hold the patient's elbow at 90° of flexion, the examiner puts his or her own elbow on the iliac crest, the arm in an almost vertical position underneath the patient's wrist. The other hand rests on the patient's ipsilateral shoulder (Fig. 15.8b). o

(b)

(a) Figure 15.6

forearm away from the body. To avoid any movement of the trunk, the other hand is put on the patient's con­ tralateral shoulder (Fig. 15.7a). Counterpressure is applied just above the wrist and care must be taken to get two details right. First, the patient should keep the elbow against the body, so that there is no element of abduction. Second, extension of the elbow during lateral rotation is avoided. This is easily checked if the examiner puts the little finger underneath the patient's wrist: extension at the elbow causes the digit to move down.

Resisted movements (a) adduction; (b) abduction.

CHAPTER 15 - CLINICAL EXAMINATION 299

(a) Figure 15.7

(b) Resisted rotation: (a) lateral; (b) medial.

(a) Figure 15.8

(b) Resisted flexion (a) and extension (b) of the elbow.

300 SECTION THREE - THE SHOULDER

PALPATION

General palpation for heat and swelling is done after the functional examination. It might be present in bacterial arthritis and in primary and secondary tumours of the humeral head, glenoid and acromion, and in acute and chronic subdeltoid bursitis. Palpation for pain is only performed when the basic examination proves the lesion to lie within the reach of a finger. As already indicated, it always follows the clin­ ical examination and never precedes it. Comparison between the two sides is essential. Palpation for tender­ ness is mainly done in acute and chronic subdeltoid bur­ sitis and in a sprained superior ligament of the acromioclavicular joint.

ACCESSORY TESTS

Sometimes the diagnosis is still not clear after the basic examination and a differential diagnosis has to be under­ taken. At other times the exact structure at fault has been identified by this stage of the examination but the precise localization of the lesion within that particular structure remains uncertain. In both cases, one or more accessory tests may be required (see Box 15.4). Passive horizontal adduction is the only one which is explained here. The other tests are discussed, together with the correspon­ ding disorders, in the following chapters.

The indications for this test are: • • •

Sprain of the acromioclavicular joint Subcoracoid bursitis Subscapularis tendinitis.

TECHNICAL INVESTIGATIONS

In shoulder problems it is rather exceptional that there is any need for further investigation. If some abnormality is found on radiographs or by any other technical aid, the question arises whether it is relevant or not. In other words, does the finding account for the clinical findings? For example, it is not sufficient to conclude that arthrosis of the shoulder seen on the radiograph of a 55-year-old man who has had shoulder pain for years is the cause of the symptom. If the diagnosis is based only on such radi­ ographic evidence, the patient cannot be treated and will be told to live with the problem. But it is quite possible that in addition to arthrosis, a simple tendinitis or chronic subdeltoid bursitis is present, neither of which will show on the radiograph. Once the lesion is treated in the proper way, the symptoms will be relieved even though a non­ troublesome arthrosis persists. The same is true of all technical aids, even the most sophisticated ones. As

Passive horizontal adduction. The patient's arm is brought horizontally in front of the body. At the end of the movement the elbow is pressed gently further towards the contralateral shoulder (Fig. 15.9). Twisting of the patient' s trunk is prevented by the examiner bringing the other hand behind this shoulder.

Box 1 5.4 Sum mary of accessory tests of the shoulder Passive horizontal adduction Passive horizontal lateral rotation Apprehension test for anterior instability Apprehension test for posterior instability Load and shift manoeuvre Sulcus sign Yergason's test R esisted horizontal adduction R esisted horizontal extension R esisted horizontal adduction with the arm forwards R esisted flexion R esisted extension Pressure against a wall Scapular adduction against resistance Figure 15.9

Passive horizontal adduction.

CHAPTER 15 - CLINICAL EXAMINATION 301

Kessel states: 'An X-ray is best used to check an hypothe­ sis which has been formed by history and clinical exam­ ination. One should eschew the temptation of a shortcut to the X-ray room or scanner',13

tial diagnosis in cases of impingement, in the absence of a rotator cuff tear. Arthroscopy

The main indications for radiography of the shoulder are evaluation of fractures and dislocations, imaging of bony disorders such as tumours and metastases and identification of calcifications in or around tendons. Plain radiographs may also be helpful in the evaluation of anterior and posterior instability. Although ultrasonogra­ phy is nowadays the most used method to evaluate rotator cuff lesions, plain X-ray examination can be of use in the detection of accompanying appearances such as changes in the coracoacromial arch, an unusual form or a spur off the acromion.I4 Radiography is also still advo­ cated in long-standing massive cuff tears. 15,16

Arthroscopy is useful for both diagnosis and treat­ ment.22-27 It should be regarded as an adjunvant I those cases where the normal diagnostic aids are insufficient.23 In that it offers an excellent view of the glenoid, labrum and capsule, it is an excellent technique in repair of shoul­ der instability.24 However, confronted with these almost perfect results of an examination technique, the physician should never forget that full and partial tears of the rotator cuff exist in a substantial part of a normal asymptomatic population. Both cadaveric studies25,26 and imaging studies27,28 on asymptomatic individuals have demonstrated that cuff defects become increas­ ingly common after the age of 40 and that most occur without substantial clinical manifestations.

Ultrasound scanning

Magnetic resonance imaging

Plain radiography

Ultrasound scanning is mainly advocated for the detec­ tion of full or partial rotator cuff lesions. In experienced hands it can reveal not only the integrity of the rotator cuff but also the thickness of its various component tendons. By careful positioning and by knowledge of the dynamic anatomy of the cuff, the experienced ultrasono­ grapher can image selectively the upper and lower sub­ scapularis, the biceps tendon, the anterior and the posterior supraspinatus, the infraspinatus and the teres minor. Ultrasonography has further advantages: it is non­ invasive and safe, bilateral examinations are quickly per­ formed, the shoulder can be examined dynamically and above all, the procedure is inexpensive. One important disadvantage, however, is that the method has a long learning curve. The results are exam­ iner-dependent and a good outcome is only to be expected in experienced hands. Specificity and sensitivity of as high as 98% and 91% respectively in comparison with surgical findings were claimed by Mack et al.I7 Others have found an overall sensitivity of 97% in diag­ nosing full cuff tears and of 91% in partial thickness tears.I8

Arthrography

Single-contrast arthrography can be helpful in diagnos­ ing complete tears of the rotator cuff, incomplete deep surface tears and in instability problems. 19 It will show loss of axillary-fold space and diminished joint capacity in adhesive capsulitis, but because this disorder is so easy to detect clinically, arthrography should never be required. It is not of assistance in clarifying the differen-

This can be helpful in the early detection of ischaemic necrosis, in primary and metastatic bone tumours and in osteomyelitis. The major advantages include its non­ invasive nature, lack of ionizing radiation, excellent contrast and anatomical resolution.29 If arthrography has been carried out recently or a steroid injection has been given, MRI should be postponed because it could lead to false-positive diagnosis. Small foci of soft tissue calcification may be missed on MRI. Other soft tissue lesions, such as subacromial bursitis, supraspinatus ten­ dinitis and tears, can be visualized.30-34 As always with new techniques, care should be taken not to be too optimistic about its possibilities or to believe that it is infallible.35-37

Computer tomography

This is an equally accurate method to MRI for evalu­ ation of the glenoid rim and labrum, the humeral head and the glenohumeral capsule. Nevertheless, MRI is to be preferred because it is more accurate in tendinopathies and no X-ray exposure occurs.32 In shoulder instability, CT-arthrography seems to be the best diagnostic method.38

Bursoscopy

Bursoscopy can be done under general or local anaesthe­ sia. Although there are almost no indications for bur­ soscopy,39 it may be of help in diagnosing lesions of the bursal part of the rotator cuff. At the same time, it offers visualization of the acromial roof.

302 SECTION THREE - THE SHOULDER

REFERENCES 1. Herberts P, Kadefors R. A study of painful shoulder in welders.

Acta Orthop Scand 1976;47:381-387.

1987;18(3):361-372.

2. Cyriax JH. Textbook of Orthopaedic Medicine, vol I, Diagnosis of

in

micro-

and

macrotraumas

of

the

shoulder.

Indications for echography and CT scanning. Rev Med Brux

capsule

to

the

rotator

cuff.

Clin

Orthop

Rei

Res

rotator cuff. J Bone Joint Surg 1990;72A(2):169-180. 23. Arens H, Van der Linden T. Artroscopie van de Schouder. Ned 24. O'Brien S, Warren R, Schwartz E. Anterior shoulder instability.

Orthop Clin North Am 1987;18(3):395-408. 25. Fukada H, Mikasa M, Yamanaka K et al. Incomplete rotator cuff

1990;254:29-34. 5. Hollingworth G, Ellis R, Hattersley T. Comparison of injection

techniques for shoulder pain: results of a double blind, ran­ M.

Schouderpijn.

Ned

tears diagnosed by subacromial bursography. Cli11 Orthop 1987;223:51-58. 26. Jerosch J, Muller T, Castro WH. The incidence of rotator cuff

domised study. BMJ 1983;287:1339-1341. 6. Kingma

22. Gartsman GM. Arthroscopic acromioplasty for lesions of the

Tijdschr Geneeskd 1984;128(49):2334.

1990;11(3):47-53. 4. Clark J, Sidles J, Matsen A. The relationship of the glenohumeral

joint

21. Uhthoff H, Sarkar K. An algorithm for shoulder pain caused by

soft-tissue disorders. Clin Orthop 1990;254:121-127.

Soft Tissue Lesions, 8th edn. Bailliere Tindall, London, 1982. 3. Annaert JM, Peetrons P, Famaey JP. Paraclinical diagnostic pro­

cedures

20. Neviaser JT. Arthroscopy of the shoulder. Orthop Clin North Am

Tijdschr

Geneeskd

rupture. An anatomic study. Acta Orthop Belg 1991;57(2):124-129. 27. Sher JS, Uribe JW, Posada A et al. Abnormal findings on mag­

1976;120(8):325-337.

humeroscapularis. Ned Tijdschr

netic resonance images of asymptomatic shoulders. J Bone Joint

8. Wirth C, Kohn D, Melzer C, Mark! A. Value of diagnostic meas­

28. Milgrom C, Schafflel' M, Gilbert S, van Holsbeeck M. Rotator­

7. B1ecourt J. De periarthritis

Surg 1995;77:933-936.

Ge11eeskd 1960;104:369. ures in soft tissue diseases and soft tissue lesions of the shoul­

cuff changes in asymptomatic adults. The effect of age, hand

der joint. Unfallchirurg 1990;93(8):339-345.

dominance and gender. J Bone Joint Surg 1995;77B:296-298.

9. Spengler D, Kirsch M, Kaufer H. Orthopaedic aspects and early

diagnosis of superior sulcus tumour of lung (Pancoast). J Bone

29. Meyer S, Dalinka M. Magnetic resonance imaging of the shoul­

der. Orthop Clin North Am 1990;21(3):497-513. 30. Seeger L. Magnetic resonance imaging of the shoulder. Clil1

Joint Surg 1973;58A:1645. 10. Postacchini F, Perugia D, Gumina S. Acromioclavicular joint

cyst associated with rotator cuff tear. Clin Orthop Rei Res

Orthop Rei Res 1989;244:48-59. 31. Ianotti J, Zlatkin M, Esterhal J, Kressel H, Dalinka M, Spindler

K. Magnetic resonance imaging of the shoulder. J Bone Joi11t Surg

1993;294:111-113. 11. Pellecchia GL, Paolino JP, Connell J. Intertester reliability of the

Cyriax evaluation in assessing patients with shoulder pain JOSPT 1996;23:34-38. 12. Vanderstraeten G, Schuermans

P,

1991;73A:17-29. 32. Rafii M, Firooznia H, Sherman 0 et al. Rotator cuff lesions:

signal patterns at MR imaging. Radiology 1990;177(3):817-823. De Neve J. Kinesiologie van

33. Gagey N, Desmoineaux P, Gagey 0, Idy-Peretti I, Mazas F.

de schouder en relatie tot de sportpathologie. Tijdschr Geneeskd

Contribution of MRI to the preoperative evaluation of rotator

1990;46(6):399-404.

cuff

13. Kessel L. Clinical Disorders of the Shoulder, 2nd edn. Churdtill

acromion and its relationship to rotator cuff tears. Orthop Trans

Chir

Orthop

Reparatrice

Appal'

Mot

Evaluation of the painu f l shoulder. J Bone Joint Surg 1991;73A(5): 707-716. 35. Ellman H. Diagnosis and treatment of incomplete rotator cuff

1986;10:228.

K,

Rev

34. Nelson M, Leather G, Nirschl R, Pettrone F, Freeman M.

Livingstone, London 1986. 14. Bigliani LU, Morrison D, April EW. The morphology of the

15. Hamada

tears.

1991;77(8):521-529.

Fukuda

H,

Mikasa

M,

Koboyashi

Y.

Roentgenographic findings in massive rotator cuff tears. Clin Orthop Rei Res 1990;254:92-96. 16. Weiner DS, Macnab 1. Superior migration of the humeral head:

a radiological aid in the diagnosis of tears of the rotator cuff. J Bone Joint Surg 1970;52B:524. 17. Mack LA, Matsen III FA, Kiloyne RF. Ultrasound: US evaluation

of the rotator cuff. Radiology 1985;157:205-209. 18. Hedmann A, Fett H. Ultrasonography of the shoulder in sub­

acromial syndromes with disorders and injuries of the rotator cuff. Orthopiide 1995;24:498-508. 19. Neviaser RJ. Radiologic assessment of the shoulder: plain and

arthrographic. Orthop Clin North Am 1987;18(3):343-349.

tears. Clin Orthop Rei Res 1990;254:64-74. 36. Heuck A, Appel M, Kaiser E, Lehner K, Luttke G. Magnetic res­

onance tomography of the shoulder. Possibilities of over inter­ pretation of normal findings. ROFO Fortschr Geb ROl1tgenstr Nuklearmed 1990;152(5):587-594. 37. Chandnani V, Ho C, Gerharter J, Neumann C, Kursunoglu­

Brahme S, Sartoris DJ. MR findings in asymptomatic shoulders: a blind analysis using symptomatic shoulders as controls. Clin Imaging 1992;16(1):25-30. 38. Van Oostayen J, Bloem J, Obermann W, Niezen R, Burgers A.

Computertomografie na artrografie bij instabiliteit van het schoudergewricht. Ned Tijdschr Geneeskd 1993;137(5):236-240. 39. Verdonk R, Van Meirhaeghe J, Van Houcke H et al. Shoulder

bursoscopy. Acta Orthop Belg 1988;54(2):233-250.

Interpretation of the clinical examination Traumatic arthritis Monarticular steroid­ sensitive arthritis Immobilizational arthritis Shoulder-hand syndrome

1-------+ Haemarthrosis Crystal synovitis Septic arthritis Primary tumours Metastases Aseptic necrosis Osteonecrosis Rheumatoid-type arthritis

Shoulder girdle problem

Acute subacromial bursitis

I----- Posterior capsular contraction

Interpretation of the clinical examination of the shoulder

[ Subcoracoid bursitis Anterior capsular contraction

1--------... Acromioclavicular sprain

Chronic subdeltoid bursitis Lesion of conoidl trapezoid ligament

1----------------..", Anterior instability

L Posterior instability L Inferior instability

303

304 SECTION THREE - THE SHOULDER

Adductor lesion

Pectoralis major Latissimus dorsi Teres major Teres minor

Pain

Acromioclavicular lesion (transmitted stress) Biceps lesion (origin)

Weakness

C7 nerve root lesion

Supraspinatus tendinitis

Musculotendinous Tenoperiosteal superficial

Pain

Tenoperiosteal deep Tenoperiosteal extended Deltoid lesion Partial rupture supraspinatus

Pain and weakness

Weakness Neurological lesion

Contractile structures

-f

Complete rupture supraspinatus C5

"'N'

.0,11 .. ;, "

Suprascapularis nerve lesion Axillary nerve lesion

Pain

Pain and weakness

Subscapularis tendinitis

Superficial

Subscapularis (partial) rupture

In isolation

Weakness

Pain

Deep

In combination with supraspinatus rupture! infraspinatus rupture C6 nerve root lesion

Infraspinatus tendinitis

Musculotendinous Superficial Deep

I

Pain and weakness

I�------------Complete rupture infraspinatus

Weakness

Extended Partial rupture infraspinatus In isolation Combined with infraspinatus rupture Combined with subscapularis rupture

Neurological lesion

C5 nerve root lesion Suprascapularis nerve lesion

Pain

Biceps lesion Brachialis lesion

Weakness

Biceps rupture C5 nerve root C6 nerve root

Pain

Painful arc? Triceps lesion

Weakness

C7 root lesion

Disorders of the inert structures

CHAPTER CONTENTS Limited range of movement Capsular pattern 305

305 306 Conditions 306

30S

Introduction

Staging

307

Traumatic arthritis

Immobilizational arthritis 312 Monoarticular 'steroid-sensitive' arthritis Shoulder-hand syndrome 315 Rheumatoid-type arthritis 315 Haemarthrosis 316 Crystal synovitis

316

Septic arthritis 316 Primary tumours 317 Metastases

LIMITED RANGE OF MOVEMENT

317

Aseptic necrosis 37 Osteoarthrosis 317

Neuropathic destructive arthropathy

Non-capsular patterns 319 Limitation of active elevation

319

Limitation of passive lateral rotation Limitation of passive medial rotation Full range of movement

318 324 326

326

Excessive range of movement: instability of the shoulder

335

313

INTRODUCTION

The capsular pattern at the shoulder joint is a propor­ tional limitation of the three passive scapulohumeral movements. There is some limitation of abduction, more limitation of external rotation and less limitation of internal rotation.1 A capsular pattern always indicates a lesion of the capsule of the joint, whatever its nature may be.2 It may be either an acute synovitis or a chronic organized reaction of the fibrous capsule. The selective limitation of movement is initially caused by involuntary muscle spasm that protects the inflamed joint from further over­ stretching. Because the ranges of movement are under­ traversed, intra capsular adhesions form and the movements become structurally limited. Long-standing capsular inflammation leads to fibrosis and thickening of the fibrous capsule. It has been demonstrated that these adhesions are mainly formed at the axilla and the ante­ rior portion of the capsule.3-6 This fits in very well with the greater loss of anterior capsular elasticity that is seen clinically more as restriction of lateral than of medial rotation (the capsular pattern; Fig. 17. 1).

Figure 1 7.1

The capsular pattern.

305

306 SECTION THREE - THE SHOULDER

Table 17.1

Capsular pattern: different degrees of limitation'

Severity of

Lateral

Scapulohumeral

limitation

rotation

abduction

Slight: Medium: Severe

30° 60-70° 90-100°

'From Cyriax:1

Medial rotation

Full range but painful 10-15° 15-25°

p. 135.

STAGING

Although only one capsular pattern at the shoulder exists, it can present clinically in different ways: magni­ tude, stage, degree of limitation. The magnitude of the limitation is expressed in its degree; limi tation can be slight, medium or gross, although always in the same (articular) proportion (Table 1 7. 1 ) A particular stage is a n indication for the severity o f the synovial inflammation. Three stages are considered. Stage I corresponds to a minor degree of inflammation: there is slight pain and thus minor or no protective muscle contraction. Stage III is the worst condition: highly inflamed synovia leads to serious pain and pro­ tective muscle spasm. Staging includes four criteria; three are provided by history, the fourth is the end-feel during lateral rotation (see Box 1 7. 1 ). Staging is of particular importance in posttraumatic arthritis and in immobilizational arthritis, because the choice of treatment depends on the actual stage. A clear distinction must be made between the degree of limitation of range and the stage. Limitation of movement and stage do not always correspond. It is quite possible,

Box 1 7. 1 Staging .-

Stage I: minor inflammation

Pain a bsent at rest Pain remains above the e l bow Patient can sleep on that side at night End-feel on lateral rotation is normal or sl ightly ha rdened Stage III: gross inflammation with all four criteria at their worst

Pain at rest Patient can not l i e on that side at night Pain spreads below the e l bow End-feel ind icates m uscle spasm

for example, to find a subtle degree of limitation in stage III or a pronounced degree of limited range in stage 1. The latter is encountered during the healing process of former stage III arthritis when the inflammation is progressively decreasing but capsular elasticity has not yet returned. To a certain extent, some relationship exists between them but this is rather unimportant from a therapeutic point of view. What matters is the stage. It should be emphasized that the diagnosis of arthritis is made purely on clinical grounds. Radiology is of no direct help7 nor is arthroscopy recommended. Although arthrography could show the diminished axillary fold and the reduced intra-articular lumen, the clinical signs and symptoms are so obvious that it should never be required.s One last point should be made about the initial phase of arthritis. When limitation has not yet set in, making a diagnosis can be very difficult. The only finding is pain at the end of all passive movements. It may be helpful to remember that passive lateral rotation is the most painful movement, accompanied by a slightly abnormal end-feel. Later an increasing limitation of lateral rotation sets in, subsequently followed by a diminishing range of both abduction and medial rotation.

CONDITIONS

Stiffness of the glenohumeral joint has classically been called ' frozen shoulder '.9 Several investigators have tried to propose a nomenclature to separate different types of shoulder stiffness.10-1 2 The subgroup typing was based on both the severity of stiffness and the presence or absence of an associated cause. The group without appar­ ent background was further subdivided into either 'post­ traumatic frozen shoulder', where an injury or a surgical intervention was at the onset of the disorder, and 'primary frozen shoulder' where no causative precursor could be found.13 Cyriax1 listed 1 3 different disorders leading to 'shoulder stiffness' in a capsular way (see Box 17.2). Whenever a capsular pattern is found, an attempt is made to categorize the lesion. Differentiation between the subgroups is achieved by history, clinical presentation and paraclinical investigations as follows: •

Stage II shows a m ixed result on the four c l inical criteria

(one or more of the criteria a re s l ightly positive and the other ones negative). Exam ple: a patient having pain below the el bow, but no pain at rest, who can l ie on that side at night and has a more or less elastic end-feel. This is on ly one example of a stage I I a rthritis, all other combinations of the four criteria a re poss i ble.

•

Try to detect an intrinsic aetiology which may be either a general disease (rheumatoid type of arthritis) or a local affection: infection, gout, haemarthrosis, or tumour. In the remaining subgroup where no intrinsic aetiology can be found and the only finding is of a progressive stiffening of the capsule, history will indicate whether the arthritis should be called posttraumatic, post­ immobilization or primary.

CHAPTER 1 7

Box

-

DISORDERS OF THE I N E RT STRUCTURES 307

17.2 _ . .

Classification of 'frozen

Cyriax's classification of

shoulder'

shoulder arthritis

With apparent aetiology - rheumatoid/infectious/ crystal l ine - osteoarthrosis Without apparent aetiology - posttraumatic frozen shoulder - primary frozen shoulder

Traumatic arthritis I mmobi l izational arthritis Monarticular 'steroid­ sensitive' arthritis Shoulder-hand syndrome Rheumatoid-type arthritis Haemarthrosis Crystal synovitis Septic arthritis Primary tumours Metastases Aseptic necrosis Osteoa rth rosis Neuropathic destructive arthropathy

To categorize capsulitis of the shoulder in this manner is extremely important because different lesions have a different development and prognosis. Furthermore categorization is of great use in deciding the course of the treatment.

T RAUMATIC A RTH RITIS

This condition is almost never encountered in patients younger than 40 years. Because the risk of traumatic arthritis in youth is virtually zero, preventive measures after injury are unnecessary for the young. NATURAL HISTORY

A capsular pattern may develop after glenohumeral (sub )luxations, contusions or surgical procedures to the shoulder.I4 Most often, however, injury need not have been severe and a traumatic arthritis may precipitate some days after the shoulder capsule sustained an indirect and sudden traction or after the joint bumped against a wall. Because it can take some weeks before the pain is bad enough to force the patient to consult his physician, it is quite possible that such a minor accident may have been forgotten. The evolution and natural history of traumatic arthri­ tis is quite typical. It takes about a year for the lesion to heal spontaneously. During this process, three stages of about 4 months each are observed (Fig. 1 7.2). In the first, the 'painful phase', both pain and limitation of move­ ment increase. In the second, ' the progressive stiffness phase', the pain diminishes but limitation remains the same. It takes until the beginning of the last 4 months before limitation begins to decrease (the resolution or 'thawing' phase), so that by a year movement is back to

� Pain

c:::::::J Limitation

6 months F i gure 17.2

1 year

Natural history of traumatic arthritis.

normaI. lS Several authors, however, have demonstrated a significant number of patients with a delayed thawing phase and one instance showed persistent stiffness for 6 years.16.17 Sometimes elevation and lateral rotation may remain permanently slightly restricted. IS

Painful phase The onset of the arthritis is very characteristic. Immediately after the injury an ache develops that may wear off in 2 days or so but which appears again a few days later to increase progressively over the next few months. During the painful phase, the intensity of the arthritis typically evolves from stage I, over stage II to stage III. In the first 2 weeks after onset, the patient complains of an ache mainly on activity. During this time, the pain does not spread beyond the elbow and sleep on the affected side is possible. A subtle capsular pattern can be detected on functional examination, for example limita­ tion of some 20° on lateral rotation and of 5° on abduc­ tion, together with a normal (but slightly painful) range on medial rotation. All these movements are also painful at the end of the achievable range. The end-feel may be slightly altered but not definitively abnormal. A clear stage I arthritis is present. As the arthritis increases, stage II will be found at 2-6 weeks from the onset: pain may interfere with sleep, pain spreads below the elbow or a spastic end-feel may be apparent on passive testing. After 2 months, the inflammation is at its worst. Now, with the features of stage III, the patient suffers from continuous pain, day and night, which spread below the elbow. A limitation of about 80° on lateral rotation, 60° on abduction and 20° on medial rotation may be present. The end-feel is abrupt (hard or muscle spasm). Progressive stiffness phase Although the severity of the synovial inflammation may progressively diminish from the fourth month, the

308 SECTION T H R E E - T H E S H O U LD E R

limitation in range remains the same for a few more months. With decreasing inflammation, pain at night and at rest gradually disappears and remains above the elbow. The end-feel changes from spastic to hard ligamentous (but still painful). The arthritis gradually returns to stage II and finally, after about 8 months, stage I.

Thawing phase The final stage of the natural evolution is the resolution or the thawing phase, characterized by a slow and gradual gain in mobility. Usually a few months (4-6) may be required to achieve full functional motion. The joint is in stage III with moderate pain and a hard ligamentous end­ feel. 19 TREATME NT

The choice of treatment for posttraumatic arthritis should always be adjusted according to the duration and sever­ ity of symptoms. Treatment techniques should also be applied in the context of the patient's needs, risk factors and tolerance. Finally, the outcome of the treatment must always be related to the expected natural history of the disease and treatment is only begun when it is expected to positively change the course of this natural history.20,21

Prophylaxis The primary management for posttraumatic arthritis in the shoulder is prevention: to suppress the natural tendency of most patients to immobilize the painful joint until comfort returns. Therefore, a patient older than 40, seen shortly after a shoulder injury, should be encour­ aged to use the arm as normally as possible with move­ ment to full range at least twice daily. When the patient has excessive pain a therapist can undertake mobilization just to maintain normal movement at the glenohumeral joint. The joint should be only gently forced actively and passively, using the capsular stretching technique. In this way, arthritis with secondary limitation of movement will not have an opportunity to develop and the pain dis­ appears. Once pain has ceased, treatment can be stopped. Passive movements If arthritis has set in, it is too late for prevention and treat­ ment to the capsule should be given. Gentle but firm passive stretching exercises have proven effective in the relief of pain and recovery of range in motion in up to 90% of patients with capsular stiffness.22-25 However, some studies report inadequate results with stretching and even exacerbation of the condition.26,27 Two main types of passive mobilization are used depending on the degree of inflammation. As a conse­ quence, clinical staging is the guide. Stages I and II with non-spastic end-feel (stage IIa) are cured by mobilization

using the capsular stretching technique. Stages lIb (spastic end-feel) and III are treated by either capsular distraction, which is a less irritating type of mobilization, or by intra-articular injections with corticosteroid. Preference is for the steroid injections but, if the patient refuses injections or if use of steroid is contraindicated, distraction can be very useful.

Capsular stretching Warning

Stretch ing manoeuvres on a highly inflamed capsule exacer­ bate the condition. The fol l owing indications of a high degree of infla mmation a re therefore considered as con­ traindications. • Arthritis in stage III or in stage II with a spastic end­ feel. • Wrong end-feel on first distraction attempt: when the thera pist brings the patient's arm up and starts the manoeuvre attention should be g iven to pain and end-feel. If it is possi ble to bring the el bow slightly further towards the couch without increasing pain too much or without provoking muscle spasm, it is a good sign that capsu lar stretching will succeed. In the oppo­ site case, stretching should not be undertaken but intra-articul a r injections or the distraction technique should be used. • After-pain lasting for more than 2 hours.

Before capsular stretching is begun, analgesic short-wave diathermy can be given for 10 minutes. The patient lies supine and brings the ipsilateral hand on to the forehead . The therapist stands on the same side, facing the patient and puts one hand on the sternum and the other on the elbow of the affected side. By pushing the elbow backwards towards the couch, the capsule of the joint is stretched (Fig. 1 7.3). In this way the inferior recess of the capsule, where most of the adhesions lie, is elongated. The hand on the sternum prevents the patient from avoiding the stretch by curving the trunk. The cap­ sular stretching is done in elevation. As this is a combined movement, the rotations improve simultaneously with the increase in abduction range. If this does not happen, the shoulder must be stretched in lateral rotation as well. Stretching is not manipulation and any tendency to 'jerk' should be avoided. Rather the manoeuvre is done by a continuous pressure gently intensified for a few seconds, then slackened off slightly for a little while and increased again. This is repeated for as long as the patient can endure and is followed by a full rest, in which the arm is brought down, avoiding pain by axial traction. Stretching should be repeated several times during one session and can be combined with hold-relax techniques. The therapist should teach the patient which mobiliz­ ing exercises can be done at home in order to maintain

Technique.

CHAPTER 1 7 - DISORDERS OF THE I N E RT STRUCTURES 309

Figure 17.3 Capsular stretching.

the mobility that has been regained. These should be per­ formed several times daily.

mobility increases. Two or three of these ruptures may be necessary to restore a full range of movement.

Force used during stretching. The stretching itself is

Distraction This technique consists of a very gentle elongation of the joint capsule performed in such a way that the fibres are stretched longitudinally. It has been suggested that this inhibits nociceptive reflexes which result from long­ standing stimulation of the nocisensors. These reflexes would be responsible for an increased sympathetic activ­ ity giving rise to a vasoconstriction of the vessels around the joint.28

given with a reasonable amount of force, sufficient to provoke some discomfort at the time. But more important than the patient' s sensation during the treatment is what is felt afterwards, which provides the information about the amount of force to be used. If there is increased pain for the first 2 hours after the procedure, the correct amount of power has been used and future treatment must be identical. If pain is not increased, the stretch power has been insufficient and, at the next session, must be increased. If the patient returns after 2 days still having increased pain attributable to the procedure the implication is not­ as one might logically assume - that the stretching was too aggressive. Rather it indicates this shoulder can not accept capsular stretching at all. Even if only stage I or IIa arthritis is present, and although all indications for stretching seem present, distraction or injections should be substituted. Sequence and duration. These sessions are given three

times a week for about 1 5-20 minutes each. Improvement is expected after 5-15 sessions, depending on the severity of the lesion. Stretching is continued until the shoulder is back to normal (pain and range) or no further gain is achieved. long-standing cases. Sometimes, in long-standing cases, it is possible to hear and feel adhesions rupture on stretching. Immediately afterwards, pain diminishes and

Indications. Patients with stage I or IIa arthritis in whom

capsular stretching is contraindicated have an open choice between steroid or distraction. Patients with a traumatic arthritis in stage lIb or III for whom steroids are refused, have been used withou t success or are contraindicated. Technique. The patient lies supine, the arm along the

side, with a small cushion beneath it, for maximum comfort. The therapist sits at the patient's painful side and brings the ipsilateral hand deep into the axilla, the other one partially on the outer aspect of the shoulder, partially reinforcing the one in the axilla (Fig. 1 7.4). The former hand will try to pull the head of the humerus out of the glenoid fossa. The direction of the pull is mainly lateral and slightly cranial and anterior. Initially the manoeuvre is done with the patient's arm in the most comfortable position. Once mobility has increased, some degree of lateral rotation and abduction can be added, so that the distraction is performed at the

3 1 0 SECTI ON TH R E E - THE S H O U L D E R

in the time course of the disease after the manipulation or they have seen too many complications. Ruptures of the subscapularis tendon, damage to the neurovascular structures and fractures and dislocations have been reported after manipulation under anaesthesia.31-35 Manipulation should be considered only if all other treatment methods fail. In fact this type of treatment is very seldom needed as almost all capsular limitations can be resolved by either mobilization techniques or a sequence of intra-articular injections with triamcinolone.

Figure 17.4 Capsular distraction.

end of the possible range. At first, when there is a lot of pain, fine vibration can be additionally incorporated so as to stimulate the mechanoreceptors and inhibit the nocisensors, resulting in pain relief. During the first sessions not much happens. It is only after a few sessions that the therapist feels a loosening of the patient's shoulder in such a way that the humeral head is felt to leave the glenoid fossa. This technique is performed with so little force that it is not at all painful during the session and is not followed by any after-pain. Sequence. As with stretching, this technique is done

three times a week for about 1 5-20 minutes each. Distraction is continued until the arthritis has regressed to stage II or IIa. Then normal capsular stretching can be performed.

Manipulation under anaesthesia Manipulation under anaesthesia has been used for over a century. Some believe in its effectiveness,28-30 others have denounced its use because they think there is no change

Intra-articular injections In an attempt to suppress the painful inflammatory response in posttraumatic capsulitis of the shoulder, intra-articular injections with corticosteroids have been used for decades. Studies that evaluate the response to intra-articular injections generally combine the injection with other treatment methods and rarely compare the efficacy of the injection alone. However, some studies could demonstrate improvement in pain scores and increase in range of motion after steroid injections alone.36--38 Other investigators are very sceptical about the injections as their studies failed to demonstrate the benefit of the treatment.39 Cyriax could initially not find benefit in intra-articular hydrocortisone injections40 but after he detected the advantages of a sequence of consecutive intra-articular injections with triamcinolone, he became a very enthusi­ astic advocate of intra-articular injections for capsulitis of the shoulder.41 Our experience is that traumatic arthritis responds very well to injections with 20 mg of triamcinobne, pro­ vided the treatment is given in stage III or stage lib and the correct sequence is followed (see below). Technique. The patient lies prone, the arm under the

abdomen and the elbow flexed to a right angle, a position which has a double advantage. First it brings the articu­ lar surface of the humeral head to point straight back­ wards, so creating a large target for the needle. Second, the patient cannot move the arm. The coracoid process is palpated in the infraclavicular fossa. The examiner puts the index finger here and places the thumb dorsally on the posterior angle where the scapular spine meets the acromion. A 4 cm needle is fitted on a 2 ml syringe filled with 20 mg of triamcinolone. It is inserted just below the thumb and aimed at the coracoid process. The same approach is nowadays used on arthroscopy via the posterior portal.42,43 After about 2-3 cm the needle is stopped by the articular surface of the head of the humerus with a typical cartilaginous sen­ sation. At this point, the needle lies intra-articularly. Just before the needle is arrested, tough resistance is felt on passing through the capsule (Fig. 1 7.5).

CHAPTER 1 7

Figure

1 7.5

-

DISORDERS OF THE I N E RT STRUCTU RES 3 1 1

Intra-articular injection.

With the needle in cartilaginous contact, 2 ml of triam­ cinolone are injected here. A reasonable amount of resist­ ance is encountered. Exceptionally, not even a single droplet can be injected, in which case the point of the needle is fully with the articular cartilage. Should this be the case, the needle should be withdrawn about 2 mm while injection pressure is maintained. Once the tip of the needle leaves the cartilage the steroid floats in. The injec­ tion is given in this position and is minimally painful. Sequence. The aim is to keep the capsule continuously under anti-inflammatory influence till the inflammation has almost fully disappeared. Therefore the next injection must be given just before the effect of the previous one has worn off.

A practical scheme, with increasing intervals between the injections, is as follows: First injection: day O. Second: after 1 week: day 7. • Third: 10 days after the second injection: day 1 7. • Fourth: 2 weeks after the third one: d ay 3 1 . • Fifth: 3 weeks later: day 52. • Sixth: 4 weeks later on day 80. • Seventh: 5 weeks later on day 115. • Eight: 6 weeks later on day 1 57. • Ninth: 6 weeks later on day 1 99. The usual sequence is that after the first injection the patient will have less pain, and from the third injection onwards the limitation of movement starts to decrease. • •

3 1 2 SECTION TH R E E - THE SHOULDER

The injections are given until the arthritis reverts to stage I. Treatment can then be stopped and the arthritis will continue to resolve spontaneously. In general, about five injections are needed. Exceptionally it happens that, even if the scheme is fol­ lowed, a patient who is temporarily better after the last injection complains of increasing pain during the days before the next appointment. This means that the interval between injections was too long and should be reduced. Sometimes the pain subsides progressively as expected but limitation of movement does not alter. In this event, capsular stretching should be tried and is started once the arthritis is at stage I. If stretching makes the pain relapse, it must be postponed for a few weeks and another injection given. A summary of the treatment of traumatic arthritis is shown in Figure 1 7.6.

Complications and side-effects Because there is a small but real risk of infection with intra-articular injections, it behooves the practitioner to prepare the skin and handle the procedure as though it were surgical . It should also b e remembered that steroid injections i n diabetic patients, even given intra-articularly and i n rather small doses, may cause blood glucose t o fluctuate and also may incur a greater risk of infection. Further side-effects may be some flushing next day and perhaps some interference with the menstrual cycle because of hormone effects.

No arthritis develops

Cure

If no improvement or contraindicated Stage I If no improvement of range, stretching is used Cure

Figure 17.6 Treatment of traumatic arthritis.

Other treatments Hydraulic distension. 'Brisement', a distensive capsular stretching and rupturing technique of the shoulder, has become increasingly popular during the last decades. The procedure is performed by insufflating the glenohumeral joint with a volume of approximatively 60-100 ml of fluid, the exact quantity depending on the distensibility of the joint.44 Advocates of the technique claim that hydraulic distension is relatively non-invasive, simple to perform and an effective mechanism to achieve sympto­ matic and lasting relief in adhesive capsu litis.45-47 However, a double-blind, prospective study, conducted on 45 patients with adhesive capsulitis compared the therapeutic efficacy of non-distensive and distension arthrography in combination with intra-articular steroid injection. After 3 months there was no significant differ­ ence between the two treatment regimens in the degree of pain or range of motion.48 The outcome of this study was later confirmed.49 As with manipulation under anaesthesia, this tech­ nique should be reserved for a few cases that do not respond to passive mobilization and injection with corticosteroids. Arthroscopic release. Recent studies have demonstrated

that arthroscopic capsulotomy may be an effective tech­ nique in the management of the frozen shoulder that does not respond to physiotherapy.50,51 During standard shoulder arthroscopy, intra-articular cautery is used to completely divide the anterior-inferior capsule, the intra­ articular portion of the subscapularis tendon and the middle glenohumeral, the superior glenohumeral and the coracohumeral ligaments. 52

IMMOBI LIZATIONA L A RTH RITIS

I n patients over 60, when the shoulder is immobilized, it is at risk of becoming stiff. The reasons for the initial immobilization may be multiple. Immobilizational arthritis is a well-known complication in hemi­ plegics.53,54 During a prospective study, conducted by Bruckner and Nye, 25% of patients with subarachnoid bleeding developed a frozen shoulder over an observa­ tion period of 6 months.55 Other neurological conditions such as Parkinson's disease may precipitate capsular stiffening.56 Immobilization of the arm for disorders such as a fracture of the elbow or the humerus is also reason enough to develop a posttraumatic arthritis.57 For many years clinicians have associated ischaemic heart disease and shoulder arthritis, 58 which eventually develops as the resul t of immobilization after an infarction or surgery.

CHAPTER 1 7 - DISORDERS OF THE I N ERT STRUCTU RES 3 1 3

Natural history The development and natural history of an immobiliza­ tional arthritis cannot be distinguished from a traumatic arthritis. Again there are three phases in the progress of the disease. In the painful phase, both pain and limitation of movement increase. In the subsequent progressive stiffness phase, the pain diminishes but the limitation remains the same. Lastly limitation decreases during the final 'thawing' phase. Altogether, it takes about a year for the lesion to recover spontaneously and movement to return to normal. Treatment This condition should never be encountered. It is very important for primary care phYSicians and physiothera­ pists to realize that immobilized shoulders should get gentle movements at least once a day, in order to prevent the development of an immobilizational shoulder arthri­ tis. This simple advice was already given by Neviaser who in 1945 wrote: 'I believe we can accept the fact that disuse and inactivity play a very important role in the etiology'.59 In prevention it is sufficient to maintain the normal range of movement from the very beginning of immobilization. If arthritis has set in by the time the patient is first seen, it should be managed the same way as traumatic arthritis: stage I is treated with capsular stretch­ ing, stage III with a series of intra-articular injections of 20 mg of triamcinolone. Stage IIa can also be treated with stretching if the end-feel is right. If this is not the case the patient should receive intra-articular injections.

MONOA RTICU LA R 'STE ROID-SENSITIVE' A RTH RITIS

A monoarticular arthritis that develops without apparent cause - neither a trauma nor immobilization can be traced in the history - is called 'idiopathic frozen shoulder' or monoarticular 'steroid-sensitive' arthritis. The latter term comes from Cyriax, who discovered that most cases of 'freezing arthritis' could be successfully treated with a series of intra-articular steroid injection.6o

Pathophysiology Although the exact cause of the capsular inflammation and the subsequent capsular fibrosis is not exactly known, recent investigators have focused on the inflammatory cellular changes and immunological response in the syn­ ovium and the capsule. Currently it is not exactly known what triggers the initial synovial inflammation. Some point to specific cytokines which may be involved in the early inflammatory stages of the disease.61 Several refer­ ences in the literature assume frozen shoulder to be an algoneurodystrophic process.62,63 Others suggest that a

proteinase may b e involved i n the pathogenesis o f both a Dupuytren's contracture and a frozen shoulder.64,65 Others have suggested that an area of focal necrosis in a degenerative tendon is the earliest lesion, followed later by a generalized chronic inflammatory reaction of the whole capsule and of the rotator cuff.66 Hannafin and colleagues have studied the histopatho­ logic evolution of monoarticular shoulder arthritis. They found an initial hypervascular synovitis, provoking a progressive fibroblastic response in the adjacent capsule, finally leading to diffuse capsular fibroplasia, thickening and contracture.67

Incidence The bulk of patients who present with primary mono­ articular arthritis of the shoulder are between 45 and 60 years of age,57 although the disease can be encountered at any age.68 Diabeti c patients are more likely to su ffer from monoarticular steroid-sensitive arthritis. Whereas in a normal population about 2% su ffer from this disorder, in diabetics the figure is almost 1 1 % .69,70 Some connection with hyper- or hypothyroidism has also been suggested although the l ink between the disorders remains obscure.71 Natural history The onset is spontaneous and involves only one shoulder at a time; sometimes the other shoulder may become involved within 5 years.72 In the spontaneous evolution of a monoarticular steroid-sensitive arthritis, four periods of about 6-9 months each are distinguished (Fig. 1 7.7). At first, the patient starts to feel pain at the shoulder for no apparent reason. This increases progressively, becomes continuous (although often worst at night) and starts to spread _p'ain

1 year

:

: 2 years

�Limitation

Figure 1 7.7 The four phases in the spontaneous evolution of monoarticular steroid-sensitive arthritis.

314 SECTION THREE - TH E SHOULDER

beyond the elbow. It causes many months of sleepless nights, a more than sufficient reason to start treatment at once. At the same time movement becomes progressively limited . During the second phase, the pain does not get worse but remains at maximum for another 6 months. Limitation does not change for about 12 months. One year (sometimes even more) after the onset the pain starts to diminish and it disappears almost fully at the end of this third phase. Restriction of movement however does not alter. Finally, in the fourth period, the limitation of move­ ment gradually decreases. At this time, only some slight discomfort and a certain degree of stiffness remains, which usually disappear fully at the end of the 2 years. These clinical phases in the natural history of idio­ pathic capsulitis of the shoulder correspond roughly with the histopathologic phases identified by Hannafin67: first hypervascularization and inflammation of the synovia (first period), then progressive fibroblastic response of the capsule (second and third periods) and finally the remodelling of the capsule (fourth period).

Functional examination The first phase is initially characterized only by pain, which occurs at the extreme of all passive movements. Almost no limitation will be present during the first few weeks. Arriving at the diagnosis at this stage may difficult. As in traumatic arthritis, it is of help to know that the pain is referred in the C5 dermatome and that full passive lateral rotation is the most painful test. Also the changing end-feel may be of clinical importance in making an early diagnosis. Later, as the pain increases, limitation of movements sets in. From now on a clear cap­ sular pattern is found that will have its maximum limita­ tion by the end of the first period (6-9 months from the onset of the complaints). By then the end-feel will certainly be that of muscle spasm. Both pain and limitation remain maximal during the entire second phase. The third phase is characterized by a gradual decrease in pain. The end-feel progressively changes towards a hard one, indicating the loss of capsular elasticity. Limitation of movement, however, does not change yet. During the final ('thawing') phase the range of move­ ment progressively increases to return to normal about 2 Table 17.2

Stages of monoarticular steroid-sensitive arthritis Stage

Pain beyond elbow? Spontaneous pain? Can lie on the affected side at night? End-feel?

I

No No Yes Normal

Stage

II

Yes Yes Mixed pattern

Stage

III

No Abrupt: hard or muscle spasm

years after the onset. Some authors have stated, however, that it may take longer for the stiffness to disappear com­ pletely or that some degree of stiffness may remain.73 In general, the duration of the recovery stage is related to the duration of the stiffness phase: the longer the stiffness phase is, the longer is the recovery phase.?4

Staging As in traumatic arthritis, three stages are distinguished, in relation to the degree of inflammation: stage I is the slightest, stage III is the worst (Table 1 7.2). The stages are based on the following criteria: • • • •

Does the pain spread beyond the elbow? Is there spontaneous pain? Can the patient lie on the affected side at night? What is the end-feel?

Although the treatment is the same for stages I, II and III, the classification helps in following the natural devel­ opment, gives an idea about the effect of the treatment and indicates when to stop the treatment.

Treatment Because spontaneous recovery takes about 2 years and the patient suffers severely in the meantime, treatment is absolutely necessary.?5,76 As a rule, a series of intra-articular injections with triamcinolone are given, despite the stage of the arthritis. Exceptionally, capsular distraction is used for those patients who do not want injections or when steroids are contraindicated. If distraction is used it should be per­ formed in the same way, frequency and duration as for traumatic arthritis (see p. 309). Injections for monoarticular steroid-sensitive arthritis are given in the same way (tech­ nique and interval) as for traumatic arthritis (see p. 310). They can be stopped once the patient can use the arm freely; the end-feel is back to normal and no relapse of pain occurs by 6 weeks after the previous injection. If some limitation of movement still exists by then, it usually disappears spontaneously during the following months. It is rare for patients not to respond to injection therapy or to remain with a painless stiff shoulder.?7 In 1 989 we did a prospective study on 54 patients with idiopathic arthritis of the shoulder. The youngest patient was 40, the oldest 71. On clinical examination all showed a clear cap­ sular pattern and none had pain on any resisted move­ ment. Laboratory tests were performed to exclude other rheumatoid types of arthritis and to check for a possible association with diabetes (only one diabetic was identified). Over 90% of the cases presented initially with stage II or stage III arthritis. All were treated by a series of intra-articular injections given at increasing intervals. The total number of injections given was between four and nine with an average of six (Fig. 1 7.8). After the first injection half the patients were less troubled at night. This

CHAPTER 1 7

6

5.8

5.6

5 4 3 2

0

1.5

1.5

Female

Male

Figure 1 7.8 Mean numbers of steroid injections given in a study of monoarticular steroid-sensitive arthritis (error bars are standard deviations).

0.90

0.90

0.80

-

DISORDERS OF THE I N E RT STRUCTURES 3 1 5

down the upper limb, in association with trophic changes in the forearm and the hand. At onset, the hand is bluish and diffusely swollen. The condition can resolve sponta­ neously or may develop into a dystrophy. Later the wrist and fingers become stiffened (flexion contracture with limitation of extension) and the skin shiny and atrophic.78 Cyriax considered the syndrome to be a variety of monoarticular steroid-sensitive arthritis because it is often associated with a capsular pattern at the shoulder.79 So far the exact cause has not been clarified al though some assume that emotional instability could be an important factor. Another view is that the disorder does not really exist and, as a theoretical legacy, has been passed on from textbook to textbook and should now be given a decent burial. Good diagnostic practice will always define some other causes in these cases, very often a cervical root problem with secondary atrophy.8o

0.70

0.40 0.30 0.20

0.16

0.10 0.00 -'-_-'--_L...---'-_--'-_-'--_'----'-_--'---' Diagn 1 inj 2 in j 3 inj 4 inj 5 inj 6 inj 7 inj 8 in j

Figure 17.9 Decay of nocturnal pain (% of total) in relation to the given number of injections.

figure increased to more than 90% after the third injec­ tion. Spontaneous pain decreased in the same way as the nocturnal pain but with some delay, being less severe and progressively less distantly referred. After eight injec­ tions, 98% of all patients had no pain (Fig. 1 7.9). The range of movement of rotation and elevations began to increase after the first injection, though this was clinically not very obvious. An increased amplitude usually became clear after the third injection. The final conclusion of the study was that 98% of all patients recov­ ered fully from their pain - only one patient continued to have a painful shoulder. As far as range of movement was concerned, there was an 80% increase after the seventh injection. The results of this study correspond roughly with what was found by Steinbrocker.66

SHOU LDE R-HAND SYNDROME

Classically, shoulder-hand syndrome has been described as a pain starting in the shoulder area and spreading

Rheumatoid arthritis (RA) is an autoimmune disorder of unknown aetiology characterized by symmetric, erosive synovitis and sometimes multisystem involvement. Any joint can be involved, but the proximal interphalangeal and metacarpophalangeal joints of the hand and the wrist are preferential sites, as well as the metatarsopha­ langeal joints of the foot, the knee joint and the joints of the shoulder, the ankle and the hip. Symmetry is the hall­ mark of joint involvement. The synovium of bursae and tendon sheaths can also be affected. It gives rise to pain and stiffness, usually greatest in the morning. There is a marked capsular pattern with a spastic end-feel. Warmth and tenderness can be palpated over the joint. Conventional radiography remains the standard imaging technique for joint studies in patients with sus­ pected RA. The first radiological signs are osteoporosis and joint space narrowing. Later chondral erosions and small bone erosions at the joint margin are seen. Marginal and central erosions follow in advanced stages. Fibrous ankylosis, joint deformities (subluxations and disloca­ tions), fractures and fragmentations are typical findings of more advanced RA.81-83 RA is best treated systemi­ cally; local intra-articular injections are used only as a secondary aid. Sometimes the shoulder is the seat of a reactive type of arthritis in which the inflammation is caused by an infec­ tion but in which no bacterial or viral agent can be isolated from the synovial fluid.84 Ankylosing spondylitis rarely starts in the peripheral joints but cases have been described with initial localiza­ tion at shoulder or hip.85 Particularly in the pediatric form of the disease (juvenile ankylosing spondylitis), peripheral joint involvement is more frequent and can

3 1 6 SECTION THREE - THE SHOULDER

precede, by many years, the onset of back features.86 I n its later course, signs and symptoms will be more localized in the spine and the sacroiliac joints. Arthritis at the shoulder from this disorder responds well to intra-articular steroids. The pain disappears fully but very often movement remains limited. Reiter 's disease seldom afflicts the shoulder joint. It is usually polyarticular in nature. Classically the triad urethritis-arthritis-conjunctivitis is present. Arthritis as a manifestation of psoriasis or lupus responds well to steroids although a slight limitation of movement may remain.

HAEMA RTH ROSIS

A patient complaining of severe pain immediately after an injury and showing a capsular pattern should always be suspected of having a haemarthrosis. In haemophilia, the haemarthrosis can develop spontaneously. It is more common at knee, elbow and ankle joints than in the shoulder. Blood is very irritant to articular cartilage and so should be aspirated at once. If it is not, it will lead to full destruction of the joint over a few years.87

C RYSTA L SYNOVITIS

Crystal synovitis at the shoulder from urate crystals is very rare.88 This disorder should be considered when a capsular pattern comes on spontaneously i n a few hours. It normally remains monoarticular but has often been preceded by earlier attacks in smaller joints (particularly in the metatarsophalangeal joint of the big toe). It disap­ pears spontaneously in the course of a week and responds very well to colchicine or phenylbutazone. Diagnosis is mainly based on the presence of urate crystals in the synovial fluid.89 Pseudogout is the result of the presence of pyrophos­ phate crystals in the joint. The term 'chondrocalcinosis' is used if calcification in the hyaline cartilage of the joint is visible on radiography.90 The knee is much more com­ monly affected than the shoulder.91 Clinically, the presen­ tation is spontaneous but is less acute in onset than gout. Crystals are also presen t in the synovial fluid. Pseudogout resolves spontaneously in about 3-4 weeks.

tion), by haematogenous dissemination or from adjacent osteomyelitis. It is mainly seen in elderly people, often in connection with other predisposing factors such as diabetes, immune deficiency, malnutrition and alco­ holism.92,93 Some cases occur after mastectomy and radio­ therapy for breast cancer,94 A joint affected by a chronic arthritis, such as rheumatoid arthritis, is more likely to develop septic arthritis. It rarely occurs in the healthy elderly or in young adults. In children it may be a sequel to adjacent osteomyelitis. In many cases Staphyloccus aureus is the causative agent.95 Sometimes a Streptococcus or Escherichia coli is present and even a gonococcal infec­ tion may be found. The history is that of an acute and very painful shoul­ der, which after a few days becomes warm and red. A previous injection is sometimes mentioned. Usually the patient is very ill with high temperature, nausea and toxaemia. In rare cases, fever may be absent. Inspection may show a swelling, which is often due to a subcutaneous abscess that communicates with the joint. On testing the shoulder, a very pronounced capsular pattern is found. In the initial stage, radiology is diag­ nostically irrelevant. In the further development, peri­ articular osteoporosis, diminution of the joint space and finally joint destruction are found. Biological features, such as raised erythrocyte sedimentation rate and increased leukocyte counts are suggestive but not confirmative. A diagnostic (and evacuating) aspiration of the joint, with a wide-bore needle (> 20 gauge) usually shows over 1 00 000 leukocytes / mm3, more than 90% being of the polymorphonuclear type. Sometimes the bacterial agent can be isolated.96

Treatment and prognosis Septic arthritis of the shoulder is more difficult to treat than septic arthritis at any other joint. It is a very severe disorder and death is not uncommon. The condition is normally managed with systemic antibiotics and daily evacuation of the pus. Also the combination of arthro­ scopic irrigation debridement and systemic antibiotic therapy is often used.97 Sometimes open surgical drainage is necessary. The erythrocyte sedimentation rate is a useful monitor of adequate treatment.98 Very often the long-term result is significant limitation of movement at the glenohumeral joint because of bone destruction. TUBERCULOSIS OF THE GLENOHUMERAL JOINT

SE PTIC A RTH RITIS SEPTIC NON-TUBERCULOUS A RTHRITIS

Septic arthritis can be provoked by a direct inoculation of a bacterium into the joint (after an intra-articular injec-

In tuberculosis of the shoulder joint, the clinical picture is far less pronounced than in septic arthritis and is slower in progression. Clinical diagnosis can be very difficult and made only late. A capsular pattern is found, often i n association with severe muscle atrophy.

CHAPTER 1 7

Aspiration of the joint followed by direct microscopic examination and culture, together with radiology (severe osteoporosis, narrowing of the joint space and erosions) are of help in diagnosis. The treatment is the same as for septic arthritis but specific antitubercular agents are administered.

PRIMA RY TUMOU RS

Primary tumours at the shoulder are mainly encountered in the young and may occur in acute leukaemia99 or be due to sarcoma.l OO The tumour often presents insidiously. In the beginning it is characterized by localized, non­ mechanical pain. From the moment that the tumour incites a synovial response, a painful capsular pattern at the shoulder will gradually develop . .In a younger patient, this should always arouse the suspicion of a primary tumour. Even the slightest limitation in a young patient is a formal indication for further careful explo­ ration of this area by techniques such as radiography, CT scan or MRI. Warning

Spontaneously developing l i m itation of shoulder movement in a young patient should prompt suspicion of a primary tumour.

METASTASES

Metastases can be localized either i n the humeral head or at the glenoid. A rapidly increasing pain around the shoulder, radiating into the arm and increasingly restricted shoulder movements in a patient with deterio­ rating general health, is strongly suggestive of a second­ ary neoplasm. Sometimes a previous operation for a primary tumour is mentioned. Localized warmth is usually the first sign, later fol­ lowed by a very pronounced capsular pattern, with much pain and limitation because both joint and muscles are affected. Moreover, the resisted movements are extremely weak and painful. Visible muscular wasting is present. A radiograph or a bone scan can help confirm the diagnosis.

Warning

A gross capsu lar pattern together with pa infu l muscular weakness and wasting coming on over a short period of time should prompt suspicion of metastases.

-

DISORDERS OF THE I N ERT STRUCTU RES 3 1 7

A SE PTIC NEC ROSIS

Osteonecrosis of the humeral head is about half as common as osteonecrosis of the hip and mainly affects middle-aged people. Its causes can be divided into three groups: traumatic (mainly a proximal humeral fracture), non-traumatic and idiopathic.1 O J Non-traumatic cases may be the result of haemoglobinopathies, 102 radiation of the joint or diving accidents.J03 Before the radiograph becomes positive necrosis may give rise to moderate or severe shoulder pain, usually worst at night, not much influenced by passive or resisted movements. The pain does not radiate far because, in the beginning, the dis­ order is osseous. If limitation of movement is found at this stage it is usually of a non-capsular type. Technetium bone scanning and MRI can detect aseptic necrosis in the early stage.104 Later on, the whole joint is destroyed, resulting clinically in a gross capsular pattern. Treatment consists of core decompression in the early cases. lOS I n very severe cases, prosthetic joint surgery may be indicated.1°6

OSTEOA RTH ROSIS

A number of different processes can destroy the gleno­ humeral joint surface. If no apparent reason for the devel­ opment of the osteoarthrosis can be found it is termed primary degenerative joint disease. It is characterized by a triad of anterior capsular contracture, posterior wear of glenoid and subchondral bone and posterior humeral subluxation.J07 Primary arthrosis does not usually evoke much pain. Indeed, a patient with an arthrotic shoulder, in the absence of any capsular inflammation, complains merely of painless crepitus on movement. During and after exertion there may be a vague ache, which usually disappears after a few hours. There is a capsular pattern with a hard, but almost painless end-feel. With shoulder movement crepitus may be detected on palpation. However, an osteoarthrotic joint is much more liable to develop arthritis, which can be the result of only a slight injury or some unusual activity. Once arthritis has set in, the limited movements also become painful. The diagno­ sis of primary arthrosis at the shoulder should be made on clinical grounds and should not be based solely on the radiograph for it is quite possible to have no arthrosis on clinical examination but signs of it present on the radi­ ograph. In contrast, secondary degenerative joint disease may be much more painful and disabling. It occurs when previ­ ous injury, surgery or another condition affects the joint surface and causes degeneration. Chronic glenohumeral subluxations often lead to severe osteoarthrosis. The

3 1 8 SECTION THREE - T H E SHOULDER

condition develops also when a chronic and massive tear of the rotator cuff subjects the uncovered humeral articu­ lar cartilage to compression against the u ndersurface of the coracoacromial arch. The resulting arthrosis is then called 'cuff arthropathy' . IOS Here, clinical examination will be that of a total rupture of the supraspinatus in com­ bination with limited movement in a capsular way. Also, in the end-stage of avascl!Jar necrosis of the shoulder, the irregular head destroys glenoid articular cartilage, which results in secondary degenerative joint disease. I09

Treatment For the primary arthrosis, not very much need be done. Limitation of movement cannot be altered either by cap­ sular mobilization or by intra-articular injections. If a traumatic arthritis or an immobilizational arthritis super­ venes, intra-articular injections have no effect. The oilly

Table 17.3

remammg treatment is capsular stretching which can oilly be executed if the arthritis is in stage I or stage II. In secondary degenerative joint disease of the shoul­ der, considerable pain and functional impairment can result, for which there is no option other than surgery.

NEU RO PATHIC DEST RUCTIVE A RTH RO PATHY

Neuropathic arthropathy arises in association with syringomyelia, diabetes or other causes of joint denerva­ tion.tlO The joint and the subchondral bone are destroyed because of the loss of trophic and protective effects of its nerve supply. In neuropathic destructive arthropathy, a gross but painless capsular pattern with a very hard bone-to-bone end-feel is found. The complete clinical

Differential diagnosis of a capsular pattern at the shoulder

Type

Disorder

Signs/symptoms

Gout Pseudogout

Urate crystals in aspirate Calcium pyrophosphate crystals Radiographic signs Severely ill Shoulder very painful, warm, red and swollen Haemophilia Injury

Monoarticular arthritis

Acute onset

Septic arthritis Haemarthrosis Slow onset

Traumatic arthritis Immobilization arthritis Monoarticular steroid-sensitive arthritis Osteoarthrosis Shoulder-hand syndrome Neuropathic destructive arthropathies

Metastases

Primary tumour Aseptic necrosis Polyarticular arthritis

Symmetrical distribution

Rheumatoid arthritis Arthritis due to systemic lupus erythematosus

Asymmetrical distribution

Ankylosing spondylitis

Unspecified distribution

Psoriatic arthritis

Patients over 40 Trauma Patients over 60 Immobilization of the arm Spontaneous onset Negative blood tests Hard end-feel Painless crepitus Hand bluish and diffusely swollen Distal dystrophy and stiffness Painless, sometimes bilateral Bony-block end-feel Neurological signs Local warmth Muscular wasting Extreme pain and weakness on all resisted movements Youngster developing a painful stiff shoulder in a short period of time Moderate or severe pain Only a few signs

CHAPTER 1 7

picture is slow to develop. By the time the painless cap­ sular pattern and bony end-feel are found the underlying condition is usually already known from other neurolog­ ical signs, such as muscular weakness and atrophy in the upper limbs occuring over a short period. Radiography provides the key to the diagnosis. 1 1 1 Table 17.3 outlines the differential diagnosis of a cap­ sular pattern at the shoulder.

Three main groups are distinguished: limitation of active elevation, limitation of passive lateral rotation and limitation of passive medial rotation.

LIMITATION OF ACTIVE E LEVATION

To recall: the term 'elevation' is used to indicate the upwards movement of the arm in a sagittal plane. Full elevation assumes a normal range of movement of the shoulder girdle and a normal range of 'abduction' at the glenohumeral joint. The latter is the upwards movement in a sagittal plane of the humerus in relation to a fixed scapu la. A limitation of active elevation may be the result of either a disorder of the inert structures of shoulder or shoulder girdle or a disorder of their contractile struc­ tures. In the latter, there is a full range of passive move­ ment, together with pain and I or weakness of resisted movements of neck, shoulder girdle or humerus. If both

-

DISORDERS OF THE I N ERT STRUCTU RES 319

active and passive elevation are limited, the problem must lie in the inert structures. Passive scapulohumeral abduction will then be most helpful in differentiating between a lesion of the shoulder joint and a disorder that causes limitation of scapular movement (Fig. 1 7. 1 0). BOTH PA SSIVE ELEVATION A N D PA SSIVE SCA PULOHUMERAL A B DUCTION LIM ITED

Acute subdeltoid bursitis This is one of the most painful disorders in orthopaedic medicine. It has a swift onset and, untreated, it recovers spontaneously in about 6 weeks. According to Cyriax 1 there is some tendency for recurrence within 5 years at one or both shoulders. For no apparent reason, pain starts and increases pro­ gressively to reach a maximum in about 3 days (Fig. 1 7.l1 t by which time it is very severe and may radiate in the entire C5 dermatome. The slightest movement of the shoulder is unbearable and, even if the arm is kept totally immobile, the pain is very pronounced, leading to sleep­ less nights. As the patient walks in, the arm is usually supported by the other hand. The lack of sleep and the severe suf­ fering show clearly on the patient's face. The pain is so excruciating that the patient refuses to move the elbow away from the body. Active and passive elevation are therefore hardly possible and an 'empty end-feel' is found on passive elevation: the movement is stopped by the patient who begs the examiner not to go any further although the examiner has the impression that it would be possible to continue because tissue resistance is not

Limitation of active elevation

Normal passive elevation

Limitation of passive elevation

Neck

Figure 1 7. 1 0 Differential diagnosis of limitation of active elevation of the shoulder.

I Shoulder girdle I I Shoulder I

320 SECTION THREE - THE S H O U L D E R

c=J

Pain Lim itation •

•

3

days Figure

17. 1 1

10

14

days days

6

weeks

Natural history o f acute subdeltoid bursitis.

encountered. Marked limitation of passive scapulo­ humeral abduction is also present. Other passive movements are also painful, sometimes only slightly limited but in a clearly non-capsular way; in acute subdeltoid bursitis, passive elevation and abduc­ tion are most restricted, whereas in arthritis it is passive lateral rotation that is most reduced. It is quite natural that in such a painful disorder some resisted movements, such as abduction and lateral rotation, may also be painful. If the patient presents at the very beginning (first day after the onset), a painful arc on elevation may be found. However, once the inflammation has become severe, this disappears because it is no longer possible to get beyond the point of painful impingement. After 7-10 days of severe pain the pain starts progressively to wear off so that at the end of 3-4 weeks only an ache remains. At this moment, active elevation is still limited to about half range. After 4-6 weeks the pain has disappeared totally and range of movement has returned to normal. During the last week, when full recovery is almost complete, a painful arc may reappear. The clinical examination is followed by palpation of the superficial part of the bursa, which is very tender and sometimes even swollen. It should be noted that in acute bursitis not only the palpable (subdeltoid part) but also the subacromial bursa is involved.

tiated by the accompanying symptoms of fever, general illness and local warmth and by the presence of a pronounced capsular pattern. Pathological fracture: mainly as a result of metastases, a pathological fracture is usually preceded by severe pain of weeks' or months' duration, together with limitation of capsular movement. Severe exacerbation of pain comes on immediately when fracture occurs. Dislocation of the shoulder: a history of an injury or of previous attacks is present here. Deformation on inspection and radiography provide the key.

Treatment. During the first 1 0 days after the onset, an

infiltration of the entire bursa with triamcinolone is most helpful. If done correctly, this is one of the most success­ ful treatments in orthopaedic medicine: in almost all patients, full cure is achieved in less than 5 days. In patients who have not presented within 10 days or those who refuse steroids, a 'figure-of-eight' bandage at night, fixing the arm to the body, avoids any involuntary move­ ment during sleep. In the day, the arm is carried in a sling for as long as the pain so warrants. Giving an infiltration into such a severely inflamed bursa is extremely painful unless a strong local anaes­ thetic is added. Two syringes are used: one with a needle of about 3 cm, used for the superficial part of the bursa,

Differential diagnosis. The clinical presence of this type of bursitis, in which a striking non-capsular pattern emerges, is so typical that differential diagnosis should not offer much in the way of difficulty. However, all conditions with a swift onset can quickly be taken into consideration: •

•

Gouty arthritis: this has a very abrupt onset but the condition lasts only 3-7 days. On clinical examination a capsular pattern is found . Septic arthritis: although very similar to acute bursitis - swift onset and very painful - this is easily differen-

Figure

17. 1 2

Infiltration of the superficial part of the subdeltoid bursa.

CHAPTER 1 7 - DISORDERS O F THE I N E RT STRUCTU RES 321

tion is not full and painless by then, some part of the bursa must have been missed. The remaining inflamma­ tion - either at the subdeltoid or the subacromial section of the bursa - is again localized and thoroughly infiltrated. Maximally, half the amount if infiltrate used at the first attempt is now used. Recurrences are not usually seen. Special cases. There are two special types of subdeltoid

bursitis: •

Figure

17.13

Infiltration of the deep part of the subdeltoid bursa.

one with a 5 cm needle used for the deep part of the bursa. Both syringes contain 1 ml of triamcinolone, 40 mg / ml mixed with 4 ml of prilocaine 2% . The tech­ nique used is the same as for chronic subdeltoid bursitis but in acute bursitis, both subacromial and subdeltoid parts of the bursa must be treated (Figs 17.12 and 17.13). Gentle palpation of the entire subdeltoid part determines the area of tenderness, which is usually much larger than in chronic subdeltoid bursitis. The subdeltoid area is mapped and infiltrated thoroughly. The second infiltra­ tion is then given via a lateral approach under the acro­ mial arch. Special care must be taken to deposit some of the product at all spots of the tender part of the subdel­ toid bursa and over the entire subacromial bursa. Immediately after the infiltrations, the pain is some­ what relieved and thereafter the patient improves gradu­ ally with time. Usually after-pain is not felt. The patient should rest the arm and return 2 days later to be re-examined. If some pain still remains and eleva-

(a)

•

Acute bursitis with calcified deposit: The clinical picture is almost the same as in ordinary acute bursitis but spon­ taneous recovery does not take so long, although the tendency for recurrence is higher. 112 The treatment is the same. In order to diminish the tendency to recur­ rence, it is worth trying to dissolve the calcification by repeated infiltrations of procaine, after the acute attack has been dealt with. For this purpose, 5 rnl of procaine 2% is infiltrated at weekly intervals for 3 or 4 weeks, each time infiltrating the part of the bursa where the calcification lies (Fig. 1 7. 14).113,114 Haemorrhagic subdeltoid bursitis: This occurs only in elderly patients. It usually comes on spontaneously or may accompany a tendinous rupture. The patient complains of moderate pain and swelling. On clinical examination, some limitation of movement is found which is mainly the result of fluid and not of pain. As in acute subdeltoid bursitis, a non-capsular pattern is present. On palpation, pain can be elicited and flucnl­ ation detected. Treatment consists of repeated aspira­ tions at weekly intervals. Infiltrations are not required. If blood keeps reaccumulating, a haemangioma has to be considered.

Psychogenic limitation Mental problems may sometimes be expressed in terms of physical behaviour. It should not be a surprise that psychogenic symptoms are often localized at the shoul­ der because the shoulder joint is closely connected with emotional tone: the outstretched arm is a symbol of

(b)

Figure 1 7 . 1 4 Acute bursitis with calcified deposit before (a) and after (b) treatment.

322 SECTION THREE - THE S H O U LD E R

pleasure and welcome; the arm held into the side expresses rejection. The diagnosis ' functional ' limitation of elevation is quite simple to make: there is a marked limitation of both active and passive elevation, the end-feel being that of an active, voluntary muscular contraction. However, active and passive elevation of the shoulder girdle (shrugging of the shoulders) is completely normal and the passive, scapulohumeral abduction is as much limited as is the passive elevation of the arm. The patient does not realize that, even if the shoulder joint is ankylosed, mobility of the scapula permits 60° of tilting and that the arm must be capable of this amount of elevation unless the scapula has also become fixed. Hence, detection of a non-physical problem is simple if, in a patient with normal scapular mobility and a normal elasticity of the pectoralis major muscle (see below)' the range of voluntary and passive elevation is contrasted with the range of passive abduction at the scapulo­ humeral joint.

PA SSIVE ELEVATION LIMITED A N D PASSIVE SCA PULOHUMERAL A B DUCTION NORMAL

This indicates that the glenohumeral joint is intact but that the disorder is due to a malfunction of structures belonging to the shoulder girdle. These lesions are dis­ cussed more extensively in Chapter 22.

Contracture after radical mastectomy After a Halsted-type operation, a limitation of about 30-60° on both active and passive elevation of the arm can occur, from a loss of elasticity of the pectoral muscle as a consequence of scarring tissues. A normal scapulo­ humeral range is found, together with full mobility of the scapula. Pain is absent. Pulmonary tumour An apical tumour of the lung (Pancoast tumour) is often initially misdiagnosed as a shoulder problem. 115,116 Tumours of the base of the lung may also give rise to pain referred to the base of the shoulder (C4) in that they may irritate the diaphragm. Once a neoplasm of the lung involves the thoracic cage, muscle spasm of the pectoralis major ensues and causes a limitation of both passive and active elevation: the arm cannot be raised beyond the horizontal. Trying to go any further is very painful and is stopped by muscular spasm. Pain and / or limitation are not found at the glenohumeral joint and the scapula is fully mobile. In addition, there is pain on resisted adduc­ tion and medial rotation of the arm. Care should be taken not to misinterpret these signs as being a psychogenic limitation.

Warning

The end-feel of muscle spasm a lways means that a serious disorder is present and should warn the exa m i ner. A plain radiog raph of the l u ngs must be taken at once.

Contracture of the costocoracoid fascia This disorder often causes diagnostic difficulties. Initially there is only pectoroscapular pain on full elevation of the arm. Later on, when the pain becomes more or less con­ stant, a slight limitation of about 5-10% of elevation can be detected. Limitation at the glenohumeral joint is not found. The possibility of a shortened costocoracoid fascia is also brought to mind when a small limitation of active and passive scapular elevation on the painful side, pro­ voking the same slight pectoroscapular discomfort, is detected and resisted movements of the scapula prove painless. Pain is not felt on resisted scapular elevation or depression. Forward movement of the scapula is slightly painful; backward movement is negative. A shortening of the costocoracoid fascia may be caused by a neoplastic invasion, healed apical tuberculosis or an injury. The contracture may also be developing without apparent reason. It should be differentiated from other subclavicular disorders such as a lesion of the subclavius muscle, sprain of the conoid and trapezoid ligaments or subcoracoid bursitis. Ankylosed acromioclavicular or sternoclavicular joint This is encow1tered in advanced cases of ankylosing spondylitis, in arthrosis or in rheumatoid arthritis. It leads to a severe limitation of elevation of the arm which cannot be raised actively or passively beyond the hori­ zontal because scapular rotation is limited. Clinical exam­ ination reveals full scapulohumeral abduction but total absence of scapular elevation and rotation. A CTIVE ELEVATION LIMITE D A N D PA SSIVE ELEVATION NORMAL

Fracture of the first rib A stress fracture rather than trauma is usually the cause. In that a fractured rib heals spontaneously in about 2 months, the condition is considered only in pain of recent onset. The patient complains of unilateral pain felt at the root of the neck. The lesion is characterized by neck, scapular and arms signs. Typically, botl1 active and passive side flexion of the neck to the painless side increases the pain because this pulls on the fractured rib via the scalene muscles. As a consequence, resisted side flexion towards the pain is also painful. All scapular movements - active, passive and resisted - are also more

CHAPTER 1 7 - DISORDERS OF THE I N E RT STRUCTU RES 323

or less painful. When the patient is asked to raise the arm actively beyond the horizontal he or she cannot do so, whereas passive elevation is of full range but only slightly painful. Radiography confirms the diagnosis.

Clay-shoveller's fracture This rare condition is a traction fracture of a spinous process in the lower cervical or upper thoracic area.ll7, Il S At this level, the trapezius, rhomboid and posterior serratus superior muscles are attached to the spinous processes. A fracture is usually the result of heavy work. Less commonly it is encountered in athletes. The patient normally feels a sudden sharp pain followed by local ten­ derness. Although neck movements are almost painless, the patient can hardly get either arm actively into slight elevation. A very pronounced limitation of active eleva­ tion of about 1 50° is found but passive elevation remains normal. Both active and resisted scapular elevation are also painful. There is local tenderness and, on the radio­ graph, avulsion of the seventh cervical or first thoracic spinous process is seen. The lesion heals spontaneously in 5-6 weeks. Immobilization is unncesssary. Long thoracic nerve palsy A lesion of the long thoracic nerve resulting in a palsy of the serratus anterior muscle may follow local invasive procedures on the anterolateral aspect of the thorax,119 a local trauma or a traction injury to the nerve.120,121 However, in the majority of cases no cause can be estab­ lished. The usual onset is with unilateral scapular pain which continues day and night for about 3 weeks. During

this period the arm becomes weak and heavy. In rare cases pain is totally absent, the patient complaining only of fatigue of the arm. The clinical examination is more specific and provides the key to the exact diagnosis. On inspection, winging of the scapula may be present. Clinical examination shows a painless limitation of active arm elevation of about 45-90°.122 Passive movements are of full range. Neck, scapular or arm movements have no influence on the pain. Weakness is present within the serratus anterior muscle and can easily be detected by the following test: the patient is asked to push against a wall with the arms stretched out horizontally in front of the body (Fig. 1 7. 15). This pushes the medial border of the scapula further away from the thoracic cage when the movement is not countered by a contraction of the serratus anterior muscle. The abnormal movement is seen as a considerable winging of the scapu la. The natural history is spontaneous recovery from the pain in about 3 weeks and full recovery of normal muscle function usually occurs in an average of 9 months.123

Accessory nerve palsy The spinal accessory nerve is the sole motor nerve of the trapezius. A palsy may result from a crush injury to the nerve124.125 after a forceful blow to the neck. Often the lesion is posttraumatic, after cervical lymph node biopsy or other surgical proceduresY6, 1 27 Sometimes no clear cause for the neuritis can be detected and in such a case the diagnosis may be quite difficult. There is a severe and continuous unilateral scapular ache with spontaneous onset and lasting for about

Figure 17. 1 5 Test for mononeuritis of the long thoracic nerve.

324 SECTION THREE - THE S H O U LD E R

3 weeks. The patient then starts to complain of weakness in the arm, which may last for months. On clinical examination, a painless limitation of about 5-10° on active elevation is found. The restriction is usually less pronounced than that in long thoracic nerve neuritis. Again passive elevation is full range and pain­ less. Passive and resisted movements of the shoulder are completely normal. The diagnosis can be confirmed by testing the strength of the trapezius muscle. The patient is asked to pull both scapulae together while counterpressure is given at the medial side of the inferior angle (Fig. 1 7. 1 6 ). In accessory nerve neuritis, the scapula can be pushed away easily. In an idiopathic mononeuritis the pain disappears after about 3 weeks but spontaneous recovery of motor function may take abou t 4-8 months.

C5 full root palsy This is usually the result of slowly but progressively increasing com pression of the C5 nerve root by an osteo­ phyte in the fourth intervertebral foramen. It may finally result in painless inability to raise the arm actively, because of pronounced weakness of the supraspinatus and the deltoid muscles. Other C5 muscles, such as the infraspinatus and the biceps, are, of course, also weak. A C5 palsy may also result from a traction injury, which is usually caused by a sudden depression of the entire shoulder girdle, in combination with a simultaneous and

forceful side flexion of the neck in the opposite direction (see p. 188).

C7 full root palsy A severe C7 palsy may cause weakness of shoulder adduction. Often, a slight limitation of active elevation is also noticed. The diagnosis is obvious when a palsy of the triceps and / or the flexors of the wrist is also found. Total rupture of the supraspinatus In full rupture of the supraspinatus tendon the patient is unable to elevate the arm actively. Passive elevation is of full range with a severe painful arc. Resisted abduction is weak and painless (see p. 359).

L IM ITAT ION OF PASSIVE LATE RAL ROTAT ION

Only a few lesions cause an isolated limitation of lateral rotation of the arm. History, end-feel and accessory tests differentiate between an anterior capsular contracture and a subcoracoid bursitis.

Anterior capsular contracture An isolated contracture of the anterior capsule results from trauma or develops gradually after a ruphue of the infraspinatus tendon. Previous shoulder injury such as subluxation is one cause. Usually the whole joint suffers from the traumatic impact and a traumatic arthritis results. Exceptionally, only the anterior portion of the capsule bears the impact of the injury. A localized synovitis and subsequent capsu­ lar contracture follow. An anterior capsular contracture may also result from a complete rupture of the infraspinatus tendon. Because the teres minor muscle is a weak and incomplete lateral rotator, it does not alone bring the arm in full lateral rota­ tion, which finally leads to a loss of the normal elasticity of the anterior portion of the capsule. The condition is characterized by a painful limitation of passive lateral rotation together with an abnormal end-feel. In the beginning the end-feel is that of muscle spasm, later, it changes to typically hard. Treatment. It is important for all patients with a rupture

Figure 1 7 . 1 6 Test for mononeuritis of the accessory nerve.

of the infraspinatus tendon to exercise on a regular basis to keep the shoulder mobile, as a means of prevention. This can be achieved by sport activities or by passive mobilizations which bring the shoulder into full lateral rotation. Patients who have already developed a contrac­ ture of the anterior capsule are best treated by capsular stretching. This can be done in the same way as for shoul­ der arthritis but stretching in lateral rotation must also be included (Fig. 1 7. 1 7).

CHAPTER 1 7 - DISORDERS OF THE I N ERT STRUCTURES 325

Figure

Figure 1 7. 1 7 Capsular stretching in lateral rotation. Technique: capsular stretching in lateral rota tion. The patient lies supine, the arm abducted to about 45°, the elbow bent to 90°. The therapist stands at the affected side and takes the arm just proximal to the elbow in both hands and the contralateral forearm pushes the patient's forearm down just above the wrist. This results in stretch­ ing of the anterior part of the joint capsule into lateral rotation. The amount of force used, the duration and the sequence are the same as for stretching in arthritis.

Subcoracoid bursitis This rare condition comes on for no apparent reason and provokes unilateral pectoral pain . On clinical examina­ tion, a painful limitation of lateral rotation is the main finding. The limitation is because of passive stretching of the pectoralis major muscle over the inflamed bursa. If the lateral rotation is performed again, and this time with disregard of the patient's pain, the range of lateral rota­ tion will be found to be increased. The limitation will even completely d isappear during a lateral rotation with the upper arm abducted to the horizontal (Fig. 17.18). Although still painful it is no longer limited since, in this

17.18

Passive horizontal lateral rotation.

position, the pectoralis major compresses the inflamed bursa less. 1 28 The main differential diagnosis is with an anterior cap­ sular contracture. Here, the limitation does not depend on the position of the upper arm and the movement always comes to a stop at the same point in range. Another accessory test that differentiates between a cap­ sular contracture and a subcoracoid bursitis is passive horizontal adduction in front of the chest which pinches the subcoracoid bursa painfully between scapula and upper arm (see p. 300). Other differential diagnoses that must be considered are subscapularis tendinitis, a lesion of the pectoralis major, sprain of the trapezoid-conoid ligament and early glenohumeral arthritis. In the former two condi tions, passive lateral rotation, al though painful, is not limited and resisted medial rotation causes pain. For a lesion of the pectoralis major, resisted adduction is also painful. A sprain of the trapezoid-conoid ligament does not give rise to lin1itation of movement; only pain at the extremes of all passive tests is present and passive horizontal adduction is painless. At the very beginning of a glenohumeral arthritis (idiopathic or traumatic), it is possible to find only a slight painful limitation on passive lateral rotation together with some pain on full passive elevation and medial rotation. The end-feel may be more or less normal. On passive lateral rotation with the arm abducted to the horizontal, the same limitation is found.

326 SECTION THREE - THE SHOULDER

Figure 1 7. 1 9

Infiltration of the subcoracoid bursa.

Treatment. The condition can be treated only by infiltra­

tion with steroid. Technique. The patient is put in the half-lying position, and asked to adduct the scapula and shrug the shoulders. Adduction brings the coracoid process into prominence and shrugging the shoulders takes it away from the top of the lung. Next the tip of the coracoid process is pal­ pated and a point chosen about 2 em below it. A 5 em needle is inserted here, pointing in a cranial-medial­ dorsal direction, aiming at the base of the coracoid bone (Fig. 1 7.19). After it hits the bone, it is withdrawn for about 1 em and 2 ml of triamcinolone is infiltrated here over several withdrawals and reinsertions (Fig. 1 7.20). The infiltration is repeated at weekly intervals until full relief is obtained. Three infiltration usually suffice.

L IM ITAT ION OF PASS IVE MED IA L ROTAT ION

Isolated limitation of the medial rotation is very rare. A discrete painful loss of internal rotation is sometimes seen in combination with a lesion of the upper / posterior rotator cuff (supraspinatus-infraspinatus). This limita­ tion is most prominent if the internal rotation is per­ formed in 90° of abduction and is thought to be caused by a thickened posterior capsule.129 The limitation usually disappears spontaneously after the tendinous lesion has been healed. A summary of the non-capsular limitation patterns at the shoulder is shown in Figure 17.2 1 .

Figure 1 7.20

Infiltration o f the subcoracoid bursa.

FU L L RANGE OF MOVEMENT

Disorders of inert structures may be characterized by a full range of passive movements and a normal end-feel. However, the passive movements are painful at the end of range or at half-range (painful arc). The resisted move­ ments from the basic functional examination are of

CHAPTER 1 7

Contractile problem of: -neck -shoulder girdle -shoulder

Figure 1 7.21

-

DISORDERS OF T H E I N ERT STRUCTURES 327

Limited scapulohumeral abduction: -glenohumeral problem -subacromial problem

Normal scapulohumeral abduction: -shoulder girdle problem

Summary of the non-capsular limitation patterns at the shoulder.

course negative - painless and strong. Only a few poten­ tial lesions correspond to this pattern. They are: a sprain of the acromioclavicular ligaments, a sprain of the cora­ coclavicular ligaments and chronic subacromial bursitis.

upwards to the trapezius, which usually in dicates involvement of the inferior capsular ligament. In this event the differentiation from a case of chronic subdeltoid bursitis may be difficult and often necessitates a diagnos­ tic infiltration with local anaesthetic.

A CROM IOCLAVICULA R SPRA IN

Functional examination There is pain at full range on passive elevation and passive lateral and medial rotation. Limitation of movement is not found. Resisted movements are usually painless although exceptionally pain may be present on resisted adduction or abduction as a result of transmitted stress on the acromioclavicular ligaments. Logically one would expect all scapular movements to hurt as well, because they all put strain on the acromioclavicular joint. Strangely enough, these tests are mostly negative in that far less stress is put on the acromioclavicular joint during active and passive scapular movements than o n using the arm as a lever on passive arm movements. Sometimes a painful arc is present, locating the lesion in the inferior acromioclav­ icular ligament. With this type of clinical pattern, an accessory and useful differential diagnostic test should be done: passive horizontal adduction across the front of the chest (see p. 300). This is the most painful movement when the acromioclavicular joint is affected and may even be limited in a severe sprain of the posterior part of the acromioclavicular ligaments. After the diagnosis has been established clinically, the joint line is palpated for local tenderness. When palpation is painful, it establishes the superior ligament at the site of the lesion. The inferior ligament is obviously beyond the finger's reach and cannot be palpated but, as previously described, if it is involved, a painful arc is usually present. Sometimes there is a combined lesion of both superior and inferior ligaments. In this event, palpation of the joint line is positive and a painful arc is also found.

The acromioclavicular joint is stabilized by capsular liga­ ments which reinforce the thin capsule all around, and by extracapsular (coracoclavicular) ligaments. Vertical stability of the joint is controlled mainly by the coraco­ clavicular ligaments, whereas horizontal stability is controlled by the acromioclavicular ligaments yo An acromioclavicular injury is most commonly the result of a fall onto the point of the shoulder with the arm at the side, as often occurs in football, hockey, alpine skiingl3l or judo.l32,l33 In this position, the acromion is driven medially and downwards in relation to the distal end of the clavicle, the latter being fixed through inter­ locking of the sternoclavicular ligaments. 1 34 Less often the trauma is a fall on the elbow or on the outstretched arm. In this event, a cranial force is exerted on the acromion. Finally, on occasion the sprain is the result of too much tension on the acromioclavicular ligaments from overuse, as can be seen in swimmers, weightlifters and body­ builders.135 In an osteoarthrotic joint, ordinary daily work may cause acromioclavicular sprain.

Symptoms Pain is felt at the shoulder during and after activity. Lying on the affected side is usually painful. In that the acro­ mioclavicular joint is derived from the C4 segment, and the C4 dermatome is rather small, little referred pain is to be expected. As a rule, when the patient is asked to point out the exact site of the pain, he or she generally puts the finger right on the acromioclavicular joint. Exceptionally the pain spreads beyond the lateral acromial rim or

328 SECTION THREE - THE S H O U LD E R

( b)

(a) A-C joint lesion

Figure

1 7.22

Grade I

A-C joint lesion

(c)

•

•

Grade I I I

Acromioclavicular joint lesions: (a) grade I; (b) grade II; (c) grade I I I .

Grades Most commonly, a sprain to the joint occurs without liga­ mentous damage and no displacement can be palpated. If the traumatic force had sufficient magnitude to disrupt the acromioclavicular ligaments, (sub )luxation of the acromioclavicular joint becomes visible. Acromio­ clavicular sprains and dislocations are classified on the integrity of the acromioclavicular and coracoclavicular ligaments. Classically there are three grades of acromio­ clavicular dislocation : 136-138 •

A-C joint lesion

Grade I I

Grade I (Fig. 1 7.22a): there is a partial lesion of the acromioclavicular ligament without any degree of clavicular displacement. No specific radiographic findings are present. Grade II (Fig. 1 7.22b): there is cranial displacement of the clavicle, of less than hal£ its width, due to rupture of the acromioclavicular ligament and subluxation of the clavicle. The degree of displacement is best esti­ mated from a radiograph centred on the sternum, so that both acromioclavicular joints are on the same picture and it is simple to compare the distance between the coracoid process and the clavicle. Grade III (Fig. 1 7.22c): this signifies a rupture of the coracoclavicular ligaments and results in a full dislo­ cation. Rupture of the trapezius and deltoid is highly probable.

Recen tly grades IV, V and VI acromioclavicular dislo­ cations have been added to the classification system.139 I n type I V injuries, the clavicle i s grossly displaced posteri­ orly into the trapezius muscle. Type V is a severe vertical separation of the clavicle and in type VI the clavicle is dislocated inferiorly into either a subacromial or subcoracoid position.

Differential diagnosis An uncomplicated sprain of the acromioclavicular joint is sometimes difficult to differentiate from chronic sub­ deltoid bursitis and early glenohumeral arthritis.

I n chronic subdeltoid bursitis, a very similar clinical picture (all passive movements are painful at full range, together with a painful arc) may be seen. The pain in bur­ sitis is usually felt in the deltoid area and spreads further down the arm in the C5 dermatome. There is usually no history of trauma. Painful passive horizontal adduction is less pronounced than in acromioclavicular sprain. If the superficial part of the bursa is at fault, palpation is posi­ tive; if the deep part is affected, certainty can only be obtained by a diagnostic infiltration of local anaesthetic. The differential diagnosis from an early arthritis of the shoulder is difficult when no notable limitation of move­ ment is present. The patient complains of pain at the shoulder, radiating down the arm. On functional exami­ nation, pain is present at the end of all passive move­ ments. The most painiul movement is full passive lateral rotation, whereas in a sprain of the acromioclavicular joint it is passive horizontal adduction. In arthritis the end-feel on lateral rotation is slightly harder than normal.

Treatment Sprain without displacement (grade I). In that adhesions do not form in a sprain of the acromioclavicular joint, it is best treated by relative rest. The only additional measure needed is to stop the inflammation. This can be achieved by deep friction (superior ligament) or by a local infiltra­ tion of steroid (superior and inierior ligaments). No matter how long the lesion has existed, the treatment remains the same. Rest on its own is usually not enough. It gives the patient a false impression of healing. The pain disappears only temporarily until normal activity is restarted, when it recurs. When sprain is the result of repeated stress on the acromioclavicular ligaments, the lesion may recur. In this event the patient must avoid these activities in the future. Technique: palpation. The patient sits with his or her arm in the neutral position and the back resting against the

CHAPTER 1 7 - D I SO R D E RS OF THE I N E RT STRUCTU RES 329

couch. The posterior angle of the scapular pine is palpated first. The finger is then brought to the lateral edge of the acromion and more medially on the flat upper surface of the acromion. A hard bony rim is felt, sticking out at approximately 2 cm medial to the lateral acromial border. This is the outer end of the clavicle, which is always slightly elevated. The joint line lies just lateral to it. Palpation may be difficult in stout patients, or in elderly people in whom a rim of osteophytes at the acro­ mial part of the acromioclavicular joint can be mistaken for the outer clavicular end. In these cases, some extra landmarks can be used. When the anterior edge of the acromion and clavicle is palpated, a depression is felt at the level of the acromioclavicular joint line. The anterior depression can be slightly opened if an assistant pulls the arm into fuJI lateral rotation. If traction is applied to the arm in a distal direction, the palpating fingers on the acromioclavicular joint can usually feel the movement between clavicle and acromion. Technique: infiltration of the superficial ligament. After exact delineation of the painful spot, a 2.5 cm needle is fitted to a syringe containing 1 ml of triamcinolone. If the deep ligament is also affected (painful arc) 2 ml is used. The patient sits in the same position as previously described for palpation. The needle is obliquely inserted at the centre of the painful area (Fig. 1 7.23a). The aim is to infiltrate the whole tender spot, at both sides of the joint line, by a series of partial withdrawals and reinsertions of the needle while depositing a few droplets into the ligament each time. A typical ligamentous resistance is encountered . It should be noted that the ligament lies superficial to the osseous structures and therefore the

needle should not be inserted deeply but must have its tip in bony contact. Technique: infiltration of the deep ligament. The same type of needle and amount of steroid are used. After the joint line has been identified, the needle is inserted from above, halfway between the anterior and posterior margins of the acromioclavicular joint. It may be useful to have an assistant who brings the arm of the patient into full lateral rotation, so as to open the acromioclavicular joint space as widely as possible. The needle is normally inserted in a craniolateral to caudomedial direction (Figs 1 7.23b and 1 7.24). First the superficial ligament is encoun­ tered, next the meniscus and finally the deep ligament. They all offer the same resistance. The deep ligament lies about 2 cm from the surface. The needle must be slid in almost to its full length until ligamentous resistance is felt. The structure is then infiltrated fanwise over its full length.

The patient rests the arm for 1 week and is reassessed. If the tests are still positive a further infiltra­ tion is done. One or two infiltrations usually suffice.

Follow up.

Technique: friction. This applies only to the superficial ligament. The patient adopts the same position as for palpation. The therapist stands behind, level with the affected shoulder. Friction is given with the index finger of the ipsilateral hand reinforced by the middle finger (Fig. 1 7.25). The fingers are placed exactly on the tender fibres of the superficial ligament at the jointline. Counterpressure is given with the thumb at the back of the shoulder (Fig. 1 7.25), placed vertically w1der the fingers. It is best to keep the index finger rather flat in order to treat the whole lesion at once. Because of the ori-

(b) (a)

Figure 17.23

Infiltration of the (a) superficial and (b) deep (lower) ligament of the acromioclavicular joint.

330 SECTION THREE - THE S H O U LD E R

Figure

1 7.24

Infiltration o f the acromioclavicular joint: deep ligament.

entation of the fibres, the friction is given in an antero­ posterior direction. As usual, the therapist alternates active and passive phases: the active moment is when the finger is pulled backwards towards the body, starting with the fingertip at the anterior portion of the ligament. Friction is done three times a week for 20 minutes each session. Cure is normally obtained after 1 0-15 sessions. Treatment of recurrences. Some cases tend to recur. In this event, sclerosant infiltrations may be useful. The technique used is the same as for steroid infiltration: 0.75 ml of P2G (phenol solution) mixed with 0.25 ml of xylocaine 2% is used per ligament and repeated twice at weekly intervals. The patient should be warned to expect severe after-pain for about 4 days.

Spra in with moderate displacement (grades II and I II).

In all but the most severe dislocations, treatment consists of a short period of standard sling immobilization and early functional rehabilitation. Many studies have reported good functional results in spite of residual deformity in patients treated by this manner of 'skillful

neglect' . 1 40-143 The treatment consists of a standard sling until the acute inflammation has subsided. If the pain and inflammation persist, a steroid infiltration can be given into the ligamentous remnants in order to sup­ press the inflammation. After 10 days the patient is allowed to mobilize the shoulder and is referred to a rehabilitation programme to strengthen the muscles of shoulder and shoulder girdle. Return to work or to sport is advised as soon as the shoulder can tolerate it. Several studies have shown that non-operatively treated patients with grade III acromioclavicular separations return to work earlier and with a lower complication rate than operated patients.144, 145 Treatment of grade IV, V and VI injuries. Because of the

severe displacement of the distal clavicle, surgical repair is advised.146

Special cases Atraumatic osteolysis of the distal clavicle. Atraumatic

osteolysis of the distal clavicle (AODC) in athletes is a

CHAPTER 1 7

-

DISORDERS OF THE I N ERT STRUCTU RES 3 3 1

athletes who have a long history of intense strength train­ ing. 1 49 Sporting endeavours with repeated episodes of significant trauma to the shoulder, or when the partici­ pant suffers repeated falls onto the point of the shoulder have also been i dentified as precipitating causes of osteolysis.ISO History and clinical findings are the same as in ordi­ nary grade I sprain. As symptoms become more estab­ lished, tenderness of the entire joint and some swelling can be palpated. Often a joint effusion can be aspirated.1 S I Diagnosis is by plain X-ray examination. Classically the radiographic changes are divided into three phases: lytic, reparative and 'burnt out' . The radiographic tech­ nique to identify the lesion is very important. Standard anteroposterior views of the shoulder are inadequate. Optimal visualization of the acromioclavicular joint is only provided by taking an anteroposterior film with the X-ray beam tilted in a 25-30° cephalic direction. 152 The natural history of the condition seems to run a self­ limiting course of 1-2 years. Symptomatic treatment con­ sists of modification of the training activities and local infiltration of the acromioclavicular ligaments with tri­ amcinolone.1S3 Operative treatment is the exception and consists of resection of the distal clavicle,ls4 which is usually performed arthroscopically. 1 55 The reported results are fair to good.1S6 Arthrosis of the acromioclavicular joint. Generally, a joint that is already arthrotic is more susceptible to the effects of exertion. This applies also to the acromioclavi­ cular joint. The arthrosis as such normally gives rise to a vague ache in the C4 dermatome for some hours after activity. The pain usually wears off spontaneously. Sometimes it persists and if this is so the clinical picture is that of a grade I acromioclavicular sprain. Cure is easily achieved by steroid infiltration. If relapse occurs, scle­ rosant infiltration of the ligaments can be tried. If this remains without success, the patient should avoid the precipitating activity for the rest of his life. Total fixation of the acromioclavicular joint is some­ times seen in ankylosing spondylitis.

Figure 17 .25

I

Deep friction to the superficial acromioclavicular ligament.

stress failure syndrome of the distal clavicle.147 It is char­ acterized by symptomatic resorption of bone over a period of weeks to many months. The origin is uncertain but the condition is usually related to strenuous physical activity.148 There is never a history of any major injury to the acromioclavicular joint. It occurs principally in young

SPRA I NED CONOID A N D TRA PEZOI D LIGA MENT

History and examination A sprain of the coracoclavicular ligaments is a particular hazard in sports such as squash or tennis, where the pre­ liminary to a 'smash' may require the arm to be pulled far back. It is also sometimes the result of a clavicular fracture. The clinical picture may be difficult to interpret. Pain is felt in the midclavicular area at the extreme of all passive arm and scapular movements. No limitation is found and resisted movements are painless. If the disorder is

332 SECTI ON THREE - THE S H O U LD E R

suspected, forced lateral rotation with the arm in hori­ zontal abduction must be added to the clinical examina­ tion (see p. 325). This is usually the most painful test. The lesion may be found at the superior side of the coracoid process or at the insertion on the inferior aspect of the clavicle. Differentiation between the two locations is made by palpation of the coracoid process, which is best done with approximated scapulae. The coracoid process is the first osseous structure that is met when pal­ pating the infraclavicular fossa in a mediolateral direc­ tion. Careful comparison with the painless side should always be done because the coracoid process is always somewhat tender to touch. In cases of doubt, a diagnostic local anaesthetic infiltration must be performed.

Differential diagnosis Di fferential diagnosis is necessary, and includes the fol lowing disorders: •

•

• •

Sprained acromioclavicular joint: the pain is felt more laterally at the tip of the shoulder. Passive horizontal adduction is the most painful test. Subcoracoid bursitis: this usually gives rise to a limitation of passive lateral rotation which disappears when the test is repeated with the arm abducted to the horizontal. Sprain of the subclavius muscle: resisted shoulder depression is painful. Subscapularis tendonitis: the pain is felt more laterally, at the level of the axillary line. Resisted medial rotation is painful as is passive lateral rotation.

Treatment Because the coracoid attachment is deeply situated and the clavicular insertion is beyond the reach of the finger, both sites are treated by an infiltration with steroid. Technique: infiltration o f the coracoid insertion. If ten­ derness is found at the coracoid process, 2 ml of triamci­ nolone are infiltrated at the superior aspect with the tip of the needle in bony contact. The typical ligamentous resistance must be felt. The whole amount is infiltrated dropwise at, say, 5-10 different places. Technique: infiltration of the cla vicular insertion. If palpation is painless the problem lies at the clavicular insertion. A 3 cm needle is fitted to a syringe containing 2 ml of triamcinolone. The needle is inserted about 2 cm distal to the centre of the ligamentous insertion at the clavicle (Fig. 1 7.26). It is then moved further in until it hits bone. When ligamentous resistance is felt the product is infiltrated drop by drop, starting just medial to the line of the acromioclavicular joint and over about 3 cm towards the midline until l igamentous resistance is no longer felt. During the whole procedure, the tip of the needle stays in bony contact. In some cases it may be of help to have the arm in full elevation, which brings the inferior aspect of the clavicle to lie anteriorly. Follow up. The patient i s reassessed I week later and reinfiltrated if necessary. Results are fairly good as long as the activity that caused the lesion is avoided.

4

(a)

2

3

Figure 1 7.26 (a) Infiltration of the clavicular insertion of the coracoclavicular ligament. (b) Anatomy: 1 , coracoid process; 2, conoid ligament; 3, trapezoid ligament; 4, coracohumeral ligament; 5, glenoid labrum.

CHAPTER 1 7

CHRONI C SUB DELTOID BURSITIS

The condition is often associated with lesions of the rotator cuff (see p. 349) but exists also in isolation. A chronic subdeltoid bursitis is not the late result of an acute subdeltoid bursitis; it is chronic from the onset. It is therefore a clinical entity in itself, being far less painful than acute bursitis. In the majority of cases, only one part of the bursa is affected. In the literature the lesion is often referred to as 'subacromial abrasion'. Local inflammation and fibrotic adhesion formation between the acromial and tendinous parts of the bursa are the anatomical sub­ strates of the lesion.l S7 Recently an increased amount of substance P was demonstrated in the subacromial bursal wall of patients with signs and symptoms that were attributed to chronic subdeltoid bursitis.I S8

History The condition may affect all ages. It comes on sponta­ neously, or after injury complicates rheumatoid arthritis. Untreated it does not show much tendency for sponta­ neous healing and it can even persist for the patient's life. It is also not exceptional for those who have been cured by proper treatment to sustain a recurrence. The pain is usually localized in the deltoid area but can spread further down the arm in the C5 dermatome. Sometimes it is felt only on activity, at other times it is felt mainly at rest or even continuously, day and night. Consequently, the pain of chronic bursitis is not readily differentiated from C5 pain caused by other shoulder dis­ orders. Functional examination The main difficulty with chronic subdeltoid bursitis remains the heterogeneity of the clinical pattern. Sometimes there is a mixed clinical picture of pain on some passive movements and pain on some resisted movements, with or without painful arc. Cyriax consid­ ered this pattern to be an 'incomprehensible bursitis'. It is highly possible that such a case is in fact a more evolved form of rotator cuff failure: a tendinous lesion of the bursal surface of the cuff tendons in combination with reactive inflammation of the bursa (see p. 352). Most typically, chronic subdeltoid bursitis is character­ ized by a painful arc in the absence of any limitation of movement. The arc is sometimes the only positive clinical finding, can be very pronounced and is usually the most painful test. Often, in addition to this, the extremes of all passive movements also hurt. Exceptionally, chronic subdeltoid bursitis may provoke limitation of movement. If this is so, it will always be in a non-capsular way. Limitation of either passive scapulo­ humeral abduction or passive internal rotation is present. All resisted movements are painless or equally painful.

-

DISORDERS OF THE I N E RT STRUCTURES 333

Box 1 7.3 Clinical patterns of chronic subdeltoid bursitis Most frequent patterns • Painful a rc only • Pronounced painful a rc

Pa i n at the extremes of a l l passive movements

• Limitation of a bd uction or med i a l rotation

All resisted movements p a i nless or eq u a l ly pai nful 'Incomprehensible b u rsitis' • Pa i n on f u l l passive lateral a nd/or med i a l rotation • Pa i n at the end of all passive movements

Painful a rc Resisted abd uction and lateral rotation painful • Full passive lateral and med i a l rotation painful Painful a rc Varying pattern of p a i n on resisted movements which a re sometimes transiently pai nfu l

Although the list given in Box 1 7.3 is not exhaustive, one of the clinical pictures corresponding to a chronic subdeltoid bursitis may be found. If subdeltoid bursitis is suspected, palpation of the superficial part always follows the functional tests. For this the patient sits on a couch, the arm in neutral position and the hand resting on the thigh for maximal relaxation. The whole deltoid area must be palpated and no single point overlooked . Palpation starts posteriorly below the outer end of the spine of the scapula and is continued laterally and anteriorly below the acromial edge. It is a good habit to start palpation away from the expected site of the lesion. It should always be done on both sides. Sometimes a local swelling or a small effusion is present.159, 1 60 It must be stressed that the diagnosis always remains doubtful until it is confirmed by an infiltration with local anaesthetic.

Differential diagnosis The diagnosis of chronic subdeltoid bursitis is not always obvious and there are several other disorders of both inert and contractile structures which must be differenti­ ated. Sprain of the acromioclavicular joint. If the upper liga­ ment is at fault, the features that reveal this are localiza­ tion of the pain at the tip of the shoulder, lack of pain reference down the arm and pain on palpation of the acromioclavicular joint line. The situation is more complicated with a sprain of the inferior ligament. In this, the pain may spread further into the deltoid area and is impossible to differentiate from the pain of subdeltoid bursitis. A point in favour of the acromioclavicular joint is severe pain on passive horizon­ tal adduction, a test which is usually less pronow1ced in bursitis. Nevertheless, the diagnosis should always be confirmed by an infiltration with local anaesthetic.161

334 SECTION THREE - THE SHOULDER

Tendinitis. Because, in chronic subdeltoid bursitis, one or more resisted movements may be positive together with pain on passive movements and a painful arc, a disorder of a contractile structure must be eliminated. Most often, differentiation from supra- or infraspinatus tendinitis is needed, less frequently the subscapularis structure. Differentiation is usually done by repeating the resisted movement in the supine position, because this relaxes most other structures except the one which is elicited. If the muscle is at fault, the resisted test remains positive to the same degree; in bursitis, the pain usually diminishes or disappears totally when repeated in the lying position. If resisted abduction is painful it may be of help to repeat the test not only lying but also with longitudinal traction. If this renders the test less positive, bursitis is most likely. Subcoracoid bursitis. In subcoracoid bursitis the pain is more localized in the outer infraclavicular area and does not radiate into the arm. A slight limitation of passive lateral rotation is present, disappearing when the test is repeated wi th the arm abducted to the horizontal (see p. 300). Sprain of the subclavius muscle. This

provokes pain in the same area as in subcoracoid bursitis but resisted shoulder depression is painful. Sprain of the coracoclavicular ligaments. Pain is felt in the mid infraclavicular area. The most painful movement is passive lateral rotation in 90° horizontal abduction.

In its early stage, aseptic necrosis may give rise to a limitation in a non-capsular way. The dis­ crepancy between symptoms and signs is striking: much pain and only slight influence of the arm movements. A diagnostic infiltration in the subdeltoid bursa can be helpful; in cases of doubt, technetium scanning should be obtained.

Aseptic necrosis.

Treatment As a rule, only one part of the bursa is affected and pal­ pation will reveal which part must be dealt with. If local tenderness is found on palpating the superficial part, this must be treated; if no local tenderness can be detected, the subacromial part must be at fault. An infiltration of to 10 ml of 0.5% procaine solution is administered. Procaine has the advantage in this disorder of being diagnostic and curative. If no lasting benefit follows the first infiltration, procaine should be substi­ tuted by steroid in a subsequent infiltration. Technique: infiltra tion of the superficial part of the

If local tenderness is found on palpation, the superficial part must be treated. The patient sits on a high couch with the arm in neutral position. The tender part of the superficial bursa is marked (Fig. 1 7.27). A 3 cm needle bursa.

Figure 1 7.27

Infiltration of the superfcial part of the subdeltoid bursa.

is fitted to a 10 ml syringe filled with a 0.5% procaine solution. The needle is inserted at the centre of the tender area and thrust in until it hits the bone. On withdrawing, a little of the procaine is injected. This manoeuvre is repeated several times until all the procaine is divided over the whole lesion. Technique: infiltration of the subacromial part of the

If palpation is negative the subacromial pc:rt of the bursa is at fault. To infiltrate this portion, the lateral edge of the acromion is first localized. A thin needle, 5 cm in length, fitted to a 10 ml syringe filled with 0.5% procaine, is inserted just underneath the middle of the outer acro­ mial edge and in a slightly cranial direction (Fig. 1 7.28). It is passed in to its full length, meeting hardly any resist­ ance. If the needle encounters resistance, either the cora­ coacromial ligament or the capsulotendinous structures have been contacted and pain is felt. The needle should be slightly withdrawn and the direction adjusted. Occasionally an effusion is encountered in the bursa and must be evacuated by aspiration before injection of local anaesthetic. Once the needle is correctly placed, the infiltration is given while withdrawing and reinserting it about four or five times. Fanwise infiltration is used in order to reach the whole of the subacromial bursa. bursa.

The patient is re-evaluated 1 week later. If there has been improvement but not full recovery, the infiltration is repeated. Usually, three infiltrations are sufficient for full cure. If no improvement is obtained Follow up.

CHAPTER 1 7

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DISORDERS OF THE I N E RT STRUCTURES 335

not cause pain, merely a vague discomfort. No treatment is known.

E XCESS IVE RANGE OF MOVE MENT: INSTABI L ITY OF T HE S HO U LDE R DEFI NITION

Glenohumeral instability is defined as ' the inability to maintain the humeral head centred in the glenoid fossa' .162 Recurrent instability may be characterized as dislocation, subluxation or apprehension. Dislocation is the complete separation of the articular surfaces without spontaneous relocation. Subluxation is defined as symp­ tomatic translation of the humeral head without com­ plete separation of the articular surfaces. Apprehension refers to the fear that the shoulder will subluxate. Instability can also be characterized according to the direction of the (sub)luxation: anterior, posterior, inferior and superior. Subluxations can also be classified accord­ ing to their cause: they may be traumatic, atraumatic or voluntary. Around 95% of (sub )luxations are anterior. Most have a traumatic origin, although instability can also result from relatively small bu t repeated movements of the arm as may occur in swimmers, volleyball players or baseball pitchers.163 Derangement of the labrum, intracapsular ligaments or joint capsule are regarded as the main underlying causes of chronic instability. l64 Exceptionally, osseous changes such as a fracture of the glenoid are found.

FA CTORS IN GLENOHUMERAL STA BILITY Figure 1 7.28

Infiltration of the deep part of the subdeltoid bursa.

after the first infiltration, 5 ml of steroid should be substituted. Some patients suffering from chronic subdeltoid bursitis never get fully well or tend to have frequent recurrences. They usually present one of the less compre­ hensible clinical pictures. This may be the consequence of a minor rupture in one of the rotator cuff structures, leading to the formation of adhesions and a self-perpet­ uating inflammation. Definitive cure for this is often difficult to obtain. In such cases, the infiltrations may be repeated on a regular basis with increasing intervals until full cure is obtained and no relapse occurs.

Crepitating bursitis After a previous bursitis with effusion, some patients may have crepitus on movements of the arm which does

A considerable range of mobility is essential at the gleno­ humeral joint. As a consequence, the shoulder has less bony and ligamentous stability than any other diarthro­ dial joint. There is a considerable incongruence between the two articulating surfaces with only 25-30% of the humeral head being covered by the glenoid fossa. This enables a wide range of positions without neck-rim contact.165 Furthermore, the glenohumeral joint does not have strong isometric articular ligaments that provide stability while the joint is flexed around a defined anatomical axis as is the case in knee, elbow and ankle joints. Instead, the glenohumeral ligaments have a stabi­ lizing function only at the extremes of motion and play no part in most functional positions of the joint.166 In spite of all this, the normal shoulder joint is quite stable and able to centre the humeral head in the glenoid cavity throughout most of the arc of movement.167 This is achieved by a set of mechanisms which classically are divided into static factors (those that do not require the

336 SECTION T H R E E - T H E S H O U LD E R

expenditu re of energy by muscles) and dynamic factors (requiring muscle energy).

Static factors Joint surfaces. Recent studies have demonstrated that,

although the bony surfaces of the joint are largely incon­ gruent (flat glenoid and round humerus), congruence is restored by the difference in thickness of cartilage. Glenoid cartilage was found to be the thickest at the periphery and thinnest centrally, whereas humeral artic­ ular cartilage was thickest centrally and thinnest periph­ erally (Fig. 1 7.29). This leads to a merely uniform contact between humeral head and glenoid surface throughout shoulder motion.168 T he glenoid labrum contributes to stability by increasing

the depth of the glenoid socket (Fig. 1 7.29) and so increas­ ing the surface area for the humeral head.169,170 Cohesion-adhesion forces. Joint surfaces, wet with joint fluid, are held together by the molecular attraction of the fluid to itself and to the joint surfaces. This is called the adhesion-cohesion mechanism (compare with two wet microscope slides pressed together) and is a very strong stabilizing factor in the glenohumeral joint. Negative pressure. There is minimal (less than 1 cc) free

fluid in the normal shoulder joint. The normal shoulder is sealed by the capsule so that external fluid cannot enter it. Osmotic action by the synovium removes free fluid, keeping a slightly negative pressure within the normal joint. The negative intra-articular pressure creates a vacuum that pulls the humerus against the glenoid.l7l The li mited joint volume effect is reduced if the joint is 'vented ' (opened to the atmosphere) or when the capsu­ lar boundaries of the joint are very compliant.l72 This will lead to the production of a 'sulcus sign' (see p. 341 ): under attempted traction on the arm, the flexible capsule is dragged into the joint.

Capsule and ligaments. The joint capsule is large, loose

and redundant (the capacity of the glenohumeral joint capsule is larger than that of the humeral head ). Capsule and ligaments alone cannot prevent glenohumeral trans­ lation when the joint is in most of its range of movement. Recent studies show that the main importance of the capsule for stability lies in the feedback mechanism of the proprioceptive innervation and contraction of the rotator cuff.173, 174

Dynamic factors Both shoulder girdle and rotator cuff muscles contribute to 'dynamic' glenohumeral stability. The muscles of the shoulder girdle (trapezius, rhomboideus, latissimus dorsi, serratus anterior and levator scapulae) stabilize the scapula as a firm platform for movement of the humeral head.175 The 'rotator cuff' (supraspinatus, infraspinatus, subscapularis and the long head of the biceps) serves three stabilizing functions: •

•

•

Dynamic ligaments. By virtue of the blending of their tendons with the glenohumeral capsule and liga­ ments, selective contraction of the cuff muscles can adjust the tension in these structures, producing dynamic ligaments. 1 76, 177 By contracting together, the rotator cuff muscles and the biceps press the humeral head into the glenoid fossa (Fig. 1 7.30), locking it into position and thus providing a secure scapulohumeral link for upper extremity function.178 By contracting selectively, the rotator cuff muscles can resist displacing forces resulting from contraction of the principal shoulder motors. 1 79 For example, when the pectoralis major and anterior deltoid muscles elevate and flex the shoulder, they tend to push the humeral head out the back of the glenoid fossa; this displacement is resisted by contraction of the sub­ scapularis, infraspinatus and teres minor (Fig. 1 7.31). When the lateral deltoid initiates shoulder abduction, the supraspinatus and the long head of the biceps

Subscapularis

Infraspinatus

Figure 1 7.29 Glenoid cartilage is thickest at the periphery (1); humeral cartilage is thickest centrally (2). The glenoid labrum increases the depth of the glenoid socket and the surface area for the humeral head (3).

Figure 1 7.30 By contracting together the rotator cuff muscles and the biceps press the humeral head into the glenoid fossa, locking it in position.

CHAPTER 1 7 - DISORDERS OF THE I N ERT STRUCTU RES 337

few moments, after which the patient is usually able to return to activities without much pain or problem. In advanced cases however, and after repeated attacks; the shoulder may be felt to slip out and clunk back into place with increasing ease and in an increasing number of activities.187 Finally the shoulder may become uncomfort­ able even with the arm at rest and by then the acute symptoms are brought about with less forceful activities such as turning the steering wheel of a car or when the patient puts the arm in the sleeve of a coat.188 FUNCTIONAL EXAMINATION

Figure 1 7.31 By contracting selectively the rotator cuff muscles can resist the displacing forces of the principal shoulder motors.

actively resist upward displacement of the humeral head relative to the glenoid fossa. HISTORY

The history and detailed physical examination are both very important for diagnosis. Unfortunately symptoms are often vague and clinical findings subtle.l80,181 The majority of patients mention a previous injury, usually a fall onto the outstretched arm in lateral rotation and abduction, which resulted in a luxation of the humeral head.182 However, it should not be assumed that there is also a record of manipulative reduction at that time because in most cases the humeral head only subluxates and imme­ diately reduces spontaneously. The earlier in life this happens, the more likely is future transient subluxation.183 Sometimes, patients are encountered without a history of earlier displacement. This situation is called atraumatic instability and is more likely to be multidirectional. Atraumatic instability is more a syndrome that may arise from a set of pathogenic disorders: a flat glenoid, compli­ ant capsule or weak neuromus-cular control. It is often referred to as the AMBRII syndrome: Atraumatic, Multidirectional, Bilateral, with Rehabilitation directed at restoring neuromuscular control, as the most important therapeutic measure; in case surgery is necessary, it should include reconstruction of the rotator Interval and tighten­ ing of the Inferior capsule.184-186 An attack of subluxation is usually described as follows: the patient experiences a sudden paralysing pain and weakness of the arm during activity. Whatever is held may be dropped. Very often the pain is brought on by unguarded movements such as raising the arm during throwing, swimming or serving at tennis. The pain is only momentary and disappears spontaneously after a

The basic functional examination may show some abnor­ mal findings, typical for a possible minor instability: an enlarged range of movement (ROM) and a loose end-feel. Momentary subluxation can also appear as a kind of painful arc.189 During active elevation of the arm, the humeral head subluxates to a certain extent, blocks the movement for a while and slips back into place as the movement is continued. Recently it has been shown that a real painful arc, caused by impingement, may coexist in subluxation of the shoulder as a secondary phenomenon to the instability.190,191 An overlap seems to exist in the concepts of instability and impingement and for this reason when a painful arc is present minor shoulder instability must always be kept in mind .192,193 On passive lateral rotation, when performed firmly, a different type of end-feel may be encountered. First resistance is felt, which then is overcome and finally gives rise to a new ligamentous end-feel. When the arm is brought back to neutral position a click is often felt. This sequence of sen­ sation - although not necessarily painful - may indicate anterior instability. The same occurs in posterior instabil­ ity for passive medial rotation.

Accessory tests If a minor instability is suggested after the history and the basic functional examination, the classical stress tests to challenge the stability of the joint in various directions must be performed. During these tests, both apprehen­ sion and palpable subluxations are sought. To differenti­ ate normal laxity from pathological instability, both shoulders should be compared. The uninvolved arm is always examined first. Apprehension test for recurrent anterior dislocation

(Fig. 1 7.32). This test can be performed with the patient either standing or supine. The fingers of the contralateral hand are placed on the anterior aspect of the humeral head, the thumb posteriorly. With the other hand the examiner brings the arm into full lateral rotation. In this position, anteriorly directed pressure is applied with the thumb to the posterior part of the humeral head. The test

338 SECTION THREE - THE SHOULDER

Figure 17.32

Anterior apprehension test.

can be repeated with increasing degrees of abduction

also state that the feeling at the end of the test is what was

varying from 90° to full elevation. The test is regarded as

felt when the shoulder was previously dislocated.

positive if the patient judges that it provokes the same impression as the one felt when the shoulder moves out of place. Pain alone is not regarded as a positive appre­ hension sigh. The examiner must be able to feel the humeral head subluxating or the patient may contract the muscles to avoid this subluxation. Relocation test (Fig.

17.33). If, with the arm still in full

load-and-shift manoeuvres (anterior and posterior drawer) (Fig.

17.35). These tests are performed with the

patient in the supine position, lying with the scapula on the couch but with the humerus beyond the edge. The contralateral hand fixates the scapula with the thumb placed on the coracoid process and the fingers on the acromion. Before assessing the amount of translation it is

elevation and lateral rotation, a posteriorly directed force

important that the humeral head is brought initially into

is applied to the anterior aspect of the humerus, it relo­

its neutral position in the glenoid fossa (i.e. 'loaded').

cates the head of the humerus within the glenoid fossa, so

This is achieved by placing the shoulder in a position of

reducing the pain and alleviating the apprehension. This

neutral rotation: the humerus in approximately 20° of

test is very valuable in differentiating a simple impinge­

abduction and forward flexion. The elbow is flexed and

ment from a real anterior subluxation and is known as

the arm directed upwards. The ipsilateral hand grasps

the 'relocation test'.

the patient's humerus in the axilla and the shift manoeu­

Apprehension test for recurrent posterior dislocation

(Fig.

17.34). The patient lies supine, with the arm

abducted to 90° and the elbow flexed to a right angle. The examiner places the contralateral hand under the gleno­ humeral joint. The shoulder is then brought very gently into medial rotation - if the test is done too quickly, the

vres are performed by moving both hands in opposite directions: the anterior shift by translating the humerus anteriorly, the posterior shift by moving the humerus posteriorly in relation to the scapula. No attempt is made to produce subluxation but hypermobility is sought. Sulcus sign. With the arm hanging down and maximally

humerus might subluxate. A positive test for posterior

relaxed, traction (Fig. 17.36) may provoke inferio� sub­

instability is indicated by a feeling of apprehension and

luxation of the head of the humerus. An increase of the

the patient's resistance to further motion. The patient may

space between humerus and acromion is shown in the

CHAPTER 17

Figure 17.33

Relocation test.

Figure 17.34

Posterior apprehension test.

-

DISORDERS OF THE INERT STRUCTURES 339

340 SECTI ON THREE - THE S H O U LD E R

(a)

(b)

Figure 1 7.35 Anterior (a) and posterior (b) load-and-shift manoeuvres.

CHAPTER 1 7

Figure

17 .36

-

DISORDERS OF THE I N E RT STRUCTU RES 341

Sulcus sign.

skin being pulled towards the bone (i.e. sulcus sign). When present it points towards inierior subluxation of the humeral head which is usually part of a multi­ directional instability.194

Diagnosis Instability tests are performed only if the patient gives a history of shoulder instability. In other conditions, for example shoulder arthritis or bursitis, these tests would be very painful. In anterior instability the apprehension and relocation tests as well as the anterior load-and-shift manoeuvre are usually positive, although sometimes very subtle.196,197 If the sulcus sign is also found, multi­ directional instability is present.198 Diagnosis of posterior instability is based on the patient's ability to reproduce the subluxation by arm positioning in flexion and medial rotation. Posterior apprehension is usually absent and posterior translation of the humeral head on the glenoid may provide the only clue to the diagnosis of posterior instability.199,2oo If inierior instability is also present, distal traction may reproduce the symptoms, suggesting multidirectional instability.201 Since a momentary subluxation of the humeral head on elevation can give rise to the impression of a painful arc, all other lesions causing a painful arc must also be included in the differential diagnosis. None of these lesions however

provokes the sensation of instabili ty. In the assessment of chronic instability of the shoulder, special X-ray views may be helpful to determine bony anatomy and patho­ logical change.202 CT scan, MRI and arthrography seem to have limited application in the routine roentgenographic diagnosis of the unstable shoulder.203

Treatment Initial treatment for minor instability is conservative204 and banks on three pillars: • • •

strengthening of the periscapular muscles training of the antagonists of the deltoid training of the neuromuscular control of the rotator cuff muscles.

Provide a firm base. Fixation of the scapula must be optimal. Therefore, the scapular rotators (trapezius, levator scapulae, serratus anterior, rhomboids and pectoralis minor) must be trained to provide a stable platform for the humeral head.205 At first only isometric exercises should be given; later isotonic contractions are added to the training session. It is important, however, not to use long levers; only the muscles of the shoulder girdle are trained and the humerus stays alongside the trunk because long-lever exercises may put excessive strain on the rotator cuff and shoulder ligaments.

342 SECTIO N TH R E E - TH E S H O U LD E R

Train strength and propriocepsis of the antagonists of the deltoid: the latissimus dorsi and the pectoralis major muscles. To start with, only isometric exercises from 90°

of abduction are given. The purpose is to train the mus­ cular feeling and active relaxation of the deltoid. A caudal movement of the humeral head is encouraged. Later on isotonic exercises are added. These consist of active adduction movements, using weights and a pulley - in the beginning only with a short lever, later with the use of the stretched arm. Finally, coordination exercises com­ plete the session: training of contractions of the antago­ nists during active elevation of the arm - this in an attempt to pull the head of the humerus in a caudal direc­ tion during active abduction of the arm. Proprioceptive exercises for the rotator cuff muscles. It has been demonstrated that the muscles of the rotator cuff serve a complementary function to adjust tension in the capsuloligamentous system.205 The simultaneous contraction of rotator cuff and biceps causes the humeral head to be compressed into the glenoid. Furthermore, selective muscular contraction of the sub­ scapularis plays an important role in limiting anterior translation206,2o7 whereas teres minor and infraspinatus have a similar function with regard to posterior insta­ bility.208 The purpose is to train the muscular response to the capsular neuroreceptor input. This is mainly

Figure

1 7.37

Exercises for infraspinatus-subscapularis.

done under eccentric conditions: the muscle is activated while being stretched. Acceleration and deceleration movements are performed under high speed while using small weights. In practice the training consists of three exercises: •

•

•

In supine lying: the elbow is held close to the body. A small weight (+ / - 1 kg) is rotated towards and away from the trunk. The speed of rotation will change from one cycle / 3--4 seconds to one cycle / second. This movement trains capsular feedback for the infra­ spinatus and subscapularis muscles (Fig. 1 7.37). In side lying: the shoulder is slightly flexed and in medial rotation. A small weight (0.5 kg) is lifted and brought back. The arm remains stretched and the movement is repeated, first slowly (one cycle / 3 seconds) and gradually speeding to one cycle / second. This movement trains capsular f­ eedback for the supraspinatus muscle (Fig. 1 7.38). Standing: the trunk is slightly flexed, the arm hanging by the side. A weight of about 2-3 kg is used. The patient is asked to let the arm hang down and to relax the deltoid muscle as much as possible. Maximal inter­ nal and external rotations are now performed. First slowly, to the very end of range, then more quickly. These acceleration-deceleration exercises, with increasing velocity, train the capsular feedback for

CHAPTER 1 7

Figure

17 .38

Exercises for supraspinatus.

Figure

17 . 39

Acceleration-deceleration exercises.

-

DISORDERS OF THE I N E RT STRU CTURES 343

344 SECTION THREE - THE S H O U LD E R

subscapularis, infraspinatus and teres minor. The deltoid should be maximally relaxed (Fig. 1 7.39).

tIVv

Practitioner's checklist

• It i s i m portant to start the exercises o n ly when the

routine basic c l i n ical exa m ination is pa i n less. • Use sma l l weights, especia l ly in the beg i n n i ng; the

exercises should be performed as relaxed as possible. • Ask the patient to repeat the exercises as often as

possi ble during the day i n order to atta i n maxi mal neuromuscular feedback.

Surgery When surgery is called for, it is extremely important that the differentiation between a posterior, anterior and multidirectional displacement is clear. If not, the opera­ tion will make the patient worse. The indications for operation depend on various factors such as disability during daily activities, pain and frequency of disloca­ tions. Operative results are fairly good in anterior insta­ bility209 depending on the type of surgical procedure21 O,2l1 but results are less good in posterior instability in which a 40% failure rate exists.212 Multidirectional instability is also not conducive to a good outcome.213

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82. Scutellari PN, Orzincolo C. Rheumatoid arthritis: sequences. Eur J Radial 1998;27(Suppl 1):S31-S38. 83. Cuomo F, Greller MJ, Zuckerman JD. The rheumatoid shoulder. Rheum Dis Clin North Am 1 998;24(1):67-82. 84. Veys B, Mielants H, Verbruggen G. Reumatologie. Omega Editions, Ghent, 1985. 85. Will R, Kennedy G, Elswood J et al. Ankylosing spondylitis and the shoulder: commonJy involved but infrequently disabling. J RheumatoI 2000;27(1):177-182. 86. Law LA, Haftel HM. Shoulder, knee, and hip pain as initial symptoms of juvenile ankylosing spondylitis: a case report. J Orthop Sports Phys Ther 1 998;27(2): 1 67-172. 87. Helm M, Horoszowski H, Martinowitz U. Haemophilic arthropathy resulting in a locked shoulder. Clin Orthop Rei Res 1986;202:169-172. 88. Dieppe P, Cal vat P. Crystals and Joint Disease. Chapman and Hall, London, 1982:145. 89. Curran J, Eilman M, Brown N . Rheumatologic aspects of painful conditions affecting the shoulder. Clin Orthop Rei Res 1983;173:27-37. 90. Zitan D, Sitai S. 1963 Articular chondrocalcinosis. Ann Rheum Dis 1963;22:142. 91. Doherty M, Dieppe P, Watt 1. Pyrophosphate arthropathy: a prospective study. Br J Rheum 1993;32:189-196. 92. Leske B, Harris J, Driscoll D. Septic arthritis of the shoulder in adults. ] Bone Joint Surg 1989;71A(10):1516-1522. 93. Hughes R, Rowe L, Shanson D, Keat A. Septic bone, joint and muscle lesions associated with human immunodeficiency virus infection. Br J RheumatoI 1992;31(6):381-388. 94. Chaudhuri K, Lonergan D, Portek J et al. Septic arthritis of the shoulder after mastectomy and radiotherapy for breast carci­ noma. J Bone Joint Surg 1993;75B(2):318-321 . 95. Dubost JJ, Soubrier M, Sauvezie B . Pyogenic arthritis i n adults. Joint Bone Spine 2000;67(1):11-2 1 . 9 6 . Kelly P, Martin W, Coventry M. Bacterial (suppurative) arthri­ tis in the adult. J Bone Joint Surg 1970;52A(8):1595-1602. 97. Stutz G, Kuster MS, Kleinstuck F, Gachter A. Arthroscopic management of septic arthritis: stages of infection and results. Knee Surg Sports Traumatol Arthrosc 2000;8(5):270-274. 98. Gardner G, Weisman M. Pyarthrosis in patients with rheuma­ toid arthritis: a report of 13 cases and a review of the literature from the past 40 years. Am J Med 1990;88(5):503-51 1 . 99. Epps C. Painful haematologic conditions affecting the shoulder. Ciin Orthop Rei Res 1983;173:38--43. 100. Marcove R. Chondrosarcoma: diagnosis and treatment. Orthop Clin North Am 1977;8(4):811-820. 1 0 1 . Hattrup SJ, Cofield RH. Osteonecrosis of the humeral head: relationship of disease stage, extent, and cause to natural history. J Shoulder Elbow Surg 1999;8(6):559-564. 102. Wingate J, Schiff CF, Friedman RJ. Osteonecrosis of the humeral head in sickle cell disease. J South Orthop Assoc 1996;5(2):101-107. 103. Wilmshurst P, Ross K. Dysbaric osteonecrosis of the shoulder in a sport scuba diver. Br J Sports Med 1998;32(4):344-345. 104. Morakkabati N, Strunk H, Gutjahr P. MRI diagnosis and follow-up of bilateral necrosis of the humeral head as a complication after chemotherapy. Aktuelle Radial 1997;7(1):41--44. 105. LaPorte DM, Mont MA, Mohan V et al. Osteonecrosis of the humeral head treated by core decompression. Clin Orthop 1998;355:254-260. 1 06. Gerber C, Hersche 0, Berberat C. The clinical relevance of posttraumatic avascular necrosis of the humeral head. J Shoulder Elbow Surg 1998;7(6):586-590.

107. Cofield RH. Degenerative and arthritis problems of the gleno­ humeral joint. In: Rockwood CA, Matsen FA III (eds) The Shoulder. Saunders, Philadelphia, 1990:678-749. 108. Neer CS III, Craig EV, Fukuda H. Cuff-tear arthropathy. J Bone Joint Surg 1983;65A:1232-1244. 109. Rutherford CS, Cofield RH. Osteoarthrosis of the shoulder. Orthop Trans 1987;11:293. 110. Mau H, Nebinger G. Arthropathy of the shoulder joint in syringomyelia. Z Orthop 1986;124:157-164. 1 1 1 . Tully JG Jr, Latteri A. Paraplegia tarde and neuropathic arthro­ sis of the shoulder. A triad. Clin Orthop 1978;134:244-248. 112. Johnson GS, Guly HR. Acute calcific periarthritis outside the shoulder: a frequently misdiagnosed condition. J Accid Emerg Med 1994;11(3):198-200. 113. Pfister J, Gerber H. Behandlung der Periarthropathia humero­ scapularis calcarea mittels SchulterkalkspiihJung: retrospek­ tive Fragenbogenanalyse. Z Orthop Ihre Grenzgeb 1994;132:300-305. 114. Gartner J. Tendinosis calcarea-Behandlungsergebnisse mit der Needling. Z Orti1op Ihre Grenzgeb 1993;313:461--469. 115. Brown C. Compressive, invasive referred pain to the shoulder. Clin Orthop ReI Res 1983;173:55-62. 1 1 6. Johnson DE, Goldberg M. Management of carcinoma of the superior pulmonary sulcus. Oncology 1997;11(6):781-785. 1 1 7. McKellar Hall. Clay shoveller's fracture. ] Bone Joint Surg 1940;12:63-75. 118. Herrick R. Clay-shoveller's fracture in power lifting. Am ] Sports Med 1981;9(1):29-30. 119. Kauppila LI, Vastamaki M. Iatrogenic serratus anterior paraly­ sis. Long-term outcome in 26 patients. Chest 1996;109(1):31-34. 120. Packer GJ, McLatchie GR, Bowden W. Scapula winging in a sports injury clinic. Br J Sports Med 1993;27(2):90-9 1 . 1 2 1 . Gregg J R , Labosky D , Harty M et al. Serratus anterior paralysis in the young athlete. ] Bone Joint Surg 1979;61A(6):825-832. 122. Wouters D, Dauwe D, Demuynk M. Geisoleerde verlamming van de musculus serratus anterior. Tijdschr Geneeskd 1922;48(7) :531-534. 123. Foo CL, Swann M. Isolated paralysis of the serratus anterior. A report of 20 cases. J Bone Joint Surg 1983;65(5):552-556. 124. Logigian EL, McInnes JM, Berger AR et af. Stretch-induced spinal accessory nerve palsy. Muscle Nerve 1988;11(2):146-150. 125. Matz PG, Barbaro NM. Diagnosis and treatment of iatrogenic spinal accessory nerve injury. Am Surg 1996;62(8):682-685. 126. Marini SG, Rook JL, Green RF, Nagler W. Spinal accessory nerve palsy: an unusual complication of coronary artery bypass. Arch Phys Med RehabiI 1991;72(3):247-249. 127. London J, London NJ, Kay SP. Iatrogenic accessory nerve injury. Ann R Call Surg EngI 1 996;78(2):146-150. 128. Grainger AJ, Tirman PF, Elliott JM et af. MR anatomy of the subcoracoid bursa and the association of subcoracoid effusion with tears of the anterior rotator cuff and the rotator interval. Am J Roentgenol 2000;174(5):1377-1380. 129. Ticker JB, Beim GM, Warner JJ. Recognition and treatment of refractory posterior capsular contracture of the shoulder. Arthroscopy 2000;16(1):27-34. 130. Fukada K, Craig EV, An K-N. B iomechanical study of the liga­ mentous system of the acromioclavicular joint. J Bone Joint Surg 1 986;68A:434--439. 1 3 1 . Kocher MS, Feagin JA Jr. Shoulder injuries during alpine skiing. Am J Sports Med 1 996;24(5):665-669. 132. Vandenbossche J, Raes R, Verdonck R. Acromioclaviculaire luxaties. Tijdschr Geneeskd 1990;46(6):393-398. 133. Neer C, Welsh P. The shoulder in sports. Orthop Clin North Am 1977;8(3):183-191 .

CHAPTER 1 7 - DISORDERS OF THE I N E RT STRUCTU RES 347

134. Beam JG. Direct observations on the function of the capsule of the sternoclavicular joint in clavicle support. J Anat 1967;101:1 59-170. 135. Oh W, Garvin W. Anterior subluxation of the distal clavicle. Orthop Ciin North Am 1980;11(4):813-818. 136. Horn J . The traumatic anatomy and treatment of acute acromio­ clavicular dislocation. J Bone Joint Surg 1954;36: 1 1 3-194. 137. Allman F. Fractures and ligamentous injuries of the clavicle and its articulation. J Bone Joint Surg 1 967;49A:774-784. 138. Tossy JD, Mead NC, Sigmond HM. Acromioclavicular separa­ tions: useful and practical classification for treatment. Ciin Orthop 1963;28:111-119. 139. Williams GR, Nguyen VD, Rockwood CA Jr. Classification and radiographic analysis of acromioclavicular dislocations. Appl Radial 1989;18:29-34. 140. Bjernfeld H, Hovelius L, Thorling J. Acromio-clavicular sepa­ rations treated conservatively: a 5-year follow-up study. Acta Orthop Scand 1983;54:743-745. 141. Dias JJ, Steingold RA, Richardson RA et al. The conservative treatment of acromioclavicular dislocation: review after five years. J Bone Joint Surg 1987;69B:71 9-722. 142. Glick JM, Milburn LH, Haggerty JF, Nishimoto D. Dislocated acromioclavicular joint: follow-up study of 35 unreduced acromioclavicular dislocations. Am J Sports Med 1977;5: 264-270. 143. MacDonald PB, Alexander MJ, Frejuk J, Johnson G . Comprehensive functional analysis o f shoulders following complete acromio-clavicular separation. Am J Sports Med 1988;16:475-480. 144. BarUlister G, Wallace W, Stabieforth P, Hutson M. The manage­ ment of acute acromioclavicular dislocation. J Bone Joint Surg 1989;71(8):848-850. 145. Larsen E, Bjerg-Nielsen A, Christensen P. Conservative or surgical treatment of acromioclavicular dislocation: A pro­ spective controlled randomised study. J Bone Joint Surg 1 986;68A:552-555. 146. Post M. Current concepts in the diagnosis and management of acromioclavicular dislocations. Ciin Orthop 1985;200:234-247. 147. Cahill BR. Atraumatic osteolysis of the distal clavicle. A review. Sports Med 1992;13(3):214-222. 148. Brunet ME, Reynolds MC, Cook SO, Brown TW. Atraumatic osteolysis of the distal clavicle: histologic evidence of synovial pathogenesis: a case report. Orthopedics 1986;9:557-559. 149. Kaplan PA, Resnick D. Stress-induced osteolysis of the clavicle. Radiology 1968;158:139-140. 150. Orava S, Virtanen K, Holopainen YVO. Post-traumatic osteo­ lysis of the distal end of the clavicle. Report of three cases. Ann Chir GynaecoI 1984;73:83-86. 151. Murphy OB, Bellamy R, Wheeler W, Brower TD. Post­ traumatic osteolysis of the distal clavicle. Clin Orthop 1975;109:108-114. 152. Levine AH, Pais ML, Schwartz EE. Posttraumatic osteolysis of the distal clavicle with emphasis on early radiologic changes. Am J Roentgeno/ 1976;127:781-784. 153. Cahill BR. Osteolysis of the distal part of the clavicle in male athletes. J Bone Joint Surg 1982;64A:1053-1058. 154. Lyons FR, Rockwood CA. Osteolysis of the clavicle. In: De Lee Je, Drez 0 (eds) Orthopaedic Sports Medicine. Saunders, Philadelphia, 1994:546. 155. Auge WK 2nd, Fischer RA. Arthroscopic distal clavicle resec­ tion for isolated atraumatic osteolysis in weight lifters. Am J Sports Med 1998;26(2): 1 89-192. 156. Zawadsky M, Marra G, Wiater JM et al. Osteolysis of the distal clavicle: long-term results of arthroscopic resection. Arthroscopy 2000;16(6):600-605.

157. Rahrne H, Nordgren H, Hamberg H, Westerberg C. The sub­ acromial bursa and the impingement syndrome. Acta Orthop Scand 1993;64(4):485-488. 158. Gotoh M, Hamada K, Yamakawa H, Inoue A, Fukuda H. Increased substance P in subacromial bursa and shoulder pain in rotator cuff diseases. J Orthop Res 1998;16(5):618-621 . 1 59. Farm P, Jaroma H , Harju A, Soimakallio S. Shoulder impinge­ ment syndrome: sonographic evaluation. Radiology 1 990; 176(3):845-849. 160. Takayama A, Ito H, Shirai Y. Subacromial bursitis mimicking a soft tissue tumor. J Shoulder Elbow Surg 2000;9(1):72-75. 161. Larson HM, O'Connor FG, Nirsch! RP. Shoulder pain: the role of diagnostic injections. Am Fam Physician 1996;53(5):1637-1647. 162. Matsen FA III, Fu FH, Hawkins RJ (eds) The Shoulder: A Balance of Mobility and Stability. American Academy of Orthopaedic Surgeons, Rosemont, IL, 1993. 163. Schwartz E, Warren R, O'Brien S, Fronek J. Posterior shoulder instability. Orthop Clin North Am 1987;18(3):409-419. 164. Schewelies S. Die habituelle Schulterluxation. Physiotherapie 1979;6:507-509. 165. Turkel SJ, Panio MW, Marshall JL, Girgis FG. Stabilizing mech­ anisms preventing anterior dislocation of the glenohumeral joint. J Bone Joint Surg 1981;63A:1208-1217. 166. Warner JJ, Deng XH, Warren RF, Torzill PA. Static capsuloliga­ mentous restraints to superior-inferior translation of the glenohumeral joint. Am J Sports Med 1 992;20:675-685. 167. Howell SM, Galinat BJ, Renzi AJ, Marone pJ. Normal and abnormal mechanisms of the glenohumeral joint in the hori­ zontal plane. J Bone Joint Surg 1988;701:227-232. 168. Soslowski LJ, Bigliani LU, Flatow EL et al. Articular geometry of the glenohumeral joint. Clin Orthop 1992;285:181-190. 169. Howell SM, Galinat BJ. The glenoid-labral socket: a con­ strained articular surface. Ciin Orthop 1 989;243: 122-125. 1 70. Bowen MK, Deng XH, Hannafin JA et al. An analysiS of the pat­ terns of glenohumeral joint contact and their relationship to the glenoid 'bare area'. Trans Orthop Res Soc 1992;17:496. 1 7 1 . Levick JR. Joint pressure-volume studies: their importance, design and interpretation. J RheumatoI 1983;10:353-357. 1 72. Gibb TO, Harryman DT II, Sidles JA et al. The effect of capsular venting on glenohumeral laxity. C/in Orthop 1991 ;268: 120-127. 173. Jerosch J, Steinbeck J, Clahsen H, Schmitz-Nahrath M, Grosse­ Hackmann A. Function of the glenohumeral ligaments in active stabilisation of the shoulder joint. Knee Surg Sports Traumatol Arthrosc 1993;1{3-4):152-158. 1 74. WUlker M, Rossig S, Korell M, Thren K. Dynamic stability of the glenohumeral joint. A biomechanical study. Sportverletz Sportschaden 1995;9:11-18. 1 75. Kronberg M, Nemeth G, Brostrom LA. Muscle activity and coordination in the normal shoulder: An electromyographic study. Clin Orthop 1990;257:76-85. 176. Terry Ge, Hammon 0, France P, Norwood L. The stabilizing function of passive shoulder restraints. Am J Sports Med 1991;19:26-34. 177. Warner JJ, Lephart S, Fu FH. Role of proprioception in patho­ etiology of shoulder instability. Clin Orthop 1 996;330:35-39. 178. Howell SM, Galinat BJ. The glenoid-labral socket. A con­ strained articular surface. Clin Orthop 1 988;243:122. 179. Loehr JF, Helmig P, Sojbjerg JO, Jung A. Shoulder instability caused by rotator cuff lesions. An in vitro study. Clin Orthop 1994;304:84-90. 180. Mizuno K, Nabeshima Y, Hirohata K. Analysis of Bankart lesion in the recurrent dislocation or subluxation of the shoulder. Clin Orthop Rei Res 1993;288:158-165.

348 SECTI ON THREE - T H E S H O U LD E R

1 8 1 . Kvitne R , Jobe F. The diagnosis and treatment o f anterior instabil ity in the throwing athlete. Clill Orthop Rei Res 1993;291:107-123. 182. Dalton S, Snyder S. Glenohumeral instability. Bailliere's Clill RheumatoI 1 989;3(3):51l -534. 183. Schwartz E, Warren R, O'Brien S, Fronelk J. Posterior shoulder instability. Orthop Clin North Am 1987;18(3):409-419. 184. Lippit SB, Harryman DT II, Sidles JA, Matsen FA III. Diagnosis of management of AMBRII syndrome techniques. Techniques Orthop 1 991;6:66-73. 185. O'Driscoli Sw. Atraumatic instability: pathology and patho­ genesis. In: Matsen FA III, Fu FH, Hawkins RJ (eds) The Shollider: A Balance of Mobility and Stability. American Academy of Orthopaedic Surgeons, Rosemont, IL, 1993:305-308. 1 86. Te Slaa R, Lim T. Multidirectioneie instabiliteit van de schouder; een nieuwe vorm van chronische schouderinsta­ biliteit. Ned Tijdschr Geneeskd 1992;136(32):1560-1563. 187. Rowe CR. Recurrent transient anterior subluxation of the shoul­ der. The dead arm syndrome. Clin Orthop Rei Res 1987;223:11-19. 1 88. Glousman R. Instability versus impingement syndrome in the throwing athlete. Orthop Clin North Am 1993;24(1):89-99. 189. Fu F, Harner C, Klein A. Shoulder impingement syndrome. Clin Orthop Rei Res 1991;269:162-1 73. 190. Schenk TJ, Brems JJ. Multidirectional instability of the shoul­ der: pathophysiology, diagnosis, and management. J Am Acad Ort/lOp Surg 1998;6(1):65-72. 191 . Jobe F, Giangarra C, Kvitne R. Anterior capsullabral recon­ struction of the shoulder in athletes in overhand sports. Am J Sports Med 1991;19:428-434. 192. Neviaser R, Neviaser T, Neviaser J. Anterior dislocation of the shoulder and rotator cuff rupture. Clin Orthop Rei Res 1993;291:103-106. 193. Silliman J, Hawkins R. Classification and physical diagnosis of instability of the shoulder. Clin Ort/lOp Rei Res 1993;291:7-19. 194. Matsen FA III, Lippitt SB, Sidles JA, Harryman DT II. Practical Evaillation and Management of the Shoulder. Saunders, Philadelphia, 1994. 1 95. McFarland EG, Torpey BM, Curl LA. Evaluation of shoulder laxity. Sports Med 1 996;22(4):264-272. 196. Zarins B, McMahon M, Rowe C. Diagnosis and treatment of traumatic anterior instability of the shoulder. Clin Orthop Rei Res 1993;291:75-84.

1 97. Magarey M, Jones M. Clinical diagnosis and management of minor shoulder instability. Aust Physio 1992;38(4):269-280. 1 98. Altchek DW, Warren RF, Skyhar MJ et ai. T-plasty modification of the Bankart procedure for multidirectional instability of the anterior and inferior types. ] Bone Joint Surg 1991;73(1):105-112. 199. Czitfer E, Habel T, Kepes P. Posterior shoulder dislocation: pit­ falls and perils. Orthopedics 1993;16(1):97-99. 200. Pollock R, Bigliani L. Recurrent posterior shoulder instability. Clin Orthop Rei Res 1993;291:85-96. 201 . An YH, Friedman RJ. Multidirectional instability of the gleno­ humeral joint. Orthop Clin North Am 2000;31(2):275-285. 202. Rokous JR, Feagin JA, Abbott HG. Modified axillary roentgenogram: a useful adjunct in the diagnOSiS of recurrent instability of the shoulder. Clin Orthop 1972;82:84-86. 203. Engebretsen L, Craig L. Radiologic features of shoulder insta­ bility. Clin Orthop Rei Res 1993;291:29-44. 204. Burkhead WZ Jr, Rockwood CA Jr. Treatnlent of instability of the shoulder with an exercise program. J Bone Joint Slirg 1992;74A(6):890-896. 205. Kamkar A, Irrgan JJ, Whitney SL. Nonoperative management of secondary shoulder impingement syndrome. J Orthop Sports Physical Therapy 1993;17:21 2-224. 206. Terry GC, Hanin10n D, France P, Norwood L. The stabilizing function of passive shoulder restraints. Am j Sports Med 1 991;19:26-34. 207. Jobe F, Moynes D, Brewster C. Rehabilitation of shoulder joint instabilities. Orthop Clin North Am 1987;18(3):473-482. 208. Oveson J, Nielsen S. Anterior and posterior instability: a cadaver study. Acta Ortl1Op Scand 1985;57:324-327. 209. Oveson J, Nielsen S. Posterior instability of the shoulder: a cadaver study. Acta Orthop Scand 1985;57:436-439. 210. Miniaci A, MacDonald P. Open surgical techniques in the athlete's shoulder. Clin Sports Med 1991;10(4):929-954. 2 1 1 . O'Driscoll S, Evans D. Long-term results of staple capsulor­ rhaphy for anterior instability of the shoulder. j Balle jOil1t Slirg 1993;75A(2):249-258. 212. Roberts SN, Taylor DE, Brown IN, Hayes MG, Saies A. Open and arthroscopic techniques for the treatment of traumatic anterior shoulder instability in Australian rules football players. J Shoulder Elbow Surg 1 999;8(5):403-409. 213. Tibone J, Bradley J. The treatment of posterior subluxation in athletes. Clin Ortl1Op Rei Res 1993;291: 1 24-137.

Disorders of the contractile structures

CHAPTER CONTENTS Introduction

349

350 Pathology 350 Incidence 351 Diagnosis and treatment

Rotator cuff

352

353 Pain 353 Painful weakness 357 Painless weakness 358

Resisted abduction

360 Pain 360 Painful weakness 362 Painless weakness 363

Resisted adduction

INTRODUCTION

363

Resisted lateral rotation

Pain 363 Painful weakness 367 Painless weakness 367 368

Resisted medial rotation

Pain 368 Painless weakness Resisted elbow flexion

Pain 371 Painless weakness

369 370 373

Resisted elbow extension

Pain 373 Painless weakness

373

373

Resisted flexion of the arm

374

Functionally, shoulder muscles are of two types: stabilizing muscles and effector muscles. Stabilizing muscles (A, Fig. 1 8. 1 ) are relatively small, with insertion tendons that lie close to, or even in, the substance of the fibrous capsule. Therefore they are not capable of causing significant shoulder movement but rather main­ tain the humeral head in the glenoid fossa. These stabi­ lizing muscles are called the rotator cuff and include supra- and infraspinatus, teres minor and subscapu­ laris. They all originate from the scapula, run partly under the acromial roof and insert on the humeral tubercles. Effector muscles (B, Fig. 1 8 . 1 ) are much larger, with tendon insertions at a greater distance from the joint. Consequently, they produce powerful movements and are not primarily involved in stabilization. They are the deltoid complex, the pectoralis major, the latissimus dorsi and the teres major.

Figure

1 8.1

(A) Rotator cuff (stabilizing) muscles; (B) large effector muscles. 349

350 SECTION THREE - THE SHOULDER

Although the standard clinical examination tests both muscle groups, the great majority of the positive findings point towards lesions of the rotator cuff, because lesions of the large effector muscles are extremely rare.

ROTATOR CUFF

Rotator cuff disorder is one of the commonest afflictions of the shoulder and a major cause of impairment of health in the young as well as in older individuals.1 Lesions of the rotator cuff should be recognized as different from those of other tendons in the body and for different reasons. The tendons of the rotator cuff blend intimately with each other and with the capsule. The insertion of the tendons, as a continuous cuff around the humeral head permits the cuff muscles to provide an almost infinite variety of movements to rotate the head and to oppose unwanted movements generated by the larger effector muscles.2 Further the long head of the biceps may be considered a functional part of the rotator cuff, because tension in the tendon helps to compress the humeral head into the glenoid (Fig. 18.2). Apart from their primary function (to rotate the humerus with respect to the scapula), the cuff muscles have two other actions: they compress the head of the humerus into the glenoid fossa and provide muscular balance (Box 1 8 . 1 ). The latter is mainly performed

Box 1 8.1 Functions of the rotator cuff 1. Rotate the humerus 2. Compress the humeral head 3. Provide muscular balance

Figure 1 8.2 Rotator cuff from above: 1, coracoacromial ligament; 2, subscapularis tendon; 3, biceps tendon; 4, supraspinatus tendon;

5, infraspinatus tendon.

through eccentric contraction of the muscle. Both func­ tions have been extensively discussed in Chapter 17. PATHO LOGY

Pathological changes associated with rotator cuff tendinopathy features are variable. Inflammatory tendinitis is a reversible process, associated with an inflammatory infiltrate, increased vascularity and hyperaemic changes within the rotator cuff tendon.3 Partial rotator cuff tears may develop within the sub­ stance of the tendon on either the acromial (bursal) or articular surface of the tendon.4 Most of the lesions occur near to the tendon insertion side. Full thickness tears are often initiated by a partial tear. They can be associated with a traumatic event or can progress with the normal daily use of the arm. Changes in the rotator cuff may also involve calcifying tendinopathy and rotator cuff arthropathy (degenerative glenohumeral osteoarthrotic disease associated with chronic massive rotator cuff tears). The pathogenesis of rotator cuff disease has been asso­ ciated with three factors: age-related degeneration, impingement and microvascular blood supply. The primary cause of tendon degeneration is age.s Changes in the rotator cuff include diminution of fibro­ cartilage at the cuff insertion, diminution of vascularity, fragmentation of the tendon and disruptions of the attachment to the bone.6,7 Changes in the coracoacromial arch have been described in association with cuff disease and it is quite clear from both cadaver and clinical data that individu­ als with full thickness rotator cuff tears have changes in the acromial shape, with spur formation on the under­ surface of the acromion and / or hypertrophy of the acromioclavicular joint.8-11 Although these data indicate a strong association between the presence of cuff tears and alterations of acromial contour, 1 2 it is still unclear whether the change in acromial shape is the cause or the result of the cuff defect or if both are consequences of ageing.13 Recent studies suggest that acromial deformity is usually developmental. Most acromial ' hooks' develop within the acromial ligament as traction spurs (analogous to the traction spur in the plantar ligament at its attachment to the calcaneus). The traction results from loading of the ligament by the cuff, which is increased when superior instability and cuff degenera­ tion are present.14,lS Changes in the microvascular supply to the rotator cuff also have a possible role in the pathogenesis of rotator cuff lesions.16 A hypovascular region exists at the 'critical zone' of the supraspinatus (the deep surface of the ante­ rior insertion).1 7,18 Microangiographic studies demon-

CHAPTER 18

strate that inadequate vascular supply to this critical zone is present in the adducted position of the arm.19 Furthermore, microvascular supply changes within the thickness of the tendon: the acromial part has a much better vascularity than the articular part.20-22 It is likely that a combination of age, anatomical changes and vascular insufficiency is responsible for rotator cuff 'failure'.23 Throughout life the cuff is sub­ jected to various adverse factors such as traction, com­ subacromial abrasion, contusion, pression, inflammation and age-related degeneration. A lesion may start where the loads are the greatest and the vas­ cular supply the lowest, i.e. at the deep surface of the anterior insertion of the supraspinatus.24 Each fibre rupture then generates other adverse effects: it increases the load on the neighbouring fibres, it compromises the blood supply of the tendon fibres by distorting the microcirculation and it exposes increasing amounts of the tendon to joint fluid that contains lytic enzymes. The cuff is gradually weakened and under increased risk for further failure. With subsequent loading episodes the pattern repeats itself, rendering the cuff weaker and progressively more susceptible to additional failure (Fig. 18.3).25

I N CID E NCE

The incidence of rotator cuff tears has been studied both in cadaveric studies and in living subjects and found to range from 5 to 80%. All the studies show a strong rela­ tionship with age: rotator cuff tears are rare before age 40 and common after age 60. However, almost all of the

-

DISORDERS OF THE CONTRACTILE STRUCTURES 351

Age Anatomical changes in the acromion Vascular insufficiency

Increasing load on the neighbouring fibres

1--------..

Compromise of blood supply Weakened tendon Exposition of the tendon to joint fluid Figure 1 8.3

Tendon f ibre failure .

reported cadaver studies failed to correlate cuff disorder with the presence of clinical symptoms (Table 18.1). Some of the most important studies in living subjects have concerned the prevalence of cuff lesions in asymp­ tomatic patients (Table 18.2). They all demonstrated a high prevalence of tears of the rotator cuff in asympto­ matic individuals, an increasing frequency with advanc­ ing age and compatibility with normal, painless functional activity. It must be concluded from these studies that cuff defects become increasingly common after the age of 40 and many occur without substantial clinical manifesta­ tions. This realization poses substantial questions about the anatomical diagnosis of shoulder pain and of its treat­ ment and in particular the indications for cuff surgery.

Table 1 8.1 Incidence of rotator cuff tears in cadaver dissections Authors

Incidence (%)

Keyes (1933)26

19

Wilson (1943)27

20-22

Grant & Smith (1948)28 Cotton & Rideaout

(1963)29

Uhtoff et al (1986)30 Osaki J et al

Increasing incidence with age

20 30

(1988)31

Kummer & Zukerman

37

Remarks

12 (complete)

(1995)32

17

None age 60

6% in cadavers 60 years

Jerosch J et al

(1991)33

28.3 (partial)

More common in women

31 (complete) Fukada et al (1987)34

13 (partial)

30% in patients older than 40 No tears in ?!:;,i� . "

Figure 50.12

:

Facet joints at L4-L5 and L5-S 1 .

ments could get pinched between the articular surfaces, which is then a probable source of backache.81-83 The facet joints are innervated from fibres of the medial branch of the dorsal root. The same nerve sup­ plies the inferior aspect of the capsule and the superior aspect of the joint below.84

LIGAMENTS

The broad and thick anterior longitudinal ligament (Fig. 50.13) originates from the anterior and basilar aspect of the occiput and ends at the upper and anterior part of the sacrum. It consists of fibres of different lengths: some extend over four to five vertebral bodies; the short fibres

attach firmly to the fibres of the outermost annular layers and the periosteum of two adjacent vertebrae. The posterior longitudinal ligament (Fig. 50.14) is smaller and thinner than its anterior counterpart: 1.4 cm wide (versus 2 cm in the anterior ligament) and 1.3 mm thick (versus 2 mm). This is another fact in favour of the theory that the lumbar spine was originally designed to be a hor­ izontal hanging structure: to withstand extension strains, the back had to be stronger anteriorly than posteriorly.5 The posterior longitudinal ligament is narrow at the level of the vertebral bodies, and gives lateral expansions to the annulus fibrosus at the level of the discus, which bestow on it a denticulated appearance.85 Although the posterior ligament is rather narrow, it is important in preventing disc protrusion.86 Its resistance is the main factor in restricting posterior prolapse and accounts for the regular occurrence of spontaneous reduction in lumbago. This characteristic is also exploited in manipulative reduction, when a small central disc displacement is moved anteriorly when the ligament is tightened. That the ligament occupies only the midline of the vertebral column is one of the predetermining factors in the progression of sciatica: as a central protrusion enlarges, it tends to move in the direction of least resist­ ance - lateral to the ligament. Once free from ligamentous

7 1 2 SECTION TEN - THE LUM BAR SPI N E

---;tlrr\\--- 3

Figure 50.15

Figure 50.14

Posterior longitudinal ligament.

resistance, it further enJarges and starts to compress the nerve root. This anatomical evolution is mirrored in the change of the clinical picture: a central backache is replaced by a unilateral sciatica. The Ligamentum flavum (Fig. SO.IS) connects two con­ secutive laminae and has a very elastic structure with an elastin content of more than 80%.72 The lateral extensions form the anterior capsule of the facet joints and run further laterally to connect the posterior and inferior borders of the pedicle above with the posterior and supe­ rior borders of the pedicle below. These lateral fibres form a portion of the foraminaI ring and the lateral recess.87,88 The interspinous ligament (see Fig. SO.13) lies deeply between two consecutive spinal processes. Unlike the longitudinal ligaments it is not a continuous fibrous band but consists of loose tissue,89 with the fibres running obliquely from posterosuperior to anteroinfe­ rior.9o This particular direction may give the ligament a function over a larger range of intervertebral motion than if the fibres were vertical.91 The ligament is also bifid, which allows the fibres to buckle laterally to both sides when the spinous processes approach each other during extension.89 The supraspinous ligament is broad, thick and cord-like. It joins the tips of two adjacent spinous processes, and

Lamina

(1) and ligamentum flavum

(2).

merges with the insertions of the lumbo-dorsal muscles. Some authors consider the supraspinous ligament not truly as a ligament, as it seems to consist largely of tendi­ nous fibres, derived from the back muscles.92 The effect of the supraspinous ligaments on the stability of the lumbar spine should not be underestimated.93 Because the ligament is positioned further away from the axis of rotation and due to its attachments with the thoracolum­ bar fascia,94 it will have more effect in resisting flexion than all the other dorsal ligaments. Pearcy95 showed that the distance between the tips of the spinous processes increases during full flexion by 360% at L3-L4 and 129% at LS-Sl. By contrast, the posterior longitudinal ligament only increases by SS% at L3-L4 and 34% at LS-Sl. This demonstrates the limiting effect of the ligament on the increasing posterior disc height during stooping. 'The importance of a strong supraspinous ligament in the prophylaxis of recurrent disc protrusions will be discussed later. The intertransverse ligaments are thin membraneous structures joining two adjacent transverse processes. They are intimately connected to the deep musculature of the back. The iliolumbar ligaments (Fig. SO.16) are thought to be related to the upright posture.96 They do not exist at birth but develop gradually from the epimysium of the quad­ ratus lumborum muscle in the first decade of life to attain full differentiation only in the second decade.97 The liga­ ment consists of an anterior and a posterior part.98 The anterior band of the iliolumbar ligament is a well-devel­ oped and broad band. Its fibres originate from the ante­ rior-inferior part of the LS transverse process from as far medially as the body of the LS vertebra to the tip of the transverse process and expands as a wide fan before

CHAPT E R 50 - APPLI E D ANATOMY 7 1 3

2 3

7

6

( a)

Figure 50.16

Iliolumbar ligaments: 1, anterior band; 2, posterior band.

inserting on the anterior part of the iliac tuberosity. The posterior band of the iliolumbar ligament originates from the apex of the L5 transverse process and is thinner than the anterior. It inserts on the iliac crest, behind the origin of the quadratus lumborum.99 The iliolumbar ligaments play an important role in the stability of the lumbosacral junction by restricting both side flexion and rotational movement at the L5-S1 joint and forward sliding of L5 on the sacrum.96,lOO,lOl The clin­ ical importance of this is that posterolateral disc protru­ sions at the level L5-S1 will not be followed by large lateral flexions of L5 on the sacrum. Marked adaptive deformity will therefore be absent here. Consequently, a large lateral tilt in a patient with acute backache means a displacement at L3-L4 or L4-L5, since these interverte­ bral joints can open up more easily.

MUSCLES AN D FASCIAE

The spine is unstable without the support of the muscles that power the trunk and position the spinal segments.102 Back muscles can be divided in four functional groups: flexors, extensors, lateral flexors and rotators (Fig. 50.17). The extensors are arranged in three layers: the most superficial is the strong erector spinae or sacrospinalis

(b) Figure 50.17 (a) Muscles of lumbar spine: 1, transversus abdominis, 2, internal oblique; 3, external oblique; 4, latissimus dorsi; 5, lumbar fascia; 6, erector spinae; 7, psoas; 8, quadratus lumborum. (b) Posterior layer of the thoracolumbar fascia: 1, thoracolumbar fascia; 2, fascia latissimus dorsi; 3, fascia of external oblique; 4, posterior superior iliac spine; 5, lateral raphe.

muscle. Its origin is in the erector spinae aponeurosis, a broad sheet of tendinous fibres attached to the iliac crest, the median and lateral sacral crests and the spinous processes of the sacrum and lumbar spine.103 The middle layer is the multifidus, which originates from the poste­ rior aspect of the sacrum and from the medial part of the iliac spine on the posterior superior aspect. It inserts into the lamina and the spinous processes. The third layer is made up of small muscles arranged from level to level, which have not only an extension function but are also rotators and lateral flexors. The extensor muscles are enveloped by the thoraco­ lumbar fascia (Fig. 50.17b) which in turn consists of three layers. The anterior layer is quite thin and covers the

7 1 4 SEGION TEN - THE L U M BAR SPI N E

anterior surface o f the quadratus lumborum. Medially, it is attached to the anterior surfaces of the lumbar transverse processes, and in the inter transverse space it merges with the intertransverse ligaments. The middle layer lies behind the quadratus lumborum muscle. Medially, it also continues into the intertransverse liga­ ment to attach to the lateral border of the lamina. The posterior layer covers the back muscles. It arises from the lumbar spinous processes and from the supraspinous ligaments to envelop the back muscles and blend with the other layers of the thoracolumbar fascia along the lateral border of the iliocostalis lumbo­ rum. The union of the fasciae is quite dense and forms a strong raphe (the lateral raphe104) which fuses with the fibres of transversus abdominis, internal oblique and latissimus dorsi muscles. The lateral raphe further inserts at the posterior segment of the iliac crest and the posterior superior iliac spine.IOS The flexors of the lumbar spine consist of an intrinsic (psoas and iliacus) and an extrinsic group (abdominal wall muscles). LateraL flexors and rotators are the internal and external oblique, the intertransverse and quadratus lumborum muscles. It should be remembered that pure lateral flexion is brought about only by the quadratus lumborum.

SPINAL CANAL

The spinal canal is made up of the canals of individual vertebrae so that bony segments alternate with interver­ tebral and articular segments. The shape of the transver­ sal section changes from round at Ll to triangular at L3 and slightly trefoil at L5 (see Fig. 50.2).106 The margins of the canal are an anterior wall and a posterior wall, connected through pedicles and inter­ vertebral foramina. The anterior waLL consists of the alternating posterior aspects of the vertebral bodies and the annulus of the intervertebral discs. In the midline these structures are covered by the posterior longitudinal ligament, which widens over each intervertebral disc. The posterior wall is formed by the uppermost portions of the laminae and the ligamenta flava. Because the superoinferior dimensions of the laminae tend to decrease at the L4 and L5 levels, the ligamenta flava consequently occupy a greater percentage of the poste­ rior wall at these levels.87 The poterolateral borders of the posterior wall are formed by the anterior capsule of the facet joint and the superior articular process, which is located well anterior of the articulating inferior articular process. The spinal canal contains the dural tube, the spinal nerves and the epidural tissue.

DURA MATER

The dura mater is a thick membraneous sac, attached cra­ nially around the greater foramen of the occiput, where its fibres blend with the inner periosteum of the skull, and anchored distally to the dorsal surface of the distal sacrum by the filum terminale. The latter descends to the coccyx where its fibres merge with the connective tissue of the sacroiliac ligaments.107 The dural sac itself ends blind, usually at 52. There is an inconstant dural attach­ ment, the 'Hofmann complex',108 made of connective tissue bands and loosely joining the anterior dura to the vertebral column (Fig. 50.18). Ventral meningovertebral ligaments pass from the ventral surface of the dura to the posterior longitudinal ligament. They are variable in structure and may present either as tight bands, bifurca­ tions in Y shape or paramedian bands.109-111 Others reported on more lateral ligaments, passing from the lateral surface of the dural sac and blending with the periosteum of the pedicles.112-115 At the lumbar level, the dura contains the distal end of the spinal cord (conus medullaris, ending at Ll), the cauda equina and the spinal nerves, all floating and buffered in the cerebrospinal fluid. The lumbar roots have an intra- and extrathecal course. Emerging in pairs from the spinal cord, they pass freely through the sub­ arachnoid space before leaving the dura mater. In their

2 •

4 .,,'(I. ,

t

.

", "

Figure 50.18 1, The dura mater; 2, nerve root in the nerve root sleeve; 3, meningovertebralligaments; 4, posterior longitudinal ligament.

CHAPTER 50

extrathecal course and down to the intervertebral foramen, they remain covered by a dural investment. At the L1 and L2 levels, the nerves exit from the dural sac almost at a right angle and pass across the lower border of the vertebra to reach the intervertebral foramen above the disc. From L2 downward, the nerves leave the dura slightly more proximally than the foramen through which they will pass, thus having a more and more oblique direction and an increasing length within the spinal canal. The practical implications of this oblique course of the roots are discussed later. The dura mater has two characteristics that are of cardinal clinical importance: mobility and sensitivity. DURAL MOBILITY

During spinal movements, the canal is subject to varia­ tions in length and shape. It is obvious that all varia­ tions in dimensions of the vertebral canal will influence its contents. The vertebral canal lengthens considerably during flexion: O'Connell1l6 showed by radiological measure­ ments that in full flexion the length of the cervical canal increases by 3 cm, compared with its neutral position. The dura mater, a structure situated in the vertebral canal but anchored at the top and at the bottom will conse­ quently move in the spinal canal. Breigll7 suggests that the dura mater unfolds and stretches. Other authors have found a gliding of the dural sac in relation to the spinal

APPLI E D ANATOMY 7 1 5

canal during flexion and extension.118-121 Using gas myel­ ography, Decker122 showed that the dura moved towards the front of the canal during flexion: like a rubber band, it shifts towards a position of less tension, and is pulled against the anterior wall. Klein12 3 demonstrated an upwards displacement of the dura by more than 5 mm at L3 level during full flexion of the spine. Straight leg raising can put considerable traction on the dural sac. During this manoeuvre the L4, L5, Sl and S2 nerve roots are dragged downwards and forwards (Fig. 50.19). At the level of the intervertebral foramen, the degree of downwards movement is about 0.5 cm.124 In that the root is connected through its dural investment with the distal part of the dura, the latter will also be involved in the downwards movement. Therefore, straight leg raising drags on the dura mater and pulls it caudally, laterally and forwards. 123,125 During neck flexion and straight leg raising, the dura thus moves slightly in relation to the anterior wall of the spinal canal, despite some loose attachments between the posterior longitudinal ligament and the dural sac. Anatomical changes at the anterior walls, for instance a disc protrusion bulging dorsally into the canal, com­ presses the dura. Conversely it can be pulled against this protrusion, whether from below during straight leg raising or from above during neck flexion. The observa­ tion that the dura is mobile thus has considerable clini­ cal significance, in that increase of lumbar pain during neck flexion or during straight leg raising implicates the

I

Figure 50.19

-

Movement of nerve root and dura mater during straight leg raising.

7 1 6 SECTION TEN - THE LU M BAR SPI N E

dura mater a s the source. I n fact, these signs have been accepted for decades to be positive in meningeal irrita­ tion (Kernig's sign and neck retraction) but this mecha­ nism of dural pain was not elucidated until Cyriax's paper was published in 1945 . 126 In the differential diag­ nosis of lumbar pain syndromes 'dural signs' are extremely important in distinguishing a lesion in which the anterior part of the dura mater is involved (disc dis­ placements) from possible lesions at the posterior wall (facet joints and ligaments). DURAL SENSITIVITY

Clinical experiments have shown that the anterior part of the dura is sensitive both to mechanical and to chemical stimulation. 1 27,128 Back pain is also well known in the context of neurological diseases in which the dura becomes inflamed129 or compressed130 Further evidence for dural pain comes from neurosurgical studies that report relief of postlaminectomy pain after resection of the nerves to the dura.1 31 From the 1 950s, numerous neuroanatomical studies have been conducted that describe the innervation of the dural tube.1 32 Several authors have shown that the ventral half of the dura mater is supplied by small branches of the sinuvertebral nerve.133,1 34 Further work has confirmed that the innervation is from the sinu­ vertebral nerves and is confined to the anterior part of the dura only. 13 5 ,1 36 During the last decade, immunohistochemical studies clearly demonstrated a significant number of free nerve endings, containing substance P, calcitonin generated peptides and other neurotransmitters contributing to nociception.1 37,1 38 All these findings have been confirmed and extended recently so that the present concept is of a dense longitudinally orientated nerve plexus in the ventral spinal dura, extending over up to eight segments, showing a great deal of overlap between adjacent levels and crossing the midline.B9,14o The anterior part of the dura mater is thus innervated by a mesh of nerve fibres which belong to different and consecutive sinuvertebral nerves (Fig. 50.20). This probably explains the phenome­ non of 'dural pain', which is a pattern of large and broad reference of pain, covering different dermatomes, com­ monly found in low back syndromes. The patient then describes lumbar pain, radiating to the abdomen or up to the chest, to the groin or to the front of both legs . 141 NERVE ROOTS DEFINITION

The spinal cord terminates at the level of T12-Ll. Consequently the lower lumbar and sacral nerve roots

Figure 50.20 The anterior part of dura mater is innervated by a mesh of nerve fibres belonging to different and consecutive sinuvertebral nerves. 1, anterior part of the dura; 2, posterior part of the dura; 3, nerve root; 4, sinuvertebral nerve. Reproduced with permission from Groen.140

must run within the vertebral canal. The motor (ventral) and dorsal (sensory) rootlets that take their origin in an uninterrupted series of attachments at the ventrolateral and the dorsolateral aspects of the cord, run freely down­ wards through the subarachnoid space of the dural sac. The rootlets that form one 'nerve root' are gathered into pairs before they leave the dural sac. They do so by taking with them an extension of dura mater and arach­ noid mater, referred to as a 'dural sleeve'. The pair of roots, covered by dura mater is called the illtraspinal, intrathecal part of the spinal nerve. The pairs of spinal roots join at the level of the foramen. Immediately proximal to its junction with' the ventral root, the dorsal root forms an enlargement - the dorsal root ganglion - which contains the cell bodies of the sensory fibres in the dorsal root. Distal to the junction at the foramen, the dura mater merges with the epineurium of the spinal nerve. From here the extraspinal part of the spinal nerve begins.l13 BOUNDARIES

The entire course of the intraspinal part of the spinal nerve is enveloped by the radicular cana[142 or spinal nerve root canal,143 The term lateral recess has been applied to the bony boundaries of this radicular canal.144 The radicular canal is a small cone-shaped osteofibrous space, which begins at the point where the nerve root leaves the dural sac and ends at the lateral border of the intervertebral foramen. It thus shelters the complete extrathecal nerve root in its dural sheath. The direction of

CHAPTE R 50 - APP LI E D ANATOM Y 717

the canal is caudal, lateral and slightly anterior. The ante­ rior wall is formed by the posterior aspects of the vertebral body and intervertebral disc, both partly covered by the posterior longitudinal ligament. The posterior wall is the ligamentum flavum, the lamina and the corresponding superior articular facet. The medial wall is the dura mater. The lateral aspect of the radicular canal is formed by the internal aspect of the pedicle and is continuous with the intervertebral foramen. The length of the radicular canal increases from L3 to 51, so making the L5 and 51 roots more liable to com­ pression. The L3 nerve root travels behind the inferior aspect of the vertebral body and the L3 disc. The L4 nerve root crosses the whole vertebral body to leave the spinal canal at the upper aspect of the L4 disc. The L5 nerve root emerges at the inferior aspect of the fourth lumbar disc and crosses the fifth vertebral body to exit at the upper aspect of the L5 disc (Fig. 50.21).1 45,146 Further clinical applications of this downward direction of the nerve roots are: • • •

At L4 levet a disc protrusion can pinch the fourth root, the fifth root or, with a larger protrusion, both roots. At L5 level, a disc can compress the fifth root, the first sacral root or both. Root L5 can be compressed by an L4 or an L5 disc.

( a)

It should, however, be remembered that aberrant courses and anastomoses exist between the lumbar nerve roots147 which may be present in about 4% of the population.148 The intervertebral foramen149 is the point of emergence of the spinal nerve from the canal (Fig. 50.22). It is located in a sagittal plane, so it can be demonstrated perfectly on a plain lateral radiograph. The foramen is limited cranially by the upper pedicle and caudally by the pedicle below. The anterior wall corresponds to the posterior aspect of the vertebral body and the disc. The posterior wall of the intervertebral foramen is formed by the articular facets. The size of the fClramen increases from T12-Ll to L4-L5, but the foramen L5-51 is the smallest of all and is located slightly more anteriorly.

ANATOMY

The radicular canal contains the intraspinal extrathecal nerve root. The nerve root consists of a sheath (dural sleeve) and the fibres. Each structure has a specific behaviour and function, responsible for typical symp­ toms and clinical signs (see Box 50.1). From a clinical point of view, disorders of the outer investment cause pain and loss of mobility, whereas problems with the

Arachnoid

(b)

Dura -------9 Subarachnoid space --�='!\Pia -------t----\\ Dorsal root ----="=�\\. Ventral root ----�,__ Dorsal root ganglion

-------"�-"---

Dural sleeve Spinal nerve

Sinuvertebral nerve

Disc

-----!Il,L,4,L,4'+!-,r//j

----I I-tI I

Pedicle

Dura

Figure 50.21

(a) Course of the lumbar nerve roots; (b) anatomy of the nerve root.

Ventral ramus Dorsal ramus

718 S E CT I O N T E N - T H E L U M BA R SPI N E

Figure 50.23

The relationship between the nerve root and dural sheath: dural pouch; 3, dural sleeve of nerve root .

1, dura mater; 2,

Figure 50.22

Intervertebral foramina.

Box 50. 1 Nerve root behaviour Sheath

Fibres

Respo n s i b l e for:

Respons i b l e for:

Seg me ntal pain

Paraesthesia

M o b i l ity

C o n d u ctivity

arachnoid space forms a bilaminar tube within the root sleeve as a whole.150 At the foramen, the epidural tissue becomes more con­ densed and forms a loose ligamentous fixation of the epineural sheath to the bony boundaries of the interver­ tebral foramen. A stronger ligament (the so-called 'lateral root ligament'; Fig. 50.24), connecting the epineural sheath to the pedicle, has also been described.151 It has been suggested that the fixation of the dural sleeve, together with the anterior attachment of the dura to the posterior longitudinal ligament could be of some impor­ tance in the mechanism of sciatica.152 Simple mechanical

nerve root itself cause symptoms and signs manifest in the territory of its supply. Pressure and inflammation of the sheath first provokes pain and impaired mobility but more substantial compression of the root will also affect the nerve fibres, which leads to paraesthesia and finally to interference with conduction. The dural sheath The dural sheath (Fig. 50.23) starts as a funnel-shaped pouch, enclosing the anterior and posterior roots at their exit from the dural sac. The dural nerve root sleeve proper is formed at the end of this short pouch and con­ tinues distally to the foramen, where it merges with the connective tissue sheath of the ganglion and the spinal nerve. The dural investment of the nerve root therefore does not extend beyond the lateral border of the vertebral foramen. In this sleeve, the anterior and posterior roots no longer lie free but are firmly bound to the dural sleeve by the arachnoid membrane. In other words, the sub-

Figure 50.24

The lateral root ligament.

CHAPTER 50

analysis suggests that pressure applied to the nerve root by a' disc protrusion is determined by the extent of the dural ligament fixation rather than by the compression of the root against the posterior wall. The dural investment of the nerve root is, as is the dural sac, sensitive and mobile. Although the intervertebral foramen represents a point of relative fixation of the nerve, some caudal migration of the latter remains possible.153 Distal traction on the sciatic nerve and lumbosacral plexus thus pulls the nerve root downwards and drags on the dural sheath and the dura. This occurs during straight leg raising, when the nerve roots of L4, LS, Sl and S2 are moved down­ wards at the level of the intervertebral foramen.124,154,155 The main range of motion of the Sl root is 4 mm, of LS 3 mm and of L4 1.5 mm. Straight leg raising does not pull directly on the L3 root. This structure can only be moved caudally during knee flexion in the prone position, which stretches the femoral nerve.156 It is not possible to test the mobility of the S3 and S4 roots, because they do not reach the lower limb. Because of the downward and anterior direction of the nerve roots and the relative fixation of the dural invest­ ment at the anterior wall, a downwards movement of the nerve always involves anterior displacement, which pulls the root against the posterolateral aspect of disc and vertebra. Restriction of nerve root mobility therefore always means anterior compression of the root. Internal rotation of the hip during straight leg raising adds more tension to the lumbosacral plexus and nerve roots.157 To clinicians this is not surprising, because it is common to see patients with considerable limitation of straight leg raising, actively rotating their hips laterally when it is performed, thus protecting the inflamed root against further traction. Cyriax drew attention to two interesting phenomena in relation to the mobility of the nerve root sheath, ncfmely the existence of a painful arc and the aggravation of the pain during neck flexion. ISS Mobility.

•

•

It is a common clinical finding that patients with sciatica show momentary pain during straight leg raising: there is pain only in a certain sector of movement (usually between 45 and 60°). The most acceptable explanation for this curious sign is that a small discal bulge exists over which the root slips and thereafter the rest of the movement is painless. This painful arc during straight leg raising always implies a small disc displacement and is a good indication that reduction by manipulation or traction is possible. The dural sheath can also be stretched from above. As we have seen previously (in the section on dural mobility), the dura can slip upwards during neck flexion. If a pain brought on by straight leg raising is

-

APPLI E D ANATOMY 7 1 9

aggravated b y neck flexion, the tissue thus stretched must run in a continuous line from the lumbosacral plexus to the neck. Only the dura mater and its continuations, the dural investments, can possibly be stretched from above and below at the same time. Sensitivity of the dural investment. Dural root sheaths are innervated by the sinuvertebral nerve,135 and each sheath receives branches from the nerve of the corre­ sponding side and level only (Fig. 50.25). In contrast to the anterior aspect of the dural sac, anastomoses between branches of adjacent sinuvertebral nerves do not exist. Pain originating from the dural sheath is therefore strictly segmental and follows the corresponding dermatomes in the limb.159 Compression of the spinal nerve beyond the interver­ tebral foramen does not generate pain but only pins and needles, numbness and paresis. This is the case when a disc protrusion has passed very laterally, when the fifth lumbar nerve is compressed between a corporo­ transverse ligament and the ala of the sacrum,52 or in some spondylolitic compressions of the nerve root. Experience during the performance of a sinuvertebral block also confirms the insensitivity of the nerve root fibres. When the needle, just before touching the

4

�+-- 2

4

5

3

Figure 50.25 Innervation of the nerve root sheath: 1, posterior ramus; 2, anterior ramus; 3, sinuvertebral nerve; 4, dura mater; 5, posterior longitudinal ligament.

720 SECTION TEN - THE LUM BAR SPINE

posterior aspect of the vertebral body, brushes against the nerve root, no pain but a sharp 'electric' shock results. As the dural investment of the root ends at the same level, it must be concluded that the latter is responsible for the radicular pain in sciatica . I ss Nerve root The structure of the nerve root differs from that of the peripheral nerves in three ways: the epineurium is less abundant, the fasciculi do not branch and the perineurium is missing. Thus, compared with a periph­ eral nerve, the parenchyma of the nerve root is more susceptible to injury, by either mechanical or chemical irritation.1 60 Irritation of the parenchyma leads to paraesthesia. Unlike 'radicular' pain, which is merely a symptom of compression of the dural sheath, pins and needles indicate that the nerve fibres are irritated as well. Paraesthesia is thus a symptom of direct involvement of the nerve root . Further irritation and destruction of the neural fibres leads to interference with conduction, resulting in a motor and/or sensory deficit. That the motor and sensory components of the nerve root remain com­ pletely separated during the course of the nerve root along the radicular canal has some clinical conse­ quences: it is possible for a nerve root compression to cause a pure motor paresis or a pure sensory deficit. If pressure is exerted from above, sensory impairment may result, whereas an impingement from below can induce a motor paresis. A larger protrusion, pressing between two roots, can result in a motor palsy of the root above, together with a sensory deficit of the nerve root below (Fig. 50.26). Controversy still exists over the mechanism of nerve root compression by a protruded disc. Inman and Saunders1 61 stated that the nerve root is rarely 'com­ pressed' between anterior and posterior wall, but is merely brought under tension by the disc herniation.

Figure 50.26

Protrusion pressing between two roots.

Others have observed that the extrathecal, intraspinal nerve root is relatively fixed to the anterior wall and the intervertebral foramen by the dural ligamentous complex and the foraminal complexlS4,162 (see p. 718). Therefore, this particular part of the root cannot easily slip away from a disc protrusion and is tethered over it, and a pressure-induced nerve lesion can develop.152 These anatomical findings probably help to explain why the magnitude of signs and symptoms in sciatica do not necessarily correspond to the magnitude of the disc protrusion and also why many asymptomatic protru­ sions exist. The amount of interference with conduction is related to the degree of the compressing force, which in turn depends not only on the magnitude of the pro­ trusion but also on the tightness of the dural fixation to anterior wall and intervertebral foramen. The involvement of nerve fibres is tested during clin­ ical examination: resisted movements and the reflexes test the integrity of the motor fibres, while cutaneous analgesia indicates loss of sensory conduction. Interference with conduction suggests that an attempt to achieve reduction by manipulation or traction will fail. In general, a disc lesion affects only one nerve root and the neural effects are rather subtle. As described above, combinations of sensory and motor effects or their independent existence may occur. It is also possi­ ble for two roots to be pinched by one disc protrusion, which can be the case at the L4 level where a combined fourth-fifth palsy can occur, probably resulting in a drop foot, or at the L5 level where a combined fifth lumbar-first sacral deficit can occur. Massive pressure may finally cause ischaemic root atrophy and then complete loss of sensitivity of the sheath occurs. Reflex hamstring contraction to protect the nerve root no longer takes place and straight leg raising becomes full range, despite the massive disc protrusion and the complete lesion. Conclusion For clinical purposes it is as well to divide the compo­ nents of the nerve root into an external aspect (the sheath), which is mobile and is responsible for pain, and an internal aspect (the nerve fibres), which serves con­ duction only. To do so helps to distinguish symptoms and signs of each, so permitting a good assessment of the location of a lesion, the magnitude of compression and the degree of functional incapacity (see Box 50.2). In nerve root compressions by a displaced disc, the development of symptoms and signs allows the anatom­ ical changes in the radicular canal to be followed: slight pressure will only involve the sheath of the �oot (Fig. 50.27), giving rise to pain in the corresponding dermatome and probably impaired mobility, reflected by alterations in straight leg raising. Greater pressure will

CH APTER 50 - APP L I E D ANATOMY

Box 50.2 Neurological deficit at each level , L 1 Compression of the L 1 root produces neither paraesthesia nor muscle weakness and cuta neous a n a lgesia is only found below the inner half of the i n g u i n a l l i g a ment

L2 Involvement of the L2 root causes p a raesthesia a n d a n a lgesia over t h e a nterior aspect o f t h e t h i g h , from the groi n to the pate l l a . M uscle wea kness is found i n the psoas.

721

result in pressure on nerve fibres, reflected in paraesthe­ sia at the distal end of the dermatome. Clinical examina­ tion will now reveal not only interference of mobility but also impaired conduction - a sensory deficit and / or loss of motor power. Greater pressure causes root atrophy, which results in loss of sensitivity of the dural sheath and gives a painless straight leg raising test. At the same time the sensory deficit and motor palsy become com­ plete (see Fig. 50.30).

L3 Interference of conduction in the L3 root causes paraesthesia at the anterior a spect of the leg from the dista l t h i rd of the thigh, over the knee a n d the lower leg, down to the a n kle. Cuta neous a n a l gesia exte nds from the pate l l a a l ong the front a n d the i n n e r aspects of the leg, a n d ends j ust a bove the a n k l e . The wea k muscles a re psoas a n d q u ad r i ceps a n d the knee jerk is slugg ish or absent. '

L4 Compression of L4 has the following c l i n ica l s i g ns: paraesthesia at the outer leg and the b i g toe, sensory deficit at the lateral aspect of the lower leg, over t h e foot u p to the b i g toe, a n d wea kness of the extensor h a l l ucis and the t i b i a l i s anterior m uscles.

L5 I nvolvement of the L5 root res u lts in p a raest h e s i a at the outer leg, t h e front of the foot and t h e b i g a n d two adjacent toes, a n d cuta neous a n a l gesia of t h e o u t e r leg, the dorsum of t h e foot a n d t h e i n n e r t h ree toes. Weakness is found at t h e exte nsor h a l l uc i s

EPI DURAL SPACE

The virtual space between the dural sac, the dural sheaths of the nerve roots, and the spinal canal is the epidural space. This space is quite narrow because the dural sac lies very close to the boundaries of the vertebral canal and is filled with a network of loose connective tissue, fat, arteries and a dense network of veinsJ63 The sinuvertebral nerve is in the anterior half of the epidural space. The venous system is extensive and valveless, with multiple cross connections. Batson1 64 has described retrograde venous flow from the lower pelvis to the lumbosacral spine, which probably provides the route for metastases and infections spreading from the pelvic organs to the spine.

long us, the peroneal a n d g l uteus med i us m uscles.

51 Compression of the S1 n e rve root shows the fol lowing signs: paraesthesia at the two outer toes, n u m bness at the calf, the heel and the latera l aspect of the foot. The weak muscles a re the calf muscles, the h a mstring, the g l uteus maximus and the peronei

52 Involvement of the S2 root results in p a raesthesia at the heel a n d cuta neous a n a lgesia at the poster i o r aspect of the t h i g h, the calf a n d the h e e l . The calf m u sc l es, the ha mstri ngs a n d the g l utea l mass a re wea k .

53 Neural deficits can not be detected i n S 3 lesions 54 Parenchymatous lesions of the S4 root res u lt in paraesthesia in the peri neum, vag i n a o r pen is, a n a l a n a l g esia, a n d funct i o n a l d i sorders o f t h e bladder a n d

INNERVATION

The spine is innervated by the sinuvertebral nerve and the posterior primary ramus. All the tissues lying poste­ rior to the plane of the intervertebral foramina at each level (i.e. the facet, the vertebral arch, the related tendi­ nous and aponeurotic attachments and the flaval and interspinous ligaments) are innervated from the posterior primary rami. Those anterior to the intervertebral foram­ ina (longitudinal ligaments, anterior dura and dural sleeves) are supplied by branches of the sinuvertebral nerves (Wyke, cited by Cyriax165).

rectum, u s u a l l y i ncontinence

SINUVERTEBRAL NERVE

pain

pain

+ +

(paraesthesia) palsy ±

pain + / ­ (paraesthesia) palsy + +

Figure 50.27 Symptoms and signs of a compressed nerve root vary according to the intensity of compression.

The sinuvertebral nerve was first described by Luschka in 1850.166 It emerges from the anterior aspect of the spinal nerve, distal to the nerve ganglion, and receives some sympathetic branches from the ramus communi­ cans.22 In the fetus the nerve is composed of several filaments which may become bound together during later life, to form the adult sinuvertebral nerve.J 32 The composite nerve is between 0.5 and 1 mm thick,167 passes through the intervertebral foramen and points upwards around the base of the pedicle, to pass along the cranial side of the corresponding disc to reach the

722 S E CT I O N T E N - T H E L U M BAR S P I N E

medial aspect of the posterior longitudinal ligament. Here it divides into ascending, descending and trans­ verse branches, which anastomose with the sinuverte­ bral nerves of the contralateral side and with those from adjacent levels. Therefore, instead of a recognizable nerve trunk, the sinuvertebral nerve is represented by a network of overlapping fine filaments from different levels and from both sides (Fig. 50.28).168 Branches of the sinuvertebral nerve supply the verte­ bral body, the outermost layers of the annulus fibrosus, the posterior longitudinal ligament, the anterior aspect of the dural sac and the dural investments around the nerve roots. Branches of the sinuvertebral nerve also surround the blood vessels of the vertebral canal. The posterior aspect of the dura is devoid of nerve endings.

There is still disagreement as to whether the ligamen­ tum flavum and the lamina are innervated by the sinu­ vertebral nerve.

POSTERIOR PRI MARY RAMUS

Distally from the intervertebral foramen, the spinal nerve divides into a large anterior branch and a smaller posterior ramus (Fig. 50.29). The latter divides almost immediately into a medial and a lateral branch,1 69 although a smaller intermediate branch has also been identified.84 The medial branch descends posteriorly to the trans­ verse process, where it lies in a groove formed by the junction of the superior articular and transverse processes. A strong fibrous band transforms this osseous groove into an osteofibrous tunnel. At this level a branch innervates the inferior part of the articular capsule of the facet joint. The nerve continues its course caudally on the lamina, to supply the dorsal muscles and the superior part of the articular capsule of the facet joint of the level below.17o Each medial branch thus supplies the facet joints above and below its course. Consequently, each facet joint is innervated by two consecutive medial branches. I 71,I 72 The lateral branch of the posterior ramus emerges between the deep layer of the lumbodorsal fascia and the lateral edge of the lamina. It supplies the muscles and the fascia. The lateral branches of the ramus posterior have cutaneous nerves and reach distally as far as the greater trochanter.134

3

Figure 50.28 Dural nerve branches. 'Cut pedicle of a vertebral arch; cv, vertebral body; di, intervertebral disc; drg, spinal ganglion; rv, ventral ramus of spinal nerve. Reproduced with permission fro m Groen GJ ( 1 990).

Figure 50.29 Posterior primary ramus: 1 , medial branch; 2, lateral branch; 3, sinuvertebral nerve.

CHAPTER 50

Symptom

Sign

Symptom

Pain

Mobility

Paraesthesia

Motor deficit

Sensory deficit

Reflex disturbances

None

None

None

Inner half inguinal ligament

None

Root

L1

:�

1\

f±J

Femoral stretch

Figure 50.30

I

r�il'

Psoas quadriceps

\)

\)

\,

�

I'

�

r

SLR

k,

Tibialis anterior, Extensor hallucis longus

Symptoms and signs of nerve root compression at each level.

Knee jerk

Knee jerk

��

��

SLR

None

J

r;i

�

L5

I

Psoas

1\

L3

L4

None (femoral stretch )

�

,r

Signs

I

lu

If

APPL I E D ANATOMY 723

Nerve fibres

Sheath

L2

-

Extensor hallucis longus, Peronei, Gluteus medius

Ankle jerk

724 SECTION TEN - T H E L U M BAR SPI N E

Nerve fibres

Sheath

Root

Figure 50.30

Symptom

Sign

Symptom

Pain

Mobility

Paraesthesia

Signs Motor deficit

Sensory deficit

Reflex disturbances

S1

SLR

Peronei, Calf muscles, Hamstrings, Gluteal muscles

S2

SLR

Calf muscles, Hamstrings, Gluteal muscles

S3

None

None

None

None

None

S4

None

Perineum

Sphincters

Perineum

None

(Continuecf)

Ankle jerk

Ankle jerk

CHAPTER 50 - APPL I E D ANATOMY 725

REFERENCES
the affected intervertebral joint opens, i.e. gives the loose fragment room to move.

CHAPTER 59 - TREATMENT OF THE LUMBAR SPINE 877

•

The manipulation is usually carried out during trac­ tion. This tautens the posterior longitudinal ligament and causes suction in the disc so exerting a centripetal force (Fig. 59 .3) .

Most o f our techniques are non-specific long-lever manipulations: the force is exerted on a part of the body some distance away from the area where it is expected to have its beneficial effect. Leverage enables the manipula­ tor to apply more force at the affected level. The normal joints are moved as far as they can go. The posterior lon­ gitudinal ligament becomes taut. At the moment resist­ ance of the blocked joints and the taut ligament is felt, a quick additional thrust is given, to act at the affected level. Manipulation of the lumbar spine is either quickly successful or fails. If, after one or two manoeuvres performed in a certain direction, signs and symptoms remain unaltered, another direction or another technique is tried. If these also prove ineffective, manipulative treat­ ment is abandoned. I f, by contrast, manipulation has led to reduction, both local and referred d iscomfort cease. Previously painful movements become normal immedi­ ately. So it is the patient, rather than the manipulator, who judges the effect of treatment. Most other manipulative schools claim to work more selectively, i.e. on the affected level only. They claim to have developed the clinical skills to localize, by palpa­ tion, the exact site of the ' fixation' or 'locking'. Several studies have failed, however, to demonstrate the reliabil­ ity of this.52-57 We support the conclusion of McKenzie58 that demystification of spinal manipulative therapy is an

urgent priority. Both chiropractice and osteopathy thrive by creating the impression that there is something complex and exclusive about the practice of passive end­ range motion that only chiropractors or osteopaths can understand or have the skills to ' feel'. They generate the belief that, in order to become skilled in the understand­ ing and delivery of spinal manipulative therapy, it is necessary to undergo 3 or 4 years of training.59 This suggestion is undermined by the fact that the majority of lay manipulators in Britain have never had any tuition at all and yet have amassed many satisfied clients and also very rarely figure in actions for damages.2o The main advantages of the methods discussed in this book are, first, that they are much simpler but at least as effective as those advocated by chiropractors and osteopaths. Second, it takes only about 180 hours of tuition, provided that the student has completed medical or physiotherapy studies. In orthopaedic medicine, the manoeuvres are always intended to relieve the actual cartilaginous displacements. This is in contradiction to other methods, where a proto­ col of regular or intermittent manipulation sessions is commonplace. The type of displacement as well as the patient has to be assessed before any kind of mani pulative manoeuvre is undertaken. •

The displacement should be cartilaginous, not too large and not placed too far laterally. Soft nuclear protrusions are

seldom reduced by manipulation unless they are small and very recent and the technique of manipulation is changed to sustained pressure. If the consistency of the

Figure 59.3 Effects of long-lever manipulations. Positioning of the spine 'opens' the intervertebral space. A combination of traction and rotation produces a torque with tautening of the posterior longitudinal ligament and helicoidal traction on the lateral part of the annulus.

878 SECTION TEN - THE LUMBAR SPINE

•

displacement is not quite clear, with symptoms and signs pointing in opposite directions, it is worth while making one attempt at manipulation. During the first session it is usually quickly apparent whether reduction by this means will prove feasible or not. If it fails, traction is substituted the next day. Reduction of cartilage displacements, together with full relief of symptoms and signs, has proved to be possible in two-thirds of all cases of backache and in one-third of all cases of sciatica.6o Just about half of all lumbago cases are relieved in one treatment.61,62 T17e patient must be mentally stable and keen to get well. If this psychogenic aspect is neglected, on some occa­ sions a patient may be treated who claims to have been made worse by a type of therapy that is regarded in retrospect as unacceptable. Hence it is important to avoid these active methods of treatment when the patient's attitude appears to be more important than the minor mechanical disorder found on examination.

INDICATIONS FOR MANIPULATION History and clinical examination almost always supply sufficient information to select those cases suited to manipulation (see Box 59.3, p. 879).

Acute annular lumbago. The attack is initiated by a click in the lower back, followed by a sudden agonizing lumbar pain fixing the back in slight flexion or lateral deformi ty. The pain radiates in an extrasegmental way and there are marked dural signs and symptoms. Reduction should always be attempted, except in hyperacute cases, where the attempt proves impossible to bear. An epidural injection is then substituted and fol­ lowed by manipu lation the next day. If such an injection is refused, it is still possible for the patient to recover in about a fortnight by bed rest and the use of McKenzie's extension mobilizations58 and anti-deviation techniques. The moment the process has ceased to be hyperacute, treatment by manipulation can be tried again. Backache. Acute or recurrent backache that has started suddenly usually responds well to manipulative treat­ ment. There are a number of symptoms and signs that are indications to expect that manipulation will be successful. The description of a click and sudden pain in the back on bending forward or on coming upright from a forward-bent or sitting position indicates displacement of a small cartilaginous fragment. Another ' favourable symptom' is the patient's age because, over the age of 60, nuclear protrusions no longer occur and a hard and mobile fragment of disc material is very likely. ' Favourable signs' are: (a) a partial articular pattern in which some movements are only painful at extreme

Box 59.1 Symptoms and signs favouring manipulative treatment of backache Favourable symptoms

Favourable signs

Patient over 60 years Sudden onset of pain: On bending forward Or on coming up

Partial articular pattern Side flexion away from the painful side hurts most Painful arc with or without momentary deviation Absence of gross deviation Absence of gross limitation on movement

range, for example flexion, extension and side flexion away from the painful side; (b) the existence of a painful arc with or without momentary deviation; (c) absence of gross deviation caused by muscle spasm on standing or during as much flexion as the patient is capable of; (d) absence of gross limitation on movement - gross devia­ tion or limitation of movement always requires several sessions of manipulation (Box 59.1). However, some small protrusions do not respond well to manipulation. Patients under 60 years of age and in whom the pain is greatest on pinching the lesion by side flexion towards the painful side are usually ' unfavourable'. If such a manoeuvre causes pain in the lower limb instead of the lumbar region or upper buttock, manipulation nearly always fails. A better response will be achieved with traction.

Sciatica. Reduction proves possible in about a third of all patients with sciatica. Again several symptoms and signs indicate those patients who can be expected to respond well (Box 59.2). Patients with mixed protrusions. If neither the symptoms and signs nor the patient's age establish the consistency of the displaced fragment, manipulation should be tried first: it is quickly clear whether this is effective or not. In contrast, traction usually requires a week before efficacy can be determined.

Box 59.2 Symptoms and signs favouring manipulative treatment of sciatica Favourable symptoms

Favourable signs

Backache still continues after root pain has begun Root pain is recent

Lumbar extension and side flexion hurt in the back not in the limb Absence of deviation or muscle spasm Straight leg raising is only moderately limited, with absence of spasm of the hamstring muscles ' Absence of neurological deficit

CHAPTER 59

Patients over the age of 60. The rules that determine a nucl�ar or an annular lesion are no longer applicable over the age of 60 years. The nucleus has become hard and dry and will react correspondingly. Bed rest is wholly ineffec­ tive because there is no great d ifference in intradiscal pressure on lying and standing and as the tension of the posterior longi tudinal ligament lessens, it becomes elon­ gated and loses its ability to apply a correcting centripetal force. Hence all discodural or discoradicular interactions in this age group are best treated by manipulation, as this is the only way to achieve reduction. However, for elderly patients, manipulative treatment should also be adapted. This means that only one or two manipulations are performed during a session. The inter­ val between two sessions is also extended, say to once a week. The intensity of each technique should not be changed, however, otherwise the centripetal forces acting on the joint at the moment of manipulative thrust are too small to influence a displacement. Lumbar manipulations are not contraindicated in osteoporosis. However, some techniques are not used for fear of fracturing a bone.

-

TREATMEN T OF THE LUMBAR SPINE 879

Box 59.3 Manipulation Indications Acute annular lumbago Backache with favourable symptoms/signs Sciatica with favourable symptoms/signs Mixed protrusions Patient over 60 years

Contraindications Danger to S4 roots Anticoagulant therapy Aortic graft Last month of pregnancy Weakened body structures Muscle spasm Seriously neurotic patients

Not useful Too painful Too large a protrusion Too soft Too long a duration of root pain Compression phenomena After laminectomy. protrusion at the same level Unfavourable articular signs in: Backache Sciatica Primary posterolateral protrusion

CONTRAIND ICAT IONS These may be divided into circumstances in which manipulation is absolutely contraindicated and those in which manipulation is of no use although not harmful to the patient (see Box 59 .3) . Appropriate selection of patients and choice of techniques can avoid such serious complications as have been reported.63,64

Absolute contraindications Da nger to the fourth sacral roots. 65-67 Although these roots lie in the centre of the spinal canal, well protected by the posterior longitudinal ligament, they may be threatened by a massive central lumbar disc prolapse which has caused considerable bulging and possibly partial rupture of the posterior longitudinal ligament. Manipulation may rupture this ligament completely, causing extrusion of the entire disc. The important symptoms of an S syndrome are rapid 4 progression of bilateral sciatica and neurological symp­ toms in both legs. Pain and paraesthesia in the perineum, rectum, genitals or anus are other symptoms suggesting this menacing lesion. Finally bladder weakness, causing frequency of micturition without a strong urge, loss of rectal tone and faecal incontinence result. Acute lumbago and bilateral sciatica with compres­ sion of the nerve roots at the same level are examples of a large central protrusion in which bulging of the pos­ terior longitudinal ligament is to be expected. Such a protrusion may also cause spinal claudication. These

patients have symptoms during walking, immediately relieved by lying down.68 In all these conditions, a high-force rotational tech­ nique in the side-lying position could rupture the last protecting fibres of the posterior longitudinal ligament with massive extrusion of the entire disc.

Anticoagulant medication. Manipulation of patients on anticoagulant therapy may lead to an intraspinal haematoma.69 A patient who has a clotting abnormality should also not be subjected to forceful manipulations. Aortic g raft. Although there has not been a report of damage at the junction of a graft in the aorta by manipu­ lation, its presence is reasonably regarded as a contra­ indication to any forceful manipulation - rotations or extension thrusts. Final month of p reg nancy. During the final month of pregnancy, lumbar manipulation is impracticable. Rest in bed or epidural local anaesthesia are alternative pos­ sibilities. There is no bar to manipulation during the first 4 months; after this, extension techniques which necessitate a prone-lying position are omitted . Manipulation should not be employed at any time if there is any predisposition to miscarriage. Wea kened bon e structure . This includes unstable fractures, severe osteoporosis, osteomyelitis, multiple myeloma and bony tumours.

880 SECTION TEN - T H E LUMBAR SPI N E

Muscle spasm. Forced movements should never b e used when there is obvious muscle spasm, which may indicate some kind of joint irritability, fracture or metastasis. Therefore, any sign of muscle spasm at the moment the lumbar spine is positioned and the manipulator starts to stress the affected intervertebral joint, should be taken as a sign to stop the procedure immediately. Of course, such a warning sign should already have been detected by an adequate clinical examination. Menta l state. Seriously mentally disturbed patients should not be treated by manipulation, even if there is an underlying disc protrusion which seems suitable for manipulative treatment. The symptoms largely exist in the patient's mind and indicate certain needs - compen­ sation or protection - and it can be expected that manip­ ulation will fai l or even aggravate the disorder. In addition, an obsessional neurosis about vertebral dis­ placement may result. This not only may make manipu­ lation troublesome to undertake but also may cause the patient to blame the treatment for making matters worse.

CASES IN WHICH MANIPULATION IS NOT USEFUL

Too much pai n. In hyperacute lumbago manipulation is impossible because of unbearable pain at any attempted movement. These patients are best treated by the imme­ diate induction of epidural anaesthesia and manipulation is postponed until dural irritation has mostly ceased. Too large a protrusion. There are two categories. Protrusions causing impaired root conduction. All such protrusions are impossible to reduce either by manipula­ tion or traction. If clinical signs of muscle weakness, cuta­ neous analgesia or reflex disturbances are p resent, the protrusion is too large (and located too far laterally) to be replaced.38,67,7o-73 Epidural local anaesthesia is the treat­ ment of choice. Sciatica with an excessive flexion or side flexion deformity.

In such cases, an attempt to move in the contrary direction causes pain to shoot down the leg. Laminectomy or chemonucleolysis is indicated.

Too soft a protrusion. Nuclear protrusions causing back­ ache and sciatica do not respond to manipulation (except in small and very recent cases, and provided that the manipulation technique is changed to sustained pres­ sure). The consistency of the protrusion is too soft to be influenced by a quick thrust. Traction is the treatment of choice. The history is rather typical and usually identifies this type of disc lesion. Acute nuclear lumbago is also an example of a protru­ sion too soft to manipulate with a thrust. The history is of pain that began gradually, after doing much stooping and

lifting, and became slowly worse over the next few hours. The following morning the patient wakes unable to get out of bed because of severe lumbar pain. The patient is always under 60 years old and, although manipulation is indicated, it must be exerted by sustained pressure. If this makes the patient better, techniques in the supine, side­ lying, and standing positions to correct a persisting lateral deviated position of the trunk should follow (see pp. 890-892). Alternatively, an epidural injection can be tried, again followed the next day by manoeuvres to correct a lateral deformity. However, if these measures all fail, constant pelvic traction in a supine position and continued for some days is called for, slowly changed to periodic half an hour daily traction. Extension mobilizations, as rec­ ommended by McKenzie,58 have also been found to be effective, a treatment explained by him on the hypothesis that the flow or displacement of fluid, nucleus or sequestrum can occur within the intact annulus of the intervertebral disc as a result of prolonged or repetitive loading. This most commonly occurs with flexion loading. He recommends well-defined extension forces in order to reverse the direction of flow or displacement.

Too long a duration of root pain. In patients under 60 years, 6 months of root pain has been shown to be the limit for manipulative reduction. However, if back­ ache persists together with root pain, manipulation should be tried because these patients often do not recover spontaneously. Compression phenomena. Central stenosis, lateral recess stenosis and the 'self-reducing' disc protrusion do not respond to manipulative treatment. In stenosis, the under­ lying condition is the reason that attempted manipulation or traction fails.71,74, 75 The self-reducing disc protrusion, with symptoms at the end of the day only, may be reduced by manipulation but will prove to be transient anyway.38 After laminectomy. New protrusions, at the same level, are seldom successfully reduced by manipulation. Traction is often more effective. Unfavourable articular signs in a patient under 60 years. In backache, side bending towards the painful side is an unfavourable sign for manipulation but this does not apply in lumbago. If any movement other than flexion hurts in the lower limb instead of the back, manipulation is almost certain to fail. If an attempted extension manipulation gives rise to root pain, the manoeuvre should be discontinued, for the protrusion is pressed harder against the nerve root. ,

Primary posterolateral protrusions. These protrusions all consist of nuclear material and therefore cannot be reduced by manipulation (see p. 756).

CHAPTER 59 - TREATMENT OF THE LUM BAR S P I N E 881

DANGERS OF MANIPULATION ,

Lumbar manipulation is quite safe.63,76 The most fre­ quently reported serious complication is further prolapse of a herniated disc, resulting in a cauda equina syn­ drome. A comprehensive search of online and biblio­ graphical databases traced 61 cases of cauda equina syndrome as a complication of spinal manipulation, its incidence being estimated to be less that 1 per 1 million treatments?7 Most of the incidents were described in patients undergoing manipulation under anaesthesia or chiropractic adjustments?8 Long-lever, high-force rota­ tion techniques in side-lying position are regarded as responsible. This is only partly true: the underlying cause is the lack of adequate examination to rule out unsuitable disorders. If, in contrast, manipulative procedures are instituted after a thorough examination, those described in this·book have never led to severe accidents. The main advantages of these manipulations are: • • •

A great deal of traction is used to exert a strong centripetal force on the intervertebral joint. Movements towards flexion, which can intensify potentially harmful centrifugal forces, are excluded. Each manoeuvre is followed by a fresh assessment of dural, root and articular signs, which affords a clear pointer to what has happened inside the joint and what the next step should be.

Other complications, such as sprains of the costoverte­ bral and costochondral junctions or fractures of a trans­ verse process, are less serious and either the result of poor technique or inappropriate indications. Should they happen, spontaneous recovery is to be expected after a short period of, say, 4-8 weeks.

However, examination during the next consu ltation shows that symptoms and signs have decreased or even disappeared. Therefore patients should be warned of some after-pain, which is due to muscular and / or capsular-ligamentous reactions. It disappears within 2-3 days and is unrelated to the lesion. Elderly patients can safely be manipulated. However, the number of manoeuvres during one session should be confined to, say, two or three. In these patients high-force long-level techniques should also be omitted.

SUCCESS RATE

Acute lumbago. If there is no deviation on standing or in the maximal forward bent position and the lumbago is of recent date, 50% will get well with one treatment.61,62 Potter73 noted 93% of such patients either fully recovered or much improved following manipulation. Backache. Uncomplicated low back pain of recent onset seems to be significantly more responsive to manipula­ tion than are chronic cases.29,73,74,79-82 However, a report37 suggests that manual therapy also produces better results than physiotherapy or medication in cases with a dura­ tion of 1 year or longer. The beneficial effect of manipula­ tion is particularly significant in low back pain with limited straight leg raising.83 Sciatica. One report has claimed the immediate complete recovery of 18 chronic cases out of 50 with unilateral sci­ atica after one manipulative session.6o This result was confirmed by J. Cyriax (personal communication, 1982). Others found up to 75% of their patients with uncompli­ cated sciatica to recover or improve considerably on spinal manipulations.39,62,7o,73,83

SIDE EFFECTS, RE MARKS AND PRECAUTIONS If it becomes clear, after the history and clinical examina­ tion, that the orthopaedic problem is less important than the psychological one, the patient is best left untreated. Even if such a patient can be helped, the improvement will not persist. The moment it is realized that there are adverse consequences of the symptoms ceasing, a post­ manipulative mental crisis is to be expected, blaming the treatment. If the backache is not of organic origin, manipulation will surely be of no help. Frequently these patients get years of futile treatment, which harms the reputation of manipulation. Manipulation should cause only minor discomfort, which is due to stretching effects on soft tissue structures. In acute lumbago a more gentle start is often necessary, to assess the patient's reaction and to gain their confidence. Sometimes the patient leaves a session pain free but, for the following 2 days, a rather strong reaction follows.

MANIPULATION TECHNIQUES The manipulative techniques used in orthopaediC medi­ cine can be divided into three groups: • • •

Rotation Extension Antideviation.

After a detailed description of each technique, the reader will find a ' practitioner's checklist' regarding choice of technique, assessment of progress, repetition of techniques and the course of a manipulative session. Symbols have proved useful to register the employed techniques. These are given for each technique.

Rotation techniques Rotation strains have been shown to be very effective in reducing displacements at a low lumbar level. A session

882 S E CTION TEN - THE L U M BAR SPI N E

o f manipula tion therefore always starts with these manoeuvres. First a 'stretch' is performed, being the smallest rotation strain. The patient lies with the painful side u ppermost in order to bring the joint surfaces apart on the side of the displacement. Then, if necessary, this technique is followed by stronger rotations, using the femur as a lever. However, the latter techniques are impracticable in patients with arthritis at the hip or in elderly patients in whom osteoporosis is suspected. If the displacement lies centrally, straight leg raising may indi­ cate which side should be treated first. However, in the absence of any symptom or sign to indicate the side, either side can be treated and the manipulator proceeds by trial and error. Five different rotation techniques are described, all of which are used frequently. +R- Stretch. The straight arrow symbolizes 'stretch'. The R indicates that the patient lies on the right-hand side. The direction of the arrow to the left indicates that the patient's trunk is rotated to left posteriorly. The couch should be stable and adjustable to about 30 cm height. Using a high couch makes it impossible to aid the d istraction of body weight, which in turn decreases the effect of manipulation. The patient lies on the painless side. The upper thigh is flexed to a right angle with the under leg extended. The manipulator stands behind the patient, level with the patient's waist. One hand is placed in front of the shoulder and rotates the thorax backwards and upwards as far as it will go. At the same time, the heel of the other hand, placed against the greater trochanter, rotates the pelvis forward and downward to the same extent. This brings the joint surfaces apart on the side of the displacement. By using the body weight and leaning well over the patient, the manipulator obtains considerable distraction at the lumbar joints. At the moment the limit of tissue tension is felt, the body is pushed forwards on the verti­ cally outstretched arms to apply overpressure (Fig. 59.4). At that moment a 'click' or 'snap' is nearly always heard and felt, after which the result of the manipulation is assessed.

"IIV Practitioner's checklist • Ang les of rotation should be equal • Hands positioned with fingers pointing in the d i rection

of movement • Elbows extended • Equal amount of pressure on both hands • Body weight over the patient but assess, depend i n g on

bui ld, for exam p le, with l ig htly built patients • Man i pu l ation is a stretch, not a rotation

Figure 59.4

Stretch.

1't Leg crossed over. The curved arrow symbolizes a ' leg crossed over' . The direction of the arrow, to the left, indicates that the patient's trunk is rotated to the left pos­ teriorly. The letter R indicates that the patient lies on the right-hand side. The couch should be stable and adjusted to about 60 cm height. The patient lies supine about 20 cm or a hand's breadth from the edge of the couch. The manipulator stands on the painless side, level with the patient's waist, facing the feet. With both hands flexing the thigh on the far side up to 90° and drawn for­ wards, the pelvis and lower back are rotated towards the operator. In this way, hip adduction is avoided. The ipsi­ lateral knee of the manipulator is applied to the pelvis, if necessary, to prevent the patient from falling from the couch. Next, the contralateral forearm is turned into supination and the palm of the hand applied to the outer side of the knee. The other hand pushes the patient's far shoulder flat on the couch (Fig. 59.5). Then rotation of the

CHAPTER 59

( a) Figure 59.5

-

TREATMENT OF THE L U M BAR S PI N E 883

(b) Leg crossed over: (a) with the leg forwards to rotate the pelvis; (b) shortly before manipulation.

pelvis is continued until tissue tension is felt to be maximal. At that moment, rotation is forcibly increased by pressing the patient's knee strongly and with high velocity towards the floor, using the thigh as a lever. At the same moment, the other hand maintains the position of the patient's far shoulder (if possible) flat on the couch.

� Leg crossed over with side flexion . The curved arrow to the left symbolizes a ' leg crossed over' with rotation of the trunk left posteriorly. The oblique arrow to the right indicates that the lumbar spine is in a side-bent position, bent to the right. The R represents the position of the patient, on the right-hand side at the moment of manipulation. This manoeuvre is a variation on the previous ' leg crossed over' technique and also achieves side flexion. The patient lies supine, both legs flexed and crossed, the

tillV Practitioner's checklist • This man i p u l ation creates max i m u m rotation but l ittle

d istracti o n • U s e o f leverage a n d g ravity means that o n ly m i nimal

force on the knee is needed In stiff patients it is i m possible to hold the far shou l der on the couch; with the pelvis rotated as described, the far shoulder is more or less off the couch and held i n that position • The degree to which the leg is flexed depends on posture i n the stand ing position: i n patients who show considerable forward and/or lateral deviation of the l umbar spi ne, the hip must be well flexed, u p to 120· if necessary, thus end-feel is reached more effectively, making the man i p u l ation more l i kely to be successfu l; patients without deviation are often best treated at first with the th igh brou g ht up to rather less than 90· •

884 SECTION TEN - T H E L U M BAR S P I N E

leg o n the painful side u nderneath. The manipul ator stands on the pai nless side, level with the patient's waist. Holding the patient's knees i n the hands, the manipulator moves the patient's hips into 90° of flexion. Then both legs are twisted, in order to tilt the pelvis lat­ erally and open up the lumbar spine on the painful side. This position is maintained at full range. The hand th at has been on the patient's uppermost knee is now freed to fix the far shoulder on the couch. The side-bent posi­ tion of the lumbar spine is ensured by the manipulator's thorax and abdomen, which are used to engage the knee from the side. Next, rotation is stepped up slowly:

under the influence of gravity the legs turn in the direc­ tion of the floor until the limit of tissue tension is felt at the end of range. At that moment the manipulator 'S thigh, engaging the uppermost knee from the side, has taken over to secure the side-bent position of the lumbar spine. Lastly, the hand at the knee is supinated to increase the manipulative force. M anipul ation is performed by pressing the knee quickly downwards (Fig. 59.6) . At the same moment, the other hand is used to maintain the position of the patient's far shoulder flat on the couch, if possible. Rotation is thus forced during side flexion.

(b)

(a)

(e)

Figure 59.6 Leg crossed over with side flexion: (a) flexion of the hips and knees

and side flexion of the pelvis; (b) rotation of the pelvis; (c) manipulation.

CHAPTER 59

�IIII Practitioner's checkl ist ,

-

• This manoeuvre must not be performed in arthritis of

the h i p and in the elderly, where osteoporosis is to be expected • Hi p of the leg underneath shou ld be flexed to 900 • Lateral flexion should be mai ntained u ntil and inclusive of the final th rust • Man ipu lation creates a q uick but short downward thrust, without releasing the patient's far shoulder

-A* Reverse stretch. The straight arrow again symbol­ izes a 'stretch' but its direction to the right indicates that the patient's trunk is now rotated right posteriorly. The R ind icates that the patient lies on the right-hand side. The couch is adjusted to about 30 cm height. The patient lies on the pain-free side, close to the edge of the couch where the manipulator stands. The patient's upper hip is extended, the lower flexed to about 45° in order to stabilize this position. The upper arm hangs off the couch, the lower lies behind the back. The manipulator stands behind the patient, distal to the pelvis and facing the patient's head. The ipsilateral hand takes hold at the anterior iliac spine and twists the pelvis backwards as far

TREATMENT OF T H E LUMBAR S P I N E 885

as it will go. In this position, the manipulator 'S arm is fully pronated, with the hand placed against the anterior aspect of the anterior iliac spine, pushing the pelvis downwards and backwards. The other hand is placed against the scapula and pushes the thorax upwards and forwards (Figure 59.7). Next, by leaning well over the patient, the joints are distracted by moving both hands in opposite directions, until tissue tension is felt to be maximal. Manipulation is performed by jerking the body downwards over the rigid arms. It is best to apply this overpressure at the moment of expiration.

�IIII Practitioner's checklist • Pelvis must be rotated well backward, otherwise the

• • • •

•

manipu lation compresses the pelvis instead of stretc h i n g the l umbar j o i nts Angles of rotation should be equal Same amount of pressure is used by both hands Elbows are extended at the moment of final thrust Body weight is brought well over the patient to reinforce the stretch but adapted accord i n g to the patient's constitution Man i pu l ation is a stretch, not a rotation

( b)

(a) Figure 59.7

-

Reverse stretch: (a) the ipsilateral hand twists the pelvis backwards; (b) manipulation.

886 S E CTION TEN - THE LU M BAR S P I N E

� Reverse rotation with thigh. The curved arrow sym­ bolizes rotation; its direction to the right means that the patient's trunk is rotated right posteriorly. The R indi­ cates that the patient lies on the right-hand side. The couch is adjusted to about 60 cm height. The patient lies on the pain-free side, the upper leg extended, the lower hip flexed to 60°, with the lower arm behind the back. The manipulator stands behind the patient, level with the lumbar spine. The upper thigh is grasped at the knee with the ipsilateral hand and flexes the hip to 90° and abducts the thigh horizontally. As a result the pelvis is twisted as far as it will go. The other hand is placed against the scapula and pushes the upper thorax to the couch (Fig. 59.8). While maintaining pressure on the thorax, the patient's upper thigh is now brought to 60° of flexion and full abduction. In some cases it is also neces­ sary to put a knee against the patient's lower buttock, to prevent the pelvis from slipping backwards. At the moment the manipulator feels the limit of tissue tension, manipulation is performed by a sharp and short rotation of the manipulator'S body. This forces the arm at the thorax down, at the same time as it jerks the thigh back­ wards. Strong rotation and extension occur in the lumbar joints. It is obvious that this manipulation must not be per­ formed in the elderly or in patients with arthritis of the hip or osteoporosis.

ments. The impulse separates L5 from Sl in a cranial direction, instead of compressing the dorsal parts of the joint. In acute lumbago and when extension pressure causes pain to shoot down the limb, extension techniques are contraindicated. Deviation, as an expression of a large displacement, provides an indication that these techniques will almost certainly fail. If a heavily built manipulator is dealing with a light patient, leaning on the patient's back using the whole weight of the body may give rise to strong resistance and therefore the amount of weight applied should be reduced.

U Central pressure. The straight arrow symbolizes the extension technique, which is exerted centrally. The level at which the manoeuvre is performed is indicated by L5. The patient lies prone on a firm couch adjusted to about 30 cm height. The manipulator stands level with the lumbar spine, facing the patient, with the knees

tI"� Practitioner's checklist • Suitable technique for l i g htly bu i lt manipu lators • Contraind icated in h i p lesions, elderly patients and

osteoporosis • Upper thigh is in not less than 60·

Extension techniques These techniques are very effective in small cartilagi­ nous d isplacements that cause backache, especially in elderly patients and in those with persistent minor pro­ trusions following incomplete reduction by a stretch in rotated position. The techniques are milder than those performed with rotation strains and may substitute the latter in osteoporosis. However, they affect one segment only. During the manoeuvre it is thought that interspinous pressure moves two adjacent vertebrae apart, so tighten­ ing the posterior longitudinal ligament and causing suction in the disc - a centripetal force which may reverse a displacement. The shape of the facets of L5-S1, which are more in a frontal plane, contributes to the better results achieved at this level than at the other lumbar seg-

Figure 59.8

Reverse rotation with thigh.

CHAPTER 59 - TREATMENT OF T H E L U M BAR S P I N E 887

against the edge of the couch. One hand is placed with its ulnat border at the interspace of two adjacent spinous processes (normally between Sl and L5). The other rein­ forces it with the heel pressing on the radial and the thumb pressing on the dorsal and ulnar sides of the lower hand (Fig. 59.9). To prevent any contact with the iliac bones, it is useful to use the right hand, standing at the patient's left-hand side, and to turn this hand through about 45°. With the upper limbs extended and kept rigid, the manipulator leans well on to the patient's back and extends the knees, one after the other. From this moment the body weight presses full on the patient's back and results in a maximum tissue tension.

""II Practitioner's checklist • Wei g ht appl ied shou l d be adapted when a heavily bui lt

manipu lator deals with a l i g ht patient: one or even both knees remain in a flexed position and lean against the edge of the couch • Lean well over the patient • Arms extended and kept rigid • If pressure of body weight shoots a pain down the l imb, stop the man i p u lation

At the moment the patient relaxes and some exten­ sion has been achieved, the final thrust is given by

(b)

( a)

Figure 59.9 (a, b) Central pressure; (c) the ulnar border of the hand is placed between two adjacent spinal processes.

(c)

888 S ECTIO N TEN - T H E L U M BAR SPI N E

bending the head and thorax abruptly forward. Usually a thud is felt or a click is heard if the manipulation is successful.

L{

U n i l ateral p ressure. The a rrow symbolizes an extension technique and also that pressure is exerted unilaterally, according to the direction of the arrow. The level at which the manoeuvre is performed is indicated by L5. If repeated central pressure has neither fully relieved the patient nor made the problem worse, this technique is used immediately after central pressure. The manipulator stands on the patient's painful side although, if the pain is central, there will be no indica­ tion whether to start on the right or on the left. The wrist of the ipsilateral hand is extended and the prominent pisiform bone is used to exert localized and unilateral pressure at the base of the spinous process of L5 or L4. It is necessary to lean well over the patient, in order to press in a slightly oblique d irection (Fig. 59. 1 0 ) . The other hand reinforces the pressure, using the heel to press on the manipulating hand. In order for the manip­ ulator to stay well balanced, both legs are moved slowly backwards at the moment the body moves forwards. The knees or thighs should stay in contact with the edge of the couch. Manipulation is all but identical to the previous technique, except that the thrust is now directed medially as well as downwards, which opens the joint on the p ainful side, at the same time also exert­ ing some rotational stress and strong extension.

vV� Practitioner's checklist • Arms kept rigid • The centre of g ravity moves beyond the centre of the

patient's body • Knees or t h i g hs stay in contact with the couch • F i n a l th rust at the moment the patient relaxes and a l l

the slack i n the tissue has been taken u p • I f pressure o f body weig ht shoots a p a i n down t h e l i mb,

stop the m a n i p u lation

Q + thigh II Uni lateral pressure with thigh I . The

arrow symbolizes extension with unilateral pressure. The level at which the technique is performed is indi­ cated by L4 / 5. Thigh I indicates the first variation of the technique. This is a much stronger technique which follows the previous extension manoeuvres but is undertaken only if partial reduction has been achieved and repetition affords no further improvement. In the absence of any

benefit, it is unwise to continue with this technique or the next one. The patient lies prone and near to the edge of a low couch. The manipulator stands on the pain-free side, level with the pelvis. With the ipsilateral hand the front of the knee is grasped at the painful side around its lateral aspect. The ulnar border of the other hand is placed just above the posterior spine of the ilium. Then the hip is extended and strongly adducted by leaning heavily towards the patient's head (Fig. 59. 11 ). This opens the joint on the side where the d isplacement lies. Manipulation is performed by a quick rotation of the manipulator 's trunk towards the patient's head. In this way, the unilateral downwards pressure of the lumbar hand, and the pull upwards of the hand on the knee, is considerably intensified . This results in a combined movement of hyperextension, side flexion and rotation at the lower lumbar joints.

vV� Practitioner's checklist

�-

• Only use if the previous extension manoeuvres have

a l ready achieved some reduction • Not possible i n a lesion of the h i p joint • Size of the patient should be comparable to that of the

m a n i pu lator

Q + thigh I

Unilateral pressure with thigh II. Dealing with a heavily built patient, added force can be exerted by employing the knee; however, this technique should not be adopted if the previous extension strains have led nowhere. The patient lies in the same position as in the previous technique. The manipulator stands on the painful . side. With the contralateral hand, the front of the patient's knee around its medial aspect is grasped and the thigh is extended and adducted until the pelvis rises just off the couch. The palm of the other hand is placed on the sacrospinalis muscle covering the fourth and fifth lumbar levels on the painful side, with the forearm fully supinated (Fig. 59.12). The manipulative thrust is per­ formed by pressing the ipsilateral knee with the hand at the same time as the patient's thigh is forced into full extension and adduction. A forced extension at the lower lumbar joints results.

tIV� Practitioner's checklist • Use only if central a nd u n i l atera l pressure tech n iques

have ach ieved some reduction and the manipu lator is dea l i n g with a heavi ly built patient • Not possible in a lesion of the hip joint

-

CHAPTER 59 - TREATMENT OF THE LU M BAR SPI N E 889

(b)

Figure 59.10 at the base.

(a) x

(a) Unilateral pressure; (b) the prominent pisiform bone is placed

R Uni lateral distraction. The crossed arrows symbolize distraction. The letter R indicates that the manoeuvre is performed on the patient's right-hand side. This technique is indicated if the previous manoeu­ vres towards extension have helped but reduction has still not been fully achieved. It may also serve to remove a generalized ache that results from any manipulative manoeuvre. The patient lies prone and side flexes the body to open the joint on the painful side as far as possible. The manipulator stands on the concave side, facing the

patient, with the arms crossed and the elbows bent almost to a right angle. The heel of one hand is placed against the iliac crest, j ust lateral to the sacrospinalis muscle. The heel of the other hand is placed just under the lowest ribs (Fig. 59. 1 3). To p revent the skin from being strained at the moment of manipul ation, the skin is first pulled u pwards with the lower hand, while the upper hand does the same downward s. Manipulation is now performed by repeated (1 0-20 ti mes) forward movements of the trunk, keeping the elbows rigid . Th is

Figure 59.1 1

Figure 59.12

Unilateral pressure with thigh I.

Unilateral pressure with thigh II.

890 SECTION TEN - T H E L U M BAR SPI N E

Figure 59.13

Unilateral distraction.

forces the hands apart and imparts rhythmic further dis­ traction together with some extension at the lumbar level.

Antideviation techniques These techniques are applied in backache and lumbago with an adapted postu re, caused by posterocentral disc protrusions. The previous rotation and / or extension techniques will have already eased the pain but when the patient stands for a few moments, the tilt of the trunk to one side quickly returns, as a result of persistent one­ sided muscle spasm . On examination, side flexion towards the contralateral convex side, and sometimes extension, is still limited . Three techniques can be used: • • •

Side bending in the supine position. Rotation-distraction in side lying. Side gliding, standing.

l' Side bending. The curved arrow symbolizes side bending. A bar at the arrowhead indicates the sustained maintenance of the position. The patient lies supine with both legs flexed and crossed, the leg on the concave side of the lumbar spine underneath. The manipulator stands on the convex side, level with the pelvis. With one hand the upper knee is pushed away from, while the other is used to pull the lower knee towards (Fig. 59.14). This simultaneous action tilts the pelvis and achieves full side flexion at the lumbar spine in the previously b locked direction. It is quickly repeated a number of times, whereafter the pressure is maintained for a few seconds. When there has been a pre­ vious nuclear protrusion, the extreme of range is better maintained for a minute or so. This position is consoli-

Figure 59.14

Side bending.

dated either by assistance of the manipulator'S ipsilateral knee, pushing from a distal position against the patient's ischial tuberosity or by the contralateral knee pushing from a lateral position against the patient's pelvis. The manipulation is repeated until the patient can keep the trunk in a neutral position on standing.

� Rotation-distraction. The straight arrow symbolizes distraction, the curved arrow rotation. The bars at the arrowheads indicate that the technique is performed in a sustained manner. The R indicates that the patient lies on the right-hand side. The patient lies on the side of the lumbar convexity with the upper thigh flexed to about 60°, thereby rotating the pelvis to just more than 90°. The manipulator stands in front of the patient, distal to the pelvis and facing the patient's head. The thigh of the uppermost lower limb is clasped between the manipulator 'S knees, just proximal to the patient's knee, to secure the position of the pelvis.

CHAPTER 59

Both hands are placed at one side of the upper thorax. Correction of the lateral tilt is achieved by pushing against the patient's thorax in an upwards and back­ wards direction (Fig. 59.15). This correcting force should be sustained as long as the patient can endure it. The manipulator must stand well balanced to prevent the entire body weight from pressing on the patient. After some repetitions the patient is re-examined in the stand­ ing position. The manoeuvre is repeated until correction has been achieved or until repetition affords no further benefit.

""')0-

Side gliding. Two straight arrows pointing to the convex curves of a scoliotic spine symbolize the side gliding. The bars at the arrowheads indicate that the technique is performed in a sustained manner. The patient stands upright, the feet about 20 cm apart to provide a stable base, with the elbow held against the lower rib cage on the side of the lumbar concavity. The manipulator stands on the same side and presses the thorax against the patient's elbow, with the hands placed on the far side of the patient's pelvis. Correction and even slight overcorrection is achieved slowly, by pressing the thorax against the patient's elbow,

-

TREATMENT OF T H E L U M BAR SPI N E 891

simultaneously pulling the pelvis from the far side towards the manipulator (Fig. 59. 1 6 ) . This pressure should be maintained for a couple of minutes and is repeated several times. It is essential that the movement is side gliding rather than side bending. Once the spine is upright, an attempt is made to restore lordosis. To this end the patient is brought into the cor­ rected position again and asked to let the hips move for­ wards at the same time as the trunk bends backwards. In this way, the body stays well balanced all the time. This movement is repeated, until the range of extension is restored. It will take at least three to four consecutive daily ses­ sions to produce a lasting result. In addition, it is essen­ tial to instruct the patient in self-correction (Fig. 59. 17). Standing in front of a full-length mirror, one hand is placed against the lower lateral rib cage at the concave side of the lumbar tilt. The other hand is placed on the opposite lateral iliac crest. Then the patient performs the side gliding movement of the pelvis in the restricted direction so as to correct the deformity. Once this has been achieved, a controlled extension movement is per­ formed: the patient supports the trunk by placing the hands at the lower back and slowly bends backwards as far as is comfortable. These exercises should be repeated every hour.

�IIII Practitioner's checklist • Correction i nvolves side g l iding. not side bending

The course of a manipulative session is summarized in Figure 59. lB. MANIPULATION PROCEDURE

Choice of technique •

•

• • •

•

Figure 59.15

Rotation-<Jistraction.

Stretch or reversed stretch in the side-lying position is usually the first technique to be tried, especially if the pain is unilateral. If rotation-stretch techniques lead to incomplete reduction in minor protrusions, it may be best to move on to extension techniques. Usually, L3-L4 protrusions respond better to rotation techniques. L5 protrusions may respond better to extension techniques, especially in elderly patients. In elderly patients it is also better to avoid long-lever techniques for fear of fracturing weakened bones. Acute lumbago is unsuitable for extension tech­ niques, whereas rotation manoeuvres usually give good results.

892 SECTION T E N - THE L U M BAR SPI N E

(a)

(b)

Figure 59.16 •

(c)

Slide gliding: (a,b) correction; (c) extension .

After the use of each technique the result is assessed and a decision taken whether to continue with the same technique or to change. If one manoeuvre has helped, it should be repeated until symptoms and signs no longer alter. Then another is tried. Experience, the result of each particular manoeuvre, end-feel during exertion, the patient's age and estimation of tolerance all affect the types of manoeuvre employed.

Assessment of progress (Box 59.4) The physical signs are reassessed after each manoeuvre. If there were dural signs, these are tested first: limitation of straight leg raising, before the manipulation, is tested afresh after the manoeuvre. If there was pain on cough­ ing, the patient is asked to cough once more and to describe how it feels. It is only after the physical signs in the lying position have disappeared that lumbar movements are examined on standing to assess articular signs. In contrast, if only lumbar movements on standing caused pain, the patient is asked at once to stand and bend backwards and side­ ways to judge whether there is any change in the degree

of pain or in the amplitude of trunk movement. Because forward flexion movement is likely to increase any dis­ placement, flexion of the trunk should not be tested before the manipulator can be sure that full reduction has been secured, i.e. all other tests have become negati.ve. Another important sign is 'centralization' of pain: a shift, after manipulation, to a more central position is regarded as an improvement.58,84 Assessment of outcome after each manoeuvre gives the manipulator the certainty that: • •

The protrusion has moved. It has moved into the right direction.

Box 59.4 Summary of improvement after manipulation Dural signs Ampl itude of stra ight leg raising Pa i n on cou g h i n g Articu l a r signs Pain Ampl itude of l u mbar movements Centra l ization of pain

C H APTE R 59 - TREAT M E N T OF TH E LU M BAR SPI N E 893

Rotation

[

Rotation

1

Reverse rotation with thigh

Better I No change ..... Worse--.... Figure 59.1 8

Unilateral pressure with thigh I-II

Unilateral distraction movements

Course of a manipulative session (see text for explanation).

manipulated and re-examination after each manoeuvre will avoid mistakes.

Figure 59.17

Self-correction.

Repetition of techniques One manipulative session continues until symptoms and signs have been modified to the greatest extent possible. If a 'thud' is felt on performing an extension thrust and considerable improvement is noted, no more should be done until the next visit. If there is only slight improve­ ment, the same technique should be repeated until no further change occurs. In young patients, another tech­ nique can still be tried. However, six to eight manoeuvres are about the maximum a patient can stand. In elderly patients, it is better to stop after two or three and to continue on the next visit. Sometimes a manoeuvre may make a patient worse. I f this i s the result o f an extension technique, a rotation manoeuvre can still be tried. If rotation is responsible, the direction of rotation can be changed. If these measures are unsuccessful, the question arises as to whether the patient is in fact suitable for manipulative treatment. Since a decision on this point is often difficult, the manip­ ulator should first report these facts to the doctor in charge. Manipulation is by no means free from danger if continued in spite of warning signals. Starting gently, paying attention to the patient's statements while being

TRACTION

Although there is still much controversy about the effec­ tiveness of traction,85 we still consider passive sustained stretching of the low back as the treatment of choice for nuclear, reducible disc protrusions causing backache and / or sciatica, mtless there are specific contraindications. Despite the poor design of most of the stud ies,86 traction has been shown to be more effective than corset, bedrest, hotpack and massages.83,87-89 HISTORICAL NOTE The Ancient Egyptians utilized the beneficial effect of axial traction.90 An illustration of traction employed by the Spanish-Arabian physician Abu'L Qasim (1 013-1106) of Cordoba is reproduced by Schi6tz and Cyriax in their book on manipulation past and present.20 In the same book, illustrations show the way in which traction was used by Hippocrates (400 Be) and Galen (AD 131-202). A 1 4th century method of manipulation during traction is illustrated in Figure 59. 19. Nowadays, two methods of performing traction are practised. The sustained manner, as described in this book and first suggested by Cyriax in 1 950,91 and several types of intermittent traction. Intermittent traction can be done either electrically (Tru Trac machine), manually (by a therapist) or by the patient (autotraction, Spina Trac).

894 S E CTION T E N - T H E L U M BAR SPI N E

I � '� I I t.. 1

� l" H I 4 '

ll:'Oq.'1 !fl 1lI1,

Figure 59.19

Manipulation during traction i n Albucasis's Surgery. Latin translation. Vienna, fourteenth century. (By courtesy of Wellcome Trustees.)

However, nearly all reported work has shown all types of intermittent traction to be ineffective.92,93

Effects of sustained traction Several studies have investigated axial traction. It has been established that during sustained traction at least three effects result (Fig. 59.20).

The space between the vertebral bodies enlarges. This is an im portant precondition for a displacement to recede. In young men sustained traction of 60 kg, applied for 1 hou r, results in an increased body length of 1 0-30 mm, which is thereafter lost at the rate of 4 mm / h.94 In an excised lumbar spine, sustained traction of 1 0-30 kg increases each joint space by 1 .5 mm.95 Vertebral separation is greatest in those subjects with wide disc spaces and least where there is evidence of disc degenera tion.96 The effect of lumbar sustained traction on stature has also been studied in 10 healthy young subjects: the inves­ tigators confirmed the significant increase in stature but also that this increase was over and above that known to

(a)

occur when the load is taken off the spine by lying down.97 The findings suggest that most of the vertebral separation takes place in the first 30 minutes. It has also been established that the enlargement between two con­ secutive lumbar endplates during a normal traction is between 1 .0 and 1 . 5 ffiffi, which is 1 0-15% of the thick­ ness of the disc.98 Other studies demonstrate a widening of the lumbar intervertebral space of between 3 and 8 mm measured on radiographs of patients undergoing gravi­ tational traction.99,l OO

The heavy lumbar paravertebral musculature nor­ mally exerts significant resistance to distraction. At least 30-35 kg of traction, not dissipated by friction, is required to influence the lumbar spine.101 Other work has demonstrated that a traction force of at least 25% of the body weight is necessary to achieve d istraction of the lumbar vertebrae against the inertia of muscular resistance of the body. 102 This supports an earlier study l o3 in which any traction power less than 25% of body weight was regarded as a placebo.

The posterior long itud inal l i ga ment is tautened. exert­ ing a centri peta l force at the back of the joint. The

(c)

Figure 59.20 Effects of sustained traction. (a) Before traction, nuclear protrusion posteriorly displaced. (b) During traction: the intervertebral space enlarges; the posterior longitudinal ligament is tautened; a negative intradiscal pressure is created. (c) After traction, reduction is maintained (after Mathews)'OS.

CHAPTE R 59

increasing tension in this ligament is certainly of great therapeutic value, particularly if the protrusion is located anterior to and remains in close contact with the ligament. Traction will therefore be less effective if the protrusion is laterally pl aced - a conclusion confirmed by CT investigation of the effect of static horizontal trac­ tion on lumbar disc herniations: 'The clinical responses of the herniation to conservative treatment and the loca­ tion of herniated nuclear material seem to be related. Traction. is more effective on median and posterolateral herniation cases, and clinical improvement is evident in these cases, but traction is not very effective on lateral herniations'. 104 Also, re-entry of ruptured or sequestered disc material into the intervertebral disc is not possible (see Fig. 59.21 ).

(a) Contained discs

-

TREATMENT OF T H E L U M BAR SPI N E 895

Suction draws the protrusion towards the centre of the joint It is believed, on the basis of biomechanical calculations, that significant intradiscal negative pressure may be produced during sustained traction.lO S A traction load of 30 kg caused a lowering of the intradiscal pressure from 30 to 1 0 kp in the L3 intervertebral disc. 106 In another study intradiscal pressure demonstrated an inverse relationship to the tension applied. Tension in the upper range was observed to decompress the nucleus pulposus significantly, to below 1 00 mmHg. 1 07 Discography has established that the decrease in i ntradiscal pressu re causes a suction effect with centripetal forces on the contents.95 An interesting

(b) Non-contained discs

Nuclear protrusion

Disc herniation

A partial radial annular tear

Nuclear material has been

has occurred and nuclear

extruded through the

material has been extruded into it

posterior longitudinal ligament into the spinal canal. There is still connection with the disc itself

Disc herniation

Disc herniation

Complete disruption of the annulus fibres and localized

A sequestered disc fragment lies free in the spinal canal

bulging of the disc. Nuclear material has not passed the posterior longitudinal ligament

Disc herniation

{)

Nuclear material has been extruded and passed the annulus fibrosus but is still contained by the posterior longitudinal ligament

Figure 59.21 (a) Contained disc herniation. Examples of displaced nuclear material that remains contained by annulus fibres and/or an intact posterior longitudinal ligament. Traction is indicated. (b) Non-contained disc herniations. Nuclear material has been extruded into the spinal canal. Traction cannot reduce the protruded material.

896 SECTION T E N - T H E L U M BAR SPI N E

Chinese study investigated the changes i n intradiscal p ressure and intervertebral disc height on 3 1 prolapsed discs under traction. It was demonstrated that the intrad iscal pressure decreased as the intervertebral distance increased in most cases under traction. J OB

Repair of d isc lesion. It has also been suggestedJ10,JJ1 that during epi sodes of disc decompression nutrition is improved, reparative collagen is deposited and natural healing of annulus tears and fissures is promoted. Sustained traction has the same effect on the intra­ di scal pressure as prolonged bed rest, but much more strongly. A few hours' traction achieves as much or more than rest in bed for weeks. Although the latter can also bring about slow reduction of a nuclear protrusion, traction has the advantage of speed. Instead of simply avoiding the compression produced by the upright postu re, it mechanically distracts the joint. In addition, the patient remains ambulant, greatly p referred to rest in bed for some weeks, which is not only bad for morale but also increases the cost in lost working days and the payment of sickness benefit. It should be emphasized that this effect can only be achieved if traction brings about more in the way of reduction in half an hour than can be reversed during the rest of the day by new loading effects. To this end, traction shou ld be sustained and must be given daily and as energetically as the patient can bear. Otherwise it is merely a placebo. There is increased motor activity of the sacrospinalis muscles on an electromyogram during traction, until the mechanoreceptors in the tendons a re stimulated.l12 From that moment, motor activity is inhibited, the inter­ vertebral joint takes the strain and reduction of the pulpy mass starts slowly. Electromyographic silence is reached after 3 minutes. This suggests that traction must be sustained . A study that measured the intradiscal pressure during 30 seconds of passive traction per­ formed by two therapists and d uring 2 minutes' auto­ traction with 50 kg weigh tll3 has established that intradiscal pressure did not alter much in passive trac­ tion, whereas autotraction increased the pressure con­ siderably. These findings strongly contrast with those of sustained traction, which makes it obvious that only the latter is able to diminish a nuclear protrusion in volume and return it to its normal position. INDICATIONS FOR TRACTION

Nuclear d i sc protrusions. Pulpy nuclear protrusions which remain contained and in contact with the posterior longitudinal ligament (Fig. 59.2 1 ) are more effectively treated by traction just as hard annular protrusions are more readily treated by manipulation. Cyriax always

said: 'You can hit a nail with a hammer, but treacle must be sucked'. It should be emphaSized that signs of irreducibility such as neurological deficit or gross lumbar deformity maintained by root pain should be absent. The typical clinical pattern of a lumbar nuclear protru­ sion is as follows. The patient is under 60 years of age. On bending forwards for a while some aching in the back is initially felt, which gets slowly worse later in the day. The next morning it is impossible to rise out of bed because of severe low back pain. Clinical examination shows a partial articular pattern and movements pinching the lesion, i.e. side flexion towards the painful side or exten­ sion, are often most painful. This is quite different from the patient with an annular protrusion, who describes a sudden onset of lumbago on bending forward, perhaps lifting up some heavy object. This may happen at any age. Again a partial articular pattern is present. A painful arc, with or without momen­ tary deviation, suggests a small mobile aIU1ular fragment and is a further encouraging sign for manipulation. The distinction between these different types of disc protrusion is not always as clear as in these examples. Nevertheless, for therapeutic reasons, it is important to differentiate between these mechanisms. The summary given in Table 59.1 may be helpful.

I ndetermi nate protrusions. If signs and symptoms do not exactly indicate the consistency of the protrusion, manip­ ulation is tried first, because it may be much more quickly effective. If it fails, or only partly succeeds after repetition, sustained traction is indicated and started the next day. The reason for this is two-fold: • •

Painful twinges may occur after release, if traction follows manipulation too quickly. It is not possible to judge the effect of a single treatment if this is combined with other forms of treatment at the same session.

Fi rst and second lumba r d isc lesions. At this level, trac­ tion is regularly successful whereas manipulation always fails. A disc lesion secondary to lower lumbar arthrodesis constitutes an exception: the fixation of the low lumbar segment alters the biomechanical relationship ih such a way that manipulation can often succeed. Recurrence after laminectomy. Manipulation can be tried first but seldom proves successful if the protrusion is sit­ uated at the level of the operation. Traction is more often effective, although the prognosis remains less favourable than for those patients who have not had su rgery. Primary posterolatera l protrusions. These protrusions may constitute a difficult therapeutic problem. Because they all consist of nuclear material, manipu lation has no

CHAPTER 59

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TR EATME NT OF T H E LUMBAR S P I N E 897

Table 59.1 Differences between nuclear and annular protrusions Nuclear protrusion

Annular protrusion

Age (years)

< 60

All ages

Onset

After much stooping and lifting

During bending forward and coming up again, abrupt

Pain increasingly evoked by sitting in a kyphotic posture

displacement with a click, initiating acute lumbago

Backache after exertion

Backache as soon as exertion starts

History

Clinical examination

Partial articular pattern

Partial articular pattern

Pain on pinching the lesion in backache (not in lumbago or

Pain on side bending away from the painful side

over the age of 60

effect. The protrusion usually responds to daily traction but the tendency to relapse after reduction is consider­ able. Epidural local anaesthesia is a good alternative but only works when the protrusion is at its maximum size. ConsiJering the therapeutic approach in a primary posterolateral protrusion, Cyriax21 (his p. 317) gives the following advice: . . . such a protrusion of a month or two's standing should be reduced by daily traction . . . [Howevel� if a relapse occurs a fter a successful reduction, or the protrusion has continued for three or four months, it is better to leave it where it is, especially in a young patient with slight pain only, which is the common situation.] Spontaneous recovery usually takes nine months from the onset of root pain, and the strong ten­ dency to recurrence is largely obviated by allowing the patient to get well of himself. [ However] he should be kept under observation until the protrusion i s stable at its maximum size, i.e. the range of straight-leg raising has stopped decreasing and is found unal tered at two examina­ tions a fortn ight apart. This is the moment for one or two inductions of epidural local anaesthesia which usually abolish the root pain in a few weeks.

Backache together with bilateral long-standing l i mita­ tion of straight leg raising. Those affected are mainly young adults with months or even years of backache associated with marked bilateral limitation of straight leg raising. Daily traction has proved to be successful but only if it is continued for about 3 months. It may take at least 1 month before any improvement is noted. Pai n with fourth sacral reference. Symptoms and espe­ cially signs of impaired conduction of the S4 root probably call for immediate surgical intervention. Nevertheless, if pain is the only symptom and paraesthesia, referred to the coccyx or the genital area, is absent, traction may first be attempted with caution. However, this measure is not entirely safe and should be only performed after discus­ sion with the physician in charge.

(ONTRA INDI (ATIONS

Acute lumbago. Because lumbago with twinges is made so much worse for several days by only a single such session of traction, such traction is absolutely contraindicated. Even in patients with lumbago, who have recently lost their twinges, the first session of traction must be undertaken very cautiously. It is not during traction, but at the moment when tension is diminished, that the patient gets agoniz­ ing twinges, making it impossible to release the traction at that moment. It may take the patient up to 3 or 4 hours to rise from the couch. Cyriax advised a very slow diminu­ tion of the traction force. Then, once released, it can take a good 15 minutes for neck flexion to cease to hurt and the range of straight leg raising to begin to increase. If, on starting movements, twinges still persist, repeated rotation manipulations (leg crossed over), gently at first, should be carried out. If this fails, epidural local anaesthesia must be induced without delay. Abdom inal surgery or hiatus hernia. Patients who have had previous abdominal surgery or hiatus hernia may not tolerate abdominal compression. Respi ratory or cardiac i nsufficiency. The patient may not be able to lie down at all, let along tolerate the harness . 1 l 4 Respi ratory i rritation. In discodural interactions pain may be evoked by coughing or sneezing as a result of the sudden increased expansion of the dura pressed against the protrusion. During traction, a strong cough or sneeze is also often painful, making it impossible for the patient to relax. For this reason, respiratory problems should be dealt with first. Painful reactions. If traction, however applied, increases pain in the back or in the leg, the patient is unsu ited to it. This often happens in chronic low back pain and sciatica where the lumbar spine is fixed in flexion. It is usually not possible to find a position in which the pain is not increased as soon as the traction starts.

898 S E CTION T E N - T H E L U M BAR SPI N E

A large protrusion. I n gross lumbar deviation any attempt to move in the contrary direction is aborted by a sharp pain, therefore traction is not applicable. Discodural and discoradicular interactions with a high degree of inflammation, for example continuing pain or pain at night, are best treated by epidural injections. M ental state. Some patients cannot tolerate restrictions such as the harness used. The moment the thoracic harness is pu t on, they become very anxious and start to hyperventilate. It is then better not to continue the treatment. CASES IN WH ICH TRACTION IS NOT USEFUL Although not really contraindicated, traction has no effect and should therefore not be applied in the follow­ ing circumstances. In patients with neurological deficit or gross lumbar deviation, the protrusion is larger than the pathway through which it emerged. Such material extruded through the outer rim of the annulus surely cannot be reduced by traction or manipulation. In the presence of a free protrusion or sequestered fragment, disc herniation traction will always fail. In all these instances, an epidural injection may relieve the symptoms and, given adequate clinical and neuro­ logical justification, surgery may be indicated.

Long-standing clin ical features. A primary posterolateral protrusion lasting longer than 3 months is better not treated by traction, especiaIly in a young patient with only slight pain. There is a strong tendency to relapse after reduction, whereas spontaneous recovery takes place within 9 months of the onset of root pain. A secondary posterolateral protrusion i n a patient under 60 years old, causing root pain for more than 6 months, has passed the time limit for traction. The treat­ ment of choice is epidural local anaesthesia. Spontaneous recovery is the rule and is to be expected within a few months. Indications for, contraindications to and cases in which traction is not useful are summarized in Box 59.5. TRACTION PROCEDURE

Traction apparatus. This consists of a couch and an elec­ trically or manually operated machine, assembled at the foot of the couch. In the non-electrical form a spring balance, attached to the traction rope, is necessary. It measures the amount of traction and ensures an even degree of traction. Whenever the pelvic belt slips slightly over the bench, the bu ffer mechanism of the spring balance intervenes to

Box 59.5 Traction Indications Contai ned n uclear protrusions I ndeterm i nate protrusions Fi rst and second l u m ba r d isc protrusions Recurrence after l a m inectomy Primary posterolateral protrusion Backache with b i latera l l i m itation of stra ight leg ra iSing Fourth sacra l root pain (7)

Contraindications Acute l u mbago Abdo m i n a l surgery H i atus hernia Respiratory or cardiac i nsufficiency Traction i ncreases the p a i n Psychogenic patients

Not useful Non-contai ned protrusion A l a rge protrusion Long-stan d i n g c l i n ical features

take up the slack and subsequently optimum force must be restored. The attendance of a therapist is consequently required, especially during the first 15 minutes of appli­ cation, when traction force is regularly lost. In the electri­ cal form, an electric device obviates this, although the therapist should remain within hearing distance because automatic machines are not 'fail-safe' . There is mechanical equipment that has the advan­ tages of the electrical appliance: constant traction force during the entire session (see Fig. 59.22). The couch should have an opening through which the patient can breathe when treated in a prone position. Frictional resistance in the system can be overcome by using a split-table model. However, with an ordinary couch the same results can be attained, although" fric­ tional resistance must be compensated for by a greater degree of traction force.

Thoracic harness. The thoracic harness is tightened over a layer of thick foam-rubber or a folded towel, applied outside the patient's shirt. This harness is placed as low down on the thorax as possible, to confine the traction to the lumbar spine. Sometimes, however, patients cannot bear this position and fixation at a higher level is then required. The harness anchors the patient at the head of the couch. The straps should clear the patient's trunk when applied above (not shown). To this end the upright, at the head of the couch, should be at least 30 cm high. Pelvic harness. This is also put over a folded towel or layer of foam-rubber and encircles the entire pelvis.' This belt takes purchase from the iliac crest, and connects to the traction rope.

CHAPTER 59 - TREATMENT OF THE L U M BAR SPI N E 899

•

•

the articular surfaces stay parallel during distraction (Fig. 59.23a-d) . Ifflexion hurts a n d extension is pain free, traction i s carried out with the lumbar spine in slight lordosis. The patient is positioned supine with a small pillow supporting the lumbar spine or lies prone. In both positions the straps of the harnesses are situated anteriorly (Fig. 59.23e,f). If extension hurts and flexion is pain free, traction is carried out with the lumbar spine in slight kyphosis. The patient is positioned supine with the lower legs supported on a small bench, the knees bent up or lies prone. In both positions the straps of the harnesses are situated posteriorly (Fig. 59.23g,h).

Thus, eight different positions may be used. In practice, howevel� the positions regularly used are: •

(a)

•

Supine (seldom prone), in kyphosis, lordosis or neutral position. 'Psoas position' with the hip and knee joints flexed to 90°. This position is particularly indicated in L3 root lesions.

Instructions to the patient. Before the session a large meal should be avoided. The patient is instructed con­ cerning the underlying disorder and the therapeutic effects that can be obtained with sustained traction and is also encouraged to keep as relaxed and as still as possible during the stretch. Coughing and sneezing should be avoided, because either may cause a twinge and after­ pain. The patient is further assured that traction must never be painful during the time it is applied, nor should it increase an already existing pain. Any discom fort should be reported at once. This explanation will allay fears engendered by the similarity of the apparatus to a medieval torture rack. (b) Figure 59.22

(a) Mechanical traction apparatus and harnesses for continuous lumbar traction. (b) Patient in position for continuous lumbar traction.

For the same reason, to clear the patient's body, when applied above, the height of the traction rope should be adjusted to 30 cm.

Patient's posture. The possibilities are prone or supine. Cyriax suggests the position that the patient finds most comlortable in bed (provided that this is either prone or supine) as the best guide for the first treatment. If this is of little help, the degree of pain and / or limitation during flexion and extension should be assessed: •

If both flexion and extension are painful (or neither) the patient may lie supine or prone. One strap is situated posteriorly, the other anteriorly. In this way

Force and duration. Theoretically the pull is as strong and for as long as the patient can tolerate. Usually this will be 40-60 kg, applied for at least half an hour to be effective. In practice the amount of traction is measured in relation to body weight. Traction with 60% of the body weight is considered to have the best effective / tolerance ratio. Interval between treatments. Traction must be given daily, for the attempt is to secure more reduction in half an hour than the patient, by bearing weight on the joint for the rest of the day, can reverse. It is remarkable that this in fact proves possible. Furthermore, traction is nor­ mally still effective with an interval over the weekend, provided that the patient spends these days in a relaxed way - lying down at regular times and not sitting for a longer time than absolutely necessary. If these rules are neglected, the protrusion is apt to have returned to the same size by the time of the next attendance. In an urgent

900 SECTION TE N - T H E L U M BAR SPI N E

- -

- -

a

b - -

- -

- -

- -

c

d - -

- -

--

- -

--

- -

- -

--

e

h

9 - -

Figure 59.23

- -

Eight positions for lumbar traction (arrows indicate position of the straps and direction of the pull).

case, traction can be performed more than once a day. Alternatively, in such circumstances, one long stretch of up to an hour has proved effective. Passive back exten­ sion and prone lying can also be useful supplements. 58 If traction has not begun to prove effective after a few days, the question is whether to use a different position on the couch or a different position for the straps. If these alter­ ations are made and the patient has not begun to improve after 2 weeks, traction should be abandoned. The physio­ therapist should not despair too soon, however, as many patients begin to get better only during the second week. Obviously, if a patient is much better but not well after a fortnight, a third week's daily treatment is justified. In young adults with backache and long-standing bilateral limitation of straight leg raising, it may even take a month before any improvement is noted.

Procedure (see Box 59.6). (Re)examination. The patient must be (re)examined before each session. Symptoms and some physical signs, for example lumbar movements and straight leg raising, are noted afresh and any alteration given due consider­ ation. However, there is no point in examining a patient immediately after a session of traction: the transient changes for better or for worse, detected then, mean very little. Traction. The patient then lies down on the couch in the position that is considered to be most effective and the harnesses are applied evenly and firmly but not in such a way that the patient tenses up. Finally, traction is started slowly, reaching 30-35 kg within a minute. As the patient becomes accustomed to the pull, traction can be increased to reach the maximum that is tolerable. However, on the first occasion, the traction force should be low, say 30 kg

for a person of moderate body weight and applied for no longer than 1 5-20 minutes. Care should be taken particu­ larly in acute lumbago when twinges have only recently ceased. The therapist should always be within earshot and from time to time must directly observe the patient. This helps to give the feeling that there is continual control of the situation. It is still useful to ask the patient regularly abou t any d iscomfort because, although instructions will have been given about reporting dis-

Box 59.6 Traction procedure 1 . I nform the patient a bout the tech n i q ue, the mechanism

and the possible side-effects. 2. Exa m i ne the patient each time before traction is

appl ied. 3 . Look for the most comfortab l e position. 4. Apply for the straps firmly but not too tight. 5 . Start the traction slowly, reaching 30-35 kg after one

6. 7. 8. 9. 10. 11.

12.

m i n ute: -first occasion: traction force may remain low -further occasions: i ncrease to 60% of the body weight. Keep the appl ied traction force steady for a bout 30 m i n utes. Release the traction force slowly - over 2-3 m i n utes. Allow the patient a few m i nutes' rest before getting up. Perform gentle active and passive movements of pelvis and h i ps before getting off the bench. Patient's back should be kept stra ight on getting off the bench. I nstruct the patient about activities of d a i ly l iving and a l low h i m/her to wal k a short d istance before getting i nto a car. G ive traction on a d a i ly basis for 2-3 weeks. Treatmerrt: must be a bandoned if no improvement is experienced after seven or eight sessions.

CHAPTER 59 - TREATMENT OF T H E L U M BAR SPI N E 901

comfort, some patients still accept painful reactions. Anything more than the minor discomfort of the harnesses cannot be disregarded. Release of traction. When traction has been completed,

particular care is exercised while the tension is being released and the harnesses loosened, for this is the time when twinges are most likely to occur. To prevent this unpleasant experience, release is slow, over say 2-3 minutes. The harnesses are then loosened carefully, the pelvic one first because this influences the lumbar seg­ ments least. The patient is also reminded of the need to remain quite still and resist the temptation to take a very deep breath as release is completed. Five minutes further rest on the couch before getting up is also advisable in that it gives the patient a chance to ' regain normal length' before compressing the joint by standing. Next, the low back is moved a little, first by flexing I extending each leg in turn slowly, then by tilting the pelvis. If this proves possible without twinges, the patient can get off the bench; this should be done keeping the back straight by rolling on to one side, putting the feet over the edge of the couch and rising sideways to a sitting and thereafter a standing position. Any pain should suggest that the patient spend another 5 minutes on the bench before trying to rise again. After-care. The patient is then shown how to put shoes

on and how to sit in a car (see p. 921 ). If the low back still feels stiff on leaving the room, it is better for the patient to take a short walk before getting into a vehicle. A lumbar support, for example a rolled towel, is often useful to prevent the patient from sagging. In this way, the intradiscal pressure is kept as low as possible. However, during the whole period of treatment the patient should be instructed to avoid sitting and stooping as much as possible.

Results. In most of those patients with disco-dural low back pain and sciatica in whom results of manipulation have been insufficient, traction proves effective. The nuclear protrusions recede in the course of 2 or 3 weeks, while the patient is ambulant. First of all, the pain eases. Gradually, straight leg raising returns to full range. Lastly, trunk movements cease to hurt. When the patient is nearly well, a painful arc often appears on straight leg raising. The effect of sustained traction on herniated nuclear material has been studied with CT. 104 Thirty patients with lumbar disc herniations were investigated. Their ages ranged from 20 to 40 years and their body weight from 55 to 68 kg. The duration of traction application was 40 minutes, with a load of 45 kg. Evaluation of the results showed a regression of herniated nuclear material in 78.5% of median herniations, i n 66.6% of posterolateral herniations and in 57. 1 % of l ateral

herniations. So the effects were variable, especially in relation to the amount and location of herniated nuclear material. This study also showed that low back and leg pain decreased i n all cases, except when the disc was fragmented or calcified. A recent study measured the effects of lumbar traction with three different amounts of force (10%, 30% and 60% of body weight) on pain-free straight leg raise test of 1 0 patients suffering from sciatica caused b y discoradicular interactions. The straight leg raise measurements were found to be significantly greater immediately following 30% and 60% of body-weight traction as compared to pretraction and 10% of body-weight traction. l I S AFTER TREATMENT Pulpy protrusions ooze out gradually. They start bulging backwards if the patient sits badly, or stands bent forward for some time with the lower back in kyphosis. They are apt to appear some hours after or even the day after exertion involving trunk flexion. Gradual nuclear protrusion is the explanation for waking with acute lumbago after, say, digging the previous afternoon. Hence any mechanism of the disorder must.be explained to the patient (at back schooO, who must be careful thenceforth to maintain the lumbar lordosis while holding any position for some time, especially seated (see p. 921 ). Several types of cushions and chairs have been developed to support the lumbar spine in a natural curved position. The patient need not avoid stooping and coming up again quickly; thus, for example, most of these patients can play tennis safely. Forgetful patients may require a belt.

A nuclear protrusion occurs in a young to middle-aged population and is characterized by a gradual onset, symp­ toms that develop with prolonged, mostly kyphotiC, postures and after activities which usually include forward bending. Reduction of such a disc displacement is gradual and often slow because it displaces under the influence of prolonged forces. Quick manipulative techniques, with short, high-velocity i mpulses have no effect on the nucleus. Techniques such as continuous traction that slowly ooze the nucleus back into place are then required. In our experience, traction is the treatment of choice for most patients with nuclear protrusions. However, some alternative techniques can also be used if the patient pres­ ents with contraindications to traction or the therapist

902 S E CTION TEN - T H E L U M BAR SPI N E

has n o traction equipment. We find the following tech­ niques most effective in these cases: oscillatory and sus­ tained Cyriax manipulations and McKenzie's reduction techniques. OSC ILLATORY AND SUSTA INED MANIPU LAT IONS Most techniques, as described by Cyriax and regularly used for reduction of annular displacements, can be per­ formed in a ' nuclear' way. The patient is positioned as described and the manipulator takes u p the slack and p robes for the articular end-feel. At this moment, instead of giving a sudden high-velocity thrust, the therapist proceeds to oscillation or sustained pressure. Slight oscillations at the end of the possible range during 1 0-15 seconds and frequently repeated may be effective in small displacements with minor signs on examination. When the symptoms and signs are more pronounced the patient will probably respond better to more sustained pressure. The pressu re is maintained for as long as the patient can support, usually 20-45 seconds. The manipul ator monitors the patient's respiration cycle and slightly increases the pressure during the expiration phase. In more difficult cases these techniques can be combined with continuous traction. Manipul ations a re done as long as the patient improves, usually a few sessions. When no further result i s obtained the patient is put in traction. When the trac­ tion does not lead to full resolution but has improved the patient, one can retu rn to the manipulative procedures, which are then likely to give further relief. MCKENZIE'S REDUCTION TECHNIQUES The thinking behind McKenzie's approach is based on Cyriax's disc theory. Being a physiotherapist, he has developed a prophylactic and therapeutic concept based primarily on self-applied repetitive exercises and / or positioning by the patient in order to reduce the nuclear displacement that leads to the ' derangement syndrome'. A classification - derangements 1 to 7 is made accord­ ing to the localization of the pain and the presence or not of deviation, either in kyphosis or in scoliosis.116,1l 7 The patient is taught how to apply progressively increasing mechanical forces that aim to cause centraliza­ tion and subsequent diminution of pain. The therapist's intervention is only necessary when the results of self­ treatment are insufficient. The choice of technique is based on the results obtained during repetitive move­ ments - flexion, extension and side gliding - in the exam­ ination. 1 1 8 Those movements that reduce, centralize or abolish symptoms during the testing are used as treat­ ment procedures. 119 The reader is referred to McKenzie's books and articles for further details.120--1 22 -

The main principles for treating three of the most common discal conditions - posterocentral prolapse - are set out below. These conditions mostly respond to exercises according to the 'extension' principle.

Acute lumbago without deviation. The patient has central or bilateral pain in the back and / or both glu tei and may be treated with nuclear Cyriax manipulations (rotation techniques in an osci llatory or sustai ned manner). If the McKenzie approach is chosen it is the treatment of ' derangement 1 ' . The patient gradually moves from one position to another. Progression follows when the pain centralizes and / or diminishes. Starting with 5 minutes of prone lying, the patient then progresses to lying prone in extension (resting on the elbows) for another 5 minutes. After a few minutes of relaxed prone lying the patient is asked to do extension movements in lying in series of 10 motions. The patient is advised to repeat this procedure on a regular basis. Acute lumbago with flexion deviation. This is ' derange­ ment 2'. The patient again has central or bilateral pain but also deviation in flexion. The deviation should be cor­ rected first. The start is in prone lying, supported by a few pillows. Very gradually - every 5 minutes - a small pillow is removed until normal prone lying is possible. After a few minutes the head of the table is raised and every 4-5 minutes it is raised a bit more until full exten­ sion - if possible - is obtained. All the time the pain should centralize and diminish . The patient is then gradually brought back to the neutral position. When ' derangement 2' has turned into ' derangement 1 ', in that the deviation has disappeared, the treatment of derange­ ment 1 (see above) can be continued. Acute lumbago with lateral deviation. The heavy nuclear lumbagos with lateral deviation are hard to manipu late as long as the lateral shift has not been corrected . Therefore the first technique is 'correction of the lateral shift' in standing. When the deviation can be corrected and even overcorrected in a prone-lying position, repeti­ tive extension movements can be tried, eventually with the therapist's assistance. When these manoeuvres lead to the disappearance of the deviation, the situation has probably returned to ' derangement l' and can be treated accordingly. Reduction of a derangement is not the only feature and is not sufficient. The patient should try to maintain the reduction by behaving according to the principles of back school ('keep your back hollow' ). If normal function is impaired as the result of the derangement, the pahent should be advised to exercise in order to obtain full normal painless range of movement in all directions.

C HAPTER 59

Based on the movements that still influence the patient's symptoms a treatment scheme is prescribed.

·

iNJ ECTIONS

EPIDUR AL LOCAL ANAESTH ESIA

INTR ODUCTI ON Discodural or discoradicular syndromes are treated by manipulation, traction or epidural injection. The aim of manipulation or traction is to remove the displaced tissue from contact with the dura mater or the nerve root sleeves. These techniques are therefore suitable for reducible disc displacements. If, however, the protrusion cannot be moved or the dura mater is too inflamed, an epidural injection is the treatment of choice. The aim of epidural injection is to deal with the second element of the interaction: the dura mater or nerve root sleeve. Because procaine 0.5% is used, only surface local anaesthesia is to be expected. The solution does not pen­ etrate the ligaments, the dural sheath of the nerve root or myelinated nerve tissue. The only structures anaes­ thetized are the free nerve endings of the surfaces tha t the solution bathes: the dura mater (both tube and sleeves), the posterior surface of the posterior longitudinal liga­ ment and the anterior surfaces of the ligamentum flavum and facet joints. Fluid injected from the distal end of the epidural space (sacral hiatus) is forced upwards and passes between disc and dura. Cessation of symptoms after the injection shows that the fluid has intervened in the discodural interaction. Epidural local anaesthesia is therefore very helpful when the existence of a disc lesion is in doubt. The procedure can be used safely on out­ patients. Often the injection is therapeutic; although pro­ caine 0.5% has only a short anaesthetic effect, permanent benefit often results. Intrasacral epidural injections were used in the treat­ ment of sciatica long before the nature and mechanism of production of sciatic pain was understood. The tech­ nique was conceived by Sicard123 and Cathelin124 in 190 1 . The first reports on cures of sciatica with epidural anaesthesia came from Caussade and Queste in 1 909125 and Viner in 1 925.126 In 1 930, Evans obtained a complete and permanent cure in 61% of his patients after one or two injections. Although he used large amounts of pro­ caine (up to 1 40 ml of a 1% solution), alarming symp­ toms occurred only in one case: cyanosis, opisthotonos, unconsciousness and incontinence of urine and faeces followed the injection of 120 ml of procaine 2% but 'consciousness returned within half an hour and sphinc­ ter control was re-established 12 hours later; recovery was complete'. 127

-

TREATM ENT OF THE L U M BAR SPI N E 903

Cyriax used the method from 1 937, first diagnostically to determine whether the cause of backache and sciatica lay outside or inside the vertebral column, later as the treatment of choice for irreducible disc lesions.128,129 In his series of 50 000 injections (50 ml of a procaine 0.5% solu­ tion was used) no disasters and only five misfortunes were noted: one case of hypersensitivity, two cases of temporary paraplegia of the lower half of the body and two cases of chemical meningitis, all of whom recovered without lasting harm (Cyriax:21 p. 325). Since 1 980, we have used the injection over 1 0 000 times on outpatients. There were only slight side effects, such as giddiness or headache, which usually did not last longer than hali an hour. In one case, paraplegia of the legs developed. The patient recovered completely within 3 hours.

INDICATI ONS FOR DIAGNOSTIC INJECTI ON Procaine 0.5% is a surface local anaesthetic and the fluid does not enter any structure, nor does it pass the myelin barrier of larger nerves. Also the posterior longitudinal ligament, the facet joint capsule and the ligamentum flavum will not be penetrated. The only structures rendered anaesthetic are those that the solution bathes. Temporary relief of symptoms shows that the solution has been able to pass between the two interacting sur­ faces - disc and dura. Therefore the injection is a very helpful diagnostic procedure, in that a positive answer is the proof of an existing discodural interaction. In non­ mechanical pain or in conditions such as uncomplicated spondylolisthesis, sacroiliac strain or arthritis, spinal or lateral recess stenosis and ligamentous or facet pain, the injection makes no difference to the pain. In practice, a diagnostic epidural injection can be used in psychogeniC backache, uncharacteristic backache or unusual referred pain.

Psychogenic pain. The history and functional examina­ tion usually settle the diagnosis (see Section 1 6 ) . However, even when a patient reacts i n a neurotic way, a small underlying discodural interaction may also be present. The psychogenic signs overshadow the organic ones and make it difficult to arrive at a conclusion as to the nature of the lesion. A diagnostic epidural injection is then indicated. Twenty minutes after the injection, clinical examina­ tion is again performed. A statement from the patient that the pain has gone identifies a minor discodural interac­ tion. Should the patient wish to make the worst of the problem, the usual statement is that the infiltration has made the pain worse. Instead of a straight leg raising limited to 20°, a limitation of 45° will occur after the injec­ tion, which supports the psychogenic nature of the pain.

904 SECTION TEN - T H E L U M BAR SPI N E

If, after injection, the pain i s unaltered, the question rem ains open whether the patient suffers from a psychogenic or a genuine non-discogenic disorder.

Uncharacteristic backache. There is a clear history of con­ stant lumbar pain and the symptoms do not vary with posture or exertion. Clinical examination shows a ful l and painless range o f lumbar movements. The latter cause little or no ache, or only one movement slightly increases the pain. The question then arises whether the pain is of dural, ligamentous or non-mechanical origin. I f it i s abolished temporarily by the induction o f a l ocal anaesthesia, d ural origin is established . Often the injec­ tion is also therapeutic. Referred pai n. A diagnostic epidural anaesthesia may be needed in cases in which it is not certain whether the symptoms are local or referred. The typical example is pain in the buttock or thigh: if lumbar movements do not hurt and no abnormalities in the sacroiliac joint, hip or buttock are detectable, the question whether the pain has a dural or a local origin arises. The epidural injection then settles the d iagnosis at once. Med icolegal cases. Contradictory opinions often exist. The presence or absence of a disco dural interaction can once again be determined by the use of local a naesthesia. INDICATIONS FOR THERAPEUTIC INJECTION The injection is used as a treatment for those disco dural interactions unsuitable for manipulation or traction, i .e. in those cases in which the bulge, for one reason or another, cannot be removed from the dura mater, or where the dura mater is too inflamed. This can be the case in all three syndromes: lumbago, backache and sciatica.

Lumbago Hyperacute lumbago is an excellent i n dication for epidural injections. Because of the severe impingement of the protrusion on the dura mater and the extreme inflammatory reaction of the latter, the dural symptoms are so profound that the patient . experiences severe twinges on the slightest movement. In such a case, even a slight attempt at manipulative reduction is aborted by severe muscle spasm and increasing pain. Traction is strongly contraindicated, for considerable worsening of the condition is to be expected. Epidural local anaesthe­ sia, in combination with manipulations from the next day onwards, is then the only alternative to several weeks of bed rest. Immediately after the injection, dural signs and symp­ toms disa ppear: a cough no longer hurts, and neck flexion and straight leg raising are of full range and pain­ less. It has been suggested (Cyriax:21 p. 320) that relief of pain leads to decrease of muscle spasm which, in combi-

nation with the recumbent position, allows a quick spon­ taneous reduction of the bulge. It follows that for the next 24 hours a horizontal position should be maintained. The patient should also be prohibited from being driven home in a sitting position. He or she should return as they came - recumbent. By the next day the symptoms have usually improved sufficiently for the patient to be able to get up and walk around, and it is even possible to travel to the therapist's office for further man ipulative reduction. It is striking that the dural symptoms and signs usually do not return when the local anaesthesia has worn off. The immobilizing twinges having been abolished, the patient can be manipulated, which secures complete relief of the articular signs after one to four sessions.

Backache Ordinary discodural backache responds very well to physical treatment: annular lesions are manipulated and nuclear displacements are treated by traction. Epidurals are reserved for those unusual cases which prove refrac­ tory to both manipul ation or traction. Also, when manip­ ulation and traction are technically not possible for one reason or anothel� epidurals are called for. There are also discodural interactions in which the dural inflammation continues, despite a total or partial reduction of the disc displacement: the approach will then be to desensitize the dural tube, in order to abolish the constant ache.

I ntractable backache. Discodural backache is called 'intractable' when it proves to be refractory to both manipulation and traction. A distinction from recurrent backache should be made. Here the displacement can be reduced but remains unstable. In intractable backache, however, every attempt to replace the bulge fails. The next approach is to give a number (one to four) of epidural injections at weekly intervals, which very often '. abolish the permanent pain. 'Bruised dura'. After an attack of acute lumbago the dura remains painfully inflamed resu lting in a chronic back­ ache, unaltered by position or movement. The clinical examination reveals a full and painless range of lumbar movement. Epidural local anaesthesia should be given at once. If inflammation lies at the origin of the symptoms, the pain disappears, not only for the anaesthetic's duration of action but very often permanently. Early morning or nocturnal backache. The history is that of a patient complaining of being woken every morning by severe backache. After the patient is out of bed the pain quickly subsides. During the day everything can be done without the slightest discomfort. Clinical examina­ tion reveals nothing but full and painless lumbar mo tion. The pain mechanism in early morning backache is probably dural. The increased intradiscal oncotic pres-

CHAPTER 59

sure during the recumbent position causes an expansion of t�e disc, which bulges against the dura mater.130- 132 In this condition no physical treatment is possible but epidural local anaesthesia succeeds in about 70% of cases.

Preg nancy. Du ring the final months of p regnancy, discodural backache cannot be treated by manipulations or tractions. The alternative is then epidural local anaes thesia. Neurosis. Sometimes the patient is too hypersensitive to accept active treatment, especially when the treatment methods are not totally devoid of some unpleasant side effects. It is therefore not always wise to manipulate the back of a psychoneurotic patient. First of all the patient is usually very anxious and not prepared to receive (brutal) active treatment to the painful back. Second, if he I she finally accepts manipulation, one will feel that the mai1ipulation actually does not take place, because of the increased muscle defence when slack is taken up. Therefore, if the physician thinks that the personality of the patient is such that manipulations will not be tolerated, it is better to treat with epidural injections.

Sciatica Only 30% of patients with sciatic pain are treated suc­ cessfully by manipulation or traction. In practice, only those protrusions which are not too large, not too long­ standing and without too much periradicular inflamma­ tion will respond. When the bulge is too large (impairment of motor and I or sensory conduction), too long standing (more than 6 months) or there is considerable nocturnal pain, the treatment of choice is epidural local anaesthesia. Epidurals are also called for when sciatica is in the recovery phase or when a bruised dural sleeve results after the bulge has disappeared.

Discoradicular d isorders with neurological deficit. Root pain together with signs of interference with conduction (motor and I or sensory) show that the protrusion has reached such an extent that reduction is impossible. The induction of local anaesthesia via the sacral route is then strongly indicated and affords lasting relief in about 80% of cases. The mode by which improvement is secured is still a matter of discussion but it seems that the solution has a lasting desensitizing effect on the free nociceptive nerve endings in the dural sleeve. It has also been sug­ gested that the fluid, which is forced between the dural sleeve and the bulge, lastingly separates both compo­ nents, and thus ends their 'conflict'. An epidural is the treatment of choice for root pain with muscle weakness or sensory deficit. As in other treatment methods recommended in this book, the injec­ tion is either quickly successful or not effective at all.

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TREATM ENT OF T H E L U M BAR SPI N E 905

The patient should therefore attend 1 week after the injection for the symptoms and signs to be re-evaluated . If the first injection has afforded no lasting benefit (objective and I or subjective), further epidural injections should be abandoned because there is almost no chance that they w i l l add to a cure. In contrast, if the first injection has afforded some benefit, further injec­ tions should be given, at intervals of 7-1 0 days, until the patient is completely pain free. There is theoretically no limit to the number of epidu ral injections that can be administered but u sually the patient needs two to four, depending on the severity and the immed iate d iagnostic response after the first injection. The diagnostic response after the first injection often has a predictive value for the number of injections required. If the straight leg raising is full and painless, one more injection will probably be needed. If there is pain at the end of range, one or two more injections are required. If straight leg raising although improved, still remains somewhat limited, several weekly injections (up to six) may be necessary. Sciatica with straight leg raising limited on the painless side usually requires more than the usual number of injections: after the first injection the range on the good side is restored immediately but it may take up to seven injections before the leg on the painiu l side can be raised painlessly to a full range. Patients with severe neurological weakness usually lose their pain very quickly. After one or two injections they are relieved of the sciatic pain although it may take some months before their strength recovers. The course during the first few days following the injection is very difficult to predict. Many patients com­ plain of increased pain during the days following the injection and then improve rapidly. Others have immedi­ ate improvement, or improve over 2-3 days and then relapse. Sometimes the patient recovers slowly but grad­ ually in the course of a week. The patient should there­ fore be warned that during the first days no prognostic conclusions can be drawn from the symptoms and that for a couple of days it may be possible that more pain is suffered than before the injection. Symptoms and signs should be assessed only after 1 week. In long-standing root pain it is even better to wait for 2 weeks, because considerable improvement often takes place during the second week after the injection. A second injection is considered if either subjective or objective improvement are detected: for instance, the patient states that pain is diminished but during clinical assessment straight leg raising is as limited as before the injection; or there is a marked increase in straight leg raising but the patient insists that the pain is as severe as ever. Improvements in symptoms and signs usually run parallel, which simplifies the decision in favour of a

906 SECTION TEN - T H E LUM BAR SPI N E

second injection. However, if there has not been a lasting change in pain and I or signs, repetition of the procedure is pointless. It is then better to try a sinuvertebral block or to refer the patient for surgical intervention. Cases that are often refractory to epidural anaesthesia are those in which the patient stands deviated in flexion and away from the pain. If every attempt at extension or side flexion in the limited direction is followed by severe pain shooting down the limb, surgery is almost unavoidable. The prognosis is also poor when the patient stands sym­ metrically but deviates markedly during forward flexion. Sciatica in the elderly and third lumbar disc lesions with root pain and deficit seldom respond to epidural injec­ tions. In both cases, we p refer to induce sinuvertebral blocks at the required level. If the immediate diagnostic response after the injection is excellent but, after 1 week, the patient remains as bad as before, the injection can be repeated with some corti­ sone or triamcinolone added to it, which may produce permanent relief.

Sciatica without neurological signs. Clinical examination shows no clear signs of impaired conduction but data drawn from the history and clinical examination strongly indicate the injection. This is the case in the following conditions: • • • • • • •

Root pain longer than 6 months' standing. Recovering root pain. Recurrence within a year, following sciatica with neurological deficit. Considerable nerve root inflammation. ' Bruised dural sleeve'. Primary posterolateral protrusion. Failure of manipulation or traction.

Root pain of longer than 6 months' duration. The chance of reduction of the bulge whether by manipulation or by traction is very small . In contrast, the induction of local anaesthesia usually affords good results. Normally, root pain caused by a disc lesion starts to recover spontaneously within 1 year. If this is not the case and pain and limitation of straight leg raising continue, one or two epidural injections should be given. It is as well to wait up to 2 weeks before the second injection. Cyriax explains the good results by the mobilization of the nerve root during local anaesthesia and by the lasting desensitization of the nerve root sleeve (Cyriax:21 p. 323). Recovering root pain. The patient has spent some days or weeks in bed and the sciatic pain is declining. Clinical examination shows limited straight leg raising but no weakness. Although this case seems to be an indication for manipulation or traction, epidural local anaesthesia usually affords better and quicker results.

Recurrent sciatica after a recent root palsy. Occasionally

a patient is encountered who, after the sciatic pain has completely gone, whether as the result of root atrophy or after a couple of epidural injections, sustains another attack of sciatica within a year. This is most uncommon, for in most patients signs and symptoms do not recur at the same side and level once they have d isappeared. Probably a small and recent protrusion underlies the 'new' pain. Therefore it could be argued that such a case would benefit from manipulation or traction. In practice, however, these measures seem to fail, whereas one or two epidural injections usually succeed. Inflammation of the nerve root sheath. If the sciatic pain

is constant and remains during recumbency, a consider­ able degree of inflammation around the nerve root sleeve should be suspected. Even although neurological signs are absent, manipulation or traction is then best avoided, for fear of considerably increasing the symptoms. The treatment of choice is epidural local anaesthesia. It is our experience that, in acute and intense nerve root inflammation, it is wise to add 40 mg of triamcinolone to the solution. Bruised nerve root sleeve. The sciatic pain is more or less continuous and not dependent on posture or movement. The clinical examination shows nothing but a full range of movement, painless straight leg raising and normal conduction of the nerve roots. No alternative causes for the pain are present. The segmental pain may be caused by a persisting inflammation of the dural nerve root sleeve after the bulge has undergone reduction, whether spontaneously or as the result of treatment. Although the nerve root lies free and has normal mobility, it remains inflamed and causes continuous sciatic pain. Epidural local anaesthesia should be induced to settle the diagnosis. Very often the pain is abolished not only for the time being but also permanently. Usually one or two epidural injections suffice for complete cure. Primary posterolateral protrusion (see p. 757). The disor­ der can be treated by traction or by epidural local anaes­ thesia, depending when the diagnosis is made. Traction very often succeeds but the recurrence rate is high. Epidural local anaesthesia affords no benefit at all when the problem is still developing. The injection therefore should only be given when signs and symptoms are at their worst. In practice, the patient should be re-exam­ ined every 2 weeks. The injection is given when the limi­ tation of straight leg raising becomes more or less stable. One to three injections may then relieve the condition. Treatment of primary posterolateral protrusion is thus neither simple nor quick. It should be explained to the patient that proper treatment can only be given at a specific moment during the development of the condi-

CHAPTER 59

tion, which may require a wait of up to 4 months. As the pain' is never severe and never appears during the night, it is usually possible for the patient to avoid premature surgery. Failure of manipulation or traction. The possibility that a

displaced disc fragment causing a discoradicular interac­ tion can be replaced by manipulation or traction is about 30% a. Cyriax, personal communication, 1982). The reason is that the bulge is located beyond the edge of the posterior longitudinal ligament. The ligament is therefore not of great help in shifting the disc back into place, as occurs in manipul ations for discodural interactions. However, manipulation and traction can always be tried first if no contraindications are present and the condition is suitable: root pain lasting no longer than 6 months, no neurological deficit and a moderate degree of inflammation. If there is no marked improvement after two or three manipulative sessions or after 10 sessions of traction, the patient should be referred for epidural local anaesthesia. Indications for epidural local anaesthesia are summa­ rized in Box 59.7. CONTRAINDICATIONS

Sensitivity. Hypersensitivity to procaine is very excep­ tional . In a series of 50 000 epidurals, Cyriax encoun­ tered it once. The rarity of the condition does not imply

Box 59.7 Indications for epidural local anaesthesia -

Diagnostic

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TREAT M E NT OF T H E L U M BAR SPI N E 907

that the physician can ignore it and the greatest care should be taken. If the patient mentions serious adverse reactions from previous local anaesthesia, it is better to test for sensitivity. If no special local or general reactions follow, the epidural injection can safely be given the next day.

Local sepsis. The existence of local skin sepsis in the neighbourhood of the site of introduction of the needle is an absolute contraindication. The introduction of bacteria into the neural canal is disastrous 133 and therefore the risk should not be taken. Also a previous local abscess or previous operations for a pilonidal sinus or anal fistula should be considered contraindications. Previous neurological infections. It has been argued that, after the recovery from a febrile neurological iniection, some septic adhesions may form at the lower end of the theca. Pressure on the epidural fluid could then reactivate the inflammation. Anticoagulant therapy. The insertion of an epidural needle into the sacral canal very often causes a venous puncture. In the presence of anticoagulant therapy, bleed­ ing could provoke serious haematoma, with the possible consequence of adhesions. SIDE EFFECTS AND DANGERS OF EPIDURALS Apart from hypersensitivity, which usually can be pre­ cluded before the injection, two main adverse reactions are possible: hypotension when the injection i s given intravenously or too rapidly, and transient para­ plegia if the solution leaks through the dura to cause spinal anaesthesia.

Psychoneurosis Uncharacteristic backache Referred pain Medicolegal cases

Hypotension. If certain precautions are taken, a drop in blood pressure should not be feared:

Therapeutic

•

Hyperacute l umbago: ( i n combi nation with m a n i pu lation) Backache: Intractable backache ' B ru ised d ura' Morning or nocturnal backache Pregnancy Psychoneurosis Sciatica: Sciatica with neuro log ica l deficit Sciatica without neurological deficit • Root pain of over 6 months' sta n d i n g • Recovering root pain • Recurrence within the year, fol lowing sciatica with neurological deficit • Considerable nerve root i nflammation • Bru ised d u ra l sleeve • Primary posterolatera l protrusion • Fa i l u re of m a n i pu lation or traction

•

•

Intravenous injection is avoided by testing for aspiration of blood after the needle has been inserted and following the injection of each 5 ml of fluid (see p. 912). The fluid is i njected very slowly at a rate of 10 ml / min. After each 10 ml there should be a pause of 30 seconds to 1 minute. During the injection a constant conversation is main­ tained with the patient. The slightest faltering in the voice is usually an indication of an incipient drop in blood pressure. The introduction of fluid is then temporarily stopped until the patient feels better.

Spinal anaesthesia. Cyriax described four cases of paral­ ysis to the mid-thorax after the epidural induction of 50 ml procaine 0.5%. The solution had obviously trans­ gressed the dural barrier and temporarily paralysed the lower limbs and the abdomen. Diaphragmatic breathing

908 SECTION TEN - T H E L U M BAR SPI N E

was retained, the patients did not need artificial ventila­ tion and all recovered from their paraplegia within 2 hours (Cyriax:38 p. 1 83). One of the present authors (L.O. ) encountered a similar instance of paraplegia up to the lower thoracic region. Weakness of the limbs became apparent during the injection, which was stopped after the in troduction of about 20 ml of procaine 0.5% . It took 3 hours before strength in the limbs reappeared sufficiently for the patient to drive home. The most likely explanation for the spinal anaesthesia is an unintentional intrathecal injection: the tip of the needle pierces the dura mater during the procedure. Even if the tip does not remain intrathecally during the injec­ tion, enough of the solution can pass through the hole to give rise to a complete sacral and lumbar root block.134 In order to avoid this complication, the injection should be given very slowly, and aspiration is made after each 5 mI, or after each unintentional movement by the patient. At each stopping point, the Achilles tendon reflex is tested, together with the force of the dorsiflexors of the toes at both sides. If weakness is discovered, the injection is stopped at once.

receive a needle, without fear of piercing the dura. Normally, the needle can be moved upwards over a dis­ tance of more than 6 cm before the tip reaches the distal end of the dural sac. 1 35

Landmarks The d istal end of the sacral canal is formed by the distal basis of the sacrum, the two sacral cornua and the inter­ cornual l igament. There is only subcuta neous fat between the borders of the sacral hiatus and the cover­ ing skin (Fig. 59.24). The most important landmarks are therefore the two cornua, bordering the distal end of the sacrum. The pal­ pation of these two bony prominences is not always easy. Some women have a thick layer of fat covering the sacrum, camouflaging the cornua. Sometimes the cornua are absent or asymmetrical. Sometimes they lie deeply between the buttocks or may appear higher up, where they can be palpated some centimetres proximal to the intergluteal line. In order to palpate the cornua the following instruc­ tions should be followed: •

TECHNIQUE The aim of the technique (summarized in Box 59.8) is to introduce the fluid into the epidural space, a space between two concentric cylinders: the outer cylinder is the bony sacral and lumbar canal, the inner cylinder the dural tube with the dural nerve root sleeves. The space is fi lled with loose connective tissue, fat and venous plexuses. The sacral canal ends at the lower end of the sacrum, where it is covered only by ligament, subcutaneous tissue and skin. The dura mater usually ends at the level of the second sacral vertebra. These anatomical peculiarities make the d istal end of the sacral canal a suitable place to

•

The patient lies prone, with the pelvis slightly tilted up by placing a small pillow under the symphYSiS. The legs are slightly spread and rotated internally (Fig. 59.25). This position moves the buttocks outwards and makes the sacrum and the hiatus more prominent. I n this position the two cornua can sometimes be seen at the upper extent of the intergluteal line.

I f the cornua are not visible, they can be located in the following way: both inferior iliac spines are palpated and a downwards-pointing equilateral triangle is drawn, the base of which is formed by the line connecting the two

Box 59.8 Sacral epidural injection: technique • Position the patient • Check the landmarks • Desensitize the skin and the intercornual l ig a ment with 1 ml l idoca i n e ( l i gnocaine) 2% • Introduce the spinal needle about 4 em into the sacral canal • Remove the stylet and check for blood or cerebrospinal

fluid • I nject slowly - no more than 5 m l/m i nute while mainta in­

ing conversation with the patient

� ' ' il --�

--

• I nterrupt the i njection after each 5 m l and:

-check for need l e placement -check b l ood pressure -check strength of dorsiflexors • After the i njection the patient remai ns prone for about 10 m i nutes and supine for another 1 5 m i n utes.

! /'

' f; I

Figure 59.24

The sacral hiatus, 1 and inferior iliac spines, 2.

CHAPTE R 59

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TREATMENT OF T H E L U M BAR SPI N E 909

Figure 59.25

Position of the patient for locating the

cornua.

spines; the ti p of the triangle point is at the sacral hiatus (Fig. 59.26). Other important landmarks are the sacral spinous processes and the two sacrospinal muscles at the first sacral level. The sacral spinous processes are palpated in order to estimate the curvature of the sacrum and the direction of the spinal canal. It is extremely important to assess the angle of the sacrum, in order to estimate the direction of the needle in the canal . Some people have a very flat sacrum with almost no curvature at alt others have a very curved sacrum; occasionally the sacrum is twisted or has a marked asymmetry. The sacrospinalis muscles are palpated to detect such asymmetry.

Preparation A cambric roll is placed in the intergluteal fold to spread the buttocks and to protect the anus and vagina from irri­ tation by the disinfectant. If hair is present, it is shaved. One thumb palpates for the cornua. If the patient cannot relax the gluteal muscles, or the cornua lie deeply, the buttocks are stretched outwards by an assistant. Care should be taken not to overstretch the skin over the cornua, for fear of obliterating the landmarks. A small syringe, filled with 0.5-1 .0 ml of a 2% lido­ caine (lignocaine) solution is fitted to a 1 inch 25 G needle. This is used to anaesthetize the skin and the sub­ cutaneous tissue over the hiatus, distal to the palpating thumb (Fig. 59.27). The needle also penetrates the inter­ cornual ligament under the thumb. The angle at which the needle enters the hiatus is noted in order to have a guide for the introduction of the larger lumbar puncture needle. So as not to obliterate the bony landmarks, it is important not to use more than 1 m!.

Introduction of the needle The insertion is made with a lumbar puncture needle equipped with a stylet. In order to be manoeuvred easily into the sacral canat the needle must have some flexibil­ ity and therefore should be long: one of 9 cm is perfect for

Figure 59.26

The triangle used to locate the sacral hiatus.

9 1 0 SECTION TE N - T H E L U M BAR S P I N E

(a)

Figure 59.27

Anaesthetizing the skin and subcutaneous tissue over the hiatus.

this purpose (21 G x 3t inches). The stylet precludes the risk of carrying in a piece of skin, which later could lead to the development of an inclusion dermoid cyst. The needle is thrust in between the two cornua just distal to the palpating thumb. After piercing the thick intercornual l igament it passes freely through the hiatus before it hits the bone of the sacral base. The needle is then partly withdrawn and slightly angled i n order to conform with the obliquity of the sacral canal; this can be done by slight pressure of the palpating thumb on the skin above the needle (see Fig. 59.28). The needle is then moved further upwards over a dis­ tance of 3-5 cm. Normally the tip then remains well distal to the lower end of the dural sac, which is repre­ sented by the line between the two lower iliac processes. Usually the needle slips intrasacrally without any problem. However, the tip may meet bone, which indi­ cates that the angle must be altered. To judge the angle of insertion of the needle is the most difficult part of the whole procedure. Important guides are the previous pal pation of the lower sacral spinous processes and the angle of the fine needle used for surface anaesthesia when it was pushed through the intercornual ligament. A difficult sacrum to approach is the very curved one, which demands a punctu re well distal to the bony ridge connecting the cornu a . The needle is then aimed almost horizontally, in the direction of the patient's head. A

(b) Figure 59.28

Insertion of the lumbar puncture needle.

patient with hyperlordosis usually has a flat, horizontal sacrum which calls for an almost vertical insertion. A particular problem is the overcurved bifid sacrum, where the sacral arches are not bony but consist of fibrous tissue. If the insertion is made too low down, the tip of the needle may slip through the ligamentous roof of the sacrum and come to l ie in the fibrous tissue closing the defect. An occasionally encountered difficulty is the sacrum with an intrasacral bony projec­ tion. If the needle catches such a bony obstacle on its way up, it must be withdrawn a short distance and thrust in again at a slightly d ifferent angle. If this proves to be impossible, the tip of the needle should b� left there and the injection made from this position, provid­ ing no palpable swelling at the hiatus appears as the fluid is administered.

CHAPTER 59 - TREATMENT OF THE L U M BAR SPI N E 9 1 1

When the needle is far enough into the sacral canal, the stylet is withdrawn. Care is taken to see that neither cerebrospinal fluid nor blood escapes. The needle pierces the theca in only the occasional case in which the dural sac ends at an abnormally low level. I n most, the dural sac terminates at the level o f 52, which i s considerably more proximal than the t i p o f the needle. If cerebrospinal fluid escapes, the needle should be removed immediately. It is a serious mistake to withdraw the needle only a little until it lies extra-durally and then to continue the injection, for enough of the procaine solu­ tion can pass through the hole to cause a spinal block. Hence, if the theca has been pierced, the whole procedure should be postponed until some days later, when the needle is not inserted so far proximally. Often blood escapes when the stylet is withdrawn, which is not surprising, considering the number of epidural veins in the sacral canal. It is sufficient to move the tip of the needle into such a position that it no longer penetrates the vein, and the injection can then be given without any danger. If the needle cannot be manoeuvred to such a position that blood ceases to escape, the injec­ tion should be postponed for 2 days.

The injection A syringe containing 50 ml of procaine 0.5% is connected to the needle. Aspiration ensures that the needle has not penetrated either the dura or a vein. The solution is then injected very slowly at a rate of no more than 5 ml / min. Normally, not much tissue resistance is felt and the patient only experiences a slight ache in the sacral region. Usually the full volume of 50 ml is injected, but the amount can be altered according to the size of the patient and the localization of the lesion. Even in a large patient with a third lumbar lesion, 50 ml is always sufficient. Smaller amounts - 30-35 ml - are adequate in slightly built women and 40 ml are sufficient for any patient with a lesion at the L5-S1 level. If the fluid cannot be injected or the patient experi­ ences considerable pain over the sacrum, a subperiosteal localization of the tip of the needle should be suspected. Although the needle lies correctly intrasacrally, the tip remains under the periosteum, which obstructs the free entrance of the fluid (Fig. 59.29). In this case, it is usually sufficient to rotate the needle through 1 80°, so that the bevel faces towards the sacral canal. If introduction of the fluid is still obstructed, the needle should be withdrawn by a millimetre or two. Before the injection is tried again, a new aspiration should be performed to ascertain that neither the theca nor a vein has been punctured. The physician keeps the palm of his free hand flat on the sacrum during the whole injection. I f the needle is inaccurately inserted and lies in the sacrospinalis muscle instead of in the sacral canal, a swelling will be felt under

Figure 59.29 I f the fiuid cannot be injected, a subperiosteal localization of the tip of the needle should be suspected.

the palpating hand after the introduction of about 1 0 ml (Fig. 59.30). A misplaced needle is more common than expected as was demonstrated by a recent study on 200 consecutive injections: only 85% of caudal epidural injections clini­ cally thought to be correctly placed were confirmed radi­ ographically.136 The hand on the sacrum is thus the main safeguard against a misplaced needle and it is therefore vital to palpate the two sacrospinalis muscles before the injection is started. Sometimes there is marked asymme­ try in the two convexities of the sacrum. If this is not ascertained before the injection, an expanding bulge in one sacrospinalis muscle during the injection will be

Figure 59.30 Palpation of the sacrum during injection detects misplacement of the needle.

9 1 2 SECTIO N TEN - T H E L U M BAR SPI N E

more difficult to identify. Although a n extrasacral injec­ tion causes no harm at all, it may cause false diagnostic conclusions or an unjustified conclusion of therapeutic failure. After each 5 ml is injected (Fig. 59.31) it is as well to interrupt the procedure and to test the strength of the dorsiflexors of the toes, in order to detect an incipient paralysis. The strength of the foot muscles will quickly weaken if the solution passes the dural barrier. Aspiration is also performed each time the patient moves. The physician should maintain conversation with the patient during the whole duration of the injection. The patient describes any pain, locally or referred, dizziness and headache. A stuttering voice is usually the first warning sign of an unfavourable effect. If the patient feels odd, or his or her voice is slightly faltering, the injection is temporarily stopped until he or she feels better. If dizzi­ ness appears rapidly during the injection, and continues for more than 5 minutes even though no more fluid is in troduced, the injection should be abandoned. Elderly people usually sustain the injection better than younger patients. The dizziness and the slight headache that follow too rapid an injection is explained by the quick raising of the pressure in cerebrospinal fluid, which causes an abrupt drop in the venous pressure in the sagittal sinus. 1 37 The injection typically causes an unpleasant feeling of pressure at the sacrum, sometimes radiating to both but­ tocks or thighs. A patient with sciatica usually declares that pain in the leg is reproduced when the fluid is injected, which probably results from increased pressure on the inflamed nerve root sheath.138 Reproduction of root pain may start after the introduction of 5-10 ml if the patient suffers from a lesion at the fifth lumbar level, but

Figure 59.31

The injection.

if the lesion lies at L3 the pain will be felt only after 35-40 ml (Troisier:1 39 p. 383). Pain reproduction during an epidural injection is a good sign, in that it indicates that the fluid is placed epidurally and has reached the affected nerve root. The intensity of the pain depends on both the degree of inflammation and the speed of injection. If the injection is done too quickly, the pressure on the inflamed nerve root may increase so rapidly that it causes unbearable pain, which should obviously be avoided. Because the injec­ tion may have to be repeated, it must be given in such a way that the patient does not fear it on the next occasion. The physician therefore adjusts the injection according to the reaction of the patient.

After the injection The patient remains prone for about 1 0 minutes and then turns into a supine-lying position, remaining there for at least 15 minutes and kept under observation the whole time. Occasionally, a patient feels faint or has a slight fall in blood pressure a few minutes after the injection. If this occurs, it is usually sufficient to raise the legs. Sometimes there is a slight numbness over the sacrum and the saddle area, and in the supine position the pressure of the couch is not felt. The feet may become warm after the injection as a consequence of sympathetic block, which indicates that the fluid has reached the second lumbar level. Within 1 5-20 minutes of the injection the inflamed dura or dural nerve root sleeves should be rendered more or less anaesthetic. The effect of the epidural is best tested by noting the change in range and pain on straight leg raising. Especially in sciatica, immediate improvement of straight leg raising has prognostic value. If full and pain­ less straight leg raising is restored immediately after the injection, one more injection will usually settle the matter. If there is only some improvement in straight leg raising, which remains very uncomfortable or even limited, two to four more injections may be required. In sciatica with a bilateral limitation of straight leg raising, the first epidural injection usually restores full and painless range of the leg on the unaffected side but the restriction on the painful side can remain unchanged; the range of straight leg raising on the affected side shows only slight improvement after the second injection and it may even take five more injections before a full and painless range is restored. Hence, it is probable that five to six epidurals are required to cure sciatica with bilateral limitation of straight leg raising. The patient is allowed to get up after 20-30 minutes. To most patients this is not a problem; they can walk out and even drive a car safely. However, occasionally a patient may feel a little lightheaded or have a slight and te�po­ rary disturbance of proprioception. Although muscle strength is completely normal, walking may be difficult.

CHAPTER 59

It has been suggested that this is merely the result of some loss of deep sensitivity.1 4o Probably a tiny amount of the local anaesthetic has leaked through the nerve root sheath. The concentration is too low to have serious clin­ ical effects1 4 1 and symptoms disappear in the course of abou t 30 minutes. Patients who complain of dizziness or show some disturbances in gait after the injection should thus remain supine until their symptoms disappear com­ pletely. As it is very difficult to foresee how a patient will react to · an epidural injection, and theoretically any patient may need to lie still for an hour or more, the tech­ nique must not be used if time is limited. The patient is advised to take relative rest for the remainder of the day. From the next day on, normal daily activities can be resumed. Some patients complain of a slight headache but this does not last longer than 24 hours. The immediate result of the injection is very difficult to predict. Some patients with sciatica may have increased pain for 2-4 days, and then improve rapidly, or have an initial improvement but relapse after a couple of days. Others have immediate and excruciating pain for 1-2 days and then gradually improve. Because the direct result of the injection is so variable, it is best not to eval­ uate the situation until a week has elapsed. In patients with long-standing sciatica it is even better to wait 2 weeks because improvement often only takes place during the second week following the injection. FOLLO W UP One to two weeks after the first injection the patient attends for re-examination. In judging the results, both subjective and objective factors are taken into consider­ ation. An improvement in either warrants a second injection. Although d iminution of signs and symptoms usually run parallel, sometimes straight leg raising is considerably increased, despite the patient declaring there has not been improvement. Alternatively, there may be significantly less pain but the nerve root mobil­ ity is as impaired as before the injection. In both situa­ tions, the condition is considered to be improved and a second injection is given (Box 59.9). However, i f there has been no lasting improvement in symptoms or signs, continuation of the treatment with epidural local anaes­ thesia is pointless and other forms of treatment shoul d b e considered . Further epidural injections at intervals of between 1 and 2 weeks are given as long as there is progressive improvement. In hyperacute lumbago one infiltration, followed by a series of daily manipulations, usually suffices for cure. Chronic backache usually requires one to two injections. In sciatica up to six infiltrations may be required.

-

TREATM ENT OF T H E L U M BAR S P I N E 9 1 3

Sometimes, in spite o f a positive diagnostic response, there is no appreciable improvement at the next atten­ dance. It is then worth giving another epidural injection, this time with 40 mg of triamcinolone mixed in the pro­ caine solution. The combination may prove successful when local anaesthesia alone has failed MECHANISM The way epidural local anaesthesia works is not yet com­ pletely understood. A clinical response may be attributa­ ble to physical effects on d isc, dura and neural structures or to pharmacological actions on the surfaces bathed by the fluid. It is also hypothesized that the fluid separates the dura from the disc and thus directly intervenes in the disco dural interaction. Because of the increased pressure in the closed epidural space, the dural sac becomes com­ pressed, narrows and is momentarily released from the disc. The epidural injection of a large volume of fluid thus has a mechanical influence on the dura mater. Instead of the disc being moved away from the nocicep­ tive structures by manipulation or by traction, the du ral tube or dural sleeves are separated from the disc by the amount of fluid injected in the epidural space, as has been experimentally demonstrated by introducing lipiodol into the dural sac and thereafter performing an epidural injection via the sacral route (Troisier: l39 pp. 390-391 ). It is likely that the separation of dura and disc is not only temporary but also causes a definite change in the relationship between disc and dura. Some support is lent to this view by the observation that the introduction of normal saline into the epidural space has a therapeutic benefit on its own J 42, 1 43 Further evidence for the separation hypothesis comes from a recent randomized double-blind study on epidural injections for postoperative lumbar spinal fibrosis. Forceful injections via the sacral hiatus of 1 25 mg pred­ nisolone acetate plus 40 ml saline showed significantly

Box 59.9 A second injection is given if there is dimi nution in symptoms or signs Symptoms Less pain No more noctu rnal pain No more p a i n at rest Pa i n has sh ifted u pwards (e.g. g l utea l instead of calf) No more p a i n d u r i n g coug h i ng or sneezing More m o b i l ity in d a i ly l ife

Signs I m provement in stra ight leg raising I mprovement in l u mbar m o b i l ity 40 mg of triamcinolone is added to the solution if injection

with procai n e helped only temporarily

9 1 4 S E CTION TEN - T H E L U M BAR SPI N E

greater improvement than injections via the same route with 125 mg prednisolone acetate alone.144 Although the hydraulic effect presumably contributes to the long-term results of caudal epidural injections, it is certainly not the only mechanism. It is reasonable to suppose that the therapeutic results also depend on a lasting effect of the anaesthesia. Although the anaesthetic only desensitizes the nerve root for a short time, this may result in the breaking of a pain cycle.145

ity at 4 weeks, which resulted in improved quality of life; at 1 year, subjective and objective measures were improved equally in both groups. One of the present authors (L.a.) performed a retro­ spective study of 94 consecutive patients treated with epidural local anaesthesia. A total of 208 injections were given without side effects and resulted in a full and pain­ less range in 69 patients.154 The findings were classified as follows.

R ES ULTS

Hyperacute lumbago. Five patients were all pain free within 5 days of combined treatment with epidural local anaesthesia followed by daily manipulations.

The first results of epidural local anaesthesia were published by Evans in 1 930.127 He obtained a 62% success rate in sciatica patients with limited straight leg raising. Coomes compared the results of epidural local anaes­ thesia and bed rest in a randomized series of 40 patients suffering from severe sciatica with signs of impaired con­ duction. For the 20 injected patients he found the average convalescence period to be 11 days, whereas for those treated with bed rest alone it took 31 days to reach the same degree of comfort.146 Goebert et al147 obtained excellent results in 73% of 1 1 3 cases of sciatica treated with a combination of local epidural anaesthesia and hydrocortisone. Knutsen and Ygge148 treated 96 patients with lumbago or sciatica with prolonged extradural anaesthesia with bupivacaine and found a good to very good effect in 82% . Beliveau149 com­ pared the results of epidural injection of procaine alone and procaine together with 80 mg of methylpred­ nisolone in patients with sciatica. There was no difference between the two groups, the overall success rate being 70% . Yates1 50 compared the effect of caudal infiltration of 50 ml of saline solution, 50 ml of lidocaine (lignocaine) 0.5%, and 47 ml of lidocaine (lignocaine) 0.5% with 30 mg triamcinolone. The best results were obtained after the induction of the steroid solution. Cyriax (personal com­ munication, 1 982) obtained an overall success rate of 68% in patients with root pain and neurological signs treated with 50 ml of procaine 0.5%. Mathews et al83 compared the effect of sacral epidural injections of 20 ml of bupivacaine 0.125% and 80 mg methylprednisolone with control injections of lidocaine (lignocaine) over the sacral hiatus and found a statistically significant difference after 3 months and 1 year. Other studies describe excellent results in 60-83% of patients suffering from sciatica and treated with sacral epidurals with a mixture of local anaesthesia and methylpred­ nisolone.1 5 1 , 1 52 Bush and Hillier1 53 compared, in a double­ blind placebo-controlled study, the effect of 25 ml of procaine 0.5% containing 80 mg of triamcinolone ace­ tonide with the introduction of 25 ml of normal saline in patients su ffering from sciatica. The active group showed significant pain relief and a significant increase in mobil-

Chronic backache. There were 21 patients: 12 successes and 9 failures. This group was divided in three subgroups: •

• •

Nine patients with a 'bruised dura mater' - dural symptoms, absence of dural and articular signs produced three cures and six failures. Three patients with morning backache were all cured after one to two injections. Nine patients with chronic intractable backache (i.e. manipulation or traction had failed to secure adequate relief): three were cured after the injection, three were pain free after injection and subsequent manipulation and there were three failures.

Root pain. There were 68 cases: 39 patients with and 23 without neurological deficit and 6 patients suffering from postlaminectomy root pain. •

•

•

•

Nineteen of the 23 patients with root pain without neurological deficit recovered and in four the treatment failed. Of the 39 patients suffering from sciatica with neurological deficit, 31 recovered with one to seven injections. 40 mg of triamcinolone was added six times to enhance an initially slow response. The figures per affected nerve root are given in Table 59.2. The average limitation of straight leg raising was 35° (70-10°) at the beginning of the treatment. The average duration of the treatment was 3 weeks (1-8 weeks). The number of epidurals given was: 7 patients - 1 injection; 9 patients 2; 11 patients 3; 2 patients - 4; 1 patient - 6; 1 patient - 7. Only two of the six postlaminectomy patients responded successfully to the epidural injection. -

•

-

NER VE ROOT BLOCKS

An injection with local anaesthetic or triamcinolone at the lateral foramen and at the corresponding sinuvertebral

C HAPTER 59 - TREATM ENT OF T H E L U M BAR SPI N E 9 1 5

Table 59.2 Result of epidural injection in sciatica with neurological deficit

Root

n

Success

Failure

L3 L4 L5 81 82

2 4 11 15

1 1 9 14

7

6

1 3 2 1 1

Total

39

31

8

nerve may be required when a patient with a discoradic­ ular interaction fails to benefit from the induction of epidural local anaesthesia. This injection is also indicated in root pain from a narrow lateral recess or in persisting root pain after laminectomy. INDICATIONS

Failure of epidural injections. Some cases are found that are suitable for epidural local anaesthesia and in which injection is followed by a good diagnostic response, but in which there is no improvement after 1 week. When repetition of the injection with 40 mg of triamcinolone added is also unsuccessful, the next step is to produce root block with local anaesthesia. If this affords immedi­ ate improvement of signs, 20 mg of triamcinolone is injected at the same level. All patients with a discodural interaction for whom epidural injection has been a failure should therefore receive a sinuvertebral block at their next attendance (Cyriax:21 p. 353). Nerve root blocks are particularly indicated in radicular pain caused by far lateral or foraminal disc herniations. Foraminal injection of local anaesthetic and steroids afforded long-standing improvement in 80-90% of patients with severe lumbar radiculopathy secondary to foraminal and extraforami­ nal disc herniation.155--1 57 l2 and l3 root syndromes. Experience shows that L3 radicular pain from a disc lesion reacts quicker and better to a root block than to epidural injections. A root block is also the treatment of choice in the very uncommon case of L2 pain due to an Ll-L2 disc lesion. lateral recess stenosis. When root pain results from compression in a narrowed lateral recess, epidural local anaesthesia always proves a therapeutic failure.91 The introduction of a steroid suspension around the nerve root is very often successful and even local anaes­ thesia alone may produce a prolonged effect.158--161 The fact that infiltration of a steroid suspension around the nerve root affords long-term relief (many patients are even permanently cured) suggests that radicular pain from a lateral recess stenosis is not simply caused by a

narrowing of the bony margins o f the canal but stems from inflammation and pressure exerted by oedema and fibrosis in the perineural soft tissues.162 The main difficulty is to distinguish between the fourth and the fifth lumbar levels. Localizing symptoms cannot be provoked by clinical tests, so the triamcinolone injec­ tion is given at the likeliest level and, if there is no clear result after 1 week, repeated at the other level. If consid­ erable benefit is achieved, one or two more injections at intervals of 2 weeks will produce complete recovery.

Patients with root pain after l a m i nectomy. The post­ operative spine with persistent or recurrent root pain is a major d iagnostic and therapeutic p roblem. Differentiation shoul d be made between a recurrent d isc displacement, scar tissue formation and an overlooked lateral canal stenosis.163 Myelography and CT, al though valuable, cannot always establish the diagnosis.164, 1 65 Epidural local anaesthesia sometimes succeeds but more often scarring prevents the solution reaching the right spot. A second or third surgical intervention should only be considered as a last resort because, as Nachemson4 has pointed out, the success rate drops dra­ matically after the first operation and second or subse­ quent procedures have only a 5% chance of success. Others have reported a similar pattern of success rates (8%166 and 10%167) after a second operation. A good alternative in persistent root pain after surgery can be a sinuvertebral / root block. However, it is not always easy to single out the right point. Several attempts with a local anaesthetic may be required but, once the appropriate level has been found, 20 mg triamcinolone is injected at the same place during the next attendance. However, results of nerve root blocks in persistent root pain after back surgery are significantly poorer than in primary nerve root irritation.168 TECHNIQUE FOR ROOTS L2-LS The patient lies prone with the arms along the body. A small pillow, p laced under the pelvis, reduces the lumbar lordosis. This position relaxes the sacrospinal muscles and facilitates palpation of the bony landmarks. The intervals between the spinous processes a re marked. The line between the fourth and the fifth spinous process usually coincides with the horizontal line joining the uppermost parts of the iliac crests (Fig. 59.32a). Care should be taken, however, not to press too much subcu­ taneous tissue between the palpating fingers and the iliac crest, which may be a particular problem in obese patients. Sometimes a patient presents with a high pelvis: the sacrum is relatively low in relation to the iliac crests. The line connecting the two iliac crests may then cross the fourth spinal process, or even lie at the L3-L4 level.

9 1 6 SECTION TEN - THE L U M BAR S P I N E

( b)

(a )

Figure 59.32

Another method of identification may be required . The levels of the pal pated spinous processes and inter­ spinous ligaments are then d istinguished by using the posterior and inferior iliac s p i nes as l a n d ma rks (Troisier: 139 p . 423) : the tip of the first sacral spinous process invariably lies 2 cm above the line connecting the inferior borders of these spines. In case of doubt, the landmarks are inferred from a radiograph of the pelvis and lower lumbar spine. The intervertebral foramen lies level with the spinous process. At the appropriate level, a point is thus chosen between two consecutive horizontal lines and about three fingers breadth from the vertical midline (Fig. 59.32a). A long and thin needle (usually a 7 cm needle will do but in obese patients 9 cm may be required) is fitted to a 2 ml syringe, filled either with procaine 2% or 20 mg of triamcinolone. The needle is introduced at an angle of approximately 60° to the horizontal, aiming at the centre of the vertebral body (Fig. 59.32b). Normally the needle passes without any particular resistance to its ful l length, where it is felt to hit the posterior aspect of the vertebral body. Sometimes the tough resistance of cartilage can be felt at full depth which indicates that the needle has engaged against the disc. I f the needle hits bone or meets some ligamentous resistance at a depth of 3-5 cm, it has confronted the lateral aspect of the lamina or the posterior aspect of the

facet joint. The needle must then be almost withdrawn and pushed in again in a straighter direction. Occasionally, the transverse process is encountered and is indicated by bony contact at a depth of 5-6 cm. In this case, the needle is partly withdrawn and redirected slightly inferiorly. If the needle touches the nerve root, the patient experi­ ences a sudden and sharp electric ' shock' shooting down the leg. The sensation is only momentary and disappears irnmedia tely. As soon as bone or cartilage is felt, aspiration is per­ formed to make sure the tip of the needle is neither inside the theca nor in a blood vessel. If clear fluid is aspirated, injection with procaine should not be made, for fear of spinal anaesthesia. The needle should therefore be with­ drawn immediately, and the whole procedure p9stponed for 2 days. If blood flows back into the syringe, the tip of the needle can be slightly altered until it lies outside the vessel. If neither blood nor cerebrospinal fluid is aspi­ rated, 1 ml is injected with the tip of the needle in contact with bone or cartilage, i.e. at the site of the sinuvertebral nerve. The needle is then d rawn back 0.5-1 .0 cm. Renewed aspiration is performed and the rest of the fluid injected at the level of the foramen and consequfntly around the nerve root. Normally no particular tissue resistance is apparent. In a postlaminectomy patient, however, fibrosis may impede the injection.

Injection of the left L4 root.

CHAPTER 59 - TREATMENT OF T H E L U M BAR SPI N E 9 1 7

Usually discomfort is not felt in the back or down the limb� Tissue resistance and increasing root pain during the injection indicate that the tip of the needle remains in the nerve root tissue or the spinal ganglion. The injection is not continued unless the needle has been withdrawn over a small distance because pressure necrosis can result.169 After the injection of local anaesthetic, the patient turns supine and nerve root mobility is tested afresh. If the correct point has been chosen, there will be marked improvement in range and pain. If not, the injection is repeated either the same day or at the next attendance at one of the other lumbar levels. If an injection with triam­ cinolone solution has been made, pain relief should be evaluated after 1 week. Improvement of symptoms calls for a second injection at the same level. If no progression is noted, another level must be tried. TECHNIQUE FOR THE FIRST SACRAL ROOT The patient adopts a prone position with the arms along­ side the body and the pelvis slightly tilted to relax the muscles and to reduce the lumbar lordosis. The edge of the ilium and the two inferior iliac processes are identified. The first sacral foramen is a large aperture which lies at the level of the apex of the first sacral spinous process.

The latter i s located about 2 cm above a horizontal line connecting the two posterior and inferior iliac p rocesses (Fig. 59.33a). The first dorsal sacral foramen lies on the line, some 3 cm from the midline. 17O A 7 cm needle with short bevel is fitted to a 2 ml syringe containing procaine 2% or 20 mg of triamci­ nolone. A point is chosen on the horizontal line as far from the midline as the ilium allows. The needle is then inserted in a 45° (oblique) direction, aiming at the dorsum of the sacrum (Fig. 59.33b). This oblique insertion is preferred because a transverse insertion could easily cross the whole sacrum, pierce the anterior foramen and eventually p uncture the bowel. This would be disastrous because contarnina tion would be transferred into the epidural space when the needle is withdrawn. The obliquely inserted needle usually meets the dorsum of the sacrum at a depth of 3-5 cm. It is then moved about in slightly different directions until the resistance of a tough ligament is felt. After the needle has penetrated this, no more resistance is felt and it passes freely for 1-2 cm into the epidural sacral space. Injection can now be made after careful aSFiration has been performed; aspiration is done because the point of a needle placed obliquely through the first sacral foramen into the sacrum can easily penetrate the dura. Cautious aspiration before injection is therefore vital. Cerebrospinal

(b ) � : "i.. _

, '

: ---�

. I

.--

:

._#

,

(a)

Figure 59.33 Injection of the first sacral root.

9 1 8 S ECTION T E N - T H E L U M BAR S PI N E

fluid flowing back into the syringe i s a n absolute contraindication for injection of the local anaesthetic.

INJECTION O F LIGAMENTS

INTER - AND SUPRASPINOUS LIGA MENTS The injection is made both for diagnostic (li docaine (lignocaine) 2%) and therapeutic (10 mg of triamcinolone) reasons when a local inflammation in the ligament or the periosteum of the spinal process is considered to be the cause of symptoms. Sclerosing injections of the inter- and supraspinous ligaments of the two lower segments are also gjven as part of the stabilizing treatment in recurrent disc displacements.

Technique The patient lies prone, with a small pillow under the pelvis. The interspinous ligaments L5-S1 and L4-L5 are easily located: usually, the horizontal line joining the upper edges of each iliac crest falls between the supraspinous processes of L4 and L5. A 2 ml syringe, fitted to a 2 inch 21 G needle, is filled with the solution. At the required level the needle is inserted vertically through the ligament and moved slightly upwards so that it touches the inferior border of the spinous process of the vertebra above; 1 ml of the fluid is then injected by a series of droplets deposited at the ligamentoperiosteal j unction (Fig. 59.34). Then the needle is partly withdrawn and reinserted in the direc­ tion of the upper surface of the spinous process of the vertebra below. Using the same procedure, another milli­ litre of the fluid is infiltrated here. In order to stay clear of any vital structures, including the structures in the spinal canal, the injection should not be made unless the tip of the needle touches bone. Considerable tissue resistance may be encountered when the fluid is forced in. For this reason, the needle should not be too thin. Should the infiltration be part of a sclerosing treatment for recurrent disc displacement, both fourth and fifth lumbar levels must be infiltrated. A mixture of 1 ml of lidocaine (lignocaine) 2% and 3 ml of sclerosant is then distributed over both levels. POSTER IOR CAPSULE OF THE LU M BAR FACET JOINT Backache seldom stems from a facet joint lesion which is not a very reliable clinical diagnosis.17o However, facet joint pain may occasionally result from traumatic over­ stretching of the dorsal capsule. Although the facet joints are richly innervated by the dorsal rami of two consecu-

Figure 59.34

Injection of the inter- and supraspinous ligaments ( L5-S 1 ).

tive roots,1 72 only the fibrous capsule contains nociceptive free nerve endings and can be the possible source of facet­ derived pain.1 73 The aim of the treatment is therefore not to inject the joint but to infiltrate the dorsal capsule. Apart from traumatic overstretching, infiltration with 20 mg triamcinolone is also indicated in ankylosing spondylitis. However, the common reason for infiltrating the facet joints is postural backache. Here a sclerosing solution is used to cause capsular sclerosis. Capsular scle­ rosis is also indicated when, after reduction, the fragment of a disc proves unstable. Some recommend that intra-articular injections should be done in the radiology department under fluoroscopic controP74, 175 or under CT guidance of the needle.176 Infiltration of the posterior capsule of the joint can, however, be performed blind. To find the facet joint liga­ ments with the tip of a needle is not difficult. It has been shown that pain relief occurs equally well with intra­ articular and periarticular injections, indicating that the pain may be of capsular origin rather than synovial inflammation.177

Technique The patient lies prone on a couch, with the pelvis slightly elevated in order to reduce the lordosis. This postu re enables better pal pation of the spinous processes and the intervals between them. The patient keeps the arms along the body so as to relax the sacrospinalis muscles. A horizontal line connecting the two iliac crests is drawn. It usually falls between spinous processes pf L4 and L5. Other horizontal lines are drawn between the processes of L3 and L4 and L5 and S1. Finally the midline is drawn. The centre of the facet joints L4-L5 and L3-L4

CHAPTER 59

usually lie on the cross-bars at about 1 .5 cm from the midl1ne. At the L5-S1 level, the joint is located slightly more lateral at 2.0-2.5 cm from the midline. A 5 cm needle is inserted at the surface marking of the joint and thrust in vertically downwards through the sacrospinalis muscle (Fig. 59.35b). Depending on the build of the patient, the needle reaches the lamina at 3-6 cm depth. The needle should encounter tough liga­ ment before reaching bone. As it meets bone, the point lies against the lamina. One millilitre of the fluid is injected at different places over the surface of the joint. Considerable tissue resistance may be encountered. In order to remain clear of any vital structures, no injection should ever be made unless the tip of the needle is felt to impinge on bone. For diagnostic purposes, 1 ml of lidocaine (ligno­ caine) 2% can be used. In traumatic overstretching of the joint or in ankylosing spondylitis, 20 mg of triamci­ nolone is injected. A sclerosant is injected in the two lower pairs of facet joints when capsular sclerosis is requi red (see p. 779) . D E EP LU M BAR FASCIA The middle layer of the thoracolumbar fascia is attached to the lumbar transverse processes and is continuous with the intertransverse ligaments. It is also attached to the edge of the lamina, where its fibres blend with those of the posterior layer of the thoracolumbar fascia.178 The transition between deep lumbar fascia and lamina at both L5 and L4 levels is infiltrated with sclerosant solu-

-

TREAT M E NT OF THE L U M BAR SPI N E 9 1 9

tion a s part o f the treatment o f chronic postural backache or to induce ligamentous contraction in the treatment of recurrent disc displacements. An injection at the lateral border of the lamina also reaches the posterior ramus, where the fibrils that supply the facet joint curl round the bone to continue on the dorsal aspect of the lamina. Injection of a sclerosant (phenol solution) at the edge of the lamina will therefore also induce a facet denervation.179-18 1

Technique The patient lies prone, the pelvis slightly tilted and the back muscles as relaxed as possible. Three transverse lines, crossing the L3-L4, L4-L5 and L5-S1 supraspinous ligaments, and the midline are drawn. Points chosen between the horizontal lines and 1 .5 cm from the midl ine lie exactly above the laminar edges (Fig. 59.36). The syringe is filled with either a local anaesthetic or a mixture of sclerosant and local anaesthetic and fitted with a needle 5 cm long. The needle is inserted at the appro­ priate level. It is then thrust vertically downward until it touches bone at a depth between 3 and 6 cm (the depth depends mainly on the size of the patient). The needle is then partly withdrawn and reinserted in a slightly more lateral direction. This is repeated until the operator feels the needle slip along the edge of the lamina: 0.5 ml of the solution is injected here. Care is taken to keep bony contact with the edge of the lamina during the injection. The needle is then partly withdrawn and reinserted in a slightly more medial direction, where it touches the surface of the lamina. Another 0.5 ml of the solution is then injected.

(a )

Figure 59.35

Injection of the posterior capsule of a lumbar facet joint.

(b)

920 S E CTION TEN - T H E LU M BAR SPI N E

(a )

Figure 59.36

Injection of the deep lumbar fascia.

ILIOLU M BAR LIGA MENTS These ligaments play an important role in stabilization of the lu mbosacral j unction.182 They are especially important in maintaining the torsional stability of the junction.183, 1 84 (See p. 712.) An iliolumbar strain can stem from overstretching.18S

Technique (Troisier:139 p . 396; Naeim et a1186) Infiltration of the ligament is made at the iliac insertion. A 5 ml syringe is filled with 4 ml of the sclerosant solution and 1 ml of procaine 2% and fitted with a 7 cm needle. The iliac crest and the posterior superior iliac spine are palpated . A horizontal line is drawn, connecting the u pper edge of each iliac crest. One thumb is held at the medial edge of the iliac crest. The needle is inserted on the horizontal line, about 3 cm lateral to the supraspinous processes (Fig. 59.37). The tip of the needle is thrust in very obliquely in the direction of the palpating thumb until it is felt to traverse a resistant ligament before touch­ ing bone. The infiltration is performed along the border, deeply and superficially by multiple withdrawals and reinsertions. It is important to realize that the zone of insertion extends over 3-4 cm. Caution must be taken to inject only when the needle touches bone.

(b)

sulphate and carbolic acid . In the late 1 950s, Ongley chose to use a dextrose-phenol-glycerol solution, origi­ nally developed for treatment of varicose veins. 1 89 This mixture has a good safety record and causes few side effects. It provokes an effective inflammatory response, which leads to fibroblast proliferation and new collagen production (0. Troisier, cited by Cyriax:21 p. 339).190 The tightening and permanent shortening that result limit vertebral mobility and thus are beneficial in preventing recurrent disc displacements. Phenol is also known as a very powerful neurolytic agent.191, 192 The fact that some of the phenol solution injected at or around the medial and lateral branches of the posterior ramus causes a

SCLEROSANT INJECTIONS AT THE LOWER LU M BAR SPINE From 1 956 onwards Hackett used sclerosant injections at the ligamentous periosteal junctions of the posterior lumbar arch as a treatment for chronic low back pain . 1 87,188 The solution initially used consisted of zinc

Figure 59.37

Injection of the right iliolumbar ligaments.

CHAPTER 59 - TREATM ENT OF T H E L U M BAR S P I N E 921

chemical denervation181 adds to the therapeutic effect of the Injections. Chemical denervation probably explains the quick relief (sometimes from the day after the injec­ tions) obtained by a number of patients treated with sclerosan t injections. Local sclerosant injection is the treatment of choice in a local posterior dysfunction syndrome. The purpose then is to create a long-standing denervation of local nociceptors or of branches of the dorsal ramus. In recurrent disc displacements, or in chronic backache caused by postural ligamentous pain, a series of infiltra­ tions is made in all the dorsal ligaments of L4-L5-S1 motion segments, or the L3-L4-L5 motion segments.

Technique Over 3 consecutive weeks, 3 ml of the solution, mixed with 1 ml of lidocaine (lignocaine) 2% is infiltrated in the different lumbar ligaments at the ligamentous periosteal junction, in the following sequence. •

•

•

The first injection is given at the interspinous and supraspinous ligaments L4-L5 and L5-S1 and at the il iac insertions of the iliolumbar ligaments. The second injection, 1 week later, reaches the posterior aspects of the apophyseal joints L4 and L5 at both sides. The third injection, 1 week later, is given at the lateral aspects of the laminae of L4 and L5, where the ligamentum flavum and the medial aspect of the deeper layer of the fascia lumborum merge.

Remarks Usually there is considerable after-pain for the 24-48 hours following each treatment session but the pain seldom necessitates bed rest or absence from work. For 6 weeks, which is the time needed to induce sufficient sclerosis of the tissues, the patient should avoid bending forwards or sitting in kyphosis, in order to avoid stretching the ligaments. If, during this period of contrac­ tion of the fibrous tissue, a new disco dural interaction develops, manipulative reduction should be carried out at once.

Results The results of these injections are reasonably good.193 In chronic postural backache, about 70% of patients become pain free after 6-8 weeks. If after 6 weeks there is improvement but no cure, the series can be repeated. If, on the other hand, no improvement is reported after 2 months, it is pointless to repeat the injections. Our personal experience with sclerosant treatment shows that there is usually little or no tendency to recurrence. Sometimes the patient has to return for a 'booster' after 2 years.

PREVENTION OF LUMBA R S PINE DI SO RDERS

INTRODUCTION Prevention is the ideal approach to low back pain. Classically, there are three types of prevention. Primary prevention aims to avoid the causes before they occur; secondary prevention endeavours to reduce the fre­ quency and severity of low back episodes; tertiary pre­ vention attempts to reduce disability in patients with chronic problems. 1 94 Primary prevention, although the best approach, is hard to achieve. It is extremely difficult to motivate change in behaviour, especially if the condition at risk is not life­ threatening. However, primary prevention programmes are important in industry. In a good one, efforts should not be focused on the worker alone. A good ergonomic approach to the workplace (plant, office and cars) is the first prerequisite; education of the employee the second.195 Secondary prevention is the responsibility of every therapiSt. Once resolution is complete and the patient has recovered from an episode of backache, the question arises how to prevent further recurrences. The pa tient should be told about the mechanism of disc protrusions and the way they can be prevented, and motivated to attend a back school programme where education about proper back care and the reduction of future episodes is more thorough.196 In tertiary prevention, the focus is on the patient in whom treatment did not completely succeed and it is necessary to adapt lifestyle to persistent pain. The causes of backache are many and prevention strategies must be adapted to the mechanical situation that pertains. PREVENTION IN DISCODURA L INTERACTIONS Once the displacement is reduced, whether by manipula­ tion, traction or the passage of time, the patient must be warned that the probability of a new attack remains very high. Because of its avascularity, repair of disc tissue is almost non-existent and what has shifted once can shift again when subject to the same provocation. Recurrent episodes of backache thus occur in up to 85% of patients. The severity and duration also tend to increase with each recurrence. 1 97,198 Recurrences therefore increase the risk of chronicity, disability and eventually surgery. These facts are reason enough to inform the patient in as detailed a way as possible about the mechanism of disc protrusions and how they can be prevented in the future. There are two basic principles: • Avoid immobil ity for long periods • Keep the back i n the ' physiolog ica l ' position, which is

l u mbar lordosis

922 SECTION T E N - T H E L U M BAR SPI N E

Immobility causes a drying out and a quicker degener­ ation of disc material and is therefore deleterious to disc tissue (see p. 728-729). The patient should be advised to change position as frequently as possible. A slight physiological lordosis, the normal and natural posture of the lower back, is the consequence of the wedge-shape of the lumbar discs. The patient should try to keep the back hollow in all positions. First, it has been demonstrated that in this position the intradiscal pres­ sure is at its lowest.1 99 Second, in a lordotic posture, the intervertebral joint is more open in front than behind. During this asymmetrical loading, the resultant of the compressive forces pushes the nucleus in a forwards direction. Bending, in contrast, results in a tensile stress on the posterior part of the annulus and is a compressive backwards force on the nucleus (Fig. 59.38). A posterior movement of the nucleus then threatens the dura and nerve roots. Several biomechanical studies have demon­ strated that the normal nucleus moves posteriorly in kyphosis and anteriorly i n lordosis.200-2o3 The patient shou l d understand the necessity of keeping the back hollow at all times. All advice is based on the simple principle ' keep your back hollow' (Fig. 59.39), and a real endeavour shoul d be made to render this second nature.

Sitting posture Nowadays, people sit for a great deal of their life: in cars, trains, buses, at the office, at home. It should be made

Figure 59.39 Correct postures for keeping the back hollow.

Figure 59.38 Analogies are useful in explaining mechanical principles to

patients. If the spine is loaded in kyphosis the disc tends to move backwards.

clear to the patient that sitting is the worst position for the back, because it increases the pressure inside the ,disc. Sitting positions should therefore be avoided but, if they are necessary, a proper position on a good chair must be chosen. A good chair allows the user to correct the hollow

CHAPTER 59

-

TR EATM ENT OF T H E L U M BAR S P I N E 923

in the back. Of importance are the height and depth of the seat-, and the inclination and shape of the back rest.

Height of the seat. This should adjust to the height of the individual (Fig. 59.40). Ideally, the thighs rest slightly on the seat when the knees are at right angles and the heels rest on the ground.204 If the seat is too low and the patient holds the legs straight, the hamstrings pull the pelvis forwards, which results in flexion of the lumbar spine from below; or the knees and hips are kept bent, which once again rotates the pelvis forwards and forces the lumbar spine into flexion.2os If the seat is too high, the whole pelvis glides forwards and the lumbar kyphosis increases.206 A slight anterior inclination of the seat may be advised when the patient sits at a desk (Fig. 59.4 1 ) . In this position the pelvis rotates forwards; the lumbar spine follows and is lll oved towards lordosis.207 The patient adopts a straight, erect posture which is more comfortable when working at a horizontal desk and keeps the lumbar spine hollow.208 Depth of the seat. The seat should be no deeper than the distance from the back of the knees to the sacrum. If it is longer, the sitter cannot position the lumbar spine against the back rest and the spine is forced into a convex posi­ tion (Fig. 59.42). Should this be the case, the gap must be filled with a hard support such as a cushion, a briefcase or rolled up coat.209 Inclination of the back rest. The angle between the seat and the back rest should not exceed 1 00°. An increase in inclination is followed by an increased backwards rota­ tion of the pelvis and kyphosis of the lumbar spine.2JO lumbar support. The chair should be fitted with a well­ stuffed hard lumbar support. The level of the support is at the L3-L4 region, which is the level at which the forearm lies when put behind the back, with the elbow bent at a right angle (Fig. 59.43). Normally, this is between 1 9 and 26 cm above the surface of the seat.211 Posture in the car. Car seats often cause a great deal of trouble. Aerodynamic principles force modern construc-

Correct seat height Figure 59.40

Seat height.

Seat too low

Seat too high

Figure 59.41

Slight anterior inclination of the seat, for sitting at a desk.

tors to design the coupe as low as possible. As a result the car seat is also low, which is harmful for the driver's back: the legs are held nearly straight and pull the pelvis for­ wards. The principles set out above can only be followed if a backwards inclination, together with a corresponding tilting of the seat is achieved. A back rest inclination of 1 1 0-120°, with a back rest-to-seat angle of 90-100° is

Seat too long Figure 59.42 Seat depth.

Correct adjustment

924 SECTION TEN - T H E L U M BAR S P I N E

Lumbar support Figure 59.43

Checking support height

Standing posture

Lumbar support.

optimal (Fig. 59.44). A hard lumbar support, approxi­ mately 8 cm thick and between 20 and 25 cm above the horizontal part of the seat, should be present to maintain the lordosis. Inclination of the seat has several advantages: •

•

•

The buttocks slide backwards and are pushed into the angle between the horizontal and the vertical part of the seat. With the thighs resting on the seat, the knees move upwards so that the angle between thighs and lower legs decreases, which relieves tension on the hamstrings. The upper trunk moves dorsally, which increases the contact between the back and the back rest. A large proportion of the body weight is then transmitted to the back rest and the axial load on the spine is reduced. The d istance between the back rest and the steering wheel should be such that the arms are nearly straight. A position with completely extended arms prevents adequate contact between chest and back rest, increases the load and forces the back into kyphosis.212,213

The patient should realize that simply having a proper and well-adjusted chair is not sufficient. It must also be used in a proper way; forcing the buttocks backwards as far as they will go, until the sacrum touches the back rest; the support on the back rest then pushes the lumbar spine forwards i nto lordosis. A random ized stu dy showed that sitting with a lumbar support at the L3-L4

Good Figure 59.44

Car seat adjustment.

level resulted in reduction of lumbar pain.21 4 All sitting positions that are performed in kyphosis should be avoided. Sitting with the legs crossed, for instance, is harmful: the uppermost thigh draws the pelvis forwards which flexes the lumbar spine from below. Also, in sitting with the legs out straight (i.e. in bed or in the bath) the hamstrings rotate the pelvis forwards, which results in considerable kyphosis.

Standing does not increase intradiscal pressure and no posterior displacements of discal tissue need be feared when a normal lordotic posture is maintained. However, to work in a standing position usually implies a slight bending of the spine (e.g. working at a desk, sweeping, vacuum cleaning), which considerably increases the intradiscal pressure.215 Proper height of the work surface and proper equipment can prevent this (Fig. 59.45). The work surface for standing should be some 8-10 cm (a fist's height) under the elbow. For most people, this is 30-40 cm higher than the top of the kitchen table and about 1 0-15 cm higher than most work surfaces. Washbasins should also be built-in higher than they usually a re . Cleaning materials - brushes, vacuum cleaners and floor-mops - should be long enough to allow a proper use, with the body kept upright.

Lifting and carrying 'Use your legs, not you r back'. In order to decrease lever­ age, it is extremely important to keep the distance between the load and the body as short as possible.216 Therefore, lifting should never be done with straight legs.217 The best way to pick up a load is by squatting (Fig. 59.46). Care should be taken to arch the back in lor­ dosis by a contraction of the sacrospinalis muscles, b(!fore lifting starts. Straightening the knees and hips, while the lumbar spine is kept as immobile as possible, then lifts the load. 'Avoid combined flexion and twisting of the trunk', A combination of torsion and bending maximally stretches the posterolateral al1J1ulus and is likely to cause annular

Wrong

Wrong

CHAPTER 59

Wrong Figure 59.45

Good

-

TREATM ENT OF T H E L U M BAR SPI N E 925

Good

Wrong

Standing posture.

spine into kyphosis and may result in gradual nuclear displacements. The mattress should therefore be firm and positioned on a hard surface (boards or laths). The best way to lie on it is prone, the chest slightly turned to one side. The upper leg is slightly bent, the lower leg out straight (Fig. 59.48). This position is excellent as it maintains the lumbar concavity. Wrong Figure 59.46

Good

Lifting.

failure and protrusion.218,219 To avoid this, the patient can be taught to pivot on the feet rather than twist the trunk.220 In carrying, the load is placed as close as possible to the body: the further the distance between body and load the larger the intradiscal pressure and the more the spine is forced into kyphosis.221 It is also a good idea to carry loads on one iliac crest (Fig. 59.47). The load is then trans­ mitted directly to the leg, rather than via the lumbar spine.

Wrong

Posture in bed A lot of backache results from sagging mattresses. Lying on the back in the hammock position forces the lumbar

Good Figure 59.47

Carrying: the load should be held close to the body

Figure 59.48

Posture in bed.

926 S ECTIO N T E N - T H E L U M BAR SPI N E

What about exercises? Exercises that enhance muscle strength cannot prevent disc displacements. The patient should be told that strong back and abdominal muscles do not prevent pos­ terior migration of disc tissue. Only the maintenance of a good posture during the activities of daily living can do this. It is not the strength of the muscles but the way they are used that is of importance. Furthermore, back exer­ cises aiming at increasing muscle power can be damaging for the disc: prone-lying extension exercises increase the intradiscal pressure five-fold, sit-up exercises six-fold.222 Exercises that augment or maintain lumbar mobility are also contraindicated. Displacements will be prevented by keeping the lumbar spine still, not by moving it. In contrast, exercises that increase strength and mobil­ ity of the hips and the knees should be encouraged.223 To transfer the stress from the spine to the legs implies good function (strength and mobility) of these; therefore exer­ cises make sense but only as a complement to instruction and postural training. Only one prophylactic 'exercise' is logically defensible and proves to be of some value in patients with recurrent attacks of back pain: extension exercise under passive traction (Cyriax:2J p. 226). The patient puts the hands on a table and straightens the arms. The legs are placed backwards as far as possible. By bringing the shoulders almost vertically above the outstretched arms, the trunk is allowed to sag. This results in passive extension during traction provided by the weight of pelvis and legs (see Fig. 59.49). The position is sustained for 20-30 seconds. The traction causes a decrease in intradiscal pressure and the extension results in a forward shift of the disc. The exercise is performed 5-10 times a day.

Figure 59.49

Extension exercise under passive traction.

hamstrings pull the pelvis forwards, which results in kyphosis. Patients with back pain should therefore avoid this sport.

What about sport? Swimming, walking and running are safe. In swimming the trunk floats, which precludes any compression strain. In running and walking the lumbar spine remains in physiological lordosis, which prevents posterior migra­ tion of the disc. Riding also seems to be quite harmless, as long as the rider uses the muscles to keep the back hollow. Ball games may p rovoke sudden annular displace­ ments. The player does not always have full control over the movements performed or the positions the body is forced to adopt. Tennis, badminton and volleyball have an especially bad reputation, because these sports are 'jerky' and require much stooping and twisting. Basketball and soccer are safer. Rowing involves ful l forward bending. Once a disc lesion has developed it is extremely difficult to continue the sport even if the performer trains to achieve perfect technique. Canoeing requires a sitting position with extended knees. This is a bad posture because the

PREVE NTIO N I N L IGA ME NTOUS DISORDERS

"

(Box 59. 1 0 ) Lumbar l igamentous pain appears when the posterior ligaments are subjected to abnormal mechanical stress: because of the decrease of intervertebral height, too much load is applied on the posterior compartment of the spinal axis. The clinical picture is intermittent pain, induced by the maintenance of prolonged positions and abolished by posture correcti on or movement. Maintenance of lordosis or hyperlordosis especially stresses the posterior facets and increases the postural pain. To prevent postural pain, the patient should avoid constant static postures. Hyperlordosis in particular should not be permitted. Much attention should be given to correction of the hyperlordotic position. Pelvic tilting in the standing position or while standing against the wall with the knees slightly flexed (Fig. 59.50) should be

CHAPTER 59

-

TREATMENT OF THE L U M BAR SPI N E 927

Figure 59.50 tilting (b).

(a)

Correction of hyperlordosis (a) by pelvic

(b)

performed several times if the patient has to stand for any length of time. In addition, moving the body weight from one leg to the other changes postural tone and thus prevents postural backache. It is also advisable, when standing, to place one foot on a small footstool or bar (1 5-20 em high; Fig. 59.5 1 ). This allows slight flexion of the hip and relieves the lordotic pressure. PREVENTION IN STENOTIC DISORDERS (Box 59. 1 1 ) Compression o f the nerve roots i n a narrowed spinal canal is not constant. The size of the canal changes in rela­ tion to posture. An axial load on a degenerated spine decreases the size of the canal: the posterior longitudinal ligament folds and buckles in a posterior direction, the superior articular process moves forwards and upwards in relation to the vertebra above and the pedicles tend to push downwards on the nerve roots. Extension further narrows the space and therefore adds to more compres­ sion on the roots. Flexion relieves the compression as it

Box 59. 1 1 Prevention in stenotic disorders • Avoid lordosis • Avoid axia l load

stretches the posterior longitudinal ligament and moves the superior articular process away from the root. Patients suffering from stenotic disorders must there­ fore be encouraged to flatten the lumbar spine as much as possible in all positions. The sitting position in kyphosis is most comfortable. In standing and walking, however, it is extremely difficult to maintain some kyphosis in the

Box 59. 1 0 Prevention in ligamentous disorders .-

• Avoid the mai ntenance of prolonged positions • Avoid hyperlordosis • Keep moving

Figure 59.51

Use of a footstool to relieve lordotic pressure.

928 SECTION TEN - T H E L U M BAR S P I N E

lumbar area. In order to achieve this the patient can be trained in pelvic tilting (active forwards movement of the pelvis, which straightens the back), first while lying on the floor, then while standing against the wall with the knees slightly flexed. Once the technique of pelvic tilting has been mastered, it should be practised for 5-10 minutes several times a day. In early cases of spinal stenosis or lateral recess stenosis, these pelvic tilting techniques have proved to be efficient. I'if�U�::tJ/II� ',.' 1

•

�SPINA L:: SUR G ERY . , �il":._�..'

",_,. C,

"

•

The incidence of spinal surgery is highly variable and differs from country to country, In the industrialized world the lowest incidence is in the UK: fewer than 1 0 / 1 00 000 Britons undergo disc excisions or lumbar fusions each year, The rate of back surgery in the US is more than five times that in England and Scotland, In the USA, it is estimated that 695 / 1 00 000 have a lumbar discectomy each year, and an additional 31 / 1 00 000 have a spinal fusion,225,226 Even within the same country there remain large differences, Volinn and colleagues have demonstrated almost IS-fold differences in low back surgery rates among counties in Washington State,227 Given that there is no difference in the incidence of sciatica and low back pain this large variation between regions and countries can only be explained by a lack of medical consensus on the indications for surgery, Also a report of the US Institute of Medicine concluded that 'surgery for chronic low back pain is overused and often misused' ,228 Moreover, recent studies demonstrate that the higher the regional disc surgery rate, the poorer the outcome229 and the higher the reoperation risk.23o Successfu l surgery to the lumbar spine is based on an unequivocal cause of symptoms; congruence between this and the findings on imaging; a lack of undue influence by the psychosocial circumstances surrounding the patient's illness; and conviction on the part of all con­ cerned that surgery will produce better results than allowing the condition to evolve naturally, Violation of these principles is the dominant cause of failure, rather than failure to choose the right operation from the variety of surgical procedures currently available,231 Surgical intervention should therefore not be lightly undertaken and adequate weight must be given to non-surgical treatment or even to natural spontaneous resolution. Sometimes, however, surgical treatment is absolutely necessary and should not be postponed, In deciding for or against surgery, the following are important. Fi rst, most of the conditions that are broad indications for lumbar spine surgery have a normal and na tu ra I recovery. 232,233 Second, the results of surgical procedu res are not perfect. Even in the best hands and

after using strict preoperative criteria for selection, the immediate successful rates of discectomy for sciatica do not exceed 90%,234 and long-term success is less than 80% ,235,236 If the main complaint has been backache, only half the patients will be relieved of symptoms.237,238 Further surgical procedures on those who have not obtained relief have, as we have already indicated, a very low chance of success.4,166 The rate of reoperation d uring the subsequent 4 years is 10%239 and increases to 1 5% if the interval is 5 years.240 Third, the risk of non­ intervention should be known, Is there a possibility of continuing disability if a patient with a commencing muscle paresis is not sent for surgery? It has been gen­ erally accepted that motor weakness and / or sensory loss is a major reason for surgical intervention. There is little or no debate that a cauda equina syndrome is an absolute and urgent indication for lumbar disc excision, This condition affects between 0,25 and 2.00% of patients with a known disc problem and is an emer­ gency. However, most muscle paresis of the lower limb is not severe and is a sign that is detected by the doctor rather than a phenomenon apparent to the patient patients with weakness are usually quite unaware of it. In a single root paresis, recovery is the ru le. Usually after some months, and sometimes before the patient loses the root pain, the muscles begin to strengthen and the skin to regain its sensitivity (Cyriax:21 p, 330). Hakel ius and Hindmarsh241 showed that delays of up to 3 months had only a minimal effect on the ul timate recovery of strength. In a retrospective study of 1 66 patients who underwent surgery and 4 1 7 patients who were treated non-surgically, Hakelius242 could not find a statistical difference between the two groups in recovery from muscle paresis and from sensory loss, Also, the classic prospective controlled study by Weber243 showed an equally good restoration of muscle weakness iri sur­ gical and non-surgical groups. However, if a disc pro­ trusion causes a double palsy of two adjacent roots, permanent weakness may be found. Such may be the case in an L4-L5 palsy caused by a protrusion at the fourth lumbar level and resulting in a drop foot. If per­ manent weakness of the dorsiflexors is feared, decom­ pression surgery should be performed without delay because delayed laminectomy does not guarantee restoration of muscle power,

SUR G ERY FOR DISCODURA L OR DISCORADICULAR INTERACTIONS

Lumbar disc herniations can be treated by different inter­ ventions: discectomy by intra laminar approach, microdis­ cectomy, percutaneous discectomy and chemonucleolysis with chymopapain. Comparison of these treatments is not

CHAPTER 59 - TREATM ENT OF T H E L U M BAR SPI N E

possible, because no controlled prospective studies have beel'l carried out. Lumbar discectomy has, in the past, been referred to as lumbar laminectomy. This term is not appropriate because it suggests a complete exposure of the neural elements. The advantages of microdiscectomy are the smaller incision and the more rapid recovery. The disadvantages are technical difficul ty, a higher infection rate, the increased risk of missing significant disorders, operating at the wrong level and the higher recurrence rate.244 In percutaneous or suction discectomy, a cannula is placed against the annulus. A cutting tool is moved into the sheath to carve a hole in the annulus. Small curved forceps are then introduced into the disc space and as much nuclear material as possible (usually 4-6 g) is evacuated. In suction discectomy a nucleotome, inserted through the cannula, functions according to the same principles as the guillotine instruments used in arthro­ scopic surgical procedures. Aspiration of the cut material is automatic and air driven.245 The success rate of the pro­ cedure is between 50 and 75%.246,247 Although the exact mechanism is not known, the benefit of the procedure presumably relies on the mechanism of disc decompres­ sion. The procedure is contraindicated for a sequestered disc. The advantages of the technique are the low risks of complications, the short duration of treatment and the quick recovery. However, the results are still too poor to consider the treatment a useful intervention: in a recent randomized clinical trial the treatment was only success­ ful in 44% of the patients.248 Chemonucleolysis is the treatment of intervertebral disc lesions by intradiscal injection of the enzyme chy­ mopapaill .249 The protease rapidly degrades proteogly­ can core protein and generates fragments containing only a few glycosaminoglycan chains. These diffuse out of the tissue and the water-binding capacity of the disc is lost, so reducing the intradiscal pressure and hence pressure on the entrapped nerve root.250 The results are slightly inferior to those of surgical excision.248 A serious disad­ vantage of the procedure is increasing low back pain for up to 6 weeks after the injection. Also, a small number of catastrophic allergic and neurological complications have been recorded.251-253 Chemonucleolysis can be a viable treatment option for younger patients with a lumbar disc protrusion causing radicular pain.254 INDI CATIONS There is little debate about the absolute indications for lumbar disc excision when the patient presents with a cauda equina syndrome or an incipient drop foot. The dominant complaint, however, in the majority of patients with lumbar disc herruation, is pain rather than significant

929

neuromuscular dysfunction. Although muscle paresis is usually considered by most neurosurgeons as an indica­ tion for early surgery, it still has to be proved that recovery from neuromuscular dysfunction occurs more rapidly with surgery than with non-surgical treatment.255,256

Absolute indications (Box 59. 12) Third and fourth sacral root palsy. Weakness of the bladder with incontinence du ring an attack of acute lumbago or sciatica calls for immediate laminectomy. 68 The outcome of a cauda equina syndrome is dependent on rapid recognition and early surgery because the com­ pression is preganglionic and therefore no recovery will take place. The important features are bilateral root pain with bilateral neurological symptoms; perineal pain, paraesthesia and / or numbness; and presence of urinary dysfunction and / or loss of rectal sphincter tone. Cyriax went further and recommended a 'prophylactic laminec­ tomy' for those patients who had, during an attack of lumbago, temporary pain or paraesthesia in the per­ ineum. Although there is no weakness and the perineal symptoms decline when the lumbago improves, he still advocated a laminectomy because 'there can be no guar­ antee that the next time the patient gets lumbago his pro­ trusion will not transect the fourth sacral root, and this may happen at a moment when urgent laminectomy is unobtainable' (Cyriax:21 p. 333 ) . Inci pient d rop foot. Dorsiflexion of the foot is controlled by the L4 and L5 motor roots. A large herruation at the fourth lumbar level may cause a pressure atrophy of both. The tibialis anterior and the dorsiflexors of the toes are then completely paralysed and usually remain so. Hence, if there is a major and rapidly progressive muscle weakness of the dorsiflexors of the foot, immediate laminectomy should be considered as the best hope of rapid restoration of muscle power. Severe intracta ble root pai n. What matters is not the severity of the lesion but the severity of the pain. This indication has nothing to do with the existence of neuro­ logical signs but with the presence of continuous and intractable pain: the patient has received all possible con­ servative treatment including epidural local anaesthesia, eventually with the addition of triamcinolone and nerve root blocks, but the symptoms remain as severe as ever. Discectomy most often proves necessary in sciatica, with Box 59. 1 2 Surgery for discoradicular interactions: indications • • • •

Fourth sacral root pa lsy Incipient drop foot Severe i ntractab l e root p a i n No res u lt after 6-12 months o f conservative treatment

930 S ECTION T E N - T H E L U M BAR SPI N E

o r without neurological deficit, accompanied b y gross lumbar deformity: the patient presents with a gross side flexion or flexion deformity and any attempt to straighten the back results in severe root pain shooting down the limb (see p. 81 6). Alternatively, there may be considerable deviation away from the side of the pain during flexion and the side flexion towards the pain is inhibited by severe root pain.

Relative indications Most surgeons consider root pain with neurological signs as a primary indication for discectomy.234 However, it is our strong belief that slight or moderate muscle weak­ ness alone does not indicate that surgical intervention will be necessary. If only one nerve root is involved, recovery from the palsy is the rule. Usually the muscle begins to recover soon after the pain has ceased. Although it is true that root atrophy may sometimes lead to permanent weakness and loss of sensitivity or a per­ manent loss of the ankle jerk, these slight inconveniences cannot always be prevented by an operation. Several ret­ rospective and prospective studies comparing surgically and non-surgically treated patients did not demonstrate any di fference in recovery from the palsy.241,243,257 Therefore weakness is not a primary indication for surgery but for epidural local anaesthesia : desensitiza­ tion of the nerve root is all that is required. Pain passes off quickly and often permanently; recovery from neuro­ logical weakness usually follows after some months. It should never be forgotten that most patients with sci­ atica recover within a year, no matter what sort of treat­ ment has been instituted. It is appropriate to recall that in the prelaminectomy era all but a few patients with sciatica recovered from their pain and disability. Therefore, a patient who suffers from tolerable root pain, even in combination with neurological signs and who does not respond to conservative treatment should be advised to wait until spontaneous recovery has had a chance to take place. If the signs and symptoms remain unchanged after, say, a year, surgery may then be considered.

FAILURE AFTER DECO MPRESSIVE SURGERY The estimated rate of failure following decompressive surgery varies widely and ranges from 5 to over 50%, with an average of 1 5% .258,259 The reason for failure is either incorrect diagnosis, surgery at the wrong level, the wrong operation, an unsuitable patient or technical prob­ lems. The history once again may be very helpful in assessing the probable cause of the failure: there are three possibili ties: 1 67

The patient has no initial relief of the symptoms. or the symptoms are worse: diagnosis. indication or level were

wrong . A major reason for failure is psychosocial: the patient is not cooperative or is not anxious to get well; there may be a compensation claim, job dissatisfaction or psychological disturbances.260,261 Operations should be considered carefully in such patients: prolonged disabil­ ity after the operation is to be expected. Even if there was genuine organic trouble, the operation will be followed by intermittent backache.262 An operation should there­ fore always be avoided if the patient's personality is though t to preclude achievement of a satisfactory outcome. Sometimes failure results from missing the actual level of involvement. This follows segmentation abnormalities or mislabelled imaging studies. The latter is not uncommon and results from the rather low specificity of diagnostic imaging.263-267 The accuracy of CT and myelography is between 80 and 87%,268,269 and therefore it should not be surprising that the wrong level can be operated upon if imaging studies only are taken into account in the decision to operate. Furthermore, one of the most important sources of continuing radicular pain is that a concomitant lateral spinal stenosis is overlooked at the time of surgery.270-272 There has been i nitial relief. fol lowed by gradual onset of recurrent radiculopathy at the same segment. It is likely that gradual scarring around the nerve root has set in; it is estimated that such root scarring accounts for 1 2% of all failures.273,274 There has been complete relief of symptoms but months or years later recurrent problems develop. A new disc displacement, either at the same or at another level may have occurred. Alternatively, the disc-space narrowing resulting from the excision is contributing to the devel­ opment of a lateral recess stenosis.

SUR G ERY FOR SPINAL STENO SI S AND LATERAL R ECESS STENO SI S

In a narrowed central canal, a wide laminectomy that extends laterally on both sides as far as the facet joints is recommended. When lateral recess stenosis is present, laminectomy and facetectomy are performed. The operation is usually executed on both sides, because the opposite side is often also narrowed. So at any one level, four nerve roots should be explored (L4-L5 at the level L4 and L5-S1 at the level L5).163 The outcome of surgery for spinal stenosis is good to fair in 75% of the patients, although about 33% continue ' to have severe backache.275 Also the reoperation rate seems to be rather high: 23% of the patients undergo reoperation of the spine during a follow-up period of 8

CHAPTER 59

years.276 Factors associated with a good outcome are: a cleat myelographic stenosis, no prior surgical interven­ tions, no diabetes, no hip joint arthrosis and no preoper­ ative fractures of the lumbar spine.277

LUM BAR ARTHRODES I S

Spinal arthrodesis may b e indicated when gross lumbar instability has set in. A number of different approaches and techniques to stabilize two consecutive vertebrae or the lumbosacral junction exist. All use bone grafts after the segment has been stabilized by different types of fixation (screws, pl ates, wires, hooks and rods). According to the localization of the bone grafts, the oper­ ation is described as posterior lumbar fusion, posterior interbody fusion or anterior interbody fusion.

INDICATIONS

Spondylolisthesis. The disorder is found in 5-7% of the population278 but surgical stabilization is only called for if specific signs and symptoms are present:279 •

•

Progressive and symptomatic slippage of more than 33% or an initial symptomatic slip of more than 50% in a child. The persistence of ligamentous lumbar pain or bilateral sciatica despite sclerosant therapy.

Degenerative spondylolisthesis. A degenerative spondy­ lolisthesis is a vertebral slip in spite of an intact neural arch. The slippage is caused by a combination of disc degeneration, general joint laxity, increase of mechanical stress and structural abnormalities of laminae and facets.28o-282 It occurs most often at the L4-L5 level and seldom progresses by more than 33% .283-285 As the dis­ placement progresses, the patient may present with back­ ache or bilateral sciatica. Arthrodesis must be considered if sclerosant injections do not provide benefit.285

-

TREATMENT O F T H E LUM BAR SPI N E 931

Lumbar instability. The patient suffers from recurrent severe low back pain caused by repetitive d iscodural interactions. The pain and the dysfunction may be promptly relieved by manipulation bu t reappear after an apparently trivial twist or strain. If the condition contin­ ues despite conservative treatment such as back school and sclerosant injections, arthrodesis should be per­ formed. The key premise, however, is that selective fusion will only relieve the symptoms if the 'unstable level' can be identified with certainty. To define the level, discography286 or sinuvertebral blocks (Cyriax:21 p. 223) can be useful. Also short-term external fixation can select those patients who will benefit from fusion.287 N uclear self-reducing protrusions. Pain comes on in the morning and gets slightly worse as the day goes on. The patient is comfortable lying down. Each morning the pain has vanished but reappears on getting up. Repeated sclerosant injections into the dorsal ligaments have not helped nor did epidurals. The only effective treatment then is arthrodesis (Cyriax:2 1 p. 338). Indications for spinal surgery are summarized in Box 59. 1 3 .

Box 59. 1 3 Indications for spinal surgery Discectomy Absol ute i n d i cations: Thi rd and fourth sacral pa lsy I n c i p ient d rop foot Severe i ntracta b l e root pain Relative ind ications: F a i l u re of conservative treatment

Laminectomy Narrowed centra l canal Narrowed latera l recess

Arthrodesis G ross l u mbar i nsta b i l ity: Spondylol isthesis Recurrent d i sc protrusions N uclear self-reducing d isc

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Neuroradiology 1998;40(1):59-62.

CHAPTER 59 - TREATM ENT OF T H E L U M BAR S P I N E 935

157. Weiner BK, Fraser RD. Foraminal injection for lateral lumbar ;:Iisc herniation. J Bone Joint Surg 1997;79B(5):804-807. 158. Krempen JF, Smith BS, De Freest LJ. Selective nerve root infiltration for the evaluation of sciatica. Orthop c/in North Am 1975;6:311-314. 159. White AH. Injection techniques for the diagnosis and treat­ ment of low back pain. Orthop c/in North Am 1983;14:553-567. 160. Haueisen De, Smith BS, Myers SR, Pryce ML. The diagnostic accuracy of spinal nerve injection studies. Clin Orthop 1985;198:179-183. 161. Tajima T, Furakawa K, Kuramochi E. Selective lumbosacral radiculography and block. Spine 1980;5:68-77. 162. Fukusaki M, Kobayashi I, Hara T, Sumikawa K. Symptoms of spinal stenosis do not improve after epidural steroid injection.

c/in j Pain 1998;14(2):148-151 . 163. Kirkaldy-Willis WH, Wedge JH, Yong Hing A. Lumbar spine nerve lateral entrapment. c/in Orthop 1982;169:171-178. 164. Irstam L . Differential diagnosis of recurrent l u mbar disc hernia and postoperative deformation by myelography. Spine 1984;9:759-763. 165 . Teplick JG, Haskin ME. Computed tomography of the post­ operative lumbar spine. AjR 1983;141:865-884. 166. Selecki BF, Ness TD, Limbers P et al. The surgical management .

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1974;56A:1435-1444. 170. Lievre JA. Traitement des lombalgies. Semin H6p Paris 1967;43:373-376. 171. Jackson RP. The facet syndrome. Myth or reality? c/in Orthop 1992;279:110-121. 172. Bogduk N . The innervation of t h e l u mbar spine. Spine 1983;8:286-293. 173. Wyke B. The neurology of low back pain. In: Jayson MIV (ed) The Lumbar Spine and Back Pain, 2nd edn. Pitman Medical, Tunbridge Wells, 1980. 174. Carrera GF. Lumbar facet injection in low back pain and sciat­ ica. Neuroradiology 1980;137:661-664. 175. Destouet JM, Murphy WA. Lumbar facet block: indications and technique. Orthop Rev 1985;14:57-65. 176. Schleifer I, Fenzl G, Wolf A, Diehl K. Treatment of lumbar facet joint syndrome by CT-guided infiltration of the intervertebral joints. Radiologe 1994;34(11):666-670. 177. Lilius G, Laasonen EM, MyUynen P. Lumbar facet joint syndrome: a randomized clinical trial. J Bone Joint Surg

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203. Serrousi RE, Krag MH, Muller DL, Pope M H . Internal defor­ mations of intact and denucleated human lumbar discs sub­ jected to compression, flexion and extension loads. I Orthop Res

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227. Volinn E, Mayer J, Diehr P et al. Small area analysis of surgery for low-back pain. Spine 1992;17:575--5 81 . 228. Osterwis M, Kleinman A, Mechanic D. Pain and Disability: Clinical, Behavioral and Public Policy Perspectives. National Academic Press, Washington DC, 1987. 229. Keller RB, Atlas SJ, Soule DN, Singer DE, Deyo RA. Relationship between rates and outcomes of operative treat­ ment for lumbar disc herniation and spinal stenosis. j Bone

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loint Surg 1999;81A(6):752-762. 230. Keskimaki I, Seitsalo S, Osterman H, Rissanen P. Reoperations

Lumbar d isc pressure and myoelectric back muscle activity during sitting. Scand I Rehabil 1974;6:104-114. 2 1 1 . Oliveri M. Richtig sitzen - ein wichtiges Element bei der Therapie und der Pravention von chronischen Schweiz R u ndschau Med (Prax) Rii ckenbesch werden.

1996;21:1 383-1387. 234. Spengler OM, Freeman CWo Patient selection for lumbar discectomy. Spine 1979;4:129-134. 235. Shannon N, Paul EA. L4-L5 and L5-S1 disc protrusion - analy­ sis of 323 cases operated on over 12 years. I Neurol Neurosurg Psychiatry 1979;42:804-809. 236. Naylor A. The lab results of laminectomy for lumbar disc pro­ lapse. I Bone Joint Surg 1974;56B:17. 237. Jackson RK. The long term effects of wide laminectomy for lumbar disc excision. J Bone joint Surg 1971;53B:609. 238. Nelson MA. Lwnbar intervertebral disc lesions. Rheulllatol Rehabi/ 1975;14:163. 239. Hu RW, Jaglal S, Axcell T, Anderson G. A population-based study of reoperations after back surgery. Spil1e 1997;22(19): 2265-2270. 240. Malter AD, McNeney B, Loeser JD, Deyo RA. 5-year reopera­ tion rates after different types of lumbar spine surgery. Spil1e 1998;23(7):814-820. 241 . Hakelius A, Hindmarsh J. The comparative reliabi lity of pre­ operative diagnostic methods in lumbar disc surgery. Acta Orthop Scand 1972;43:234-238. 242. Hakelius A. Prognosis in sciatica: a clinical follow-up of surgical and non-surgical treatment. Acta Orthop Scal1d 1970;

1988;77(25):706-711 . 212. Keegan JJ. Evaluation and improvement of seats. Industr Med Surg 1962;31 : 1 37. 213. Andersson BJ, brtengren R, Nachemson A, Elfstrom G . Lumbar disc pressure and myoelectric back muscle activity during sitting; I I I . Studies on a car driver's seat. Scand J Rehabil

Med 1974;6:1 28-133. 214. Williams MM, Hawley JA, McKenzie RA, Van Wijmen PM. A comparison of the effects of two sitting postures on back and referred pain. Spine 1991 ;16: 1185-1191. 2 1 5. Andersson G , brtengren R , Nachemson A. Quantitative studies of the back in different working postures. Scand I Rehabil Med 1 978;6(suppl):1 73. 216. Andersson G, brtengren R, Nachemson A. Intradiscal pres­ sure, intra-abdominal pressure and myoelectric back muscle activity related to posture and loading. Clill Orthop

1 977;129 : 1 56. 217. Mundt OJ, Kelsey JL, Golden AL et al An epidemiologic study of non-occupational lifting as a risk factor for herniated lumbar intervertebral disc. Spine 1993;18:595-602. 218. Adams MA, Hu tton We. Gradual disc prolapse. Spine 1 985;10:524-531 . 219. Gordon SJ, King HY, Mayer PJ et al Mechanism of disc rupture. A preliminary report. Spine 1991;16:450-456. 220. Gagnon M, Plamondon A, Gravel D. Pivoting with the loa d . A n alternative for protecting the back in asymmetrical lifting.

Spine 1 993;18:1515-1524. 221 . White III A, Panjabi M. Clinical Biomechanics of the Spine. Lippincott, Philadelphia, 1978:331. 222. Nachemson A. Review of mechanics of the lumbar disc.

Rhellmatol Rehabi/ 1975;14:129. 223. Trafimow JH, Schipplein 00, Novak GJ et al. The effects of quadriceps fatigue on the technique of lifting. Spine 1993; 18:364-367. 224. Cherkin DC, Deyo RA, Loeser JD et al. An international com­ parison of back surgery rates. Spine 1994;19:1201-1 206. 225. Rutkow [M. Orthopaedic operations in the US, 1979 through 1983. j BOlle joint SlIrg 1986;68A:71 6--7 19. 226. Frymoyer JW. Are we performing too much spinal surgery? Iowa Orthop 1 ] 989;9:32-36.

after lumbar disc surgery: a population-based study of regional and interspecialty variations. Spine 2000;25(12):1500-1508. 231 . Frymoyer JW (ed) Radiculopathies: lumbar disc herniation and recess stenosis. Patient selection, predictors of success and failure, and non-surgical treatment options. In: The Adult Spine. Raven Press, New York, 1991 :1 719-1 731 . 232. Weber H. The natural history of disc herniation and the influence of intervention. Spine 1994;19(9):2234-2238. 233. Postacchini F. Spine Update: Results of surgery compared with conservative management for lumbar disc herniations. Spine

129(suppl):1-76.

243. Weber H. 1982 Volvo award in clinical science. Lumbar disc herniation. A controlled, prospective study with ten years of observation. Spine 1983;8:131-140. 244. Williams RW. Microlumbar d iscectomy. A 1 2-year statistical review. Spine 1986;11:851-852. 245. Mooney V. Percutaneous and suction discectomy. In: Frymoyer JW (ed ) The Adult Spine. Raven Press, New York, 1991:

1 751-1763. 246. Kahanovitz N, Viola K, Goldstein T, Dawson E. A multicenter analysis of percutaneous discectomy. Spine 1990;15:713-715. 247. Schweigel J. Comparison of chymopapain and percutaneous d iscectomy. In: Onik G, Helms CA (eds) Alltolllated Percu taneous Lumbar Discectol11Y. Radiology Research and Education Foundation, San Francisco, 1988:85-92. 248. Revel M, Payan C, Vallee C et al Automated percutaneous lumbar discectomy versus chemonucleolysis in the treatment of sciatica. A randomized multicenter trial. Spine 1993;13:1-7. 249. Smith 1. Chemonucleolysis. Ciil1 Orthop Rei Res 1969;67:72-80. 250. Suguru T, Oegema TR, Bradford OS. The effect of chymo­ papain on prolapsed human intervertebral disc. Clil1 Orthop

Rei Res 1986;213&:223-231 .

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251 . Bouillet R. Complications de la nucleolyse discale par la �hymopapaine. Acta Ortilop Belg 1987;53:250-260. 252. Bernstein DE, Gallagher IS, Ulmer A. Prospective evaluation of chymopapain sensitivity in patients undergoing chemo­ nucleolysis. J Allergy Clin Tmmun 1985;6:458-465. 253. Agre K, Wilson RR, Brim M, McDermott OJ. Chymodiactin postmarketing surveil lance - demographic and adverse experience data in 29,075 patients. Spine 1984;9:479-485. 254. Nordby EJ, Fraser RD, Manucher JJ. Spine Update: Chemonucleolysis. Spine 1996;22:1102-1105. 255. Hakelius A, Hindmarsh J. The comparative reliability of pre­ operative diagnostic methods in lumbar disc surgery. Acta

Orti7op Scand 1972;43:234-238. 256. Weber H. Lumbar disc herniation: a prospective study of prognostic factors including a controlled trial. Part I I . J Oslo City Hosp 1978;28:89-113. 257. Nashold BS, Hrubec Z. Lumbar Disc Disease: A Twenty-year Clinical Follow-up Stlldy. Mosby, St Louis, 1971 . 258. Gill K, Frymoyer JW. The management of treatment failures after decompressive surgery. In: Frymoyer JW (ed) The Adult .Spine. Raven Press, New York, 1991 : 1 849. 259. Fritsch EW, Heisel J, Rupp S. The failed back surgery syn­ drome. Reasons, intraoperative findings and long-term results: a report of 182 operative treatments. Spine 1996;21:626--633. 260. Dvorak J, Valach L, Fuhrimann P, Heim E. The outcome of surgery for lumbar disc herniation. II. A 4-17 years' follow-up with emphasis on psychosocial aspects. Spine 1 988;13:

1423-1427. 261 . Long OM, Filtzer DL, Ben Debba M, Hendler N H . Clinical features of the failed-back syndrome. J Neurosurg 1988;69:61-71 . 262. Spengler OM, Freeman C, Westbrook R, Miller JW. Low-back pain following multiple lumbar spine procedures. Failure of initial selection. Spine 1980;5:356-360. 263. Hitselberger WE, Whitten RM. Abnormal myelograms in asymptomatic patients. j Neurosurg 1968;28:204. 264. Wiesel SW, Tsourmas N, Feffer HL, Citrin CM, Patronas N. A study of computer-assisted tomography: 1 . The incidence of positive CAT scans in an asymptomatic group of patients.

Spine 1984;9:549-551 . 265. Powell Me, Wilson M , Szypryt P, Symonds E M . Prevalence of

lumbar disc degeneration observed by magnetic resonance in symptomless women. Lancet 1986;13:1366-1367. 266. Weinreb JC, Wolbarsht LB, Cohen JM, Brown CE, Maravilla KR. Prevalence of lumbosacral intervertebral disc abnormali­ ties on MR images in pregnant and asymptomatic non­ pregnant women. RadiolofSlJ 1989;170:125-128. 267. Boden SD, Davis DO, Dina TS, Patronas MJ, Wiesel Sw. Abnormal magnetic resonance scans of the lumbar spine in asymptomatic subjects. J Bone joint Surg 1990;72A:403-408. 268. Zsernavicky J, Juppe M. A comparison of myelography and computer tomography in lumbar disc herniation. Intern Orthop

1989;13:51-55.

269. Bell GR, Rothman RH, Booth RE. Study of computer assisted tomography. Spine 1984;9:552-556. 270. Burton CV, Kirkaldy-Willis WH, Yong-Hing K, Heithoff KB. Causes of failure of surgery on the lumbar spine. Clin Ortirop Rei Res 1981;157:191-199. 271 . MacNab 1. Negative disc exploration: an analysis of the causes of nerve-root involvement in 68 patients. J Bone joint SlIrg 1971;53:891-903. 272. Shiraishi T, Crock HY. Re-exploration of the lumbar spine fol­ lowing simple discectomy: a review of 23 cases. Eur Spine J 1995;4(2):84-87. 273. Frymoyer JW, Hanley EN Jr, Howe J, Kuhlmann D, Matterie

274. 275. 276. 277. 278.

RE. A comparison of radiographic findings in fusion and non­ fusion patients, ten or more years following lumbar disc surgery. Spine 1979;4(5):435-440. Jonsson B, Stromqvist B. Clinical characteristics of recurrent sciatica after lumbar discectomy. Spine 1996;21:500-505. Amw1dsen T, Weber H, Nordal HJ et al Lumbar spinal steno­ sis: conservative or surgical management? A prospective 10year study. Spine 2000;25(11):1424-1435. Katz IN, Lipson SJ, Chang LC et al. Seven to ten-year outcome of decompressive surgery for degenerative lumbar spinal stenosis. Spine 1996;21:92-98. Airaksinen 0, Herno A, Turunen V, Saari T, Suomla inen O. Surgical outcome of 438 patients treated surgical l y for lumbar spinal stenosis. Spine 1997;22:21 78-2182. Fredrickson BE, Baker 0, McHolick WI, Yan H, Lubicky JP. The natural history of spondylolysis and spondylolisthesis. J Bone

Joint Surg 1984;66A:699-707. 279. Moller H, Hedlund R. Surgery versus conservative manage­ ment in adult isthmic spondylolisthesis - a prospective ran­ domized study: part 1 . Spine 2000;25(13): 1 71 1-1 715. 280. Tai l lard WF. Etiology of spondyloli sthesis. Clin Orti7op

1976;117:30-39. 281 . Porter RW, Hibbert C. Vertebral displacement in spondylo­ listhesis. Clin Biomeci7 1989;4:58-63. 282. Fitzgerald JAW, Newman PH. Degenerative spondylolisthesis. J Bone Joint Surg 1976;58B(2):1 84-192. 283. Newman PH. Stenosis of the lumbar spine in spondylolisthe­ sis. Clin Orti7op 1976;115:116-1 2 1 . 284. Cauchoix J , Benoist M, Chassaing V. Degenerative spondylo­ listhesis. Clin Orti7op 1976;115: 122-129. 285. Feffer HL, Wiesel SW, Cuckler JM, Rothman RH. Degenerative spondylolisthesis: to fuse or not to fuse. Spine 1985;10:287-289. 286. Grubb SA, Lipscomb HI, Guilford WB. The relative value of lumbar roentgenograms, metrazamide myelography and discography in the assessment of patients with chronic low­ back syndrome. Spine 1987;122:282-286. 287. Esses SI, Botsford OJ, Kostuik JP. The role of external spinal skeletal fixation in the assessment of low back disorders. Spine

1989;14:594-601 .

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SECTION ELEVEN

The sacroiliac joint and coccyx

SECTION CONTENTS 60. Applied anatomy of the sacroiliac joint

The joint 941 Joint capsule and ligaments Muscles 943 Innervation 943 Biomechanical aspects 943

942

61. Clinical examination of the sacroiliac joint

Introduction 947 Referred pain 948 History 949 Functional examination 949 Epidural local anaesthesia 953 Radiology 953 62. Interpretation of the clinical examination 63. Disorders of the sacroiliac joint 957 Introduction Sacroiliac arthritis 957 Ankylosing spondylitis 957 Psoriasis 960 Reiter's syndrome 960 Septic arth ritis 960 Gout 961 Osteoarthritis 961 Sacroiliac joint syndrome 961 Introduction 961 History 961 Clinical examination 962 Treatment 962 Bony disorders of the pelvis 964 Tumours 964 Fractures of the sacrum 964 64. Anatomy and disorders of the coccyx

Anatomy of the coccyx Disorders of the coccyx

967 967

955

THIS PAGE INTENTIONALLY LEFT BLANK

CHAPTER CONTENTS The joint

941

Joint capsule and ligaments Muscles

942

Applied anatomy of the sacroiliac joint

943

Innervation

943

Biomechanical aspects 943 Nutation-counternutation More complex movements Torsion of the pelvis 945

944 944

THE JOINT The sacroiliac joint possesses all the characteristics of a true joint: a joint cavity containing synovial fluid,l adja­ cent bones having ligamentous com1ections, cartilagi­ nous surfaces which permit movements and an outer fibrous joint capsule with an inner synovial lining.2-5 The joint most commonly links the posterosuperior part of the medial aspect of the iliac bones with the first, second and the upper part of the third segment of the sacrum (Fig. 60.1). A transverse section shows that the joint is situated rather anteriorly (Fig. 60.2). The clinical consequence of this is that it is not possible to elicit ten­ derness by digital pressure at the joint. The sacrum can be regarded as a wedge that fits verti­ cally between the two iliac bones. The sacrum also fits between these bones in the transversal plane.6 The dorsal width of the sacrum exceeds the ventral width only in the middle portion of the joint (Fig. 60.4c). At the lower and upper parts, the wedge shape is quite reversed (Fig. 60.2). Several investigators, however, have demonstrated a high degree of variability in the plane of sacroiliac joints, in both the vertical and transverse directions.1,7,8

Figure 60.1

Articular surfaces of the sacroiliac jOint. 941

942 SECTION ELEVEN - THE SACROILIAC JOINT AND COCCYX

2

Male Figure 60.2 Tranverse section at the iliacus; 3, gluteus; 4, erector spinae; 5,

level of the sacroiliac joint: 1, psoas; 2, sacroiliac joint.

The articular surfaces are ear- or C-shaped and exhibit irregular ridges and depressions that fit into each

Female

Differences between the position of the centre of gravity in the male and female. The position of the centre of gravity lies in line with the axis of the support (male), or lies dorsally (female).

Figure 60.3

axis of movement of the sacrum and it is therefore also known as the axial ligament.

other.9,ID The anatomical configuration, together with

The strong posterior sacroiliac ligament consists of several

strong ligaments, make the joint very stable. These fea­

fascicles of different lengths which overlie the interosseus

tures are more pronounced in men than in women, sug­

ligament and pass in an oblique direction from the lateral

gesting the likelihood of increased mobility in the latter.

crests of the sacrum to the posterior superior iliac spine

Some authors also associate this increased mobility with

and the posterior end of the inner lip of the iliac crest.

the position of the centre of gravity, which in women lies

Those fibres from the third and fourth sacral segments

dorsal to the hip joint and not in line with the axis of support (Fig.

60.3). This exerts a strong rotational force in

the sacroiliac jOint.11,12

are longer and constitute the long posterior sacroiliac ligaments.13

The thin anterior sacroiliac ligament consists of two bands

Cartilage covers the joint surfaces. It is thicker and smoother at the sacral than at the iliac surface.s

which reinforce the anterior and inferior parts of the fibrous capsule and also pass across the joint obliquely from sacrum to ilium.

The sacrotuberous ligament is attached to the posterior JOINT CAPSULE AND LIGAMENTS

iliac spines, the lower part of the sacrum and the upper

A tight articular capsule is attached close to the margins

and laterally to insert at the medial margin of the ischial

part of the coccyx. Its fibres run obliquely downwards of the articular surfaces of the ilium and sacrum. Powerful ligaments support the joint and sharply limit movements (Fig. into

the

60.4). These ligaments can be divided

massive

interosseous

sacroiliac

ligament,

tuberosity. The gluteus maximus, the thoracolumbar fascia, the multifidus muscle and, in some individuals (especially females), long head of biceps femoris are partly attached to this ligament.

the posterior and anterior ligaments, and three accessory

The thin triangular sacrospinous ligament attaches to the

ligaments, - the sacrotuberous, sacrospinous and iliolum­

lateral margins of sacrum and coccyx in front of the

bar ligaments.

The interosseous ligament fills the irregular space between sacrum and ilium at the level of 51 and 52,

attachments of the sacrotuberous ligament. The fibres run in a lateral, caudal and anterior direction to insert at)he spine of the ilium.

immediately behind and above the joint. The shortest and

The iliolumbar ligament takes origin at the lower part of

strongest part of this ligament is in the frontal, horizontal

the transverse processes of the fourth and particularly the

CHAPTER 60 - APPLIED ANATOMY 943

2

fifth lumbar vertebrae. Its fibres radiate to the anterior part of the upper surface of the sacrum as well as to the crest of the ilium.

MUSCLES

2

(b)

6--+-�------����

5

The sacroiliac joint is surrounded by some of the largest and most powerful muscles of the body, i.e. the erector spinae, psoas, quadratus lumborum, piriformis, abdomi­ nal obliques, gluteal and hamstrings. However, there are no muscles designed to act on the sacroiliac joint to produce active, physiological movements. All muscles that cross the joint are designed to act on the hip or the lumbar spine.I,2,14-16 None of the small movements of the sacroiliac joint is produced by active movements of the sacrum. The movements are indirectly imposed by gravity and muscles acting on trunk and lower limbs. Whether these muscles could contribute to active stability of the joint (force closure) is still open to debate. Some authors suggest that the latissimus dorsi and the contralateral gluteus maximus are coupled via the thora­ columbar fascia. The forces of these two synergists cross the sacroiliac joints perpendicularly and it is hypothe­ cated that this could stabilize the joint indirectly.

INNERVATION

No authoritative anatomical studies exist today but most authors report a posterior innervation from the lateral branches of the posterior rami L4-S3 and an anterior innervation from the L2-L3 segments.21 The fact that capsule and ligaments contain nocicep­ tors suggests that the sacroiliac joint is a possible source of low back pain and also plays a role in somatic referred pain. 22 The wide range of segmental innervation probably accounts for the variable referred pain patterns seen in sacroiliac joint lesions,1,23 although pain is localized most commonly at the buttock and the posterior thigh.

BIOMECHANICAL ASPECTS

(a) Posterior and (b) anterior aspect. 1, 2, superior and inferior bands of iliolumbar ligaments; 3, sacrospinous ligament; 4, sacrotuberous ligament; 5, posterior sacroiliac ligaments; 6, anterior sacroiliac ligaments. (c) Transection through the sacroiliac joint: 7, sacroiliac joint.

Figure 60.4

In essence the sacroiliac joint is a stress-relieving joint that serves as a buffer between the lumbosacral and hip joint.lO The sacroiliac joint transmits forces from the ver­ tebral column sideways into the pelvis and then to the lower limbs. Conversely, forces from the lower limbs can be transmitted through pelvis and sacrum to the vertebral column. Despite its size, the sacroiliac joint cannot be considered like any other major joint of the body: its ranges of movement (nutation-counternuta-

944 SECTION ELEVEN - THE SACROILIAC JOINT AND COCCYX

tion, more complex movements and pelvic torsion) are very small and are not controlled by active muscular contractions. The precise nature of motion in the normal joint is still unclear and joints such as the sacroiliac joint with exten­ sive ridges and depressions can be expected to have a very limited amount of mobility. In Kapandji's words: 'There is more a tendency to movement than actual movement since the extremely powerful ligaments pre­ clude any movement from the start'.6 Both in vivo and in vitro kinematic studies have demon­ strated various types of minor motion in the sacroiliac joints, such as gliding, rotation, tilting, nodding and translation.24-26 Mobility is always increased temporarily at the end of pregnancy and for up to 3 months after­ wards.15,27,28 It decreases in men at between 40 and 50 years, and after the age of 50 in women.29

the short upper part of the posterior sacroiliac ligament and the sacrospinous and sacrotuberous ligaments. During counternutation (posterior rotation), the promontory of the sacrum moves superiorly and poste­ riorly while the apex and the coccyx move anteriorly (Fig. 60.5b). As a result, the iliac bones move apart, whereas the ischial tuberosities are approximated. Coun­ ternutation is limited by the tension of the posterior sacroiliac ligaments, especially the long part of these ligaments.6 WeisPo showed that the length of the anterior­ posterior diameter of the superior aperture of the pelvis changed by 5-6 mm during combined nutation­ counternutation. This mobility pattern has been confirmed in women.34

MORE COMPLEX MOVEMENTS NUTATION-COUNTERNUTATION

Most authors 1,15,30-33 Accept that there is a small rotatory movement about a frontal, horizontal axis at the level of 51-52, constituted by the shortest and strongest part of the interosseous (' axial') ligament. During anterior rotation, called nutation, the promon­ tory of the sacrum moves inferiorly and anteriorly while the apex of the sacrum and the coccyx move posteriorly (Fig. 60.5a). As a result of the converging planes of the sacral joint surfaces, the iliac bones are approximated, whereas the ischial tuberosities move apart (Fig. 60.6). This movement also results in slight distraction of the symphysis pubis. Nutation is limited by the tension of the anterior sacroiliac ligament, the interosseus ligament,

Figure 60.5

Movement of nutation (a), counternutation (b).

Radiological stereophotogrammetrical analysis35 has identified very small movements in the sacroiliac joints. In changing position from supine to standing or sitting and between standing and hyperextenSion of the leg, the movements proved even to be three-dimensional, although again most constant around the frontal, hori­ zontal axis. The mean values obtained were: 2.5°, transla­ tion 0.7mm. In a recent study of sacroiliac kinematics for recipro­ cal straddle positions in relatively young subjects, it was established that the pelvis showed a tendency to move in three directions - flexion-extension, side flexion and rotation.36 Another study, using rigidly fixed external devices in 21 volunteers, examined the range o� motion of the sacroiliac joint during maximal flexion and

CHAPTER 60 - APPLIED ANATOMY 945

Figure 60.6 Nutation of the sacrum. The iliac bones approximate, whereas the ischial bones move apart.

extension of the trunk and during standing on one leg. The conclusion was that there was a small range of movement (less than 1°) but with an irregular direction - during flexion of the trunk, the sacrum was just as likely to flex as to extend around a transverse axis. Consequently, in a sample of individuals and for one particular test the true range of motion of the sacroiliac joint is 0°.37

TORSION OF THE PELVIS

Cramer discusses more complex movements.38 During walking (Fig. 60.7), when a person lifts one leg and puts the entire body weight on the other leg, the load of the trunk moves the sacrum forward and caudally but also causes forward rotation. The ilium on the weight­ bearing side is pushed cranially and rotates dorsally and externally. On the non-weight-bearing side, the movement of the sacrum is dorsal and cranial, with pos­ terior rotation; on this side the ilium slides caudally and rotates forward in relation to the sacrum. Overall, the movements of the iliac are torsional. This mobility of the sacroiliac joints incontrovertibly relieves part of the strain on the lumbar spine and is therefore clearly beneficial. It has been conjectured that jumping from a height or stepping onto a high stool increases these complex movements and perhaps even subluxates the joint. Vleeming et a139,40 have stated that: 'Abnormal loading conditions could theoretically force the sacroiliac joint in a new position where ridges and depressions are no longer complementary. Such an abnormal joint position could be regarded as a blocked joint. Being part of the complex kinematic chain between legs and spine, even a small displacement of the sacrum or ilium could be responsible for abnormal displacement or stress of the

Figure 60.7 Complex movements of the iliac bones and sacrum during walking (from Cramer A38, with ppermission). (a) Rotation of the iliac bone at the non­ weight-bearing side, around a frontal, horizontal axis. (b) Rotation of the iliac bone at the weight-bearing side around a vertical axis.

lumbar vertebrae'. In the literature, however, they found (as yet) no definite proof of this phenomenon. In the radiological stereophotogrammetrical analysis men­ tioned earlier, Sturesson et al35 also found that the mobil­ ity of symptomatic joints had a mean value equal to that of asymptomatic joints. Mobility normally decreases with age, which is regu­ larly shown on the radiograph in elderly patients with osteophytes at the lower margin of the joints or even bony ankylosis. In middle age the joint has already reduced in width and becomes obliterated by fibrous and fibrocartilagenous adhesions.4 In ankylosing spondylitis complete fusion is found even in young adults.

Conclusion: movements at the sacroiliac joint are small in extent. At the end of pregnancy (and for some months after­ wards), mobility is increased temporarily due to hormonal influences which favour the process of childbirth. Rotatory movements of the sacrum about a frontal and horizontal axis (nutation and counternutation) seem to occur but strong sacroiliac ligaments, as well as ridges and depressions at the articular surfaces, restrict these move­ ments. Radiological stereophotogrammetical analysis shows movements to be three-dimensional, although rotation about a frontal and horizontal axis is most significant. Mobility normally decreases with age. Subluxation and dysfunction are as yet unproven phenomena.

946 SECTION ELEVEN - THE SACROILIAC JOINT AND COCCYX

REFERENCES 1. Solonen KA. The sacroiliac joint in the light of anatomical, roentgenological and clinical studies.

Acta

Orthop

Scand

2. Albee FH. A study of the anatomy and the clinical importance 3. Gardner E, Gray OJ, O'Rahilly R. Anatomy: A Regional Study of

(eds) The Adult Spine: Principles and Practice. Raven Press, New

4. Brooke R. The sacro-iliac joint. J Anat 1923-24;58:299-305. 5. Sashin DA. A critical analysis of the anatomy and pathological sacroiliac

joints.

j

Bone

joint

23. Bernard TN, Cassidy JD. The sacro-iliac joint syndrome: patho­ physiology, diagnosis and management. In: Frymoyer JW et al

HlIllIan Structure. 4th edn. Saunders, Philadelphia, 1975.

the

on the Sacro-iliac Joint, Maastricht, 1991. ECO, PO Box 25327, Rotterdam, NL.

of the sacro-iliac joint. JAMA 1909;53(16):1273-1276.

of

iliac joint: its role in posture and dysfunction. Segmental signs of sacro-iliac joint dysfunction. First International Symposium

1957;27(suppl):27:1-127.

changes

22. Oostendorp RAB, Elvers JWH, van Gool JJ, Clarijs JP. The sacro­

Surg.

York 1991:chapter 101. 24. Beal MC. The sacro-iliac problem: review of anatomy, mechan­ ics and diagnosis. J Am Obstet Organ 1982;81(10):667-679.

1930;12:891-910. 6. Kapandji IA. The Physiology of the joints, vol 3 Trunk and Vertebral Column, 2nd edn. Churchill Livingstone, New York, 1974. 7. Fischer LP, Gonon GP, Carret JP, Dimmet J. Biomecanique artic­

25. Kim LYS. Pelvic torsion, a common cause of low back pain. Orthop Rev 1984;13(4):206-211. 26. LavignoU B. An approacll to the functional anatomy of the sacro-iliac joints in vivo. Anatomica Clinica 1983;5:169-] 76.

ulaire. Ass Corp Med 1976;2:33-36. 8. Bakland 0, Hansen JH. The axial sacroiliac joint. Anat Clin

27. Clarke WE. Legros: The Tissues of the Body: All Introduction to the Study of Anatomy. Clarendon Press, Oxford: 1952.

1984;6:29-36. 9. V leeming A, Stoeckaert R, Volkers ACW, Snijders CJ. Relation

28. Lynch FW. The pelvic articulation during pregnancy, labor and

between form and function in the sacro-iliac joint. Part I:

the

Clinical anatomical aspects. Spine 1990;15:130-132.

1920;30:575-580.

puerperium.

An

X-ray

study.

Surg

Gynecol

Obstet

10. Bowen V, Cassidy JD. Macroscopic anatomy of the sacro-iliac

29. MacDonald GR, Hunt TE. Sacro-iliac joints: observation on the

joint from embryonic life until the eighth decade. Spine

gross and histological changes in the various age groups. Canad Med Assoc J 1952;66:157-163.

1981;6:620-628. 11. Tischauer ER, Miller M, Nathan 1M. Lordosimetry. A new tech­ nique for the measurement of postural response to materials 12. Bellamy N, Park W, Rooney PJ. What do we know about the sacro-iliac joint? Sel1lin Arthritis Rheum 1983;12:282-313. PL.

(ed)

Gray's

Anatomy,

38th

edn.

Churchill

Livingstone, Edinburgh, 1995. 14. 14.

1955;23:80-91. 31. Duncan JM. The behaviour of the pelvic articulations in the

handling. Am j Indust Hyg Ass 1973;1:1-12.

13. Williams

30. Weisl H. The movements of the sacro-iliac joint. Acta Anat

Miller JA, Schultz AB, Andersson GB. Load displacement

behaviour of sacro-iliac joints. J Orthop Res 1987;592-101. 15. Colachis Sc, Warden RE, Becthal CO et al. Movement of the sacro-iliac joint in the adult male. Arch Phys Med Rehabil 1963;44:490-498. 16. Bogduk N. Clinical Anatomy of the Lumbar Spine and Sacrum. Churchill Livingstone, Edinburgh, 1997. 17. Snijders CJ. Transfer of lumbosacral load to the iliac bones and legs. Part 2: Loading of the sacroiliac joints when lifting in stooped posture. j Clin Biolnech 1993;8:295-301. 18. Snijders CJ, Slagter AHE, Van Strik R et al. Why leg crossing? The influence of common postures on abdominal muscle activ­ ity. Spine 1995;20:1989-1993. 19. V leeming A, Snijders CJ, Stoeckaert R. The posterior layer of the

mechanism of parturition. Dublin

Q j Med Sci 1854;18:60-69.

32. Egund N, Olsson TH, Schmid H, Selvik G. Movement in the sacroiliac joints demonstrated with roentgen stereophotogram­ metry. Acta Radial (Diagn) 1978;19:833. 33. V leeming A, Stoeckart R, Snijders CJ et al. Mobility in the sacro­ iliac joints in the elderly. A kinematic and roentgenologic study. Clin Biomech 1992;7:170-176. 34. Brunner C, Kissling R, Jacob HAC. The effects of morphology and histopathologic findings on the mobility of the sacro-iliac joint. Spine 1991;16(9):221-224. 35. Sturesson B, Selvik G, Uden A. Movements of the sacro-iliac joints. A roentgen stereophotogrammetric analysis. Spine 1969;14:162-165. 36. Smidt GL, McQuade K, Wei SH et al. Sacro-iliac kinematics for reciprocal straddle positions. Spine 1995;20(9):1047-1054. 37. Jacob HAC, Kissling RO. The mobility of the SI joints in healthy volunteers between 20 and 50 years of age. Clill Biomech 1995;10:352-361.

thoraco-lumbar fascia: its function in load transfer from spine to

38. Cramer A. Iliosakralmechanik. Asklepsios 1965;6:261-262.

legs. Spine 1995;20:753-758.

39. Vleeming A, van Wingerden JF, Snijders CJ, Stoeckart R, Stijnen

20. Hodges PW. Is there a role for transversus abdominis in lumbo­ pelvic stability? Manual Therapy 1999;4(2):74-86. 21. Bernard TN, Cassidy JD. The sacroiliac joint syndrome. Pathophysiology, diagnosis and management. In: Frymoyer JW (ed) The Adult Spine: Principles and Practice. Raven Press, New York, 1991:2107-2130.

T. Load application to the sacrotuberous ligament; influences on sacro-iliac joint mechanics. First International Symposium on the Sacro-iliac Joint, Maastricht, 1991. ECO, PO Box 25327, Rotterdam NL. 40. V leeming A, Volkers ACW, Snijders CJ, Stoeckart R. Relation between form and function in the sacro-iliac joint. Part 2: bio­ mechanical aspects. Spine 1990;15(2):133-135.

CHAPTER CONTENTS Intr� duction

947

Referred pain 948

Pain referred to the region of the sacroiliac joint Pain referred from the sacroiliac joint 948

History

948

Clinical examination of the sacroiliac joint

949

Functional examination

Introduction 949 Sacroiliac tests 949

949

Epidural local anaesthesia Radiology

953

INTRODUCTION

953

Whether the sacroiliac joint is a primary source of backache remains controversial. There is still much dis­ agreement between those who believe that subluxations of the sacroiliac joint exist and those who doubt their existence.1,2 The occurrence of sacroiliac arthritis, both rheumatic and septic, cannot be denied because the sacroiliac joint is a true synovial joint and is therefore subject to the same inflammatory and infectious condi­ tions affecting other synovial joints. Difficulties arise when labels such as 'sacroiliac dysfunction' or 'sacroil­ iac subluxation' are given. These diagnoses remain ill defined and are difficult to substantiate.3-s Much of the controversy is caused by lack of agreement on clinical criteria that justify diagnosis of sacroiliac lesions. If the diagnosis is made only on the basis of pain localization or tenderness on palpation, sacroiliac lesions will be seen frequently. The clinical key to diagnosis must be to exert tension on the sacroiliac ligaments without affect­ ing the lumbar spine and the hip joint. Numerous tests to detect sacroiliac joint pain lack this requirement, which may explain differences of opinion between examiners. Several authors6-9 Are of the opinion that unilateral pain and tenderness in the region of the sacroiliac joint is usually a manifestation of the confusing phenomena of referred pain and referred tenderness from a dura mater at a low lumbar level. Cyriax even states that lesions of this joint are as rare as referred lumbar pain at the medial aspect of the buttock and that the side of the sacrum is common. A discussion of the disorders affecting the joint requires definition of the terms used: •

Sacroiliac strain/sprain is overstretch or rupture of the capsuloligamentous structures as a result of abnormal joint movement.

•

Sacroiliac instability is a condition of abnormal joint mobility caused by capsuloligamentous laxity.

•

Sacroiliac subluxation is permanent displacement of the bony parts forming the joint. 947

948 SECTION ELEVEN - THE SACROILIAC JOINT AND COCCYX

• •

Sacroiliac dysfunction is a reversible decreased

upper part of the buttock because of segmental reference

mobility of the joint, the result of articular causes.

of this joint in the third lumbar segment (see p. 000).

Sacroiliac arthritis is an inflammatory condition of the joint.

PAIN REFERRED FROM THE SACROILIAC JOINT14

The concept of a 'sacroiliac sprain' as a common cause of backache and sciatica was introduced by Goldthwait and Osgood in 1905 and reinforced by otherslo,l1 And it still persists. However, MacNab8 noticed that sacroiliac sprains only occur below the age of 45 and in circum­ stances creating considerable force on the joint, such as those generated by falls from heights or motor vehicle accidents. Cyriax? (his p. 364) advised reserving the term for cases of pain arising from the sacroiliac ligaments in the absence of arthritis. However, difficulty arises in those examples of early sacroilitis (14%) in which pain and clinical signs precede the appearance of radiographic sclerosis. Diagnosis of lesions at the sacroiliac joint is still based on clinical examination and radiographs rarely add any useful information.12 In a study of childhood arthritis13

Cyriax states that the sacroiliac ligaments are of first and second sacral origin. It has been confirmed IS That, in par­ ticular, the posterior capsule and ligaments are inner­ vated by articular branches of the posterior primary rami from 51.16 In sacroiliac strain or arthritis, pain is felt most often in the buttock with radiation to the back of the thigh and the calf but never the foot. A typical distribution of pain is shown in Figure 6 1.1. In a series of 17 cases of sacroiliac arthritis in children, Reilly et all? found the usual complaint to be pain in the hip, buttock and thigh. Only one child with septic arthri­ tis also mentioned pain in the groin. This corresponds with referred pain from the superior part of the joint which is innervated by articular branches of the anterior primary rami of L2.

12 of 17 plain radiographs were negative, and initial bone scans were negative in six cases. Of these letter, five had septic arthritis and one juvenile rheumatoid arthritis. Diagnosis can be suggested by negative findings. For example, absence of articular signs in the lumbar spine, full range on straight leg raising, a normal end-feel of the hip joint and the absence of neurological and arterial signs suggest possible involvement of the sacroiliac joint, when there is pain in the buttock, posterior thigh and calf. Clinical

assessment

does

not

differ

from

that

described for the lumbar spine in low back pain disor­ ders (see Ch. 55). When data from the history and func­ tional examination suggest the possibility of a sacroiliac lesion, special tests can be performed.

REFERRED PAIN In sacroiliac joint lesions pain may be either localized or referred into the buttock and leg. The distinction between pain referred to and from the joint is very important and should be the first consideration.

PAIN REFERRED TO THE REGION OF THE SACROILIAC JOINT Most instances are the result of lumbar disc protrusions with segmental (LI, L2, L3 and 51, 52) or multisegmental (lumbar dural) reference of pain. Arthritis of the hip joint is another possibility: pain may be felt in the inner and

Figure 61.1 Pain referred from the sacroiliac joint. (Right) Typical pain referred from the posterior capsule and ligaments. (Left) Pain in the groin may refer from the superior part of the jOint.

CHAPTER 61

-

CLINICAL EXAMINATION 949

Box 61.1 Indications specific sacroiliac tests

HISTORY

-

• Positive sacroiliac distraction test during the routine

History taking should cover preceding disease, trauma, pregnancy and delivery, occupation and working habits, as well as sports and recreational activities. Family and social history are of similar importance.18 In pelvic peri­

lumbar examination • Discrepancy between gross lumbo pelvic pain and slight signs during routine lumbar examination • Suggestive history for sacroiliac disorder and negative routine lumbar examination

partum instability the pain often starts in the third month or within the first few weeks after delivery. In sacroiliac lesions, a typical finding is that there is unilateral gluteal pain

(often deep,

dull and ill­

defined1 9-21), perhaps together with reference in the

5 1-52 dermatomes, chiefly the posterior thigh. Pain may alternate in the right and left buttock and then strongly suggests a manifestation of early ankylosing spondyli­ tis, particularly when it is found in males aged between

15 and 35. Coughing usually jars the buttock or posterior thigh as the result of the sudden increase in abdominal pressure which distracts the ilium from the sacrum. This sign may be interpreted as being of dural origin, based on the assumption that a disc lesion is present at a low lumbar level. However, if such a lesion is present, pain is nor­ mally felt in the lumbar area rather than the buttock. Some authors describe the adoption of an antalgic gait in painful disorders of the sacroiliac joint22,23 And a tilt of the trunk, most frequently towards the painless side.22 Some patients avoid sitting on the buttock of the affected side.23 Neurological symptoms, such as paraesthesia, weak­ ness or numbness, are absent.

tion of possible sacroiliac involvement because of low back pain and / or sciatica. In sacroiliac strain, basic tests are usually not capable of evoking pain.24,25 It is only when movements really stretch the ligament and when this is prolonged that an injured ligament may react painfully. A diagnosis of ligamentous strain is thus based on the history, painful reactions after prolonged load and the outcome of special sacroiliac tests (Box 6 1.1).

SACROILIAC These tests can be divided into those that assess move­ ment or position by palpation (palpation tests) and those that stress the structure to reproduce the patient's symp­ toms (pain provocation tests).

Palpation tests The best-known palpation tests are the standing and sitting flexion palpation tests and the Gillett test.26 The Gillett test is performed as follows. The patient stands with the back to the examiner (Fig. 6 1.2) who places one thumb just underneath the posterior superior iliac spine and the other on the second sacral spinous process or on the contralateral superior

FUNCTIONAL EXAMINATION

iliac spine. The patient is asked to lift one knee as high as

INTRODUCTION

and therefore moves the posterior superior iliac spine

Clinical examination of the sacroiliac joint is not routinely

sacroiliac joint prevents this movement or, paradoxically,

undertaken in low back pain and sciatica, except for one test - sacroiliac distraction (Fig. 61.3) - because this is the most sensitive test to detect inflammation in the joint. Apart from positive sacroiliac distraction test, atten­ tion may be drawn to the sacroiliac joint by some dis­ crepancies between gross symptoms and slight signs during standing lumbar movements. For instance, in acute sacroiliac arthritis full trunk flexion and side bending to the painful side may provoke pain but the pain is much more severe as soon as the sacroiliac joints are directly tested. Movements of the hip joint may also prove painful, especially both rotations, as the result of an indirect strain on the sacroiliac joint at the end of the movement. Routine clinical examination of the lumbar spine can be negative but some symptoms may point in the direc-

possible which rotates the ilium on that side posteriorly inferiorly relative to the opposite side. Fixation of the even gives rise to elevation of the posterior superior iliac spine as the patient compensates by tilting the pelvis at the point of maximal hip flexion. This manoeuvre is usually painful in symptomatic patients. The test presupposes normal hip joint function; inter­ pretation is difficult and even impossible in leg-length inequality, lumbar scoliosis and particularly in obese patients, in whom the bony landmarks are difficult to palpate. To date palpation tests have not had acceptable levels of reliability, despite claims to the contrary27-29 and there­ fore we do not use them.

Pain provocation tests Pain provocation tests aim to stress the structures in an attempt to reproduce the patient's symptoms. Studies

950 SECTION ELEVEN - THE SACROILIAC JOINT AND COCCYX

Figure 61.3

Anterior gapping test.

The patient lies supine. The examiner applies increas­ ing pressure to the anterior superior spines of the ilia in a downward and outward direction. The examiner crosses the arms to do this, in order to increase the strain on the ligaments. If the patient states that the test is painful, it must be ascertained whether pain is located unilaterally gluteal or posteriorly crural. All other outcomes, such as lumbar pain or tenderness at the anterior superior iliac spines, are not relevant. In gluteal or posterior crural pain the test is repeated, with the lumbar region supported by the patient's forearm so as to stabilize the lumbar joints and also prevent compression of a tender part of the sacrum or ilium on the couch. If this does not alter the Figure 61.2 Gillett test to estimate rotation of the sacroiliac joints. The knee on the right-hand side is raised as high as possible. The ilium on that side rotates posteriorly, which can be established by palpation of the posterior superior iliac spine.

intensity of pain, it is almost certain that the anterior sacroiliac ligament is at fault. Other tests to stretch the anterior sacroiliac ligament exist but are less specific because tension is also applied to other structures. Forced lateral rotation at the hip joint

that have examined these tests show a good interexam­

with the leg held in 90° flexion is one example and is a

iner agreement.30--32

routine test in the basic functional examination of the lumbar spine.

The main tests are: • •

Distraction test or anterior gapping test

Posterior gapping test (Fig.

Compression test or posterior gapping test

painless side. The examiner stands behind the patient

• Sacral thrust or downwards pressure test

6 1.4). The patient lies on the

and exerts pressure to the uppermost iliac crest, directing it towards the opposite iliac crest. The test stretches the

•

Cranial shear test

•

Posterior shear or thigh trust test

posterior sacroiliac ligaments and compresses the ante­

•

Pelvic torsion or Gaenslen's test

rior part of the sacroiliac joint. This test has the advantage

•

Yeoman test

that the sacrum and the iliac spine are not in contact with

•

Patrick's or 'faber' test.

Anterior gapping test

(Fig. 6 1.3). This test, always

performed routinely in the basic functional examination of the lumbar spine, is particularly sensitive and therefore

the couch, excluding the possibility of pain being a result of pressure on a tender area. Sacral thrust or downwards pressure test (Fig.

6 1.5).

Pressure is applied directly to the sacrum whil e the

specific in arthritis because the weakest part of the sacroil­

patient lies prone. The heel of one hand, reinforced by

iac joint is involved.

the other hand is on the centre of the sacrum (52) and

CHAPTER 61 - CLINICAL EXAMINATION 951

Figure 61.4

Posterior gapping test.

the force is directed anteriorly against the ilia which are fixed against the examining couch. In sacroiliac lesions, gluteal pain may be provoked on attempted

Figure 61.5

Downwards pressure on the sacrum.

extension by similar pressure on the lumbar spine but is much more severe when pressure is directed to the sacrum. In the cranial shear test, the hand is on the coc­ cygeal end of the sacrum and the pressure is applied in

same shoulder, axial pressure is believed to tense the sacrotuberal ligament.25 Pelvic torsion or Gaenslen's test (Fig.

a cranial direction.

6 1.7). This test is

The following set of sacroiliac pain provocation tests

performed with the patient in a supine-lying position.34

all use the femur as a lever. The results should therefore

One hip is passively flexed and pushed to the chest. The opposing leg is extended passively, hanging over

be interpreted cautiously. Posterior shear or thigh thrust test (Fig.

6 1.6). The patient

lies supine and the examiner stands at the painful side. The hip is flexed and slightly adducted. The examiner applies a posterior shearing stress to the sacroiliac joint and ligaments through the femur. Excessive (to the end­ feel) adduction of the hip is avoided and the stress should

the edge of the couch. Overpressure is applied to force the sacroiliac joints to their end of range: nutation on one side and counternutation on the other. Inter­ pretation of the test should be done with care because this test also stresses the psoas muscle, the hip joints and the femoral nerve.

be in a longitudinal direction and not towards further

Yeoman's test35 (Fig.

adduction. Some authors believe that this test in particu­

patient lying prone. The examiner stands at the painful

6 1.8). This test is performed with the

lar puts strain on the iliolumbar ligaments and that, if the

side and puts one hand on the sacrum. The other hand

thigh is maximally flexed and adducted towards the

extends the hip and at maximum range forces the ilium

opposite shoulder, axial pressure falls on the posterior

into anterior rotation. A positive test produces pain over

sacroiliac ligaments; if the thigh is pushed towards the

the sacroiliac joint. This test also stretches other struc-

952 SECTION ELEVEN - THE SACROILIAC JOINT AND COCCYX

Figure 61.S Figure 61.6 thrust test).

Yeoman's test.

Alternative test to stretch the posterior sacroiliac ligaments (thigh

tures: hip joint and psoas muscle and via the latter also puts tension on the lumbar spine. For this reason this test is not always reliable and should at a minimum be com­ pared with the results of hip extension with the ilium fixed (the stabilizing hand on the ilium instead of on the sacrum). Patrick's test (Fig.

6 1.9). This test flexes, abducts and

externally rotates (J-ab-er) the femur at the hip joint. After reaching the end of movement, the femur is fixed in relation to the pelvis. The examiner holds down the anterior superior iliac spine on the opposite site and increases the pressure at the medial side of the knee. This stresses the anterior sacroiliac ligaments, in part­ icular on the side of the abducted leg. It is good to recall that almost all routine functional tests of the hip (summarized in Box 61.2) indirectly put stress on the sacroiliac joints. • Forced lateral rotation with the leg held in

90° of

flexion and resisted adduction of the thigh exert a distraction force at the sacroiliac joints and indirectly stretch the anterior sacroiliac ligaments.

Box 61.2 Sacroiliac pain provocation tests Anterior ligaments Anterior gapping test Patrick's test

Posterior ligaments Posterior gapping test

Anterior and posterior ligaments Sacral thrust test Cranial shear test Thigh thrust test Pelvic torsion test (Gaenslen's) Yeoman's test Figure 61.7

Gaenslen's test.

CHAPTER 61

-

CLINICAL EXAMINATION 953

patients with what appears to be genuine complaints, painful lumbar and sacroiliac tests and an uninforma­ tive radiograph.

RADIOLOGY In sacroiliac strain nothing is revealed by the radiograph. In arthritis, radiological assessment of the sacroiliac joints is of vital importance. However, clinical signs may precede by months or years the appearance of early scle­ rosis (Cyriax? p. 360). A normal appearance of the sacroil­ iac joint therefore does not exclude a diagnosis of ankylosing spondylitis. If symptoms persist, radiological examination should be repeated after 3 months. Pelvic instability may be detected if the X-ray is taken Figure 61.9

Patrick's test

• Forced medial rotation at the hip joint with the hip

and knee held in 90° of flexion and resisted abduction

while standing on one leg. A shift of the pubic bone on the non-weight-bearing side to a more caudal position implies an unstable symphysis pubis and sacroiliac joint.

of the thigh pull the ilium away from the sacrum. In the absence of hip joint disease, pain experienced over the sacroiliac joint is highly suggestive of a sacroiliac lesion.s

EPIDURAL LOCAL ANAESTHESIA Positive confirmation by local anaesthesia, normally so useful in difficult cases, is impracticable here, because the anterior sacroiliac ligaments cannot be infiltrated and the posterior mass of ligaments is too large. Cyriax advises the induction of epidural local anaesthesia in

Conclusion: the diagnosis of sacroiliac joint disorders should be established from the findings of a careful history and the outcome of physical examination. If two or more specific tests to stress the joint prove to be positive, such a disorder is especially to be expected. However, these tests are only significant when the history and remaining physical findings rule out other syndromes. It should also be remembered that patients with sacroiliac joint lesions can have coexisting sources of pain, for example lateral recess spinal stenosis or a herniated disc lesion. Arthritis and strain are accepted conditions affecting these joints. Dysfunction and subluxation are difficult to prove, remain obscure and may not exist.

REFERENCES 1. Bradley KC. The anatomy of backache. Aust NZ J Surg 1974;44:227-232. 2. Grieve GP. COIIIIIIOIl Vertebral Joillt Problems. 2nd edn. Churchill

Livingstone, New York, 1988. 3. Dreyfuss P, Dryer S, Griffin J et al. Positive sacroiliac screening

tests in asymptomatic adults. Spine 1994;19(10):1138-1143. 4. Sturesson B, Selvik G, Uden A et af. Movements of the sacroiliac

joints; a roentgen stereogrammetic analysis. Spine 1989;14: 162-165.

5. Tullberg A, Bromberg S, Branth B et af. Manipulation does not

alter the position of the sacro-iliac jOint. A roentgen stereogram­ metic analysis. Spine 1998;23:1124-1129.

10. Brooke R. The sacro-iliac joint. J Anat 1924;58:299-305. 11. Sashin DA. A critical analysis of the anatomy and the pathologic

changes of the sacroiliac joints. J Joint Bone Surg 1930;12:891-910. 12. Lawson TL, Foley WD, Carrera GF, Berland LL. The sacroiliac

joints: anatomic, plain roentgenographic and computed tomo­ graphic analysis. J Comput Assist TOl11ogr 1982;6(2):307-314. 13. Wurff v d F, Hagmeyer RM, Meyne W et af. Sacro-iliacaael

gewricht getest. Inter- en intra beoordelaars betrouwbaarheid. Ned Tijd Fysiotherapie 1996;1:78-184. 14. Schwarzer AC, Aprill CN, Bogduk N. The sacroiliac joint in

chronic low back pain. Spine 1995;20:3 1-31. 15. Oostendorp RAB, Elvers JWH, van Gool JJ, C1arijs JP. Segmental

6. Fitzgerald RTD. Sacro-iliac strain. BMJ 1979;1:1285-1286.

signs

7. Cyriax J. Textbook of Orthopaedic Medicine, vol. 1, 8th edn.

SympOSium on the Sacroiliac Joint, Maastricht, 1991. ECO, PO

Bailliere Tindall, London, 1982. 8. McNab I. Backache. Williams & Wilkins, Baltimore, 1979. 9. Goldthwait JE, Osgood RB. A consideration of the pelvic articu­

lations from an anatomical pathological and clinical standpoint. Bostoll Med Surg J 1905;152:593--601.

of sacro-iliac joint dysfunction.

First International

Box 25327, Rotterdam, The Netherlands. 16. Grob KR, Neuhuber WL, Kissling RO. Innervation of the

sacroiliac joint of the human. Z RlzeumatoI1995;54(2):117-122. 17. Reilly JF, Gross RH, Emans

Jl3,

Yingve DA. Disorders of the

sacro-iliac joint in children. J Balle Joint Surg 1988;70A(1):31-40.

954 SECTION ELEVEN - THE SACROILIAC JOINT AND COCCYX

18. Bellamy N, Park W, Rooney PJ. W hat do we know about the sacroiliac joint? Semin Arthritis Rheum 1983;12(3):282-313.

history and physical examination in diagnosing sacroiliac joint

19. Inman VT, Saunders JB. Referred pain from skeletal structures. J Nerv Ment Dis 1944;99:660-667.

lower back with special reference to the sacro-iliac joints in health and inflammation. Ciin Rheum 1985;4(4):426-432. clinical studies. Acta

Orthop

Scand

1957;27(suppD:1-127. Clinical Considerations, Roentgenology, Pathologic Anatomy and Treatment. (Translation of the original French edition of 1951 by

Des Jardins, AW Springfield, CC Thomas, 1946.) sacroiliac joint. Ciin Orthop 1976;118:113-117. Semiologie et

Traitement des

flexion

test.

Manual

Therapy

Phys Ther 1999;79(11):1043-1057.

30. Broadhurst NA. Pain provocation tests for the assessment of

Medizin

im

Rahmen

341-345. 31. Laslett M. The reliability of selected pain provocation tests for sacroiliac joint pathology. Spine 1994;19(11):1243-1249. sacroiliac joint tests in patients with and without low back pain.

Discales et

33. IlIouz G, Coste F. Le signe du trepied dans I'exporation clinique

medizinischen

34. Hoppenfeld S. Physical Examination of the Spine and Extremities.

Algies

des sacro-iliacques. Press Med 1979;72:66-67. der

Rehabilitation, 2e auflage. Johann Ambrosius Barth, Leipzig, 1977.

26. Gillett H, Liekens M. Belgian Chiropractic Research Notes, 10th edn. Brussels, 1973.

standing

J Orthop Sports Phys Ther 1999;29(2):83-89.

Ligamentaires du Rachis. Masson, Paris, 1972. Manuelle

the

32. Cibulka J, Koldehoff D. Clinical usefulness of a cluster of

23. Dunn EJ, Byron OM, Nugent JT et al. Pyogenic infections of the

K.

of

1999;4(2):87-93.

sacro-iliac joint dysfunction. J Spinal Disorders 1998;11(4):

22. Forestier J, Jacqueline F, Rotes-Querol J. Ankylosing Spondylitis,

25. Lewit

reliability

29. Levangie PK. Four clinical tests of sacro-iliac joint dysfunction.

21. Solonen KA. The sacroiliac joint in the light of anatomical,

24. Troisier O.

pain. Spine 1996;21(22):2594-2602. 28. Vincent-Smith B, Gibbons P. Inter-examiner and intra-examiner

20. Jacobsson H, Vesterkold L. The thermographic pattern of the

roentgenological and

27. Dreyfuss P, Michaelsen M, Pauza K et at. The value of medical

Appleton-Century-Crofts, New York, 1976. 35. Yeoman W. The relation of arthritis of the sacroiliac joint to sciatica. Lancet 1928;215:1119-1122.

Interpretation of the clinical examination of the sacroiliac joint and coccyx

Interpretation of the clinical examination of the sacroiliac joint

955

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CHAPTER CONTENTS ,

Introduction

9S7

Sacroiliac arthritis 9S7 Ankylosing spondylitis 957 Psoriasis 960 Reiter's syndrome 960 Septic arthritis 960 Gout 961 Osteoarthritis 961 Sacroiliac joint syndrome 961 Introduction 961 History 961 Clinical examination 962 Treatment 962 Bony disorders of the pelvis 964 Tumours 964 Fractures of the sacrum 964

Disorders of the sacroiliac joint

INTRODUCTION

Sacroiliac joints are true synovial joints and thus subject to various forms of arthritis and degenerative processes. Although they are relatively immobile - the joint can only rotate 3-50 in the younger subject - they may be suscep­ tible to mechanical trauma. After the fifth decade of life, fibrosis takes place between the cartilage surfaces and by the seventh decade the joint has usually undergone fibrous ankylosis. The available range of movement decreases as fibrous ankyl­ osis increases. 1 Most pain in the sacroiliac or gluteal region does not originate from the sacroiliac joint but is referred pain of disco dural origin (see Ch. 52) and every diagnosis of a 'sacroiliac lesion' should be made with caution and only after other common sources of 'sacroiliac pain' have been ruled out. The pathological conditions affecting the sacroiliac joint are inflammatory and mechanical. The latter is usually referred to as 'sacroiliac joint syndrome'.2 The exact nature of the syndrome is not known but it is generally accepted that mechanical pain stems from minor subluxations and/ or ligamentous strain. "

SACROILIAC ARTHRITIS

In the assessment of patients with pain in one buttock, perhaps radiating to the back of thigh and calf, the clinician must always bear in mind the possibility of an inflammatory lesion of the sacroiliac joint. Sacroiliitis is usually the first manifestation of ankylosing spondylitis but may also be associated with inflammatory bowel disease, psoriasis and other more uncommon rheumatic disorders. Sacroiliac gout has been observed. Pyogenic infection of the sacroiliac joints are rare. ANKYLOSING SPONDYLITIS INTRODUCTION

Once considered a rare disease, ankylosing spondylitis (AS) is now recognized as relatively common, affecting 957

958 SECTION ELEVEN - THE SACROILIAC JOINT AND COCCYX

up to 0.5-1.0% of the population.3 The ratio of occur­ rence in males and females is approximately 5 : 1 although it was previously thought to be 20 : 1. Several studies now suggest that it may occur almost as fre­ quently in females as in males, although in a milder form and with more peripheral localization.4,5 The disease is characterized by fibrosis and ossification of ligaments and capsules rather than the joint destruction so typical of rheumatoid disease.6 Ankylosing spondylitis almost invariably starts at the sacroiliac joints and then extends upwards to involve the spine at increasingly higher levels. However, the sacroiliitis very often remains silent. It has been esti­ mated that no more than 1 case in 10 ever has pain in the buttock. Most spondylitis begins as a diffuse lumbar ache, and sometimes the earlier symptoms are thoracic or cervical (Cyriax? p. 366). Ankylosing spondyliitis fre­ quently involves extraspinal joints, tendons and liga­ ments. The disorder may affect all body systems: iritis, pulmonary diseases, chronic prostatitis and cardiovas­ cular diseases are now recognized as possible complica­ tions of the disease.8-12 Diagnosis of AS is not always easy, particularly in the early stages when only the pelvis is affected. Clinical cri­ teria have been developed during recent decades.13,14 These criteria are usually not appropriate. Radiologically documented sacroiliitis is obligatory for making a definite diagnosis but it may take years before the radio­ logical abnormalities of the sacroiliac joints can be demonstrated without doubt;15 the clinical criteria, such as decreased chest expansion and symmetrical limitation of spinal movements, also occur relatively late in the course of AS, at a time when the disease should be obvious on other grounds (see Box 63.1). The natural history of the disease in an individual patient is extremely difficult to define or predict. Some patients have disease limited to the pelvis and the major-

Box 63.1 Modified 'New York' criteria for ankylosing spondylitis (AS) -

Clinical criteria Low back pain and stiffness for more than 3 months not relieved by rest Symmetrical limitation of lumbar movement Limitation of chest expansion to 2.5 cm

Radiological criteria Bilateral sacroiliitis, grade II or more Unilateral sacroiliitis, grades III-IV

Definite AS is diagnosed if the radiological feature is associ­ ated with at least one of the clinical criteria Probable AS is considered if three clinical criteria are present

ity have a good outlook for a successful life pattern. Only in a small minority of patients does AS progress to the well-known total ankylosis.16 SACROILIITIS

It is well recognized that ankylosing spondylitis begins at the sacroiliac joints but it is not widely appreciated that here the disease may be silent. Many patients with advanced disease cannot recollect ever having pain in the sacroiliac region or the buttock. Even if at its onset sacroiliitis causes symptoms, these may be taken for a SI disc lesion. However, routine clinical examination of the spine performed carefully can always detect the lesion. Symptoms

The patient is usually between 15 and 40 years old and complains of unilateral gluteal pain. Because the sacro­ iliac joints are largely derived from the first and second sacral segments, the pain commonly radiates to the back of the leg as far as the heel. The localization of the pain is thus the same as in SI or S2 nerve root compression. However, in sacroiliac arthritis it never spreads to the foot, and paraesthesia is absent. As in discodural prob­ lems, coughing (which increases intra-abdominal pres­ sure) may cause pain in the buttock and down the leg. The localization and the extent of pain, together with the painful cough, may lead to the assumption that an ordi­ nary discoradicular conflict is present.l7 Some specific characteristics then help to distinguish sacroiliac arthritis from disc diseases. The main feature is that the pain comes and goes in an irregular and unpredictable way. During a flare-up the pain is constantly present, during a remission the patient can exercise freely without an increase in symptoms. An attack is usually unprovoked: if pain is present it is usually increased by exertion, but if it is absent it cannot be stimulated. This is the reverse of the history in disc lesions, where the pain always follows certain activities and subsides after their avoidance. Another important feature is that sacroiliac pain often alternates from one side to the other though it is seldom bilateral except as it changes sides.18 Signs

Given the similarity with SI or S2 root compression, the index of suspicion usually remains low and the diagnosis is often missed (Table 63. 1). During the examination in a standing position no sus­ picion arises: there may be a slight increase in gluteal pain during extension and bending towards the painful side; flexion is limited because of increasing pain in the buttock and thigh; sometimes a slight deviation tow�rds the painful side can be noted during flexion.19 Straight leg raising may also cause pain at the end of range.20

CHAPTER 63 - DISORDERS OF THE SACROILIAC JOINT 959

Table 63.1 Differential diagnosis of sacroiliac arthritis and S1-S2 disc lesions Arthritis

51-52 root compression

History Gluteal pain

Spreading in S1-S2 dermatomes

Spreading in S1-S2 dermatomes

Flaring/constant pain

Flares

Constant

Coughing

Painful

Painful

Morning symptoms

Pain on awakening improved by walking

Pain on leaving the bed

Prolonged morning stiffness Association with activity

Pain irrespective of exertion

Pain localization

Alternating

Unilateral

Not beyond the ankle

Often in the foot

Never present

In foot or toes

Extension and side flexion

Full

Often limited

Flexion

May be slightly limited

Usually grossly limited

Straight leg raiSing

May be painful at the end

Usually limited

Sacroiliac distraction test

Painful

Painless

Paraesthesia

Pain follows certain activities

Clinical examination

It is only when the anterior part of the sacroiliac joint is tested (see Ch. 61) that the diagnosis becomes obvious. Unilateral or gluteal or posterior crural pain during the test incriminates the sacroiliac joint. This manoeuvre is an extremely sensitive method of deciding whether the sacroiliac joint is affected and a positive distraction test often precedes radiological evidence of sacroiliac arthri­ tis by years. Although many other tests for the sacroiliac joints have been described, the distraction technique as described earlier is the most significant test for the status of the joint: it applies immediate stress to the anterior part of the joint, without using a lever - distraction forces using the patient's femur as a lever are very non­ specific and should therefore not be used as screening tests. Because of the specificity of the sacroiliac distrac­ tion test, it is an essential part of the routine clinical examination of the lumbar spine. If the patient is examined during a flare-up, passive and resisted hip movements can also cause the gluteal pain, especially passive external rotation and resisted flexion, abduction and extension. Although some authors find tenderness over the sacroiliac joint highly indicative of the existence of sacroiliac arthritis,21 we believe that palpating for tender­ ness adds no further information and only confuses the examiner. First, the joint, covered as it is by the overhang of the ilium and the sacral extent of the sacrospinalis muscle, remains beyond the direct reach of the palpating finger. Second, the sacroiliac region is a common site for referred tenderness in lumbar discodural conflicts.

by months or even years. In the early stages, radiological signs may be minimal and of questionable significance. Sometimes it is necessary to use CT, which is more useful for demonstrating joint narrowing and fusion.22 If radio­ graphs appear to be within normal limits, radiological examination should be repeated in 3 months. The changes are classified according to the New York criteria in five grades (grades 0 to IV; Table 63.2). Initially there is a patchy periarticular osteoporosis, leading to loss of definition of the subchondral bone plate. The joint thus appears to be widened. Further evolution of the process results in superficial erosion, together with focal sclerosis of subchondral bone. Further proliferative changes result in irregular bridging across the articular cavity. This causes blurring and indistinct margins on both sides of the joint. Finally, the radiograph shows a complete osseous fusion. Some authors stress that radionuclide scanning may be more sensitive than radiography in detecting early sacroiliac disease.24,25 Others, however, have questioned the advantages of the technique and have also demon­ strated its lack of specifity.26,27

Table 63.2 Sacroiliac changes in ankylosing spondylitis23 Grade

Changes

o I II

None Suspicious

Patchy periarticular osteoporosis

Minimal

Loss of definition at the edge of the joints Some sclerosis Minimal erosion

Further examination

Radiological evidence of sacroiliitis is accepted as being obligatory for the diagnosis of AS. However, the clinical symptoms may predate the radiological abnormalities

III Definite

Definite sclerosis on both sides Blurring and indistinct margins Loss of joint space

IV Ankylosis

Complete fusion of the joint

960 SECTION ELEVEN - THE SACROILIAC JOINT AND COCCYX

Association with HLA-B27

The association between the genetic marker HLA-B27 and AS is well known:28,29 The frequency of HLA-B27 in healthy populations is between 1% (Japanese and African) and 14% (Caucasian) whereas the marker is present in 90% of the AS population.4 However, the pres­ ence of HLA-B27 plays little or no role in the diagnosis of the diseases: a patient with repeatedly normal radio­ graphs is unlikely to have the disease, regardless of the HLA status; in contrast a B27-negative individual with symptoms suggesting AS has the disease if the radiograph shows the typical changes.3D Natural history

The prognosis for an individual patient is difficult to predict. Some patients have the disorder limited to the pelvis whereas others quickly develop spinal and extraskeletal disease. The younger the patient is at the age of onset, the worse the outcome, and men usually do worse than women.31 When sacroiliac arthritis appears after the age of 25 years, the disease is likely to follow a mild course: bilateral sacroiliitis goes on flaring up and subsiding for some years until bony ankylosis is com­ plete and the pain disappears. If the disease spreads upwards, its spread is very slow and the thoracic spine is only affected when the patient is 40 or 50 years. In these patients the cervical spine usually remains unaffected and the hips retain full mobility. In contrast, when the sacroiliac arthritis appears before the age of 20 years, or the spondylitis has reached the lumbar spine before the age of 25 years, early and severe disablement is very probable: pain and stiffness spread upwards along the spine very quickly and there is also a great chance of hip involvement within 20 years of the onset.32 Treatment

It is vital that patients have some knowledge of the natural history of the disease. They should be told that the concept of inevitable progressive stiffening of the joints, ending in complete ankylosis and crippling dis­ ability, is not correct. The diagnosis of AS is usually not as sombre as is generally believed. The patient should be made aware that the majority have a good prognosis, for a normal social, family and professional life, and that the disease leads to incapacity in only a few cases. No specific treatment of a curative nature presently exists. The aim of treatment is therefore preventive and symptomatic: avoidance of pain and deformity. In order to prevent further deformity, the patient should adopt an appropriate routine. A strict daily routine of positioning and extension exercises is more valuable than physiotherapy. Sleeping on a hard mat­ tress and avoiding lying bent on the side are basic. To lay face downwards on a rigid surface at least once a day for

half an hour is also recommended. During the day, extension exercises should be performed as often as pos­ sible. Attention should also be given to the position used at work and all opportunities for mobility exploited. Swimming is the best routine sport. Pain and inflammation are treated by non-steroidal anti-inflammatory drugs (NSAIDs). Although phenyl­ butazone appears to be the most efficacious,33 It is potentially irreversibly toxic. Therefore indometacin is considered the drug of choice. The patient must be informed that therapy should be continuous and that the purpose of medication is to allow normal activities to be followed and the daily posture and exercise routine to be carried out.

PSORIASIS

The true prevalence of sacroiliitis in psoriasis is unknown. The majority of estimates are in the range of 20-30%.34,35 The link between the skin condition and the joint disease is unknown. The disease is frequently unilateral or asym­ metrical and can be asymptomatic. The clinical presenta­ tion is pain and a positive sacroiliac distraction test - the same as in ankylosing spondylitis. Treatment of the sacroiliitis is with NSAIDs.

REITER'S SYNDROME

Reiter's syndrome is the classical triad of arthritis, conjunctivitis and non-bacterial urethritis. The arthritis affects several joints, usually asymmetrically. The cause is unknown but evidence tends to point to an infectious agent. Males are predominantly affected and the onset of the disease is usually between the ages of 20 and 40 years. Although a high percentage (more than 30%) of patients with the syndrome show severe radiological sacroiliitis,36 only a small percentage develop clinical evi­ dence of unilateral or bilateral sacroiliac arthritis. Clinical evidence of sacroiliac joint involvement may occur as early as 3 months from the onset of the illness.37

SEPTIC ARTHRITIS

A pyogenic infection of the sacroiliac joints is rare although in recent years more reports have been pub­ lished on this topic.38-4D The infection reaches the joint by the haematogenous route or by direct extension from a contiguous abscess. Predisposing factors are pregnancy, ' intravenous drug abuse and immunosuppression. The initial diagnosis is often overlooked because of its rarity and the poorly localized symptoms and signs. The

CHAPTER 63

condition should be considered in cases of acute or sub­ acute onset of pain in the gluteal region, hip or low back accompanied by fever. An apparent acute abdomen may be present, especially in children.41,42 The disease may also present with symptoms and signs of femoral or sciatic nerve root irritation if the distended anterior joint capsule comes into contact with the lumbosacral plexus. The diagnosis is highly suspect when the 'sign of the buttock' is found during clinical examination of the back (see p. 1007). Roentgenograms are often normal. CT scan and MRI may be useful tools but radionuclide scanning with 99mTc or 67Ga usually affords an early confirmation of the condition.43-45 Generally antibiotic treatment leads to complete recovery.

GOUT

Gout is usually considered to be a disorder of the periph­ eral joints. However, since 1965 it has been recognized that the sacroiliac joint is also radiologically affected in a late stage in a significant percentage (7-17%) of patients with tophaceous gout.46,47 The sacroiliitis usually remains clinically silent, acute attacks being rare.48

- DISORDERS OF THE

SACROILIAC JOINT 961

and around the sacroiliac joint as possible sources of 'dys­ functional' pain. It is, however, more difficult to identify a 'blocked sacroiliac subluxation' as the main cause of the dysfunction. Numerous tests to detect dysfunction of the sacroiliac joint have been described in the chiropractic and manual medicine literature. Although commonly used, many of these tests are difficult to perform or to interpret and consequently their intertester reliability is low (see p. 949). In particular those tests that assess motion (or the lack of it) in a sacroiliac joint are not reliable. Pain provo­ cation tests - stressing the structures in an attempt to reproduce the patient's symptoms - have a much better intertester reliability and can be used to detect sacroiliac joint syndrome. We therefore do not discuss blocked sacroiliac joints as a possible source of sacroiliac dysfunction. The issue is too controversial and today there exists no clear evidence for the disorder. Sacroiliac strain by contrast is a well­ delineated entity with typical signs and symptoms. Recent studies demonstrated temporary pain relief after local blocks of the sacroiliac joint, thus confirming the sacroiliac joint as a real source of low back pain.53,54 However, it is worth repeating that the diagnosis requires typical physical findings and that tenderness over the sacral sulcus and the posterior sacroiliac joint line are not alone sufficient to make the diagnosis.

OSTEOARTHROSIS

The incidence of degenerative arthritis in the sacroiliac joints increases with age.49 It is not considered to be a cause of symptoms. Osteoarthrosis of the sacroiliac joints is a radiological finding only and has no clinical significance (Cyriax:7 p. 372).

SACROILIAC JOINT SYNDROME INTRODUCTION

That mechanical lesions of the sacroiliac joint could cause backache and referred pain to the buttock and posterior leg was first recognized by Goldthwait and Osgood in 1905.50 Some schools of thought have put great emphaSiS on the joint and consider the sacroiliac joint syndrome as a common source of low back and pelvic pain.51 Although it is generally accepted that most pain in the sacroiliac region is of dural origin and has nothing to do with an actual lesion of the joint/,52 it is logical to accept the sacroiliac joint as a prime cause for pain because it is a synovial joint and thus subject to the same dysfunctional conditions that affect other synovial joints. It is not hard to accept ligamentous sprain and overuse phenomena in

HISTORY

Sacroiliac joint syndrome or strain occurs usually in women between the ages of 15 and 35 years. It may be that the ligaments have been strained by an accident such as a fall on the buttocks or a motor vehicle accident. Because the sacroiliac joint is extremely stable and is sur­ rounded by powerful, massive interosseus and accessory ligaments, considerable force is usually required to drive the joint beyond their physiological range. Alternatively, the strain can be associated with pregnancy. Hormonal changes can cause relaxation of the sacroiliac ligaments; during pregnancy and parturition the joint will therefore be more susceptible to strain. Pain is usually unilateral (although bilateral pain may occur), is never alternating and is localized in the sacro­ iliac region with reference to the buttock and the postero­ lateral aspect of the thigh and calf. The pain has typical postural characteristics in that it appears only after prolonged or increased loading of the ligaments. A typical complaint will therefore be that the pain is brought on by the maintenance of prolonged pos­ tures.55 As a rule, it is increased by excessive standing or by strolling and is abolished by correction of posture or by movement. Resting will also decrease the symptoms,

962 SECTION ELEVEN - THE SACROILIAC JOINT AND COCCYX

although lying down, for example in a fixed position, may cause pain. Pain is often aggravated by bending and climbing stairs. Dural signs such as pain during coughing and sneezing are absent. Neurological symptoms paraesthesia and weakness - do not occur. The condition is persistent, though rare cases of spontaneous recovery do occur.

CLINICAL EXAMINATION

Because pain at the sacroiliac area is usually of dural origin, the diagnosis of sacroiliac strain (summarized in Box 63.2) must always be made with some reserve. Examination of the lumbar spine shows a full range of movement, sometimes with pain at the end of range of flexion or extension. There may be pain if weight is borne on the ipsilateral extremity. Straight leg raising is full range, although pain at the end of range may be encoun­ tered. In severe cases, some hip movements (flexion, medial rotation and extension) may be painful at the end of range. Resisted abduction and resisted extension of the leg may also provoke pain. Box 63.2 Summary of the diagnosis of sacroiliac strain Postural pain in the sacroiliac region after: Pregnancy A fall or motor accident Negative lumbar examination Negative examination of the hip Positive sacroiliac tests

It is possible that the sacroiliac distraction test (inclu­ ded in the basic lumbar clinical examination) remains negative. Because this test merely pulls on the anterior ligaments, the stress is not always adequate.to provoke pain in the posterior ligaments. More vigorous move­ ments, performed with leverage of the hip, will then be required to stress the posterior ligaments (see pp. 949-952). It is worth emphasizing again that most of these tests are non-specific in that they assume that the hip is completely normal. A positive test is therefore significant only when the clinical examination has ruled out lumbar and hip disorders.

TREATMENT

Vleeming et al consider an inadequate 'force closure' of the sacroiliac joints as an important cause of sacroiliac strain. Force closure is defined as the compressive stabi­ lizing forces exerted by ligaments and coupled bilateral gluteal and back muscles. The authors hypothesize that

ligaments alone are not capable of transferring lumbo­ sacral load effectively from the spine to the iliac bones. This is particularly the case in heavy load situations and conditions of sustained load such as sitting and standing for a longer time in a relatively counternutated position of the sacrum.56--59 Muscle weakness and inadequate coordination between muscles diminish force closure which consequently increases the load on the pelvic liga­ ments. The ligaments become strained, leading to pain and laxity. The authors advise a specific training programme as one of the treatment measures to compensate for the lack of force closure. Strength and coordination of the gluteus medius and contralat�ral latissimus dorsi should be trained. The erector spinae, the multifidus muscle fasci­ cles and the oblique and transverse abdominals should also be part of the active stabilizing training programme because of their direct or indirect attachments with the sacroiliac ligaments. The active straight leg raising test, described by Mens et al60 seems to have some prognostic value. Lying supine the patient is asked to lift the leg about 5 cm off the couch. In a serious pelvic dysfunction the patient is unable to do so or the strength on one side is considerably less. The test is repeated after stabilizing the pelvis with a belt or by manual pressure on the iliac spines from the lateral side. If this lateral pressure converts a painful active straight leg raising into a painless one, wearing a belt will lead to a good result. BELT

The symptoms may be abolished permanently if the joint and the ligaments are protected for a month or so by the wearing of an appropriate belt. The most suitable type is a very tight, non-elastic 6 cm belt, placed around· the pelvis between the iliac crest and the greater trochanter (Fig. 63.1). The biomechanical effects of such a belt in human pelvis-spine preparations was studied by Vleeming et al58 who found that it caused a significant decrease in rotation at the sacroiliac joints. Both the location of the belt and the degree of loading were crucial. An optimal decrease in movement was reached with a belt worn at the level just cranial to the trochanter. SCLEROSING INJECTIONS

If wearing a pelvic belt fails, sclerosing injections into the posterior sacroiliac ligaments are indicated. We use Ongley's solution (2% phenol, 25% dextrose, 15% glyc­ erol). This mixture has a good safety record and, apart from considerable pain for up to 2 days after the injec­ tion, it causes no side effects. It induces an inflammatory

CHAPTER 63 - DISORDERS OF THE SACROILIAC JOINT 963

response which leads to fibroblast proliferation and new collagen production (see p. 125). Because of pain, the solution must be mixed with 2% lidocaine (ligno­ caine) in a proportion of 80% sclerosant and 20% lido­ caine (lignocaine). Usually all the sacroiliac ligaments are treated at their ligamentoperiosteal junction. Although it is possible to be very selective and to infiltrate only small groups of liga­ ments, better results will be achieved if all the ligaments on both sides are infiltrated.61 Technique. A 10 ml syringe, filled with 8 ml sclerosant

Figure 63.1

A belt for sacroiliac strain.

(b)

(a) Figure 63.2

and 2 ml lidocaine (lignocaine) is fitted to a 7 cm long needle. One skin puncture is made at the level of the tip of the first sacral spine. From this puncture the following ligaments on both sides can be infiltrated: the posterior sacroiliac, the interosseous sacroiliac, the sacrotuberous and the sacrospinous (the latter two form the sacral attachments). To reach the posterior sacroiliac ligament, the tip of the needle is directed at an angle of 30° to the skin and thrust laterally until it touches bone. Four to five small injections are made along the posterior aspect of the posterior superior spine. It should be stressed that no fluid is introduced unless the tip of the needle is felt to impinge on bone (Fig. 63.2). The needle is then partly withdrawn and reinserted at an angle of about 45° to the horizontal to reach the iliac attachments of the interosseous sacroiliac ligaments. Bone is reached at a depth of 5-7 cm, where small infiltrations are made. To reach the sacral attachments of the sacrotuberous and the sacrospinous ligaments the needle should be almost

Sclerosant infiltration of the posterior sacroiliac ligament.

964 SECTION ELEVEN - THE SACROILIAC JOINT AND COCCYX

completely withdrawn and, together with the skin and subcutaneous tissue, moved down towards the coccyx as far as possible. The free thumb palpates the lateral side of the sacrum at the lower three levels. The needle is then pushed under the palpating thumb and small infiltra­ tions (with bony contact) are made. The iliac insertion of the iliolumbar ligament is infiltrated via a separate skin puncture. The needle is inserted about 3 cm lateral to the fifth supraspinous process. The palpating thumb is placed at the medial edge of the iliac crest. The tip of the needle is thrust in very obliquely in the direction of the thumb, until it is felt to traverse a resistant ligament before touching bone (Fig. 63.3). An infiltration of 1 ml is performed along the border, deeply and superficially, by multiple withdrawals and reinsertions. Care is taken to inject only when the needle touches bone. Follow

up. There is considerable pain at the time of injec­

tion but the anaesthetic soon takes effect. After an hour and subsequently for up to 2 days the back is painful, sometimes to such an extent that the patient is forced to rest in bed. This disagreeable reaction usually lasts no longer than 2 days. The infiltration is repeated twice, at weekly intervals. For 6 weeks after the last infiltration the patient should avoid all movements and postures that strain the sacroiliac joints, such as standing, bending and climbing stairs. The result should be judged after 6 weeks. Insufficient relief indicates the need for another infiltration.

BONY DISORDERS OF THE PELVIS TUMOURS

Sacral tumours, both primary and secondary, are rare lesions. They often escape early diagnosis. Most patients with sacral tumours have a non-specific complaint of low back pain. However, the history will reveal some unusual features typical for non-mechanical lesions in the lumbar spine, currently referred to as 'warning symptoms' (see p. 852). • • • •

Continuous pain, not altered by changing positions or activities Increasing pain, slowly getting worse Expanding pain Bilateral sciatica.

Late in the course of a serious sacral lesion, dis­ turbance of urinary and I or bowel control may occur. Clinical examination may reveal local tenderness and swelling. Both lumbar examination and sacroiliac pain provocation tests may be positive. The most striking clin­ ical finding is usually the appearance of a 'sign of the buttock' (see p. 1007) which draws immediate attention to a serious pelvic lesion. Apart from metastases, a sacrococcygeal chordoma is the most common type of malignant sacral tumour. The neoplasm is believed to take its origin from remnants of the notochord, grows slowly but is locally infiltrative and destructive. Symptoms may initially be mild and may present months or years before the diagnosis is made. As the disease progresses the pain may become intractable. Death usually results from complications or extensive local tumour growth. Diagnosis can be made via a careful rectal examination which almost always reveals the firm, presacral tumour mass, extrarectal and fixed to the sacrum. Radical resection is the treatment of choice for sacral chordomas. Addition of radiation after subtotal resection improves the disease-free interval, although radiation therapy can generally be used only once.62,63

FRACTURES OF THE SACRUM

Figure 63.3 ligament.

Sclerosant infiltration of the iliac insertion of the iliolumbar

The increased incidence in motor vehicle and industrial trauma during the last decades has led to an increase in fractures of the sacrum. The diagnosis and treatment of these lesions is beyond the scope of this book. However, insufficiency fractures of the sacrum usually develop in the absence of obvious trauma and must therefore be included in the differential

CHAPTER 63 - DISORDERS OF THE SACROILIAC JOINT 965

diagnosis of sacroiliac lesions. Insufficiency fractures of the -sacrum usually occur in elderly women with post­ menopausal osteoporosis. They are often confused with disc lesions, spinal stenosis and cauda equina syndrome.

Sacroiliac tests are very painful and there is a 'sign of the buttock'. A CT scan is often necessary to demonstrate the fracture line. Treatment consists of rest.64,65

REFERENCES 1. Bowen V, Cassidy JO. Macroscopic and microscopic anatomy of the sacroiliac joint from embryonic life until the eighth decade.

22. Wilkinson M, Meikle JAK. Tomography of the sacro-iliac joints. Anll Rheul1l Dis 1966;25:433-439. 23. Gofton JP. Report from the subcommittee on diagnostic criteria

Spil1e 1981;6:620-628. 2. Bernard TN, Cassidy JO. The sacroiliac joint syndrome. In: Frymoyer ]W (ed) The Adult Spine: Principles and Treatment. Raven Press, New York, 1991:2107-2130. 3. Gran JT, Husby G, Hordvik M. Prevalence of ankylosing

24. Russel AS, Lentle BC, Percy JS. Investigation of sacro-iliac

spondylitis in males and females, in a young middle-aged

disease: comparative evaluation of radiological and radio­

population in Tromso, northern Norway. Ann Rheum Dis

nuclide techniques.] RheumatoI1975;2:45. 25. Namey TC, McIntyre J, Buse M. Nucleographic studies of axial spondarthritides: 1. Quantitative sacroiliac scintigraphy in early HLA B27 sacroilitis. Arthritis RheulIl 1977;20:1058-1064. 26. Goldber RP, Genant HK, Shimshak R et af. Applications and limitations of quantitative sacroiliac joint scintigraphy. Nllcl Med 1978;128:683-686. 27. Oequeker J, Godderis T, Walravens M et al. Evaluation of

1985;44:359. 4. Calin A, Fries JF. The striking prevalence of ankylosing spondylitis in "healthy" W27 positive males and females. A controlled study. N Ellgl' Med 1975;293:835. 5. Oequeker J, Oecock T, Walravens M, Van de Putte 1. A system­ atic survey of the HLA-B27 prevalence in inflammatory rheumatic diseases.' Rheumatol 1978;5:453.

6. Ball J. Enthesopathy of rheumatoid and ankylosing spondylitis. Ann RI,ertlll Dis 1971;30:213. 7. Cyriax JH. Textbook of Orthopaedic Medicine, vol 1, 8th edn. BaiJIiere Tindall, London, 1982. 8. Blumberg B, Ragan C. The natural history of rheumatoid spondylitis. Medicine 1956;35:1. 9. Anonymous. The lungs in ankylosing spondylitis (editorial). BM] 1971;3:492. 10. Mason RM, Murray RS, Oates JK. Prostatitis and ankylosing spondylitis. BM] 1958;1:748. 11. Tucker CR, Fowles RE, Calin A. Aortitis in ankylosing spondyl­ itis: early detection of aortic root abnormalities with two­ dimensional echocardiography. Am ] CardioI1982;9:680.

12. Bergfeldt L, HLA B27 associated rheumatic diseases with severe cardiac bradyarrhythmias: clinical features and prevalence in

223 men with permanent pacemakers. Am, Med 1983;75:210. 13. Van der Linden SJ, Valkenburg HA, Cats A. Evaluation of diagnostic criteria for ankylosing spondylitis. Arthritis Rheum 1984;27:361. 14. Cats A, Van der Linden SJ, Goeithe HS, Khan MA. Proposals for diagnostic criteria of ankylosing spondylitis and allied dis­ orders. c/ill Exp RheumatoI1987;5:167-171.

15. Agarwal A. Pre-ankylosing spondylitis. In: Moll JMH (ed) Ankylosing Spondylitis. Churchill Livingstone, New York, 1980. 16. Calin A. Ankylosing spondylitis. In: Fries JF, Ehrlich GE (eds) Prognosis: Contemporary Outcomes of Disease. The Charles Press, Bowie, MD, 1981:357-359. 17. Rosen PS, Graham oc. Ankylosing (Strumpell-Marie) spondylitis - a clinical review of 128 cases. Arch Interam Rheum 1962;5:158. 18. Ogryzlo MO. Ankylosing spondylitis. In: Hollander JL, McCarthy OJ (eds) Arthritis and Allied Conditions. Lea & Febiger, Philadelphia, 1972:699-723. 19. Solonen KA. The sacroiliac joint in the light of anatomical, roentgenological and clinical studies. Acta Orthop Scand 1957;27(suppl):1-127. 20. Grieve GP. The sacro-iliac joint. Physiotherapy 1976;62:384-400. 21. Bellamy N, Park W, Rooney PJ. What do we know about the sacro-iliac joint? Sem Arthritis Rheum 1983;12(3):282-313.

for ankylosing spondylitis. In: Bennett PH, Wood PHN (eds)

Population Studies of the Rheumatic Disease. International COl/gress, Series 148. Excerpta Medica Foundation, Amsterdam, 1968.

sacroiliitis: comparison of radiological and quantitative radio­ nuclide techniques:] RadioI1978;128:687-689.

28. Brewerton OA, Caffrey M, Hart FD. Ankylosing spondylitis and HL-A 27. Lancet 1973;1:994. 29. SchJosstein L, Trasaki PI, Bruestone R et al. High association of an HL-A antigen W 27, with ankylosing spondylitis. N Engl ] Med 1973;288:704. 30. Calin A. HLA-B27 in 1982. Reappraisal of a clinical test. AnI/ Illtern Med 1982;96:114. 31. Marks SH, Barnett M, Calin A. Ankylosing spondylitis in women and men: a case-controlled study., RheulIlatoI1983;10:624-628. 32. Calin A, Elswood J. Ankylosing spondylitis (AS) - a nationwide analytical review: entry variables determining surgical inter­ vention and outcome. Br J RheulIlato/ 1987;26(suppl):53. 33. Godfrey RG, Calabrao II, Mills D et al. A double-blind cross­ over trial of aspirin, indomethacin and phenylbutazone in ankylosing spondylitis. Arthritis Rheum 1972;15:110. 34. Barraclough D, Russel AS, Percy JS. Psoriatic spondylitis: a clinical, radiological and scintigraphic survey. ] RheulIlatol 1977;4:282-287. 35. Moller P, Vinje O. Arthropathy and sacroiliitis in severe psoria­ sis. Scand , RheumatoI1980;9:113-117. 36. McEwen C, Di Tata D, Lincc C et af. Ankylosing spondylitis and spondylitis accompanying ulcerative colitis, regional enteritis, psoriasis and Reiter's disease: a comparative study. Arthritis

Rheum 1971;14:291. 37. Russel AS, Davis P, Percy JS et al. The sacroiliitis of acute Reiter's syndrome. J RheumatoI1977;4:293-296. 38. Haug M, Ovesen J. Psoas abscess in pyogenic sacroiliitis. , Ugeskr Laeger 1999;161(8):1123-1124. 39. Gutierrez Macias A, Barreiro Garcia G, Ribacoba Bajo L et al. Pyogenic sacroiJiitis. Presentation of 10 cases. C Rev c/ill Esp 1993;193(5):235-238. 40. Moyer RA, Bross JE, Harrington TM. Pyogenic sacroiliitis in a rural population., Rheumato/1990;17(10):1364-1368. 41. Cohn SM, Schouetz OJ. Pyogenic sacro-iliitis: another imitator of the acute abdomen. Surgery 1989;100:95. 42. Metis K, Roland J, Appel B et al. Pyogene Sacro-iliitis bij kinderen. Tijdschr Genees 1994;50:14-15, 1145-1148.

966 SECTION ELEVEN - THE SACROILIAC JOINT AND COCCYX

43. Lenfant ], ]ourneau P, Touzet P, Rigault P. Pyogenic sacroiliitis in children. Apropos of 11 cases. Rev ChiI' Orthop Reparatrice Appal' Mot 1997;83(2):139-147. 44. Haliloglu M, Kleiman MB, Siddiqui AR, Cohen MD. Osteomyelitis and pyogenic infection of the sacroiliac joint. MRl findings and review. Pediatr Radio/1994;24(5):333-335.

45. Bittini A, Dominguez PL, Martinez P et al. Comparison of bone and gallium-67 imaging in heroin user's arthritis. J Nucl Med 1985;26:1377-1381. 46. Malawista SE, Seegmiller JE, Hathaway BE et al. Sacroiliac gout. lAMA 1965;194:106-108. 47. Alarcon-Segovia D, Cetina JA, Diaz-Jouanen E. Sarco-iliac joints in primary gout. Am J Roentgel1oI1973;118:438-443. 48. Lipson RL, Slocumb CH. The progressive nature of gout with inadequate therapy. Arthritis Rheum 1965;8:80-81. 49. Cohen AS, McNeil JM, Calkins E et al. The "normal" sacroiliac joint: analysis of 88 sacroiliac joints. Am J Roel1tgenol 1967;100:559-563. 50. Goldthwait JE, Osgood RB. A consideration of the pelvic articu­ lations from an anatomical, pathological and clinical stand­ point. Boston Med Surg J 1905;152:593-601. 51. Bernard TN Jr, Kirkaldy-Willis WHo Recognizing specific characteristics of nonspecific low back pain. Ciin Orthop 1987;217:266-280. 52. Macnab 1. Backache. Williams & Wilkins, Baltimore, 1983:64. 53. Maigne J-Y, Aivalikis A, Pfefer F. Results of sacroiliac joint double block and the value of sacroiliac pain provocation tests in 54 patients with low back pain. Spine 1996;21(16): 1889-1892.

54. Broadhurst NA, Bond MJ. Pain provocation tests for the assessment of sacroiliac joint dysfunction. J Spinal Disord 1998;11(4):341-345.

55. Troisier O.

Semiologie et Traitement des Algies Discales et Ligall7entaires du Rachis. Masson, Paris, 1973.

56. Vleeming A. The sacroiliac joint. A clinical, biomechanical and radiological study (dissertation). Rotterdam Erasmus University, 1990. 57. Vleeming A, Stoeckaert R, Volkers ACW, Snijders CJ. Relation between form and function in the sacroiliac joint. Part 1: Clinical anatomical aspects. Spine 1990;15:l30-132. 58. Vleeming A, Stoeckaert R, Volkers ACW, Snijders CJ. Relation between form and function in the sacroiliac joint. Part 2: Biomechanical aspects. Spine 1990;15:l30-l32. 59. Pool-Goudzwaard AL, Vleeming A, Stoeckaert R, Snijders CJ, Mens JMA. Insufficient lumbopelvic

stability: a clinical,

anatomical and biomechanical approach to 'a specific' low back pain. Mal1ual T herapy 1998;3(1):12-20. 60. Mens JMA, Vleeming A, Snijders CJ et al. Active straight leg raising. A clinical approach to the load transfer function of the pelvic girdle. In: Vleeming A (ed) Secolld Interdisciplinary World

Congress 011 Low Back Pain and its Relation to the Sacro-iliac Joint. Rotterdarn ECO 207-220, 1995. 61. Barbor R. Sclerosant therapy. In: Cyriax JH (ed) Orthopaedic Medicine, vol II, 8th edn. Bailliere Tindall, London, 1974. 62. York JE, Kaczaraj A, Abi-Said D et al. Sacral chordoma: 40-year experience at a major cancer center. Neurosurgery 1999;44(1):74-79. 63. Cheng EY, Ozerdemoglu RA, Transfeldt EE, T hompson RC Jr. Lumbosacral chordoma. Prognostic factors and treatment. Spille 1999;24(16):1639-1645. 64. West SG, Troubler JL, Baker MR, Place HM. Sacral insufficiency fractures in rheumatoid arthritis. Spine 1994;19(18):2117-2121. 65. Mumber MP, Greven KM, Haygood TM. Pelvic insufficiency fractures associated with radiation atrophy: clinical recognition and diagnostic evaluation. Skeletal RadioI1997;26:94-99.

CHAPTER CONTENTS ,

Anatomy of the coccyx

967

Disorders of the coccyx 967 Referred coccygodynia 968 Local coccygodynia 968 Psychogenic coccygodynia 969

Anatomy and disorders of the coccyx

ANATOMY OF THE COCCYX The coccyx is formed by fusion of four rudimentary ver­ tebrae. The first coccygeal vertebra has a base for articu­ lation with the apex of the sacrum and two cornua (curnua coccygea) that are usually large enough to artic­ ulate with the cornua sacralia. The sacrococcygeal joint is a true joint with a joint capsule and ligaments. Other lig­ aments covering the posterior aspect of the coccyx are the posterior intercoccygeal ligaments. The gluteus maximus partly inserts at the dorsolateral aspect of the coccyx via its coccygeal fibres (Fig. 64.1). The coccyx and overlying skin are innervated via the dorsal rami of 54 and 55'

DISORDERS OF THE COCCYX Usually coccygeal pain results from a local lesion but referred coccygodynia is possible and psychogenic pain also occurs.

3

2

The coccyx (1), showing its articulation with the sacrum, the insertion of the gluteus maximus (2), and the two cornua (3) intercoccygeal ligaments. Figure 64.1

967

968 SECTION ELEVEN - THE SACROILIAC JOINT AND COCCYX

REFERRED COCCYGODYNIA

Palpation starts at mid-sacrum and four types of

That coccygodynia can arise from a lumbar disc lesion, usually as the result of extrasegmental reference, is well

coccygodynia may be found:1 •

of lower pelvic structures (neoplasms of rectum or

•

prostate).2 The history and clinical examination can

•

easily distinguish referred pain from a local disorder. In

•

referred coccygodynia from a disc lesion the pain arises

Contusion of the tip of the coccyx and the immediate surrounding tissue. This is the most common type.

known.1 Coccygodynia may also arise from irritation

Sprain of the posterior intercoccygeal ligaments. Sprain of the sacrococcygeal joint. Irritation of the coccygeal fibres of the gluteus maximus muscle. In this condition the pain is uni­

not only during sitting but also during lumbar move­

lateral and may spread slightly to one buttock.

ments. Coughing is also painful. Physical examination

Occasionally the patient complains that walking is

further

uncomfortable.

shows

pain

during

lumbar

movements

and straight leg raising often increases the pain. However, palpation does not assist in diagnosis because

Treatment

local tenderness is to be expected whichever variety of

Apart from seating modifications that transfer the

coccygodynia is present. Tumours or other causes of

weight to the ischia, treatment may consist of deep

inflammation affecting the sacrum should be suspected if the pain is not relieved by lying down or if there is

transverse friction, steroid infiltrations or surgery.

nocturnal pain. When there is doubt, epidural local anaesthesia can be useful.

Deep transverse friction. When applied to the affected ligaments, this is very often quickly effective. Six to eight sessions two or three times a week usually suffice, except in contusion of the tip of the coccyx, where

LOCAL COCCYGODYNIA True coccygodynia nearly always affects women and the

infiltration of a local steroid usually affords better and quicker results.

most common cause is traumatic. Usually a direct contu­

Technique. The patient lies prone with a pillow under

sion during a faU in the half-sitting position is responsi­

the pelvis. The legs are slightly abducted and internally

ble. Because the coccyx usually lies 2 cm above the two

rotated. The physiotherapist sits next to the patient and

ischial tuberosities it can only be contused when the body

places one thumb on the affected spot. If the lesion is at

is tilted backwards during a fall on the buttocks.

the sacrococcygeal or dorsal intercoccygeal ligaments,

Alternatively in a fall onto a narrow object the force may

the friction is given by alternating, up-and-down move­

strike the coccyx rather than the ischial tuberosities.

ments of the thumb. If the lesion lies at the insertion of

In 'idiopathic' coccygodynia, no particular injury is

the gluteal fibres, the thumb should be pressed deeply

noted. It has been suggested that certain anatomical vari­

between the muscle and the lateral border of the coccyx.

ations of the coccyx predispose to repeated micro­

Friction is then given by drawing the thumb up and

traumata which then cause chronic irritation. A coccyx

down along the edge of the bone.

with a sharp forwards angle seems to be more prone to being painfully stretched.3 Childbirth also sometimes causes injury and post­ partum coccygodynia is a well-recognized entity. Coccygodynia is related to sitting. The pain is felt at the coccyx only and does not spread in any direction. Sitting on a hard surface or with the buttocks over the

Steroid infiltration. This can be done if the lesion lies at the tip of the coccyx or when deep friction does not succeed. The injection is usually very effective but if the patient does not take some preventive measures in the form of seating modifications then relapses may be

encountered. 4

border of the chair relieves the pain. Lumbar movements,

Technique. The patient lies prone on the couch, the

standing and lying down do not provoke the pain.

pelvis slightly tilted and the legs internally rotated. The

Coughing and sneezing is painless but defecation some­

tenderness is carefully sought. Sometimes it is necessary

times hurts. As a rule, walking is painless except when

to perform rectal palpation (Fig. 64.2). The coccyx is

the coccygeal fibres of the gluteus maximus muscle are

then pressed between the index finger and the thumb. In

involved.

this position the injection can be given precisely and

The routine clinical examination of the lumbar spine,

without fear of penetrating the rectum. This precaution

sacroiliac joints and hips will be found to be completely

is particularly appropriate if the sacrococcygeal joint or

normal. Palpation will reveal a localized tender area. As

the apex of the coccyx is infiltrated.

already mentioned, tenderness is also present in referred

Al ml tuberculin syringe, filled with 10 mg of triamci­

and in psychogenic coccygodynia, so the diagnosis

nolone, is fitted to a thin 2 cm needle. After careful prepa­

should be made before palpation starts.

ration of the skin, the needle is introduced at the localized

CHAPTER 64 - ANATOMY AND DISORDERS OF THE COCCYX 969

after 2 weeks. A second infiltration is made if some residual tenderness remains. If the condition recurs frequently, the steroid solution should be replaced by two infiltrations of sclerosant solu­ tion (1.5 ml of sclerosant and 0.5 ml of lidocaine (ligno­ caine) 2%). Although very painful during the days following the injections, it usually affords permanent results.

Coccygectomy. This is only considered in intractable inca­ pacitating pain persisting in spite of adequate conserva­ tive treatment. However, the operation is very rarely indicated and the results are far from goOd.5.6 Furthermore a high incidence of Gram-negative infection following coccygectomy has been reported?

PSYCHOGENIC COCCYGODYNIA Coccygeal pain may be of psychogeniC origin. Because Figure 64.2

Steroid infiltration of the coccyx.

the diagnosis is usually made by elicitation of tenderness, the elimination of a psychogenic case is extremely impor­ tant. Usually the history helps: genuine local coccygo­ dynia does not spread and psychogeniC pain is usually

spot until it hits bone. By half-withdrawing the needle

vague and radiates in various (impossible) directions. In

and reinserting at a slightly different angle, the entire

local coccygodynia the lumbar or hip movements do not

lesion is then infiltrated with a series of tiny neighbour­

elicit pain, whereas they all hurt in a psychogenic case. If

ing punctures. The palpating thumb and index finger feel

the suspicion of psychogenic coccygodynia arises, the

exactly where each droplet is deposited.

patient must be given enough freedom during history

After injection the coccyx remains sore for a few days before the symptoms abate. The patient is re-examined

and functional examination for contradictions to emerge (see Section 16).

REFERENCES 1. 2.

3.

Cyriax JH. Textbook of Orthopaedic Medicine, vol I, 8th edn. Bailliere Tindall, London, 1982;302. Traycoff RB, Crayton H, Dodson R. Sacrococcygeal pain syn­ dromes: diagnosis and treatment. Orthopedics 1989;12(16):

4.

Kersey PJ. Non-operative management of coccygodynia.

Lancet 1980;1:318. 5.

1373-1377.

6.

Postachini F, Massobrio M. Idiopathic coccygodynia. Analysis of fifty-one operative cases and a radiographic study of the normal coccyx. J Bone Joint Surg 1983;65:1116-1124.

7.

Beinhaker NA, Ranawat CS, Marchisello P. Coccygodynia: surgical versus conservative treatment. Orthop Trans 1977;1:162. Pyper JB . Excision of the coccyx for coccygodynia. A study of the results in twenty-eight cases J Bone Joint Surg 1957;39B: 733-737.

Bayne 0, Bateman JE, Cameron HU. Influence of etiology 011 the results of coccygectomy. Clin Orthop 1984;190:266-272.

THIS PAGE INTENTIONALLY LEFT BLANK

SECTION TWELVE

The hip and buttock

SECTION CONTENTS 65. Applied anatomy of the hip and buttock The hip joint 973

973

Capsule and ligaments 974 Muscles 975 Bursae 979 Nerves 979 Blood vessels 980 Topographical anatomy 980 Joint movements 980

Stress fracture of the femoral neck 1012 Internal derangement in the hip 1012 Psoas bursitis 1015 Haemorrhagic psoas bursitis 1016 Gluteal bursitis 1017 Trochanteric bursitis 1018 Ischial bursitis 1019 Psychogenic pain 1019 69. Disorders of the contractile structures

66. Clinical examination of the hip and buttock Introduction 985

Referred pain 986 History 987 Inspection 988 Functional examination Palpation 994 Accessory tests 994 Technical investigations

985

989

1023

Resisted flexion 1023 Resisted extension 1025 Resisted adduction 1026 Resisted abduction 1028 Resisted medial rotation 1029 Resisted lateral rotation 1029 Resisted extension of the knee 1029 Resisted flexion of the knee 1030

994

67. Interpretation of the clinical examination 68. Disorders of the inert structures

997

999

The capsular pattern 999 Traumatic arthritis 999 Monoarticular steroid-sensitive arthritis 1000 Rheumatoid conditions 1000 Septic arthritis 1002 Tuberculous arthritis 1002 Chondrocalcinosis and gout 1002 Monoarticular arthritis in middle-aged people 1002 Osteoarthrosis 1002 The non-capsular patterns 1007 1007 Disorders with a positive 'buttock sign' Aseptic necrosis of the hip 1010

70. Groin pain 1035 Introduction 1035

History 1035 Clinical examination Interpretation 1036

1036

71. Hip disorders in children 1043 Congenital dislocation of the hip 1043 Congenital limitation of extension 1045 Arthritis of the hip in children 1045 Perthes' disease (pseudocoxalgia) 1046

Slipped epiphysis 1046 Avulsion fractures about the hip 72. Summary of hip pain

1049

1046

THIS PAGE INTENTIONALLY LEFT BLANK

CHAPTER CONTENTS ,

The hip joint

973

Capsule and ligaments Muscles

974

Applied anatomy of the hip and buttock

975

Flexor muscles 975 Extensor muscles 976 Abductor muscles 978 Adductor muscles 978 Lateral rotator muscles 979 Medial rotator muscles 979

Bursae

979

Nerves

979

Blood vessels

THE HIP JOINT

980

Topographical anatomy

Anterior side 981 Lateral side 981 Posterior side 981

Joint movements

981

981

The hip joint is a ball-and-socket joint, formed by the femoral head and the acetabulum (Fig. 65.1). The articu­ lar surfaces are spherical with a marked congruity; this limits the range of movement but contributes to the con­ siderable stability of the joint. In the anatomical position the anterior / superior part of the femoral head is not covered by the acetabulum. This is because the axes of the femoral head and of the acetabulum are not in line with each other. The axis of the femoral head points superiorly, medially and anteriorly, while the axis of the acetabulum is directed inferiorly, laterally and anteriorly. The cup-shaped acetabulum is a little below the middle third of the inguinal ligament. The acetabular articular surface is an incomplete cartilaginous ring, thickest and broadest above, where the pressure of body weight falls in the erect posture, narrowest in the pubic region. The rough lower part of the cup, the acetabular notch, is not covered by cartilage. The centre of the cup, the acetabular

Figure 65.1

The hip joint: 1, ilium; 2, femur; 3, ligamentum teres; 4, labrum acetabulare; 5, transverse acetabular ligament; 6, joint capsule.

973

974 SECTION TWELVE - THE HIP AND BUnOCK

fossa, is also devoid of cartilage but contains fibroelastic fat. The acetabular labrum, a fibrocartilaginous ring attached to the acetabular rim, deepens the cup and enlarges the contact area with the femoral head. The part of the labrum that bridges the acetabular notch does not have cartilage cells and is called the transverse acetabular ligament. If forms a foramen through which vessels and nerves may enter the joint. The acetabular labrum is tri­ angular in section. The base is attached to the acetabular rim and the apex is free. The femoral head is ovoid or spheroid but not com­ pletely congruent with the reciprocal acetabulum. It is covered by articular cartilage except for a rough pit for the ligamentu111 teres, a flattened fibrous band, embedded in adipose tissue and lined by the synovial membrane (Figs 65.2 and 65.3). The ligament connects the central part of the femoral head with the acetabular notch and its transverse acetabular ligament. The ligament is extra­ articular and contains a tiny branch of the obturator artery partly responsible for the vascular supply of the femoral head. The femoral head and neck also receive arterial supply from the capsular vessels, arising from the medial and lateral circumflex arteries (Fig. 65.3).

CAPSULE AND LIGAMENTS

The capsule is a cylindrical sleeve, running from the acetabular rim to the base of the femoral neck. It is supported by powerful ligaments. Anteriorly these are two ligaments: the fan-shaped iliofemoral ligament of Bertin situated craniolaterally; and the pubofemoral ligament, in a more caudomedial orientation. Together they resemble the letter Z (Fig. 65.4).

7

f'H-"""":"-- 2 6

3

5

Figure 65.3 Coronal section through the hip: 1, ilium; 2, ligamentum teres; 3, branch of obturator artery; 4, branch of medial circumflex artery; 5, femur; 6, branch of lateral circumflex artery; 7, joint capsule strengthened by the iliofemoral ligament (lateral part).

Posteriorly the capsule is strengthened by the ischio­ femoral ligament. These three ligaments are coiled round the femoral neck. Extension 'winds up' and tautens the ligaments, thus stabilizing the joint passively (Fig. 65.5a); flexion slackens them (Fig. 65.5b). Lateral rotation tightens the iliofemoral ligament and also the pubofemoral ligament. Medial rotation tightens the ischiofemoral ligament. Abduction tightens the pubofemoral and the ischiofemoral ligaments. Adduction tightens the lateral part of the iliofemoral ligament.

2

'i'l-wt--- 3 4

Figure 65.2 The acetabulum: 1, articular cartilage; 2, acetabular fossa; 3, ligamentum teres; 4, labrum acetabulare; 5, transverse acetabular ligament.

Figure 65.4 Anterior ligaments: 1, iliofemoral, lateral part; 2, iliofemoral, medial part; 3, pubofemoral.

CHAPTER 65

-

APPLIED ANATOMY 975

(b)

Figure 65.5

Lateral view of the ligaments in extension (a) and flexion (b): 1, iliofemoral, lateral part; 2, iliofemoral, medial part; 3, pubofemoral.

The ligamentum teres plays only a minor role in the control of hip movements. Adduction from a semi-flexed position is the only movement where this ligament is under tension.

Table 65.1

Innervation

MUSCLES

The hip joint is surrounded by a large number of muscles. According to their function these are divided into six groups: (1) flexors, (2) extensors, (3) abductors, (4) adductors, (5) lateral rotators, (6) medial rotators. In this chapter the anatomical and kinesiological aspects of particular importance in orthopaedic medicine are discussed. FLEXOR MUSCLES

The flexor muscles of the hip joint (Table 65.1) are ante­ rior to the axis of flexion and extension. The iliopsoas is the most powerful of the flexors (Fig. 65.6). It originates at the lumbar vertebrae and the cor­ responding intervertebral discs of the last thoracic and all the lumbar vertebrae, the superior two-thirds of the bony iliac fossa and the iliolumbar and ventral sacroil­ iac ligaments. The insertion is to the lesser trochanter. Although its main function is flexion, it is also a weak adductor and lateral rotator. The distal part of the muscle is palpable just deep to the inguinal ligament, where it lies bordered by the sartorius muscle laterally and the femoral artery medially (Fig. 65.7).

Flexor muscles

•

Muscle

Peripheral nerve

Spinal

Iliopsoas'

Femoral and lumbar plexus

L2, L3

Sartorius'

Femoral

L2, L3

Rectus femoris'

Femoral

L3

Tensor fasciae latae

Superior gluteal

L5

Pectineus

Femoral and obturator

L2, L3

Adductor longus'

Obturator

L2, L3

Adductor brevis

Obturator

L2, L3

Adductor magnus

Obturator and sciatic

L3, L4

Gluteus medius

Superior gluteal

L5

Gluteus minimus

Superior gluteal

L5

Clinically important muscles.

The sartorius is mainly a flexor of the hip, originating at the anterior superior iliac spine and inserting at the proximal part of the medial surface of the tibia (Fig. 65.7). Consequently the muscle acts on two joints, with the accessory function of lateral rotation and abduction of the hip as well as flexion and medial rota­ tion of the knee. At the surface, the muscle divides the anterior aspect of the thigh into a medial and a lateral femoral triangle. During active flexion, abduction and lateral rotation at the hip and 90° flexion at the knee, the muscle becomes prominent and is easily palpable. The rectus femoris combines movements of flexion at the hip and extension at the knee. Its origin is at the ante­ rior inferior iliac spine, a groove above the acetabulum and the fibrous capsule of the hip joint and inserts into

976 SECTION TWELVE - THE HIP AND BUTTOCK

5

4 ---/-----.. 3 --/------'Ir 2 -++�l--ff

Figure 65.6

The iliopsoas and associated structures: 1, psoas; 2, pectineus; 3, iliopsoas tendon; 4, inguinal ligament; 5, iliacus.

the common quadriceps tendon at the proximal border of the patella (Fig. 65.7). The origin can be palpated only in a sitting position because of tension in the overlying structures. The tendon and muscle belly are bordered medially by the sartorius muscle, and laterally by the tensor fasciae latae and the vastus lateralis, the largest part of the quadriceps. The tensor fasciae latae (Fig. 65.7) originates at the outer surface of the anterior superior iliac spine, and inserts into the proximal part of the iliotibial tract - a strong band which thickens the fascia lata at its lateral aspect. Thus the course of the tensor is dorsal and distal. Acting through the iliotibial tract the muscle extends and rotates the knee laterally. It may also assist in flexion, abduction and medial rotation of the hip. In the erect posture, it helps to steady the pelvis on the head of the femur (Fig. 65.8). The muscle can be palpated easily during resisted flexion and abduction of the hip with the knee extended. A number of other muscles are also active during flexion of the hip joint but only via their accessory func­ tion. These are the pectineus, adductor longus and brevis, and the most anterior fibres of the adductor magnus and the glutei (medius and minimus).

EXTENSOR MUSCLES

These (Table 65.2) are posterior to the axis of flexion and extension of the hip. Gluteus maximus

The most important extensor is the gluteus maximus (Fig. 65.9) which takes origin from the posterior gluteal line and crest of the ilium, the lower part of the sacrum, the coccyx and the sacrotuberous ligament, and runs in a lateral and caudal direction. Three-quarters of the muscle inserts at the proximal part of the iliotibial tract (see Fig. 65.8) and the other part into the gluteal tuberos­ ity of the femur. It is a strong extensor. The lower fibres also have a function in lateral rotation and adduction and the upper fibres assist in powerful abduction. In

Table 65.2

Extensor muscles

Innervation Peripheral nerve

Spinal

Gluteus maximus'

Inferior gluteal

Mainly S1

Semimembranosus

Sciatic

S1, S2

Semitendinosus

Sciatic

S1, S2

Biceps femoris

Sciatic

S1, S2

Muscle

Figure 65.7

Anterior view of the hip muscles: 1, inguinal ligament; 2, iliopsoas; 3, femoral artery; 4, pectineus; 5, adductor longus; 6, gracilis; 7, sartorius; 8, rectus femoris; 9, tensor fasciae latae.

'Clinically important muscle.

CHAPTER 65 - APPLIED ANATOMY 977

Hamstrings: semimembranosus, semitendinosus and biceps femoris

These muscles (Fig. 65.10) are also important extensors of the hip. Because the muscles cross two joints, their efficiency at the hip depends on the (extended) position of the knee. Their origins are from the upper area of the ischial tuberosity. The semimembranosus inserts at the posterior aspect of the medial condyle of the tibia. An additional attach­ ment is to the posterior capsule of the knee joint. Throughout its extent the muscle is partly overlapped by the semitendinosus and is therefore only palpable on each side of the latter. The semitendinosus inserts at the proximal part of the medial surface of the tibia, behind the attachments of the sartorius and gracilis. Both muscles have accessory func­ tions in medial rotation and adduction of the thigh, and in flexion and medial rotation of the knee joint. The tendon of the biceps femoris splits round the fibular collateral ligament and inserts into the lateral side of the head of the fibula. The accessory function of this muscle is lateral rotation and adduction of the thigh, and flexion and lateral rotation of the knee.

3 ----1'--1

2

Figure 65.8

Lateral view of the hip muscles: 1, gluteus maximus; 2, iliotibial tract; 3, tensor fasciae latae.

standing, the muscle is inactive and remains so during the forward bending at the hip joint. However, in con­ junction with the hamstrings, it is active in raising the trunk after stooping.

3

2

2

3

Figure 65.9 maximus.

1, Posterior superior iliac spine; 2, gluteus medius; 3, gluteus

Figure 65.10

Extensors of the hip (hamstrings): 1, semitendinosus; 2, semimembranosus; 3, biceps femoris.

978 SECTION TWELVE - THE HIP AND BUTTOCK

The collective origin of these muscles at the tuberosity of the ischium is best palpated in the side-lying position or supine lying, with the hip flexed to 90°. This position moves the gluteus maximus upwards so permitting direct palpation of the tuberosity. Palpation of the muscle bellies is performed in prone lying, with the knee flexed to less than 90° and during slight contraction of the muscles. Resisted medial rotation of the lower leg makes semitendinosus and semimembranosus prominent. Resisted lateral rotation of the lower leg tenses the biceps and also makes the tendon visible and palpable at the lateral and distal part of the thigh. ABDUCTOR MUSCLES

The main abductor muscle is the gluteus medius (Fig. 65.11). It originates from the external surface of the ilium, just below the iliac crest. Insertion is on the lateral surface of the greater trochanter of the femur. The muscle is partially covered by two other muscles: anteriorly the tensor fasciae latae, posteriorly the gluteus maximus. The gluteus medius stabilizes the pelvis in the trans­ verse direction. Standing on one limb, strong action of the gluteus medius, powerfully assisted by gluteus minimus and tensor fasciae latae, keeps the pelvis horizontal. This stabilization of the pelvis is essential for normal walking. In mild or moderate weakness of these muscles, the char­ acteristic sign of Duchenne-Trendelenburg syndrome is demonstrated, i.e. the patient is unable to keep the pelvis horizontal, which is tilted to the opposite side. In gross weakness an excessive movement of the trunk towards the affected side compensates the paralysed hip abduc­ tors ('abduction lurch').

2

Figure 65.1 1

The gluteus medius muscle - the main abductor of the hip joint:

1, gluteus medius; 2, gluteus maximus (reflected back); 3, quadratus femoris; 4, gluteal bursa; 5, gemelli; 6, piriformis; 7, ischial bursa.

Table 65.3

Abductor muscles

Innervation Muscle

Peripheral nerve

Spinal

Gluteus medius

Superior gluteal

L5

Gluteus minimus

Superior gluteal

L5

Tensor fasciae latae

Superior gluteal

L5

Gluteus maximus

Inferior gluteal

Mainly S1

The other important abductors are the gluteus minimus, the tensor fasciae latae and the upper part of the gluteus maximus (Table 65.3). The lateral aspect of the hip is covered by a wide mus­ cular fan (see Fig. 65.8) made up of two muscle bellies: anteriorly the tensor fasciae latae, posteriorly the superficial fibres of the gluteus maximus. Both insert into the anterior and posterior borders of the iliotibial tract at its proximal aspect. Because of the triangular shape and the anatomical and functional similarity to the deltoid muscle of the shoulder joint, these muscles are sometimes known as the 'deltoid of the hip'. The iliotibial tract is a long and strong band, which is part of the fascia lata and attached to the anterior aspect of the lateral tibial condyle. This structural arrangement permits the muscles to influence the stability of the extended knee joint and thus help to maintain the erect posture. The iliotibial tract overrides the greater trochanter, where it is vulnerable to strain. ADDUCTOR MUSCLES

The adductors lie medial to the central axis of the hip joint. Although the adductor magnus is the most pow­ erful it is clinically not important. The adductor longus (see Fig. 65.7) is more easily strained. Its origin is at the anterior aspect of the pubis at the junction of the pubic crest and symphysis, and it inserts at the middle third of the linea aspera of the femur. During resisted adduction the adductor longus is the most prominent muscle of the adductor group and forms the medial border of the femoral triangle. Its accessory function is flexion of the hip. Other adductors are the pectineus, adductor magnus, quadratus femoris, external obturator and the greatest part of the gluteus maximus. Another adductor is the gracilis, the most superficial of the adductor group. It arises broadly from the inferior ramus of the pubis. The muscle belly lies just dorsal to the adductor longus (see Fig. 65.7). The tendon of this biarticular muscle passes across the medial condyle of the femur, posterior to the tendon of the sartorius, and is attached to the uppe� part of the medial surface of the tibia. Because of this course it is also a flexor and medial rotator of the knee.

CHAPTER 65

Table 65.4

Table 65.6

Adductor muscles

-

APPLIED ANATOMY 979

Medial rotator muscles

Innervation

Innervation Muscle

Peripheral nerve

Spinal

Muscle

Peripheral nerve

Spinal

Adductor longus'

Obturator

L2, L3

Tensor fasciae latae

Superior gluteal

L5

Adductor magnus

Obturator and sciatic

L3, L4

Gluteus medius

Superior gluteal

L5

Gracilis

Obturator

L2, L3, L4

Gluteus minimus

Superior gluteal

L5

External obturator

Obturator

L3, L4

Semimembranosus

Sciatic

S1, S2

Pectineus

Femoral and obturator

L2, L3

Semitendinosus

Sciatic

S1, S2

Quadratus femoris

Sacral plexus

L4, L5, S1

Semimembranosus

Sciatic

S1, S2

Semitendinosus

Sciatic

S1, S2

Biceps femoris

Sciatic

S1, S2

Anteriorly, the sartorius and iliopsoas have only an accessory function during lateral rotation.

'Clinically important muscle

MEDIAL ROTATOR MUSCLES

Finally, the semitendinosus, semimembranosus and biceps femoris also assist in adduction of the hip (TabJe 65.4). There is a strong functional relationship between the abdominal muscles and the adductors of the hip joint. 'Adductor tendinitis' and 'rectus abdominus tendinitis' are often seen simultaneously.

BURSAE

LATERAL ROTATOR MUSCLES

When the resisted lateral rotation test is painful, the quadratus femoris should be sought first because the lesion is usually in this muscle (see Fig. 65.11). This flat quadrilateral muscle arises from the upper part of the lateral border of the tuberosity of the ischium and inserts just distally from the intertrochanteric crest of the femur. Other lateral rotators of the hip (Table 65.5) that cross the joint posteriorly, such as the piriformis, the obturator muscles, pectineus, the posterior fibres of the adductor magnus, the gluteus maximus and the posterior fibres of gluteus medius, are clinically unimportant. The long head of biceps also laterally rotates the thigh when the hip is extended. Table 65.5

The medial rotators (Table 65.6) that cross the hip anteri­ orly are the tensor fasciae latae and the anterior fibres of gluteus medius and minimus. Posteriorly, semimembra­ nosus and semitendinosus have an accessory function in medial rotation when the hip is extended.

Lateral rotator muscles

The gluteal bursae are situated deeply, just above and behind the greater trochanter underneath the gluteus medius and maximus (see Fig. 65.11). The trochanteric bursa is situated more superficially, laterally between the greater trochanter and the iliotibial tract. The psoas bursa, also called the bursa iliopectinea, lies deep to the iliopsoas muscle at the floor of the femoral triangle and just in front of the hip joint, with which it may communicate (Fig. 65.12). The ischial bursa lies distally at the tuberosity just covered by the edge of the gluteus maximus (see Fig. 65.11). In a flexed, i.e. sitting, position the muscle is pulled up slightly so that in bursitis pain results because of compression of the inflamed bursa between the seat and the tuberosity.

Innervation

•

Muscle

Peripheral nerve

Spinal

Quadratus femoris'

Sacral plexus

L4, L5, S1

Piriformis

Sacral plexus

S1, S2

Internal obturator

Sacral plexus

L5, S1, S2 L3, L4

External obturator

Obturator

Pectineus

Femoral! obturator

L2, L3

Adductor magnus

Obturator

L3, L4 L4, L5, S1

Gluteus medius

Superior gluteal

Gluteus maxim us

Inferior gluteal

L5, S1, S2

Biceps femoris

Sciatic

S1, S2

Sartorius

Femoral

L2, L3

Iliopsoas

Femoral

L2, L3

Clinically important muscle.

NERVES

The femoral nerve (see Fig. 65.14) arises mainly from the second and third lumbar spinal nerves. It passes down between the psoas major and iliacus muscles, then behind the inguinal ligament to enter the thigh. At this proximal level, the nerve lies just lateral to the femoral artery. Muscular branches supply the iliacus, pectineus, sartorius and quadriceps muscles. The skin on the front of the thigh is supplied by several cutaneous branches. The lateral cutaneous nerve of the thigh arises from the second and third lumbar spinal nerves. It passes behind

980 SECTION TWELVE - THE HIP AND BUTTOCK

2 3

4

8 9

5 6

3 I 4 7

Figure 65.13

Arteries: 1, aorta; 2, right common iliac artery; 3, left common iliac artery; 4, external iliac artery; 5, superior gluteal artery; 6, obturator artery; 7, internal obturator muscle; 8, internal iliac artery; 9, inferior gluteal artery.

Figure 65.12

The psoas bursa, 1; 2, psoas (resected); 3, sartorius; 4, pectineus.

or through the inguinal ligament about 1 cm medial to the anterior superior iliac spine. At the proximal part of the sartorius it divides into two branches to supply the anterolateral part of the thigh as far as the knee. The obturator nerve arises mainly from the third and fourth lumbar spinal nerves. It enters the thigh through the obturator foramen. Some cutaneous branches are given to the skin on the medial side of the thigh, whereas another branch supplies the capsule of the hip joint. Muscular branches are distributed to the pectineus, adductor longus, gracilis, adductor brevis, external obturator and adductor magnus. The sciatic nerve (see Fig. 65.16), the largest nerve in the body, arises from the fourth and fifth lumbar and first and second sacral spinal nerves. It passes out of the pelvis through the greater sciatic foramen below the piriformis muscle. On its medial side it is accompanied by the infe­ rior gluteal artery and the posterior cutaneous nerve of the thigh. The nerve descends just medial to the midpoint of a line joining the greater trochanter of the femur and the tuberosity of the ischium. Muscular branches are dis­ tributed to the semimembranosus, semitendinosus and biceps femoris muscles. It also supplies the capsule of the hip joint through articular branches.

At the level of the sacroiliac joint, these vessels divide into external and internal iliac arteries. Passing behind the inguinal ligament just midway between symphysis pubis and anterior superior iliac spine, the external artery becomes the femoral artery. The internal iliac arteries divide into three: the superior and inferior gluteal arteries supplying the buttock and the obturator artery which supplies the hip joint and the adductor muscles (see Fig. 65.14).

6

--------'j,-'(

5 ---�--���

���r---- 2 �----- 3 1iiii/!'il'�--- 4

BLOOD VESSELS

The abdominal aorta bifurcates at the level of the fourth lumbar vertebrae into right and left common iliac arteries (Fig. 65.13).

Figure 65.14

Iliopsoas tendon and neurovascular structures of the groin: 1, inguingal ligament; 2, femoral artery; 3, femoral vein; 4, pectineus; . 5, femoral nerve; 6, iliopsoas; 7, psoas bursa; 8, lymph vessels, 9, Iliac nerve.

CHAPTER 65 - APPLIED ANATOMY 981

TOPOGRAPHICAL ANATOMY ANTERIOR SIDE

The anterior superior iliac spines (ASIS) are easily palpa­ ble except in obese patients. They form the point of origin of the sartorius muscle anteriorly and the tensor fasciae latae laterally. The spines are not level when there is leg length difference. The same occurs in pelvic torsion. However, the level of the posterior superior iliac spine (PSIS) on the same side is then just reversed, i.e. in a pos­ terior rotation of the right innominate bone the ASIS on that side is higher whereas the PSIS is lower compared with the other side. The anterior inferior iliac spines, lying just beneath the superior ones, are best palpated in a sitting position, with the hip flexed to 90°. These are the points of origin of the rectus femoris muscles. Towards the midline, the pubic tubercles provide attachment for the medial end of the inguinal ligament. They are palpable as bony prominences lying at the same level as the superior aspect of the greater trochanters. The rectus abdominus inserts with a medial and lateral head just cranial to these tubercles at the crest of the pubic bone. For topographical reasons, it is also important to have an understanding of the anatomy of the femoral triangle (Fig. 65.7), whjch is defined superiorly by the inguinal lig­ ament, medially by the adductor longus and laterally by the sartorius. The floor of the triangle is formed by por­ tions of the iliopsoas on the lateral side and the pectineus on the medial side. The femoral artery lies superficial and medial to the iliopsoas muscle and is easily found by pal­ pation of the pulse as it emerges from behind the inguinal ligament (Fig. 65.14). Deep to the iliopsoas lies the psoas bursa and still deeper the hip joint. The femoral head, however, is not palpable because of the presence of the overlying muscles. The femoral nerve and vein (lateral and medial to the artery, respectively ) are not palpable. Several lymph nodes are situated medially in the femoral triangle. They can be palpated only when they are enlarged. LATERAL SIDE

Palpation of the greater trochanter is relatively easy at its posterior edge, where the bone is not covered by muscles. The greater trochanter is an important landmark and, in the standing position, both greater trochanters should be level and at the same distance from the iliac crest and the anterior superior iliac spines. Their upper aspects should also be on the same level as the pubic tubercles.

2 Figure 65.15

The bursa at the ischial tuberosity: 1, gluteus maxim us; 2, ischial

bursa.

POSTERIOR SIDE

The ischial tuberosity is covered by the gluteus maximus and adipose tissue (Fig. 65.15). If the hip is flexed, the gluteus maximus moves upwards and the ischial tuberosity becomes easily palpable. It provides attachment for the hamstring muscles posteriorly and the quadratus femoris laterally. At its distal aspect, the bone is covered by a bursa (Fig. 65.11). Midway between the greater trochanter and the ischial tuberosity the sciatic nerve passes to the leg (Fig. 65.16). With the hip in a flexed position this nerve may be palpable underneath the adipose tissue. The posterior superior iliac spines (see Fig. 65.9) are easily palpable, where they lie directly underneath the visible dimples just above and medial to the buttocks.

JOINT MOVEMENTS

The hip has three degrees of freedom: flexion-extension, adduction-abduction, and medial and lateral rotation. Flexion is forward movement in the sagittal plane (Fig. 65.17a). The range depends on the position of the knee. With the knee flexed and the movement per­ formed passively, the anterior aspect of the thigh comes in close contact with the abdomen, so that the range exceeds 140°. With the knee extended, flexion is limited by the tension of the hamstrings. These muscles are biarticular and therefore restrict hip flexion when the knee is extended - the constant-length phenomenon.

982 SECTION TWELVE - THE HIP AND BUnOCK

2

3 4

5

Figure 65.1 6 The sciatic nerve: 1, piriformis; 2, gemellus superior; 3, sciatic nerve; 4, gluteus maximus (resected); 5, ischial tuberosity.

Extension backward movement in the sagittal plane (Fig. 65.17b) is considerably restricted by the tension of the iliofemoral ligament. Passively an average range of 30° can be reached. Adduction and abduction are movements in the frontal plane (Fig. 65.18). The average range of adduction

Figure

65.17

Flexion (a) and extension (b).

(b) Figure

65.18

Abduction (a) and adduction (b).

Figure

65.19

Medial (a) and lateral (b) rotation.

CHAPTER 65 - APPLIED ANATOMY 983

is 30°, and abduction 45°. In the latter, the constant-length phen6menon again plays a vital part. Here the biarticular gracilis restricts the range of abduction when the knee joint is fully extended. Rotational movements of the hip are measured in the supine position, with the thigh in 90° of flexion

(Fig. 65.19), or lying face down, the hip at 0° and the knee flexed to 90°. The normal range of medial rotation is about 45°, whereas lateral rotation reaches about 60°. With the thigh flexed, lateral rotation can be increased, because of relaxation of the iliofemoral and pubo­ femoral ligaments.

BIBLIOGRAPHY Cyriax

J.

Textbook of Orthopaedic Medicine. Vol 1, 8th edn. Bailliere

Tindall, London, 1982. Hoppenfeld S. Physical Examination of the Spine and Extremities. Appleton-Century-Crofts, New York, 1976. Kapandji IA. T he PhysiolofSlJ of the Joints. Vol 2, Lower Limb, 2nd edn. Churchill Livingstone, London, 1970.

Kendall HO, Kendall FP, Wadsworth CE. Muscle Testing and Function, 2dn edn. Williams & Wilkins, Baltimore, 1971.

Martens M, Hansen C, Mulier J. Adductor tendinitis and musculus rectus abdominus tendopathy. J Sports Med 1987;4:156-158. Warwick R, Williams PL. Gray's Anatomy, 35th edn. Longman, London, 1973.

THIS PAGE INTENTIONALLY LEFT BLANK

CHAPTER CONTENTS Introduction

98S

Referred pain

986 Pain referred to the buttock and hip region 986 Pain referred from the buttock and hip region 986

History 987 Onset 987 Evolution 987 Current symptoms

987

Inspection 988 Gait, facial expression and movement

Posture 988 Hip joint position 988 Muscle contours 988 Skin folds 988 Functional examination 989 Preliminary examination 989 .. Basic functional examination 989 Palpation

994

Accessory tests

994

Technical investigation

Clinical examination of the hip and buttock

994

988

INTRODUCTION

Pain felt in the hip and buttock does not necessarily orig­ inate from a lesion in these areas. Cyriax stated that most pain in the buttock derived from the lumbar spine (refer­ ence from L1 and 52), whereas pain in the thigh is as often referred from the lwnbar spine and hip region as it is of local origin. When dealing with pain in this area, it is often not easy at first to determine if there is a problem in the lower back, the sacroiliac joint or the hip. The examiner has to perform a preliminary examination that includes the whole region from the lumbar spine, over the sacroiliac and hip joints to the upper leg. From the moment it is clear that the symptoms do not arise from the lumbar spine or sacroiliac joint, the structures of the hip are examined more intensively. It may also be helpful to realize that some disorders are age related. Mechanical low back pain rarely occurs below the age of 15 and is most frequent between 30 and 55; the hip joint is a more common problem in the elderly. However, symptoms may start in middle age. Lesions of the hip joint (such as congenital dislocation, Perthes' disease and epiphysio­ lysis) are also quite common in young children. A careful, detailed and chronologically ordered history is first taken as described for the lumbar spine (p. 799). Past and present symptoms are noted and the examiner is informed about the exact site and nature of the pain. The development of symptoms and how they produce dis­ ability are also noted and may give the examiner an impression of the source of the complaints. Functional tests are performed and interpreted and it is rarely difficult to identify the origin of the lesion if the principles of applied anatomy are logically practised. An example makes this clear: bending backwards places strain on the abdominal muscles, the lumbar spine, the sacroiliac joint, the hip joint and the flexor muscles of the hip. Pain in the thigh brought on by this test must be the result of a capsular lesion of the hip joint if the same test done with the hip joint flexed and resisted flexion at the hip are pain free. If the diagnosis is still obscure after taking the history and making a physical examination, focus should turn to disorders outside orthopaedics that could be responsible 985

986 SECTION TWELVE - THE HIP AND BUnOCK

REFERRED PAIN

the back of the thigh and the lower half of the posterior aspect of the leg, the sole of the foot and the outer two toes. The second sacral dermatome is also represented at the back of the whole thigh and leg, the sole and plantar aspect of the heel. In cases of multisegmental pain in the buttock, for example with dural reference, the pain may spread diffusely in both legs excluding the feet. Pain in the groin may also result from intra-abdominal pathological conditions: appendicitis, gynaecological disorders or inguinal or femoral hernia.

PAIN REFERRED TO THE BUTTOCK AND HIP

PAIN REFERRED FROM THE BUTTOCK AND HIP

REGION

REGION

for the symptoms - usually intra-abdominal lesions. In such conditions the pain is usually unrelated to move­ ments that have been undertaken during the examina­ tion. Another cause of pain in the buttock of non-orthopaedic origin is occlusion of the common iliac artery with intermittent claudication. Finally it must be remembered that hip complaints may be claimed but can have a non-physical basis in the psyche.

Most pain in the buttock and hip results from a lumbar lesion with a segmental (L1-S2) or multisegmental (dural) reference of pain. Knowledge of the dermatomes that meet in the buttock and hip is therefore essential. The first lumbar dermatome is represented by an area of skin at the outer and upper buttock and hip region. Parts of the second and third lumbar dermatomes also partly overlap the first dermatome at the inner and upper quadrant (Fig. 66.1). The skin of the lower part of the buttock is derived from the first and second sacral segments. The fourth and fifth lumbar segments are not present in the buttock. In spite of this, fourth and fifth lumbar disc protrusions are the commonest cause of pain in the buttock,] which results from pressure on the dura mater. It is worth remembering that the first lumbar der­ matome also covers the lower abdomen and the groin. The second lumbar dermatome is also found more dis­ tally, from the front of the thigh to the patella. The third lumbar dermatome is positioned over the inner aspect and the front of the thigh, then down the leg to just above the ankJe anteriorly. The first sacral dermatome covers

L1

Muscles The muscles of the buttock are derived from the fourth and fifth lumbar and first sacral myotomes. Lesions are a rarity and so is referred pain from these muscles. The seg­ mental distribution of the most frequently injured muscles is: • • • • • •

Iliopsoas - L2 and L3. Adductor longus - L2 and L3. Rectus femoris - L3. Quadratus femoris - L5 and Sl. Semimembranosus/ semitendinosus - Sl and S2. Biceps femoris - Sl and S2.

Hip joint The hip joint is formed largely from the third lumbar segment. Therefore pain referred from the joint may be felt in the upper and inner part of the buttock, the inner aspect and front of the thigh and leg as far as the medial malleolus. Rarely, the joint has developed mainly from the fourth lumbar segment. In such cases, the pain spreads along the outer side of the mid-thigh and leg and may reach the big toe. Because referred pain does not

L3

S2

Figure 66.1

Dermatomes at the hip and buttock.

CHAPTER 66

Box 66.1 Summary of referred pain ,

Pain referred to the buttock and hip region Segmental:

Groin Thigh Buttock

L 1-L2 L2-L3 52

did the problem start, what was its evolution and what are the current symptoms (see Box 66.2)?

•

Pain referred from the buttock and hip region Hip joint Gluteal bursitis Psoas bursitis Muscles:

Iliopsoas and adductor longus Rectus femoris Quadratus femoris Hamstrings

CLINICAL EXAMINATION 987

ONSET

Multisegmental from the lumbar dura

Sacroiliac joint

-

L3 51 -52 (L3-L4?) L4-LS L2-L3 L2-L3 L3 LS-51 51-52

•

Sacroiliac joint The sacroiliac joint normally gives rise to pain along the back of the thigh and calf. In rare instances, pain is felt in the groin as well (see p. 948).

Bursae The bursae may also give rise to referred pain in the same way as other soft tissues. In gluteal bursitis, pain is felt at the lateral or posterior trochanteric area and may be referred to the outer thigh, i.e. a lesion in a tissue derived from the fourth or fifth lumbar segments. The psoas bursa is developed from the second and third lumbar segments. Pain is felt in the groin and may spread to the front of the thigh. Referred pain in the buttock and hip is summarised in Box 66.1.

What brought it on or how did it start? Was there an injury or did the pain appear without obvious reason? If there was an injury:

• •

always occupy the whole dermatome, it is possible for a hip lesion to refer pain to the knee only, perhaps also spreading along the front of the tibia.1,2 But pain felt only at the upper inner quadrant of the buttock strongly points to the low back or the sacroiliac joint.

When did it start? Is it an acute, subacute or chronic problem?

How did it happen? In what position was the body and what forces were applied to the hip? What were the immediate symptoms? Where was the pain? Was there any swelling? Was there any func­ tional disablement? If there was no injury:

•

Did the symptoms come on suddenly or gradually?

EVOLUTION

In long-standing cases or in traumatic conditions it is important to have an idea of the degree and localization of the complaints: •

•

•

What was the development of the pain? Was it gradually worse, gradually better, persistent, ups and downs with complete or no complete relief between attacks? What was the development of the pain localization? A pain moving from one side to another is characteristic of a loose body. What sort of treatment did you have and with what result?

CURRENT SYMPTOMS •

What is the problem now? The examiner makes further enquiries about pain, pins and needles, instability or functional disability.

HISTORY

History taking is largely the same as in lumbar spine dis­ orders (see p. 799) because it is not always clear from the onset if the patient has a lumbar, a sacroiliac or a hip problem. However, once it has become more or less apparent that the complaints are the outcome of a hip lesion, some particular questions should be asked. After the usual questions on the patient's age, sex, occupation and hobbies, the examiner tries to find out what the actual problem is: pain, functional disability or instability? The problem should then be worked out sys­ tematically via a chronological approach: when and how

Box 66.2 Summary of symptoms -

Onset: congenital/acquired (traumatic/non-traumatic) Evolution Current symptoms Site of pain Influence of posture, movement Nocturnal pain Twinges Coughing and pain Instability Functional disablement Symptoms in other parts of the body

988 SECTION TWELVE - THE HIP AND BUnOCK

• •

•

• • •

• •

•

•

•

Where do you feel the pain (which dermatome)? As exact a description as possible must be obtained.

Did you have pain at rest or during the night? Nocturnal pain indicates a high degree of inflammation and may point to a serious disorder such as arthritis, haemarthrosis, tumoUl� metastasis or fracture. However, in an ordinary gluteal bursitis, lying on the affected side at night is also often painful. What brings the pain 011? Sitting, standing up, walking, running or sport activities may bring pain on. If the pain starts after walking a certain distance, ask if it disappears at rather a short time of standing still and appears again after having walked the same distance: this suggests claudication in the buttock. Does a particular movement provoke the pain? Does the pain appear at the beginning, during or after some exertion? Do you have twinges, and when? This symptom is defined as a sudden, sharp and unexpected pain and is clearly indicative of momentary subluxation of a loose body. On walking, a severe twinge is felt shoot­ ing down the front of the thigh and the leg gives way at this moment. Is allY 1I10vement attended with a click? Clicking may be indicative of loose bodies or acetabular labrum tears.3,4 Does coughing hurt? This dural sign is very suggestive of a lumbar intervertebral disc lesion but is also found in sacroiliac arthritis. Do you have a feeling of instability? Any disorder alter­ ing the anatomical relations in the hip region, for example congenital dislocation, coxa vara or epiphys­ iolysis, may be a reason for instability. Painful condi­ tions at the hip or neurological disorders, such as paresis of the fifth lumbar root involving the gluteus medius, or of the third lumbar root involving the quad riceps, are other possibilities. Do you have any functional disability? This may be stiff­ ness on standing up, starting to walk or inability to put the shoes on. All these direct attention to an arthrotic joint. Do you have complaints in other parts of the body? The possibility of systemic diseases arises, for example rheumatoid arthritis or ankylosing spondylitis.

INSPECTION GAIT, FACIAL EXPRESSION AND MOVEMENT

When the patient enters the room, observe the gait. Disorders that affect the hip joint or any other joint of the lower extremity become especially perceptible during walking. The patient's gait can be restricted so as to avoid a painful component. An excessive movement of

the pelvis may compensate for a stiff hip joint. In gross weakness of the gluteus medius or gluteus maximus, an abduction or extension lurch are respectively present. The patient's face should be in harmony with his com­ plaints, for example haggard due to sleepless nights. While the patient lmdresses, note should be taken of any manoeuvre that seems painful or awkward.

POSTURE

Next posture is assessed, especially in relation to the lower back, pelvis and lower extremities. Details of observing the patient's posture are dealt with in the chapter on the lumbar spine (see p. 802).

HIP JOINT POSITION

The position of the hip joint can be informative about a pathological condition. In acute arthritis and gross osteoarthrosis, the hip joint is often in flexion, which is compensated for by an anterior tilt of the pelvis together with increased lordosis of the lumbar spine. The femur is also slightly adducted and laterally rotated. This in turn influences the position of the knee and foot, which are also rotated. It must be remembered, however, that exces­ sive external rotation of the leg, with 'toeing out' also occurs in external femoral neck retroversion or a slipped upper femoral epiphysis and in pelvic torsion. Also a posterior rotation of the innominate hone may be respon­ sible for slight external rotation of the leg. In contrast, 'toeing in' may be the result of extreme femoral neck anteversion.5 In third lumbar root pain, patients may also adopt a flexed position to relax the nerve root. The combination of excessive internal rotation together with adduction is typical for a non-organic cause.

MUSCLE CONTOURS

The contours of the glutei, hamstrings and quadriceps muscles are observed. Unilateral or bilateral muscular atrophy is noted.

SKIN FOLDS

Lastly the skin folds, i.e. gluteal folds and groin, are assessed. These are normally situated symmetrically. Asymmetrical folds may be the result of underlying anatomical alterations, such as muscular atrophy, pelvic obliquity, leg-length discrepancy or congenital disroca­ tion of the hip joint. Box 66.3 summarizes the aspect of inspection.

CHAPTER 66

-

CLINICAL EXAMINATION 989

Box 66.3 Summary of inspection ,

Observation of: Gait Face Unusual movements Posture/position of the hip Contours of muscles Skin folds

FUNCTIONAL EXAMINATION PRELIMINARY EXAMINATION

Before starting the clinical examination of the buttock and hip, a preliminary examination of the lumbar spine and sacroiliac joint (summarized in Box 66.5, p. 994) should be performed to ascertain the absence of any lesion in these regions. BASIC FUNCTIONAL EXAMINATION

Routine clinical examination consists of 15 func­ tional tests (Box 66.4). If signs warrant or the history is indicative, complementary tests can be performed.

The range, painfulness and end-feel of passive flexion, lateral and medial rotation, adduction and abduction are noted, carefully comparing both sides. Passive movements.

flexion. The anterior thigh is moved upwards until it touches the abdomen (Fig. 66.2). The average range of movement is 140°, with a soft end-feel caused by tissue approximation. It must be remembered that the last 30° of this apparent hip movement takes place by the pelvis flexing at the lumbar joints. This backward tilt of the pelvis also moves the other thigh towards extenPassive

Box 66.4

Fifteen functional tests

Supine

Prone lying

Passive tests

Passive tests

Flexion

Extension

Medial rotation

Bilateral medial rotation

Lateral rotation Adduction Abduction Resisted tests

The hip and knee are bent to 90°, to examine rotation movements (Fig. 66.3). The contralateral hand is used to stabilize the femur at the knee, while the other hand, placed at the distal end of the lower leg, performs the rotation movement. At the end of range, a capsular elastic end-feel should be found. The average range of passive lateral rotation is 60°, of medial rotation is 45°. In advanced arthrosis or arthritis, the end-feel is hard. However, a soft end-feel replaces a hard one when swift erosion of the femoral head occurs in arthrosis. In gross arthritis or arthrosis there is 90° limitation of flexion and no range of medial rotation although lateral rotation is full. In very early arthrosis or arthritis, medial rotation is the first movement to become measurably restricted, soon followed by slight limitation of flexion. In arthrosis or arthritis, medial rotation is the most painful passive movement. In bursitis or an impacted loose body in a joint not yet arthrotic, the end-feel is soft. Usually, in these last two disorders, lateral rotation hurts and is the only clinical finding.

Resisted tests Bilateral lateral rotation

Extension

Bilateral medial rotation

Adduction

Flexion knee

Abduction

Extension knee

Passive rotation.

This is tested after raising up the other leg, so as to get it out of the way (Fig. 66.4). The range of movement is on average 30°. In a normal joint, the end-feel is elastic, caused by stretching of the capsule and muscles that lie on the outer side of the hip. When movement is painful at the outer side of the hip, a lesion of the iliotibial tractl should be considered. If some o

Flexion

Passive flexion.

sion, and when there is a restriction of extension in the other hip joint, the thigh will move upward (this is Thomas's sign of flexion contracture of the hip). o

Supine

o

Figure 66.2

Passive adduction.

990 SECTION TWELVE - THE HIP AND BUTTOCK

trochanter and the ilium. In arthritis and arthrosis, movement is restricted because of muscle spasm and bone-to-bone contact, respectively. Resisted movements. Four resisted movements are then tested: resisted flexion, extension, adduction and abduc­ tion. Because muscle lesions in the buttock are very rare, pain on resisted abduction or extension usually results from compression of a nearby tender bursa. Muscle sprains in the thigh do occur and are mainly found in young adults as the result of sports injury. o

Resisted flexion. This is performed with the hip joint flexed to 90°. Both hands are placed at the

(a)

(a)

(b) Figure 66.3

Passive rotation: (a) lateral; (b) medial.

resisted movements are also painful, gluteal bursitis is probably the cause. The ipsilateral hand is placed at the medial and dorsal side of the thigh, as far distal as possible. The knee is put into 90° flexion, which eliminates the influence on the movement of the biartic­ ular part of the adductors, i.e. the semitendinosus, semi­ membranosus and gracilis. The other hand stabilizes the pelvis (Fig. 66.4). On full passive abduction, the structures on the medial side of the thigh are stretched, while on the outer side the bursae may become compressed between the greater o

Passive abduction.

(b) Figure 66.4

Passive adduction (a) and abduction (b).

CHAPTER 66

anterior and distal end of the thigh so as to exert coun­ terpressure, while the patient endeavours to flex the hip. The lower leg is supported in 90° of flexion at the knee. To stabilize the ilium the examiner places one knee against the tuberosity of the ischium (Fig. 66.5). Pain and weakness are noted and again carefully compared with the other hip. This test gives a positive result in the fol­ lowing circumstances: •

If pain alone is provoked, the possible lesions are: strain in the' psoas, sartorius or rectus femoris muscle; obturator hernia is another possibility.

-

CLINICAL EXAMINATION 991

Painful weakness is found in avulsion fracture of the lesser trochanter, abdominal neoplasm infiltrating the psoas muscle or metastasis in the upper femur. Painless weakness is the result of paresis of the psoas muscle, usually the consequence of a second lumbar root palsy but rarely a third. If the palsy is bilateral, neoplasm at the second lumbar level should always be suspect.

•

•

Resisted extension. This tests the gluteus maximus and the hamstrings. The hip joint is slightly flexed and the knee joint remains extended. The examiner places both hands at the heel of the foot and resists extension (Fig. 66.5). Pain and weakness are noted: o

Pain usually results from a hamstring lesion but gluteal

•

bursitis or sacroiliac strain are also possibilities. Weakness indicates a lesion of the first sacral root.

•

adduction. The examiner places the (clenched) fist between both knees and asks the patient to squeeze it (Fig. 66.6). o

Resisted

Pain is usually the result of an adductor longus lesion.6 A fracture, neoplastic invasion of the pubic bone or a sacroiliac lesion are other possibilities.

•

Resisted abduction. The hip joints are placed in a slightly abducted position. The examiner resists the abduction movement at the ankles (Fig. 66.6). This test primarily activates the gluteus medius, gluteus minimus and tensor fasciae latae. o

Pain is usually the result of the compression of under­ lying structures, such as an inflamed gluteal bursa, or is the consequence of stress placed upon strained or inflamed sacroiliac ligaments. Weakness is found in a palsy of the fifth lumbar root from a disc herniation at the same level. It may also be the result of anatomical changes, as in congenital dislocation of the hip or coxa vara; in such circum­ stances the muscle's origin lies closer to its insertion which makes the contraction less efficient.

•

(a)

•

Prone Passive movements. There are two passive movements.

The ipsilateral hand is placed over the mid-buttock. The other hand grasps the thigh just below the patella. The test is performed by a simultaneous movement of both hands in opposite direc­ tions. The knee should stay extended, to prevent tension on the rectus femoris. By pressing the pelvis firmly onto the couch, the examiner prevents any stress reaching the sacroiliac and the lumbar joints (Fig. 66.7). The average range of movement is 30°. The normal end-feel is o

(b) Figure 66.5

Resisted flexion (a) and extension (b).

Passive extension.

992 SECTION TWELVE - THE HIP AND BUnOCK

Figure 66.7

(a)

•

Passive extension.

Minor limitation is often important, for this is the first movement to become restricted at the onset of arthritis.I

Resisted movements. There are four resisted movements. Bilateral resisted lateral rotation. This is performed with the knees flexed to a right angle. With crossed arms, the examiner presses his hands against the inner side of both legs at the internal malleoli of the ankle (Fig. 66.9). o

•

Pain may be the result of muscle strain, i.e. the quadra­ tus femoris. More commonly, as has been said before, it results from compression of an inflamed bursa.

(b) Figure 66.6

Resisted adduction (a) and abduction (b).

capsular-elastic. Extension is one of the movements that becomes restricted in arthritis or arthrosis. Passive medial rotation. Both hips are examined together, even though a separate assessment will have been made in the supine position. The knees are flexed to a right angle. The thighs are rotated by pressing the feet apart (Fig. 66.8). Care should be taken to ensure that the buttocks are level. A small amount of limitation of medial rotation can now be ascertained. o

Figure 66.8

Passive medial rotation.

CHAPTER 66 - CLINICAL EXAMINATION 993

(b)

(a) Figure 66.9

Bilateral resisted lateral (a) and medial (b) rotation.

medial rotation. This is per formed in the same way but both hands are pressed against the outer malleoli (Fig. 66.9). This creates tension in the medial part of the hamstrings, tensor fasciae latae and gluteus medius and minimus. However, pain is more often the result of compression of an inflamed bursa. o

o

Bilateral resisted

This tests the ham strings. The knee is positioned in 70° of flexion. One

Resisted flexion of the knee.

(a) Figure 66.10

hand fixes the ilium, the other hand presses against the distal end of the lower leg (Fig. 66.10). •

•

(b) Resisted flexion (a) and extension (b) of the knee.

Pain in the thigh results from a lesion in the semitendi­ nosus, semimembranosus or biceps femoris. Pain at the ischial tuberosity indicates a tendinitis of one of the same muscles or a lesion of the sacrotuberous ligament. Weakness is present in first and second sacral root palsy and is usually the result of a disc herniation at the fifth lumbar level.

994 SECTION TWELVE - THE HIP AND BUTTOCK

Resisted extension of the knee. This tests the quadriceps. The knee is held in 70° of flexion. The ipsilateral hand is used to stabilize the thigh on the couch. The elbow of the other arm is placed at the distal end of the lower leg to resist extension movement (Fig. 66. 10). In order to be able to withstand even the strongest extension, the hand of this arm may grasp the stabilizing arm. o

• •

provokes gluteal pain in claudication due to a block in the common iliac or internal iliac arteries. Trendelenburg test in obturator hernia. The patient lies for at least 10 minutes in the Trendelenburg position oblique with the legs up and the trunk down. Thereafter, pain on resisted flexion abates because the psoas muscle no longer interferes with the obturator hernia.

Pain in the thigh is from a lesion in the quadriceps. Weakness results from a third lumbar root lesion. TECHNICAL INVESTIGATIONS

PALPATION

When tendinitis is suspected, points of tenderness are sought. Both sides should be compared. However, it is only when a resisted test is positive that it is worthwhile palpating for the exact site of the lesion. In bursitis, palpation affords little assistance. It is the response to resisted movements that helps to indicate the bursal relationship with a muscle. ACCESSORY TESTS

Interpretation of the results of technical investigations without previous clinical diagnosis may often be mis­ leading. The classical example is that an asymptomatic osteoarthrosis, easily visible on the X-ray but not causing any pain, or a loose body in an osteoarthrotic

Box 66.5 Summary of examination Preliminary examination Lumbar spine Sacroiliac joint

If signs warrant or the history is indicative, accessory tests can be performed. Palpation of the femoral arterial pulse (see p. 828).

The pulse is just inferior to the inguinal ligament, halfway between the anterior superior iliac spine and the pubic symphysis.

Basic functional examination Supine Five passive movements Four resisted movements Prone Two passive movements Four resisted movements

Palpation

This test should be interpreted with care, because it includes several struc­ tures. It may be a localizing sign both in tendinitis of the rectus femoris and in psoas bursitis. The implication is that the lesion lies in a position where it can be com­ pressed. The test is also painful in arthritis of the hip joint and in sacroiliac conditions (see p. 952).

Trendelenburg test

Sustained active extension of the hip in the prone posi­

Technical investigations

Combined passive flexion/adduction.

tion.

Tendinitis Bursitis?

Accessory tests Palpation of femoral arterial pulse Passive flexion/adduction Sustained active extension of the hip

This test (Fig. 66.11), continued for several minutes,

Figure 66.11 Sustained active extension of the hip in the prone position.

CHAPTER 66 - CLINICAL EXAMINATION 995

joint, where the radiograph shows the arthrosis but not the subluxated piece of cartilage. However, if symptoms and clinical signs warrant, technical investigations become an obligatory part of assessment. This is especially the case in: • • •

Hip joint lesions in children Suspected aseptic necrosis Positive sign of the buttock (see p. 1007).

In these circumstances radiography, CT, MRI, sonogra­ phy or arthroscopy will be performed to confirm or exclude a particular diagnosis.

Two diagnostic techniques have become popular during the last decades. Ultrasonography (ultrasound) is an excellent method to detect intra-articular fluid.7,8 It may also be a very useful auxiliary method in estimating the degree of tendon and muscle ruptures9 and in localiz­ ing bursitis.1° However, the method requires much expe­ rience and diagnostic precision depends entirely on the skill of the examiner. There is general agreement that hip arthroscopy is valu­ able as a diagnostic investigation in patients with catch­ ing or transient locking of the hip (loose bodies, synovial tags and lesions of the labrum)Y-14

REFERENCES 1. Cyriax j. Textbook of Orthopaedic Medicille. Vol I. Bailliere Tindall,

9. Fornage BO. Ultrasonography of Muscles alld Tendons. Springer,

2. Adams JC, Hamblen D. Outline of Orthopaedics, 12th edn.

10. Flanagan FL, Sant S, Coughlan Rj, O'Connell O. Symptomatic

London, 1982.

Churchill Livingstone, Edinburgh, 1 995:282-324. 3. Fitzgerald R. Acetabular labral tears. Ciill Orthop ReI Res 1995;311:60-68.

New York, 1988. enlarged iliopsoas bursae in the presence of a normal plain hip radiograph. Rheumatology 1995;34:365-369. 11. Dorfmann H. Pathologie du bourrelet cotyloi"dien. Lecture pre­

4. McCarthy J, Busconi B. The role of hip arthroscopy in the diag­

sented at the 6th AlUlual Meeting of Reeducation Medecine.

nosis and treatment of hip disease. Orthopedics 1995;18:753-756.

Vlemes Journees de Medecine et de Reeducation de l'Est

5. Hoppenfeld S. Physical Examination of the Spine and Extremities. Appleton-Century-Crofts, New York, 1976. 6. Renstrom

P,

Peterson L. Groin injuries in athletes. Br J Sports

Med 1980;21:30.

Parisien, 1995. 12. Locker B, Chiron P, Oorfmann H, Kelberine F. Arthroscopie de hanche. Conference d'enseignement SFA. Annales de la SFA,

1992:74-97. Reported in Rev ChiI' Orthop 1993;79:327-329.

7. Marchal GJ, Van Holsbeeck MT, Raes M et al. Transient synovi­

13. Suzuki S, Awaya G, Okada Y et al. Arthroscopic diagnosis

tis of the hip in children: role of US. RadioIogJJ 1987;162:825-828.

of ruptured acetabular labrum. Acta Orthop Scalld 1986;57:

8. Moss SG, Schweitzer ME, Jacobson JA et al. Hip joint fluid: detection and distribution at MR imaging and US with cadaveric correlating. Radiology 1998;208:43-48.

513-515. 14. Farjo LA, Glick JM, Sampson TG. Hip arthroscopy for aceta­ bular labral tears. Arthroscopy 1999;15:132-137.

THIS PAGE INTENTIONALLY LEFT BLANK

I�terpretation of the clinical examination of the hip and buttock

!-----------...... Traumatic arthritis Monoarticular steroid­ sensitive arthritis Rheumatoid-type arthritis Septic arthritis Tuberculous arthritis Haemarthrosis Crystal synovitis Beginning of arthrosis Disorders with a positive buttock sign

Interpretation of the clinical examination of the hip and buttock

1---.... Septic bursitis Ischiorectal abscess Fractured sacrum Neoplasm at the upper femur Neoplasm in the ilium Osteomyelitis of the upper femur Septic sacroiliac arthritis Loose femoral prosthesis

Disorders without a positive 1---"'I"'Aseptic necrosis buttock sign Advanced arthrosis

Internal derangement Psoas bursitis Haemorrhagic psoas bursitis Gluteal bursitis Trochanteric bursitis Psychogenic pain

t-----------.. lschial bursitis Gluteal bursitis Femoral neck stress fracture Pubic ramus stress fracture Osteitis pubis Inguinal hernia

997

998 SECTION TWELVE - THE HIP AND BUnOCK

I---..-Psoas tendinitis Rectus femoris tendinitis Sartorius tendinitis Obturator hernia

!---..-Avulsion fracture of trochanter Metastasis of femur Avulsion fracture of anterior superior iliac spine Abdominal neoplasm

1---... L2 root palsy L3 root palsy Psychoneurosis

1---... Inflamed gluteal bursa Intermittent claudication Hamstrings tendinitis Gluteus maximus lesion

1----51 root palsy I---..-Adductor longus tendinitis Fracture or neoplasm in upper femur Osteitis pubis Lesions of the sacroiliac joint 1-----L2-L4 root lesions

1---..-Lesion of gluteus medius/minimus Lesion of tensor fasciae latae Sprain of iliotibial tract Sacroiliac joint lesions

I---..-Avulsion fracture of the greater trochanter Iliac apophysitis

1---... L5 root palsy Lesions with raised greater trochanter I-----Gluteal bursitis !-----L5 root lesion I-----Gluteal bursitis I---T-- endinitis rectus femoris I---P -- artial rupture of rectus femoris 1----- L3 root lesion I---H -- amstring syndrome

1----51, 52 root palsy

CHAPTER CONTENTS

Disorders of the inert structures

The capsular pattern

999 Traumatic arthritis 999

Monoarticular steroid-sensitive arthritis Rheumatoid conditions

Septic arthritis

1002

1000

1000

Tuberculous arthritis 1002 Chondrocalcinosis and gout 1002 Monoarticular arthritis in middle-aged people Osteoarthrosis 1002

The non-capsular patterns

1007

Disorders with a positive 'buttock sign' Aseptic necrosis of the hip 1010 Stress fracture of the femoral neck Internal derangement of the hip Psoas bursitis 1015 Haemorrhagic psoas bursitis Gluteal bursitis

1017

Trochanteric bursitis 1018 Ischial bursitis 1019 . Psychogenic pain 1019

1016

1002

1007

1012 1012

THE CAPSULAR PATTERN The capsular pattern at the hip joint is gross limitation of medial rotation, abduction and flexion, less limitation of extension and little or no limitation of addu ction and lateral rotation (Fig. 68.1). In an advanced arthritis, abduction and internal rotation are impossible and asso­ ciated with obvious limitation of flexion and extension. A capsular pattern in the hip joint of a child or adoles­ cent always implies a serious problem. The slightest lim­ itation of movement should be reason enough to put the child on bed rest and start diagnostic procedures to detect the cause. Weight bearing is prohibited until the reason for the capsulitis is discovered (see Ch. 71). If a capsular pattern is present at the hip, and resisted movements do not hurt, the conditions discussed in this section should be considered.

TRAUM ATIC ARTHRITIS This results more often from overuse of a stiffened and arthrotic joint than from one single injury. When it occurs

Figure 68.1

The capsular pattern at the hip joint. 999

1000 SECTI O N TWELVE - T H E H I P A N D BUn OCK

in a child, transitory arthritis or the beginning of Perthes' disease should always be suspected (see p. 1046). In traumatic arthritis in adults, a single intra articular injection with 40 mg of triamcinolone often leads to permanent cure.

MONOARTICULAR STEROID-SENSITIVE ARTHRITIS The patient complains of considerable aching in the L3 dermatome, first during exertion, later also at night. In an early case there is only slight limitation of movement with a capsular pattern, which gradually becomes more obvious. The end-feel is that of muscle spasm and resisted movements are negative. Radiographs are negative in early cases, whereas in more advanced arthritis a generalized loss of joint space may be seen. If the disorder is left untreated, there is a risk that early osteoarthrosis supervenes, which then complicates the condition. As in idiopathic monoarticular arthritis of shoulder, knee and elbow, the true aetiology remains unclear but the condition subsides i mmediately and lastingly with two intra-articular injections of 50 mg of triamcinolone.

RHEUMATOID CONDITIONS In rheumatoid conditions, the hip is affected only late in the evolution of the disease. In ankylosing spondylitis, the arthritis progresses with ups and downs until the hip becomes almost completely fixed in flexion. Apart from systemic treatment, an intra­ articular injection can be given during flares but caution should be taken with repeated injections of triamci­ nolone, for fear of a steroid arthropathy; no more than three injections per year should be given. During periods when the symptoms subside, gentle stretching can be undertaken to counteract the progressive stiffening.

Technique: injection. Although there are many different

approaches to the hip joint, the safest is from the lateral aspect because there are no important blood vessels or nerves on this aspect (Fig. 68.2). The patient lies on the painless side, with out­ stretched legs and a small pillow between the knees, or with the upper leg supported. This relaxes the iliotibial tract and makes the upper border of the trochanter more easily palpable. The femu r is kept in an anatomical posi­ tion and the leg not allowed to rotate internally. In this position, the trochanteric border lies vertically above the acetabulum. A point is chosen at the middle of the border and a 7 cm needle is thrust in vertically down­ wards. At 4-7 cm depth the tip of the needle is felt to pierce the thick ligamentous structu re of the capsule, before striking the bone of the femoral neck; 50 mg of triamcinol one is injected. No particular resistance is experienced when the fluid is forced i n but the patient may feel some aching down the leg. Although some a fter-pain may be present for the next 12 hou rs, there is considerable subjective improvement from the second day on and the following night the patient will have what is probably the fi rst undis­ tu rbed sleep for months. The injection is repeated after 2 weeks. The patient should be told to avoid hard work and exercises for a further 2 weeks. Usually, there are no recurrences.

(a)

(b) Figure 68.2

Intra·articular injection of the hip joint.

CHAPTER 68

In polymyalgia rheumatica, both shoulders and hips are iavolved early in the course of the disease. Systemic therapy quickly relieves signs and symptoms. 1

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DISORDERS OF T H E I N ERT STRU CTURES 1001

OSTEOARTHROSIS

AETIOLOGY SEPTIC ARTHRITIS As a rule, this is caused by a haematogenous dissemina­ tion, although it can also be the result of an intra­ articularinjection. Septic arthritis at the hip is not only a disaster for the joint but can also threaten life.2 Acute pain in the L3 dermatome, together with fever and a gross capsular pattern, draws attention to this disease. Local aspiration should be carried out and systemic antibiotic therapy should be administered at once. 3

TUBERCULOUS ARTHRITIS Insidious onset and slow progression of a mono articular arthritis together with muscle wasting are the first features to draw attention to this disorder. The capsular pattern is gross, the hip sometimes fixed in flexion. At the onset, systemic manifestations may be minimal or absent. The diagnosis is made on radiography and the exami­ nation of the synovial fluid .

CHONDROCALCINOSIS A N D GOUT The lesions very rarely affect the hip joint. The diagnosis is suspected when acute hip pain and a gross capsular pattern are encountered, especially if there is a previous history of attacks of acute pain in other joints. The diag­ nosis is confirmed by the demonstration of crystals in the synovial fluid.

MONOARTICULAR ARTHRITIS IN MIDDLE­ AGED PEOPLE This condition was described by Cyriax4 (his p. 386). For no special reason, a middle-aged patient experiences aching at the anterior aspect of the thigh during exertion. Clinical examination of the hip shows only a slight cap­ sular pattern, with some limitation of internal rotation and flexion. There is pain at the end of range and the end­ feel is elastic. The radiograph reveals nothing but a normal hip joint. The condition continues unchanged for months. Intra-articular injection with triamcinolone seems to be ineffective, but the lesion responds very well to stretching of the capsule, which relieves the pain quickly and permanently (see p. 1000 for technique).

It is widely accepted that the most likely causative factor in the development of arthrosis of the hip is the incapac­ ity of (parts of) the hip to withstand mechanical stresses. In the literature, a distinction is made between primary and secondary arthrosis.s Secondary arthrosis originates from a pre-existing anomaly at the hip, such as Perthes' disease, acetabular dysplasia and epiphysial dysplasia. Rapidly developing osteoarthrosis results most often from aseptic necrosis. When the osteoarthrosis results from an undetermined abnormality of the cartilage or the subchondral bone, the condition is called idiopathic or p rimary. Prim ary osteoarthrosis is extremely rare - in more than 90% of cases, previous abnormalities in the hip joint can be demonstrated .6-8. Initiation and progression of osteoarthrosis at the hip seem to be caused by a continuous interaction between such factors as deterioration of articular cartilage, changes in the subchondral bone, stiffening of the capsule, dys­ function in the neuromuscular system and chemical changes in the composition of the synovial fluid.

Cartilage fibrillation Articular cartilage is a viscoelastic substance. It deforms slightly under load. The main purposes of the tissue are (a) to transmit joint forces to underlying bone struc­ tures, (b ) to minimize the frictional d rag of joint motion and (c) to maximize the contact area of the joint under load. Strain may induce loss of proteoglycan molecules in the collagen network.9 This results in an increase in hydration and loss of tensile strength, and initiates the fibrillation of the cartilage. 1 °, ll Subchondral bone The health of articular cartilage depends largely on the mechanical qualities of its bony subchondral bed : the greater the discontinuity in elasticity between cartilage and subchondral bone, the more shear stress will occur. 1 2 The p resence of stiffened subchondral bone thus increases the likelihood of the progression of cartilage lesions. 1 3 Capsule of the joint Inflammation of the synovial membrane can also be responsible for the degeneration of cartilage: connective tissue activating pep tides and catabolites are set free during inflammatory reactions and have a negative influence on cartilage and subchond ral bone,1 4,lS

1 002 S ECT I O N TWELV E - T H E H I P A N D B UTTOCK

In addition, rigidity of the capsule, so often seen in the early stages of arthrosis,16 plays a role in its progression: because of the loss of laxity, the normal gliding move­ ment of the cartilage surfaces is altered, which imposes a change in load distribution and thus increases stresses on particular areas of the joint.

Synovial fluid The composition of the synovial fluid may enhance the development of osteoarthrosis: a decrease in viscoelastic quality provokes more friction between the joint surface. It is well to remember that immobilization also decreases synovial fluid hyaluronan levels and may thus contribute to the progression of osteoartruosisY Muscular dysfunction Muscular dysfunction and a disturbed neuromuscular balance are quite common in osteoarthrosis of the hip. They cause the joint to work under abnormal conditions and may play a role in the development or continuation of hip osteoarthrosis. 1 8 A pattern of tightness and over­ activity of the psoas, adductors, tensor fasciae latae and rectus femoris is typical in arthrosis of the hip joint, whereas the gluteals show a tendency towards weakness and inhibition. 19,2o The continuous interaction between the changing structures of the joint imposes a physiological imbalance, which starts the process of degeneration. Vigorous and persistent attempts to repair the degenerative changes aggravate the already d isordered joint function and acti­ vate a vicious circle. Hypervascularity, weakening of the subchondral bone, fatigue fractures, localized zones of collapse, flattening of the femoral head and formation of osteophytes then become inevitable (Fig. 68.3). This whole process can lead to rapid destruction of the joint; howevel� this is not always the case and spontaneous clinical and radiological improvements can occurY Conclusion: osteoarthritis is a 'joint failure', similar to 'heart failure'. The aetiology is multiple but each of the compo­ nents of the joint (cartilage, subchondral bone, synovial fluid and joint capsule) plays a role in the pathogenesis.

SYMPTOMS AND SIGNS Although the diagnosis of advanced arthrosis of the hip is easy, it may be difficult to diagnose the early stages. Also, there is sometimes a striking lack of correspon­ dence between the clinical picture and the radiographic appearance.

Symptoms The pain is located in part of the L3 dermatome: the groin, the anterior aspect of the thigh, the knee and the

Attempts to repair:

Hypervascularity Sclerosis of the bone Osteophytosis Figure 68.3

The aetiology of osteoarthrosis.

leg as far as the ankle joint. It should not be forgotten that a separate part of the dermatome is located in the region of the sacroiliac joint, so patients with arthrosis of the hip may also present with unilateral pain in the lower back. In the early stage pain is only present during and after exercise but later it becomes continuous and can even d isturb sleep. It is suggested that pain at night in cox arthrosis is associated with an increase in intracapsu­ lar pressure and subsequent joint contracture.22 If the patient mentions twinges during normal walking, the disorder is considered to be complicated by impacted loose bodies (see later).

Signs The examination often reveals a capsular pattern, with internal rotation the most limited and some limitation of flexion, extension and abduction but this is certainly not always so. Many cases of hip osteoartruosis present with other movement restriction patterns, for instance gross limitation of both internal and external rotation. 23 As a rule there is considerable difference between the clinical signs of an early osteoarthrosis and those found in advanced cases. In the early stage, there is merely a capsular stiffening and not yet much erosion of cartilage or osteophyte formation. The cl inical findings are therefore a capsular

CHAPTER 68 - DIS O R D E RS OF T H E I N E RT STRUCTU RES 1003

pattern with a less elastic end-feel. Most commonly, inter'hal rotation is found to be the most painful and limited, followed by limitation of flexion, abduction and extension. In advanced instances, gross limitation is found, with loss of all rotational movement. In extreme cases, a 'hinge joint', allowing only flexion and extension in an oblique plane, develops: the femur moves laterally when flexion is forced. The end-feel is hard and marked coarse crepitus can be palpated. Muscle tightness can sometimes be detected by performing muscle length test procedures such as described by Janda and Lewit.24--26

into four grades (Kellgren 1-4). Classically, there are three radiographic types of arthrosis of the hip, according to the direction of migration of the femoral head. •

•

RADIOGRAPHY 'Osteoarthrosis of the hip' must be a clinical diagnosis and it is unwise to rely entirely on the radiograph for estima­ tion of the functional incapacity and for deciding on optimal treatment. First, there is a considerable lack of correspondence between the degree of pain, the mobility of the joint and the radiograph appearances.27 Second, the patient may suffer from other lesions at or around the arthrotic hip. These lesions - loose body, psoas or gluteal bursitis (see pp. 112-119) - are not radiographically visible. If a radiological examination is performed without a full history and proper clinical examination of the hip, such conditions will be missed and the painless arthrosis will be blamed for the pain. The radiological changes in hip osteoarthrosis are: presence of subchondral sclerosis in femoral head and acetabu lum, joint space narrowing, femoral head defor­ mi ty, marginal osteophytes, cystic changes in the femoral head and the acetabulum and migration of the femoral head. The severity of the radiological changes is classified

Figure 68.4

•

Most osteoarthrotic hips show a superolateral migration of the femoral head with localized erosion of cartilage at the lateral border of the labrum and a widening of the inferomedial part of the joint.28 Cameron and MacNab suggest that this is the form of osteoarthrosis that is primarily related to capsular restrictions and responds well to capsular stretching. 29 A medial-axial migration occurs in about 10-15% of cases. This presentation is usually associated with gross osteophytosis at the lower border of the femur and labrum. Another 10-15% of cases are non-migratory hip osteoarthrosis, associated with superior or concentric loss of cartilage space and concentric formation of osteophytes (Fig. 68.4).

TREATMENT Early treatment of osteoarthrosis is vital. There is evi­ dence that reduced motion of the hip (from capsular tightening and muscular imbalance) further increases the degenerative process in cartilage and subchondral bone. Several studies have demonstrated the beneficial effect of exercise on pain and disability.3D The treatment of choice is therefore early stretching of the joint (grade B mobi­ lizations). Treatment with injections has only a limited indication . In later stages or in quickly developing osteoarthrosis, conservative treatment is u seless and surgery is indicated (see Box 68.1, p . 1 004).

Migration of the femoral head: (a) superolateral migration; (b) non-migratory hip osteoarthrosis; (c) medial-axial migration.

1004 SECTI O N TWELVE - T H E H I P AND BUTTOC K

Capsular stretching It is generally believed that early stretching of a tight capsule may prevent joint damage or at least slow further progression. 3 1 Therefore, stretching is the treatment of choice in the early stage of the disease. The decision to use it depends largely on the clinical findings: early arthrosis with a slight capsular end-feel u sually responds quite well to such treatment. Stretching is of no use in ad vanced arthrosis with gross limitation of movement, a hard end-feel and coarse crepitus, because these are the clinical indications of gross cartilaginous destruction and formation of large osteophytes. It is vital to start stretching treatment as early as possi­ ble. A stiff and inflamed capsule is one of the reasons for disturbed load distribu tion, responsible for further pro­ gression of degeneration. Furthermore, overuse at a stiff­ ened capsule provokes consecu tive strains, resulting in traumatic inflammation and pai n. Treatment is given two to three times a week, for 10-20 sessions. The joint is mobilized in three directions flexion, extension and internal rotation - for 5-1 0 minutes each. The patient may experience slight aching for 1 or 2 hours after the forcing. This is an important criterion to the therapist, who must adjust the vigour of the treatment to the length of time of the increased pain. Slight after-pain for 1-2 hours is acceptable. If the patient suffers from increasing pain over 1 or 2 days, it i s clear that the joint has been forced too much. If neither after-pain nor improve­ ment follows, greater stress, more persistently applied, is used during the next visit.

The resu It to be expected is not a marked increase in range but merely a decrease in pain . It is remarkable that pain at night, even of many months' standing, can often be abolished by a few sessions of capsular stretching. Used in an early stage, years of relief can often be obtained although it may be necessary to repeat the mobilizations once or twice a year to keep the capsule as mobile as possible. Tech n ique: forced flexion. The patient adopts a ha lf­

lying position on the couch. The therapist stands at the affected side, level with the patient's knee. The hip is flexed as far as is comfortably possible. One hand rests on the anterior aspect of the knee, the other presses the opposite thigh downwards to the couch. Wi th steadily increasing pressure applied to the knee, the thigh is forced towards flexion (Fig. 68.5). This position is main­ tained for as long as the patient can bear it, for instance 1 minute. The pressure is then slowly released to give some pause and the same procedure repeated. 1 . The patient lies prone on a high couch. The therapist stands level with the thighs. To prevent stress on the lumbar spine, it is vital to keep the pelvis on the couch when extension of the hip is forced . Therefore with one hand the therapist presses on the lower part of the bu ttock, which will obstruct movements at the lower back and the sacroiliac joint. With the other hand, he grasps the thigh from the medial side, just above the patella. Both arms are kept rigid. By a sideways bending of the body, the Tec h n i q ue: forced extension

-

Box 68.1 Treatment of osteoarthrosis of the hip -

Early and/or slowly developing osteoarthrosis (capsular pattern, ligamentous end-feel and absence of coarse crepitus)

Capsular stretching Angular mobilizations in: - flexion - extension - medial rotation Tractions (manual or mechanical): - in maximally loose packed positions - in other positions Muscular re-education Stretching of shortened muscles Activation of inhibited muscles Gait control (intra-articular injections) Advanced and/or quickly developing osteoarthrosis (non-capsular pattern, hard end-feel and coarse crepitus)

Surgery (Intra-articular injections may give temporary relief) Figure 68.5

Forced flexion of the right hip.

CHAPT E R 68

therapist then pulls the patient's thigh upwards, while the patient's pel vis is pushed forcefully downwards. (Fig. 68.6). 2. Some elderly people have difficulty lying on their stomach for any length of time and an alternative method can be used. The patient lies flat on the back, with the head supported with a cushion. The painless hip is now forced into as much flexion as possible, which tilts the pelvis and makes the other thigh rise from the couch. Sufficient extension can now be forced when sustained downwards pressure is applied just above the patella (Fig. 68.7). Technique: forced extension

-

Technique: forced medial rotation. The patient adopts a

prone-lying position on a high couch. The knee at the affected side is bent to a right angle. The therapist stands at the affected side and level with the pelvis. The ipsi­ lateral hand is pressed onto the ilium. The other hand is placed at the medial malleolus and forces the hip into medial rotation. The pelvis rotates and moves the iliac crest backwards on the opposite side. Pressure applied on the pelvic region now forces the iliac crest downwards again. When the thigh at the affected side is held firmly in the rotated position, this downwards pressure will considerably increase the outwards stress on the affected hip (Fig. 68.8).

Traction Traction (either manual or mechanical) is an alternative technique to stretch the joint capsule.34-36

Figure 68.6

Forced extension of the right hip - 1.

vVII

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DISORDERS OF TH E I N E RT STRUCTU RES 1005

Practitioner's checklist

• The ratio of pain to end-feel will indicate the degree

of the applied force (see general principles of treatment, p. 109). Movements should be performed to the point of discomfort but not of pain. In suitable cases the force can be gradually increased during the session. A whole session takes about 20-30 minutes with pauses after every 30 seconds to 1 minute. • Slight passive oscillatory movements can be added: mechanoreceptors type I and II come into action and suppress a painful reaction to the nococeptors (see p. 103). To prevent adaptation of the mechanoreceptors, oscillations should be constantly changed in rhythm, amplitude and direction. • Although osteoarthrosis and osteoporosis do not seem to appear simultaneously, the former protecting from the latter and vice versa·32.33 forcing medial rotation in elderly people should always be carried out with caution, for fear of fracturing the neck of the femur.

Manual traction (distraction) can be given in two dif­ ferent ways: with an extended knee, by which the trac­ tion is performed via the ankle; or with the leg flexed to more than 90°. Traction is then carried out via the prox­ imal part of the upper leg. Because of the direction of the hemispherical acetabulum, in either case the femoral head moves inferiorly, anteriorly and lateral ly. Depending on the position of the joint, some parts of the capsule are stretched more intensively.

Figure 68.7

Forced extension of the right hip -2.

1006 SECT I O N TWELVE - T H E H I P AND BUnOC K

Figure 68.8

Forced medial rotation of the right hip. Figure 68.9

Manual traction.

Traction I. The patient lies supine near the edge of the

couch. To prevent the pelvis being pulled down, side­ ways or lifted off the couch, two bands are used for fixation: one at the groin, the other transverse over the pelvis just beneath the anterior superior iliac spines. The therapist grasps the patient's ankle. According to the direction of the acetabulum - inferiorly, laterally and anteriorly and in agreement with the maximally loose packed position of the joint capsule - the leg should be brought into a position of about 30° of flexion, 30° of abduction and slight lateral rotation. Traction is performed by leaning backwards with straight arms (Fig. 68.9). At the moment the therapist feels the patient relaxing the muscles, a jerk can be tried by pulling the arms towards the body. At the moment slight separation of the femoral head from the acetabulum can be felt. Traction II. The therapist sits or stands at the level of the

pelvis. The leg should be flexed to at least 90° and slightly laterally rotated. Both hands take hold at the upper part of the upper leg (Fig. 68.10a). Traction is per­ formed in the direction of the acetabulum - inferiorly, laterally and anteriorly. Use of a band makes it possible to lessen the effort of the therapist a great deal. Both hands then hold the leg in position at the knee (Fig. 68.10b). Traction results by leaning backwards. Traction II is not suitable to manipulate the joint. It must be noted that distraction of the hip joint can only be effective if the pelvis is completely immobilized, otherwise the lumbar spine will compensate the move­ ment. To this end two fixation belts are used . One should

resist the movement of the pelvis caudally, the other resists an anterior and lateral displacement.

Muscular re-education In order to correct the pattern of muscular dysfunction and a disturbed neuromuscular balance, selective activa­ tion of inhibited, weak muscles and stretching of tight, shortened muscles is advocated by several authors.37-40 The second measure is of even more importance because tight, hyperactive muscles interfere with the activation of inhibited muscles. These muscles (usually psoas, tensor fasciae latae and rectus femoris) are stretched slowly without straining the joint. Activation of inhibited muscles is achieved by exercises with low loads to prevent overflow into other muscles. It is also advisable to perform exercises as closely as possible to their functional manner. For this purpose closed kinetic chain exercises are advocated, because the weight-bearing component effectively stimulates mechanoreceptors around the joint, so improving muscular contractions.41 Hip extensors can be activated lying supine, the lower leg over the edge of the couch, the hip extended and the knee in 90° of flexion. Pushing the foot on the floor facil­ itates both the gluteus maximus and the posterior part of the gluteus medius. Activation of the hip abductors is performed first sitting near to the edge and at the corner of the couch, one, leg extended and in contact with the floor. Taking support on this leg the patient activates the hip abductors. Standing, with the feet about 10 inches apart, and resisting a pressure against the pelvis from the contralateral side, is another

C HAPT ER 68

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DISORD E RS OF T H E I N ERT ST RUCTU RES 1 007

inflammation and the pain but increased mobility will not follow. For fear of arthropa thy, this injection should not be repeated.42

(a)

(b) Figure 68.10

Mechanical traction.

effective exercise to activate the ipsilateral hip abductors. This can also be attained if the patient is asked to lower and raise the contralateral pelvis. Taking support with the hands on a chair at each side of the body reduces the load. In order to reduce the harmful effect of a limp, a walking stick in the contralateral hand may at first be necessary. It decreases the contraction of the ipsilateral hip abductors and thereby reduces compressive forces on the joint. Finally, it is necessary to be aware of any harmful effect of the trunk or lower limb that might influence the devel­ opment and continuation of the hip joint problems, i.e. stiffness of the lumbar spine, leg-length differences or dys­ function at the knee, the talocrural or the subtalar joint.

Intra-articular injections If the patient suffers from a subacute exacerbation because of traumatic arthritis superimposed on a stiff­ ened arthrotic capsule, one intra-articular injection with 50 mg of triamcinolone will relieve the traumatic

Surgery A McMurray intertrochanteric osteotomy is ind icated in a painful hip that has good mobility. It has the advantage of diminishing pain while maintaining a useful range of motion in the ' natural hip'. Total hip rep lacement is indicated in advanced osteoarthrosis. The prosthesis is made up of two parts: an acetabular component made of a metal shell with a plastic inner socket (the socket portion) that replaces the acetabu l um and a femoral component made of metal (the stem portion) that replaces the femoral head . There are two major types of artificial h i p replacement: cemented and uncemented. Cemented total hip replace­ ment uses cement to secure an implant to the bone, while with cementless technology the bone heals directly to the prostheSiS. The choice is usually made on age, body weight and lifestyle. Nowadays it is accepted that young, active or heavy patients are most likely to loosen a cemented total hip replacement. For these patients, the cementless total hip replacement appears to be the most durable design. Patients with poor bone quality or with less active lifestyles are candidates for cemented total hip replacement. The life expectancy of the prosthesis is between 15 and 20 years.43 Aseptic loosening with or without osteolysis is the major problem and constitutes 71% of the revisions but the incidence had decreased three times during the past 15 years to less than 3% at 10 years in Sweden.44 However, the long-term du rability of the acetabular com­ ponents remains a major concern.45

THE NON-CAPSULAR PATTERN S A non-capsular pattern on clinical examination of the hip indicates the possibility of lesions of the joint itsel f or disorders of nearby tissues such as the bu ttock and the groin. The straight leg raising test and resisted movements help to differentiate the two possibilities. Serious lesions in the buttock are characterized by an interesting pattern of physical signs, called the 'bu ttock sign', summarized in Box 68.2 (p. 1008). Non-capsular lesions of the hip itself comprise loose bodies, bu rsitis and aseptic necrosis of the femoral head.

DISORDERS WITH A POSITIVE 'BUTTOCK SIGN' This clinical syndrome, described by Cyriax4 (his p. 375) always indicates a major lesion in the bu ttock.

1008 SECTION TWELVE - T H E HIP AND B UnOC K

Box 68.2 'Sign of the buttock'

More limitation of passive hip flexion (with flexed knee) than of straight leg raising Other hip movements are limited in a non-capsular way Lesions:

Septic bursitis Ischiorectal abscess Fractured sacrum Neoplasm at the upper femur Neoplasm in the ilium Osteomyelitis of the upper femur Septic sacroiliac arthritis Loose femoral prosthesis

The buttock sign is characterized by more limitation of and lor pain on passive hip flexion with a flexed knee than with an extended knee (i.e. straight leg raising; Fig. 68.11). The other passive movements at the hip joint are limited in a non-capsular way. This strange pattern immediately d raws attention to the gluteal region. Were the hip joint itself affected, straight leg raising would not be limited, except in those gross articular patterns in which flexion cannot reach 90°. Were the nerve roots, the sciatic nerve or the hamstrings affected, hip flexion with a flexed knee would not be painful or limited, because it does not stretch these structures. The fact that both movements are limited and painful implicates other structures in the gluteal region.

Checking for the buttock sign is very important in pain syndromes at the gluteal region. Because there will probably be nothing characteristic about the pain, only a comparison between the results of the straight leg raising test and passive hip flexion can detect serious disorders in the buttock. When this typical combination of signs emerges, a very careful examination of passive and resisted movements must follow. Passive move­ ments disclose a non-capsu lar pattern, with almost always a full range of medial rotation. The end-feel of the limited movements is 'empty': as a consequence of the increasing pain, the examiner has to stop the move­ ment even though it is felt that the end of range has not been reached. Some resisted movements are painful and weak as well because they increase the tension on the affected tissues. As a rule, resisted extension and inter­ nal rotation are the most painful. Palpation may disclose a painful swelling. To refine the diagnosis, the general temperature must be noted, a rectal examination performed and radio­ graphs and I or bone scans done.

SEPTIC BURSITIS This is by far the commonest cause of a positive 'buttock sign' . The condition usually occurs after direct inocula­ tion du ring an intramuscul a r injection, although a haematogenous dissemination is also possible, especially in the elderly.

History The history is often rather trivial, with increaSing gluteal pain spreading down the back of the thigh to the knee and calf. During the first hours or days the pain eases at rest and increases during movement. Coughing does· not hurt. The features do not draw immediate attention to the buttock but rather suggest a nuclear disc lesion.

(a)

./

Figure 68.11 The buttock sign: passive hip flexion is more limited and/or painful than straight leg raising.

Clinical examination The patient's gait is hobbling, as if weight can hardly be borne on the affected leg.46 This major disability contrasts markedly with the minor degree of discomfort and is the first warning for the examiner. Examination of the lumbar spine shows limitation of flexion, sometimes with a list towards the pain. This is logical since the pain increases when tension on the affected tissues increases during forward flexion of the spine. The other lumbar movements are of full range and painless and straight leg raising is painful and somewhat limited. ' These clinical examination findings correspond per­ fectly with the classical findings of a disc protrusion, so the diagnosis will be missed if the examination is not

C HAPTER 68 - DISORD E RS OF T H E I N ERT STRUCTU RES 1009

properly performed. When passive flexion at the hip joint is tested, the buttock sign will be apparent at once. The local temperature is raised and palpation reveals a tender area just above and behind the greater trochanter. In advanced cases, abscess formation may have taken place, revealed by a swollen, tense and fluctuating area in the buttock.

Treatment Treatment consists of ice packs, bed rest and antibiotic therapy. If there is abscess formation, the lesion must be drained. Sometimes the buttock sign and the localized and fluctuating swelling result from an acute haemorrhage after a trauma, for example a fall on the buttocks. Here the history of a trauma is informative and the tempera­ ture is normal. Aspiration usually leads to complete cure. ISCHIORECTAL ABSCESS Occasionally, an anorectal abscess points towards the ischiorectal fossa instead of to the rectal region - an ischiorectal abscess.47 Usually, the patient complains of gluteal pain, rather than of local rectal pain, and nothing in the history sug­ gests an infection of rectal origin: the pain is related to movement and posture and not to the function of the bowel. Sitting is impossible. The patient limps badly and even putting his foot to the ground causes considerable pain. The hip is held constantly i n slight flexion but further flexion is prevented by increasing pain, as is straight leg raising indicating the buttock sign. Apart from fever, other toxic symptoms may be present. The abscess may be felt during bidigital rectal examination with the index finger in the rectum and the thumb external. The treatment is surgical and consists of prompt incision and adequate drainage.48

FRACTURED SACRUM Sacral fractures are associated with pain, swelling, ecchy­ mosis and tenderness on palpation. In the presence of neurological symptoms, the diagnosis is usually not difficult. Neurological damage is not present, however, if the fracture line lies through the ala. Because of the posi­ tion of the sacroiliac ligaments, the fracture remains stable and the diagnosis is then frequently missed.49 The patient may ascribe discomfort to a local bruising and sometimes continues to be mobile. In a spontaneous sacral insufficiency fracture in an elderly woman the diagnosis is even more difficult.50,5 1 There is pain during walking and standing but also local tenderness during sitting or lying. A cough and a

sneeze also hurt. Careful clinical examination discloses the buttock sign. Sacroiliac tests are very painful. During digital rectal palpation of the sacrum, the anterior part is found to be as painful as the posterior, a strong sign of sacral fracture. Because the sacrum is curved, diagnosis on a radio­ graph is not always easy. It is therefore advisible to obtain anteroposterior and lateral tomograms.52 If the fracture is markedly displaced or associated with neurological deficit, surgical reduction and stabilization must be performed. In uncomplicated fractures, treat­ ment consists of aspiration of the haem atoma and rest over 4-6 weeks, although bony union without deformity seems to take place whether the patient rests or not.53

NEOPLASM AT THE UPPER FEMUR Metastases or primary hlmours in the upper femur give rise to increasing pain in buttock and thigh. After a short development of the disease process, the functional dis­ ability may be so gross that it prevents the patient bearing weight on the affected side. There is also pain at rest.54 Examination reveals the buttock sign. If the lesion lies in the neighbourhood of the lesser trochanter, resisted hip flexion is painful and weak. Marked wasting of the thigh muscles is present in advanced cases. The diagnosis is confirmed by radiography.

NEOPLASM IN THE ILIUM Again the patient complains of increasing gluteal pain, not only during movement (the patient can only hobble with assistance) but also at rest. The buttock sign is present but the other passive movements are of full range and almost painless. Some resisted movements are painful and weak, and marked muscular atrophy is seen. The contrast between the extreme pain and the almost full range of passive movement, in combination with the buttock sign, makes the diagnosis obvious. The radio­ graph confirms it.

OSTEOMYELITIS OF THE UPPER FEMUR Osteomyelitis is suspected when local symptoms and signs are accompanied by high fever and toxic manifesta­ tions. Sometimes, however, the patient is afebrile, and then only complains of local symptoms - increasing and continuous pain in the buttock and thigh. This contrasts with the signs: hobbling in with a bad limp, suggesting gross arthritis, but further clinical examination reveals a non-capsular pattern at the hip joint together with a clear sign of the buttock. Early in the evolution it is possible for the radiograph to be negative. If there is doubt, a bone scan should be obtained.

1010 SECTION TWELVE - T H E H I P AND BUnOC K

SEPTIC SACROILIAC ARTHRITIS This disease affects young patients. Predisposing factors are immunosu ppression, d ru g addiction and child­ birth.55,56 In addition to the positive buttock sign, the sacroiliac distraction test is extremely painful. Fever and general illness,57 together with local tenderness over the joint are present. Radiological examination remains negative58 in the early stage but CT or bone scan usually confirms the diagnosis.59

LOOSE FEMORAL PROSTHESIS A sign of the buttock in a patient who underwent a hip arthroplasty may indicate a loose femoral prosthesis. Radiological diagnosis may be difficult and obscured by artefacts.60

inflammatory exudate and increased intraosseous bone marrow pressure. Elevation of intra osseous pressure is transmitted to small venules and capillaries within the bone, causing a decrease in blood flow to the bone. This uncompensated increase in intraosseous pressure is thought to result in irreversible circulatory disturbances and subsequent tissue damage, which further magnifies the initial result.68 The problem with osteonecrosis is that the radiological evidence only appears months after the process has started: necrosis of bone is only the irrevers­ ible end result of severe and prolonged ischaemia. Furthermore, it is not the necrosis itself but the reaction of the tissue on the ischaemia that shows up on a radiograph. For these reasons, a standard radiograph cannot assist in early diagnosis. However, diagnosis and treatment at an early stage are extremely important to avoid gross damage to the femoral head.

DIAGNOSIS ASEPTIC NECROSIS OF THE HIP Aseptic necrosis (osteonecrosis, ischaemic necrosis and avascular necrosis are synonymous) of the hip is an osteoarticular disorder characterized by bone marrow ischaemia and death of trabecular bone of the femoral hea d . As bone repair occurs, weight-bearing bone becomes mechanically weakened and flattened and may eventually collapse. Secondarily this leads to a quickly developing osteoarthritis of the hip. In children it is called Perthes' disease (see p. 1 096). Aseptic necrosis of the hip in adults was first described in the German Jiterature.61 Two types - a posttraumatic (complicating fractures or dislocations) and an idiopathic - exist. The latter has been the subject of many experi­ mental and clinical studies over recent decades. All observations show an increasing incidence,62 although this is probably due to improved diagnostic techniques. That the disease is not uncommon was shown by Streda in 1971,63 who found that 68% of patients with actual osteoarthritis had pre-existent osteonecrosis.

PATHOGENESIS It has been accepted for years that non-traumatic osteonecrosis of the hip results from progressive ischaemia, caused by interruption of the arterial supply of the femoral head.64 Experimental and clinical studies, however, indicate that other mechanisms can induce bone necrosis. The fact that aseptic necrosis occurs most fre­ quently in patients treated with high-dose corticosteroids65 and in those with a history of alcohol abuse66 suggests a direct toxic effect on the osteocytes.67 This results in local

Early diagnosis of aseptic necrosis is important, because the disease occurs in relatively young individuals (average age 20-50 for idiopathic forms) and treatment options for more advanced disease are frequently unsuccessful. Any sudden and progressive groin pain - eventually spreading down the L3 dermatome - in a patient under age 50 should immediately arouse suspicion of the onset of aseptic necrosis, especially if there is a clear disrepancy between marked symptoms (pain) and nearly absent signs (full range of movement in the hip). The classical radiological techniques (plain radi­ ographs and a CT scan) are inefficient in making an early diagnosis and other methods of investigation should be used.

Bone scan A bone scan usually shows an increased uptake of the radionuclide from the very beginning of the disease the sensitivity is about 70% .69 Both sides should be compared. Functional exploration of bone This technique was promoted by Ficat and Hungerford . Before the introduction of MRI, it was the best technique for establishing the diagnosis with certainty in the early stages: a painful hip without obvious clinical appearances and with a normal radiograph. Magnetic resonance imaging (MRI) Nowadays MRI is the most sensitive non-inv� sive method for the diagnosis of aseptic necrosis which is diagnosed when a peripheral band of low signal inten­ sity is present on all imaging sequences, typically in the

C HAPT E R 68 - D I SORDERS OF T H E I N E RT STRUCTU RES 1 0 1 1

superior portion of the femoral head, outlining a central area of marrow. This peripheral band is most apparent on T 1 -weighted sequences.71-74 Because both hips are frequently involved, it is necessary to image both hips, not just the symptomatic one. The sensitivity of MRI is between 75 and 1 00% .

Table 68.2

M R I staging o f aseptic necrosis76

Class

T1

T2

Definition

A B C D

Bright Bright Intermediate Dark

Intermediate Bright Bright Dark

'Fat' signal 'Blood' signal 'Fluid' or 'oedema' signal 'Fibrosis' signal

STAGING There are two staging classifications of aseptic necrosis, one based on radiographs (Table 68. 1 ) (Ficat and Arlet7S) and the other on MR signal intensities76 (Table 68.2). The staging of Ficat and Arlet is based on clinical fea­ tures, radiographic signs and scintigraphy. The accuracy of radiographic staging may be improved using CT to detect a subchondral lucency. However, CT does not depict the earliest marrow abnormalities.

Stage 0 This is a theoretical, preclinical and preradiological stage. Stage I The earliest clinical manifestations are sudden groin pain (sometimes referred to the L3 dermatome), often pain at night and increasing pain on weight bearing,78 Coughing may hurt. Clinical examination normally shows a full range of movement. Sometimes there is pain in a non-capsular pattern: external rotation and flexion hurt at the end of range,79 This could suggest the presence of a psoas bursa or an impacted loose body. Sometimes a forceful axial and upwards blow on the heel also provokes groin pain. Standard anteroposterior and lateral radiographs are entirely normal but a bone scan shows an increased uptake of the radionuclide.8o The MRI is positive.

Table 68.1

Stage /I T his early radiographic stage can continue for several months. The clinical symptoms and signs persist or increase. Radiographic changes, although very subtle, appear: slight diffuse sclerosis and slight decalci fication, either generalized or in the form of small cysts. Again, the bone scan shows an increased uptake and the MRI is positive. Stage 11/ There is increasing L3 pain. The patient limps or enters the room leaning on a stick. The clinical examination shows a slight capsular pattern, and forceful axial thrust on the heel provokes the pain. T his stage is characterized by pathognomonic radiographic appearances: • •

A 'crescent line', due to a subchondral fracture and a segmental flattening of the femoral head. Later a sequestrum becomes manifest, followed by collapse of the femoral head.

Stage IV This is the terminal phase of the necrotic process. There is clinical evidence of gross arthrosis. The radiographic picture is that of an arthrosis, superimposed on a deformed femoral head.

The stages of bone necrosis of the femoral head adapted from RP Ficat17

Stage

Clinical features

Radiographic signs

Bone scan

Preclinical Preradiographic Before flattening of head or sequestrum formation

0

0 0

Reduced uptake? Increased uptake

+

Diffuse porosis, sclerosis, or cysts

+

Collapse

++

Flattening

+

+++

Broken contour of head Sequestrum Flattened contour Decreased joint space Collapse of head

+

Early

0

I II

+

Late

III Crescent sign

IV

Osteoarthrosis

1012 SECT I O N TWELVE - T H E H I P AND BUnOC K

MRI staging of aseptic necrosis is based on the signal intensity of the centre of the marrow inside the dark line of necrosis?6 Radiographically occult aseptic necrosis will generally be depicted on MRI as any of classes A to C. Unlike radiographic staging, MR classes have little pre­ dictive value regarding the prognosis for collapse of the femoral head . However, the MRI size and the position of the necrotic lesion are related to prognosis.

Box 68.3 Summary of aseptic necrosis of the hip -

Symptoms

Age between 30 and 50 years Frequently a history of steroid treatment or excessive alcohol intake Sudden groin pain or pain in the L3 dermatome during weight bearing Sometimes nocturnal pain Signs

TREATMENT The most important factor in effective treatment of non-traumatic osteonecrosis of the hip remains early diagnosis.8] Early decompression of bone before irreversible damage may break the cycle of ischaemia and increased marrow pressure. Bone decompression, or coring, has a success rate ranging from 40 to 90%.87 The therapeutic effect of a core decompression is probably the result of the reduction of medullary hypertension, one of the factors in the vicious circle which causes aseptic necrosis.83 The success of decompression appears to be directly related to the stage of the disease:84 hips without radio­ logical evidence or only 25% involvement of the femoral head have no collapse of the femoral head, while 73% of cases with more advanced disease have femoral head collapse. Thus, early diagnosis of aseptic necrosis with MRI is criti cal for patient management and successful therapeutic outcome. Other treatment options include rotational osteotomy and joint fusion.85 The symptoms, signs, technical investigations and treatment of aseptic necrosis are summarized in Box 68.3.

Walking with a limp contrasts with the normal movements or the slight non-capsular pattern found at the hip Upwards thrust to the heel sometimes evokes hip pain Technical investigations

Early stage: MRI (radiography is not informative) Later stages: radiography Treatment

Early stage: core decompression and modified rest Advanced stage: osteotomy or arthroplasty

seems to be the most accurate diagnostic tool in the early detection of a femoral neck stress fracture.92 The sequelae of undetected spontaneous fractures are subcapital fracture with displacement, angular deformity and avascular necrosis of the femoral head. Treatment depends on the radiological differentiation of the lesion. A transverse stress fracture is potentially unstable and the recommended treatment is prompt internal fixation. The compression stress fracture has a benign prognosis. Restriction of weight bearing for a few weeks i s usually sufficient to relieve symptoms. Prophylactic internal fixation should be considered only in cases of significant weakening of the trabecular bone mass.

STRESS FR ACTURE OF THE FEMOR AL N ECK IN TERN AL DER ANGEMEN T IN THE HIP Stress fractures of the femoral neck are not uncommon. The disorder presents in athletes,86 military recruits87,88 and in the elderly89 with specific symptoms and findings. However, the d iagnosis can be easily missed. Patients present with unremitting, localized hip and groin pain without a history of significant trauma or unusual increase in daily activity. As in the initial stages of aseptic necrosis of the hip, there is a discrepancy between the obvious symptoms (localized pain and limping) and the minimal clinical signs. There is a non­ capsular pattern with full and painless range of flexion and extension but considerable pain at the end of internal and external rotation of the hip. Resisted movements are painless.9o The initial radiographic features may prove negative. An early diagnosis of spontaneous stress fracture of the femoral neck may be made when the scintigraphic exami­ nation shows increased focal radionuclide uptake.91 MRI

Internal derangement in the hip is not uncommon but is frequently overlooked. It is caused by a loose body, a torn portion of the labrum or impingement of a small focus of synovitis. In all cases the plain radiographs are negative or show only some osteoarthrosis. Cyriax4 suggested that a small piece of exfoliated articular cartilage, secondary to trauma or osteoarthrosis, becomes loose in the joint. When the fragment lies inside the capsular fold, level with the femoral neck, it is harm­ less and painless but when it is pinched at the acetabular edge, sudden twinges result. During arthroscopy, Dorfmann and Boyer sometimes found a small focus of synovitis on the anterior and anteroinferior aspects of the femoral neck in patients with symptoms of internal derangement. They hypothesized that this was probably due to impingement of the capsule by the psoas muscle tendon.93

C HAPTER 68 - D I SO RDERS OF THE I N E RT STRUCTU RES 1 0 13

Recent arthroscopic studies suggest that most internal deraagement may be the result of impingement of acetabular labral tears.94 Anatomical studies have shown that the labrum is richly innervated with free nerve endings, capable of nociception. This may cause a direct painful response from the nipped flap.95 Most tears are radial flaps, located in the anterior section of the acetabu­ lum and are more tag-like than massive.96

SYMPTOMS The pathognomonic sensation in internal derangement of the hip is the presence of a 'twinge' - a sharp and severe pain in the groin or the trochanteric area. It appears sud­ denly and unexpectedly during ordinary walking or descending stairs. The patient feels a pain shooting down the thigh to the knee and the leg feels like it 'might let the patient down'. Sometimes the pain disappears immedi­ ately or the patient has to stand on the good leg for a while. This painful twinge may be repeated on each step, some 100 metres later or not at all for the first few weeks. If the patient has many twinges a day he will be severely disabled, because they happen at any moment without warning and nothing can be done to prevent them.

SIGNS There is a difference in signs between an impacted loose body in a normal joint and the presence of a loose fragment in an osteoarthrotic joint. Examination of a joint not complicated by osteoarthro­ sis shows a full range of movement, with some dis­ comfort at the end of one or two movements, as a rule external rotation and flexion. As these two movements are also painful in psoas bursitis (see later), the differen­ tial diagnosis will be supplied by the existence of twinges and the slightly different end-feel. Some authors report successful diagnosis of impingement lesions with the so­ called Thomas test.97 This involves flexion and external rotation of the hip, then allowing the extremity to abduct. The hip is then moved into extension, internal rotation and adduction. A positive test result is indicated by a palpable or audible click and the production of pain. The commonest occurrence of a loose body, however, is as a complication of osteoarthrosis. Unfortunately, these cases are often missed because the twinges men­ tioned by the patient are usually ignored, all attention being given to the radiograph. Examination shows not only the capsular pattern with the usual hard end-feel but one or two movements may have a softer end-feel and cause pain. Sometimes only the capsular pattern of osteoarthrosis is present, and then the diagnosis will rely entirely on the characteristic history of twinges. Current modalities for imaging the hip joint, including arthrography and magnetic resonance imaging, are poor

for directly identifying a l ab ral tear (sensitivity is between 13 and 24%).98

TREATMENT The ultimate proof of the existence of a loose body is the immediate and usually lasting improvement after a manipulative reduction, which means the fragment has been moved to a position within the joint where it no longer becomes ' nipped' on movement. Technique: reduction of a loose body - 1 . The manipula­

tion is a combination of three movements conducted simultaneously: a movement towards extension during strong traction, in combination with medial or lateral rotation. The patient lies supine on a low couch. An assistant presses on both anterior superior iliac spines in order to fix the pelvis firmly to the couch during the whole proce­ dure (Fig. 68.12). To prevent local pain a thick layer of foam may be placed between the hands and iliac crests. The pressure on the iliac spines should be directed downwards and cranially to withstand the force of the traction. The manipulator stands on the end of the couch, holding the patient's ankle. From this point, the proce­ dure depends on the direction of rotation required. Medial rotation. The contralateral hand encircles the heel. The other hand is placed at the distal side of the leg, level with the malleoli (Fig. 68.13). This position of the hands is vital in protecting the ligaments of the ankle when rotation is performed . The manipulator raises the outstretched leg to 70 or 80° and leans backwards, induc­ ing as much traction as possible. As soon as the muscles are felt to relax, the manipulator steps gradually off the couch, meanwhile rotating the leg with a jerk to full medial rotation and back to the neutral position as the leg is extended. This manoeuvre is repeated three or four times during extension. Lateral rotation. The ipsilateral hand is used to grasp the heel. The foot is held at a right angle and the other hand encircles the medial border of the foot (Fig. 68.14). The manipulator leans backwards after having lifted the patient's leg to about 70°. Again when the muscles relax a backward movement is made and then downwards, meanwhile rotating the leg laterally. At the end of the rotational movement, a sharp jerk is added and the leg is turned back into the neutral position. This rotational movement is performed three or four times as the leg is extended. As a rule, the manipulation in the most comfortable direction is done first. After each manoeuvre the joint is re-examined to find out whether there is an improve­ ment. The most effective rotation is then carried out several times during the same session.

1014 SECT I O N TWELVE - T H E H I P AND BUTTOC K

(b)

(a)

Reduction of a loose body in the hip joint - technique 1: start (a) and end (b) of the manipulation.

Figure 68.12

(c)

Attention should be given to two important technical points. •

•

The rotation must have the largest possible amplitude. Thus, starting at least from the neutral position, the leg has to be rotated until the end-feel is reached. It is then rotated back to the initial position, to restart the same procedure. Traction should not be lost during extension. Care should be taken to maintain strong traction throughout the whole manipulation until the joint is extended completely. Therefore, the manipulator keeps one foot on the couch, in order to maintain sufficient traction.

2. If the previous manipulation did not reduce the subluxated loose body, an alternative technique should then be tried, applying stronger traction and rotation which can be achieve,d by using the lower leg as a lever. The patient adopts a supine-lying position on a low couch. As in the previous manipulation, an assistant holds

Tech n ique: reduction of a loose body

Figure 68.13

Position of the hands during medial rotation.

-

C HAPT E R 68

Figure 68.14

-

DISORDERS OF T H E I N ERT ST RUCTU RES 101 5

Position of the hands during lateral rotation.

the pelvis down on the couch, putting all the body weight on the anterior superior iliac spines. The manipulator places the contralateral foot on the couch, just beyond the patient's buttock and puts the back of the patient's bent knee over the thigh. The contralateral hand holds the knee and the other hand grasps the ankle (Fig. 68.15). Considerable traction on the hip can now be achieved when the lower leg of the patient, used as a lever, is pushed down. This levers the buttock off the couch. In the meantime the assistant applies as much counter­ pressure as possible. At the moment the muscles are felt to relax, the femu r is rotated by means of the lever pro­ vided by the patient's leg. At the end of range, a quick rotational thrust is added. The direction of rotation can be chosen at random but usu ally the rotation found to be the most beneficial during the previous manipulation is done first. Resu lts. This manipulation can lead

to spectacular results. The patient no longer has the repeated twinges that make walking so d ifficult. This happy outcome can be attained in two-thirds of patients complaining of twinges at the hip. The osteoarthrosis itself, if present,

Warning

Because the leverage of both traction and rotation is considerable, the manipulation should never be performed in elderly people, for fear of fracture of the femoral neck.

Figure 68.15

Reduction of a loose body i n the hip jOint - technique 2.

will not be changed but it seldom causes more problems than some d iscomfort after a long walk. As a rule, two or three manipulation sessions will be su fficient. If no improvement is achieved by then, defeat must be conceded and the patient referred for arthroscopy.

PSOAS BURSITIS The psoas bursa is one of the largest bursae in the human body. 99 Located between the lesser trochan ter, the musculotendinous portion of the iliopsoas muscle and the anterior capsule of the hip joint, it can be up to 7 cm long and 4 cm wide.I OO As the bursa is derived from the second and third lumbar segments, pain is usually felt in the groin, ante­ rior thigh, knee and leg. It appears during walking and during specific movements, for example crossing the legs. IO} Untreated, the disorder can go on for years.

1016 SEC T I O N TWELVE - T H E H I P AND B UnOC K

The lesion is generally overlooked and the symptoms are usually blamed on the slight arthrosis visible on a radiograph rather than the (invisible) psoas bursa. 1 02 Clinical examination, however, shows a non-capsular pattern: lateral rotation is painful and the end-feel soft, and flexion is slightly painful at the end of range. Sometimes there is also pain at the end of extension or adduction. lo3 An accessory test is that passive adduction in flexion is the most painful movement because it squeezes the bursa. This test also provokes considerable stretching of sacroiliac ligaments and tissues in the bu ttock, so it is essential to ascertain that the reproduced pain is in the groin and is not some vague sensation of pulling in the buttock. Resisted movements are strong and painless. The bursa may be palpably enl a rged, as sometimes is the case in rheumatoid conditions. 1 0 1 , 1 04, 1 05 Differential diagnosis should be made from a loose body in the hip and early aseptic necrosis. In the former the patient complains of sudden twinges and in the latter there will often be a gross discrepancy between the func­ tional incapacity and the moderate signs. Ultrasonography is the best confirmatory diagnostic test. 1 °6 The diagnosis is also confirmed when a diagnostic infiltration with local anaesthetic is found to abolish the clinical features. This injection, eventually repeated once or twice, is very often also therapeutic. lo7 Tech nique: infi ltration. The patient adopts a half-lying position on the couch, keeping the legs out-stretched, which relaxes the tissues at the groin. Three landmarks are identi fied: the anterior superior spine of the ilium, the femoral artery and the greater tuberosity. A perpendicu­ lar line is d rawn from the anterior superior spine, and a horizontal line 5 cm under the tip of the greater tuberos­ ity. The needle is inserted at the crosspoint, which is well lateral to the inguinal vessels. A needle 7 cm long is fitted to a 50 ml syringe, filled with p rocaine 0.5%. The needle is inserted at the identified spot, and thrust in at a 45° medial and upwards direction (Fig. 68.16). At the same time the free hand is used to continuously palpate the femoral artery as a safeguard to avoid the inguinal vessels. If the tip of the needle hits bone, it lies near the junction of the femoral head and neck, where the infiltration is given, using the classical technique of withdrawals and reinsertions. If the needle pierces the capsule, it must be withdrawn somewhat until the fluid can be p laced without resistance. Results. The diagnostic infiltration often has a lasting therapeutic result, regardless of the duration of the symp­ toms. If necessary, the infiltration can be repeated once or twice, at weekly intervals. If no lasting relief is afforded, and the injection only acts temporarily, 50 mg of triam­ cinolone should be injected at the same place during the next attendance. l os

Figure 68.16

Infiltration of the psoas bursa.

H AEMORRH AGIC PSOAS BURSITIS As in haemorrhagic bursitis at the shoulder, this condi­ tion sometimes occurs in the elderly. The patient states that the hip was hurt during a sideways slip of the leg, which was immediately followed by extreme pain at the front of the thigh and knee. Spontaneous haemorrhage complicating a pigmented villonodular synovitis of the bursa has also been reported. 1 09 Examination shows a gross non-capsular pattern, with up to 90° limitation of flexion, gross limitation of lateral rotation and extension, but almost full range of medial rotation. n o Resisted movements are full range and pain­ less. Sometimes a tense and tender swelling can be palpated in the groin. Aspiration confirms the diagnosis and is also the required treatment.

C HAPTER 68

-

D I SORDERS OF T H E I N E RT STRUCTU RES 1017

GLUTEAL BURSITIS This is one of the most frequent causes of pseudoradicu­ lar pain in the limb. 1 1 1 The condition shows little ten­ dency to spontaneous cure. The patient is usually in the forties or fifties and complains of pain at the gluteal or tronchanteric area, spreading to the outer or posterior thigh and down to the calf muscles and outer malleo­ lus. 1l 2 Unlike the pain caused by a disc lesion, the symp­ toms are not related to sitting but only to walking, and going upstairs can be very painful. ll 3 The patient will not mention the twinges that are so typical of an impacted loose body but may state that a particular movement causes a sharp pain down to the leg. Sometimes the patient has nocturnal pain when lying on the affected side. Sitting with the painful leg crossed over the other also hurtS. 11 4 Coughing is painless. The combination of long-standing leg pain, related to hip movements and without symptoms typical of disc lesions suggests the existence of gluteal bursitis. 11 5 There is a full range of movement but some movements hurt in a non-capsular way at the end of range. The end­ feel is normal. Some resisted movements may be painful because they squeeze the tender bursa. A typical pattern is pain on passive external rotation and passive abduction and resisted external rotation or resisted abduction. 1 1 6 The cause of the gluteal pain during resisted hip movements is not a muscular lesion but compression of the bursa. Most of the affected bursae are located near the greater trochanter and between the gluteus maximus and gluteus medius (Fig. 68.17). Localization depends on the findings on palpation, although sometimes the approximate area can be deduced from the general examination: when full passive internal rotation together with resisted external rotation causes pain, the bursa at the insertion of the piri­ formis is affected; pain on passive abduction and passive flexion together with resisted abduction indicates that the bursa between the gluteus medius and gluteus maximus is at fault. ll 7 Caution is required in drawing conclusions from palpation. Because the gluteal region is an awkward area and the affected tissues lie deeply, tenderness can be elicited in a normal buttock if the pressure applied is considerable. It is therefore always wise to compare the unaffected side with the one affected. The diagnosis is settled by local anaesthesia. If, after infiltration, the movements known to hurt are tested again and are no longer painful, the right point has been found.us This diagnostic injection often has a lasting result; therefore the patient should attend after a week for re-examination. If there is considerable and lasting relief, the injection is repeated two or three times at weekly intervals. If there is no therapeutic result, 50 mg of triam­ cinolone is injected in the same place. This injection may also have to be repeated once or twice but this time at an interval of 2 weeks. l1 9 Sometimes an intractable case is

Figure 68.17

The gluteal bursae.

encountered; though the injections relieve the symptoms for 2 or 3 weeks, they subsequently recur; as operative exploration of the buttock is a very difficult procedure and rarely effects a cure, it is best to admit defeat and hope a spontaneous remission will take place. l 2O 1 . When the patient has evidence of a highly localized bursitis, the lateral approach is used (Fig. 68.18). The patient lies prone and the physician sits or stands at the affected side. A 7 cm needle is fitted to a syringe containing 50 rnl of procaine 0.5%. The tender area is localized and the needle inserted horizontally until it reaches the ilium. It is then withdrawn 1 or 2 cm and a large area is infiltrated using the classical technique, using withdrawals and reinsertions at different angles.

Technique: injection

-

2. When the bursitis is located at the upper or inner edge of the trochanter, this alternative tech­ nique must be used. The patient lies prone on a high couch but with the affected thigh hanging vertically downwards over the edge. In order to support the leg, a low support is placed under the bent knee. Slight adduction of the hip is preferable in order to make the inner portion of the trochanter more accessible. In this position, it is easy to palpate the upper part of the trochanter from above. The tender spot is identified. The needle is inserted from above and medially and thrust downwards until the tip touches bone. It is then slightly withdrawn and the affected area is infiltrated all over with 50 rnl of procaine 0.5% . Technique: injection

-

TROCHAN TERIC BURSITIS The trochanteric bursa (Fig. 68.19) lies at the lateral aspect of the trochanter tip, between the iliotibial tract and the bone, level with the insertion of the gluteus medius and

1018 S ECTION TWELVE - T H E H I P AND BUnOC K

during walking or running. Walking upstairs is most painfu l . Occasionally, lying on the affected side is also painful and can disturb sleep. Clinical examination shows a non-capsular pattern: external rotation is very painful and sometimes limited, with a soft end-feel; however, when external rotation is retested with the hip and the knee extended, there is no pain at all. Passive abduction may also be painful. The resisted movements are painless, except sometimes abduction. 1 24 Palpation reveals a tender area at the lateral aspect of the trochanter. Treatment consists of infiltration with procaine. i nfiltra t i o n . The patient lies prone, the tender spot is identified and the needle (7 cm long) inserted locally. It pierces the thick structure of the iliotibial tract before hitting bone. The needle is partly withdrawn and the la rge a rea between bone and tendinous tissue is infiltrated in the classical way, first with 20-30 ml of procaine 0.5% to prove the diagnosis. If no lasting benefit results, 50 mg of triamcinolone is substituted. A condition similar to acute subdeltoid bursitis can occur in the trochanteric bursa. The patient complains of serious and rapidly increasing pain at the trochanteric area. Clinical examination shows a non-capsular pattern, with limited external rotation and an extremely tender trochanteric area. The radiograph often reveals calcification. 1 25 Treatment consists of local infiltration of the whole bursal wall with triamcinolone which, as in acute subdeltoid bursitis, affords immediate and lasting relief. Tec h n i q u e:

(a)

(b) Figure 68.18

Infiltration of a gluteal bursa by technique 1 (a) and technique 2 (b).

the tensor fasciae latae. It can become inflamed after a local blow, 1 2 1 although trochanteric bursitis may also result from overuse in long-distance runners.122 The inci­ dence of trochanteric bursitis peaks between the fourth and sixth decades of life and is more common in women (male:female ratio 1 : 1 0). 1 23 The symptoms are increasing pain at the trochanteric area, spreading down to the lateral aspect of the knee,

Figure 68.19

Location of the trochanteric bursa.

CHAPTER 68 - DISORDERS OF T H E I N E RT STR U CTURES 1019

ISCHIAL BURSITIS The ischial bursa is painfully squeezed between the ischial tuberosity and the hard surface of a chair during sitting. Because the condition is not very common, it will not be the first thing thought of in the presence of ischial pain. When a patient complains of pain at the buttock, coming on during sitting and easing as soon as he is upright, the first condition to come to mind is a disc lesion at a low lumbar level. However, in ischial bursitis the patient experiences pain as soon as his buttocks touch the chair, whereas in a discodural lesion the pain gradually increases during sitting or the moment the patient comes upright again. If the routine lumbal� sacroiliac and hip examinations are negative, this condition should be considered. The only clinical finding is local tenderness at the ischial tuberosity. The diagnosis can be confirmed by introducing some local anaesthetic but the injection seldom gives lasting relief. Treatment consists of one or two infiltrations with 20 mg of triamcinolone and avoidance of further compression.

PSYCHOGENIC PAIN Sometimes pain at the hip or in the buttock does not have an organic basis. It is possible for a psychogenic pain to make the hip almost functionless. The label 'hysteria' is

given to the patient who has a firm belief in the reality of the symptoms. If the patient is faking pain and disability, the term ' malingerer' is used . Psychogenic pain affecting the hip has, just like the other and more organic lesions at the hip joint, a specific and typical pattern. The patient walks in with a remark­ able gait: the hip is fixed in internal rotation, which is completely the reverse of the fixation in external rotation of a capsular pattern. Suspicion arises immediately when this type of gait is seen and the patient must be subjected to a thorough examination from the lumbar spine to the toes. A good routine is to start with the examination of movements not relevant to the hip - ankle and foot. Only few patients with psychogenic pain will be able to resist the clear invitation to allege hip pain when several tests of, say, the foot are performed. When, finally, the hip is examined other and multiple inconsistencies will be revealed: passive hip flexion is limited to 90°, but rotations are of full range, or there is complete weakness of the psoas muscle in the supine-lying position although the patient can step off the couch without elevating the limb manually. If a movement is found to be grossly limited, sustained pressure in the direction of limitation will, in the end, afford a full range of movement with a normal end-feel, proving that the limitation was voluntary. The differential diagnosis of non-capsular patterns of the hip is summarized in Table 68.3.

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3. Goldenberg DL, Brandt KD, Cohen AS et al. Treatment of septic arthritis. Comparison of needle aspiration and surgery as initial modes of joint drainage. Arthritis Rheum 1975;18:83. 4. Cyriax JH. Textbook of Orthopaedic Medicine, Vol I, 8th edn. Bailliere Tindall, London, 1982. 5. Murray RO. The aetiology of primary osteoarthrosis of the hip. Br J RadioI 1965;38:81 0-824. 6. Solomon L. Patterns of osteoarthrosis of the hip. J Bone Joint Surg 1 976;58B(2) : 1 76-183. 7. Harris WHo Etiology of osteoarthritis of the hip. Ciin Orthop Rei Res 1986;213:20-33.

tissue

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1020 SECTION TWELVE - T H E H I P A N D B UTTOCK

Table 65.3 Differential diagnosis of non-capsular patterns of the hip Disorder

Diagnosis

Treatment

Majors disorders (All have a positive buttock sign)

Septic bursitis

Ischiorectal abscess

Fractured sacrum

Neoplasm at upper femur

Osteomyelitis of ilium

Osteomyelitis of femur Septic sacroiliac arthritis

Intramuscular injection? Raised temperature Localized swelling Sitting is not possible Raised temperature Rectal examination Bilateral buttock sign Positive sacroiliac tests Radiograph Increasing! gross disability Painful and weak resisted flexion Radiograph! bone scan Increasing pain Normal rotations Radiograph! bone scan Discrepancy between symtoms and signs Radiograph! bone scan Temperature Positive sacroiliac tests Bone scan

Antibiotics

Surgery

Rest

Antibiotics

Antibiotics Antibiotics

Minor disorders

Loose body Loose body complicating osteoarthritis

Aseptic necrosis of the hip

Psoas bursitis

Haemorrhagic psoas bursitis

Gluteal bursitis

Trochanteric bursitis

Ischial bursitis

Psychogenic pain

Twinges Often pain at the end of flexion and lateral rotation Twinges Painless capsular pattern Some painful movements in a non-capsular way Corticosteroid treatment or excessive alcohol intake? Sudden pain in the groin!nocturnal pain! pain during coughing, sneezing Discrepancy between symptoms and signs Early stages: Slight noncapsular pattern! pain during axial compression Diagnosis by bone scan! MRI or functional examination of bone Later: Gross osteoarthrosis!radiological evidence Pain at the anterior aspect of thigh Full range of non-capsular way Painless resisted movements Elderly patient! blow or fall Sudden pain in groin and thigh Limitation of flexion to 90° Echography Pain at posterolateral aspect of buttock and thigh Full range with some movements painful at the end of range Some resisted movements hurting Local tenderness Trochanteric and lateral thigh pain Passive external rotation painful and limited Local tenderness Localized pain on sitting, immediately relieved when standing up Completely negative examination of lumbar spine, and sacroiliac and hip joint Local tenderness Limping in internal rotation Multiple inconsistencies

Manipulation Manipulation

Early diagnosis essential

Early stage: core decompression

Later: osteotomy or hip arthroplasty Infiltration with procaine or triamcinolone Aspiration

Infiltration with procaine or triamcinolone

Infiltration with procaine or triamcinolone Infiltration with triamcinolone

CHAPTER 6 8 - D I S O R D E R S OF TH E I N ERT STRUCTU RES 1021

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Disorders of the contractile structures

CHAPTER CONTENTS ,

Resisted flexion Pain 1023

1023

Pain and weakness 1025 Painless weakness 1025 Resisted extension Pain 1025

Painless weakness

1025 1026

Resisted adduction Pain 1026

1026

Resisted abduction Pain 1028

1028

Pain in the buttock usually results from a lesion of the lumbar spine, the hip joint or the sacroiliac joint.

Pain and weakness 1029 Painless weakness 1029

Muscular lesions are very uncommon. Even if resisted movements elicit pain in the buttock, gluteal bursitis is

Resisted medial rotation Pain 1029

1029

Resisted lateral rotation Pain 1029

1029

more likely to be the cause, especially if one or more passive movements also elicit the pain. Pain in the groin may also result from a lesion of the lumbar spine, the hip joint or uncommonly the sacroiliac

Resisted extension of the knee Pain 1029

1029

Pain and weakness 1030 Painless weakness 1030 Resisted flexion of the knee

Pain 1030 Painless weakness

1031

joint. However, pain frequently results from a tendinous or muscular lesion; then resisted movements provoke the pain. These conditions must be differentiated from a number of intra-abdominal pathological conditions, such

1030

as appendicitis, gynaecological disorders and inguinal or femoral hernia.1 The list of causes that can result in groin pain is, however, extensive and is discussed in a separate chapter (Ch.

70).

RESISTED FLEXION This test primarily examines the psoas muscle. However, a strain or weakness may be obscured because of active contraction of other synergistic muscles such as the rectus femoris, sartorius, tensor fasciae latae and some of the adductors.

PAIN If resisted flexion is strongly opposed and is painful, the following conditions should be considered. •

Tendinitis of the: - psoas - rectus femoris - sartorius

• Obturator hernia.

Tendinitis of the psoas Tendinitis of the psoas is rare.2-6 It is always located in the femoral triangle. The lesion is therefore accessible to the palpating finger and can be identified just below the inguinal ligament between the pulsating femoral artery medially and the sartorius muscle laterally. In bilateral 1023

1024 SECTION TWELVE - THE HIP AND BUTTOCK

and used as a fulcrum (Fig.

69.1).

The transverse move­

ment of friction is imparted by alternating flexion and extension of the wrist and elbow together with some adduction-abduction movement at the shoulder. In acute cases, treatment can be started the day after onset. However, really deep friction should not take more than

1 minute and is repeated daily, with a gradual increase in the treatment time. In the second week, treatment is per­ formed on alternate days. It is then carried out deeply all the time and for about expected in

2 weeks.

15 minutes.

A good result is to be

Chronic strain requires

15 minutes

of friction, two or three times weekly, depending on the result of each session. A lesion that has continued for years will respond to six to eight sessions of deep trans­ verse friction. Treatment is very painful but, in our opinion, there is no alternative. To find the exact point is not easy and requires a good understanding of local topographical anatomy.

Tendinitis of the rectus femoris The lesion is located just below the inferior iliac spine (in the body of the tendon). Alternatively, the tender point lies at the proximal part of the muscle belly.8 In both instances, resisted flexion of the hip provokes slight dis­ comfort only, whereas resisted extension of the knee with the patient prone and the hip extended, evokes the pain more readily. This is the outcome of the constant-length phenomenon of this muscle, which crosses two joints. Treatment is deep transverse friction. The same stress that causes a muscle strain in an adult can cause an avulsion fracture in an adolescent. The frac­ ture occurs at the apophysis, which becomes separated from the underlying bone. The fracture is never widely

Inguinal ligament

Psoas tendon

Femoral nerve Figure 69.1

Deep transverse friction to the psoas tendon.

displaced because of the surrounding thick periosteum.9 Most patients can be treated non-operatively with

6-10

weeks of relative rest.

Lesions of the sartorius Lesions of the sartorius muscle are rare and typically occur in soccer players. Resisted flexion of the hip is

tenderness, palpation may be misleading but the induc­ tion of local anaesthesia is then diagnostic.

Treatment. Deep transverse friction seems to be the only effective treatment?

painful, especially if some external rotation with a flexed knee is added to the movement. Palpation reveals the localization of the lesion which is either at the tenoperi­ osteal insertion or

1

or

2 cm

more distal in the tendon.

Treatment consists either of deep transverse friction or, if

Technique.

The patient sits upright on the couch with the

the lesion is tenoperiosteal, of one or two infiltrations

hip joint in

90° of flexion and the knees

with triamcinolone.

extended - with

the hip extended in the supine position, it is not possible for the finger to penetrate deeply enough because of the

In young athletes (aged

15-18)

who are skeletally

immature, an avulsion fracture of the anterior superior

taut overlying tissues. The therapist sits at the patient's

spine of the ilium is more common than a muscle strain

side facing the thigh, with the index and middle fingers

or tendinitis (see Pain and weakness, p.

1025).

placed at the painful tendon in the femoral triangle, just lateral to the femoral artery and medial to the sartorius

Obturator hernia

muscle. The thumb is placed at the outer part of the hip

This lesion is principally found in old, thin women, often

CHAPTER 69

- DISORDERS OF THE CONTRACTILE STRUCTURES

1025

with a history of recent weight loss, obstipation or

groin pain during walking. Clinical examination shows a

chronic respiratory disease. The patient complains of

normal range of passive movement but resisted flexion is

numbness or pins and needles which may eventually cul­

weak and provokes pain. This should be reason enough

minate in intense pain at the anterior and medial side of

to obtain a radiograph, which shows separation at the

the thigh down to the knee. These symptoms result from

lesser trochanter. In most instances

compression of the obturator nerve at the obturator

bed in a half-sitting position will be enough for recovery

foramen by a prolapsed fold of peritoneum. Absence of

to take place. From the moment the patient can walk

the adductor reflex test is a sign of involvement of motor

without pain, standing is allowed.

2 or 3

weeks' rest in

conduction of the same nerve.IO Pain on resisted hip

It is well to remember that avulsion fractures of the

flexion is explained by pressure by the psoas on the

lesser trochanter in adults are almost always the result of

hernia. The differential diagnosis can be made when

metastatic bone disease.14

resisted flexion becomes negative after the patient has been in the Trendelenburg position for upwards of

2 minutes; this effect of gravity is to reduce the prolapse which is no longer painfully squeezed during active con­ traction of the psoas.

PAIN AND WEAKNESS Pain and weakness on resisted flexion can be present in the following conditions.

Abdominal neoplasm Infiltration of an abdominal neoplasm into the psoas muscle is another, although rare, cause of considerable weakness of hip flexion and pain in the iliac fossa.

Metastasis in the upper femur Weakness and pain in the thigh will be accompanied by marked articular signs in the hip joint and probably a 'buttock sign' (p.

1007).

Avulsion fracture of the anterior superior iliac spine

PAINLESS WEAKNESS

Avulsion fractures occur more commonly in skeletally

Lumbar root palsy

immature athletes than in adults because young patients' tendons are stronger than their cartilaginous growth centres. The same stress that causes a sartorius tendinitis in an adult can cause an avulsion fracture of the anterior superior iliac spine in an adolescent. The fracture does not become widely displaced because of the surrounding thick periosteum. The lesion is well known in young sprinters, soccer players and jumpers. While running, the subject feels a sudden painful click in the groin and upper part of the thigh. From that moment further activity is impossible and the athlete leaves the track with a limp; even walking is painfuJ. ll,12 On examination, resisted flexion and resisted lateral rotation of the hip and resisted flexion of the knee are all painful. Palpation reveals ecchymosis and palpable tenderness at the anterior superior iliac spine where the sartorius muscle is attached. Radiography shows slight separation of the iliac spine. Spontaneous recovery is the rule and takes

2-3 weeks. During that time, however, it is

Painless weakness is a major sign in the rare condition of a second lumbar root palsy in a second lumbar disc pro­ trusion. In a third lumbar root palsy, it is less obvious and is also accompanied by weakness of the quadriceps.

Psychoneurosis Weakness of hip flexion is also a common finding in psy­ choneurotic patients complaining of pain in the lower back or thigh. The diagnosis can then only be made if this sign is accompanied by other inconsistencies in the history and clinical examination (see Section

16).

Serious non-specific disorder Because discoradicular conflicts at the second lumbar level almost never occur, painless weakness of hip flexion should always arouse suspicion of a serious non-specific disorder (see p.

852)

such as inflammatory disease or

neoplasm.

not necessary for the patient to rest completely in bed. Movement should be permitted to the limits of pain but return to sports activity should be allowed only from the time that clinical examination becomes fully negative.

Avulsion fracture at the apophysis of the lesser trochanter

RESISTED EXTENSION PAIN Pain on resisted extension has hardly ever anything to do with the gluteus maximus, in which a lesion occurs only

This may be seen in schoolboys and young athletes.

after a direct blow and recovers spontaneously within a

There is no history of sudden onset because the lesion appears to be caused by overuse. 1 3 The complaint is of

few days. However, a contracting gluteus maxim us may compress an inflamed gluteal bursa and thus indirectly

1026 SECTION TWELVE - THE HIP AND BUnOCK

provoke pain in an inert structure (transmitted stress).

players.21, 22 Lastly, it is a well-known lesion ('rider 's

Pain after prolonged contraction of the gluteal muscles

sprain') in horse sports.

indicates a particular form of intermittent claudication. If there is hamstring tendinitis or sprain of the sacro­ tuberous ligament, resisted flexion of the knee is then also painful (see Resisted flexion of the knee, p.

1029).

Inflamed gluteal bursa An inflamed gluteal bursa is a much more frequent cause of pain on resisted extension, especially if one or more passive movements also elicit the pain (see Gluteal bursi­ tis, p.

1017).

Intermittent claudication

Pain is provoked mainly on resisted adduction but full passive abduction may also hurt because it stretches the injured muscle fibres. Imaging procedures are usually unnecessary. However, ultrasound, although operator dependent, can confirm the diagnosis.23 There are three possible locations of the lesion: • tenoperiosteal • musculotendinous • proximal extent of the muscle belly.

The exact site of the lesion is found on palpation and is more often musculotendinous, a few centimetres below

Another possibility in gluteal pain produced by resisted

the pubic bone, than tenoperiosteal. Exceptionally the

extension is intermittent claudication in the buttock,

uppermost part of the muscle belly itself is at fault.

because of obstruction of the common or internal iliac artery. Here the routine clinical examination is com­ pletely negative but the history is classic and pain is reproduced by maintained contraction of the muscles for

2 or more minutes. These features are pathognomonic for the arterial disorder.

Differential diagnosis Although pain in the groin during resisted adduction usually indicates a lesion of the adductor longus, this is not always so. Strong adduction indirectly pulls on bones and ligaments of the pelvic ring and, if a pathological condition is present there, the transmitted stress causes

PAINLESS WEAKNESS Painless weakness on resisted extension is indicative of a first sacral root palsy. In the exceptional instance of an extensive paralysis of the gluteus maximus, an 'extensor ' or 'gluteus maximus' lurch may be found; the patient has to thrust the trunk posteriorly to maintain hip extension during walking.

pain. A detailed discussion of pubic lesions can be found in the chapter on groin pain (eh.

70). The following three

lesions are the most important.

Fracture or neoplasm in the pubic bone. Palpation of the adductor muscles reveals nothing, whereas a radiograph establishes the presence of a lesion.24

Osteitis pubis (periostitis at the pubic symphysis), This occurs in soccer players and race walkers as the result of repeated shearing of the pubic bones at the symphysis.25

RESISTED ADDUCTION

Palpation of the adductor muscles reveals nothing but the pubic symphysis is very tender.26

PAIN Adductor longus Pain on resisted adduction and localized to the groin usually points to the adductors. While the adductor longus, adductor magnus, adductor brevis and pectineal muscles are all adductors of the hip, of these the adduc­ tor longus is most often injured in sports.2,1 5-18 The mechanism of an acute injury is usually that of a sharp cutting movement, which causes a forceful eccen­ tric contraction of the muscle. Acute lesions are common in soccer players and often result from a sudden slip on a

lesions of the sacroiliac joint. Sacroiliitis or sacroiliac strain may also be responsible for painful resisted adduc­ tion at the hip, caused by distraction of the ilium from the sacrum. Because the pain is felt in the buttock, attention is immediately directed to the sacroiliac joint.

Treatment Deep transverse friction is usually effective in tendinous or musculotendinous lesions, whereas tenoperiosteal lesions can be treated by friction or infiltration with tri­ amcinolone. Muscular lesions react well to infiltration

muddy field, which stretches or tears the muscle or tendon fibres. 1 9 Alternatively the lesion starts as an

with local anaesthetics or to deep friction.

overuse phenomenon, such as repetitive ab- and adduc­

rest to avoid further strain on the involved structure. In

tion movements of the leg in the skating stride or in defence movements in basketball. It also occurs in high jumping athletes and ballet dancers20 and has been described in middle-aged cricket bowlers and ice-hockey

Treatment should always be associated with relative persistent cases, surgery is indicated.27,28 The proceg ure used includes division of the adductor longus tendon close to its origin from the pubis. The results seem to be good and most athletes can return to sports after

8 weeks.

CHAPTER 69

Technique: deep friction.

-

DISORDERS OF THE CONTRACTILE STRUCTURES 1027

The patient adopts a half-lying

posifion on the couch with the affected thigh in slight abduction and lateral rotation. The therapist sits level with the patient's knees and facing the body. In musculo­ tendinous lesions, the affected area is grasped between the thumb and index and middle fingers (Fig. 69.2). Friction is imparted by a drawing movement of the hand medially. At the end of range, the affected structures have passed beyond the fingers and the movement is then repeated. In tenoperiosteal lesions, the index finger, reinforced by the middle finger, is placed on the pubic bone (Fig.

69.3) and friction is done by alternately flexing and

extending the elbow, together with a slight adduction and abduction movement at the shoulder. In the acute stage, treatment should be brief and not vigorous but can be repeated daily for the first few days and on alternate days thereafter. Long-standing scars that may have formed in the absence of treatment at an early stage are given truly

Pubis

Gracilis

Femoral artery

Adductor longus

Figure 69.3 Deep transverse friction to the adductor longus muscle (tenoperiosteal junction).

deep friction for as long as possible, say

20 minutes, twice

a week. The results are good in all recent and most chronic cases. Exertion is best avoided until the patient is symptom free.

Technique: injection.

The patient adopts a half-lying

position on a high couch and puts the thigh into slight abduction. The affected spot is identified at the teno­ periosteal junction on the pubic bone. A

2 ml syringe is 4 cm needle.

filled with triamcinolone and fitted with a

The needle is inserted just distal from the palpating finger on the periosteum and directed upwards until it strikes the bone (Fig.

69.4).

By a series of small with­

drawals and reinsertions at slightly different points, the

Adductor longus Figure 69.2 Deep transverse friction to the adductor longus muscle (musculotendinous junction).

whole area is infiltrated. Meanwhile, the palpating finger is kept on the spot, to detect where the tiny bulges of fluid appear.

1028 SECTION TWELVE - THE HIP AND BUnOCK

be painless, especially in the prone-lying position with the hip extended. When a sprain of the tensor is sus­ pected, resisted abduction should be performed in the side-lying position, with the uppermost hip (test limb) flexed to

45°.

Alternatively, an accessory test is per­

formed: in a standing position, the patient crosses the painful leg behind the other and bends sideways towards the painless side, taking all the body weight on the affected limb. Pain - sometimes severe - indicates a lesion of the tensor fasciae latae. Palpation then reveals a painful spot between the iliac crest and the greater trochanter.

Treatment. Treatment of a local lesion of the tensor fasciae latae is by deep transverse friction. Figure 69.4

Infiltration of the adductor longus (tenoperiosteal junction).

Technique.

The patient lies on the painless side. The

upper leg rests on the couch in an extended and slightly adducted position to stretch the iliotibial tract. The lower leg is flexed to about Another injection may be required when the patient is seen

2 weeks after injection if the resisted adduction test

remains positive.

45° to stabilize the pelvis.

The ther­

apist stands level with the hip and dorsal to the patient. The thumbs are placed on top of each other at the affected area with the fingers opposite the thumbs for counter­ pressure. Friction is imparted by moving the thumbs for­ wards over the iliotibial tract in a transverse direction (Fig.

RESISTED ABDUCTION

69.5).

At the same time, the elbows are slightly

extended together with a flexion movement at the shoul­ ders. Friction is continued for

PAIN

20 minutes and is repeated

twice a week. Even in long-standing and neglected cases,

Lesions of the hip abductors are rare. The diagnosis is often difficult because pain on resisted abduction of the hip is often caused by transmitted stress on inflamed bursae (trochanter and gluteal) or strained sacroiliac

it will take no more than six to eight sessions to get a satisfactory result.

Sprain of the iliotibial tract

ligaments.

This lesion is often described as the 'lateral snapping hip

Glutei medius and minimus muscles

band over the posterior part of the greater trochanter and

syndrome'. It is caused by the slipping of the iliotibial

Muscular lesions seem not to occur. Local pain during resisted abduction is far more likely caused by the com­ pression of an underlying inflamed bursa which takes place during contraction of the gluteal muscles.29 If passive abduction is also painful, bursitis is almost a cer­ tainty and results from compression of the bursa between the greater trochanter and the ilium (p.

1017).

Lesion of the tensor fasciae latae This muscular overuse lesion may occur in dancers and athletes. It is often caused by repetitive increased tension on the iliotibial band which results from pelvic tilt or certain activities such as habitual running on the sides of the road ('downside leg'). Localized pain is felt between pelvic crest and trochanter. The signs are characteristic: lumbar examination reveals pain on side flexion of the trunk towards the painless side, although the other lumbar movements are free. Passive and resisted move­ ments of the hip are normal. Resisted abduction may also

is frequent in runners, dancers and basketball players.30,31 In addition to the audible snapping phenomenon, the syndrome is characterized by pain in the region of the greater trochanter which radiates to the buttocks or thighs. The painful snapping can be observed by placing the palm of the hand on the trochanteric area during walking. Signs on examination of the hip may be identi­ cal to those of an inflamed bursa underlying the iliotibial tract (see p.

1018).

The non-operative treatment of choice is infiltration with triamcinolone. In refractory circumstances, surgical treatment is indicated. The procedure usually consists of excising an ellipsoid-shaped portion of the band overlying the greater trochanter.32

Sacroiliac joint

MacNab33 also points to the sacroiliac joint as a possible source of the pain. When the gluteus medius contracts to abduct the hip, it pulls the ilium away from the sacrum. In

CHAPTER 69

-

DISORDERS OF THE CONTRACTILE STRUCTURES 1029

placing the centre of gravity over the hip joint, the patient forces a lurch towards the involved side. Such a move­ ment is called an 'abductor ' or a 'gluteus medius' lurch. In slight examples, only a Trendelenburg gait is found characteristic dipping of the pelvis towards the leg that is off the ground.

RESISTED MEDIAL ROTATION PAIN Pain produced during this resisted movement is rare and usually attributable to an inflamed gluteal bursa. The muscles (the gluteus medius, the anterior fibres of minimus and the tensor fasciae latae) are involved only following a direct blow that causes bruising.

RESISTED LATERAL ROTATION PAIN When pain is produced, the quadratus femoris, gemelli and piriformis are first suspected of containing the Figure 69.5

Deep friction to a lesion of the transfasiae latae.

lesion35 but, except in a direct injury, they are seldom affected. Pain during resisted lateral rotation of the hip is most often the result of transmitted stress of the contract­ ing muscles acting on an inflamed gluteal or trochanteric

the absence of hip joint disease, pain experienced over the

bursa (see Gluteal bursitis, p.

1017).

sacroiliac joint on resisted abduction of the leg is then highly suggestive of a lesion of the sacroiliac joint (see p.953).

RESISTED EXTENSION OF THE KNEE PAIN

PAIN AND WEAKNESS

Tendinitis of the rectus femoris presents as pain felt in

12% of all groin injuries.2

In adolescents, painful weakness of abduction is indica­

the groin. It has been found in

tive of an avulsion fracture of the greater trochanter but

It is usually an overuse phenomenon that occurs as a

iliac apophysitis can be another possibility. It develops

result of prolonged, repetitive strengthening exercise or

in young long-distance runners as the result of repeated

intensive goal-shooting training in soccer.36 Pain is pro­

contractions of the gluteus medius and tensor fasciae

voked more on resisted extension of the knee than on

latae on an immature iliac apophysis.34

resisted flexion of the hip, particularly when the patient lies prone with the hip extended. This finding has

PAINLESS WEAKNESS

already

been mentioned and is the result of the

constant-length phenomenon.

Painless weakness usually has a neurological cause -

Pain is also felt on full passive flexion of the hip and

weakness of the gluteus medius in a fifth lumbar root

even more in a combined movement of flexion and

palsy. It is also a common finding in disorders of the

adduction, when the tender part is pinched between the

hip joint and femoral neck and leads to a raised greater

upper femur and the anterior spine of the ilium.37

trochanter - protrusion of the acetabulum, epiphysioly­

Additionally, full passive rotation of the hip, done with

sis, congenital dysplasia and malunion after a fracture of

the hip and knee held in 90° of flexion, can sometimes

the femoral neck. In these instances, resisted abduction is

cause enough localized stretch to be painful.

weak and the pelvic-trochanteric muscles are ineffective in stabilizing the pelvis on the leg during walking. In

Lesions of the muscle bellies of the quadriceps are discussed in the chapter on the knee (eh.

78).

1030 SECTION TWELVE - THE HIP AND BUTTOCK

is usually reached in six to eight sessions. During this

Differential diagnosis Tendinitis of the rectus femoris should be differentiated from lesions of the second and third lumbar roots, usually the result of a disc lesion. Pain is reported over the anterior aspect of the thigh. Knee flexion with the patient in a prone-lying position may provoke the pain. However, testing the muscle for strength is painless, although there may be some weakness. When there is doubt, an epidural local anaesthetic can be given and confirms the diagnosis.

period, all activities that risk aggravation should be avoided.

Technique: infiltration.

The patient adopts a half-lying

position on a high couch. The affected spot is identified at the tenoperiosteal junction in the triangle between the muscle bellies of sartorius and tensor fasciae latae. A 2 ml syringe is filled with triamcinolone and fitted with a 4 cm needle. The needle is inserted just distal from the palpat­ ing finger on the periosteum and directed upwards until it strikes the bone. By a series of small withdrawals and

Treatment Deep transverse friction of the tendon or infiltration with triamcinolone are both effective.

Technique: deep friction. The patient sits on a couch, with the hip joint in flexion, in order to make it possible for the palpating fingers to reach the overlying tissues. The ther­ apist sits at the patient's side facing the thigh. The painful tendon is found about

8 cm

below the anterior superior

iliac spine and in line with it, bordered by the sartorius muscle medially and the tensor fasciae latae laterally. Two or three fingers are placed just medial to the tendon, using the thumb at the outer side of the thigh for counterpressure (Fig.

69.6).

Friction is imparted by repetitively pulling the fingers over the tendon in a transverse direction. During this movement, the wrist is extended and the shoulder adducted. In acute cases, treatment is started the day

reinsertions at slightly different points, the whole area is infiltrated. Meanwhile, the palpating finger is kept on the spot, to ascertain where the tiny bulges of fluid appear. Another injection may be required if the resisted adduc­ tion test remains positive when the patient is seen

2 weeks after injection. PAIN AND WEAKNESS This characterizes a partial muscle rupture (see Ch.

18).

PAINLESS WEAKNESS Painless weakness of the quadriceps is present in third lumbar nerve root compression (see p.

760). If

weakness

is bilateral, myopathy or myositis should be suspected.

after onset. At this time, deep friction will not take more than

1 minute and is repeated daily, with a slow increase

in duration. During the second week, treatment is undertaken on alternate days. In chronic examples treat­ ment takes about

20

minutes, twice a week. Recovery

RESISTED FLEXION OF THE KNEE PAIN Painful resisted flexion of the knee implicates the ham­ strings (biceps femoris, semitendinosus and semi­ membranosus).

Lesions

of

the

muscle

bellies

of

the hamstrings are discussed in the chapter on the knee (Ch.

78).

Tendinous and tenoperiosteal lesions also

occur, cause pain in the gluteal area and posterior aspect of the thigh and are generally referred to as the 'hamstrings syndrome'.38

Hamstrings syndrome The lesion is common in hurdlers and ballet dancers and is also found in all athletes who engage in rapid acceler­ ation and short intense sprinting such as baseball, tennis and soccer players.39 The cause of a hamstring strain is not fully understood but most authors today agree that the basic causative reason for its development is the muscle strength imbalance between the hamstrings muscle group and the quadriceps femoris muscle.4o Figure 69.6

Deep friction to the rectus femoris.

Clinical features of the hamstrings syndrome include

CHAPTER 69

-

DISORD,ERS OF THE CONTRACTILE STRUCTURES 1031

pain in the lower gluteal area which radiates down the

shoulder and a slight flexion-extension movement at the

posterior thigh to the popliteal area. The pain typically

wrist. The thumb supplies counterpressure and acts as a

increases during performances that stress the hamstring

fulcrum at the outer aspect of the thigh (Fig.

muscles (sprinting or hurdling). Another characteristic

Treatment is given for

20

69.7).

minutes, two or three times a

complaint is pain felt while sitting. Driving a car typically

week. Recent onset cases respond sufficiently in about

provokes the pain because of local pressure on the lesion

weeks. In chronic cases,

and the increased tension of the hamstring muscles in

response, therefore infiltration with steroid suspension is

that position.

the preferred treatment.

Clinical examination shows painful resisted flexion of the knee and resisted extension of the hip. Straight leg raising is of full range but quite painful at the extreme of range. A common clinical test that may induce the pain is the 'shoe wiping test' of Pecina:41 it consists of having the patient imitate movements typically used when wiping shoes on a doormat; the hamstrings are stretched and at the same time are contracting which causes the typical pain. Palpation reveals tenderness either in the tendon or at the tenoperiosteal insertion. The tendons are usually affected at the upper

5 cm

of their extent. In tenoperi­

osteal lesions, the sprain lies at the tuberosity of the ischium.

Technique: infiltration.

2 months may be required

2

for a

Unless the hip is slightly flexed,

the origin of the hamstrings at the ischium remains covered by the gluteus maximus. In order to render the insertion palpable, the patient must adopt a prone posi­ tion, the pelvis well supported on a high cushion. The origin of the hamstrings is then palpable just distal to the lower gluteal border. The physician stands next to the patient's hip and pal­ pates for the tender spot. A

2 ml syringe is filled with tri­ 5 cm needle. The needle is

amcinolone and fitted with a

inserted well distally and the tip is moved upwards until it strikes bone. By a series of small withdrawals and reinsertions at slightly different points, the whole area is infiltrated. Another injection may be required if the

Differential diagnosis

resisted flexion test remains positive when the patient is

First and second sacral root lesions. Tendinitis should be

seen

2 weeks

after injection.

differentiated from these lesions which are usually the result of disc protrusion at the fifth lumbar level. Pain may be reported in the thigh and there is probably also pain at the end of lumbar flexion or straight leg raising but testing the muscle for strength is painless. Local ten­ derness is also absent. When there is doubt epidural local anaesthetic is given.

PAINLESS WEAKNESS Painless weakness of knee flexion is typical of a full root syndrome at

51 and/or 52.

Disorders of the contractile structures of the hip and buttock are summarized in Table

69.1.

Ischial bursitis. Resisted movements are also painless in ischial bursitis or 'weaver 's bottom'. Local tenderness is then the only clinical finding and points to involvement of the bursa (see p.

1019).

Treatment In tendinous lesions, the patient is treated with deep transverse friction or infiltration with triamcinolone. Persistent lesions can be treated surgically.38

Technique: deep friction.

The patient adopts a side-lying

position or a supine one with hip and knee flexed to

90°

and a chair supporting the lower leg. This position is nec­ essary to move the gluteus maximus upwards, bringing the tuberosity of the ischium directly within reach. It also keeps the tendon fairly stretched, otherwise it lies too lax and deep to be properly subject to friction. The therapist stands on the ipsilateral side level with the patent's hip. Friction is imparted by applying two or three fingers at the medial aspect of the affected area and moving across the tendon by alternating adduction-abduction at the

Figure 69.7

Deep transverse friction to the hamstring tendons.

1032 SECTION TWELVE - THE HIP AND BUTTOCK

Table 69.1 Summary of disorders of the contractile structures Test

Pain

Painful weakness

Painless weakness

Resisted flexion

Psoas tendinitis Rectus femoris tendinitis Sartorius tendinitis Obturator hernia

Avulsion fracture anterior superior iliac spine Avulsion fracture lesser trochanter Abdominal neoplasm Metastasis upper femur

Psychoneurosis Serious non-specific disorder

Resisted extension

Inflamed gluteal bursa

2nd (3rd) lumbar root

1 st sacral nerve root palsy

Intermittent claudication Hamstrings tendinitis Sprained sacrotuberous ligament Resisted adduction

Adductor longus lesion Fracture/neoplasm pubic bone Osteitis pubis Sacroiliac joint lesion Hip joint lesion

Resisted abduction

Inflamed gluteal bursa Lesion of the tensor fasciae latae Sacroiliac joint lesion

Avulsion fracture greater trochanter iliac apophysitis

5th lumbar nerve root palsy Raised greater trochanter

Sprain of iliotibial tract Resisted medial rotation

Inflamed gluteal bursa (tensor fasciae latae)

Resisted lateral rotation

Quadratus femoris lesion Inflamed bursa Gluteus maximus or medius lesion

Resisted extension knee

Tendinitis rectus femoris

Partial rupture rectus femoris

3rd lumbar nerve root palsy Myopathy Myositis

Resisted flexion knee

Hamstrings tendinitis

Partial rupture hamstrings

1 st/2nd sacral nerve root lesion

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CHAPTER 69

23. Kalebo P, Karlsson J, Sward L, Peterson L. Ultrasonography of ch,onic tendon injuries in the groin. Am ] Sports Med 1992; 20(6):634-639. 24. McBryde AM Jr. Stress fractures in runners. Clin Sports Med 1985;4:737-752. 25. Hanson PG et al. Osteitis pubis in sports activities. Phys Sports Med 1978;7(10):111-114 26. Rubenstein NH. Chronic abdominal pain due to periostitis pubis. A new syndrome. Postgrad Med 1991;91(1):147-150. 27. Akermark C, Johansson e. Tenotomy of the adductor longus tendon in the treatment of chronic groin pain in athletes. Am J Sports 1992;20(6):640-643 28. Martens M, Hansen C, Mulier J. Adductor tendinitis and muscu­ lus rectus abdominis tendopathy. AmJ Sports Med 1987;4:231-233. 29. Collee G, Dijkmans BA, Vandenbroucke JP, Cats A. Greater trochanteric pain syndrome (trochanteric bursitis) in low back pain. ScandJ RheumatoL 1991;20(4):262-266. 30. Sutker AN, Barber FA, Jackson DW, Pagliano JW. Iliotibial band syndrome in distance runners. Sports Med 1985;2(6):447-451. 31. Schaberg JE, Harper MC, Allen We. The snapping hip syn­ drome. AmJ Sports Med 1984;12:361-365.

-

DISORDERS OF THE CONTRACTILE STRUCTURES

1033

32. Zoltan DJ, Clancy WG, Keene JS. A new operative approach to snapping hip and refractory trochanteric bursitis in athletes. Am J Sports Med 1986;4:201-204. 33. MacNab 1. Backache. Williams & Wilkins, Baltimore, 1977. 34. Clancy WG, Faltz AS. Iliac apophysitis and stress fractures in adolescent runners. Am] Sports Med 1976;4:214--218. 35. Yeoman W. The relation of arthritis of the sacro-i1iac joint to sciatica. Lancet 1928;ii:1119-1122. 36. Becker W, Krahl H. Die Tendopathien. T hieme, Stuttgart, 1977. 37. Samson M, Lequesne M. Tendinites de la region de la hanche. Rev-Prat 1991;41(18):1667-1671. 38. Puranen J, Orava S. The hamstrings syndrome. AmJ Sports Med 1988;16:517-521. 39. Puranen J, Orava S. The hamstring syndrome - a new gluteal sciatica. Ann Chir GynaecoI1991;80(2):212-214. 40. Pilardeau P, Richard R, Pignel R, Mussi R, Teillet T. L'appareil extenseur de la jambe dans Ie syndrome de Lucy. Actual Sports Med 1991;12:45-47. 41. Pecina MM, Bojanic 1. Overuse Injuries of the Musculoskeletal System. CRC Press, Boca Raton, FL. 1993:152.

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CHAPTER CONTENTS ,

Introduction History

Groin pain

103S

103S

Clinical examination Interpretation

1036

1036

Femora I neck stress fracture 1036 Acetabular labral tears 1037 Pubic ramus stress fracture 1037 Osteitis pubis 1038 Groin hernia 1038 'Sports hernia' or groin disruption Ilioinguinal neuralgia

1039

1039

INTRODUCTION Groin injuries tax the diagnostic and therapeutic abilities of the clinician.1,2 Although they are considered to be common and the most frequent overuse syndromes in some athletic activities such as soccer,3 they are difficult to manage correctly. First, groin lesions involve a complex regional anatomy and often produce unusual presentations. Second, the lesions are often described using inaccurate terminology. For example, groin is a confusing term and groin injury usually describes multiple clinical conditions without clearly defining location or cause. It can, as is usually the case, mean a thigh muscle strain; it may refer to the geni­ talia; it can indicate hip disorders; or it may mean a problem in the lower abdominal wall. Finally, lesions in the back, in the sacroiliac region and within the abdomen may cause pain referred to the region of the groin.

HISTORY The clinician confronted with the prospect of evaluating a patient who complains of groin pain should first of all ask the patient to point to the pain and also establish whether it is localized or diffuse. The groin area is not only the crossing site of trunk and lower extremity muscles but is also a region of considerable dermatomical overlap which includes TIl, T12,

11, L2, 13 and S4 (Fig. 70.1). Pain

in the groin can also be of extrasegmental origin. Once the localization and any radiation of the pain have been clarified, the examiner continues with the routine history which relates to problems in the back, sacroiliac region and the hip (see Chapters

55, 61 and 66).

Finally questions related to possible intra-abdominal dis­ orders may be indicated. For example: • Are fever, sweats or chills present (infection or neoplasm)? • Has there been weight loss (neoplasm)? • Are urinary symptoms such as dysuria, urgency, frequency

or haematuria present? • Are there bowel symptoms - diarrhoea, mucus or blood in

the stool? 1035

1036 SECTION TWELVE - THE HIP AND BUnOCK

L1

L2

./

Figure 70.1

The groin is a region of intense dermatomic overlap.

followed. However, occasionally the results may be con­

CLINIC AL EXAMINATION

fusing. This is usually caused by the fact that resisted

The physical examination of the groin region should

activated contractile structures but often also induce

proceed through several steps to search for various dis­ orders. A start is always made with a routine examination of the lumbar spine, always followed with a similar pro­ cedure on the thoracic spine. A thorough examination of the hip follows. If the signs and symptoms warrant, a complete accessory examination of the sacroiliac joints must also be performed. Finally, and if appropriate, an abdominal examination may be added: palpation for pain, rebound and guard­ ing, pulses, nodes, hernia and masses such as an abdom­ inal aortic aneurysm.

movements in and around the groin not only stress the transmitted stress on inert structures (bones, ligaments). For example, resisted ad- and abduction movements of the hip may indirectly put stress on the sacroiliac or iliolumbar ligaments or on the pubic symphysis. Most lesions have been discussed in the chapters on the hip and the thoracic spine. However, there remain some common sport lesions that cause groin pain and deserve particular attention.

FEMORAL NECK STRESS FRACTURE This overuse injury occurs primarily in endurance ath­ letes (often in thin women who are frequently amenor­

INTERPRETATION

rhoeic). Risk factors include training errors, inadequate

The causes that can result in groin pain are numerous and are summarized in Table

70.1.

Differential diagnosis is

not difficult if the guidelines and principles for a good functional examination of the lumbar spine and hip are

footwear, running on poor surfaces and coxa vara (angular deformity of the hip).

, The fracture causes groin pain, sometimes radiating

down the anterior part of the thigh. The pain (often merely an ache) increases with walking or running and is

CHAPTER 70

- GROIN PAIN

1037

Table 70.1 Lesions that can cause groin pain Abdominal organs

Abdominal wall

Pelvis

Hip

Extrasegmental

Bowel

Rectus abdominis tendinitis

Sacroiliac strain

Capsular lesions

(dural) pain

•

appendicitis

•

diverticulitis

Iliolumbar strain

Loose body

Pubic ramus fracture

Avascular necrosis

Osteitis pubis

Psoas bursitis

Referred pain

Inguinal hernia

T12 L1

Aortic aneurism

'Groin disruption'

L2

Genitalia

lIioinguina neuralgial

L3

•

ovarian cyst

Femoral neck stress

•

ectopic pregnancy and

fracture

•

prostatitis

•

testicular torsion

other pelvic inflammation S2

Avulsion fracture of anterior superior iliac spine

S3

Avulsion fracture of

Urinary tract •

infection

•

lithiasis

lesser trochanter Adductor tendinitis Tendinitis of •

relieved on cessation of activity. Pain at night may be present in long-standing instances. Examination reveals an antalgic gait. There is usually a discrepancy between the obvious gait and the rather subtle signs on clinical examination: a full range of motion with pain produced at the extremes of hip rotation and on axial compression. Plain radiographs taken soon after injury may be neg­ ative. The tension (superior) side fracture may show periosteal callus or an overt fracture line. The compres­ sion (inferior) side fracture may show sclerosis or a cor­ tical break. A bone scan should be positive

2-8

days

after symptoms appear. Further imaging studies such as computed tomography (CT) or magnetic resonance imaging (MRI) should be undertaken early if clinical suspicion warrants it. Treatment is based on the type of fracture. If the bone

scan is positive but there is no visible fracture on plain film, initial treatment will consist of modified bed rest. This leads on to non-weight bearing with crutches and then pain-free weight bearing.3 If there is visible fracture

psoas

•

sartorius

•

rectus femoris

ACETABULAR LABRAL TEARS Recent arthroscopic studies suggest that most internal derangement in the hip may be the result of impingement of acetabular labral tears.4 The history is that of internal derangement: a feeling of giving way or a sharp 'twinge' in the groin that radiates into the anterior thigh, espe­ cially with a rotation of the hip while rising from a seated position. On examination, a non-capsular pattern of limitation is found, with limitation of lateral rotation. Some authors report successful diagnosis of impinge­ ment lesions with the so-called Thomas test.3 This involves flexion and external rotation of the hip and then allowing the extremity to abduct. The hip is then moved into extension, internal rotation and adduction. A posi­ tive test result is indicated by a palpable or audible click and the production of typical pain. Arthrography, MRl and arthroscopy can be used to confirm the diagnosis. Treatment consists of manipulation (p.

1012)

although

arthroscopic or open operative excision may be necessary in recalcitrant cases.

on the plain film, open reduction and internal fixation is the treatment of choice because of the high risk of dis­ placement. An already displaced fracture is considered an orthopaedic emergency and requires open reduction

PUBIC RAMUS STRESS FRACTURE Stress fractures of the pubic ramus occur mostly in dis­ tance runners and joggers, with a higher incidence in

and internal fixation. Athletes must be told that stress fractures of the femoral

females. Traction forces produced by the muscles attached

neck are serious injuries that can compromise an athletic

to the pelvis have been implicated as possible aetiological

career. Even in a successful recovery, return to participa­

factors. Pain in the inguinal, perineal or adductor region is

tion in the chosen sport may take as long as

the usual presenting symptom.

4-5 months.

1038 SECTION TWELVE - THE HIP AND BUnOCK

On examination there is a considerable discrepancy between the marked signs on standing and walking (an

8-12

weeks. One or two infiltrations with

20 mg

triam­

cinolone into the symphysis may hasten healing.9

antalgic gait with an inability to stand unsupported on

However, the condition may be chronic or recurrent. If

the affected leg) and the full and painless passive range of

symptoms persist, three infiltrations with sclerosant solu­

hip motion in the supine-lying position. However, resis­

tion at weekly intervals usually give good results.

ted movements of the hip (especially resisted adduction) do provoke the pain. Exquisite tenderness over the affected pubic ramus is also common.

GROIN HERNIA

Plain radiographs may not show a fracture until

Inguinal and femoral hernias are sufficiently common

several weeks after the injury. Bone scan is necessary for

that every patient who suffers from groin pain should be

early diagnosis.

examined specifically to eliminate this cause.

Treatment consists of cessation of running activities.

An inguinal hernia is located above and at the medial

Most athletes will show complete union of bone at

end of the inguinal ligament. A femoral hernia, more

3-5 months.3

common in female patients, is below and lateral to the inguinal ligament (Fig.

70.2).

The more common type of inguinal hernia is direct

OSTEITIS PUBIS

which pushes out through the posterior wall of the

Although osteitis pubis is a well-known entity following

inguinal canal lateral to the lateral border of the rectus

surgery of the bladder or the prostate,S it has also been

abdominis muscle. It is usually the consequence of a

reported after athletic endeavours.

weakness which has developed in the posterior wall of

Osteitis pubis (an inflammatory lesion of the bone

the inguinal canal (fascia of the transverse abdominal

adjacent to the symphysis pubiS) in athletes is thought to

muscle). Most direct inguinal hernias are symptomless

be the result of mechanical strain from trauma, excessive

apart from the presence of a bulge.

twisting and turning in sports such as soccer or repetitive

An indirect inguinal hernia is congenital in origin and

shear stress from excessive side-to-side motion.6 It is

is caused by a failure of the processus vaginalis of the

quite common in ice-hockey and soccer players and in

peritoneum soundly to close. It therefore originates at the

long-distance runners. It is also frequent in women who

internal inguinal ring, appears at the external ring and

exercise in the postpartum period because of the particu­

may extend into the scrotum. The relationship to injury is

lar instability of the symphysis after birth?

uncertain and, in contrast to the 'sports hernia' described

Complaints develop gradually and the patient cam10t

below, many authorities consider that it develops from a

link the onset to any known injury. Pain is described as

weakness or tear of the posterior wall of the inguinal

originating from the pubic region, with radiation into the

canal more lateral than that in a direct inguinal hernia in

lower abdomen, the groin and the adductor regions. The

the presence of a potentially patent processus vaginalis.1o

pain is linked to the athletic activity and gradually disap­ pears upon resting. Coughing or sneezing may be painful.8 In severe examples the athlete may develop an antalgic or waddling gait. On examination there is a full range of passive move­ ment of the hips with pain elecited by passive abduction and resisted adduction. The fact that the pain is repro­ duced during the examination of both lower extremities should help in the differentiation with a tendinitis of the adductor longus (p.

1026).

Palpation also causes pain

along the pubic bones and the symphysis itself and not at the tendinous junction of the adductor muscles. Bone scintigraphy, which typically shows increased uptake unilaterally or bilaterally at the pubic bones, is effective in making an early diagnosis. Radiographic changes may not be visible for

2-3

weeks but then

show a symmetric resorption of the medial ends of the pubic bone, widening of the symphysis and rarefaction or sclerosis along the pubic rami. Treatment initially includes relative rest because the

condition is usually considered as self-limiting within

Figure 70.2

Hernia localization: 1, inguinal hernia; 2, femoral hernia.

CHAPTER 70 - GROIN PAIN 1039

In most instances, activities that significantly increase

hernia', usually involves the posterior wall of the

intra�abdominal pressure or may involve repeated

inguinal canal and can appear as a tear of the transversus

Valsalva manoeuvres, for example weight lifting, cause

abdominis muscle or as a disruption to the conjoined

or exacerbate inguinal hernia. While the pain might ini­

tendon - the tendon of insertion of both the transversus

tially occur only after activity, it typically will increase in

abdominis and internal oblique muscles (Fig.

frequency to the point of occurring during activity and

sports hernia may, however, also involve a lesion of the

even with simple trunk and hip movements. In males the

external oblique aponeurosis and cause a dilatation of the

pain may radiate into the proximal thigh or the scrotum.

external inguinal ring.13

70.4).12

A

Examination for both types of inguinal hernia involves

A sports hernia should be differentiated from the more

invaginating the scrotal skin along the spermatic cord

common inguinal hernia in that it does not involve a

70.3) or direct palpa­

clinically detectable hernia (there is not a protrusion of

tion in females. A palpable mass may or may not be

any abdominal tissue through the walls of the abdominal

detected.

cavity).14 The term 'disruption' is therefore more appro­

using the index finger in males (Fig.

Manoeuvres to increase intra-abdominal pressure,

priate to describe this type of lesion.

such as coughing or tensing the abdominal musculature,

A sports hernia typically produces unilateral groin

may produce a cough impulse (a sign of hernia), or may

pain during exercises. In chronic cases, however, the

make a mass more prominent. Treatment of inguinal hernias should be by surgical

patient may have symptoms during activities of daily living. Onset of pain is usually insidious but may occur

repair, not only to relieve pain and discomfort but also to

suddenly. It is typically localized to the conjoined tendon

prevent complications - incarceration, obstruction and

but can involve the inguinal canal more laterally. Sudden

strangulation with infarction of the bowel.

movements often exacerbate the pain.1S Examination for a sports hernia is generally done by

'SPORTS HERNIA' OR 'GROIN DISRUPTION' Athletes in fast-moving sports that involve twisting and

inverting the scrotal skin with a finger and palpating the inguinal ring and canal. The uninvolved side should be examined first so that the examiner may put the patient

turning - such as soccer, rugby and ice hockey - may be

at ease and also assess the normal structures. The exam­

at particular risk of a tendinous disruption in the area of

ining finger is inserted into the scrotal sac just below its

the inguinal canaPl This injury, often called a 'sports

junction with the abdominal wall and carried superiorly over the pubis up to the external inguinal ring. The ring, conjoined tendon, pubic tubercle and midinguinal region are checked for size and the presence of abnor­

.�-.

mal tenderness. Conventional imaging modalities such as bone scan, ultrasound, CT and MRI all fail to reveal the defect. Surgical exploration is currently the only method to confirm the diagnosis. Treatment generally surgical and involves restoration of

the normal anatomy by repairing the conjoined tendon and / or the external oblique aponeurosis.

ILIOINGUINAL NEURALGIA 16 The ilioinguinal nerve originates from the

LJ-L2

nerve

roots. It passes between the ilium and psoas major to per­ forate the transversus abdominis near the anterior supe­ rior iliac spine (Fig.

70.5). The

nerve pierces the internal

oblique, transverses the inguinal canal below the sper­ matic cord, emerging with it from the superficial inguinal ring to supply the proximomedial skin over the penile root and the scrotum or that covering the mons pubis and the adjoining labium majus. During its course it inner­ vates the lowest portions of the transversus abdominis and internal oblique muscles as well as the skin overlying Figure 70.3

Palpation of the inguinal canal via invagination of the scrotal skin.

the inguinal ligament.

1040 SECTION TWELVE - THE HIP AND BUnOCK

(a)

(b)

Figure 70.4 Anatomy of the inguinal canal. A (overview): 1, external oblique muscle and aponeurosis; 2, rectus abdominis muscle; 3, transversus abdominis muscle; 4, external inguinal ring; 5, spermatic cord. B (insert): 1, falx inguinalis (conjoined tendon); 2, spermatic cord; 3, transversus abdominis muscle; 4, external oblique muscle; 5, inguinal ligarnent.

Ilioinguinal nerve entrapment is a well-established cause of chronic inguinal pain in patients who have had lower

abdominal

and

inguinal

hernia

surgery

(e.g. appendectomy or inguinal herniorrhaphy).' 7 Direct trauma, intense abdominal muscle training or inflam­ matory conditions can also lead to entrapment of this nerve as it passes through or close to the abdominal muscle layers.18,19 Patients describe a burning or shooting pain in the distribution of the nerve. Light-touch sensation in the inguinal area may be altered and pain may be exacer­ bated by hyperextension of the hip. There is usually a well-circumscribed trigger point medial and below the anterior superior iliac spine where the ilioinguinal nerve pierces the fascia. Relief of pain by infiltration of a local anaesthetic confirms the diagnosis.

\ \ \

(

� :::

Treatment consists of three infiltrations at weekly inter­

vals at the confirmed site with In severe cases

5 ml procaine 0.5 to 1%.20

20 mg triamcinolone may be added to the

solution. Nerve ablation may be indicated if the lesion does not respond to infiltrations.

8 Figure 70.5 Course of the ilioinguinal nerve: 1, anterior superior iliac spine; 2, transversus abdominis muscle; 3, external oblique muscle; 4, inguinal ligament; 5, ilioinguinal nerve; 6, spermatic cord; 7, pubic tubercle; 8, superficial inguinal ring.

CHAPTER 70 - GROIN PAIN 1041

REFERENCES ,

1. Renstrom PA. Tendon and muscle injuries in the groin area. c/in

Sports Med 1992;11(4):815-831. 2. Jaeger JH. La pubalagie. In: Catonne Y, Saillant G (eds) Lesions

Tralllllntique des Tendons chez Ie Portif. Masson, Paris, 1992. 3. Gross ML, Nasser S, Finerman G AM. Hip and pelvis. In: DeLee

Ie,

Drez D Jr (eds) Orthopaedic Sports Medicille Principles alld

Prnctice. Saunders, PhiJadelphia, 1994:1063-1085. 4. Fitzgerald RH Jr. Acetabular labrum tears. Diagnosis and treat­

ment. C/ill Orthop 1995;3(11):60-68. 5. Seigne JD, Pisters LL, von Eschenbach AC. Osteitis pubis as a

complication of prostate cryotherapy. J Ural 1996;156(I):182. 6. Fricker PA, Taunton JE, Ammann W. Osteitis pubis in athletes.

11. Lacroix

VJ,

Kilmear DG, Mulder DS. Lower abdominal pain

syndrome in National Hockey League players: a report of cases. c/ill Sports Med 1998;8(1):5-9. 12. Gilmore OJA. Gilmore's groin: a ten year experience of groin

disruption. Sports Med Soft T issue Traullla 1991;3:5-7. 13. Hackney RG. The 'sports hernia': a cause of groin pain. Br

J

Sports Med 1993;27(1):58-62. 14. Lovell G. The diagnosis of chronic groin pain in athletes: a

review of 189 cases. Aust J Sci Med Sport 1995;27(3):76-79. 15. Kemp S, Batt ME. The 'sports hernia': a common cause of groin

pain. Phys Sports Med 1998;26(1):36-44. 16. Starling JR, Harms BA, Schroeder ME, Eichman PL. Diagnosis

Infection, inflammation or injury? Sports Med 1991;12(4):

and treatment of genitofemoral and ilioinguinal entrapment

266-279.

neuralgia. Surgery 1987;102(4):581-586.

7. Gonik B, Stringer CA. Postpartum osteitis pubis. South Med J 1985;78(2):213-214. 8. Smedberg SG, Broome AE, Gullmo A, Ross H. Herniography in

athletes with groin pain. Am J Surg 1985;149:378-382. 9. Holt MA, Keene JS, Graf BK, Helwig DC. Treatment of osteitis

pubis in athletes. Results of corticosteroid injections. Am J Sports Med 1995;23(5):601-606.

10. Ruane Jj, Rossi TA. When groin pain is more than 'just a strain':

navigating a broad differential. Phys Sports Med 1998;26(4): 78-103.

17. Monga M, Ghoniem GM. Ilioinguinal nerve entrapment follow­

ing needle bladder suspension procedures. UrologlJ 1994;44(3): 447-450. 18. Kopell HP, Thompson WAL, Postel AH. Entrapment neuro­

pathy of the iJioinguinal nerve. N Engl J Med 1962;266:16-19. 19. Ziprin P, Williams P, Foster ME. External oblique aponeurosis

nerve entrapment as a cause of groin pain in the athlete. Br J Surg 1999;86(4):566-568. 20. Knockaert DC, D'Heygere FG, Bobbaers HJ. Ilioinguinal nerve

entrapment: a little-known cause of iliac fossa pain. Postgrad Med J 1989;65(767):632-635.

THIS PAGE INTENTIONALLY LEFT BLANK

CHAPTER CONTENTS

g

Con enital dislocation of the hip

Clinical tests 1044 Technical investigations Treatment 1045

1043

1044

Congenital limitation of extension Arthritis of the hip in children

Hip disorders in children

1045

1045

Transitory arthritis 1045 Tuberculosis of the hip 1045 Haemarthrosis 1045

Perthes' disease (pseudocoxalgia) Slipped epiphysis

1046

1046

Avulsion fractures about the hip

1046

Every complaint of groin, thigh or knee pain in a child should be taken seriously and examined very carefully without delay. Furthermore, any child who limps or shows limitation of movement at the hip joint should undergo a thorough examination. Most hip lesions in children can be diagnosed adequately with the help of a radiograph. For almost all these lesions, there are good and effective treatments, provided the diagnosis is made early enough.

CONGENITAL DISLOCATION OF THE HIP The incidence of congenital dislocation is between 1 and 2 cases per 1 000, but it is four times as frequent in girls as in boyS.l There seems to be a hereditary factor, because there is about a 5% chance of a second child being affected. This rises to 36% if one of the parents also had congenital dislocation of the hip.2 Although there are still questions about its aetiology, the condition seems to occur in the presence of some weakness of the joint capsule and elongation of the liga­ mentum teres.3 A deficiency of the rim of the acetabulum may also contribute in the development of the disease.4 However, the most important aetiological factor seems to be an imbalance between the action of the psoas muscle and the hip extensors.s A relative shortening of the psoas presses the head of the femur upwards and laterally when the hip is extended by the contraction of the stronger hip extensors. In the presence of a weakness of the capsule, dislocation then occurs. It is vital to make the diagnosis of a congenital disloca­ tion as soon after birth as possible. Conservative treat­ ment with an abduction brace6 before the child begins to walk is completely adequate but after the age of 4 even surgical repositioning is difficult and after the age of 7 it is almost impossible. Without treatment the dislocation may lead to a shorter leg, the formation of a neoacetabu­ lum at the blade of the ilium and the supervention of early arthrosis. Radiographs are not reliable in making the diagnosis of congenital hip dislocation in newborn babies. Early diagnosis therefore relies entirely on clinical tests. Those most used are known as Ortolani's and Barlow's tests.7,8 1043

1044 SECTION TWELVE - THE HIP AND BUTTOCK

It should be remembered, however, that positive tests only indicate a capsular laxity and therefore the possibil­ ity of dislocation. For instance, the incidence of positive Ortolani's and Barlow's signs in newborns is about 10-20 per 1000, which is 10 times more than at the age of 2 months, which suggests that there is a tendency towards resolution of the capsular laxity.9 CLINICAL TESTS Orto/ani's test During this test the luxated hip is replaced manually. Technique. The baby lies on the back, hips flexed to 90° and the knees completely flexed (Fig. 71.1a). The exam­ iner grasps the leg with the contralateral hand in such a way that the thumb presses on the inner side of the thigh. The ring and middle fingers are placed along the outer thigh, so that the fingertips touch the trochanter. The other hand fixes the opposite hip. Abduction of the hip is now performed (Fig. 71.1b). In a subluxated hip, resist­ ance will be felt at 45-60°. The moment the resistance is overcome, the femoral head rides over the acetabular edge and reduces. This is felt by the examiner. This sensation has wrongly been called a click, whereas the feeling is rather that of moving two knuckles of the wrist over each other. Ortoloni described this as a 'segno dello

scatto' (ridge sign). Under this definition, the sensation has to be felt rather than heard. Bar/ow's test The purpose here is to dislocate the hip first and then replace it. The hips of the baby are grasped in the same way as Ortolani's test. Technique. In this test, the thumb is placed further prox­ imally on the femur. If the capsule is elongated or weak, the examiner can easily push the femoral head over the posterior rim of the acetabulum. This is indicated by a click. Pressure with the middle finger behind the trochanter then moves the head anteriorly, where it comes to lie in the acetabulum again (Fig. 71.2). This to-and-fro movement of the femoral head over the acetabular rim indicates that the joint is unstable. TECHNICAL INVESTIGATIONS

The diagnosis can usually be made with plain radio­ graphs. However, during recent decades sonographic screening examinations have been shown to be superior in the early detection of congenital dislocations of the hip.10,1J In a recent study of sonographic screening examinations on 4177 newborns, all cases of congenital

\ (a)

(b) Figure 71.1

Ortolani's test for congenital dislocation of the hip: (a) position of the baby, (b) reposition of the dislocated hip by abduction.

CHAPTER 71 - HIP DISORDERS IN CHILDREN

1045

joints. They walk with a hyperlordosis, extending at the back instead of at their hips. This limitation is probably the result of a shortening of the psoas muscles. Treatment consist of stretching the psoas and capsule in the same way as in early osteoarthrosis (see p. 1 005).

ARTHRITIS OF THE HIP IN CHILDREN TRANSITORY ARTHRITIS Figure 71.2

Barlow's test for congenital dislocation of the hip.

dislocation of the hip joint were found and classified. The results of early treatment were 100%.12 TREATMENT

The majority of unstable hips at birth stabilize in a very short tim�,B but since the outcome of an 'unstable hip' is impossible to predict, all cases of hip instability in new­ borns must be taken seriously and treated. Hence, as soon as a positive Ortolarti's or Barlow's test is found, an abduction brace is given until these clinical signs disap­ pear. 1 4-16 If the diagnosis is made when the child starts to walk, surgical repositioning is required. Surgical reduction is almost impossible after the age of 7 years. If a 'false acetabulum' develops at the iliac bone, the functional dis­ ability may be small, especially if the disorder is bilat­ eralY Pain and serious disability then start only in the fourth or fifth decade, when pseudarthrosis has occurred. If pain is not too severe, treatment can be conservative;18 often some relief is obtained by one or two infiltrations with 50 ml of procaine 0.5% at the posterior aspect of the capsule.19 Technique: infiltration. The patient lies prone on a high couch, with the hip flexed to a right angle and the knee supported on a chair. The posterior aspect of the capsule can now be reached and a 7 cm needle is introduced medially from the trochanter and advanced in a medial and downwards direction. The tough capsule can easily be felt with the tip of the needle, and the whole posterior aspect is infiltrated applying the classical technique of withdrawals and reinsertions. Should conservative treatment fail, surgery is required.2o

CONGENITAL LIMITATION OF EXTENSION Some children have an excessive forward tilt of the pelvis, as the result of congenital limitation of extension at the hip

This is the commonest cause of hip pain in children and usually occurs under the age of 10 years. The child com­ plains of pain in the groin, thigh and knee after some pre­ vious exertion. Sometimes only knee pain is present. The child limps and clinical examination of the hip shows a capsular pattern. Although the pathogenesis of the disorder remains obscure the conventional view is that it results from ordi­ nary overuse. However, a correlation between transient arthritis and the development of Perthes' disease has been shown repeatedly.21,22 Sonographic examination, together with X-ray exami­ nation, represent the first choices in the evaluation of a capsular pattern in a child and in the follow-up of transient synovitis.23 In transient synovitis there is effusion but the effusion persists for less than 2 weeks. In the early stage of Legg-Calve-Perthes' disease the capsular distension persists for more than 6 weeks. A differential diagnOSis between transient synovitis and Legg-Calve-Perthes' disease is therefore only possible by observing the ultra­ sonographic course of the disease.24 Treatment is bed rest and non-weight bearing. It is advisable, if excessive intra-articular effusion is demon­ strated by ultrasonography, to aspirate the fluid.25 Most cases recover completely and without sequelae after a few weeks of bed rest.26 TUBERCULOSIS OF THE HIP

The child complains of pain in the groin, thigh and knee, and limps. Clinical examination shows a gross capsular pattern, sometimes to such an extent that the hip is fixed in flexion, abduction and lateral rotation. There is consid­ erable wasting of the thigh muscles. Symptoms of general illness, with slight fever and fatigue complete the picture. Radiography and examination of articular fluid give a decisive answer. HAEMARTHROSIS

The hip is very rarely affected in haemophilia. Acute hip pain and gross articular pattern in a haemophiliac reveal the diagnosis. Prompt aspiration and specific

1046 SECTION TWELVE - THE HIP AND BUnOCK

anti-haemophyliac measures must be taken in order to protect the cartilage against the erosive effects of the presence of the blood.

PERTHES' DISEASE (PSEUDOCOXALGIA) This disorder was described in 1910 by Legg as 'an obscure affection of the hip joint?7 by Calve as 'pseudocoxalgia'28 and by Perthes as 'arthritis defor­ mans juvenilis',29 and is an aseptic necrosis of the femoral head. It affects children (male:female ratio is 5:1 ) between 4 and 1 2 years of age. The disease occurs bilat­ erally in 1 5% of cases. Although it is generally accepted that the necrosis is the result of a change in the blood supply to the femoral head,3D there still remains much controversy about the way this occurs. There have been reports suggesting retarded skeletal ageing in relation to the chronological age.31 Some studies have also demonstrated an association with pituitary growth hormone deficiency.32 However the most likely aetiol­ ogy for Legg-Calve-Perthes' disease seems to be the hypothesis of clotting abnormalities with vascular thrombosis.33 In the early stage, the only symptom is a slight ache in the knee. Sometimes the parents notice a limp. Clinical examination may reveal marked limitation of movement at the hip joint but the earliest physical sign is very often limitation of adduction during flexion - as passive flexion is performed, the knee gradually moves into abduction. When the flexed hip is now drawn toward the opposite side, limitation, pain and a hard end-feel are noted. The diagnosis is confirmed on radiography, which shows flattening and lysis of the femoral head, broadening of the epiphysis and enlargement of the joint space. Treatment and prognosis depend on the age of onset (the younger the age of onset the better the prognosis), the physical signs and the radiological changes.34 Late sequelae of the disease are leg-length shortening and degenerative joint disease that develops in the major­ ity of patients by the sixth or seventh decade of life.35

The symptoms are knee and hip pain and limping.39 Trendelenburg's sign is usually positive (when the patient stands on one leg, pain in the weight-bearing hip or weakness of the ipsilateral gluteus medius results in a downwards pelvic tilt on the contralateral side). Clinical examination reveals a capsular pattern in the hip joint but external rotation is often increased.4D Resisted move­ ments are strong and painless. The radiograph reveals the slip. Treatment and prognosis depend largely on the degree of the slip.41 42 It is therefore vital to make the diagnosis as soon as possible, and a child or teenager in whom epi­ physiolysis is suspected should not be allowed to walk around until the result of radiography is known. .

Epiphysiolysis is an orthopaedic medical emergency and requires immediate relief of weight bearing.43 Treatment is sur­

gical and consists of in situ cannulated-screw fixation44 of the slipped capital femoral epiphysis or an open replace­ ment of the femoral head.45

AVULSION FRACTURES ABOUT THE HIP Avulsion fractures occur more commonly in skeletally immature athletes than in adults because young patients'

. ..Afm\

-·· '�7

,-_...

. . _..

((f;) 7'::':":'::.:

SLIPPED EPIPHYSIS Due to gravity, a lysis of the proximal epiphysial junction results in downwards and backwards slipping of the epi­ physis in relation to the neck of the femur. This causes a varus position and slight outwards rotation of the leg coxa vara in adolescence. It is a disorder of teenagers (aged between 1 2 and 1 7 years), with an incidence of 510 per 1 00 000.36 The epiphysial junction softens for an unknown reason, although there is strong suspicion that some hormone imbalance could cause the weakening.37,38

3

Figure 71.3 Bony sites of the pelvis: 1, anterior superior iliac spine;48,49 2, anterior inferior iliac spine;50,51 3, ischial tuberosity; 4, lesser tubercie,s2

CHAPTER 71

tendons are stronger than their cartilaginous growth centres. The same stress that causes a muscle strain in an adult can cause an avulsion fracture in an adolescent. These fractures occur at the secondary growth centres, or apophyses, which become separated from the underlying bone. The fractures do not become widely displaced because of the surrounding thick periosteum.46 The mechanism of injury is a sudden, violent muscle contraction or excessive repetitive action across the apophysis. Hip avulsion fractures are common in young sprinters, soccer players and jumpers.47 Patients typically describe local pain and swelling after an extreme effort and report no external trauma. Physical examination reveals pain during the resisted movements that activate the contractile structures insert­ ing at or nearby the fracture line: •

the anterior superior iliac spine - sartorius muscle

• • •

-

HIP DISORDERS IN CHILDREN 1047

the anterior inferior iliac spine, where the rectus femoris muscle attaches the ischial tuberosity, where the hamstring muscles attach the lesser tubercle - insertion of the psoas muscles.

There is also palpable tenderness (and often ecchymo­ sis) at the specific bony sites (see Fig. 71.3). Plain radiographs reveal the avulsion fracture. It is useful to compare the injured side with the contralateral side. During the healing phase of an avulsion fracture the abundant reactive ossification in the soft tissues may clinically and radiographically be mistaken for neoplasia.53 Treatment is rest. Most patients can be treated non­ operatively over 6-12 weeks although some authors recommend surgery for severely displaced fragments in rare cases.

REFERENCES 1. MacKenzie IG, Wilson JG. Problems encountered in the early

16. Burger BJ, Burger JD, Bos CF et al. Frejka pillow and Becker

diagnosis and management of congenital dislocation of the hip.

device for congenital dislocation of the hip. Acta Orthop Scand

J Balle Joillt Surg 1981;63B:38.

1993;64(3):305-311.

2. Wynne-Davies R. Acetabular dysplasia and familial joint laxity.

Two etiological factors in congenital dislocation of the hip.

17. Crawford AW, Slovek RW. Fate of the untreated congenitally

dislocated hip. Orthop Trans 1978;2:73. 18. Wedge JH, Wasylenko MJ. The natural history of congenital

J Bone Joint Slirg 1970;52B:704-716. 3. Catteral A. What is congenital dislocation of the hip? 1 Bone loint

Surg 1984;66B:469-471. 4. Wilkinson JA. Prime factors in the etiology of congenital dislo­

cation of the hip. 1 Bone Joint Surg 1963;45B:268-283. 5. McKibbin B. The action of the iliopsoas muscle in the newborn.

disease of the hip. J Bone Joint Surg 1979;61B:334-338. 19. Cyriax JH. Textbook of Orthopaedic Medicine, Vol I, Diagnosis of

Soft Tissue Lesions, 8th edn. Bailliere Tindall, London, 1982:388. 20. Henderson RS. Osteotomy for unreduced congenital disloca­

tions of the hips in adults. I Bone Joint Surg 1970;52B:468. 21. Kemp HBS. Perthes disease. Ann R CoIL Surg 1973;5:18.

I Bone loint Surg 1968;50B:161-165. 6. Frejka B. Pravention der angeborene Hiiftgelenkensubluxation

durch Abduktionspolster Wiener Med Wochenschr 1941;91:

22. Inoue A, Freeman MAR, Vernon-Roberts B, Mizuno S. The

pathogenesis of Perthes' disease. I Bone 10int Surg 1976;58B:453. 23. de Pellegrin M, Fracassetti D, Ciampi P. Coxitis fugax. The role

523-524. 7. Ortolani, M. Un segno poco noto e sua importanza per la diag­

nosi precoce di prelussazione congenita dell'anca. Pediatria

of diagnostic imaging. Orthopiide 1997;26(10):858-867. 24. Konermann W, de Pellegrin M. The differential diagnosis of

juvenile hip pain in the ultrasonographic picture. Transient

1937;45:129. 8. Barlow TG. Early diagnosis and treatment of congenital dislo­

cation of the hip. 1 Bone loint Surg 1962;268(45B):292-301. 9. Visser JD, Nielsen HKL. Lichamelijk Onderzoek bij aangeboren

heupontwrichting.

Ned

Tijdschr

Geneeskd

1984;128(26):

1217-1220. 10. Graf R. The diagnosis of congenital hip-joint dislocation by

coxitis, Legg-Calve-Perthes disease, epiphysiolysis of the femur head. M Orthopiide 1993;22(5):280-287. 25. Bernd L, Niethard FU, Graf J, Kaps HP. Transient hip joint

inflammation. Z Orthop Grenzgeb 1992;130(6):529-535. 26. Monty CP. Prognosis of 'observation hip in children'. ArdiS Dis

Child 1962;37:539.

Z Orthop Trauma Surg

27. Legg AT. An obscure affection of the hip joint. Bosto/1 Med Surg

11. Schule B, Wissel H, Neumann W, Merk H. Follow-up control of

28. Calve J. Sur une forme particuliere de pseudocoxalgie. Rev ChiI'

ultrasound compound treatment. 1980;97:117-133.

ultrasonographic neonatal screening of the hip. Ultraschall Med 1999;20(4):161-164. 12. Merk H, Mahlfeld K, Wissel H, Kayser R. The congenital dislo­

cation of the hip joint in ultrasound examination - frequency, diagnosis and treatment. Klin Piidiatr 1999;211(1):18-21. 13. Coleman SS. CongenitaL DyspLasia and DisLocation of the Hip.

Mosby, St. Louis, 1978. 14. Vasser JD. Functional treatment of congenital dislocation of the

hip. Acta Orthop Scand 1984;55(suppl):206. 15. Lempichi A,

Wierusz-Koslowska, Kruczynski J. Abduction

treatment in late diagnosed congenital dislocation of the hip. Acta Chir Scand 1990;61(suppl):236.

11910;162:202. 1910;42:54. 29. Perthes Gc. Uber Arthritis deformans juvenilis. Dtsch Z ChiI' 1910;107:111. 30. Trueta J. Normal vascular anatomy of human femoral head

during growth. I Bone Joint Surg 1975;39B:358.

31. Harrison MHM, Turner MH, Jacobs P. Skeletal immaturity in

Perthes disease. 1 Bone Joint Surg 1976;58B:37. 32. Rayner PHW,

Schwalbe SL, Hall

DJ. An assessment of

endocrine function in boys with Perthes' disease. c/in Orthop 1986;209:124-128. 33. Wall

EJ.

Legg-Calve-Perthes' disease.

1999;11(1):76-79.

Curr

Opin Pediatr

1048 SECTION TWELVE - THE HIP AND BUTTOCK

34. Menelaus

MB.

Lessons

learned

in

the

management

of

44. Givon U, Bowen JR. 1999 Chronic slipped capital femoral epi­ physis: treatment by pilming in situ. j Pediatr Orthop 1999;8(3):

Legg-Calve-Perthes disease. Ciin Orthop 1986;209:41-48. 35. Yrjonen T. Long-term prognosis of Legg-Calve-Perthes disease:

216-222. 45. Dunn OM, Angel Je. Replacement of the femoral head by open

a meta-analysis. J Pediatr Orthop 1999;8(3):169-172. 36. Kelsey J, Wayne 0, Keggi K, Southwick WOo The incidence and distribution of slipped capital femoral epiphysis in Connecticut

operation in severe adolescent slipping of the upper femoral epiphysis. j Bone Joint Surg 1978;60B:394.

and Southwestern of U.S. j Bone joint Surg 1970;52A:1203-1215.

46. Gross ML, Nasser S, Finerman GAM. Hip and pelviS. Tn: DeLee

37. Harris WR. The endocrine basis for slipping of the upper

JC, Drez D Jr (eds) Orthopaedic Sports Medicille: Prillciples lind

femoral epiphysis. An experimental study. J Bone Joint Surg 38. Tachdjian MO.

Practice. Saunders, Philadelphia, 1994:1063-1085. 47. Kling ThF. Pelvic and acetabular fractures. In: Steinberg ME

1950;32B:5-11. Pediatric Orthopedics, 2nd edn.

Saunders,

Philadelphia, 1990:1016-1081.

(ed) T he Hip and its Disorders. Saunders, Philadelphia, 1991: 173-197.

39. Matava MJ, Patton CM, Luhmann S, Gordon IE, Schoenecker

48. Draper DO, Dustman AJ. Avulsion fracture of the anterior

PL. Knee pain as the initial symptom of slipped capital femoral

superior iliac spine in a collegiate distance runner. Arch Phys

epiphysis: an analysis of initial presentation and treatment.

Med Rehabi/1992;73(9):881-882. 49. Lambert MJ, Fligner OJ. Avulsion of the iliac crest apophysis: a

J Pediatr Ortilop 1999;19(4):455-460. 40. Van den Berg ME, Keesen W, Van der Hoeven H. Epiphysiolysis van de heupkop. Ned Tijdschr Geneeskd 1992;136:1339-1343. 41. Dunn DM. Severe slipped capital femoral epiphysis and open replacement by cervical osteotomy. Proceedings of the Third

rare fracture in adolescent athletes. Anll Ell/erg Med 1993; 22(7):1218-1220. 50. Schothorst AE. Avulsion fractures of the inferior-anterior iliac spine. Arch Chir Neerl1978;1:55-59.

Louis,

51. Mader T. Avulsion of the rectus femoris tendon: an unusual

42. Ordeberg G, Hansson Ll, Sandstrom S. Slipped capital femoral

52. Theologis TN, Epps H, Latz K, Cole WG. Isolated fractures of

Open

Scientific Meeting

of

the

Hip

Society.

St.

1975:125-126 epiphysis in southern Sweden. Long-term result with closed reduction and hip plaster. Spica Ciin Orthop 1987;220:148-154. 43. Birch JG. Slipped capital femoral epiphysis: still an emergency. Report of a case. j Pediatr Ortilop 1987;7:334-337.

type of pelvic fracture. Pediatr El11erg Care 1990;6(3):198-199. the lesser trochanter in children. Injury 1997;28(5-6):363-364. 53. Resnick JM, Carrasco CH, Edeiken J et III. Avulsion fracture of the anterior inferior iliac spine with abundant reactive ossification in the soft tissue. Skeletal Rlldio/1996;25(6):580-584.

Summary of hip pain

Multisegmental (dural) pain about the hip can be classified into pain in the groin, lateral trochanteric pain and pain in the buttock.

1049

1050 SECTION TWELVE - THE HIP AND BUTTOCK

Referred from visceral pathological conditions

Bowel Aneurysms Genitalia Urinary tract

Abdominal wall lesions

Rectus abdominis Inguinal hernia

Pain in the groin Segmentally referred from T12,L1,L2,L3(S2,S3)

Groin disruption Ilioinguinal hernia

Pelvic lesions

Sacroiliac strain Iliolumbar strain Pubic ramus fracture Osteitis pubis

Hip lesions

Capsular lesions Non-capsular lesions

Avulsion fractures

E

Loose body Avascular necrosis Psoas bursitis Femoral neck fracture

.... Lesser trochanter

____

L Anterior superior iliac spine

�

Tendinitis -------.... Adductor psoas Sartorius Rectus femoris Lateral trochanteric pain Segmentally referred from L1 (L2,L3)

1-----------"""'1.. Gluteal bursitis Bursitis underlying the iliotibial tract Sprain of the iliotibial tract Lesion of the tensor fasciae latae

Pain in the buttock Segmentally referred from L1,L2 and L3 (upper part of the buttock) and from 81, S2(lower part of the buttock)

Avulsion fracture of the greater trochanter

1-

"""'1.. Hip joint lesions (articular lesions)

__________

"" " SacrO!"I"lac Jomt I eSlons

Major lesions presenting with the 'sign of the buttock' Hamstrings syndrome Muscle lesion of the quadratus femoris Ischial bursitis Intermittent claudication due to obstruction of the internal iliac artery

SECTION THIRTEEN

The knee

SECTION CONTENTS 73. Applied anatomy of the knee

1053

Articular surfaces 1053 The patella 1054 The menisci 1055 Joint capsule and ligaments 1056 Muscles and tendons 1058 Nerve structures and blood vessels: the popliteal fossa The upper tibiofibular joint 1061 74. Clinical examination of the knee

Referred pain 1063 History 1064 Inspection 1065 Functional examination Palpation 1070 Accessory tests 1072

1060

1063

1066

75. Interpretation of the clinical examination of the knee

1075

76. Disorders of the inert structures: capsular and non-capsular patterns

The capsular pattern 1077 Traumatic arthritis 1077 Rheumatoid and reactive arthritis 1078 Osteoarthrosis 1078 Monoarticular steroid-sensitive arthritis 1080 Crystal synovitis 1080 Haemarthrosis 1081 Septic arth ritis 1081 Non-capsular patterns 1082 Internal derangement 1082 Plica synovialis syndrome 1092 Intra-articular adhesions 1093 Subsynovial haematoma 1094 Adherent vastus intermedius 1094 Posterior capsular strain 1094 Cysts and bursitis 1094 77. Disorders of the inert structures: ligaments

Introduction 1099 Isolated sprains 1102 Ligamentous instability

1099

1113

78. Disorders of the contractile structures

1131

Extensor mechanism 1131 Patellofemoral disorders 1138 Strained iliotibial band 1143 Flexor mechanism 1144 79.

Differential diagnosis of lesions at the knee

1153

1077

THIS PAGE INTENTIONALLY LEFT BLANK

Applied anatomy of the knee

CHAPTER CONTENTS ,

Articular surfaces The patella

1053

1054

1055 Movements of the menisci

The menisci

Joint capsule and ligaments

1055 1056

Capsule 1056 Ligaments 1057 1058 The extensor mechanism 1058 Flexors of the knee 1059 Innervation of the muscles 1060

Muscles and tendons

Nerve structures and blood vessels: the popliteal fossa The upper tibiofibular joint

1061

1060

In nearly all circumstances, the knee works in axial com­ pression under the action of gravity. It must therefore rec­ oncile two opposed requirements, namely mobility and stability. This problem is resolved by an ingenious arrangement of ligaments, menisci and tendons: the ligaments and menisci provide static stability and the muscles and tendons dynamic stability. Nevertheless, the exposure of the knee to external forces makes it very vulnerable in many occupations and sports. The main movement of the knee is flexion-extension; secondary movement - internal and external rotations of the tibia in relation to the femur - is possible only when the knee is flexed. To measure the extent of internal and external rotation, the knee must therefore be flexed to a right angle.

ARTICULAR SURFACES

During flexion-extension, the knee acts as a hinge joint, whereby the articular surfaces of the femur roll (and glide) over the tibial surface. The distal femur can be compared with a double wheel, in which the medial and lateral condyles are the components and the intercondylar notch the junction between them (see Fig. 73.1). The condyles are convex in both planes. The medial condyle extends a little more distally than the lateral. The greater prominence of the lateral femoral condyle prevents the patella from sliding laterally.

(a)

(b)

Figure 73.1

(a) The knee as a hinge joint: the femoral condyles (twin wheel) in relation to the tibial and patellar surfaces ('rails'). (b) By flattening the anterior and posterior end of the 'rail', rotational movements become possible; the intercondylar spines act as the central pivot. 1053

1054 SECTION THIRTEEN - THE KNEE

The tibial aspect of the joint is two curved 'gutters', separated by an anteroposterior eminence. These gutters are not congruent with the corresponding condyles but this lack of compatibility is corrected by the menisci. The anteroposterior elevation between the tibial condyles corresponds with the femoral intercondylar notch. If the surfaces of the tibial condyles are projected anteriorly, they coincide with the articular surface of the patella which corresponds to, and is almost congruent with, the anterior surfaces of the femoral condyles. If the intercondylar eminence of the tibia is projected anteriorly, its plane is continuous with the vertical ridge on the patella just as the intercondylar notch of the femur con­ tinues in the central groove of the patellar surface of the femur. This arrangement resembles a twin-wheel rolling on a central rail (Fig. 73.1a). During flexion and extension, tibia and patella act as one structure in relation to the femur. I The rounded surfaces of the femoral condyles in rela­ tion to the flatter tibial ones might suggest that the former roll during flexion-extension. In fact this is not so. As long ago as 1836 the Weber brothers demonstrated that the femoral condyles roll and slide almost simultane­ ously, and that these movements are in opposite direc­ tions. During flexion, the femoral condyles roll backwards and slide forwards on the tibia, whereas during extension they roll forwards and slide backwards. The ratio of rolling to sliding differs with the degree of flexion or extension, which means that during the first 30° of flexion the movement is almost entirely rolling, whereas at nearly full flexion the condyles slip over the tibial plateau without rolling.2 The knee joint is thus primarily a hinge, with the wheel-shaped surfaces of the femoral condyles gliding and rolling in a twin set of concave curved gutters: the tibial and patellar surfaces. However, while this is a sat­ isfactory concept in terms of flexion and extension, in reality the situation is more complex because the knee

Figure 73.2

Surfaces of the patella: (a) anterior; (b) posterior.

allows not only gliding and rotation around a horizontal axis but also rotation through a vertical axis, i.e. internal and external rotation of the tibia in relation to the femur. Were the knee to be only as so far described - a hinge joint with a long tibial intercondylar eminence gliding between the two femoral condyles - rotation would be precluded. However, if the anterior and posterior ends are flattened, rotation becomes possible (Fig. 73.1b). The remaining middle part of the eminence, forming the 'intercondylar spines', is then the central pivot about which the movements of axial rotation occur. The knee joint is a hinge joint during flexion-extension but in a flexed position modifications enable axial rotation around a central pivot.

THE PATELLA

The patella is a flat, triangular bone, situated on the front of the knee joint (Fig. 73.2). It is usually regarded as a sesamoid bone, developed in the quadriceps femoris tendon. Its convex anterior surface is covered by an expansion from the tendon of the quadriceps femoris which is continuous below with the superficial fibres of the ligamentum patellae. It is separated from the skin by a bursa (prepatellar bursa). The posterior surface presents above a smooth, oval, cartilaginous area, which is divided by a rounded vertical ridge into a larger, lateral portion, for articulation with the lateral condyle of the femur, and a smaller, medial portion, for articulation with the medial condyle of the femur. Below the articular surface is a rough, convex, non-articular area, the lower half of which gives attach­ ment to the ligamentum patellae; the upper half is sepa­ rated from the head of the tibia by adipose tissue.

CHAPTER 73 - APPLIED ANATOMY 1055

The superior border of the patella is thick, and sloped from'behind, downwards and forwards; it gives attach­ ment to that portion of the quadriceps which is derived from the rectus femoris and the vastus intermedius muscles. The medial and lateral borders are thinner and give attachment to those portions of the quadriceps femoris which are derived from the vasti lateralis and medialis. The apex is pointed and gives attachment to the ligamentum patellae. The patella serves to protect the front of the joint and increases the leverage of the quadriceps femoris by making it act at a greater angle.

THE MENISCI

There are two menisci in the space between the femoral and tibial condyles. They are crescent-shaped lamellae, each with an anterior and a posterior horn, and are trian­ gular in cross section. The superior and inferior surfaces are in contact with the femoral and tibial condyles, respectively, and the peripheral surfaces are adherent to the synovial membrane of the capsule. The anterior and posterior horns are anchored to the tibial condyle in the anterior and posterior intercondylar fossae, respectively. The horns of the medial meniscus are further apart than those of the lateral, which makes the former nearly semi­ lunar and the latter almost circular. The menisci correct the lack of congruence between the articular surfaces of tibia and femur, increase the area of contact and improve weight distribution and shock absorption.3-6 They also help to guide and coordinate knee motion, making them very important stabilizers of the knee. Movement between the tibial surface and the menisci is limited by the coronary ligaments, cOlmecting the outer meniscal borders with the tibial edge (see Fig. 73.3). The coronary ligaments of the medial meniscus are shorter (4-55 mm) and stronger than those of the lateral menis­ cus (13-20 mm)? The medial collateral ligament of the knee is attached by its deep fibres to the outer border of the medial meniscus. In contrast, there is no connection between the lateral meniscus and the corresponding col­ lateral ligament (Fig. 73.4). These anatomical differences between the medial and the lateral meniscus may explain the lesser mobility and the greater vulnerability of the former (Fig. 73.3).8 There are only a few muscle fibres attached to the menisci. The popliteus sends a fibrous expansion to the posterior border of the lateral meniscus and a few fibres of the semimembranosus tendon run to the posterior edge of the medial meniscus. Menisci do not contain pain-sensitive structures and are consequently insensitive to trauma. Their outer third

5 7

6

Figure 73.3 Superior view of the menisci and their attachments (right knee). 1, lateral collateral ligament; 2, medial collateral ligament; 3, medial coronary ligament; 4, lateral coronary ligament; 5, popliteus tendon; 6, posterior cruciate ligament; 7, semimembranosus tendon.

has some blood supply and therefore a slight ability to heal. The inner non-vascularized part receives nutrition through diffusion of synovial fluid.9,lD MOVEMENTS OF THE MENISCI

The inner sides of the menisci, attached by their horns to the tibial plateau, move with the tibia. The body of each meniscus is fixed around the femoral condyle and moves with the femur. Therefore, during movement between tibia and femur, distortion of the menisci is inevitable. Because the horns of the lateral meniscus are attached closer together and its body is more mobile, distortion is more marked in it.

4

3 2

Figure 73.4 Anterior view of the menisci and their relations with the collateral ligaments: 1 , medial meniscus; 2, medial collateral ligament; 3, lateral collateral ligament; 4, lateral meniscus.

1056 SECTION THIRTEEN - THE KNEE

(a)

wards (Fig. 73.5a). On the medial aspect the anterior part of the medial coronary ligament then comes under tension. The same effect occurs in the medial rotation: the medial meniscus is pressed forwards and the lateral meniscus drawn backwards (Fig. 73.5b), which causes tension in the anterior part of the lateral coronary ligament.

JOINT CAPSULE AND LIGAMENTS CAPSULE

(b)

.....

Figure 73.5 Relative movement between tibia and menisci during rotation under 90° of fiexion: (a) lateral rotation of the tibia; (b) medial rotation of the tibia.

During flexion of the knee, the body of the meniscus moves posteriorly and during extension it moves anteri­ orly. In lateral (axial) rotation, the menisci will follow exactly the displacement of the femoral condyles, which means that the lateral meniscus will be pushed forwards on the tibia and the medial meniscus will be pulled back-

(a)

(b)

The capsule connects the distal end of the femur with the proximal border of the tibia. It consists of a fibrous sleeve and a synovial membrane, the attachments of which do not always coincide: only the synovial membrane is adherent to the peripheral surface of the menisci. Reinforcements in, or along the fibrous capsule keep the bones in contact, giving the joint passive stability. The tibial attachment of the capsule (Fig. 73.6a) is attached to the borders of the articular surfaces of the tibia and therefore follows its anterior, medial and lateral edges. At the posterior border the synovial membrane follows the edges of the medial and lateral condyles, to form a loop around the insertion of the anterior cruciate ligament. At the anterior border the synovial membrane is projected backwards by a sizeable pad of adipose tissue - the infrapatellar pad. The femoral attachment of the capsule also follows the articular surfaces of the femur, although there are some points to be noted: •

Anteriorly the capsule is attached proximal to the edge of the articular surface, thus forming the suprapatellar pouch (Fig. 73.6b).

(c)

----

fibrous capsule

----- synovial capsule Figure 73.6 (a) Insertions of the capsule into the tibia, and its relations with the cruciate ligaments (shaded). (b) Anterior and medial insertions of the capsule into the femur. (c) Lateral insertion and relationship of the capsule and the popliteus tendon.

CHAPTER 73

•

•

-

APPLIED ANATOMY 1057

On the lateral condyle the attachment of the fibrous capsule lies above the insertion of the popliteus tendon, which makes the latter lie intra-articularly, covered only by the synovial membrane (Fig. 73.6c). Posteriorly and following the articular surfaces of the femoral condyles, the attachment of the synovial membrane dives into the intercondylar notch to form a loop around the femoral insertions of the cruciate ligaments. The cruciate ligaments are thus kept outside the capsule by an invagination of the synovial membrane, which forms a partition in the sagittal plane of the joint space.

At the patella, the capsule follows the margins of the bone. 2

LIGAMENTS The medial ligamentous complex

The medial ligamentous complex has two layers: the deeply situated capsular reinforcements with an anterior, medial and posterior part, and the strong and more superficially localized medial collateral ligament (MCL). The MCL is the primary stabilizer of the medial side of the knee. It is a broad, flat and almost triangular band with a large femoral attachment on the posterosuperior aspect of the epicondyle. Its fibres run obliquely anteri­ orly and inferiorly to insert at the medial aspect of the tibia, just behind and slightly under the insertions of the semitendinosus muscle. The anterior fibres of the liga­ ment are separated from those of the deep capsular reinforcements and therefore the anterior border of the ligament can be palpated easily. The posterior fibres, however, blend intimately with the capsule and with the medial border of the medial meniscus (Fig. 73.7),u The strong MCL stabilizes the knee against excessive valgus forces and external rotation. Although it slackens during flexion, the posterior fibres attached to the menis­ cus remain taut, an observation that is important in the consideration of chronic ligamentous adhesions of the MCL (see p. 1102). The lateral collateral ligament

The lateral collateral ligament (LCL) is part of the so­ called lateral quadruple complex (biceps tendon, iliotib­ ial tract, popliteus and LCL), responsible for the lateral stability of the knee. It is round in cross-section and runs from the lateral epicondyle of the femur to the head of the fibula, deep to the insertion of the biceps. The ligament lies completely free, separated from the capsule and the lateral meniscus by the popliteus tendon (see Figs 73.3 and 73.10). It stabilizes the knee against excessive varus movement. A small bursa lies between the popliteus tendon and the LCL.

Figure 73.1

The medial collateral ligament (1 ) and medial meniscus (2).

The posterior capsular reinforcements

The posterior capsule is strengthened by two irregular lig­ amentous structures: the oblique popliteal and the arcuate popliteal ligaments. The former is an expansion of the semimembranosus tendon and reinforces the central poste­ rior part of the joint capsule. The fibres of the latter run obliquely medially and upwards from the rear side of the fibular head to the posterior aspect of the femur. The cruciate ligaments

Although the cruciate ligaments lie in the centre of the joint (Fig. 73.8), they remain extrasynovial because of the posterior invagination of the synovial membrane. They ensure the anteroposterior stability of the knee and, together with the collateral ligaments, prevent rotational movements during extension. The anterior cruciate ligament. This is attached to the

anterior intercondylar area of the tibia, between the anterior horns of the medial and lateral menisci. Its fibres run laterally and posteriorly to the internal aspect of the lateral condyle of the femur. It has three coiled bundles (anteromedial, intermediate and anterolateral), which spiral from one insertion to the other. In extension, the anterior bundle is tight but in flexion the posterior fibres are stretched, which causes the anterior cruciate to be tightest at the extremes of range.

1058 SECTION THIRTEEN - THE KNEE

9

2

3

6

Figure 73.8

Posteromedial view of the cruciate ligaments: 1, anterior; 2, posterior.

During flexion, the femoral condyles tend to roll back­ wards over the tibia. This is checked by the anterior cru­ ciate ligament, which induces a simultaneous anterior gliding of the femur. The anterior cruciate ligament also prevents excessive external rotation and varus movement of the tibia. The posterior cruciate ligament. The tibial attachment of the posterior cruciate ligament is at the posterior inter­ condylar area but fans out at the posterior border of the tibial plateau. The ligament runs in a medial and anterior direction and crosses the anterior cruciate ligament from medial and from behind to insert at the lateral surface of the medial condyle, deeply in the intercondylar fossa. Like the anterior cruciate, the posterior cruciate ligament has a complex architecture but is twice as strong. It is a basic knee stabilizer, tightest in mid-position. During extension, the posterior cruciate ligament pulls on the femur, causing backwards sliding during its anterior rolling. The posterior cruciate ligament also prevents anterior gliding of the femur during squatting, resists hyperextension and has an important role in the medial stability of the knee.13 The coronary ligaments

The meniscotibial or coronary ligaments connect the periphery of the menisci with the edge of the tibial condyle (Fig. 73.9).14,15 Some anatomists do not consider them to be real ligaments but merely reinforcements in the synovial membrane.16

Figure 73.9 Anterior view of the coronary ligaments, with the knee in flexion: 1, medial collateral ligament: 2, lateral collateral ligament; 3, popliteus tendon; 4, medial meniscus; 5, lateral meniscus; 6, lateral coronary ligament; 7, medial coronary ligament; S, posterior cruciate ligament; 9, anterior cruciate ligament.

The fibres of the medial coronary ligament are 4-5 mm long, while those of the lateral coronary ligament are 2 cm long at the front and 1.3 cm at the back. The fibres of the lateral ligament are also looser than the medial ones. The medial coronary ligament is stretched during external rotation, while the lateral is stretched during internal rotation.

MUSCLES AND TENDONS THE EXTENSOR MECHANISM (Fig. 73.10)

The extensor of the knee is the quadriceps; it consists of four muscle bellies. Three are monoarticular muscles - the vastus medialis, the vastus intermedius and the vastus lateralis. One is biarticular and spans knee and hip joints - the rectus femoris. These separate bellies have a common tendon, which inserts into the anterior tibial tuberosity. Imbedded in the tendon is the patella, a trian­ gular sesamoid bone. The function of the patella is to increase the efficiency of the quadriceps contractions. It is important to note that the patella lies fully within the tendon, which means there are tendon fibres all around the patellar edge. This has significant clinical conse­ quences, since a tenoperiosteal tendinitis at the patella will occur not only at the distal but also at the proximal' and sometimes even at the medial and lateral sides of the patella. For convenience, we call the part of the tendon

CHAPTER 73 - APPLIED ANATOMY 1059

•

t.\\bf----f-- Quadriceps •

-'-.-\-\-t-\\:\----+ Suprapatellar tendon

"r--+-- Medial expansion

Lateral expansion

•

Patella ----+--+--c:+--\lt--,--! t-7"'-1I-flf'o'..;,,;.o.."';"r-l--- nfrapatellar tendon •

Figure 73.10

The extensor mechanism of the knee.

above the patella the suprapatellar tendon (quadriceps tendon), the inferior part the inirapatellar tendon (or patel­ lar ligament), and the medial and lateral fibres the medial and lateral quadriceps expansions; they are, nevertheless, only parts of a single tendon. The biarticular nature of the rectus femoris and the fact that it runs anterior to the flexion-extension axis of the hip gives it the specific function of a hip flexor (see Ch. 65). Some deeply situated fibres of the vastus intermedius run to the superior capsule of the knee joint, where they pull the loose capsule away from the joint and prevent the suprapatellar pouch from being pinched during knee motion. Another, but weak, extensor of the knee is the tensor fasciae latae, which acts through the iliotibial tract, but only when the knee is extended. In flexion greater than 30°, the iliotibial tract becomes a weak knee flexor and an external rotator. The main function of the tract is to create static lateral stabilization of the knee.

The gastrocnemii although strong plantiflexors and invertors of the heel, are only weak flexors of the knee. They also help in active stabilization of the joint. The medial head is a weak internal and the lateral head a weak external rotator. The semitendinosus, gracilis and sartorius insert under and in front of the medial condyle of the tibia in the so-called 'pes anserinus', just medial to the tibial tuberosity and anterior to the tibial insertion of the MCL. They are flexors and internal rotators of the knee (Fig. 73.11). The semimembranosus inserts at the medial condyle of the tibia but has some fascicles attaching to the oblique popliteal ligament and a few fibres attaching to the posterior edge of the medial meniscus. It is a flexor and an internal rotator. The popliteus muscle originates within the joint at the lateral epicondyle of the femur (Fig. 73.12). Other origins are situated at the dorsal aspect of the capsule and the lateral meniscus. The muscle belly lies deeply in the popliteal fossa under the lateral gastrocnemius and the plantaris. The broad insertion is at the upper and posterior aspect of the tibia. The popli teus is a flexor and an internal rotator of the knee. It also spans the posterior capsule of the knee and pulls the lateral meniscus in a posterior direction during

1I!/IIJfWh'lj1f--- 4

FLEXORS OF THE KNEE

The knee flexors are the hamstrings (semitendinosus, semimembranosus and biceps femoris), the sartorius and the gracilis, the popliteus and the gastrocnemii.

Figure 73.11 Medial view of the knee showing the relations between the tendons: 1, insertion of the pes anserinus; 2, semitendinosus; 3 and 4, semimembranosus; 5, gracilis; 6, sartorius.

1060 SECTION THIRTEEN - THE KNEE

•

flexion. Another important function of the muscle is to prevent the femur from slipping forwards on the tibia during squatting. This active function of the popliteus is very similar to the static role of the posterior cruciate ligament. The biceps femoris or lateral hamstring inserts at the top and posterior aspect of the fibular head in front of and behind the insertion of the lateral collateral ligament (see Fig. 73.12). Some fibres also attach to the posterolateral aspect of the tibia and the lateral part of the joint capsule. It is a strong flexor and external rotator of the knee.

2

liV�,",+"-=----JHt- 3

Muscular function of the knee is summarized in Box 73.1. INNERVATION OF THE MUSCLES

This is detailed in Table 73.1.

Box 73.1 Summary of muscular function

Figure 73.12 Lateral view of the knee, showing the relations between the lateral muscles and ligaments: 1 , biceps femoris; 2, lateral collateral ligament; 3, popliteus; 4, iliotibial tract

Extension

Quadriceps femoris (Iliotibial tract)

.

Flexion

Internal rotators Gracilis Sartorius Semitendinosus Semimembranosus Popliteus External rotators Biceps femoris Iliotibial tract

NERVE STRUCTURES AND BLOOD VESSELS: THE POPLITEAL FOSSA

The lozenge-shaped popliteal fossa is an anatomical space of particular importance because it contains the

Stretching the capsule

Medial Semimembranosus Lateral Popliteus Anterior Vastus intermedius

Table 73.1

Innervation of the muscles

Extension Quadriceps Flexion Semitendinosus Semimembranosus Gracilis Sartorius Popliteus Biceps femoris Tensor fasciae latae Gastrocnemius

Peripheral nerve

Spinal innervation

Femoral

L2, L3, L4

Tibial Tibial Obturator Femoral Tibial Sciatic Superior gluteal Tibial

L5, S1, S2 L5, S1, S2 L2, L3, L4 L2. L3 L4, L5, S1 L5, S1 L4, L5 S1, S2

Figure 73.13 The popliteal fossa: 1 , biceps femoris; 2, tibial nerve; 3, popliteal vein; 4, popliteal artery; 5, common peroneal nerve; 6, lateral gastrocnemius; 7, medial gastrocnemius; 8, semimembranosus; 9, gracilis; 10, semitendinosus.

CHAPTER 73

vessels and nerves of the lower limb (Fig. 73.13). Its lower borders are formed by the heads of the gastronemius. The upper lateral border is the biceps femoris and the upper medial border the semitendinosus and semimembra­ nosus muscles. Its floor is the posterior capsule and the popliteus muscle. The popliteal fossa is bounded posteri­ orly by the deep popliteal fascia. The lozenge is traversed vertically by (from lateral to medial) the tibial nerve, the popliteal vein and the popliteal artery. The common peroneal nerve descends along the inner border of the biceps. At the head of the fibula it splits into a deep peroneal branch, which curls around the fibular head to enter the anterior compartment

-

APPLIED ANATOMY 1061

of the leg, and a superficial peroneal branch, which sup­ plies the peroneal muscles in the lateral compartment.

THE UPPER TIBIOFIBULAR JOINT

This joint is separate from the knee. The capsule is rein­ forced in front and behind by two tibiofibular ligaments. Little movement takes place at the tibiofibular joint. The biceps femoris can pull the fibular head slightly back­ wards during active knee flexion, and slight passive upwards and downwards movements of the fibula may follow valgus and varus movements of the talus.

REFERENCES 1.

Kapandji IA. The Physiology of the JOillts, vol 2: Lower Lil1lb, 5th edn. Churchill Livingstone, Edinburgh, 1987.

2.

10. Danzig L, Resnick D, Gonsalves M, Akeson WHo Blood supply

and dynamic behavior of the human knee in vivo. J Biomech

to the normal and abnormal menisci of the human knee. Ciill

Seedbom BB, Dowson D, Wright V. F unctions of the menisci a preliminary study. J Balle Joint Surg 1974;56B:381.

4.

Seedholm BB, Hargraves DJ. Transmission of load in the knee

Amsterdam, 1966:150.

Shrive NG, O'Connor JJ, Goodfellow lW. Load bearing in the Walker PS, Erkman MJ. The role of the menisci in force trans­ Seedhom BB, Dowson 0, Wright V. The load-bearing function of the menisci: a preliminary study. In: Ingwersen OS, Van Linge B, Van Rens TJG, Rosingh GE, Veraart B, Le Vau D (eds) The Knee Joint. Excerpta Medica and American Elsevier, 1974:37-42.

8.

1:

Teil

mission across the knee. Ciin Orthap 1975;109:184. 7.

Wolfe, London, 1977:308-310. 12. Spalteholz W, Spanner R. Hllndlltllls der Anlltolllie des Menschel1.

experimental results, discussion and conclusions. Eng Med

knee joint. Ciin Orthop 1978;131:129. 6.

Orthop 1983;172:27l. 11. McMinn RMH, Hutchings RT. A Colour AtillS of HUIIIIlII AlIlltomy.

joint with special reference to the role of the menisci. Part II: 1979;8:220. 5.

and its response to injury. Alii J Sports Med 1983;11:131.

Pope MH, Crowninshield R, Miller R, Johnson R. The static 1976;9:449-452.

3.

9. Arnoczky SP, Warren RF. T he micro-vasculature of the meniscus

McDermott LJ. Development of the human knee joint. Arch Surg 1943;46:705-719.

Bewegungsapparat,

16th

edn.

Scheltema

Holkema,

13. Girgis F G, Marshall JL, Monajem ARS. The cruciate ligaments

of the knee joint. Anatomical, fwlctional and experimental analysis. Ciin Orthop 1975;106:216-23l. 14. Gollehon DL, Torzill PA, Warren RF. The role of the postero­

lateral and cruciate ligaments in the stability of the human knee. A biomedlanical study. J Bone Joillt Surg 1987;69A:233-242. 15. Williams

P,

Warwick R. Grny's Anlltomy. Churchill Livingstone,

London, 1980. 16. Sobotta

J, Becher H. Atlas of HUII/Illl Allatol11Y.

Smwarzenberg, Munich, 1975.

Urban &

THIS PAGE INTENTIONALLY LEFT BLANK

Clinical examination of the knee

CHAPTER CONTENTS R�ferred pain 1063 Pain referred to the knee 1063 Pain referred from the knee 1064 History 1064 Onset 1064 Evolution 1065 Current symptoms

1065

Inspection 1065 In the standing position 1065 In the sitting position 1065 In the supine position 1065

REFERRED PAIN

Functional examination 1066 Two primary movements for the joint 1066 Eight secondary movements for the ligaments Two resisted movements for the contractile 1069 structures Palpation 1070 Fluid 1070 Heat 1071 Synovial thickening 1072 Deform ities 1072 Tenderness 1072 Palpation of the moving joint

1072

Accessory tests 1072 Bilateral passive rotations 1072 Resisted internal and external rotation Squatting 1073 Other tests 1073

1073

1066

PAIN REFERRED TO THE KNEE

The front of the knee represents the second and third lumbar dermatomes. Two structures, the hip and third lumbar nerve root, are apt to give referred pain in this area. When a referred pain to the knee is suspected, the diagnostic points in the history are the indefinite area of complaint and radiation 'upwards' along the anterior aspect of the thigh. Asked for the exact site of pain, the patient points to the whole suprapatellar area and the front of the thigh. In vague anterior knee pain, the lumbar spine and the hip joint must he examined immediately. This is especially so in children complain­ ing of knee pain but who are in fact developing hip disease, such as aseptic necrosis or epiphysiolysis. Another common error is to take a radiograph of an elderly person's knee because the pain is felt here, only to almost certainly find some osteoarthrosis at the knee but to miss the osteoarthrotic hip. The back of the knee is innervated by the first and second sacral segments. Disorders of the first and second sacral roots, and also the sacroiliac joints, can refer pain to this area. Again, the patient cannot point exactly to the site of pain. The pain distribution remains vague and spreads upwards along the thigh or down­ wards in the calf. There is also no history of relevant trauma. Also compression of 51, caused either by a primary posterolateral protrusion in a young adult or by a narrowed lateral recess in an elderly person, may provoke pain at the back of the knee only. As pain is not felt in the back or buttock at the onset, the symptoms do not draw immediate attention to the possibility of a lumbar disorder. Once again a careful history suggests the diagnosis. With a primary posterolateral protrusion, the patient will have noticed that sitting and coughing hurts the knee, whereas walking does not. In compres­ sion of the nerve root in a narrow lateral canal, com­ plaints are related to walking and standing, whereas bending usually relieves the pain.

1063

1064 SECTION THIRTEEN - THE KNEE

PAIN REFERRED FROM THE KNEE

Lesions of the knee are usually located accurately by the patient at or in the knee. Sometimes an impacted loose body complicating osteoarthrosis can cause pain referred down the leg and slightly up the thigh but this is rather exceptional.

In knee problems there are three important symptoms that provide a great deal of information: 'locking', 'twinge' and 'feeling of giving way'. Because the meaning of these words is not always totally understood and patients fre­ quently confuse them, it is vital to describe what is exactly meant when asking about these symptoms. •

HISTORY

Knee problems are always difficult and hard to evaluate and every possible assistance is needed to make a proper diagnosis. A chronological history, as summarized in Box 74.1, is therefore the first, and sometimes even the most important, feature: Cyriax used to say that one who 'doesn't have a diagnosis after the history, will hardly get one after the clinical examination'. Age is a very important factor, because some disorders at the knee appear only during a certain period of life. Anterior knee pain in an adolescent can be the outcome of Osgood-Schlatter disease, whereas the same pain in a 30-year-old sportsman is the result of infrapatellar ten­ dinitis and in a 50-year-old lady patello-femoral arthro­ sis. Symptoms of internal derangement in a 17-year-old boy almost certainly indicate an osteochondritis disse­ cans, in a 25-year-old sportsman may suggest a meniscus lesion and in a 60-year-old lady probably are the result of impaction of a small loose body. The patient should be queried about occupation and sporting activities.

•

•

In order to work out the diagnosis systematically and chronologically, it is as well to start with the onset of the symptoms before concentrating on the symptoms at the time of examination. ONSET • •

Box 74.1 Summary of history taking Age, sex, occupation and sport Site of pain Onset Trauma Mechanism Immediate symptoms Symptoms after 24 hours Non-traumatic Sudden or gradual onset What affects it? Evolution Better/worse Changing localization Treatments and results Current symptoms Localization Swelling Influence of movements Instability Twinges Clicks

Locking: sudden (painful) limitation occurs during one movement, whereas other movements are free and painless. The knee can be locked in flexion (extension being limited) or extension (flexion being impossible). Twinge: a sudden, sharp and unexpected pain is felt. For instance the patient feels an abrupt, unforeseen and sharp pain at the inner side of the knee during walking. The pain disappears immediately and normal walking again becomes possible. Feeling of giving way: this is the typical sensation in instability; a sudden feeling of weakness. It feels as if the knee cannot bear the body weight during a particular movement. The knee tends to 'collapse'.

When did it start? Is this an acute, a subacute or a chronic problem? How did it start? Did the pain come on for no apparent reason or was there an injury?

If there was a trauma

Describe the exact mechanism: • •

In what position was the body and the leg? What forces were acting on the knee?

Describe the immediate symptoms: • •

• •

Where was the initial pain? At one side, all over or inside the joint?

Was there any swelling? Immediately or after some time? An immediate effusion is always haemorrhagic and therefore indicates a serious lesion. If a swelling appears after some time, it is the consequence of a synovial reaction. Did the knee give way? Immediately or after some time? Was there any locking? If so, was the knee locked in flexion (which is typical for meniscal lesions) or V'vas it in extension (as in impacted loose bodies from osteochondritis dissecans)? How did the knee

CHAPTER 74

become unlocked? By manipulation (meniscus) or spontaneously (loose body)? •

• •

Did the pain come on suddenly or gradually? What were you doing when the pain first appeared? Describe the first symptoms. These may include local­ ization, swelling, locking or loss of function (see earlier).

EVOLUTION

In long-standing cases or in traumatic conditions, it is very important to have an exact idea of the evolution of the complaints. •

Did the pain change from one side of the joint to the other or did the pain spread? A pain moving from one side of the joint to another is characteristic of a loose body: the localization of the pain travels with the impacted loose fragment.

• • • •

What was the evolution of the swelling? For how long were you disabled? What treatment did you have and with what effect? Have there been any recurrences? If so, what brought them on and how did they progress?

CURRENT SYM PTOMS

Finally we arrive where we started the investigation: the current complaint is discussed. • • •

•

• • • •

CLINICAL EXAMINATION

1065

At the end of history taking, the patient must be asked about the general state of health.

Were you still able to walk home after the accident?

If there was no trauma •

-

Describe the exact localization. What brings the pain on? Do you have nocturnal pain or morning stiffness? Pain at night usually indicates a high degree of inflamma­ tion. It occurs in acute ligamentous lesions, haemarthrosis and arthritis. Long-standing morning stiffness is usually an indication of rheumatic inflammation.

What is the effect of going up and down stairs and which is the more troublesome? Going down stairs not only loads the extensor mechanism but also the posterior cruciate ligament and the popliteus tendon. Going down stairs is also very painful in impacted loose bodies. Do you have twinges? Very often a twinge means an impacted loose body or a meniscus. Does the knee give way? Either actually or feel as though it might.

Does the knee click or grate? Have any other joints been affected?

IN SPECTION IN THE STANDING POSITION

The lower extremities are first viewed with the patient standing. Alignment of the femur, varus or valgus posi­ tions of the lower leg, pronation of the feet and align­ ment of the patella are observed from the front. Some genu valgum deformity in children is normal and usually disappears with growth. When the cause is some valgus position of the heel and inversion of the forefoot, appropriate measures can be taken. Excessive genu valgum deformity in elderly patients may suggest osteitis deformans. A view from the side detects any recurvatum or lack of complete extension. Observation for tibial torsion is done standing above the patient's knees and gazing downwards along the tibial tuberosi ty and anterior tibial crest. The coronal plane of the knee is then compared with an imaginary line connecting the medial and lateral malleoli of the ankle. Tibial torsion between a and 40° is normal.

IN THE SITTING POSITION

The most important observations of the patellar pOSition are made with the patient seated on the examination table, the legs hanging free and the knees flexed to 90°. The examiner first assesses the patellar position and the position of the tibial tuberosity and patellar ligament by viewing the knee from the lateral aspect. Thereafter the examiner views the knees from the anterior aspect while the patient holds both knees together. Normally posi­ tioned patellae face straight ahead. Malalignment of the kneecap is seen as a patella looking up and over the shoulders of the examiner (see p. 1139).

IN THE SUPINE POSITION

The supine-lying position is the best from which to observe swelling at the knee joint. Diffuse swelling indicates fluid in the joint and/ or synovial swelling. In advanced arthritis, or in large blood effusions, the knee may adopt a slightly flexed position. Diffuse swelling with muscular wasting may indicate severe and long-standing arthritis. Swelling with redden­ ing of the skin suggests sepsis or gout. Localized swellings are caused by bony outcrops, cysts or inflamed bursae, such as a prepatellar or infrapatellar

1066 SECTION THIRTEEN - THE KNEE

bursa, a semitendinosus bursa, a bursa under the medial collateral ligament, a lateral or medial meniscus cyst or a Baker's cyst.

FUNCTION AL EXAMIN ATION

The routine clinical examination of the knee consists of 10 passive movements, two for the joint and eight for the ligaments and two resisted movements (Table 74.1). If signs warrant, or if suspicion of meniscal lesions or instability arises from the history, complementary tests can be performed. o

LIG AMENTS

•

Movements

Joints

Flexion

Extension

Ligaments

Varus

Valgus

Medial rotation

Lateral rotation

Resisted tests

•

Anterior drawer test

Posterior drawer test

Medial shearing

Lateral shearing

Resisted flexion

Resisted extension

(ReSisted medial rotation)

(Resisted lateral rotation)

Retest for heat, swelling, tenderness

Palpation for tenderness is only sought along the struc­ ture identified by the functional examination and therefore only performed after this examination. However, palpa­ tion for heat, fluid and synovial thickening is performed before the functional examination. TWO PRIM ARY MOVEM ENTS FOR THE JOINT

As in the elbow, the range of rotation becomes restricted only in advanced arthritis. Therefore extension and flexion (Fig. 74.1) are the two movements used to test the mobility of the joint. Extension

Normally, the knee can be extended until the tibia comes into line with the femur but in young people some hyperextension can occur and is normal. Extension is limited by the posterior cruciate ligament and the pos­ terior capsule. The end-feel is hard. The evaluation of the end-feel during extension is extremely important and can only be tested if a correct technique is used. One hand takes the heel of the patient; the fingers of the other hand carry the knee, while the thumb presses on the tibia, just below the patella. A quick and short extension movement is now performed by simultaneous upwards movement of the heel and down­ wards pressure on the tibia. o

A normal knee can be flexed until the heel reaches the buttock. Flexion is normally limited by contact between the thigh and calf muscles; the end-feel is there­ fore of the extra-articular type - softish. A painful arc during flexion-extension is rather excep­ tional. When present, it indicates an impacted loose body, a torn meniscus or localized erosion of the articular edge of the femur. A painful arc can also be present in lesions of the iliotibial tract (friction syndrome or bursitis). Here pain is elicited as the tract rides over the lateral femoral condyle. o

EIGHT SECONDARY MOVEMENTS FOR THE

Table 74.1 Functional examination Test for heat, swelling, synovial thickening Testing

Flexion

Stretching the ligaments tests them for pain and laxity. Valgus strain

Strong valgus movement applied with counterpres sure at the lateral femoral condyle tests the medial collateral ligament (Fig. 74.2a). Normally this is done in full extension. In a minor sprain or in a minor degree of instability resulting from previous overstretching, pain and laxity are probably better disclosed if the test is repeated in slight flexion (30°). o

Varus strain

Strong varus movement is applied during counter pressure at the medial femoral condyle and tests the lateral collateral ligament (Fig. 74.2b). Again the test can be repeated in slight flexion (30°). o

Lateral rotation

Lateral rotation of the knee puts stress on the medial coronary ligament and the posterior fibres of the medial collateral ligament. The knee is flexed to a right angle and the heel rests on the couch. To prevent rotation in the hip, the examiner places the contralateral shoulder against the knee, the arm under the lower leg and a hand under the heel. The other hand is placed at the inner side of the foot, which is pressed upwards in dorsiflexion. Lateral rotation is now easily performed by using the foot as a lever (Fig. 74.3a). The normal end-feel is elastic. o

Medial rotation

Medial rotation puts stress on the lateral coronary ligament and the anterior cruciate ligament. The hip and knee are flexed to right angles. The lower leg is sup­ ported by the contralateral forearm of the examiner. The hands are clasped tightly about the patient's heel, which is forced into dorsiflexion. By a combined �10ve­ ment of both wrists, the leg is turned into medial rotation (Fig. 74.3b). In order to protect the lateral ligaments of the o

CHAPTER 74

Extension (a) and flexion (b) of the knee.

ankle, it is important to exert the pressure at the ankle and not beyond the calcaneocuboid joint line. The normal end-feel is elastic. Anterior drawer test

The knee is flexed to a right angle, the examiner sits on the patient's foot and places one hand on the patella. The other hand is placed at the back of the upper tibia, which is drawn forwards with a strong jerk

to test for pain if the anterior cruciate ligament is damaged (Fig. 74.4a). The anterior drawer test in 30° of flexion ('Lachman's test') seems to be more precise in disclosing elongation or rupture in the anterior cruciate ligament (see Ch. 77). Posterior drawer test o

(b)

(a) Figure 74.2

CLINICAL EXAMINATION 1067

(b)

(a) Figure 74.1

-

Valgus (a) and varus (b) movement.

The examiner once again sits on the patient's foot. One hand is placed on the tibial tuberosity, the other

1068 SECTION THIRTEEN - THE KNEE

(b)

(a) Figure 74.3

Lateral (a) and medial (b) rotation.

rests at the back of the knee. A strong backwards jerk is exerted on the tibia to test the integrity of the posterior cruciate ligament (Fig. 74.4b). In a normal joint, no move­ ment takes place and the test is completely painless.

The knee is held at a right angle. The examiner sits opposite the patient, interlocks his fingers and places the heel of one hand at the lateral tibial condyle,

(a)

(b)

Figure 74.4

The anterior (a) and posterior (b) drawer tests.

Medial shearing strain o

CHAPTER 74

the heel of the other hand at the medial femoral condyle. By applying a strong shearing strain, an attempt is made to move the tibia medially on the femur (Fig. 74.5a). Pain may be elicited when a loose body is present. In a tear of the lateral meniscus, this manoeuvre can displace part of the meniscus to the other side of the femoral condyle. A loud click is then heard and full range of passive exten­ sion immediately becomes lost. Lateral shearing strain

This action is the reverse of medial shearing strain. The heel of one hand is placed on the lateral femoral condyle and the heel of the other on the medial tibial condyle (Fig. 74.5b). A strong shearing force moves the tibia laterally on the femur and may provoke a click when a loose body or a longitudinal tear of the medial o

(a)

(b) Figure 74.5

Medial (a) and lateral (b) shearing strain.

-

CLINICAL EXAMINATION 1069

meniscus is present. It also elicits pain when a strain of the posterior cruciate ligament is present. TWO RESISTED MOVEM ENTS FOR THE CONTRACTILE STRUCTURES

For convenience, resisted flexion and extension are tested with the patient supine but stronger force can be exerted if he or she is prone. Resisted extension

The knee is kept slightly bent. The examiner places one arm under the knee. The other hand is placed on the distal end of the tibia, where it resists extension by the patient (Fig. 74.6a). Pain and weakness are noted. If there is pain, a lesion of the quadriceps mechanism is o

1070 SECTION THIRTEEN - THE KNEE

likely. If there is weakness, a lesion of the nerve supply, usually the third lumbar nerve root, is present. Pain and weakness occur in a fractured patella or after a major rupture of the muscle belly.

the knee is held passively flexed. This test distinguishes between lateral (biceps) and medial (semimembranosus, semitendinosus and popliteus) rotators of the knee.

Resisted flexion

PALPATION

The hip and knee are bent to right angles. The heel o is supported by the hands of the examiner. The patient tries to move the heel downwards while the examiner applies strong counterpressure (Fig. 74.6b). If flexion is painful, the test is repeated, this time in almost full extension, to disclose lesions of the tibiofibular ligament and the posterior cruciate liga­ ment. Then, with the patient in a sitting position, medial and lateral rotation are tested against resistance, while

Palpation for warmth and fluid in the stationary joint is done before the clinical examination, and palpation for synovial thickening, tenderness, warmth and irregulari­ ties is done after the clinical examination. Finally, crepitus is sought during movement (see Box 74.2). FLUID

Fluid in the knee joint is a sign common to many dis­ orders (traumatic, inflammatory or crystalline). Therefore, 'water on the knee' is only a statement of a sign, never a diagnosis. Testing for fluid in the joint can be done in three ways. Patellar tap

This is the classical test. Manual pressure empties the suprapatellar pouch and moves the fluid under the patella. In the meantime, the thumb and middle finger of the other hand are used to press on the medial and lateral recesses until they empty. Any fluid now lies between the patella and femur. Next the index finger of the lower hand pushes the patella downwards (Fig. 74.7a). If fluid is present, the patella is felt to move. When it strikes the femur, a palpable tap is felt followed by an immediate upwards movement. This is the sensa­ tion of an ice-cube pushed downwards in a glass of water: although the patella moves downwards, the pressure of the fluid immediately shifts the bone upwards against the palpating finger. In a normal knee, the patellar tap is not elicited. o

(a)

Eliciting fluctuation

The examiner's thumb and index finger are placed at each side of the knee, just beyond the patella. With the interdigital web I-II of the other hand, the examiner squeezes the suprapatellar pouch, pushing all the fluid downwards under the patella, which forces the o

Box 74.2 Palpation For fluid (three tests) For heat For synovial thickening For irregularities For crepitus (For tenderness)

(b) Figure 74.6

Resisted extension (a) and fiexion (b).

CHAPTER 74 - CLINICAL EXAMINATION 1071

(a)

(a)

(b) Figure 74.7

Testing for fluid in the joint by patellar tap (a) and by eliciting

fluctuation (b).

two fingers of the palpating hand apart (Fig. 74.7b). This sensitive test will detect even very small volumes of fluid and enables an experienced examiner to differenti­ ate between blood and clear fluid. Blood fluctuates en bloc, like a jelly mass, whereas a clear effusion flows like water. (b)

Visual testing by eliciting fluctuation

This test is not strictly palpation but relies on vision. Stroking in a sweeping motion with the back of the hand over the lateral recess and the suprapatellar pouch moves the fluid upwards and medially (Fig. 74.8a). In minor effusion, all the fluid is moved to the medial part of the suprapatellar pouch. The lateral recess is then empty and can be seen as a groove between patella and lateral femoral condyle. Sweeping with the back of the hand over the suprapatellar pouch, and downwards over the medial recess will now transfer the fluid laterally (Fig. 74.8b), where a small prominence appears. This is the most delicate test for effusion in the knee joint and demonstrates as little as 2 or 3 ml of fluid. o

HEAT

Palpation for heat is performed before and after the functional examination. Heat, whether localized or generalized, means that the lesion is in an active stage. Generalized heat indicates

Figure 74.8 Visual testing for fluid by eliciting fluctuation. (a) A sweeping motion over the lateral recess moves the fluid upwards and medially. (b) Sweeping downwards over the medial recess transfers the fluid laterally where a small prominence appears.

capsulitis. Localized heat, sometimes appearing only after the clinical examination, indicates the presence of a minor lesion. Heat appears in the following conditions: • • • • • • • •

Blood in the joint Recent trauma or operation Arthritis of rheumatoid, crystalline, traumatic or bacterial origin Loose body impacted in an osteoarthrotic joint or an impacted meniscus Fracture Metastases Osteitis deformans Ligamentous lesions.

1072 SECTION THIRTEEN - THE KNEE

SYNOVIAL THICKENING

TENDERNESS

Synovial thickening is a vital clinical finding. It indicates primary inflammation of the synovia and differentiates this from a secondary synovitis. Synovial swelling is best detected at the medial and lateral condyles of the femur, about 2 cm posterior to the medial and lateral edges of the patella (Fig. 74.9). Here the synovium lies almost superficially, covered only by skin and subcutaneous fat. It is palpated by rolling the structures between fingertip and bone. Normally nothing except skin can be felt. In synovial thickening, a dense structure can be felt.

Tenderness can be sought in the structure identified by history and functional examination, provided the lesion lies within reach of the fingers. The two knees must always be compared carefully. Because most of the struc­ tures affected can be palpated, great diagnostic accuracy is possible.

DEFORM ITIES

After a fracture, or when osteophytes are present, bony deformities may be felt. Previous Osgood-Schlatter disease results in a prominence of the tibial tuberosity. Long-standing infrapatellar tendinitis may cause a bony outcrop at the patellar tip. Calcified areas in the supra­ patellar pouch may form a palpable thickening but are not of clinical significance. In osteitis deformans at the tibia, the sharp anterior edge of the tibial plateau may be lost and is eventually accompanied by localized warmth. Localized swellings may be felt all over the knee. Some swellings are more obvious with the knee straight, whereas others are thrown into relief by flexing the knee. Ganglia and cysts related to tendons or menisci feel tense or even hard. Inflamed bursae feel softer and bimanual palpation can usually disclose some fluctuation.

PALPATION OF THE MOVING JOINT

This can give an idea of the state of the opposed surfaces of the articular cartilage. However, it should be remem­ bered that crepitus, cracking and clicking may very well appear without any pain or disablement. Some fine crepi­ tus is also normal in middle-aged individuals. In con­ trast, rough crepitus indicates marked fragmentation of the surface of articular cartilage and hard creaking of bone against bone indicates that cartilage has been com­ pletely eroded. In patellofemoral arthrosis, the marked crepitus characteristic of this condition is felt only during squatting.

ACCESSORY TESTS

These tests, summarized in Box 74.3, are performed only if the history or clinical examination warrants them. Meniscus tests are thus performed when the history includes periods of locking. Stability tests are used when the patient mentions a feeling of giving way, or when some laxity is detected during the routine functional examination. Patello­ femoral tests are used if the history is that of anterior knee pain or patellofemoral dysfunction. BILATERAL PASSIVE ROTATIONS

The range of knee rotation can best be compared with that of the contralateral side by performing the move­ ment simultaneously at both knees. The patient lies prone and flexes both knees to a right angle. The examiner stands at the end of the couch, grasps the feet, pushes them in dorsiflexion and then simultaneously rotates

Box 74.3 Accessory tests Bilateral passive internal and external rotation Resisted internal and external rotation Stability tests

Figure 74.9 Synovial swelling is most easily detected at the medial and lateral condyles of the femur.

Meniscus tests Patellofemoral tests Squatting

CHAPTER 74

-

CLINICAL EXAMINATION

1073

wards and inwards, meanwhile maintaining the neutral position with both hands. Internal (medial) rotation tests the medial hamstrings and popliteus (Fig. 74.10a). External (lateral) rotation tests the biceps femoris and the upper tibiofibular joint (Fig. 74.lOb). SQUAITING

Palpation during squatting is performed when a lesion at the patellofemoral joint is suspected. The palpating hand ascertains whether there is crepitus, which is typical in patellofemoral disorders. OTHER TESTS

Tests for capsuloligamentous instability, meniscal lesions and patello-femoral disorders are described in Chapters 76, 77 and 78 respectively. Clinical examination of the knee is summarized in Box 74.4.

(a)

Box 74.4 Summary of the clinical examination of the knee Inspection Standing Sitting Supine-lying

Basic functional examination Two primary movements for the joint Passive flexion Passive extension Eight secondary movements for the ligaments Valgus strain Varus strain Lateral rotation Medial rotation Anterior drawer test Posterior drawer test Medial shearing strain Lateral shearing strain Two resisted movements Extension Flexion

(b) Figure 74.10

Resisted internal (a) and external (b) rotation.

both feet laterally to test external rotations and medially to test internal rotations. Range of movement and end­ feel are compared. RESISTED INTERNAL AND EXTERNAL ROTATION

The patient sits on the table, the knee flexed to a right angle and the legs hanging over the border. The examiner holds the foot in dorsiflexion and asks the patient to press out-

Palpation Fluid Synovial thickening Deformities Tenderness Palpation of the moving joint Accessory tests Bilateral passive internal and external rotation Resisted internal and external rotation Stability tests Meniscus tests Patellofemoral tests Squatting

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In,terpretation of the clinical examination of the knee 1---------------.. Traumatic arthritis Haemarthrosis Monoarticular steroid-sensitive arthritis Crystal synovitis Septic arthritis Rheumatoid-type arthritis Early arthrosis Discoid meniscus Bucket-handle lesions Posterior lesion Cysts of the meniscus

Interpretation of the clinical examination of the knee

In adolescents Complicating arthrosis

1-------.. Medial collateral ligament Intra-articular adhesions

1-------... Advanced arthrosis Subsynovial haematoma Medial collateral ligament bursitis Patellar bursitis Popliteal cyst Adherent vastus intermedius

1---------------.. Chronic non-adherent ligamentous lesion Plica synovialis syndrome Posterior capsular strain Iliotibial tract bursitis (Patellar bursitis)

�

Patellofemoral disorders Tendinous lesions about the patella Suprapatellar Infra patellar Quadriceps expansion Lesions at tibial tuberosity Quadriceps lesion Strained iliotibial band Rupture of the quadriceps Patellar fracture

I

K

Weakness

Rupture of the patellar tendon Neurological lesions

t

L3 root lesions Femoral nerve lesions

Hamstrings lesions Biceps tendinitis Lesion of upper tibiofibular joint

I

r--t Weakness

Lesions of pes anserinus Strained popliteus muscle Gastrocnemius lesions

51 root lesion 52 root lesion

1------------.... Straight instability Rotatory instability

1075

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CHAPTER CONTENTS The capsular pattern

1077 Traumatic arthritis 1077 Rheumatoid and reactive arthritis

1078

Osteoarthrosis 1078 Monoarticular steroid-sensitive arthritis Crystal synovitis 1080 Haemarthrosis 1081 Septic arthritis

1081

Non-capsular patterns

1082

1080

Disorders of the inert structures: capsular and non-capsular patterns

Internal derangement 1082 Plica synovialis syndrome 1092

1093 1093 Adherent vastus intermedius 1094 Posterior capsular strain 1094 Cysts and bursitis 1094 Intra-articular adhesions Subsynovial haematoma

THE CAPSULAR PATTERN

The normal capsular pattern at the knee joint is gross lim­ itation of flexion and slight limitation of extension; the ratio of flexion:extension is roughly 1:10 (Fig. 76.1). Thus 5° of limited extension corresponds to 45-60° limitation of flexion and 10° to 90-100°. The range of rotation becomes restricted only in advanced arthritis. Recently the concept of a capsular pattern of motion restriction at the knee was supported by a study on patients with inflamed knees. 1 A number o f conditions o f the knee show a l imited range in a capsular way but all can be differentiated by findings from history and clinical examination. The important features of capsular disorders, then, are a trau­ matic or non-traumatic, slow or sudden onset, synovial thickening, redness, nocturnal pain and so on. TRAUMATIC ARTHRITIS

Trauma to the capsule invariably leads to a traumatic arthritis. Depending on the site and the stage of the Flexion External

Internal

Extension

Figure 76.1

Capsular pattern at the knee joint. 1 077

1078 SECTION T H I RTEEN - THE K N E E

lesion, the capsular pattern may be gross (acute sprain of the medial collateral ligament) or more subtle (coronary sprain). The diagnosis is relatively simple: after an injury, a capsular pattern appears with effusion but without cap­ sular thickening. Caution must be taken not to overlook a traumatic haemarthrosis and, when the question of blood in the knee joint arises, diagnostic aspiration must be carried out at once. If blood is present in the aspirate, not only does it indicate a serious lesion but also the joint must be fully aspirated. On the other hand, if the aspi­ rated fluid is clear, there is no point in emptying the joint, because it is not the fluid that matters but the primary lesion . Hence the treatment of a traumatic arthritis showing only clear effusion during aspiration is to deal with the underlying primary disorder.

RHEUMATOID AND REACTIVE ARTHRITIS

Rheu matoid arthritis is a common cause of knee inflammation. The symmetrical distribution of the affected joints is typical for this disease (Fig. 76.2). Reactive arthritis is an inflammation of the joint secondary to a generalized infection but in which the articular fluid remains aseptic (Crohn's disease, Reiter 's syndrome, aseptic gonococcal arthritis).2,3 The arthritis can remain monoarticular but may involve other joints in an asymmetrical manner.

In rheumatoid and reactive arthritis, intra-articular injections with triamcinolone give excellent but often only temporary results. Steroids injected in weight­ bearing j oints can cause arthropathy if injected too often .4,s Therefore, injections must be restricted to two or three a year, which is enough to keep the patient com­ fortable. Nevertheless, considerable doubts about the dangers of repeated intra-articular steroid injections have arisen since a study report by Balch et al.6 They studied 65 patients with rheu matoid arthritis, who each received a minimum of 15 and a maximum of 167 injections at monthly intervals. Only two showed gross osteoarthro­ sis. These findings were confirmed la ter?

OSTEOARTHROSIS

The prime cause for gross degeneration in the knee joint is a disturbed distribution of load which happens for instance when the patient suffers repeatedly from attacks of internal derangement because of a torn meniscus.B,9 Early osteoarthrosis will also occur if a valgus deformity is present from youth or there is an old mal-united frac­ ture that produces uneven load and repeated shearing strains. This also occurs if the meniscus is totally removed and its load-bearing function is therefore lost; the femoral condyles then exert pressure on the tibial platform over a much smaller area and the joint is apt to wear out rapidly. lO,ll The knee is often affected in osteitis

•

Figure 76.2

•

The reactive (a) and rheumatoid (b) patterns of joint involvement.

CHAPTER 76

Figure 76.3 Localised arthrosis at the knee: 1, medial compartment; 2, lateral compartment; 3, patellofemoral compartment.

deformans and marked osteoarthrosis can then super­ vene. Aseptic necrosis of the medial condyle has been blamed as the cause of rapidly progressive, symptomatic osteoarthrosis in the elderly.12- 14 The loss of articular cartilage, the structural changes of subchondral bone and the reactive osteophyte formation are typical and well-known radiological appearances of progressive degenerative arthritis at the knee.1S It may be localized at the lateral, medial or patellofemoral com­ partment or may be generalized throughout the joint (Fig. 76.3). Although osteoarthrosis at the knee is considered very common, its prevalence is overestimated. The reason is quite simple: radiographs taken in a middle-aged or elderly patient complaining of knee pain will always show some evidence of cartilaginous degeneration. As age advances some narrowing of the joint space and osteophyte formation always appear, are normal and cause no harm. Therefore the diagnosis of symptomatic osteoarthrosis should be made not by radiography but by the typical findings on clinical examination. A minor degree of osteoarthrosis does not give rise to symptoms and it is only when gross osteoarthrosis with disintegra­ tion of the cartilage supervenes that the complaints can be attributed to it. What commonly, but incorrectly, receives the label 'osteoarthrosis' is a monarticular steroid-sensitive arthritis or an impacted loose body. Both occur in middle-aged or elderly patients with osteo­ phytes showing radiologically and the diagnosis is missed if full clinical examination is not carried out properly. The symptom of osteoarthrosis is pain during weight bearing which disappears at rest. In gross arthrosis with complete erosion of cartilage, nocturnal pain from an

-

DISORDERS OF T H E I N E RT STRUCTURES 1 079

increase of venous pressure in the tibial bone may some­ times supervene. The characteristic clinical features in an uncomplicated osteoarthrosis of the knee joint are a cold joint, devoid of synovial thickening with limitation of movement in the capsular pattern. The end-feel is bony and hard. In severe osteoarthrosis the marked limitation of movement of the capsular pattern is accompanied by loud creaking of bone against bone. However, the typical capsular proportion of limitation may be absent if the osteoarthrosis, although severe, remains localized. This is often the case in localized arthrosis of the patellofemoral compartment: passive flexion may be markedly limited and painful but passive extension remains normal. The flexion-extension move­ ment is here accompanied by rough crepitus. The approaches to the treatment of osteoarthrosis are mainly non-steroidal anti-inf lammatory drugs (NSAIDs) and intra-articular injections with steroids. NSAIDs provide some relief of the symptoms bu t have clinically important side effects - they are estimated to cause 3300 deaths annually among the elderly in the US .1 6 Intra­ articular injections with steroids also improve symptoms but the benefits are usually short lived17 and there is always the potential for long-term joint deteriorations if repeated too often. During the last decade a number of promising reports on the effect of intra-articular injections with hyaluronic acid have been published. Hyaluronic acid is an important component of healthy synovial fluid and cartilage tissue and is thought to protect the articular cartilage and soft tissue surfaces of the knee by acting as a lubricant and, because of i ts high viscosi ty, by imparting viscoelastic properties to the joint. Because the intra-articular hyaluronic acid concentra­ tions are lower in the synovial fluid of arthrotic knees,18 intra-articular injections with hyaluronic acid have been proposed as a means of restoring the viscoelastic proper­ ties of the knee joint, thereby providing symptom relief and improving joint function. Efficacy and safety of hyaluronic acid have been compared with th at of saline,19- 21 corticosteroids22 and NSAIDs. All the double­ blind and randomized studies on the effect of hyaluronic acid on osteoarthrosis of the knee confirm that five intra­ articular injections of sodium hyaluronate at weekly intervals are superior to placebo and well tolerated in patients with osteoarthrosis of the knee with a sympto­ matic benefit which persisted for 6 months.23,24 As hyaluronic acid seems to provide beneficial effects with minimal adverse reactions in a significant number of patients, it may be considered as a substantive addition to the therapeutic armamentarium in osteoarthrosis. When the condition is too advanced, joint replacement is the only solution.

1 080 SECTION T H I RTEEN - T H E K N E E

MONOARTICULAR STEROID-SENSITIVE ARTHRITIS

Cyriax described a monoarticular arthritis in the knee with some similarities with monoarticular arthritis in the shoulder and elbow. The cause and pathogenesis of this arthritis remain unclear but it heals immediately and l astingly after two injections of triamcinolone, thus earning it the title of 'steroid sensitive' arthritis (Cyriax:25 p. 404). The patient complains of gradual onset of unprovoked swelling in one or both knees. At first the swelling is com­ pletely painless. After some weeks or months the knee starts to hurt all over. The pain is not provoked by move­ ment and is often nocturnal. In the initial stage, clinical examination shows only some diffuse warmth, fluid and synovial thickening. These marked symptoms and signs contrast strongly with the almost completely normal functional examina­ tion. Only in advanced cases does a clear capsular pattern supervene.

have an acute onset with an immediate and gross articular pattern.

• Gout and pseudogout

Treatment

The treatment of monoarticular 'steroid sensitive' arthri­ tis at the knee is two injections of 40 lng of triamcinolone at an interval of 2 weeks (Fig. 76.4). Technique: injection of monoarticular steroid-sensitive

The patient lies on the couch and relaxes the quadriceps muscle (Fig. 76.4a). If gross arthritis is present it may be necessary to place a small cushion under the knee in order to keep it in slight flexion. The operator stands level with the other knee. With one hand the patella is pushed up and towards the operator, which makes the medial edge more prominent. A 5 ml syringe is filled with steroid suspension and fitted with a thin needle, 4 em long, which is placed near the upper border of the patella and thrust in horizontally just between the patellar edge and the medial femoral condyle (Fig. 76.4b). It lies intra-articularly at about 2 em depth.36 arthritis.

Differential diagnosis

CRYSTAL SYNOVITIS

The d ifferential diagnosis of a monoarticular steroid­ sensitive arthritis, summarized in Table 76.1, must be made from the following conditions:26

GOUT

in monoarticular steroid-sensitive arthritis, the disease does not spread to other joints and the laboratory findings remain normal, distinguishing it from rheumatoid and reactive arthritis.27,28 Villonodular arthritis of Jaffe and Lichtenstein29 is an advanced arthritis, with marked synovial hyperplasia and thickening of the capsule.3o This type of arthritis is frequently complicated by spontaneous and recurrent haemarthrosis.31 ,32 In doubtful cases, arthroscopic biopsy is indicated.33 Treatment with steroid injections usually fails. Synovectomy is then advised.34 Good results have also been reported with intra-articular injections of thiotepa.35 In middle age, a loose body complicating osteoarthrosis may be very difficult to distinguish. The distinct features of a loose body are sudden twinges, localized warmth and absence of synovial thickening. In long-standing arthritis, secondary wasting of the quadriceps muscle may make the knee feel weak and climbing stairs difficult; consequently, complaint of twinges is not always a good indication. The only certain criterion may then be synovial thickening, which is not always ascertained easily, especially in middle-aged women, whose subcutaneous tissues are already somewhat thickened . In such ci rcumstances, manipulation for a suspected loose body can be tried and, if several attempts do not succeed, the joint should be injected.

• Polyarthritis:

•

•

An acute arthritis at the knee occurs in 25% of all attacks of gout.37 There is considerable pain, swelling and redness, which makes the condition difficult to differenti­ ate from septic arthritis, haemarthrosis or pseudogout. Sometimes analysis of the joint fluid is necessary to distinguish these conditions. PSEUDOGOUT

Calcium pyrophosphate crystals are believed to induce the synovitis of pseudogout. The term chondrocalcinosis refers to the presence of these calcium-containing salts in the articular cartilage,38 which are seen on radiographs. The disease may be familial and is also commonly associated with a wide variety of metabolic disorders, for example haemochromatosis, hyperparathyroidism, ochronosis and diabetes mellitis, and also in patients undergoing dialysis.39 As a rule, victims are over 60 years of age. Ninety percent of attacks of pseudogout are localized to the knees and there is an acute and recurrent arthritis which, untreated, lasts 1-4 weeks. Plain radiography may show calcification of the articular cartilage or menisci. Diagnosis is by aspiration, which demonstrates calcium pyrophosphate crystals in the fluid. Pseudogout is best treated by an immediate intra­ articular injection of triamcinolone. Alternatively, some of the oral anti-inflammatory agents can be prescribed.

CHAPTE R 76 - DISORDERS OF T H E I N E RT STR UCTU R ES 1 08 1

(b)

(a)

2

Figure 76.4

Intra-articular injection of the knee. Structures in (b) 1, patella; 2, suprapatellar pouch.

HAEMARTHROSIS POSTTRAUMATIC HAEMARTHROSIS

This usually indicates a serious lesion, most commonly a rupture of a cruciate ligament or an intra-articular frac­ ture40,41 (see p. 1101). Sometimes it is the result of a direct capsular contusion.42 The patient states that after the injury the knee became painfully swollen within 2-3 minutes. The speed of swelling, together with the severe pain, indicates an intra-articular haemorrhage; blood fills the joint at once and is a strong irritant. Blood left within the joint for weeks can cause severe arthritis and serious erosion of the articular cartilage. It should be removed at once.43--45 After a few days it may be necessary to aspirate the remaining blood-tinged synovial effusion. HAEMOPHILIA

About half of all haemophiliac articular effusions occur at the knee joint. The patient is an adolescent who states that suddenly, and without apparent reason, the knee became swollen and very painful. Clinical examination shows a hot and swollen knee, with a severe capsular pattern (900 limi­ tation of flexion and up to 700 limitation of extension). Even if the patient is seen some weeks after the onset, the limitation of movement remains unaltered. When the ten­ dency to bleeding is only minor, the patient is probably not known as a haemophiliac but the acute onset in the absence

of a causative injury, the hot and swollen joint and the extreme capsular pattern should arouse suspicion. Aspiration will reveal a haemarthrosis but the diagnosis must be confirmed by haematological investigations. S PONTANEOUS HAEMARTHROSIS IN THE ELDERLY

Sudden pain and swelling without previous injury in an elderly patient will often be caused by an intra-articular haemorrhage, presumably as the result of the rupture of an intra-articular vein. Haemarthrosis should particularly be suspected when the patient is on anticoagulant therapy. Treatment is aspiration, repeated after a few days. VILLONODULAR SYNOVITIS

Haemarthrosis can occur in villonodular synovitis.46 Localized pigmented villonodular synovitis is a rare lesion that may affect any joint but is most often found in the knee. Treatment usually involves arthroscopic resec­ tion of the lesion.47

SEPTIC ARTHRITIS

Bacterial infection of the knee is an extremely serious dis­ order. Badly treated, it will not only lead to total destruc­ tion of the joint but can also threaten life.

1 082 SECTION T H I RTEEN - T H E K N E E

Table 76.1 Differential diagnosis o f a capsular pattern a t the knee Type

Disorder

Signslsymptoms

Haemarthrosis

Trauma Haemophilia Spontaneous Intra-articular injections? Predisposing factors? Fever-illness

Monoarticular arthritis Acute onset

Septic arthritis

Gout Pseudogout Slow onset

Steroid-sensitive Arthrosis

Twinges

Typical X-ray Typical aspirate Typical history Synovial thickening Hard end-feel No fluid No synovial thickening

Loose body complicating arthrosis

Polyarticular arthritis Symmetrical distribution Asymmetrical distribution

Symptoms and signs in internal derangement are quite typical. The pain is localized, of the mechanical type and appears with a sudden onset. 'Locking of the joint' and 'twinges' are typical sensations. The former describes a sudden and painful limitation of one movement; the latter is an abrupt, unforeseen and sharp pain that appears during weight bearing. The clinical signs are a non-capsular pattern and a typical bouncing or springy end-feel. The second is typi­ cally found during passive extension. A thorough clinical assessment can usually provide sufficient information to make a definitive diagnosis of internal derangement.52 Plain radiographs are of no use in the diagnosis of internal derangement. Arthroscopy may be useful but should never be per­ formed without first completing a full preoperative examination. LESIONS OF THE MENISCUS

Rheumatoid arthritis Reactive arthritis

These can be grouped into congenital anomalies, trau­ matic conditions, cysts and metabolic disorders.

Septic arthritis can follow haematogenous dissemina­ tion from focal infections, such as urethritis, cystitis, skin infections48 or dental abscesses. This is particularly so when resistance is decreased : diabetes, rheumatoid arthritis, renal failure or a deficient immune system are all possible causes of decreased resistance.49 Intravenous d rugs and gonococcal infections, particularly with antibiotic-resistant gonococci,50 have also been blamed for the increased incidence of septic arthritis of the knee. Another cause of septic arthritis is direct inoculation of organisms during intra-articular injection. The symptoms of septic arthritis are hyperacute pain, swelling, redness and a gross articular pattern. The local symptoms are accompanied by high fever, chills and nausea. Treatment is by high doses of antibiotics intravenously and daily aspiration of the knee.51

Congenital anomalies

The most common congenital anomaly with pathological sequelae is a discoid lateral meniscus. The incidence in autopsy specimens is between 0% and 7%,53 but most do not cause problems.54 Symptomatic disorder seems to occur only in the Wrisberg ligament type of discoid meniscus. This type is classically described as lacking a posterior capsular attachment and presents in childhood with a 'snapping' knee: the meniscus rolls up in front of the lateral compartment during flexion, as a consequence of increased friction and the greater mobility; during extension the rolled meniscus becomes trapped anteri­ orly, until it reduces suddenly with a dramatic audible snap (Fig. 76.5).55

-�;:.,

NON-CAPSULAR PATTERNS

. _�;: -.� _

INTERNAL DERANGEMENT INTRODUCTION

Impaction of loose tissue within the joint cavity, causing mechanical interference with the normal movement between femur and tibia is usually referred to as 'internal derangement of the knee'. The loose tissue consists of meniscal parts, cartilaginous tissue peeled off from meniscus, joint cartilage or bony fragments as is the case in osteochondritis dissecans.

Discoid lateral meniscus: the meniscus which roll� up i n flexion , (left) is trapped during extension (centre) until It reduces With a snap, allOWing full extension (right).

Figure 76.5

CHAPTER 76

The disorder affects children and adolescents. The pre­ senting symptom is internal derangement at the lateral side of the knee. Clinical examination reveals an audible click and a visible alteration of the knee at approximately 10-200 of extension. Treatment of a congenital discoid meniscus is complete or partial meniscectomy.56 Traumatic meniscal lesions

Disruption of collagen fibres within the meniscus occurs as the result of either an acute injury or gradual age­ dependent degeneration (Fig. 76.6). The split may be either horizontal or vertical. Vertical tears. Vertical tears are the most important clini­ copathological condition of the meniscus and usually result from excessive force applied to a normal meniscus. Transverse tears are less common than longitudinal ones. The latter frequently involve the thin inner edge of the meniscus which, when it separates, creates the bucket­ handle tear, so characteristic of the locking knee.57 Peripheral longitudinal tears are defined as those occur­ ring within 3 mm of the meniscosynovial junction and comprise about 30% of all vertical tears.58 Left untreated, most of these peripheral lesions heal spontaneously.59 The less mobile medial meniscus is much more com­ monly involved than is the lateral meniscus. The medial meniscus is closely bound to the medial collateral liga­ ment and the medial coronary ligament, which attaches the meniscus to the tibia, is only 4-5 mm long. The lateral meniscus, however, is separated from the lateral collat­ eral ligament by the popliteus tendon and its coronary

Figure 76.6 Main types of meniscal tear: 1, horizontal; 2, longitudinal; 3, radial; 4, degenerative; 5, flap.

-

DISORDERS OF T H E I N ERT STR UCTU R ES 1 083

ligament is much longer (13-20 mm).8 This difference in mobility is the reason for the h igher proportion of torn medial menisci. The typical vertically torn meniscus, which results in a bucket-handle lesion, occurs between the ages of 15 and 30 years. The mechanism of injury is as follows: during flexion-extension, the menisci move with the tibia, to which they are attached (see p. 1055) but during rota­ tional movements they follow the femoral condyles. During combined movements, the normal displacement of both menici may be prevented and the menisci become trapped between tibia and femur. This happens typically in a football player who, in an attempt to kick the ball sideways, severely twists on the slightly flexed and weight-bearing knee: the rotation force of the femur on the immobilized tibia then fractures the cartilage. It has also been suggested that meniscal lesions may appear as the result of knee instability, in particular after anterior cruciate lesions.60,6 1 The typical history of a bucket-handle lesion is that of a patient, usually a male soccer player aged between 16 and 30 years, who felt an agonizing and localized pain, usually at the inner side of the knee, during a vigorous rotation with weight bearing. The knee gave way and the victim fell to the ground. Standing up again, the knee could not be straightened; although it could be bent, it was impossible to force it into extension. Full extension was only regained when either the patient, the trainer or the doctor, forced the knee to unlock by a combined rota­ tional and extension movement. After an audible click, full extension immediately became possible again. After reduction, the knee became swollen and sore for a couple of days. After a week or two the patient may then find the knee 'cured', providing it was not twisted while weight bearing. Should that happen, something painfully ' going out' in the joint would be felt and, as before, straightened the joint would not be possible. Again the limitation of movement disappears only if the knee is manipulated. The biomechanical basis for the locking is that, in a normal knee, the collateral ligaments and the posterior aspect of the joint capsule all become taut during exten­ sion. When the slack in the ligaments has been taken up, the tibia and femur are strongly approximated and exten­ sion beyond 1800 is prevented. At full extension there is no room for a displaced piece of cartilage between the two bones and therefore the movement must be somewhat limited by its presence. Sudden locking of the knee in partial flexion, with immediate unlocking on manipula­ tion, is therefore pathognomonic of a bucket-handle tear. Horizontal and posterior cracks. I t is generally accepted that these lesions result from normal forces acting on a degenerating meniscus.62 Degenerative horizontal cleav­ age lesions are therefore more common in individuals of

1 084 SECTION T H I RTEEN - T H E K N E E

more than 4 0 years o f age and usually occupy the poste­ rior half of the menisci.63,64 They are so common that most authors regard them as part of the usual degenera­ tive processes in the knee (Noble and Turner,65 Fahmy et al,66 Smillie:9 pp. 79, 97, 108, 145, 153). In a posterior crack, the history is less dramatic than in that of a vertical tear.63 For instance, the patient finds that, if there is a twist on the knee, something is occasionally felt to 'give way', usually at the back of the joint. It is immediately difficult to straighten the leg but when it is shaken or kicked out, a click is heard and the limb is fit for normal use again. Sometimes the patient gives a dif­ ferent history: slight rotation and flexion during weight bearing, for example getting out of a car, give rise to an uncomfortable click which is relieved immediately as the leg is straightened. Diagnosis Ruptures with displacement. In a longitudinal vertical tear, the history is most informative: the patient states that on twisting the leg during weight bearing a click is heard, localized unilateral pain is felt and the knee imme­ diately locked in flexion. All unassisted attempts to straighten the knee fail. The patient enters the room with a characteristic gait: hopping on one leg with the knee on the affected side flexed and the foot plantiflexed with the toes just touch­ ing the ground. Clinical examination reveals a warm and slightly swollen joint. Flexion is normal or somewhat limited by the traumatic arthritis but when extension is attempted,

(a)

Figure 76.7

(b)

limitation of 5-10°, with a characteristic springy block, is detectable. Rotation away from but not towards the affected side is painful. Palpation usually reveals a very tender joint line at the affected side, because of a coincident sprain of the coronary ligament. When a middle-aged patient presents with a posterior displacement, extension may be just possible but very painful and once again the end-feel of a springy block is informative. In this type of lesion, tenderness is not found on palpation. In a horizontal lesion, a visible and palpable 'tag' can form, which then projects at the joint line. Often digital pressure will suffice for reduction but this is seldom permanent. If the patient is seen some time after reduction of the meniscus, the knee may appear normal or merely show a sprained coronary liga­ ment. Alternatively, the patient presents with a history of a minor posterior crack but the routine functional exam­ ination is normal. In these cases, the following tests can be used to elicit signs of a ruptured meniscus (Fig. 76.7). Ruptures without displacement.

Test 1. The knee is fully flexed. The examiner holds his index finger and thumb at both sides of the infrapatellar tendon, level with the joint line. With the other hand the heel is grasped and the leg rotated quickly to and fro. When clicks are felt at the joint line, a ruptured meniscus should be suspected.

The knee is fully flexed and rotated. One hand is placed on the knee, the index finger at the side to be

Test 2.

(c)

(a) Test 1: to detect clicks during rotation in full flexion. (b) Test 2: to detect a click during extension movement under external rotation. (c) Test 3: palpation of a displaced rim.

C H APTE R 76

tested and level with the joint line. The examiner now slowly extends the knee, while the pressure maintaining rotation is continued. As extension proceeds, a click indi­ cating a meniscal tear may be felt, usually as the leg approaches the neutral position at almost full extension. This test can also be performed during varus or valgus compression and is then called McMurray test. Test 3. The knee is held well flexed. The examiner passes the flexed thurnbtip from above downwards over the joint line at the affected side. A ruptured meniscus should be suspected when it is possible to hook the rim of the meniscus and pull it downwards until it jumps back into place again. Normally this is accompanied by an audible click. Test 4. Medial and lateral shearing strain have been dis­ cussed in the chapter on clinical examination (p. 1068). The knee is flexed at a right angle. The examiner sits at the foot of the couch and interlocks the fingers on the knee. A strong shearing strain can now be exerted to move the tibia laterally or medially on the femur. This manoeuvre may elicit pain or even displace the loose part of the meniscus to the other side of the condyle. A loud click is heard, with immediate loss of full passive extension. A torn meniscus is obvious, in that the test has provoked a subluxation. Manipulative reduction must of course follow. Test 5. If there is a horizontal split, a ' tag' of cartilage can be felt to protrude at the joint line, and can be pushed back into place by the palpating finger. The discomfort on full extension then immediately ceases but recurrences are common. If this is the case, the patient can learn to undertake the 'manipulation'.

During recent decades, arthroscopy has made the diagnosis and treatment of a torn meniscus much easier.67,68 Nevertheless, arthroscopy does not make a clinical d iagnosis redundant and routine arthroscopy without a previous and thorough functional examination can lead to wrong conclusions and treat­ ment. Because meniscal lesions are so common that they are a frequent finding in middle-aged people, it is very possible that a meniscal tear, found incidentally during 'routine' arthroscopy, is not the cause of the patient's complaints. For instance, if a patient with a chronic liga­ mentous lesion of the medial collateral band or the coro­ nary ligaments is subjected to an arthroscopy before a clinical diagnosis has been made, the damaged meniscus will be blamed and thus unnecessarily removed. The use of the arthroscope has encouraged the wide­ spread assumption that the source of chronic pain in the area of the knee is to be found in the interior of the joint itself. The more likely cause of the pain, however, is in the surrounding ligaments but this can only be demonstrated Arthroscopy.

-

DISORDERS OF T H E I N E RT STRUCTU RES 1 085

by a thorough clinical assessment.69 We, like Goodfellow (' He who hesitates is saved'), 7o believe that, although meniscal tears can be detected by arthroscopy with almost 100% accuracy, one should be cautious in ascrib­ ing symptoms at the knee to meniscal lesions. Diagnosis of meniscal lesions should be made clinically and arthroscopy should be reserved for confirmation of clini­ cal findings as an aid in therapeutic decision making. Treatment Manipulative reduction. Manipulation should be tried at once in a patient who presents with a displaced menis­ cus. The manipulation is not completely painless and anaesthesia may sometimes be required, especially if the patient is tense or anxious. Although some authors advise general anaesthesia, sufficient pain relief can be obtained after an intra-articular injection of 5 ml of lido­ caine (lignocaine) 2%. Technique: starting position. The patient lies supine on the couch and flexes the hip and knee to right angles. Every endeavour must be made to make the patient relax the muscles as much as possible. In a displaced medial meniscus, the manipulator must open up as far as possible the inner aspect of the knee. Therefore, strong valgus pressure must be exerted during the whole procedure. In order to achieve this, one hand is placed at the outer side of the knee, so that the thumb lies at the back of the knee. This thumb position is important in controlling extension during the preparatory phase of the manipulation. The other hand encircles the heel to rotate the leg to and fro during the manipulation.

The hip is slightly rotated medially and strong valgus pressure is exerted at the knee (Fig. 76.8). In this position, repeated extensions are performed but not beyond the end of range - i.e. if the extension range is limited by 10°, the movement should stop at about 15°. In order to ensure this, the thumb placed in the popliteal fossa is used as a brake during the procedure. Once flexion and extension movements have been performed several times in this way, rapid to-and­ fro rotations of the knee are added. Technique: preparative phase.

Technique: manipulation. The movements are now per­ formed rapidly and repeatedly. When the patient is most relaxed, one quick thrust towards further extension is added. This is achieved by a strong and swift down­ wards and inwards pressure of the hand at the knee joint at the end of the extension. As the ful l range of extension is reached, reduction is signalled by a small click, whereupon extension at the knee immediately becomes free. If symptoms of a sprained coronary ligament persist after successful manipulation, deep transverse friction

1 086 SECTION T H I RTEEN - T H E K N E E

left without removal or repair as they will remain asymptomatic,?4 Furthermore, laboratory studies have demonstrated that torn menisci can function biomechan­ ically normally if the peripheral circumferential fibres remain intact.75,76 A l though surgery of the meniscus should not be undertaken l ightly, it is unwise to permit repeated attacks of internal derangement, because they initiate a premature, troublesome and in tractable osteoarthrosis .66,77 The choice lies, then, between total or partial menisc­ ectomy or repair. Total meniscectomy leads to loss of integrity of the articular cartilage and impairment of joint stability?8-82 It is no longer considered the treatment of choice because of the increasing dissatisfaction with the long-term results.1° ,83 Instead, and if this is technically possible, only the loose fragment is removed and the outer part of the meniscus, together with the coronary ligament, left alone.84 The result is there is no increase in weight-bearing stress on the tibia.85 The outer rim of the meniscus can still bear weight and thus preserve the articular cartilage as well as play a useful role in stabiliz­ ing the joint. In experienced hands, this partial removal of the meniscus using arthroscopy is much less damaging to the joint and requires only 2 days' bed rest. Subsequent return to work and sport is also quicker.86 Several long-term studies have demonstrated the technique'S superiority over total meniscectomy.87-91 In recent years, suturing of the relatively vascular outer edge of the meniscus has been shown to result in healing by fibrous tissue.9 2-98 Meniscal repair is nowa­ days considered as the treatment of choice i::l single, vertical, longitudinal tears in the outer one-third of the meniscal substance.99 Good to very good long-term results are to be expected if the longitudinal tear is less than 3 cm long, within 3 mm of the periphery and the meniscal tissue is not degenerating. 1oo Ligamentous instability is a relative contraindication to repair. In com­ bination with insufficiency of the anterior cruciate liga­ ment, the rate of re-tearing approaches 40% and therefore anterior cruciate ligament reconstruction should be performed at the same surgical intervention.1°1 Surgery.

Figure 76.8

Manipulative reduction of a displaced medial meniscus.

should also be applied. Further splinting or immobiliza­ tion, in order to heel the tear, is of no use. Natural history. The meniscal lesion itself does not cause any pain because the body of the meniscus is almost com­ pletely insensitive. Pain is the result of ligamentous strain caused by the repeated luxations and subluxations. However, damaged menisci frequently do not provoke any symptoms. In a postmortem study in patients above and below the age of 50, Noble and Hambden found up to 60% of the former and 19% of the latter to have meniscal tears.71,72 It is important to realize that most complaints follow­ ing subluxation of a meniscus stem from a sprained coro­ nary ligament. If a patient with a history of a former locked meniscus complains of persistent and localized pain but proves to have a full range of movement with a normal end-feel, a sprained coronary ligament should be suspected and appropriate treatment given. After successful manipulation, the reduced piece of cartilage sometimes never subluxates again and the patient is cured for good. This was emphasized by Casscells, 73 who stated that not all meniscal tears need surgical treatment. Asymptomatic meniscal tears identified at the time of arthroscopic examination for ligamentous lesions are best

Cysts of the meniscus

When cysts form, they are almost always at the lateral meniscus; a cyst of the medial meniscus is extremely rare.102 There is evidently a connection between cyst formation and the existence of ruptured menisci, because half the cystic menisci are also torn.103 The history can be indicative of internal derangement or the patient may complain of localized pain when standing for some time. Clinical examination reveals a normal range of move­ ment and a normal end-feel. Ligamentous tests are nega-

CHAPTER 76 - DISORDERS OF THE I NERT STRUCTURES 1 087

tive. When the joint line is palpated during full extension, the ..cyst is felt there as a small firm mass that varies in apparent size depending on the position of the knee, usually being most prominent in 20-30° of flexion and disappearing on full flexion (Pisani's 'disappearing' sign).104 Some tenderness is elicited at the joint line and over the cyst. The diagnosis can be confirmed with magnetic resonance imaging. lOS Treatment is aspiration of the cyst. It is important to use a large-bore needle and to insert it in several different directions, for the cyst is often multilocular.106 Arthroscopic treatment is used if the cyst recurs.107-109 Metabolic disorders affecting the meniscus

The most important metabolic condition affecting the menisci is chondrocalcinosis. A recent random autopsy study found calcium pyrophosphate dihydrate crystals in 7% of the menisci examined yo Chondrocalcinosis of the meniscus is considered in the previous section of this chapter, the Capsular pattern. LOOSE BODY IN YOUNG PATIENTS

Loose bodies, which are often multiple, can form in the knee in teenagers and young adults. They are usually the result of osteochondritis dissecans but sometimes originate from chondromalacia patellae or a small osteo­ chondral chip fracture. Osteochondritis dissecans is well known, although the true cause is still not completely understood. In those under the age of 13 years, the condition seems to result from an abnormality of ossification. In teenagers and adults, however, trauma may have a significant part to play in the development of the lesion.m,112 More than 75% of the osteochondral lesions are on the lateral side of the medial femoral condyle.l l3 About 10-15% are situated at the lateral femoral condyle and in less than 10% of the patients the lesions are bilateral.114 Few symptoms result as long as the osteochondral lesion remains stable and embedded in the condyle (Fig. 76.9). There is some vague pain during weight bearing which can also be elicited during pressure over the medial condyle. Symptoms of intermittent pain and locking of the joint occur only when the fragment has (a)

(b)

Figure 76.9 Stable osteochondral lesion (a) and loose fragment (b) at the lateral aspect of the medial femoral condyle of the left knee (interior view).

become loose, which typically happens between the age of 16 and 20 years. The history is of a sudden and temporary locking in extension. The patient finds that, from time to time while walking along, the knee suddenly locks. If this happens while doing athletics, a fall to the ground is usual because the knee is locked straight when it is expected it could be bent. When flexion is attempted again, this is successful and walking on is immediately possible. Some aching and traumatic arthritis results for the next few days. Recurrence of this sequence is common and the location of the pain may vary, indicating that the loose body has shifted to another part of the joint. After the attack of internal derangement, there are signs of a traumatic arthritis only: the knee is warm, con­ tains some fluid and shows a slight capsular pattern. The ligamentous tests are normal and there is no local tender­ ness. Sometimes the loose body can be felt in the supra­ patellar pouch. Wilson115 describes a test that aids in the diagnosis. The knee is flexed to a right angle and the tibia rotated internally; the examiner then slowly extends the knee. At about 30° of extension, pain may occur, presum­ ably arising from the lesion at the inner condyle pressing against the tibial spine. Loose bodies have an osseous nucleus and therefore show up on the radiograph. In true osteochondritis dis­ secans, the gap at the lateral side of the medial femoral condyle is also seen on an anteroposterior and a tunnel view. The treatment is surgery and the method used depends upon the size of the defect and the congruity of the fragment with its bed. Sometimes replacement is tried, sometimes removal of the loose fragments by arthroscope.116 The differential diagnosis and treatment of loose body and meniscal tear in a young patient is summarized in Table 76.2. Table 76,2 Differential diagnosis and treatment of loose body and meniscal

tear in a young patient

Age group

Loose body

Vertical tear of the meniscus

Teenager or young adult

Young adult

Locking

In extension

In flexion

Unlocking

Spontaneous

Manipulative

Examination findings

T raumatic arthritis Positive radiograph

After unlocking: Traumatic arthritis Sprained coronary ligament During locking: Limited extension Springy block

Treatment

Surgery

Manipulative reduction (Deep friction to coronary ligament) Surgery

1 088 SECTION T H I RTEEN - THE KNEE

LOOSE BODY COMPLICATING OSTEOARTHROSIS

Cyriax25 (his p. 403) pointed out that: When a midd le-aged or an elderly patient presents with signs of a l igamentous spra in, or a tra u matic a rthritis, and there has been n o i nj u ry, it is h i g h ly probable that he suffers from a loose body.

Contrary to popular belief, minor or moderate osteoarthrosis at the knee does not cause symptoms. However, if there is some crepitating osteoarthrosis, the articular cartilage is roughened. A small piece may then exfoliate. Alternatively, a small piece of degenerated meniscal cartilage may peel off and escape into the joint space. Such a loose fragment can occupy a harmless posi­ tion at the back of the joint, or in the suprapatellar pouch, but sometimes impacts between the articular surfaces, where it occupies space, induces overstretching of the ligaments and causes localized pain.

• •

•

History

The history of a loose body is typical. The patient is middle aged or elderly and states that, for no reason, swelling and localized pain appeared in one knee, usually at the medial side. Pain may be present on waking or suddenJy each step hurts when walking. Sometimes it is felt at the lateral side, or right in the joint, but never all over the joint. Curiously, the pain can sometimes spread up to the distal part of the thigh or down to the proximal part of the leg. If the pain moves from one side of the j �int to the other, the diagnosis is obvious because movmg pain suggests a moving (and free-lying) lesion. The patient is afraid to go downstairs for fear of a sudden twinge, which makes the knee give way. Therefore descent is usually one step at a time, firmly holding on to the bannister. Less often, the twinges and the feeling of instability are experienced during ordinary walking. Twinges indicate a momentary impaction in the knee joint and in middle-aged people they are almost pathognomonic of the existence of a loose body. Sometimes pain also occurs at night; this is likely to happen when it is at the medial side of the knee. A possi­ ble explanation could be local tenderness at the medial collateral ligament when the knees are held together while the patient lies on the side. Clinical examination

The signs vary with the position of the loose fragment within the joint but there are some that are always present and draw attention to the condition: There is localized warmth on the painf u l side of the joint. If the joint is not warm at the beginning of the clinical examina tion, the examiner

• Localized warmth:

•

proceeds with the functional tests and repeats the palpation at the end. Local heat is then found which has been provoked by the minor stresses imposed on the joint during examination. Fluid: often, some fluid is present. Non-capsular pattern: there is usually a non-capsular pattern. It is obvious that when extension is limited by, say, 5° and flexion is not, or flexion is 30° limited but extension is of full range, a block due to internal derangement should be suspected. Such an obvious non-capsular pattern is rather uncommon and, as a rule, the signs are rather subtle. Extension is full but painful and with a smoother end-feel than on the opposite side, while flexion is full and painless. Alternatively, full extension is free from pain but flexion is slightly limited, with localized pain and a soft end-feel. In other words, the stop is not hard, as if muscle spasm due to arthritis was present, but feels as if it would go further, the limiting factor being pain. A varus movement h u rts at the inner side of the joint: this indicates that a space-occupying lesion is present in the medial compartment. Alternatively, lateral or medial shearing strain may hurt at the inner or the outer side of the joint. Care should be taken not to press on the tender medial collateral ligament during these tests. Localized pain and positive ligamentous tests: there is localized pain at the end of range and some ligamentous tests are positive. As a rule, valgus strain and external rotation hurt at the medial side. The medial collateral ligament is also very tender to the touch. Usually these findings, together with localized warmth, fluid and absence of synovial thickening, are characteristic of a sprained ligament. However, the patient does not mention trauma. The conclusion is that, if the ligament is not being strained by external forces, the cause of the sprain must lie within the joint: the ligament becomes sprained when a small cartilaginous loose body is displaced between femoral condyle and tibial plateau, where it will pu t stress on the ligaments on every attempt to extend the joint. Cyriax called this ' a sprain without a sprain'.

If, after the clinical examination, the conclusion is that there is an impacted loose body, an attempt should be made to move the piece of cartilage to a site where it no longer interferes with joint mobility. Confirmation that the diagnosis is correct comes from the immediate disap­ pearance of symptoms and signs after manipulation Special investigations

,

The knees of elderly patients always show radiological evidence of osteoarthrosis. Loose bodies, however, usually being composed entirely of cartilage, are not

CHAPTER 76 - D I SO R D ERS OF T H E I N ERT STR U CTU RES 1 089

visible on radiography. When the radiograph shows osteeJarthritis, the current tendency to depend on diagno­ sis by such means rather than by good clinical assessment can result in the clinical features being ignored and the patient being erroneously regarded as suffering from osteoarthrosis of the knee. The acute onset and the warmth are then mistakenly labelled as 'acute episodes' of a progressing osteoarthrosis. It is also apparently very difficult to see small loose bodies during a diagnostic arthroscopy. It is striking, however, to hear that surgeons often see improvement of symptoms and signs in an 'arthrotic' knee after such a procedure.ll 7 In all likelihood, the loose bodies are washed out inadvertently during the drainage necessary for the arthroscopic investigation and it is a consequence of this that the patient notices an improvement. Differential diagnosis (Table 76.3) Spontaneous osteonecrosis of the knee occurs in elderly patients, usually at the medial femoral condyle.12 The condition causes continuous pain which gets worse at night, but twinges are not mentioned. Clinical and radio­ logical examinations are negative during the first few weeks of the condition's development,l18-120 and early diagnosis must be made from a bone scanl 2l ,122 or by the use of MRI. The treatment is proximal osteotomy or prosthetic replacement.123 The most common error, however, is to regard the patient with a loose body as suffering from osteoarthro­ sis or a monoarticular steroid-sensitive arthritis. Because all these lesions occur i n middle-age or in the elderly and the signs are sometimes subtle, the distinc­ tion is not always apparent. In cases of doubt, it is always wise to manipulate the knee and see whether there is any improvement.

Treatment

As soon as impaction of a loose body in a knee is diag­ nosed, manipulation must be performed. The intention behind the manipulation is to move the loose body from its position between the tibial and femoral articular sur­ faces into a position in the joint where it is no longer pinched, i.e. under the posterior recess. To make room between the tibia and femur, the whole procedure is performed during strong traction. First manipulation . The principles of performing a manipulation for a loose body are: • • •

Traction as strong as possible. The manipulation starts with the ligaments in a relaxed position (knee in flexion). During movement towards extension, the knee is rotated three or four times, first in one direction and, if no improvement results, then in the other.

Technique: starting position. The patient lies prone on a low couch, the knee flexed to a right angle. An assistant holds the thigh just above the popliteal fossa. The manip­ ulator stands level with the patient's knee. The ipsilateral hand grasps the calcaneus. The other hand is placed at the dorsum of the foot in such a way that the second metacarpal bone presses against the neck of the talus (Fig. 76. l Oa). The pressure against the talus and the simultane­ ous traction on the calcaneus hold the foot in dorsiflexion during the whole procedure (Fig. 76.10b). The manipulator places the contralateral foot on the couch, just in front of the patient's knee. The patient's thigh is lifted off the couch and the foot is hooked on the manipulator's knee. The assistant now presses the thigh downwards as hard as feasible. This ensures maximal traction on the relaxed ligaments and creates some dis-

Table 76.3 Differential diagnosis and treatment of an impacted loose body complicating arthrosis at the knee Osteoarthrosis

Monoarticular steroid-sensitive arthritis

Loose body

General pain throughout the joint during weight bearing No

Gradual, with swelling and pain throughout the joint Yes

Sudden, localized, with pain Twinges/apprehension Sometimes localized pain

Absent None Absent Slight capsular Hard Crepitus

Present Generalized Present Capsular (±) Muscular spasm

Present Localized Absent Non-capsular Soft Painful varus or shearing strains Painful ligamentous tests

Hyaluronic acid Surgery

Two injections with triamcinolone

Manipulative reduction

History

Onset Pain at rest? Examination

Fluid Warmth Synovial thickening Pattern End-feel Other Treatment

1 090 SECTION T H I RTE E N - T H E K N E E

(a)

(b)

(e)

(d)

Figure 76. 1 0

First manipulation for a loose body impacted in the knee.

traction of the joint surfaces. This position is maintained for a few seconds until the manipulator feels the quadri­ ceps muscle relax, and the tibia is distracted from the femur. Technique: manipulation. The manipulator now removes the leg from the couch and, leaning sideways towards the end of the couch, places the foot as distally (in relation to the patient) as possible (Fig. 7S. 10c). By doing so, maximum traction during the whole procedure is ensured. Extension is accompanied by a series of full lateral or medial rota tions. To this end, both shoulders and elbows must be used in order to reach the very end of rotation. The end-feel will once again guide in decid­ ing whether the knee is at full range. In practice, one tries rotation first in one direction and, if this does not succeed, in the other. The assistant holding the leg down, feels the

click, indicating that reduction has taken place but the manipulator does not feel anything. After each manipu­ lation, whether the knee has clicked or not, the joint is examined again. If there is improvement after a particu­ lar manoeuvre, the same manipulation is done again. If the manipulation only incompletely reduces an impacted loose body, then other techniques must be tried. This manipulation is painless and it can be repeated up to 10-20 times during one session. Usually one or two sessions suffice for full relief, even if the condition has been present for months. Results.

' If the previous manoeuvre has only partially improved flexion, but has not completely reduced the loose body, techniques with the use of lever-

Second man i pulation .

CHAPTER 76 - D ISORDERS OF T H E I N E RT STR U CTURES 1 091

age can next be employed. If the wrist is placed at the back of the patient's knee, forced flexion of the tibia on the femur will strongly distract the joint surfaces and thus make room for the loose fragment to move. Technique. The patient lies supine on the couch. The manipulator places one wrist in the popliteal fossa, between tibia and femur, while the other hand presses at the distal end of the tibia. The knee is then bent as far as it will go (Fig. 76.11a). When progressive ligamentous resistance indicates that the slack has been taken up, the tibia is quickly forced into greater flexion by a small thrust. A click may be felt. Re-examination will show whether further reduction has taken place. If this manipulation fails, the same movement can be repeated during rotation. The manipulator places a firm

( a)

rolled bandage in the popliteal fossa (Fig. 76. 1 1 b). This permits holding the patient's foot and wrist with both hands. Doing this, rotational movements can be added during the forced flexion. First one rotation is tried; should this fail, rotation in the opposite direction is tried. It is important to verify the range of extension after each attempt, because full and painless extension at the knee is more important than some improvement of flexion. Should the range of flexion improve but exten­ sion become painful or limited, this manipulation should be terminated immediately. This technique is used when the first manipulation does not achieve full and painless exten­ sion. In most cases, extension is not limited but is painful and has an altered end-feel.

Third mani pulation.

Technique. The patient lies supine. The manipulator stands level with the knee, and bends it to a righ t angle while the hip is flexed and laterally rotated. The hand is applied at the limer side of the knee and the other hand at the lateral border of the distal tibia in such a way that a strong varus movement is achieved (Fig. 76.12). The patient's cooperation is now sought because the knee must be actively and slowly extended while the manipulator maintains the varus pressure. At almost full extension, and maintaining as much varus pressure as possible, the manipulator adds a quick jerk towards full extension. If this final jerk proves to be too painful, it should only be done a few times, after repeated active extension by the patient. Once again, re-examination should follow each attempt and the end-feel will indicate whether reduction has taken place (Fig. 76.13).

(b)

Figure 76.1 1 Second manipulation for a loose body impacted in the knee: two alternative methods are shown.

Figure 76.12

Third manipulation for a loose body impacted in the knee.

1 092 SECTION T H I RTEEN - T H E K N E E

Figure 76.1 3

Manipulative session for a loose body.

During the following days the patient must repeat the manipulation several times a day. To do this, the patient sits on a low chair or on the ground, the knee flexed and the hip laterally rotated. The lateral border of the foot now rests on the floor. Pressing strongly on the inner side of the knee, and at the same time actively extending the leg, results in a varus movement during active extension (Fig. 76.14). Fixation of the lateral border of the foot against the floor ensures the counterpressure needed for a good varus stress. At nearly full extension, a small thrust is added. Instructions on after-treatment.

Results. Most impacted loose . bodies complicating osteoarthrosis are reduced by one or two manipulative sessions. No after-treatment to the strained ligaments or the slight traumatic arthritis is necessary, because they will recover within a few days without specific treatment. Recurrences of the impaction are always possible, mainly after kneeling or keeping the knee bent for some time. The patients should therefore be told not to squat or to sit sideways on a couch with the legs tucked underneath, a sitting position often adopted by women.

PLICA SYNOVIALIS SYNDROME

Plicae synoviales are remnants of the embryological dividing walls in the knee. Arthroscopy has recently brought their existence into prominence. They are present in more than 20% of all kness 1 24 but it is only when pathological changes take place that pain and dis­ ability are likely to occur. Injuries and excessive strains are thought to be responsible for these pathological a l tera ti ons .125, 126

Figure 76.14

After-treatment exercise by the patient.

Although there are several types of synovial plicae, it is the plica mediopatellaris, or medial shelf (Fig. 76. 15), which seems to cause most problems.127 This plica was first described by lino in 1939.128 It has its origin on the medial wall of the knee joint and runs obliquely down towards and inserts into the synovium, covering the medial infrapatellar fat pad. During flexion it glides over the medial condyle like a wiper over a windscreen, which in normal circumstances is harmless and painless but, if the plica is pathologically altered or the medial condyle has undergone arthrotic changes, some symptoms may result. One of the symptoms is a sudden twinge when the inflamed plica gets pinched between the patella and the medial condyle of the femur. Sometimes there is pain and a slightly modified end-feel at the end of extension. A painful arc during flexion-extension can occur when a damaged and thickened plica rides over a chondral defect at the medial condyle, and it can be aggravated when this movement is performed during lateral rota tion.129 The clinical diagnosis of a symptomatic medial plica is made from a history of localized pain during flexion-extension or pain at the end of extension.t3o The plica can sometimes be felt if the examiner rolls the medial capsule of a slightly (45°) flexed knee under the

CHAPTER 76 - D I SO R DE RS OF T H E I N E RT STRUCTURES 1 093

Clinical examination immediately reveals the gross non-capsular pattern. Furthermore, the joint is cold, not swollen and without any capsular thickening. The com­ bination of the non-capsular pattern, the gross limitation of flexion and the absence of local signs is so striking that this remarkable condition will be recognized easily, especially if there is a history of trauma or surgery. The only lesion that can be confused with these intra­ articular adhesions is Stieda-Pellegrini disease, in which the calcified medial collateral ligament can cause a similar selective limitation of flexion. A radiograph establishes the diagnosis. Treatment

Gentle forcing d oes not prevent the progressive decrease of flexion and any conservative treatment, except forceful manipulation towards flexion, is futile. It is easiest to force the knee when the patient adopts a prone position.

Figure 76. 1 5

Medial plica ( 1).

thumb. 131 When this rolling is painful, 20 mg of triam­ cinolone is locally infiltrated.132,133 Some authors have reported good to fair results with flexibility training of the flexor and extensor muscles of the knee.133 If the symptoms persist, arthroscopic resection is performed.B4 Because the presence of a medial shelf is normal,135 one should be cautious in ascribing symptoms to it. The diag­ nosis should be made clinically and not by relying on accidental findings during arthroscopy.

INTRA-ARTICULAR ADHESIONS

There is an unusual disorder of the knee, characterized by an increasing limitation of flexion while extension remains full and painless. In that this pattern occurs after operation or an unexceptional sprain, Cyriax ascribed it to intra-articular adhesions. The history is as follows. There has been surgery to the medial side of the knee or an atypical sprain (hyper­ extension or hyperflexion) giving rise to the lesion. In spite of vigorous physiotherapy, the knee stiffens progres­ sively and almost painlessly, the main symptom being inability to flex the joint. During the initial weeks, 15-30° of flexion are lost; after a month there is loss of about 90° of flexion. While the range of flexion decreases day by day, extension remains full and painless. Finally, the knee may stiffen with a flexion range of 45°, extension still being full range.

Technique. The manipulator stands at the level of the knee, which is bent as much as possible. The elbow is curved around the distal aspect of the tibia. The other forearm is placed at the back of the knee, just above the popliteal fossa. The hands are locked. Flexion is now performed by a side bending of the body towards the patient's head. Great power can be obtained if the manipulator keeps the arms still. The arm on the thigh keeps the knee on the couch, while the other arm uses the tibia as a lever. The manipulation is executed during a quick side bending of the whole body, with as much force as possible. Often a loud sound of ripping tense tissue can be heard; flexion can be achieved immediately, thus proving that there were adhesions. Follow up. Within 24 hours, there is considerably more pain than before the manipulation and the patient has symptoms of significant arthritis: a warm joint, full of fluid and with an articular pattern. During the following days, active and passive exercises are prescribed in order to maintain the range of flexion. When arthritis is gross and pain severe, an intra-articular injection with 50 mg of triamcinolone can be given in order to diminish the traumatic capsulitis.

SUBSYNOVIAL HAEMATOMA

A severe blow on the front of the thigh may cause a local­ ized haematoma between the suprapatellar pouch and the front of the femur (Fig. 76.16). Flexion is limited but extension remains free. The history is typical: a severe knock just above the patella has caused immediate pain and localized swelling.

1 094 SECTION TH I RT E E N - T H E K N E E

POSTERIOR CAPSULAR STRAIN

There is a history of a severe hyperextension strain. When traumatic arthritis has subsided and flexion becomes full and painless, extension continues to hurt at the back of the knee. The rest of the clinical examination shows the knee to be normal and therefore strains of anterior or pos­ terior cruciate ligaments are excluded. In long-standing cases an X-ray may show the typical appearance of slight calcification in the posterior capsule. Treatment consists of infiltration with triamcinolone at the appropriate side, using the same technique as for posterior strains of the posterior cruciate ligament (see pp. 1113-1114).

CYSTS AND BURSITIS

Figure 76.1 6

Subsynovial haematoma , 1 .

It is important to note that localized swellings may limit movements in a non-capsular way (Fig. 76. 17). For example, a bursa underlying the medial collateral liga­ ment, a prepatellar bursa or a cyst under the iliotibial tract can each cause a specific pattern.

During clinical examination, the knee is found to be warm and swollen. Extension is full but probably painful at the end of its range. Passive flexion is grossly limited and there is localized pain just above the patella. Resisted extension is painless, which indicates that neither the quad riceps tendon nor the patella is to blame. Palpation reveals some fluid in the joint and a solid and tender swelling at the suprapatellar pouch. Fluid aspi rated from the joint is clear or slightly blood stained. There is no improvement in range after aspiration, which establishes the effusion as a second­ ary one. If the needle is passed just above the patella, in the direction of the femur, blood from the haematoma can be obtained and confirms the d iagnosis. It is important to note that aspiration is possible only during the initial days because the haematoma organizes rapid ly. After aspi ration the knee should be mobilized during the following days in order to prevent persistent adhesions.

ADHERENT VASTUS INTERMEDIUS

The vastus intermedius may become adherent to the femur after a fracture of the latter. Gross limitation of flexion then results. Only surgical treatment gives a satisfactory outcome.

Figure 76. 1 7 Cysts and bursitis around the knee: 1, patellar bursitis; 2, medial collateral ligament bursitis; 3, meniscal cysts; 4, pes anserinus bursitis; 5, bursa between the iliotibial tract and lateral epicondyle.

CHAPTE R 76

MEDIAL COLLATERAL LIGAMENT BURSITIS ,

The patient is usually middle aged and complains of localized pain at the medial side of the knee, which has appeared without a specific cause (Fig. 76.18). The pain is worse during activity and eases at rest, but nocturnal pain may occur. There is no symptomatic evidence of internal derangement - such as twinges, locking and fear of giving way.136 Spontaneous cure is uncommon:137 one of our patients had had unchanged symptoms for more than 6 years. Clinical examination reveals a cold joint, without fluid or synovial thickening. Extension is normal, flexion is limited by 15-45°. The end-feel is soft, the limiting factor being pain, which is strictly confined to the inner side of the knee. Valgus strain and lateral rotation are painful. Palpation reveals a solid swelling under the medial col­ lateral ligament, level with the joint, which can be so hard that it is mistaken for a large osteophyte. Unlike a cyst of the meniscus, the bulge does not disappear during flexion, but enlarges and becomes firmer, especially when it lies at the dorsal aspect of the ligamentJ38 It is important to differentiate between chronic liga­ mentous sprain and bursitis under the medial collateral ligament, the signs of which are very similar. In sprain, the distinct factors are a history of previous trauma and absence of palpable swelling. The treatment required deep friction and manipulation - would undoubtedly worsen bursitis, and therefore the differential diagnosis

-

DISORDERS OF THE I N E RT STR U CTU RES 1 095

should be made carefully. In case of doubt, MR imaging can very well demonstrate the fluid collection under the medial collateral band.139 Treatment is aspiration. A thick needle (19G x 1 � i nches) should be used because the fluid is so viscous that it is very difficult to remove. Injecting 10-20 mg of triam­ cinolone into the cavity will prevent early recurrence of symptoms. After the aspiration, immediate full and pain­ less flexion can be achieved. Permanent cure is often achieved.1 4o PATELLAR BURSITIS

Prepatellar bursitis is by far the most frequent type of bur­ sitis, especially in patients who have to kneel repeatedly in their work (e.g. gardeners, bricklayers). The infra patellar bursa can also become inflamed ('clergyman's knee'). The patient complains of pain and swelling in front of the knee. The diagnosis is made on simple inspection. If the swelling is gross, it can result in limitation of flexion, because of the painful stretching of bursa and skin. Palpation shows the effusion to lie between skin and patella. The presence of heat suggests haemorrhage into the bursa, whereas heat and redness indicate the possi­ bility of sepsisJ41 Aspiration should be performed to disclose the nature of the fluid. If the bursa refills repeatedly, surgical removal must be considered.142 BURSA BETWEEN THE ILIOTIBIAL TRACT AND THE LATERAL E PICONDYLE

A bursa can form under the iliotibial tract where it rides over the lateral condyle. This is a common condition in long-distance runners, cyclists and skiers. The patient complains of localized pain while walking or rumung. Clinical examination reveals a painful arc at 30° of flexion. Resisted flexion and extension of the knee are negative. A swelling can be palpated between the condyle and the iliotibial tract. Bursitis at this site must be differentiated from a strained iliotibial band which also occurs in athletes and gives rise to localized pain at the outer side of the knee. In tlus con­ dition, pain is the result of a lesion of the tract itself, confirmed by discomfort on resisted extension and lateral rotation (see p. 1143). Aspiration, followed by local infiltration with corticos­ teroid suspension, is the remedy. If the condition fails to respond to this treatment, the posterior 2 cm of the band should be transversely sectioned.143 PES ANSERINUS BURSITIS Figure 76.18

Medial coliateral ligament bursitis (1).

The pes anserinus bursa is situated between the medial collateral ligament and the overlying pes anserinus

1 096 SECTION T H I RTEEN - T H E K N E E

(tendons o f sartorius, gracilis a n d semitendinosus). Inflammation of this bursa commonly occurs in long­ distance runners. 144 Clinical examination reveals a full range of movement. Sometimes resisted flexion and medial rotation cause pain because these movements painfully squeeze the bursa. A tender mass can be palpated at the tibial inser­ tion of the medial collateral ligament. Treatment is local aspiration and infiltration with triamcinolone.145

MENISCAL CYSTS

Asymptomatic cysts need not be treated. If symptoms arise, treatment is by aspiration (see earlier). PO PLITEAL CYST

If a cyst forms at the back of the knee, the result may be some limitation of flexion. The end-feel will be of soft tissue approximation. There is only slight pain.146 Treatment consists of aspiration; surgical removal is seldom necessary.

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71B:518-522. 113. Aircroth PM. Osteochondritis dissecans of the knee. J Bone Joint

Surg 1971;32B:440-447. 114. Greenspan A. Orthopaedic Radiology: A Practical Approach. Raven Press, New York, 1992:8.22-8.25. 1 1 5. Wilson IN. Wilson's sign. A diagnostic sign in osteochondrosis dissecans of the knee. J Bone Joint Surg 1967;49A:477. 116. Anderson AF, Pagnani MJ. Osteochondritis d issecans of the femoral condyles: long-term results of excision of the frag­ ment. Am } Sports Med 1997;25(6):830-834. 1 1 7. Guhl FG. Operative arthroscopy. AIJI J Sports Med 1 979;7(6): 328-335.

118. Lotke PA, Ecker ML. Osteonecrosis of the knee. Current con­ cepts review. J Bone Joint Surg 1988;70A(3):470-473. 119. Lotke PA, Ecker ML. Osteonecrosis of the knee. Orthop Clin North Am 1985;16:797-808. 120. Marmor L. Osteonecrosis of the knee. Lateral and medial involvement. Clin Orthop 1984;185:195-196. 1 2 1 . Bauer GCH, Smith EM Sr. Scintimetry in osteoarthritis of the knee. ] Nucl Med 1969;10:109-116. 122. Insall IN, Aglietti P, Bullough PG. Osteonecrosis. In: Insall IN (ed) Surgery of the Knee. Churchill Livi ngstone, New York, 1984:527-549. 123. Koshino T. The treatment of spontaneous osteonecrosis of the knee by high tibial osteotomy with and without bone-grafting or drilling of the lesion. J Bone Joint Surg 1982;64A:47-58. 124. Hardaker WT, Whipple TL, Basset FH. Diagnosis and treat­ ment of the plica syndrome of the knee. ] Balle Joint Surg

1980;62A:221. 125. Blackburn TA et al. An introduction to the plica. J OrtllOp Sp Phys Ther 1982;4:85-87. 126. Vaughan-Lane T, Dandy OJ. The synovial shelf syndrome.

J Bone Joint Surg 1982;64B:475-476. 127. Platel D. Plica as a cause of anterior knee pain. Orthop Clin North Am 1986;17:273-277. 128. lino S. Normal arthroscopic findings of the knee joint in adult cadavers. J Jpn Orthop Assoc 1939;14:467-523. 129. Broom HI, Fulkerson JP. The plica syndrome: a new perspec­ tive. Orthop Clin North Am 1986;17:279-281 . 130. Johnson D P, Eastwood OM, Witherow PJ. Symptomatic synovial plicae of the knee. J Bone Joillt Surg 1993;75A: 1485-1495. 1 31 . Dupont JY. Synovial plicae of the knee. Controversies and review. Clin Sports Med 1997;16(1):87-122. 132. Rovere GO, Adair D. Medial synovial shelf plica syndrome: treatment by intraplical steroid injection. Am J. Sports Med

1985;13:383-386. 1 33. Amatuzzi MM, Fazzi A, Varel la MH. Pathologic synovial plica of the knee. Results of conservative treatment. Am J Sports Med 1990;18(5) :466-469. 134. Calvo RD et at. Managing plica syndrome of the knee. Phys

Sportsmed 1990;18:64-74. 135. Sakakibara JO, Watanabe M. Arthroscopy study on lino's band. J Jpn Ort/wp Assoc 1976;50:513-522. 1 36. Lee JK, Yao L. Tibial collateral ligament bursa: MR imaging. Radiology 1991;178(3):855-857. 137. Keflan R, Glousman R. Tibial collateral ligament bursitis. Am J Sports Med 1988;16(4):344-346. 138. Schuldt DR, Wol fe RD. Clinical and arthrographic findings in menisca! cysts. Radiology 1980;134:49-52. 139. Rothstein C P, Laorr A, Helms CA, Tirman PF. Semimembranosus-tibial col l a teral ligament bursitis: MR imaging findings. Alii J RoentgenoI 1996;166(4):875-877. 140. Ombregt L. Bursitis ter hoogte van het ligamentum collaterale mediale van de knie. Cyriax Info 1 989;2:5-6. 1 4 1 . Ho G, Tice AD. Comparison of nonseptic and septic bursitis.

Arch Intern Med 1979;139:1269-1273. 142. Quayle ]8, Robinson MP. An operation for chronic prepatellar bursitis. J Bone Joint Surg 1976;58B:504-506. 143. Noble CA. Iliotibial band friction syndrome in runners. Am J Sports Med 1980;4:232-234. 144. Reilly JP, Nicholas JA. The chronically inflamed bursa. Clin Sports Med 1987;6:345-370. 145. Larsson LG, Baun J. The syndrome of anserina bursitis: an overlooked diagnosis. Arthritis RheulII 1985;28:1062-1065.' 146. Massari L, Faccini R, Lupi L, Bighi S. Diagnosis and treatment of popliteal cysts. ChiI' Orgalli Mov 1990;75(3):245-252.

CHAPTER CONTENTS ,

Introduction

1099 Classification 1100 Diagnosis 1100

Treatment: the principle of early mobilization

Isolated sprains

1101

Disorders of the inert structures: ligaments

1102

Medial collateral ligament Lateral collateral ligament Coronary ligaments 1108 Anterior cruciate ligament Posterior cruciate ligament

Ligamentous instability

1102 1107 1110 1111

1113 1114 Functional examination 1117 Treatment 1121 Types of instability

INTRODUCTION

Ligamentous lesions at the knee are quite common. The joint is relatively uncovered by muscles, which makes it vulnerable to direct injury. Furthermore, the iJ1direct forces acting on the knee have a large leverage, whereas the active and passive stabilizers of the joint have only a small leverage (Fig. 77. 1 ) and thus give very inadequate protection. Few other sports injuries cause as much concern as lig­ amentous lesions. Each contusion, even a slight damage to the medial collateral or the coronary ligaments, can cause serious trouble. Knee traumas should always be taken seri­ ously, because a neglected knee injury may lead not only to instability but also to the formation of adhesions. There are great differences in attitudes towards the treatment regimes for the d ifferent injuries. The wide variety of traumas, the different degrees of damage and the combination of various lesions make it very difficul t to

Figure 77.1

Forces on the knee: direct (small arrow) and indirect (large arrow) . 1 099

1100 SECTI O N T H I RT E E N - THE K N E E

compile a list o f clear recommendations for treatment. In the more classical textbooks, it is advised that minor liga­ mentous sprains are immobilized, whereas for serious or combined lesions, surgical intervention is generally rec­ ommended, especially when the patient is a young athlete or when development of later instability is feared. We firmly believe that immobilization is never a good method. If there is a serious grade III lesion (see below) in a young athlete, and instability is feared, the patient should be sent for surgery. If for one reason or another the patient is not treated surgically, early mobilization, deep transverse friction and functional treatment should be used. This treatment regime gives the needed physio­ logical stimulus for quick and proper healing of the lesion and prevents the formation of adhesions, so often the cause of persistent trouble.!

This temporal division is important in choice of treat­ ment (see Table 77.1). DIAGNOSIS

Even in the era of arthroscopy, a clinical approach to ligamentous lesions continues to be vital. In the acute stage, information obtained from history and clinical examination enables the examiner to make the distinction between serious and mild lesions. If symp­ toms and signs warrant, the patient is then referred for further assessment by arthroscopy.5 In the chronic stage, only a thorough functional exam­ ination can lead to the diagnosis of ligamentous adhe­ sions or estimate the degree of functional instability. History

CLASSIFICATION

Most accounts divide ligamentous injuries into three grades: grade I i s slight overstretching with some microtears within the structure of the l igament; grade II is a severe sprain with a partial tear of the ligamentous fibres; grade III implies a ligament which is completely torn across. In our opinion, this classification is rather arbitrary and, although it might be possible to distinguish a small lesion from a total rupture, the difference between grade I and grade II will always remain subjective. Ligamentous injuries can also be classified according to which structure has been damaged. The commonest injuries are at the medial collateral and the anterior cruci­ ate ligaments. Sometimes these occur together and in combination with a torn medial meniscus - the 'unhappy triad', or the triad of O'Donoghue2,3 - or in combination with a tear of the lateral meniscus.4 Lesions at the lateral collateral ligament and the posterior cruciate ligament are rare. In our experience, tears at the medial coronary ligament are very common; however, these are often mis­ diagnosed as medial collateral tears or meniscus lesions. Sprained knees can also be classified according to the time elapsed since the causative accident. Here the terms acu te, subacute and chronic are used: • • •

It is vital to obtain a very detailed history of the mech­ anism that has led to the injury, as summarized in Box 77.1, especially in acute sprains of the knee.

injury: at the moment of injury, what was the position of the knee, what forces acted where on the knee and in which directions were they applied? The initial symptoms: what was the immediate result of the trauma? Where was the initial pain? Was there immediate swelling? Was there immediate functional incapacity caused by locking or instability or coul d the patient continue activities? Did pain, swelling and functional di sability appear only after a certain lapse of time?

• The

•

Box 77.1 History of knee injury The injury

Position of the knee Direction and severity of the forces

Initial symptoms

Localization of pain Swelling Functional disability

Evolution

Problem now

Acute: less than 2 weeks since injury Subacute: 2-6 weeks. Chronic: more than 6 weeks.

Pain Swelling Functional disability Pain? Where? What provokes It? Swelling Instability? What provokes it?

Table 77.1 Classification of ligamentous injuries according to severity, structure and time Severity

Structure

Time

Grade I: slight overstretching

Isolated sprain

Acute: less than 2 weeks

Grade II: partial tear

Combined sprains

Subacute: between 2 and 6 weeks

Grade III: complete tear

In combination with meniscal tears

Chronic: more than 6 weeks

CHAPTER 77

what was the evolution of pain, swell ing and disability after the first few days? Treatment received: what sort of treatment did the patient receive and what was the result?

• The evolution: •

In long-standing cases, the current symptoms should be ascertained: is it still present? What is its localization and when does it appear? Swelling: does the knee swell? Instability: is there any feeling of instability and giving way?

• Pain: • •

Examination

The functional examination described in Chapter 74 is carried out. In acute cases the ligamentous tests will sometimes be overshadowed by the capsular pattern of the traumatic arthritis, whidl makes it very difficult to estimate the degree of damage. In subacute and mronic cases, the cap­ sular signs have largely subsided and the tests of ligamen­ tous integrity become more informative. Sometime laxity is found during the routine examination, in which case instability tests are then carried out (see pp. 1117-1121). Sometimes not so much instability but pain and limitation of a non-capsular type are detected which indicate the formation of adhesions around the healed tissue.

-

D I SORDERS OF THE LIGAM E NTS 1 101

Chronic ligamentous lesions

Because the treatment is quite different, it is vital to differentiate between instability as the result of a total ligamentous rupture and chronic ligamentous adhesions leading to a 'self-perpetuating inflammation'. Once again, history and clinical examination are the first approach to differentiate between both and, in instability, estimate its degree (Table 77.3). Posttraumatic adhesions at the knee have the follow­ ing signs and symptoms. The knee hurts locally after (vigorous) exertion or during the first few steps after it has been kept still for a while (e.g. in the morning or after sitting for a few hours). Sometimes slight swelling is also induced. Ordinary walking does not hurt. Clinical exam­ ination reveals slight limitation of movement, positive ligamentous tests and local tenderness. Instability is characterized by a 'giving way' sensation during unexpected movements under load. There may be accompanying pain and discomfort, sometimes lasting for a day or two. Additional instability tests will usually detect the type and degree of ligamentous insu fficiency (see p. 111 7). Treatment for a 'chronic ligamentous sprain', whether it is an adhesion with nearby structures or a self-perpet­ uati ng inflammation in the ligament itsel f, is relatively simple and as a rule gives quick and permanent resu l ts. Treatment of an unstable knee is more di fficult and often requires surgical intervention.

Acute ligamentous lesions

In acute ligamentous lesions at the knee, the history will be what first indicates the severity. A few hours after a serious sprain, the knee will start to hurt considerably and develop a distinct capsular pattern, protected by muscle spasm that makes it almost impossible to perform liga­ mentous tests. In order to distinguish between a serious injury and a less important lesion, a number of elements, grained from the history may be of value (Table 77.2). When the history indicates a serious lesion, especially if the patient is an athlete, it is wise to arrange him for arthroscopic evaluation. In contrast, in a more modest lesion, a conservative approach is indicated.

TREATMENT: THE PRINCIPLE OF EARLY MOBILIZATION

To most orthopaedic surgeons, ligamentous lesions of the knee, especially if they are grade I I I, require immobiliza­ tion or surgical repair. The reasoning is purely anatomical: there is a rupture and the main medical act must be to repair both ends, either by immobilization or by surgery. Our opinion tends more in the direction of mobilization and functional management of l igamentous lesions. Experimental studies over the past several decades have demonstrated that regeneration of injured C0l1l1eC-

Table 77.2 Acute ligamentous lesions: contrasting histories of serious and less serious lesions Serious lesions

Less serious lesions

Impairment of function

Immediate inability to continue the sport or activity

Swelling

Immediate or developing during the first hour, indicating haemarthrosis5 Yes Blood may be present Triad of O'Donoghue? Isolated rupture of a cruciate?

Most initial pain disappears and sports and activities can be continued after a short time Appears, with functional incapacity and generalized pain, a few hours after the accident No Clear fluid is obtained Isolated sprain of a collateral, coronary or cruciate ligament

Feeling of instability? Aspiration Possible diagnoses

1 102 SECTION T H I RT E E N - THE K N E E

Table 77.3 Differential diagnosis o f chronic ligamentous sprain a n d instability Chronic ligamentous sprain

Instability

Stiffness after the knee has been kept still for some time The knee hurts at one small spot during and after exercises

Feeling of 'giving way' during unexpected movements under load Slight discomfort over the whole joint after the initial unstable feeling

History

Stiffness/'giving way' Pain localization Swelling

Some recurrent swelling

Clinical examination

Local pain Range Instability

During ligamentous tests Sometimes limited in a non-capsular way None

tive tissue is significantly better with the application of continuous passive motion. Under functional load, the collagen fibres are oriented in a longitudinal direction and the mechanical properties are optimized.6 Therefore, func­ tional conservative treatment is advised for all coronary ligament sprains and all isolated grade I, II or III sprains of medial collateral ligament7 and posterior cruciate liga­ ment and isolated grade I or II lesions of the anterior cru­ ciate ligament (ACL).8 However, in combined lesions and in anterior cruciate ligament tears with a positive pivot shift phenomenon, su rgery is the treatment of choice.9 Mobilization is not only the best promotor of l iga­ mentous repair but also prevents ligamentous adhe­ sions within or around the healing structure. Another advantage of early mobilization is the positive effect on muscle strength 10 and proprioceptive reflexes, 1 1 which ensures the active stability of the joint. This conservative and functional approach to recent and isolated tears was first advocated by Cyriax12 and has recently received much support. Several stu dies have demonstrated that the non-operative management of an isolated medial collateral ligament inj ury, espe­ cially of grade I and II, is as good if not better than a primary surgical approach. 13-18 The conservative treat­ ment of grade III sprains of the med ial collateral liga­ ments also gives results equally as good as the surgical approach but with significan tly quicker rehabil ita­ tion .19-21 Jones et a/22 treated 24 high school football players with an isolated grade III injury of the medial collateral ligament. They administered mobilization, using a regime of muscle strengthening and agility exer­ cises. Knee stability was achieved in 22 cases, with an average recovery time of 29 days. The players returned to competitive sport after a mean of 34 days. Similar results were obtained in a long-term study of 21 grade III medial collateral ligament tears.23 The overall conclu­ sion was that the non-surgical treatment of a complete

None Sometimes increased range of movement Detection of instability during the additional tests

tear of the medial collateral l igament was extremely successful, provided there was no associa ted structural dam age to the anterior cruciate ligament. However, in advocating ea rly mobilizati on, one common difficulty arises: the serious traumatic arthritis and the intense pain during the slightest movement are very strong impediments to early activity. As for ligamentous lesions at the ankle, this problem can be solved in two ways: •

•

Relieve the inflamma tion and pain as soon as possible so the patient can mobilize the knee. This can be achieved by local infiltration of a small amount of triamcinolone. As advised by Cyriax, mobilize the ligament over the bone by deep transverse friction instead of moving the bone under the ligament as in ordinary mobilizations. The relative movement will be the same, as is the mechanical stimulus to the regenerating fibrils.

In long-standing and chronic ligamentous lesions, where scars have been allowed to form abnormal attachments in or around the healing tissues, the approach is to break the adhesions and remodel the fibrils in the functional longi­ tudinal direction. This can be achieved by deep friction, sometimes with manipulation in addition.

ISOLATED SPRAINS MEDIAL COllATERAL LIGAMENT

The medial collateral ligament prevents valgus deviation of the knee and through its posterior fibres checks exter­ nal rotation of the tibia.24 An understanding of this IS of importance in the interpretation of clinical tests in a torn medial collateral ligament.

CHAPTER 77

Diagnosis

The classical mechanism of a medial collateral injury is a forced valgus movement on a partly flexed and externally rotated knee, 25 which occurs typically when a soccer or football player receives a kick or blow at the outer side of the weight-bearing knee.26 The patient experiences a crack and feels a sudden pain at the inner aspect of the knee. Most of the pain disappears fairly quickly and probable return to the game or walking off the field is possible. At first, the knee is not swollen and there is only slight disability. The real incapacity, with increasing swelling and pain, starts after a few hours. By the next day, the patient can hardly stand and is hobbling only with assistance. Clinical examination shows a hot and tender knee full of fluid. There is a gross articular pattern, with muscle spasm at the end of the range of movement: extension is probably 5-10° limited and flexion can be limited up to 90°. In this acute stage, it is impossible to perform proper ligamentous tests but the patient knows that the inner side of the knee was initially sprained, and localized tenderness is easily found at some point along the ligament. The tear can be proximal, be related to the mid-portion of the ligament or situated at the distal, tibial portion (Fig. 77.2). Mid-portion tears are the most common, but also the most disruptive, because they also involve the deeply situated meniscotibial and meniscofemoral por­ tions of the ligament. In a proximal tear, it is wise to take

Figure 77.2 Medial collateral ligament lesions: 1, avulsion of a bony fragment; 2, proximal tear; 3, mid-portion tear; 4, distal tear .

-

D I SORDERS OF THE LIGAM E NTS 1 1 03

a radiography to exclude avulsion of a bony fragment, which is an indication for surgical repair.27,28 The natural history of an injured medial collateral liga­ ment is as follows, In the acute stage there is a traumatic arthritis, lasting about 2 weeks, Thereafter, during the subacute stage, lasting 4-6 weeks, the limitation of move­ ment slowly diminishes. Although the joint remains warm at the inner side, the swelling declines. Testing the ligament by applying a strong valgus pressure (in 0° and in 30° of flexion) will elicit pain and, if the ligament has been totally ruptured (grade III), an excessive range will be detected. This is an indication for further stability testing. After 2-3 months the traumatic arthritis has totally subsided. At this stage, three situations are possible: • • •

There has been good healing, with a strong non­ adherent ligament. The ligament is permanently lengthened, resulting in an unstable knee. The ligament is adherent, leaving the patient with recurrent and localized disability.

If an abnormal and adherent scar forms between the ligament and the surrounding tissues, any vigorous effort will sprain the impaired ligament afresh, In this case the history is typical: the knee is quite adequate for ordinary walking and even running but one small area at the inner side hurts when the patient takes vigorous exercise. The knee also feels stiff after it has been kept still for some time. Clinical examination shows a non-capsular pattern of limitation with, as a rule, painful full extension and lim­ itation of flexion by 5-10°, External rotation and valgus strain hurt at the medial side of the knee. The other liga­ mentous tests are painless and instability cannot be detected. Resisted movements are strong and painless. There is no fluid or warmth, unless the patient is seen the day after some additional exertion. Tenderness should be sought along the medial collateral ligament. The usual localization is at the joint line, However, if a full range of movement is found after a former sprain but there is a clear history suggesting a chronic sprain and examination shows the medial collateral ligament to be at fault, tenderness is usually found at the femoral origin of the medial collateral ligament. Stieda-Pellegrini disease. Sometimes calcification of the medial collateral ligament develops after an apparently ordinary sprain of the inner side of the knee. Suspicion arises when increasing limitation of flexion, together with a hard end-feel, is found 4-6 weeks after the accident. Examination reveals the lesion to lie at the medial collat­ eral ligament at its upper extent. Radiography shows a linear shadow along the inner side of the medial femoral condyle.

1 1 04 SECTION T H I RT E E N - THE K N E E

Treatment is ineffective and spontaneous recovery takes 6 months to 1 year.29 Treatment

All grade I and grade II sprains (partial tears), as well as isolated grade III sprains (complete tears) of the medial collateral ligament (MCL) should be treated conserva­ tively. Surgery is indicated only in combined lesions of MCL and meniscus and / or anterior cruciate ligament. The chosen technique depends on the stage of the lesion, as summarized in Box 77.2. If the patient is seen during the first 24 hours after the accident, a local infil tration with triamcinolone can be considered. Deep transverse friction in combination with early mobi­ lization can be applied during the first 6 weeks following the accident. If the patient is seen after more than 6 weeks, the lesion must be considered as chronic and manipula­ tion is given. Acute stage

Infiltration and cold compression. Immediately after the accident an ice compress is applied in order to prevent excessive inflammatory reaction. As soon as the patient is seen, a small dose of triamcinolone (20 mg) can be injected at the site of the tear. Because this injection is extremely painful, a local anaesthetic must always be added. During the next 24 hours, the patient remains in bed with an ice bag on the affected area. From the second day on, flexion is strongly encouraged as is extension without weight bearing. During the first week, however, an attempt should not be made to straighten the knee com­ pletely on walking; the medial collateral ligament is taut in extension and too much stretching at the point of injury would do harm. On account of the anti-inflamma­ tory effect of the triamcinolone, pain and swelling abate very quickly and normal gait is restored after 1-2 weeks. Walking and modest movement of the knee should be encouraged because they provide the best stimulus to normal healing and prevent the formation of adhesions. The patient can usually return to sports after 6 weeks.3o By that time, movements are of fu ll range and ligamen-

tous tests negative. It is wise to recommend a protective knee brace during the first few weeks of sporting activity, especially if the patient returns to contact sports. Technique: infiltration. The patient lies supine, with a

pillow under the knee. The physician, standing at the inner side of the knee, outlines the correct area. A fine needle is fitted to the syringe, filled with a mixture of 1 ml of lidocaine (lignocaine) 2% and 20 mg of triamcinolone. The needle is thrust in al most horizontally (Fig. 77.3) and the whole tender area is infiltrated by a series of small droplets. Friction. Because a steroid injection, even a small amount, undoubtedly not only abates the excessive inflammation but also interferes in the union of the ruptured ligament, it is wise to use an alternative way of treatment if the patient is a young or professional athlete. Deep friction, applied from the first day, is an excellent alternative and gives identical results, providing the massage is given correctly. Friction serves a double purpose: it prevents any fibrils binding the ligament to bone and provokes a positive stimulus to the healing cOlU1ective tissue. As adhesions have not yet formed in the acute stage, only 2 minutes of deep friction are required in both flexion and extension, though the preparatory phase of gentle massage, followed by slight and superficial friction (which renders the liga­ ment anaesthetized), may take up to 20 minutes. The patient is given this deep friction every day during the first week, after which the subacute stage is entered. If the massage is given adequately, the range of flexion increases

Box 77.2 Treatment of medial collateral ligament sprains Acute stage

Infiltration with triamcinolone (if performed during the first 24 hours following the accident) + active mobilizations Deep transverse frictions + mobilizations

Subacute stage

within pain-free range Deep transverse frictions

Chronic stage

movements in flexion/extension/external rotation Manipulation in the limited direction,

+

gentle passive

preceded by vigorous deep friction

Figure 77.3

Infiltration of the medial collateral ligament.

CHAPTER 77

- DISORDERS OF TH E L I G A M E NTS 1105

dramatically during the first few days. The patient should be encouraged to walk and to move actively, although straightening the last 20° or flexing the last 60° must be avoided during the first week, because these movements put too much longitudinal strain on the ligament.3 1 The joint can be protected by a partial mobile brace, the coronal straps of which prevent excessive valgus movement.32 Technique: deep friction. The patient lies supine on the couch and the exact point is identified. Friction is first given in as much extension as possible, followed by in as much flexion as possible. The therapist places the index finger at the exact point, which is most usually the central part of the ligament at the joint line. The index finger is reinforced by the middle finger, and the thumb is placed at the outer side of the joint so that it can be used as a fulcrum (Fig. 77.4). Friction is imparted by an extension movement at the wrist, which draws the index finger anteriorly over the ligament. Releasing the grip and flexion of the wrist moves the index finger back to the starting position. Subacute stage. In the subacute stage the massage is given more thoroughly and for longer, applying the same technique as described for the acute stage (see Fig. 77.4). By moving the ligament across the bone, the normal movement of bone over ligament is mimicked. Immediately after the massage, gentle movements in flexion, extension and external rotation are carried out by the therapist (passive movement). In order to prevent atrophy of the thigh muscles, a programme of resisted exercises should also be followed. Two weeks of treat­ ment, three times a week, usually suffice for full recovery. Return to competitive sports is allowed only when running ability has become normal again. This may take up to 6 weeks.33 Chronic stage. When the patient is first seen in the chronic stage, adhesions have already formed between the ligament and bone - a situation that would never have been reached if the patient had received proper treatment from the beginning but which is often encountered when the knee has been immobilized. The principle of treatment is to restore a full range of movement by rupturing the abnormal adhesions. In order to do so, vigorous deep fric­ tion to the affected part of the ligament is applied for 20 minutes: 10 minutes in as much flexion as possible and 10 minutes in as much extension as possible (see Fig. 77.4). This massage anaesthetizes the affected tissue. Mani­ pulation in all the impaired directions is now performed. It is important that the manipulations must be within the normal physiological limits: it is no part of restoration of range at the knee joint to attempt to overstretch the MeL and so create instability.

(a)

(b) Figure 77.4 Friction to the medial collateral ligament: (a) in extension; (b) in fiexion.

1 1 06 SECTION T H I RT E E N - T H E K N E E

Manipulation techniques.

There are four techniques.

Manipulation in flexion. The patient lies supine or adopts a half-lying position on the couch. The hip is bent and the knee flexed as far as it will go. The therapist presses the ipsilateral hand just above the ankle. The other hand is placed on the knee (Fig. 77.5a), with the fingers on the ligament to feel the 'tearing' during the manipulation. The slack is taken up at the end of flexion and the tibia is forced vigorously backwards to the end of range. A snap is heard, which demonstrates the tearing of adhesions. Manipulation in extension. The patient lies supine on the couch, the knee extended as much as possible. The thera­ pist stands to the side, level with the knee. The ipsilateral hand supports the heel and the other hand encircles the knee, just below the patella (Fig. 77.5b). The knee is slightly flexed and suddenly moved into full extension by a strong and quick jerk. A tiny snap is heard, which indicates that the adhesion has broken. Manipulation in lateral (external) rotation. The patient

(a)

adopts the half-lying position, with the hip flexed and the knee at 90°. The therapist stands level with the patient. The ipsilateral hand is clasped behind the heel, which rests on the couch. The foot is dorsiflexed, the inner side against the therapist's forearm. The contralateral hand is used to stabilize the knee and the femur (Fig. 77.6a). Lateral rotation is now easily performed by using the foot as a lever. The slack is taken up at the end of range and the manipulation performed by a quick adduction move­ ment of the shoulder. Manipulation in medial (internal) rotation. It is unusual for an adhesion of the medial collateral ligament to cause pain on medial rotation. If it does, this technique is used. The patient adopts a half-lying position, with the hip and knee well flexed. The therapist stands at the affected side, level with the thigh, and encircles the heel with both hands. The contralateral hand clasps the inner side of the foot, while the arm passes behind the leg, and carries it (Fig. 77.6b). In order to protect the lateral ligaments of the ankle, fixation is applied to the distal end of the leg and not to the foot. If the outer hand is kept on the calcaneus and fibula, the lateral ligaments of the foot are protected. The foot is brought into as much medial rotation as possible and the manipulation is performed by a quick movement of both hands. After-treatment and results. Immediately after manipu­

lation there is a full and painless range of movement. It is remarkable that pain or a reaction in the joint does not occur. Du ring the first few days after the manipulation, the patient must repeatedly perform flexion, extension and

(b) Figure 77.5

Manipulation to rupture medial collateral ligament adhesions: (a) in flexion; (b) in extension.

rotation movements in order to maintain the regained mobility at the knee. Flexion is performed by squatting and extension by a hyperextension movement during weight bearing. Rotational movements in a lateral or a medial direction are achieved during weight bearing with a slightly bent knee, whereby the femur rotates ' inwards or outwards on the stationary tibia. These exercises are performed every few hours during the following days.

CHAPTER 77

D ISORDERS OF T H E LIGAM E NTS 1 1 07

(b)

(a) Figure 77.6

-

Manipulation to rupture medial collateral adhesions: (a) in lateral rotation; (b) in medial rotation.

Usually, one single manipulation followed by the appropriate after-treatment suffices to cure chronic ligamentous adhesions of the medial collateral band, no matter how long the problem has lasted. The symptoms / signs and treatment of isolated medial collateral ligament injuries are summarized in Table 77.4. LATERAL COLLATERAL LIGAMENT Diagnosis

The lateral collateral ligament is very rarely sprained. The mechanism of sprain is a forced varus movement on an outstretched knee. Since the ligament lies relatively distant from the joint, the immediate articular signs are less dra­ matic than in sprains of the medial collateral ligament.

VII"

Practitioner's checklist

• When the uppermost and immobile part of the medial collateral ligament is affected, limitation does not occur in the chronic stage: manipulation is of no use and localized deep friction without forcing the joint suffices. • When ligamentous strain is secondary to a loose body at the inner side of the joint (see p. 1088), deep friction is ineffective and manipulation makes matters worse. • Friction and manipulation also worsen an inflamed bursa under a ligament; treatment is aspiration (see p. 1195)

Although the knee is warm and contains some fluid, the capsular pattern is mmor or even absent. Varus strain hurts and palpation reveals the exact localization.

Table 77.4 Summary of isolated medial collateral ligament injuries Symptoms/signs

Treatment

Acute stage

Typical history Swelling Capsular pattern Three localizations

Infiltration with triamcinolone or daily deep frictions followed by progressive active movements

Subacute stage

Decreasing traumatic arthritis Positive valgus test

Deep frictions (20 minutes) 3 times a week, followed by active movements

Chronic stage

Localized pain after exercises Slight limitation of movements Positive valgus (and external rotation)

Manipulation in all the impaired movements after vigorous deep friction, followed by active exercises

Differential diagnosis

Medial collateral ligament bursitis Loose body

1 1 08 SECTION T H I RT E E N - T H E K N E E

The natural history of a lateral collateral ligament injury is as follows. The acute stage, with light traumatic arthritis, lasts 2 weeks. Thereafter, the lesion enters into the subacute stage: pain and discomfort during movement only, a further decline of the capsulitis and a painful varus test. A chronic sprain of the lateral collateral ligament causes no adhesions, thus all movements will be free but a strong varus movement remains painful. Treatment

Grade III lateral collateral ligament tears, especially if they are combined with ruptures of the posterolateral lig­ ament complex, should be repaired immediately after the injury. Isolated grade I or grade II lesions of the lateral collateral ligament are treated conservatively. Treatment in the acute stage consists of infiltration with triamcinolone (only during the first 48 hours) or daily deep friction. During the subacute or chronic stage, only deep fric­ tion is effective. Because adhesions never form in this condition, manipulation is not performed. Technique: deep friction. The patient lies supine, the knee in extension. The therapist sits on the opposite side. The index finger, reinforced by the middle finger, covers the affected part of the ligament. The thumb is placed at the inner side of the knee, to be used as a fulcrum (Fig. 77.7). By alternate flexion and extension of the wrist, the forefinger will be moved to and fro over the ligament, while the thumb is kept still. In a recent injury, when there is much local tenderness, a gradual start to the friction is necessary - preparing the area for the 2 minutes of thorough friction which is required. In chronic cases, 20 minutes' friction may be necessary, three times a week, for about 2 weeks.

Figure 77.7

Friction to the lateral collateral ligament.

CORONARY LIGAMENTS

Cyriax34 was the first to draw attention to sprains of the coronary ligaments, which are very common but mostly go undiagnosed because the localiza tion of the pain and nature of the onset resemble a meniscus lesion or a sprain of the medial collateral ligament. Recent MRI examina­ tion has confirmed the existence of coronary ligament lesions.35,36 The treatment is simple but effective and the injury is usually cured after 1 or 2 weeks' deep friction or after one infiltration. Without treatment, the lesion recovers spontaneously in about 3 months, although in some cases it can go on indefinitely. Diagnosis

The classical mechanism of a coronary ligament sprain is almost identical to that of a torn meniscus. The patient describes a rotational strain, usually during slight flexion of the knee. As in meniscal lesions, the medial side is more often damaged than the lateral. This is the typical lesion of a tennis player, twisting the body, and thus the femur, on the stationary tibia during a forced and unin­ tentional forehand drive. If the foot is anchored to the ground, the medial coronary ligament may be over­ stretched. The important fact which differentiates a coro­ nary ligament sprain from a meniscal lesion is that in the former the knee is not locked after the accident. The patient can straighten the knee and walk normally and is often able to continue playing. It is only after some hours that serious pain, swelling and limitation of movements appear. The next day, the patient is unable to walk without a limp. Clinical examination reveals a traumatic arthritis: warmth, fluid and a capsular pattern. Medial rotation is painful when the lateral coronary ligament is over­ stretched and painful lateral rotation implicates the medial coronary ligament. Applying valgus and varus strain does not hurt, so eliminating a lesion of the collat­ eral ligaments. The appropriate ligament is found to be tender. Palpation must be performed with the knee well bent and in rotation away from the affected side. During the subacute stage, the capsular pattern sub­ sides slowly but if adequate treatment is not given warmth and fluid can persist for several months: During this time, not only lateral or medial rotation but also passive extension remain painful. These features can be explained by the fact that the menisci are forced forwards during full extension of the knee, which pinches the inflamed ligaments and elicits pain. In the absence of adequate treatment, the lesion can become chronic. Although no adhesions will form here, a self-perpetuating inflammation will persist il'l. the healed tissue, giving rise to recurrent although slight disability.

CHAPTER 77

Differential diagnosis, history and examination

The ' differential diagnosis from a meniscal lesion is extremely important and once again relies almost entirely on history and clinical examination. In our opinion, it is unwise to refer a patient for arthroscopy before a lesion of the coronary ligament has been excluded. Meniscal lesions are so common that certainly not all cause symp­ toms.37,38 Although arthroscopy detects meniscus tears with almost 1 00% accuracy, it does not necessarily follow that the· detected tears are necessarily the cause of the patient's symptoms.39 The differential diagnosis between a meniscus lesion and a coronary ligament sprain is thus made on information gained from the history and clinical examination. Although the same mechanism is responsible for both a torn meniscus and a sprained coronary ligament, there is an essential difference between their histories. In a subluxated meniscus, passive extension is lost at once, whereas in a coronary ligament sprain extension becomes impaired only when the traumatic arthritis is established. In the acute stage of a coronary ligament sprain the clinical examination shows some extension to be lost, because of the posttraumatic arthritis, which implies more limitation of flexion (probably 45-60°). The end-feel is muscle spasm. In an impacted meniscus, however, lim­ itation of extension contrasts with a full range of flexion, the end-feel of extension being a springy block. In the subacute stage of a coronary ligament sprain, when extension is painful at the end of range or only slightly limited, the end-feel is never springy but rather is ligamentous. Treatment

The treatment of a coronary ligament sprain, whether acute, subacute or chronic, is the same: deep friction. Although it is reasonable to infiltrate the ligament with steroid, this hardly ever succeeds because it is technically almost impossible to infiltrate adequately the thin line of tissue between the meniscus and the tibia. However, an infiltration of the coronary ligament can be considered in two instances: if the lesion is located on the tibial border, at the ligamento-periosteal insertion of the ligament and in persistent problems after meniscectomy; here the hypertrophied scar tissue in the intersection line often causes permanent trouble but infiltration with triam­ cinolone usually gives very good results. Technique: friction to the medial coronary ligament. The patient lies on the couch with the knee flexed to 120°. Lateral rotation moves the medial tibial condyle further away from the meniscus, rendering the medial coronary ligament more accessible to the palpating finger. The phYSiotherapist sits or stands level with the injured knee.

-

DISORDERS OF T H E LIGAME NTS 1 1 09

The tibial condyle is identified and the site of the lesion ascertained. The index finger of the ipsilateral hand is placed on the lesion, and reinforced by the middle finger. Because deep friction only works if it is applied to exactly the right point, it is important to make sure that the fingertip lies on the coronary ligament and not elsewhere. Therefore the fingertip m ust press downwards on the tibial condyle, moving the coronary ligament between finger and tibial condyle. Consequently the index fingernail lies horizontally and the finger is slightly flexed.

The thumb is placed at the lateral side of the knee, where it is used as a fulcrum. The therapist ensures a vertical and downwards pressure of the index finger by placing the thumb as distally as possible on the leg. The massage is now given by drawing the fingertip horizon­ tally along the condyle, around the fixed thumb (Fig. 77.8). As usual, there is an active phase of sweeping the index finger anteriorly and a relaxing phase when the finger is moved backwards to the previous position. In order to give sufficient excursion to the fingertip, the therapist should not sit or stand too close to the patient, so that the entire arm, elbow and wrist can be moved during the massage. Technique: friction to the lateral coronary ligament. The technique is the same as described for the medial coro­ nary ligament but the therapist stands on the opposite side of the damaged knee. The well-bent knee is now brought into an inward rotation. The friction is per­ formed by the contralateral hand. Once again the fingertip of the index finger is placed horizontally on the affected ligament. The thumb now lies downwards on the inner side of the knee to act as a fulcrum (Fig. 77.9). The friction is given by a movement of the whole arm, drawing the index finger along the tibial condyle. Comments. In acute sprains the friction is given daily for 10 minutes, in subacute or chronic cases on alternate days for 10-15 minutes. As no alternative treatment exists for coronary ligament sprains, the technique must be absolutely correct. To reach the ligament it is vital to put the index finger flat on the ligament and the thumb on the opposite side of the leg as caudally as possible. If these principles are observed, all patients recover after 2-3 weeks' treatment regardless of whether they are first seen the day after the sprain or many months later. If appro­ priate friction is unsuccessful, considerable doubt must arise about the diagnosis and the patient must be re­ examined at once. Technique: infiltration of the medial (lateral) coronary lig­ ament. The knee is well bent and brought into lateral

(medial) rotation. The tibial condyle is identified and the site of the lesion ascertained. A small and thin needle is

1 1 1 0 SECTION T H I RTE E N - T H E K N E E

Figure 77.9

Friction to the lateral coronary ligament.

the knee is loaded in valgus position, with the femur internally rotated and the pivot shifted to the lateral femorotibial compartment.41 Both situations occur fre­ quently in soccer and basketball. Combined lesions of the anterior cruciate and medial collateral ligaments, together with a torn meniscus, occur in contact sports (e.g. rugby, football and judo).42A3 It has also been

Figure 77.8

Friction t o the medial coronary ligament.

fitted to a 1 ml syringe, filled with 10 mg of triamcinolone and inserted from above until it hits bone. A series of small droplets are injected all over the tender area (Fig. 77.10). ANTERIOR CRUCIATE LIGAMENT

An isolated tear of the anterior cruciate ligament may be caused by a hyperextension strain combined with medial rotation.4o Alternatively, the ligament may tear when

Figure 77.10

Infiltration of the medial coronary ligament.

CHAPTER 77

demonstrated that chronic anterior cruciate deficiencies can result in longitudinal meniscal tears.44,45 Diagnosis

Immediate swelling after the injury indicates a haemarthrosis, which suggests a complete rupture of the ligament.46--48 In moderate sprain, only a mild traumatic arthritis may result. Blood is a strong irritant to capsule and cartilage49 and should be removed at once. If the patient is an athlete competing in high-performance sport, arthroscopic assessment of the integrity of the anterior cruciate ligament must always follow the detec­ tion of a traumatic haemarthrosis. Alternatively, the patient is referred for MRI examination because this technique has become the imaging method of choice to evaluate the integrity of the anterior cruciate ligament.50 Further clinical examination discloses whether the unmodified anterior drawer test and its modification at 30° are painful or have an excessive range. Excessive anteroposterior movement shows the ligament to be ruptured or elongated. If the patient complains only of pain and no instability is detected during this test, inflammation at the ligamentoperiosteal border is present. It is very important to distinguish an inflamed but strong ligament from a painless and elongated one. In painful inflammation, treatment is infiltration with 20 mg of triamcinolone at the ligamentoperiosteal junc­ tion, no matter whether the lesion is new or of long standing. Because the ligament does not lie within the reach of the palpating finger, massage is not an alterna­ tive treatment. Spontaneous cure of a sprained anterior cruciate ligament is very slow; it can take months or years or the lesion may fail to recover. Sometimes a sprain leads to permanent lengthening, resulting in serious instability. The problem of instability is discussed later but it is as well to remember that lengthening of the anterior cruciate ligament, or even a complete ruphlre, does not always lead to permanent functional instability.5J -53 For its anterior stability, the knee depends not only on the anterior cruciate ligament but also on the capsular ligaments, the integrity of the menisci and good proprioceptive reflexes from the quadriceps and hamstrings muscles.54 Messner and Maletius re-examined 22 patients with minor knee insta­ bility caused by a partial rupture of the anterior cruciate ligament after a mean of 12 years and found excellent knee function that showed no differences from that of a control group.55 Treatment

Treatment of a painful but strong anterior cruciate liga­ ment consists of one or two injections at the site of the lesion. These injections should be given as soon as possi­ ble, regardless of whether the lesion is in an acute or

-

DIS O R D E RS OF T H E LIGAM E NTS 1 1 1 1

chronic stage. The lesion always lies at the ligamento­ periosteal j unction but sometimes it is hard to decide at which end. If there is doubt about localization, the anterior end is infiltrated first and, if no benefit has been gained within a week, the other end is then treated similarly. Technique: infiltration of the anterior end of the anterior cruciate ligament. The patient lies on the couch, with the

knee bent to a right angle. The border of the medial tibial condyle is identified, together with the medial side of the patella and the infrapatellar tendon. A point is chosen just medial to the inferior edge of the patella, about 3 em above the tibial rim. A needle 5 em long is introduced here, in a backwards and medial direction, aiming at the spine of the tibia (Fig. 77.11 ). The needle must cross dense tissue before it touches bone. If bone is hit immediately, this indicates that the needle does not lie within the liga­ ment. If the correct position is reached, an area 1 cm2 is infiltrated with 20 mg of triamcinolone, by means of a series of small withdrawals and reinsertions. It is impor­ tant to note that the infiltration must be made only at the ligamentoperiosteal junction, which is when the tip of the needle hits bone. If the entire area has been infiltrated correctly, recovery will be complete within 2 weeks. If the injection has only afforded partial relief, a second injection can be given. More than two injections are seldom required. Technique: infiltration of the posterior end of the anterior cruciate ligament. The patient lies prone, with the

knee extended. The medial and lateral femoral condyles form the landmarks. The free thumb is placed on the lateral condyle. The femoral attachment of the anterior cruciate ligament lies at the medial surface of the lateral condyle. It cannot be reached by a downwards thrust and the needle must be brought in from a medial aspect, using an almost horizontal insertion. A needle 6 em long is inserted at the apex of the medial condyle and moved at an angle of 30° to the horizontal in the direction of the lateral condyle. This approach ensures that the needle passes well posterior to the popliteal vessels (Fig. 77.12). The needle has to penetrate a tough ligamentous struc­ ture before it touches bone. The infiltration is given by a series of small droplets at different spots of the teno­ periosteal junction. More than two injections are hardly ever required. The results are uniformly good, provided the right point has been reached. Obviously, these injections have effect only on inflammation and pain but do not alter instability. POSTERIOR CRUCIATE LIGAMENT

A severe lesion of the posterior cruciate ligament (peL) is always a serious disorder because the ligament creates the axis about which the knee rotates.56

1 1 1 2 SECTI O N T H I RT E E N - T H E K N E E

\.

Figure 77.12

Figure 77.11

Infiltration of the anterior end of the anterior cruciate ligament.

Furthermore, most patients with PCL injuries have combined ligamentous and / or chondral knee damage.57 Therefore, rupture of the ligament will often lead to con­ siderable instability and limited function of the knee.58

Infiltration of the posterior end of the anterior cruciate ligament.

A mild and isolated sprain at the tibial or femoral insertion does not lead to gross instability but can induce persistent trouble by the formation of a painful self­ perpetua ting inflamma tion. In this section we deal only with mild sprains. Complete and / or combined ruptures of the PCL are discussed in the section on ligamentous instabili ty (pp. 1113-1127). A severe lesion should always be suspected if haemarthrosis is present. Escape of blood through a rupture of the posterior capsule may mask this sign. Diagnosis

Motor vehicle accidents are the most common cause of the injury, but sports-related traumas (football, skiing)

CHAPTER 77

have increased in recent years. The usual mechanism of injury {n motor vehicle accidents is a ' dashboard' injury: during a car crash the femur is forced forwards on the immobilized tibia.59 Sports-related injuries result from severe hyperextension of the knee or from hyperflexion with the foot typically plantarflexed. The l atter mechanism is the most common cause of isolated peL injuries.6o During the initial days after the accident, examination shows traumatic arthritis, with a warm and swollen knee containing clear fluid. Tests for the collateral ligaments are negative but internal rotation can be painful at the end of range. The posterior drawer test demonstrates pain rather than laxity. Shearing the tibia laterally on the femur is also painful, as is resisted flexion with the knee in a 90° flexed position. As a rule, the lesion lies at the tibial border. Sometimes a small bony chip may be avulsed and is visible on a plain radiograph.61 During the last decades magnetic resonance imaging has proven to be very accurate in the diagnosis of peL lesions and in demonstrating associated injury.62,63 After the traumatic arthritis has subsided, the poste­ rior drawer test remains painful, sometimes for years, and without proper treatment the patient will be perma­ nently unable to run or play sports. Treatment

Treatment of peL lesions depends on the severity, the existence of concomitant lesions and the presence and degree of laxity.64 Isolated, partial peL injuries (grades I and II) can best be treated non-operatively while com­ plete injuries (grade III) may require operative treatment based on clinical features. All combined ligamentous injuries usually respond best with surgical management. In recent years, several studies have demonstrated that knees with an isolated injury to the peL without con­ comitant articular damage may be successfully managed conservatively and that the majority of athletes with iso­ lated peL injuries who maintain muscle strength return to sports without functional disability.65-67 When there is no gross instability but merely pain, treatment consists of one or two injections at the site of the lesions; if given during the acute stage this may avoid many months of traumatic arthritis. The results are remarkable, and after only a few weeks the patient is able to return to activity, for example football. In chronic sprain the infiltration pro­ duces equally good results. The lesion is inaccessible to friction, and therefore infiltration is the only successful form of treatment. The posterior end of the ligament is much more frequently affected than the anterior. Therefore, this end should be infiltrated first. If the condition has not improved after 2 weeks, the anterior side should be treated.

- DISORDERS OF THE LIGAME NTS 1 1 1 3

Technique: infiltration of the posterior end of the poste­ rior cruciate ligament. The patient lies prone, with the

knee extended. The landmarks here are the lateral femoral condyle - which is easily identified - the popliteal artery and the posterior margin of the tibia. The latter cannot be palpated directly and must be marked by palpation of the joint line at the anterolateral side. The level of the poste­ rior edge of the tibia can then be estimated. The posterior end of the posterior cruciate ligament is at the mid-point of the tibia, extending somewhat to the lateral side. A needle 5 em long is inserted at the apex of the lateral femoral condyle, about 2 cm above the estimated level of the tibial surface and directed inferiorly and medially, at about 60° to the horizontal. The palpating index finger is placed on the popliteal artery and the joint line. The lateral approach, together with palpation of the artery, avoids the popliteal vessels. The tip of the needle is advanced until the characteristic feel of a ligament is encountered before bone is felt (Fig. 77.13). If the needle passes without obstruction and hits cartilage, this indi­ cates that it has passed into the knee joint. This is too far proximal and the tip should be moved in a more oblique direction until it penetrates ligament and then touches bone. This is the exact area to reach, just below the articu­ lar edge of the tibia. Infiltration of 20 mg of triamcinolone should be given here by a series of small insertions and withdrawals along the mediolateral borders. T echnique: infiltration of the anterior end of the poste­ rior cruciate ligament. The patient lies supine, with the

knee extended. The medial and lateral femoral condyles are identified. The anterior end of the ligament lies at the lateral surface of the medial condyle and is covered by the patella, so that direct access from above is not possible. The physician has to move the patella as far as possible medially and upwards by tilting the outer edge with the thumb. A needle 5 cm long is now inserted just under the inferolateral edge of the patella, and pushed up in the direction of the medial condyle, until it hits bone (Fig. 77. 14). It is then moved little by little, until ligamentous resistance is felt. A series of small droplets are injected when the needle is felt to touch bone after piercing the ligament. Ligamentous lesions of the knee are summarized in Table 77.5. LIGA MENTOUS INSTA BILITY

If the knee becomes unstable after a ligamentous injury, permanent problems may result, especially if the patient is an athlete with high functional demand. If the history indicates that there is possibly instability, an examination to detect the exact localization and

1 1 1 4 SECTION TH I RT E E N - T H E K N E E

Figure 77.14

Figure 77.13

Infiltration o f the posterior end o f the posterior cruciate ligament.

degree of this is performed. It is important to make this supplementary examination only when symptoms and signs found in the routine clinical assessment indicate lig­ amentous instability to be the cause of disability. Indeed, it is important to realize that not every lengthened liga­ ment leads to problems.68 If the athlete's muscles are

Infiltration of the anterior end of the posterior cruciate ligament.

strong enough to provide dynamic stability, a slightly unstable knee will not cause trouble. Conversely, it is quite possible that an athlete with slight laxity of one or more ligaments has a chronic painful lesion as well. If the diagnosis of the latter is missed because the routine func­ tional examination is not performed, it may well be that the patient is sent for surgery, which will solve the slight instability but does not cure the main problem. TYPES OF INSTABILITY

Knee instability is the result of loss of static and dynamic function. Stability depends on the tautness of the liga-

CHAPTER 77

Table 77.5

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DISORDERS OF T H E LIGAM E NTS 1 1 1 5

Summary of ligamentous lesions

Acute major lesions (gross or combined sprains)

Immediate swelling Immediate functional incapacity I-Iaemarthrosis Lesions: Rupture of a cruciate 'Unhappy triad' Isolated sprains

History: Information about the injury should be as detailed as possible Swelling and functional incapacity appear some time after the accident Examination findings and treatment depend on the stage of the lesion: Stage

Medial collateral ligament

Lateral collateral ligament

Coronary ligaments

Cruciate ligaments

Present Gross Present Infiltration or friction

Present Slight Present Infiltration or friction

Present Moderate Present Friction

Present Slight Absent Infiltration

Reduces Reduces Valgus External rotation Friction and mobilization

Reduces Reduces Varus

Reduces Reduces Rotation

Reduces Reduces Drawer

Friction

Friction

Infiltration

Yes Yes Manipulation

No No Friction

No No Friction

No No Infiltration

Acute

Warmth and fluid Capsular pattern Local tenderness Treatment Subacute

Warmth and fluid Capsular pattern Positive ligamentous tests Treatment Chronic

Formation of adhesions? Limited range of motion? Treatment

ments, congruency of joint surfaces, effectiveness of the menisci and the well-balanced action of all musculo­ tendinous units acting across the knee joint. Of these structures, muscles and tendons play a central role in joint stabilization. They are said to be the 'first defenders' in distortion and loading situations.69 Degree of instability

The degree of instability is demonstrated during stress tests and can be graded on the following scale (Fig. 77.15): • mild/l + • •

5 mm or less separation of joint surfaces. moderate/2+ between 5 and 10 mm separation. severe/3+ > 10 mm separation or more. =

=

This scale is not very precise but is effective for clini­ cal and therapeutic purposes. It should be remembered, however, that under anaesthesia the results of the stress tests are often exaggerated so that patients with 2+ instability often show 3+ instability in the test.

Classification of instability

Instability may be classified as straight or rotatory. Straight instability. This is defined as an increased range of angular movement in the frontal plane, i.e. valgu s / abduction or varus / ad du ction movement (Fig. 77.1 6), or an increased range of gliding movement in the sagittal plane, i.e. the simultaneous forward or backward gliding movement of the tibial condyles in relation to the femoral condyles (Fig. 77.1 7). Rotatory instability. This implies increased rotation movement of the tibia on the femur. The posterior cruciate ligament, located in the centre of the joint, is the fundamental stabilizer and is the axis of the joint, both in flexion-extension and in rotation. Consequently, this ligament is always intact in rotatory instabilities; from the moment the ligament is completely torn, there is no longer a centre of rotation and any kind of straight instability can result.70,71

1 1 1 6 SECTIO N T H I RT E E N - T H E K N E E

/; "

, '

3+

A

Figure 77.15

B

c

Degrees of straight instability in the frontal plane: A. mild; B. severe; C. moderate.

There are three types of rotatory instability: there is an abnormal forward gliding movement of the medial tibial plateau with respect to the medial femoral condyle, while the lateral tibial plateau retains a relatively normal relationship with the lateral femoral condyle (Fig. 77.18a) . Anterolateral rotatory instability: there is an abnormal forward gliding movement of the lateral tibial plateau with respect to the lateral femoral condyle, while the medial tibial plateau retains a relatively normal relationship with the medial femoral condyle (Fig. 77.1 8b).

• Anteromedial rotatory instability:

•

2+

there is an abnormal backward gliding movement of the lateral tibial plateau with respect to the lateral femoral condyle. Again, as in anterolateral rotatory instability, the medial tibial plateau remains in normal contact with the corresponding femoral condyle (Fig. 77.1 8c).

• Posterolateral rotatory instability:

Various combinations of these rotatory instabilities can occur. The most commonly encountered are combined anterolateral and anteromedial, and combined antero­ lateral and posterolateral. Posteromedial rotatory instability does not exist because an intact posterior cruciate ligament prevents any backward gliding movement of the medial tibial condyle in relation to the medial femoral condyle.

11\

3+ 2+ 1 +

Figure 77.16

Degrees of straight instability in the sagittal plane.

Figure 77.17 Straight instability: increased range of gliding movement in the sagittal plane.

CHAPTER 77

(a) Figure 77.18

(b)

(c)

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DISORDERS OF T H E LIGAM E NTS 1 1 1 7

(d)

Rotatory instability: (a) starting position; (b) anteromedial; (c) anterolateral; (d) posterolateral

FUNCTIONAL EXAMINATION

If the history or routine clinical examination indicates the possibility of instability, a supplementary examination is performed to detect the exact localization and degree of ligamentous insufficiency. Acute stage

In the acute stage, only the first few hours after the acci­ dent are suitable for clinical detection of ligamentous laxity. After this, effusion and muscle spasm resulting from the capsulitis will prevent a detailed examination. This is particularly the case in lesions of the medial col­ lateral ligament because of its close relationship with the capsule. So assessment should be made as soon as possible, preferably at the scene of the accident. If intra­ articular bleeding is present, which especially accompa­ nies tears of the anterior and posterior cruciate ligaments as well as of the medial collateral ligament, the first few minutes are often the only time available to make a proper clinical assessment of ligamentous laxity. When time has elapsed, examination under general anaesthesia, eventually followed by arthroscopy, is the only course of action. However, if the lesion seems to be less serious, supplementary examination can wait until a proper clinical evaluation can be made.

gently and repeatedly, gradually increasing up to the point of pain. The degree of movement and the end-feel are estimated. The normal limb is assessed first, especially in acutely injured patients, because this shows the patient that the examination will not be rough and is unlikely to be painful. The examiner also gets a measure of the stability of the unaffected knee. Instability indicates a tear limited to one or more of the medial compartment ligaments, i.e. the medial collateral ligament, meniscotibial or meniscofemoral capsular liga­ ments and the posterior oblique ligament. If the abduction stress test in full extension also shows instability, the posterior cruciate ligament is probably also ruptured. It should be borne in mind that, in the fully

Chronic stage

In the chronic stage thorough clinical examination suffices to estimate, in almost all instances, the degree of functional instability and to determine the type of treatment required. Tests Passive abduction or valgus stress test in 30° of flexion.

The patient is placed supine on the couch, the head resting on a pillow to enable observation of the exam­ iner without active raising of the head (which often causes tightening of the hamstrings). The thigh rests on the couch, the lower leg hangs over the side, with the knee in 30° of flexion. One hand is placed about the lateral aspect of the knee, the other grasps the lower leg at the ankle (Fig. 77.19). Then abduction stress is applied

Figure 77.19

Passive abduction or valgus stress test in 30° of fiexion.

1 1 1 8 SECTION T H I RT E E N - T H E K N E E

extended position, an intact posterior cruciate ligament still holds the joint surfaces in firm apposition, even in complete tears of the medial compartment ligaments. Passive adduction or varus stress test in 30° of flexion.

This test is performed in the same position as the previ­ ous one, but the hands are changed, so one hand is placed about the medial aspect of the knee while the other grasps the lower leg at the outer side of the ankle (Fig. 77.20). The degree of movement and end-feel are estimated. Adduction stress is applied to test the stability of the lateral compartment ligaments: the lateral collateral liga­ ment, meniscotibial or meniscofemoral capsular ligaments and the arcuate ligament. Instability of the lateral compartment is less common but causes significantly more disability than a compara­ ble amount of instability medially. Lateral instability cannot be detected when the test is performed with the knee in full extension because the intact tight posterior cruciate ligament precludes any movement in this position. If an adduction stress test in full extension shows lateral instability, rupture of both the lateral compartment ligaments and the posterior cruciate ligament should be feared. The test is performed with the patient supine and the knee in 20-30° of flexion. The distal femur is grasped from the lateral side to obtain control just above the lateral femoral condyle. The examiner uses the opposite hand to displace the proximal tibia directly anteriorly (Fig. 77.2 1 ). In acute rupture of the anterior cruciate ligament this test is preferred to the anterior drawer test in the 90° flexed position because muscle defence by the hamLachman test.

Figure 77.20

Passive adduction or varus stress test i n 30° of flexion.

Figure 77.21

Lachman test.

strings may prevent the forward movement of the tibia and give rise to a false-negative result.72 Liljedahl et a[73 found only 3 of 35 patients to have a positive anterior drawer test in 90° of flexion, whereas with anaesthesia 31 and on arthrography 29 were positive. Anterior drawer test in external and internal rotation.

The patient is positioned as for the abduction-adduction stress tests. The hip is flexed to 45°, the knee to 80-90°. The foot is placed on the couch, well fixed by a portion of the examiner 's buttock resting on the dorsum of the fore­ foot. The examiner places both hands around the upper part of the tibia with the index fingers palpating the ham­ string tendons to make sure they are relaxed. Both thumbs are placed at the anterior border of the joint so that they can estimate the range of movement. Then the proximal part of the lower leg is pulled forward repeat­ edly, first gently then with a somewhat stronger pull. The test is first performed with the lower leg and foot externally rotated beyond the neutral position and as far as is comfortably possible, then internally rotated (Fig. 77.22). The findings are compared with those of the basic examination, for example in 0° rotation, as well as with the other knee. With the tibia in external rotation. Anteromedial rota­ tory instability is indicative of a tear of one or more of the medial compartment ligaments: the medial collateral lig­ ament, meniscotibial or meniscofemoral capsular liga­ ments and the posterior oblique ligament. An associated anterior cruciate ligament tear increases the amount of subluxation of the medial tibial condyle. This ligam;nt is the second line of defence; in an acute isolated tear of the anterior cruciate the anterior drawer test will be negative.

CHAPTER 77

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DISORDERS OF T H E LIGAM E NTS 1 1 1 9

\ \

(a) Figure 77.22

(b) Anterior drawer test in external (a) and internal rotation (b).

With the tibia internally rotated. In patients with a medial compartment laxity, the test becomes negative because of the increased tension of the posterior cruciate ligament. Simultaneous forward subluxation of the tibial condyles indicates that the posterior cruciate ligament is torn. In this case, the rotational element is eliminated and straightforward instability exists.

Isolated forward subluxation of the lateral tibial plateau, for example anterolateral rotatory instability, can only be demonstrated if the knee is held in the neutral position, because internal rotation of the tibia will tighten an intact posterior cruciate ligament and prevent any subluxation. This type of instability is indicative of a tear of the middle third of the lateral capsular ligaments. Prone rotation test. 12

Sometimes doubt remains as to whether the range of rotation has been increased. A deci­ sive assessment can be made with the patient prone and the knees flexed to a right angle (Fig. 77.23). The movement of external or internal rotation is performed bilaterally and the range of movement is assessed by the twisted position of the feet.

An increased range of lateral rotation results from a lack of stability of inert structures at the medial compart­ ment (medial collateral ligament, meniscotibial and meniscofemoral capsular ligaments and the posterior oblique ligament) and / or the arcuate complex (arcuate ligament, lateral collateral ligament). An associated tear of the anterior cruciate ligament still increases the amount of rotation. An increased range of medial rotation is indicative of laxity of the middle third of the lateral capsular liga­ ments, the anterior and the posterior cruciate ligaments. The patient is in supine position with the hip flexed to 45° and the knee to 90°. The foot is flat on the couch, in neutral position. The heels of both hands are placed anteriorly against the proximal part of the tibia (Fig. 77.24). Both thumbs at the anterior border of the joint can estimate the range of movement. The proximal part of the tibia is then pushed backwards repeatedly, first gently then with a strong jerk. The posterior drawer test, which includes palpation of the tibia-femur step-off, was recently demonstrated to be the most sensitive and specific clinical test for posterior

Posterior drawer test.

1 1 20 SECTION T H I RTE E N - T H E K N E E

Figure 77.24

Posterior drawer test.

capsular ligaments. Frequently, the anterior cruciate liga­ ment and / or menisci are also ruptured and increase the instability. Anterolateral instability can also be demonstrated by carrying out the manoeuvre in the reverse direction, starting from a position of a few degrees of flexion: the pivot-shift test.

Figure 77.23

Prone rotation test.

cruciate ligament deficiency (accuracy 96% with a 90% sensitivity and a 99% specificity)?4 'Jerk' test and pivot-shift test. The patient lies supine, the hip flexed to about 45°, the knee to 90°. The examiner sup­ ports the patient's leg, with one hand at the foot, the other at the proximal end of tibia and fibula. The hand at the foot rotates the tibia slightly internally while the other hand exerts a mild valgus stress at the knee (Fig. 77.25). Extreme internal rotation may d ampen a shift significantly. Maintaining slight internal rotation and mild valgus stress, the examiner gradually extends the knee. A positive result is indicated if, on attaining about 30° of flexion, relocation occurs with a sudden movement, which is called a 'jerk'. The forwards shift can be seen and felt by the examiner. At the same moment, the patient will recognize the feeling of instability. The test demonstrates an anterolateral rotatory insta­ bility because of a tear in the middle third of the lateral

Figure 77.25

The 'jerk' test.

CHAPTER 77

-

D I SORDERS OF THE LIGAME NTS 1 1 21

Bach et afs found that the degree of pivot shift, proba­ bly b�cause of the role of the iliotibial band, strongly cor­ relates with the position of the hip and knee joint. They advised 30° of hip abduction and 20° of tibial external rotation as the position in which instability is most clearly demonstrated. The examiner stands at the foot of the couch in order to monitor hip position carefully. The ipsilateral hand cradles and holds the foot in external rotation. The other hand, slightly supinated, holds the proximal and lateral leg. An axial load and valgus movement are applied simultaneously as the knee is slowly flexed passively from the extended position.

"V"

Practitioner's checklist

• An associated acute partial tear of the medial compartment ligamentous structures makes the test too painful to undertake • A false-positive test may occur in the presence of a torn meniscus • In children, and in patients who have mild to moderate congential genu recurvatu m without symptoms, it is normal to find the 'jerk' and pivot-shift tests and the anterior drawer test with the tibia in 0° rotation to be mildly positive on both sides

External rotation-recurvatum test. The patient lies supine on the couch. Both legs are lifted simultaneously by grasping the big toes (Fig. 77.26). The amount of exter­ nal rotation of the proximal end of the tibia and the degree of recurvatum are observed. In a positive test, unilateral excess of external rotation and recurvatum is obvious, which is seen as increased tibia vara. The test demonstrates posterolateral rotatory instabil­ ity, which is located in the structures of the arcuate complex: the arcuate ligament, lateral collateral ligament and possibly the popliteus tendon. It is also advisable to observe the patient standing and actively extending the knees maximally or to observe a barefoot walk. Sometimes external rotation-hyperextension is absent, while these patients often walk with a slightly bent knee to avoid terminal extension.

Clinical tests for knee instability are summarized in Table 77.6. TREATMENT

The best chance of success in treating a knee affected by ligamentous instability is within days of the original injury.76 Management can be non-surgical or by surgical repair. Which is chosen depends on the structure(s) at fault, the degree of rupture and the extent of the lesion.

Figure 77.26

External rotation-recurvaturn test.

Conservative treatment. In general, conservative treat­ ment is indicated in all grade I and I I sprains and in iso­ lated grade I I I sprains of the medial collateral ligament. Acute complete tears of the anterior cruciate ligament, with an absent (0) or mild graded (1+) pivot-shift test, show excellent or good results in half of the cases. 77 The results of conservative treatment of isolated grade I I I sprains of the lateral ligament compartment are gener­ ally poor and not acceptable.78 Surgery. Surgical treatment of knee ligament injuries, particularly of the anterior cruciate ligament, is still con­ troversial because the complex functional role of these ligaments makes them difficult to reconstruct effectively.79 Given that reconstruction is performed using high­ strength bone-ligament-bone autogenous graft, placed isometrically and securely fixed internally, failure rates after 2 years' follow-up decreased to about 30%.80

Conservative treatment in acute instability Medial collateral ligament. Isolated acute grade I I I lesions of the medial collateral ligament seldom result in lasting instability. Successful conservative treatment of these lesions has been reported, with only a very small number of patients requiring subsequent reconstruction.13,19,22,81,82 However, this applies only to isolated injuries in which, for example, valgus stability in full extension is normal. The key to success in non-surgical management of com­ plete tears of the medial collateral ligament is to exclude those with concurrent damage to the anterior cruciate ligament or menisci.20,22,23,82 Therapy must also include a structural rehabilitation programme with early protected motion, followed by progressive strengthening. A small residual amount of medial laxity does not appear to have any influence on the ability to return to competitive athletics.23

1 1 22 S ECTION T H I RT E E N - T H E K N E E

Table 77.6 Summary o f clinical tests for instability Type of instability

Structures probably ruptured

Diagnostic test

Straight valgus

Capsuloligamentous structures of medial and posteromedial compartment, and posterior cruciate ligament

Abduction stress test in full extension

Straight varus

Lateral compartment ligaments and posterior cruciate ligament

Adduction stress test in full extension

Straight anterior

Middle third of medial and lateral compartment ligaments, and anterior cruciate ligament

Anterior drawer test Lachman test

Straight posterior

Posterior cruciate ligament and arcuate complex

Posterior drawer test

Rotatory anteromedial

Medial and posteromedial compartment ligaments, and anterior cruciate ligament

Anterior drawer test from mid-position and in internal rotation Abduction in 30° flexion Lachman test

Rotatory anterolateral

Middle third of lateral compartment ligaments, and anterior cruciate ligament

Anterior drawer test from mid-position Adduction in 30° flexion 'Jerk' test Pivot-shift test

Rotatory posterolateral

Arcuate complex

External rotation-recurvatum test Posterior drawer test from mid-position and in external rotation Adduction in 30° flexion

When surgical and non-surgical treatment are compared in isolated acute grade III lesions of the medial collateral ligament, similar results are obtained. However, non-surgi­ cally treated patients are rehabilitated in significantly less tirne.22 In combined injuries, it has been shown that the non-surgical management is successful only in 15%. Rehabilitation in non-operated, acute complete tears. 23

In the first 2 weeks the knee is partially immobilized in a rehabilitative brace that prevents the joint from moving beyond the painful range and protects against hyper­ extension, excessive lateral rotation and valgus strain. In order to maintain mobility while healing, Cyriax advo­ cates moving the ligament by deep transverse friction to and fro over the adjacent bone in imitation of its normal behaviou r.83 The first day, 1 minute's friction thus suffices, in that no unwanted adhesions have yet formed. Friction is followed by passive flexion and extension movements, within the limits of pain. This treatment is repeated daily. Within a week, tenderness is declining and friction is performed for an increasing time, for up to 15 minutes, on alternate days during the second week (see p. 1 1 04). From the moment the patient can undertake straight leg raising, weight bearing with crutches is started, pro­ vided the patient can tolerate it. At this time, isometric exercises are commenced (three times daily, 15 contrac­ tions) in order to avoid muscle wasting.

This period is followed by 4 weeks of controlled mobi­ lization in a rehabilitative knee brace that allows a range of motion to be set within the limits of pain; hyperexten­ sion should still be prevented. This provides the oppor­ tunity to perform stationary biking and to start isotonic exercises for the quadriceps and hamstrings muscles. Thereafter, isokinetic exercises are added. After 6 weeks, the orthosis is replaced by a functional knee brace. Isotonic and isokinetic muscle training are continued. Running exercises can be started from the moment the quadriceps has reached at least 60% of the strength of the unaffected muscle. At this stage, hamstrings strength is equal to that of the opposite leg. If quadriceps strength has returned to 80% of normal, agility drills can be undertaken. At this stage training is, if necessary, intensified to reach the level required for competitive sports. Strength, power and endurance should be compared with the unaffected leg. Contact drills are allowed although still with a functional brace on the knee to protect as much as is possible against valgus stress. The average time from injury to return to full activity and competitive sports is about 9 weeks. Anterior cruciate ligament. In acute complete ruptu re of the

anterior cruciate ligament, surgical repair is the treatment of choice,3,24,84 although secondary repair operations can still be undertaken.

CHAPTER 77

Non-surgically treated complete ruptures of the ante­ rior' cruciate ligament commonJy lead to recurring effu­ sion into the joint after slight trauma and, because of the integrated nature of the whole stabilizing complex, intact restraining structures may gradually be stretched as well so that a number of structures are eventually involved and chronic instability results. After some years an advanced arthrosis is often the rule. Buckley et al,8s in their study of conservatively treated partial anterior cruciate ligament tears, found that most patients developed a symptomatic knee but the majority did not have a sufficiently significant functional disabil­ ity to warrant reconstructive surgery. Furthermore, they found that knee function following a partial tear did not appear to deteriorate with time (49 months after injury). Rehabilitation programme in conser vatively treated grade /I ruptures. 79 In the first 2 weeks the knee is immo­

bilized in 30° of flexion. Isometric hamstrings and quadri­ ceps exercises are instituted within the first 3 days. Hamstring muscle function is essential, because the ham­ strings act as dynamic agonists to the anterior cruciate ligament in preventing forward gliding of the tibial plateau du ring walking, running and twisting. After 2 weeks, limited motion in flexion between 30-60° degrees is allowed and can be increased to 30-70° after 4 weeks. Flexing the hip should be avoided until week 3 or 4, because quadriceps activity during this movement may stretch the injured ligament. Partial weight bearing, using crutches, is permitted approximately 2-4 weeks after the injury. Full weight bearing is allowed after 4-6 weeks. Approximately 6-10 weeks after the injury the patient may start resisted exercises, such as swimming and stationary biking, while wearing a functional brace. Terminal extensions and body-weight load should still be avoided. Jogging is allowed about 3-6 months after the injury. Muscle exercises must be continued until there are no differences between the legs in hamstring and quadriceps strength. Athletes are not allowed to return to competi­ tive sports earlier than 6-12 months after the injury. Any swelling during the entire course of rehabilitation indicates that some overload has taken place and the programme should be modified accordingly. Recent studies have shown that conservative management is also acceptable in iso­ lated complete ruptures of the posterior cruciate ligament. Good results are obtainable even in athletes who wish to return to competitive sport. 86--90 In contrast, as found by Fowler and Messieh,89 surgical techniques of posterior cruciate ligament repair and reconstructions are generally difficult and the long-term results are unpredictable. Posterior cruciate ligament.

- DISORDERS OF T H E LIGAME NTS 1 1 23

Rehabilitation programme. This resembles the pro­

gramme for the anterior cruciate ligament. However, in posterior cruciate ligament instability, it seems to be essential that quadriceps atrophy is avoided. The long-term results of non-surgically treated grade II sprains of the lateral liga­ ment compartment of the knee are reported as good and acceptable; however, in grade III sprains the results are mostly poor and unacceptable, resulting in an unstable knee with severe symptoms and posttraumatic osteoarthritis.?8 On examination in 30° of flexion, these grade III sprains showed a severe (3+ ) adduction instabil­ ity. In full extension there is still some adduction instabil­ ity, graded as mild (1+) or moderate (2+). Kannus78 emphaSizes that in grade III sprains the anterior cruciate ligament is often injured as well, and the damage to it may be missed by clinical methods at the initial examination. Such ligamentous laxity seems too severe to be fully com­ pensated for by muscle strength, i.e. dynamic stability. Lateral ligament compartment.

Conservative treatment in chronic instability

chronic instability the action of the mechanical recep­ tors in the lengthened ligaments is normally decreased. This loss of reflex activity influences the 'protective reflex arc' formed by the ligaments and their companion muscles and leads to lack of active stability. In chronic grade III instability it is impossible to improve upon the loss of proprioception within the joint without surgical repair. Such repair is thereby limited to young and well-motivated patients with no radiological evidence of degenerative disease.91 Late examples of posterior cruciate and isolated lateral ligament instability cannot be repaired with confidence. 76 Thus early detection and repair are most important. In all cases of chronic instability the patient should still be encouraged to undertake an intensive programme of muscular training to improve the strength and endurance of all related muscles - knee flexors, extensors, internal and external rotators. Meanwhile the surgeon and therapist are able to judge the patient's motivation and to select patients appropriate for surgical treatment. Exercises include isometric, isotonic and isokinetic con­ tractions performed daily. Care should be taken again not to overload the joint, because this can lead to capsulitis, patellofemoral pain or increasing crepitus. Such symp­ toms should be seen as a sign that progress with exercises has been too quick. During more functional actions, such as jogging on even or uneven ground, running in figures of eight and jumping, it is advisable that the patient ini­ tially wears a knee brace to control the instability. Which appliance is appropriate is determined by the type of instability that is to be controlled. The level of muscular condition determines the grade of sport activity and the types of sport that are appropriate for each individual. In

1 1 24 SECTION T H I RT E E N - T H E K N E E

Rehabilitation management after surgical repair

Rehabilitation takes at least 6 months. It should be insti­ tuted carefully, because revascularization and structural conversion of any transplanted tissue is a very slow process. The fi nal result is obtained about 1 year after the operation.92-94 The rehabilitation programme can be divided into four phases:95 • • • •

assisted ambulatory phase early strength training phase intensive strength training phase retu rn to sports.

Assisted ambulatory phase

During the last decade a trend has developed to replace the period of immobilization after surgical repair by early mobilization in order to decrease the risk of contracture building up and to prevent detrimental effects on carti­ lage. For example, after complete rupture of the ante�ior cruciate ligament, the use of a high-strength bone-lIga­ ment-bone au togenous graft, placed isometrically and securely internally fixed, made it possible to commence joint motion, muscle re-education and, with the protec­ tion of a knee orthosis, even weight bearing up to 50% from the first week.96-100 A study of the results of accelerated programmes of rehabi litation after anterior cruciate ligament reconstruc­ tion indicated the need not only for individualized, eval­ uation-based rehabil i tation but also that caution should be used when introducing high loads or repetitive exercises within the first few months after su rgery.IOI For this reason postoperative clinical evaluation of graft failure, excessive pain and effusion must be strict�y and regularly performed until termination of the rehabIl­ itation. This includes joint arthrometer tests and stress diagnosis after the first week of rehabilitation and at every second week during the first 6 weeks so as to have an accurate and objective evaluation of anterior displace­ ment before progression to a more strenuous phase of rehabilitation.9s Any increase in join t displacement of 2 mm or more than the last result is an indication for adjustment of the reha­ bilitation programme. Weight bearing must be delayed, joint motion limited to between 20 and 90° and resisted exercises for hamstrings and quadriceps limited at an angle of 70°. These measures decrease the tension on the graft. After 1 week the arthrometer test is repeat:d. Excessive synovial fluid may be another SIgn that therapy has been too aggressive. It inhibits not onl r quadriceps contraction102-104 but also may degrade cartI­ lage matrix.1Os Pain must also be controlled to block harmful effects on circulation and muscular action. This can be achieved by

medication and physical agents such as cool packs (loOe) and transcutaneous electrical nerve stimulation (TENS). Signs of sympathetic reflex dystrophy contraindicate the use of low temperature methods. Programmes that are performed too aggressively, with running and agility drills 5 to 6 weeks after surgery and return to full activity and competition 16 weeks' post­ operatively, show 11-52% abnormal displacements at follow Up. l06-108 In a less aggressive rehabilitation programme, with delay of high loads and strenuous activities for at least 4 months after surgery, abnormal displacements decreased to 15%, from which only 5% . showed failure ( 6 mm or more 0f mcrease ) . 1 0 1 Early strength training p hase

On the second day after surgery active assisted exercises are started. This prevents formation of adhesions which usually occurs within 2 weeks of immobilization. Excessive scar production is estimated in 1 0-20% of cases. Because structures of the supra- and infrapatellar region and the posterior joint capsule are particularly prone to the development of contractures, motion exer­ . cises must include passive mobilizations of the patella m all directions. Several studies recommend con tinuous passive motion via an externally applied force, especially if postoperative joint motion causes difficulties.97,109,110 It has been shown not to increase effusion or haemarthrosis.lOo However, if pain and muscle spasm cause patients to resist th:se passive motions, strong forces could damage the healmg graft and contraindicate the measure. Isometric con tractions and electrical s timulation of the quadriceps also start from the second day and are per­ . formed daily. Electrical stimulation not only stImulates quadriceps contraction but also increases pain thresh­ old. From the moment contraction of the quadriceps muscle is normal again, isotonic contractions, which cause higher muscular forces, are necessary to maintain strength. Because the effects on the maturing graft are unknown, and a direct relationship exists between the inert and contractile structures, it is advisable to start with a low load which is applied close to the knee joint. Movements shoul d also not pass 30° of extension because studies on strain in the normal and recon­ structed anterior cruciate ligament during isotonic con­ traction have shown the final 30° of extension to be seven times tha t of full flexion to 30°.1 11 A training programme for the hamstrings, gracilis, tensor fasciae latae and gluteal muscles is also instituted. After the first week, s tretching exercises of the gastroc­ nemius, hamstrings and hip flexor muscles are inclu �ed. When the patient has achieved 50% weight bearing, nor­ mally about 1 0 days after surgery, balance training can be added. The patient tries for 5-1 0 minutes to stay with both

CHAPTER 77 - DISORDERS OF T H E LIGAME NTS 1 1 25

feet on a balance board. This stimulates proprioceptive activity and arthrokinetic reflexes that increase the action of the knee muscles, which in turn protects the graft. Attention should be paid to a normal, symmetrical gait, which maintains normal articular cartilage and muscle re-education.112,113 Any abnormalities during gait must therefore be identified and treated before weight bearing is increased. Intensive strength training phase

To regain muscular condition resisted exercises may start the fourth week after su rgery. These are performed sub­ maximally (about 60% of maximum effort), with a short lever arm and progressive repetition. Three sets of 1 0 repetitions are prescribed. Increase o f strength i s to be expected if the limits of fatigue are reached after each session. Isotonic contractions of the hamstrings may be per­ formed prone, with the patella lying free from the edge of the table. As for the quadriceps, three sets of 10 repeti­ tions are performed two times a day. Because there is no fear of stretching the graft, this exercise may be per­ formed throughout the full range of motion. Isotonic contractions of the quadriceps beyond 30° of extension should still be avoided. Because of its posterior drawing force, co-contraction of the hamstrings during quadriceps action is an effective measure to decrease strain on the anterior cruciate ligament. In a study on this matter during standing, knee flexion of 30° or more, together with trunk flexion of 30° or more, increased the protective posterior drawer force of the hamstrings.114 Mini-squats and wall sits (patient leans backwards against a wall with the knees flexed, ranging between 30° of extension and 90° or more of flexion) are also recom­ mended exercises, not only to increased strength but also endurance, without stretching the graft. Bending the trunk forward still increases the protective action of the hamstrings on the graft. These so-called close-kinetic exercises (standing with continued ground reaction force) also seem to reduce forces on the patellofemoral joint. From the moment the patient has achieved ful l weight bearing, which is normally 6 weeks after surgery, it is advisable to start progressive muscle training with an overload at each exercise but only on condition that there is no pain, effusion or difference of tibial anterior translation between the involved and uninvolved limb and there is a full and painless range of motion. Patients with palpable patellofemoral crepitus are at risk of deterioration and are better to avoid strong resisted exercises. The improvement of quadriceps and hamstrings must be evaluated weekly by isometric manual tests on strength and by the measurement of thigh circumference.

Proprioceptive neuromuscular facilitation (PNF) tmill ing is another recommended exercise to increase motor activity. It improves strength and endu rance of the whole limb, from proximal to distal. With allowance for pain and weakness, resistance can be performed in an isometric or a concentric manner (either eccentric or isotonic). After 2 months, training is broadened with more functional elements such as walking, pool walking and stepping. The use of a knee orthosis to control rotatory movements and the flexion-extension range within 60° and 20°, respectively, must be continued. Isokinetic con tractions have their own value. Because muscular defects have been shown to be more likely d iagnosed at special velocities, it is of great advantage to investigate that aspect of muscu lar deficiency. With the use of a device, resistance can be adjusted accurately at the indicated velocity.l15 It is advisable to perform three sets of 10 repetitions twice a day on every other day and the load should not exceed 70% of maximum effort. However, because of the process of incorporation of the graft, it seems better not to start such exercises before the sixth postoperative week and also in the absence of pain and swelling. The effect of isokinetic exercises on force and endurance have been shown to be greater than that of isotonic exercises. The high loading contra indicates these exercises when there is patellofemoral crepitus, unless this is limited to the range of motion outside the crepitus.

Return to sports

After 3 months, bicycling can be started, which is stimu­ lating for the quadriceps and hamstrings with little effect on the graft. At the beginning duration is 15-20 minutes. At that time resisted exercises are still increased although muscular effort must not exceed 75% of maximum. R u n n ing is allowed from the sixth postoperative month and, according to the patient's goals, turning, twisting, cutting and jumping may gradually be added. The use of a knee orthosis is still continued, especially in new training situations that impose high loads on the graft. 'Joint reactions', such as recurrence of pain and effusion, patellofemoral crepitus and any increase in anterior trans­ lation of the tibia, should always modify the programme. To be successful in rehabilitation, exercises must also be similar to the specific demands of the individual sport or activity.1 1 6 Strenuous and difficult aspects are trained in isolation until proficiency has again been obtained. From that moment, and on condition that pain, effusion and patellofemoral crepitus are absent and forward translation of the tibia stays normal, training in the group can restart. Return to competition is thereafter a matter of time and methodical building of strength. The level required for competitive sport can be judged from the following

1 1 26 SECTI O N T H I RT E E N - T H E K N E E

schedule: s i x 6 0 metre runs at full speed with 30 seconds' rest after each run; six 60 metre runs with small side jumps; 1 00 metre running with 10 left and right turns without losing speed. The whole question of successful rehabi litation is primarily one of motivation. Older and athletically inactive patients tend to do less well.

Tables 77.7 and 77.8 give a survey of the whole reha­ bilitation programme after anterior cruciate ligament (ACL) reconstruction.95 Table 77.9 summarizes the treat­ ment of ligamentous lesions in both the acute and the chronic phase.

Table 77.7 Evaluation-based rehabilitation advanced weight bearing and minimal protection programme: range of motion after ACL reconstruction. Weeks 1 -5a Week 1

Weeks 2-3

Weeks 4-5

When

Weight bearing with two crutches when: - postoperative pain is controlled - haemarthrosis is controlled - patellar mobility is normal - voluntary quadriceps contraction

Weight bearing with one crutch when: - pain is controlled without narcotics - effusion is controlled - ROM 1 0-100° - muscle control throughout ROM

Independent ambulation when: - pain is controlled - effusion is controlled - ROM 5-1 1 5 ° - muscle control throughout ROM - joint arthrometer results are within 2 mm

Evaluation

Pain Haemarthrosis Patellar mobility Joint arthrometer ROM Quadriceps contraction and muscle spasm Soft tissue contracture

Pain Effusion Patellar mobility Joint arthrometer ROM Muscle control Active extension Inflammatory response

Pain Effusion Patellar mobility Joint arthrometer ROM Muscle control Complete extension Inflammatory response Gait

Treatment

Pain management Control haemarthrosis Mobilize patella Motion exercises Flexibility programme Muscle re-education Knee orthosis CPM - perform ankle pumps 5 minutes every hour to maintain blood flow

Pain management Control effusion Mobilize patella Motion exercise 0-125° Flexibility Increase quadriceps exercises and add mini-squats Muscle re-education Knee orthosis Balance training Increase in joint arthrometer result Continue ankle pumps

Pain management Control effusion Motion exercises Flexibility Continue quadriceps exercises and mini­ squats Knee orthosis Endurance and advanced muscle exercises Balance training Increase joint arthrometer Address gait abnormalities

Goals

ROM 20-70° Adequate quadriceps contraction control, inflammation and effusion 25-50% full weight bearing

ROM 0-125° Muscle control Control inflammation and effusion to prevent scarring Joint arthrometer remains within 2 mm of last test 50-75% full weight bearing

ROM 0-135° Maintain ROM Muscle endurance Control inflammation and effusion to prevent scarring Joint arthrometer remains within 2 mni of last test 1 00% full weight bearing with a normal gait Early recognition of complications (motion loss, RSD, laxity)

aRationale: Achieve full weight bearing and full range of motion without compromising graft fixation or graft maturation. CPM, continuous passive motion; ROM, range of motion; RSD, reflex sympathetic dystrophy.

CHAPTER 77

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D I SO R D E RS OF THE LIGAM E NTS 1 1 27

Table 77.8 Evaluation-based rehabilitation advanced muscle training after ACL reconstruction. Weeks 6-52a Weeks 6-1 2

Weeks 1 3-24

Weeks 25-52

Evaluation

Hamstrings & quadriceps strength testing Swelling Joint arthrometer Patellar mobility & crepitus

Hamstrings & quadriceps strength testing Swelling Joint arthrometer Patellar mobility & crepitus

Hamstrings & quadriceps strength and endurance testing Swelling Joint arthrometer Patellar mobility & crepitus Function tests

Treatment

Discontinue EMS Increase isotonic exercise Start isokinetic exercises Start proprioceptive neuromuscular facilitation Start aerobic conditioning Proprioceptive training Therapeutic modalities Knee orthosis

Increase speed & resistance for isotonic & closed chain kinetic exercises Advance isokinetic exercises Continue aerobic conditioning Advance proprioceptive training Start plyometrics Knee orthosis

Increase isotonic exercise Advance isokinetic exercises Continue aerobic conditioning Advance running & start functional running programme Continue proprioceptive training Knee orthosis Sport-specific training

Increase strength endurance so there is no fatigue with ADL

Increase strength & endurance of lower extremity for limited activity

Goals

Increase function Maintain strength & endurance Return to previous activity level

'General criteria: No effuSion, painless range of motion, joint stability; performs activities of daily living without pain; range of knee motion

0-125°; full weight bearing.

ADL, activities of daily living; EMS, electrical muscle stimulation.

Table 77.9 Treatment of ligamentous lesions Phase

Treatment (1 )

Treatment (2)

Compression Elevation Effleurage + Deep transverse massage Controlled movements (active and passive) Gait instruction

Alternative (within 48 hours) Steroid infiltration Controlled movements (active and passive) Gait instruction

Deep transverse massage Immobilization

Infiltration (steroid or sclerosant) Immobilization

Deep transverse friction + Manipulation Strength-building exercises Proprioceptive training

(Steroid infiltration)

Acute phase Joints controlled by muscles

First day Following days

Joints not controlled by muscles

Chronic phase Adhesive scar formation Lasting instability

Surgical reconstruction (Infiltration with sclerosant)

1 1 28 SECTI ON T H I RT E E N - T H E K N E E

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1 1 . Jaervinen M. Healing o f a crush injury i n rat striated muscle.

With special reference to treatment by early mobilization or immobilization. Academic Dissertation, University of Turku, Turku, Finland, 1976. Cyriax JH. Textbook of Orthopaedic Medicine, vol 1 , Diagnosis of Soft Tissue Lesiolls, 8th edn. Bailliere Tindall, London, 1982. Ellsasser JC, Reynolds FC, Omohundro JR. The non-operative treatment of collateral ligament injuries of the knee in profes­ sional football players. ] Bone Joint S u rg 1974;56A:1185. Godshall RW, Hansen CA. The classification, treatment and follow-up evaluation of medial collateral ligament injuries of the knee. ] Balle loint S u rg 1974;56A: 1316. Balkfors B. The cou rse of knee ligament injuries. Acta Orthop

the

medial collateral ligament of the human knee under single and combined loads. ] Biomech 1996;29(2):199-206. 26. Reider B. Medial collateral ligament injuries in athletes. Sports

6. Lynch SA, Renstrom PA. Treatment of acute lateral ankle liga­

ment rupture in the athlete. Conservative versus surgical treat­ ment. Sports Med 1999;27(1):61-71 . Reider B, Sathy MR, Talkington J, Blyznak N, Kollias S. Treatment of isolated medial collateral ligament injuries in ath­ letes with early functional rehabilitation. A five-year follow-up study. Am I Sports Med 1994;22(4):470-477. Buss DO, Min R, Skyhar M et a/. Nonoperative treatment of acute anterior cruciate ligament injuries in a selected group of patients. Am I Sports Med 1 995;23(2) : 1 60-165. Jarvinen M, Kannus P, Johnson RJ. How to treat knee ligament injuries? A n ll Chir GynaecoI 1 991 ;80(2) : 1 34-140. Cooper RR. Alterations during immobilization and regenera­ tion of skeletal muscles in cats. ] Balle loillt S u rg

of

25. Hull ML, Berns GS, Verma H, Patterson HA. Strain in the

Arthroscopy 1990;6(3):

221-225.

l i gament

1997;40(3) : 1 76-1 8 1 .

39.

abnormal medial meniscocapsular structures: MR imaging and sonography in cadavers. Am [ RoelltgenoI 1995;171(4):969-976. George J, Saw KY, Ramlan AA et al. Radiological classification of meniscocapsular tears of the anterolateral portion of the lateral meniscus of the knee. Austrnlas Radial 2000;44(1): 19-22. Noble J. Lesions of the menisci: autopsy incidence in adults less than fifty-five years old. ] Bone [oint Surg 1977;59A:480-483. Noble J, Hamblen DL. The pathology of the degenerated menis­ cus. [ Bone Joint Surg 1975;57B : 1 80-186. Goodfellow J. He who hesitates is saved. I Bone loint Surg 1980;62B: 1-2.

17. Holden 01, Eggert AW, Butler JE. The non-operative treatment

40. Kanamori A, Woo SL, Ma CB et al. The forces in the anterior cru­

of grade I and I I medial collateral ligament injuries to the knee. Am ] Sports Med 1983;11:340. 18. Ritter MA, McCarroll J, Wilson FD, Carlson SR. Ambulatory care of medial collateral ligament tears. Phys Sports Med

ciate ligament and knee kinematics during a simulated pivot shift test: a human cadaveric study using robotic technology.

1983;11 :47. 19. Fetto JF, Marshall JL. Medial collateral ligament injuries to the

knee: a rationale for treahllent. Clin Orthop 1978;132:206. 20. Hastings DE. The non-operative management of collateral liga­

ment injuries of the knee joint. Clin Orthop 1980;147:22. 21 . Indelicato PA. Non-operative treatment of complete tears of the

Arthroscopy 2000;16(6):633-639.

·

4 1 . Ebstrup JF, Bojse-Moller F. Anterior cruciate ligament injury in

indoor ball games. Scand I Med Sci Sports 2000;10(2) :114-116.

42. Delfico AJ, Garrett WE Jr. Mechanisms of injury of the anterior

cruciate

ligament

in

soccer

players.

Clin

Sports

Med

1998;17(4):779-785. 43. Peterson TR. Knee injuries due to blocking: a continuous

problem. Phys Sportsllled 1975;3(1) :440-447.

medial collateral ligament of the knee. ] Bone loint S u rg

44. Paterson FWN, Trickey EL. Meniscectomy for tears of the

1983;65A:323.

meniscus combined with rupture of the anterior cruciate liga­ ment: a follow-up study. ] Bone [oint Surg 1983;65B :388-390. 45. Bray RC, Dandy DJ. Meniscal lesions and chronic anterior cruciate ligament deficiency. ] Balle [oillt S u rg 1989;71 B:128-130.

22. Jones RE, Bradford Henley M, Francis P. Non-operative manage­

ment of isolated grade I I I collateral ligament injury in high school football players. Clill Orthop Rei Res 1986;213;137-140.

CHAPTER 77 - DISORDERS OF T H E LIGAM ENTS 1 1 29

46. Goudernak

T. Der posttraumatische H a marthros des I6

hours

hours to 6 weeks weeks

7 Tendons of extensor d i g itorum longus

8 Ligaments of cuboid-fifth metata rsal j o i nt and

Table 84.4 Classification by severity of lesion

cuboid-fou rth metata rsal joint

Grade69

Lesion

Elongation of ligaments without macroscopic rupture

5

3

4

III

Complete ligamentous rupture

NATURAL HISTORY

Sites of inversion sprain - see Box 84. 1 for details.

1 Figure 84.20

Partial and macroscopic ligamentous rupture

age or there is localized bone tenderness of the posterior edge or tip of either malleolus or the patient is unable to bear weight i mmediately after the injury?O This rule was 1 00% sensitive and 40.1 % specific for detecting malleolar fractures and would allow a reduction of 36.0% of ankle radiographic series ordered. 71

2

Figure 84.19

II

Malleolar fractures occurring with so-called varus sprain.

During the first hours after the trauma, regardless of the size of the lesion, a traumatic inflammatory reaction with warmth, pain, swelling and loss of function will result and lasts a couple of days. In this period, damaged tissue and noxious substances are eliminated and diluted. Very soon there is in-growth of blood and lymph vessels from the adjacent intact structu res, together with migration of fibroblasts. The latter synthesize new collagen in an effort to form a scar. It has been well established that the alignment of the collagen fibres in the scar is anarchic and disorderly if insufficient external stimulus is applied to the healing tissue. Some tension to the granulation is necessary to improve and accelerate the development of the fibrillary network into orderly layers.72 Immobilization leads to a scar that is adherent to capsule and bone. The sprained ankle then proceeds to a chronic stage: prolonged disability for several months. Sometimes the patient never recovers, unless the adhesions are ruptured by manipulation. The discussion of diagnosis and treatment of ankle sprains follows the natural history sequence: •

First or acute stage: traumatic reaction immediatel y

•

following the trauma; the first 24-48 hours. Second or subacute stage: traumatic reaction disappears; period of repair; from the second day to 6 weeks.

CHAPTER 84

•

Third o r chronic stage: the scar has definitely formed; if tliere are adhesions, permanent disability results after 6 weeks to 2 months.

DISORDERS OF T H E AN KLE A N D SU BTALAR J O I NTS 1 2 1 9

-

Table 84.5 Patterns of acute ligamentous and tendinous disorders in

inversion sprains Structure Ligaments

DIAGNOSIS There is nothing so easy as to make a diagnosis of a sprained ankle. But to locate the lesion precisely, to esti­ mate the degree of damage and to predict the prognosis is not so simple. A thorough and patient clinical exami­ nation by an experienced practitioner is the best basis for an accurate diagnosis. The value of technical investiga­ tions should not be overestimated.

Anterior talofibular

Combined plantiflexionl inversion Plantiflexion

Calcaneofibular

Inversion Varus

Calcaneocuboid

I nversion Adduction and supination in the midtarsal joint

Anterior tibiotalar

Plantiflexion

Acute stage

There has been an inversion injury, with sudden pain and sometimes an audible 'snap'. Afterwards there is swelling and more pain, together with some degree of dysfunction. Sometimes there is nocturnal pain; if this is the case, haemarthrosis should be strongly suspected. If the patient has immediate inability to stand on the affected leg, a fracture should be considered.

Tendons

Peroneal

Combined plantiflexionl inversion Resisted eversion

Extensor digitorum longus

Passive plantiflexion Resisted dorsiflexion of foot and toes

History.

This should include the normal examination for the ankle and foot. In ankle sprains of short duration, the clinical examination serves a double purpose: it detects serious lesions and localizes the exact site of the sprain: Clinical exam ination.

•

To detect serious lesions in recent ankle sprains, some 'warning signs' are built into the history and the clinical tests. These make it possible to identify cases of sprained ankle that have a high risk of complications: avulsion fractures, malleolar fractures, fractures of the fifth metatarsal base, haemarthrosis and total ruptures of the lateral ligaments. Warning Serious compl ications of ankle spra i n should be suspected if one or more of the following symptoms and signs is present: Wa r n i ng signs in the h i story are:

• Aged over 60 years (risk of fractures) • I m mediate and conti nuous i n a b i l ity to bear weight (fracture)

• Nocturnal pain d u r i n g the first 48 h o u rs (haemarthrosis) Wa rning signs i n the exa m i nation are:

• Capsu l a r pattern at the a n k l e j o i nt or subta l a r j o i nt (haemarth rosis/su bcho n d ra l lesion)

• G ross pain during va lgus (compression of a fractured fibular m a l l eol us)

• Pa i n and wea kness d u r i n g resisted exte nsion (fracture of the fifth metata rsal basis)

• Loca l i zed tenderness over the tip of either mal leolus (fractured mal leol us)

• Little pain during passive movement of the foot (eventua l ly in combination with a larger range of

movement) is suggestive of a total l igamentous rupture .1 3-7S

Positive tests

The site of the lesion can be deduced from the pattern that emerges when passive and resisted movements are tested. Once the site of the sprain has been identified by clinical examination, tenderness of the appropriate structures can be sought. It is important to make the diagnosis purely by inference from the study of the clinical tests and not by palpation. In recent cases, oedema and generalized tenderness are often so gross that palpation does not yield reliable information. The patterns of acute ligamentous and tendinous dis­ orders are given in Table 84.5. In combined lesions (two or more ligaments, or a ligament and a tendon) the clini­ cal examination may be more puzzling. The information that emerges during the standard examination is summa­ rized in Table 84.6.

•

investigations: rad iography. Radiography is widely used in the assessment of inversion ankle injuries and accounts for about 10% of all radiographic examina­ tions performed in accident departments. 76 Several authors have shown that the predictive value of a plain radiograph examination in relation to fractures is rather poor when clinical warning signs are absent.77-79 A routine radiograph of the ankle is only necessary in those cases where a fracture is suspected. It is of no value in the diagnosis of a total ligamentous rupture or a haemarthrosis. In order to diagnose a complete rupture, other radio­ logical procedures have been suggested: stress radio­ graphy (evaluation of talar tilt), arth rography and tenography. The accuracy and the prognostic value of these tests however have been seriously questioned: Technical

•

Stress radiography: talar tilt (the angle between the inferior border of the tibia and the superior edge of

1 220 SECTION FOURTEEN - T H E LOWER LEG, ANKLE A N D FOOT

Table 84.6 Summary of the diagnosis of recent inversion sprains

•

•

Positive test

Lesion

Warning sign

Tiptoe rising

Peroneal tendons

Not possible: fractures of malleolus or 5th metatarsal

Plantifiexion Dorsifiexion

Anterior talofibular/calcaneocuboid ligament

A capsular pattern: haemarthrosis in the ankle

Varus Valgus Mortice

Calcaneofibular ligament

Excessive movement: total rupture Lateral pain: lateral avulsion fracture of the fibula Medial pain: medial compression fracture

Plantifiexion/inversion Plantiflexion/eversion

All lateral ligaments and peroneal tendons

Excessive movement: total rupture Lateral pain: lateral avulsion fracture of the fibula

Plantiflexion Dorsiflexion Pronation

Calcaneocuboid ligament

Supination Abduction

Calcaneocuboid ligament

Adduction

Calcaneocuboid ligament

Resisted plantifiexion

Peroneal tendons

Resisted dorsifiexion Resisted inversion

Tendons of extensor digitorum longus

Resisted eversion

Peroneal tendons

the talus, du ring varus stress) depends not only on the degree of ligamentous rupture but also on the use of anaesthesia,so the degree of applied force and the direction of the X-ray beam. The sensitivity and selectivity of stress pictures are seriously questioned.s1,82 Arthrography: this can show some leakage of the contrast medium to the surrounding tissues, supporting a rupture of the capsuloligamentous compartment. S3 However, this is likely to happen in almost every sprained ankle and the amount of leakage will not always be consistent with the degree of rupture or with the probability of complications. Nilsson84 arthrographed all patients in his study and gave them the same treatment - early mobilization no matter what the extent of the lesion. There was no correlation between the extent of ligament injury evaluated arthrographically and the end result. This supports the poor prognostic value of arthrography in recent ankle sprains. Furthermore, it is an expensive and invasive examination, not without risks. Tenography: recently, stress pictures after injection of contrast into the synovial sheath of the peroneal tendons has been suggested as a good method of testing for ruptures of the calcaneofibular ligament. S5,86 If contrast medium leaks from the tendon sheath into the joint, this implies rupture of the calcaneofibular ligament. The same remarks as for arthrography apply to this use of tenography.

In our opinion, plain radiographs are advised only if the signs warrant them. Stress radiography, arthrography

Weakness: avulsion fracture of 5th metatarsal

and tenography should not be performed, because their diagnostic and prognostic value is poor. Furthermore, because the majority of severe (grade III) ankle sprains may be treated non-operatively and, if resi dual instability occurs, late reconstruction achieves satisfactory results,87 early detection of severe grade III lesions by means of expensive and potentially dangerous investigations is obsolete. Chronic stage H i story. The patient describes a previous ankle sprain from which nearly complete recovery has been made, probably after some weeks of immobilization. The foot is functionally adequate for ordinary purposes but is apt to swell and ache after vigorous or prolonged use. The patient is fit to walk and even to run although playing football is painful, especially at the beginning of and after the game. This history might indicate that scars have formed abnormal attachments as the result of healing in the absence of enough movement. Another possibility is that the ligamentous sprain has recovered but a chronic tendinitis remains. Additionally, apart from adhesions and tendinitis, persistent trouble after a previous ankle sprain may also be caused by instability, immobiliza­ tional stiffness or a loose body in the ankle joint.

Clinical examination (see Table 84.4)

These can form at the talofibular and the cal­ caneocuboid ligament. In both instances, there is pain at

Adhesions.

CHAPTER 84

the outer side of the ankle on f u l l inversion and plarttiflexion. Pain during supination at the mid-tarsal joint implicates the calcaneocuboid ligament. Slight limi­ tation of movement can occur and the end-feel is harder than on the unaffected side. There is no pain when resisted movements are tested. Persistent tendi nitis. Here passive plantiflexion-inver­ sion movement is also painful but the end-feel is normal. Pain during resisted eversion suggests that the peroneal tendons are at fault. Painful resisted dorsiflexion of foot and toes is caused by inflammation of the extensor digitorum longus tendons. Other sources of persistent ankle trouble. These include instability, traumatic arthritis, immobilizational stiffness and impaction of a loose body; they are disclosed during the clinical examina tion. Immobilizational stiffness, traumatic arthritis (p. 1212) and loose body (p. 1214) have been discussed earlier. Instability at the ankle, because of a persisten t rupture of the tibiofibular and talofibular ligaments or delayed contraction of peroneal muscles, is discussed later.

TREATMENT Nowadays it is generally accepted that ' functional treat­ ment' with early mobilization and weight bearing and neuromuscular training exercises is the treatment of choice in grade I and grade II sprains.88-90 This approach achieves much better results than treatment with plaster immobilization.91 -97 Early surgery may claim equally good results in the short term but long-term studies clearly demonstrated much better results when early mobilization was used.82,98,99 Other prospective and randomized studies also showed the best results with early functional treatment.100- 1 02 Treatment for grade III injuries remains more contro­ versial but recent research indicates that even for total ruptures of the lateral ligaments of the ankle the treat­ ment of choice is still functional rehabilitation. Several prospective studies103,J04 and a meta-analysislOS showed that early functional treatment provided the fastest recovery of ankle mobility, with earliest return to work and physical activity, without affecting late mechanical stability. A prospective and randomized study on 85 patients with acute grade II or grade III lateral l igament ruptures, concluded that functional treatment was free from complication, resulted in shorter sick leave and facilitated an earlier return to sports than did surgery. 106 Furthermore, secondary surgical repair, even years after an injury, has results comparable to those of primary repair107, 108 so even competitive athletes can receive initial conservative treatment.1°9

-

DISORDERS OF T H E ANKLE A N D SU BTALAR J O I NTS 1 22 1

Early mobilization

In the management of ruptures at the ankle, most physi­ cians and surgeons reason anatomical ly: a ru pture is sus­ pected or established radiologically and their approach is to repair the defect as soon as possible, by partial or total immobilization or by early suture. Their philoso­ phy of treatment in ligamentous sprains is the same as in fractures: immobilize the two separated ends to build a strong scar. This anatomical way of thinking does not correspond to the functional reality. The function of a lig­ ament is in no way comparable with the function of a bone. Bone must be strong and have solidity. In contrast, the function of ligaments is mobili ty. Ligaments must allow movement and conduct movement between certain limits. To serve that purpose, ligamentous tissue must be mobile enough to change its position continu­ ously during the imposed movement. Therefore the scar must be not only strong enough to prevent excessive instability but also mobile enough to allow sufficient movement. If this is not the case, and if abnormal attach­ ments have formed between scar and bone, continuing functional problems may result. Furthermore, immobi­ lization reduces p roprioception and increases the peroneal reaction time, thus increasing the chance of functional instability. Thus early mobilization of the healing ligament is important for full recovery. However, in advocating this, we encounter one main difficulty: in a serious ankle sprain, the intensity of the inflamma tory response leads to secondary effects that impair mobility. The slightest movement causes pain, which forces the patient to immobilize joint and ligaments. The regener­ ating fibrils, however, rapidly spread in all directions, leading to disorganized scar tissue structure and to the possibility of adhesion formation, which is a sufficient reason to start the mobilization at the earliest possible moment. The problem can be solved in two ways: •

•

Abolish the inflammation and pain as soon as possible, so that the patient can start mobilizing exercises (passive or active). This can be done by a local infiltration of triamcinolone into the sprained structures. A small amount of steroid suffices, without danger of causing permanent weakness of the ligament. Move the ligament over the (stationary) joint: Cyriax used to say: 'If the joint cannot be moved in relation to the ligament, since pain and inflammation force the joint in muscle spasm, it will probably be possible to move the ligament in relation to the joint'. The relative move­ ment is the same, as is the mechanical stimulus to the regenerating fibrils. This can be achieved by gentle passive movements at the developing scar. This is the reasoning behind deep transverse friction applied to the sprained ankle. no

1 222 SECTION FOURT E E N - T H E LOWER LEG, ANKLE A N D FOOT

Table 84.6 Patterns of ligamentous and tendinous lesions in chronic inversion sprains Findings Lesions of the:

Talofibular ligament

Passive plantiflexion-in version: painful, slightly limited, tight end-feel Midtarsal tests: negative Resisted movements: negative

Calcaneocuboid ligament

Passive plantiflexion-inversion: painful, slightly limited, tight end-feel Passive midtarsal supination: painful Resisted movements: negative

Calcaneofibular ligament

Passive varus: painful

Peroneal tendon

Passive plantiflexion-inversion: painful Midtarsal tests: negative Resisted eversion: positive

Extensor digitorum tendon

Passive plantiflexion-(inversion): painful Midtarsal tests: negative Resisted dorsiflexion: positive

Differential diagnosis:

Immobilizational stiffness

Equal limitation of varus/valgus Rest of clinical examination: normal

Loose body

'Twinges' Clinical examination; negative

Instability

Clinical examination: negative Specific tests: positive

Subacute posttraumatic arthritis

Capsular pattern at the subtalar jOint and spasm of the peronei

Treatment procedures

If the patient refuses infiltration or is seen too late after the injury (after a couple of days), deep transverse massage is applied. First some effleurage is given, to diminish the oedema and to render the lesion more accessible to the fingertips. Then very gentle massage is applied for 10-1 5 minutes. The intention is merely to anaesthetize the injured liga­ ment so that the patient can bear the 30 seconds of harder friction. The massage will not be vigorous, only deep enough to move the ligament on the subjacent bone and give it the necessary stimulus for correct healing. The patient should be treated daily for 10 days to 2 weeks. Between sessions walking for short distances must be attempted. It is important to give instructions on how to walk slowly, with a heel-and-toe gait, without limp.

The treatment chosen depends on the stage of the lesion (Box 84.2). Immediate infiltration with a small dose of triamcinolone at the exact point is indi­ cated. The sooner after the injury the infiltration is made, the more spectacular the results. Because it is not easy to palpate a recently sprained ankle, the exact site of the lesion must be determined by an accurate functional examination. To facilitate the injection, most of the oedema must be removed by deep effleurage, before the needle is introduced. Because of the anti-inflammatory reaction of the steroid, the resolution of swelling and posttraumatic inflammation is hastened. The pain abates quickly and gradual functional improvement can be expected from the second day after the injection. Sometimes simple strapping in sligh t valgus is applied, which can give the patient confidence. It is also possible that the tape brings on a 'musculocutaneous reflex', whereby proprioception of the ankle is activated and so prevents an early recurrence of the sprain.90, 111 Strapping must be loose enough to enable the patient to walk and to move the ankle as much as possible.

Acute stage: first 2 d a ys.

Subacute stage. Infiltration with steroid suspension is of no use after 2 days have elapsed since the injury. Massage is the treatment of choice. It moves the ligament over the joint and the bone, in imitation of its normal behaviour, and gives a mechanical stimulus to the ingrowing fibrils, which prevents their adhesion to the surrounding tissues. Once again effleurage is applied first, in order to reduce the oedema. Gentle massage causes some local anaesthesia, after which a few minutes of firmer friction,

C HAPTER 84

-

DISORDERS OF T H E A N K LE A N D S U BTALAR J O I NTS 1 223

Bo� 84.2 Treatment of acute and chronic ankle sprain Uncomplicated lig a mentous l e si ons Acute lesion

« 48 h)

E ither:

I nfi ltration with

10

mg triamcinolone

Figu re-of-e i g ht bandage Followed by mobil ization a n d 'functional treatment' Or:

Deep transverse massage, daily for

30 seconds, after prepa rative

'effleurage', u nti l the

a n k l e is in the s u bacute stage Figu re-of-eight bandage Fu nctional treatment S u bacui:e lesion

Deep transverse massage, d a i ly for a few m i n utes, fol lowed by gentle passive movements Fu nctional treatment

Chronic lesion

(>6 weeks)

Deep tra n sverse massage as preparation for: m a n i p u lation in the l i m ited d i rection Fu ncti onal treatment

Tendinous lesions

Deep transverse massage Relative rest

applied deeply to the actual site of the ligamentous tear is used. After the friction, gentle passive movement is per­ formed to the limit of the possible range, which is the range of discomfort but not of pain. Therefore it is impor­ tant to perform the movement firmly but gently and prevent an excessive range by observing the patient's reactions. Unless the therapist is needlessly rough, there is no danger of overstretching the sprained ligaments. Active movements follow passive ones. The patient must be persuaded to execute them repeatedly during the day. Active movements are very u seful, because they further the effect of deep friction in preventing scar tissue forming abnormal adhesions. The main difficulty is to get the patient to understand how much greater the painless range is than believed. Chronic stage. Scars have been allowed to form abnor­ mal attachments as the result of healing in the absence of sufficient movement. The foot functions well enough for ordinary purposes but it aches and swells after prolonged or strenuous use. The only logical and effective treatment is to break the adhesions by manipulation. This is quite easy to perform and, apart from some deep friction, it does not need anaesthesia. One manipulation session often suffices to cure chronic adhesions that have caused continuous disability for months. After the manipulation there is no pain and after-treatment is not required. Before the decision to manipulate is made, the diag­ nosis must be certain. It is obvious that an inversion sprain which has resulted in peroneal tendinitis will not benefit from manipulation of the j oint. The distinction between tendinitis and chronic adhesions is made by the end-feel during passive inversion and the negative

findings during resisted eversion. Another di fferential diagnosis is 'subacute traumatic arthritis' at the sub­ talar joint. Because this condition can also be the result of a previous ankle sprain, it can very easily be mistaken for posttraumatic adhesions. In subacute traumatic arthritis there is also some limitation of movement in the calcaneocuboid joint, which is caused by spasm of the peronei. In chronic ligamentous adhesions, however, the movement at the talocalcaneal joint is normal and the end-feel is not spastic but rigid. It is clear that the arthritis will be aggravated if manipula­ tion is undertaken. Early mobilization is not used if a tendon is affected . In all stages, the treatment consists of deep transverse friction. The patient should also avoid any exertion that causes pain. Usually the lesion is too diffuse for injection of steroid but, if a small stretch of tendon remains refractory to friction, infiltration with triamcinolone suspension can be given.

Ten di n o u s lesions.

Treatment techniques Technique: infiltration of the fibular extent of the

The injection technique is the same for both ligaments. The patient lies supine on a couch, with the lower limb in internal rotation to bring the lateral malleolus upper­ most. The foot must be held in as much planti.flexion and inversion as possible to make the lateral side accessible by the needle. After removing most of the oedema, tenderness is palpated along the inferior border of the malleolus and a line is defined from end to end. A 2 mJ syringe is filled with triamcinolone, mixed with some local anaesthetic. A thin needle, 3 cm long, is fitted and inserted at a point 2 cm talofibular and calcaneofibular ligament.

1 224 SECTION FOURTEEN - T H E LOWER LEG, AN KLE AND FOOT

distal from the edge of the fibula. The needle is now moved almost parallel to the ligament, in the direction of the fibular edge (Fig. 84.21 ). A series of small droplets is in­ jected from end to end at the ligamentoperiosteal insertion. It is vital to infiltrate the whole tender area and to inject only when the needle touches bone. The injection is only half as painful as the previous examination and pal­ pation but some after-pain may occur for 1 or 2 days. From the next d ay onwards, the patient should use the foot and must be encouraged to walk with a proper heel­ and-toe gait, without limping. Technique: infiltration of the calcaneocuboid ligament.

The patient adopts a supine-lying position with the limb in internal rotation. This brings the outer side of the foot uppermost. With one hand the forefoot is supinated and adducted to bring the ligament under some tension. Tenderness along the ligament is sought in the following manner. The therapist places the interphalangeal joint of the thumb on the base of the fifth metacarpal bone and aims in the direction of the midpoint between the two malleoli. The tip of the thumb now lies exactly on the lateral calcaneo­ cuboid li gament (Fig. 84.22a). The line of tenderness along the ligament is marked from end to end. A 2 ml syringe is filled with steroid suspension and fitted to a fine needle, 2 cm long. The needle is thrust in at the lateral border of the ligament (Fig. 84.22b). It is first moved to the calcaneal extent, where a series of droplets is placed along the ligamentoperiosteal border. The infiltration is made when the needle touches bone. Once the calcaneal border has been infiltrated, the needle is withdrawn slightly and pushed on to the cuboid border where the same procedure is repeated.

Figure 84.21

Infiltration of the fibular extent of the talofibular ligament.

Technique: deep friction to the fibular extent of the

The patient lies supine, with the leg outstretched and in medial rotation so that the outer border of the foot faces upwards. The therapist sits at the medi al side of the foot. With the contralateral hand the patient' s foot is held in plantiflexion and inversion. This position stretches the ligaments as far as is comfortably possible. In recent sprains, some effleurage is given first, so as to move most of the oedema and to define bony landmarks and tender­ ness more easily. The index finger of the ipsilateral hand, reinforced by the m iddle finger, is now placed on the site of the lesion. talofibular ligament.

(b)

Figure 84.22 Calcaneocuboid ligament: (a) palpation technique; (b) infiltration.

CHAPTER 84 - D ISORDERS OF TH E A N K LE A N D SU BTALAR J O I NTS 1 225

To reach the exact localization under the fibula, the foreaTm must be pronated, so the pressure will be upwards and inwards and the ligament is pressed between finger and bone. The thumb is placed proximal to the medial malleolus to give counterpressure during the massage (Fig. 84.23). The friction is imparted by drawing the fingers for­ wards during an adduction movement of the shoulder. The pressure is then slightly released and the finger turned to the previous position, where the whole proce­ dure is repeated. In recent sprains, the massage is given very gently, only deep enough to move the ligament on the subjacent bone. There should be only gentle and slight pressure for 15 minutes, after which some anaesthesia will occur; another 30 seconds of proper massage can then follow. More thorough friction must be applied in the subacute stage. In chronic stages, strong and vigorous friction is given to break some adhesions and to anaesthetize the ligament for the subsequent manipulation. Technique: deep friction to the talar extent of the

The position of the patient's foot is the same as in the previous technique. The therapist uses the contralateral hand to force the foot slightly into plantiflexion and inversion to stretch the ligament. The neck of the talus is sought, and the talar insertion of the ligament identified. The tip of the index finger of the other hand, reinforced by the middle finger, is placed on the talar extent (Fig. 84.24). The pressure is directed purely medially to the bone, so the forearm is not pronated . The friction is given by drawing the hand to talofibular ligament.

Figure 84.24

Friction to the talar extent of the talofibular ligament.

and fro over the ligament. The thumb placed at the medial side of the foot acts as a fulcrum. The sweep will not be as large as in the previous technique because the talar extent of the ligament is much less. In recent sprains, the massage is gentle, whereas in chronic cases, strong friction must be given in order to anaesthetize the ligament for the subsequent manipulation. Technique: deep friction to the fibular extent of the

The patient lies supine. The therapist sits at the distal end of the foot and with the ipsilateral hand fixes the heel in varus position. The index finger of the contralateral hand, reinforced by the middle finger, is placed under the fibular tip. The thumb is held at the medial malleolus so as to give counterpressure (Fig. 84.25). The friction is imparted by a flexion-exten­ sion movement at the wrist. calcaneofibular ligament.

Technique: deep friction to the calcaneocuboid ligament.

Figure 84.23 Deep friction of the fibular extent of the talofibular ligament.

The patient lies face upwards, with the lower limb extended and in medial rotati on. In this positi on, the outer border of the foot faces upwards. The ligament is palpated by using the technique explained above (Fig. 84.22a). To check the right position, the patient is asked to contract the peroneal tendons, which should lie just plantar to the fingertip. The therapist sits at the inner side of tlle foot, facing its medial aspect. The foot is steadied with the contralateral hand, which forces the forefoot into adduction and supination. This brings the calcaneocuboid joint to prominence and stretches the ligament. The index finger of the other hand, reinforced by the middle finger, is placed on the joint line at the tender point (Fig. 84.26). Friction is given by a vertical movement of the finger, imparted by an adduction movement of the whole arm.

1 226 SECTION FOURTE E N - T H E LOWER LEG, ANKLE A N D FOOT

Figure 84.25

Friction to the fibular extent of the calcaneofibular ligament.

This moves the finger along the joint line and across the tender ligament in a transverse direction to the fibres. In recent sprains, the friction is not vigorous. The intention is merely to anaesthetize the tender area by 10 minutes of gentle massage, just deep enough to move the liga­ ment slightly on the bone. This is followed by 30 seconds of more thorough friction. In subacute treat­ ment sessions the friction may be more vigorous and in chronic cases the intention is to rub really hard, but still within the limits of comfort, as a preparation for manipul ation . Technique: manipulation of adherent lateral ligaments.

The technique is the same for both the anterior fasciculus of the fibular collateral ligament and the calcaneocuboid ligament. The intention is to rupture the adhesions at the ankle joint and the calcaneocuboid joint. Before the manipulation, vigorous friction must be given at the exact point for 1 5 minutes so as to decentralize the ligament. The patient lies supine on a high couch, the leg extended. The manipulator stands at the patient's foot, facing it, grasps the heel with the ipsilateral hand and by an abduction movement of the arm forces it into full varus. The dorsum of this hand will remain on the couch during the whole procedure. The contralateral hand is now placed on the dorsum of the foot, whereby the fingers curl round the shaft of the first metatarsal bone and the heel of the hand rests on the lateral border of the foot (Fig. 84.27). The hand must do three things at the same time: plantiflex, medially rotate and adduct the foot. These three movements must be performed simultaneously,

Figure 84.26

Friction to the calcaneocuboid ligament.

quickly and with a small amplitude at the end of range. Although the movement must be strong enough to break the adhesions, the physiological range must be respected. The manipulating hand must be ' motor and sensor' at the same time and the end-feel is the guide to manipulation, informing the manipulator whether it should be continued or not. In order to carry out this triple movement perfectly, the manipulator abducts the arm and flexes the elbow to a right angle, the hand flat on the patient's foot: • • •

The hand presses the foot downwards to the floor, which evokes plantiflexion. If the manipulator exerts a greater pressure at the outer border of the foot, it is forced into inversion. An adduction movement in the foot is now obtained, when the heel of the manipulating hand is brought inwards, pivoting around the fingers at the inner side of the forefoot.

During the whole movement the elbow is pressed downwards and towards the manipulator. Therefore, unless the manipulator holds the elbow well away from the body before the whole procedure starts, little force can be exerted in the final movement. The manipulation does not have a large amplitude. The downwards, inwards and rotational movement is per­ formed slowly, until the characteristic resistance of the adherent ligament becomes perceptible. Here a final, quick and strong thrust is given by an adduction move­ ment at the shoulder, in order to restore the 1 or 2° of impaired movement.

CHAPTER 84

There are a number of contraindications to manipula­ tior( (see Box 84.3).

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DISORDERS OF THE ANKLE A N D SU BTALAR J O I NTS 1 227

Box 84.3 Contraind ications to manipulation • •

RECURRENT VARUS SPRAIN - INSTABILITY The patient states that after a previous varus sprain, the ankle turns over easily and there is fear of the ankle ' giving way'. It lacks stability and is subjected to a succession of minor sprains. This is apt to happen more frequently in athletes, who make heavy demands on the joint. Instability at the ankle, resulting in repeated minor sprains, may have different causes (Fig. 84.28):

(a)

Figure 84.27

No l i m itation of movement and a normal end-feel. If inversion sprain has resulted in peroneal tendin itis, no advanta g e accrues from man i pu lation; the only suitable treatment is deep transverse friction to the peroneal tendons.

• •

It is obvious that forced movements are not suited to recent sprains. If laxity of the j oint rather thatn adhesions causes a permanent or recurrent problem at the ankle, manipu lation will of course not be the treatment of choice.

•

Posttraumatic arthritis which occurs occasionally after a n ankle sprain: the differential d i a g nosis is made by the detection of a capsular pattern, tog ether with peroneal spasm.

(b)

Manipulation of adherent lateral ligaments: start of manipulation (left) and end of manipulation (right).

1 228 S ECTIO N FOURTE E N - T H E LOWER LEG, ANKLE A N D FOOT

The diagnosis can be confirmed by radiography. If the radiograph is taken during strong varus movement, widening of the joint space between the tibia and fibula is seen. These must always be tried first, before the patient is referred for surgery. Sometimes excellent results can be obtained. The injections are given at weekly intervals over 3 weeks. The patient must take relative rest over another 4 weeks, to allow the injected ligaments to sclerose. To make the injection easier, it is as well to measure on an anteroposterior radiograph the distances between the tip of the lateral malleolus and the articular surface of the tibia, together with the respective widths of tibia and fibula (Fig. 84.29). The ligament must be infiltrated from behind and from in front, each time with 1 .5 ml of the sclerosant mixed with 0.5 ml of lidocaine (lignocaine) 2%. A thin needle, 4 cm long, is used.

Treatment: sclerosing i njections.

2

3

Figure 84.28 Causes of instability at the ankle: 1 , lengthened or ruptured distal tibiofibular ligament; 2, lengthened or ruptured anterior talofibular ligament; 3, proprioceptive defects affecting the peroneal muscles.

• •

•

A ru ptured distal tibiofibular ligament, with a so-called unstable mortice. A permanent lengthening of the anterior talofibular ligament, with an anteroposterior instability of the ankle joint. Proprioceptive deficits secondary to neurological injury to ankle ligaments and capsule. As a result, the peroneal muscles are brought into play too slowly to prevent further sprains when the ankle starts turning over.1 2, 13

Technique: infiltration from behind. The patient lies prone; the lines indicating the inferior border of the tibia and the joint line between tibia and fibula are drawn at right angles. The needle is thrust in vertically down­ wards, a few millimetres above the intersection of these two lines. Tough ligament must be felt to be penetrated before hitting bone. This happens at about 3 cm depth. If the needle immediately hits bone, its point is too far to one or the other side of the joint: the needle is withdrawn somewhat and reinserted in a slightly different direction until it first traverses the ligament and then hits bone. A

The unstable mortice

The common complaint is an ' unstable ankle' after a pre­ vious sprain. The patient finds that the foot turns over easily, often with an audible click and momentary severe pain in the ankle. The pain does not last very long and, after a few moments, walking can continue. The ankle merely feels sore for a couple of days. 114 Clinical examination reveals nothing except a positive test for the mortice, which is included in the standard clinical examination of the ankle. This is a strong a quick varus movement at the ankle, with the joint in the neutral position. If there is rupture or elongation at the distal tibiofibular ligament, an excessive range of varus move­ ment can be demonstrated. A click can be produced at the ankle when the force is released and the two bones meet again. If this varus movement is repeated with the examiner's fingers palpating the two malleoli, they can be felt to move apart.

1

Figure 84.29 Landmarks and measurements on a plain frontal radiograph taken preparatory to sclerosing injections for an unstable mortice.

CHAPTER 84

series of intraligamentous infiltrations along the vertical line'of the ligament follows. Technique: infiltration from in front. The patient lies supine. The two lines are drawn again, to cross each other anteriorly. The injection is now repeated from in front. Here the tendons of the extensor digitorum longus must be held apart before the needle is inserted. Again, one must pierce ligament first before hitting bone.

Ligamentous insufficiency of the an terior talofibular ligament

The patient has a history of previous ankle sprain, from which recovery is largely complete. There remains, however, some fear of the ankle 'giving way' and the patient is unable to rely on using the foot. Routine clinical examination shows nothing, except probably a greater range of inversion movement. The anterior drawer test can be used to demonstrate a rupture or elongation of the anterior talofibular I igament. ll5

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DISORDERS OF T H E ANKLE A N D SU BTALAR J O I NTS 1 229

Diagnostic technique: anterior drawer test. 1 1 6- 1 18

The ankle is held in slight plantiflexion. The examiner stands at the opposite side and stabilizes the lower leg with h is ipsilateral hand. The contralateral hand encircles the foot and displaces the foot forwards. The lateral margin of the trochlea tali is thus shifted forwards in relation to the lateral malleolus (Fig. 84.30). It is important to notice that there is not only a forward gliding but also a medial rotation of the talus around a vertical axis at the medial malleolus. Because the anterior talofibular ligament is tense in all plantiflexion positions of the ankle, this anterior move­ ment will only be possible jf the ligament is not intact. The movement of the talus can be seen and be felt. Often a depression between talus and malleolus is noticed when the talus is moved forwards (Fig. 84.3 1 ) . If a posi­ tive anterior drawer sign is present in a patient with recurrent ankle sprains or the patient fears the ankle 'giving away', a lax anterior talofibular ligament must be blamed for the symptoms. ll9 However, the reverse does not hold, because only half of the patients with a positive anterior d rawer sign

Anterior

Medial

Posterior Figure 84.30 Anterior drawer test for ligamentous insufficiency of the anterior talofibular ligament.

1 230 SECTION F O U RTEEN - T H E LOWER LEG, ANKLE A N D FOOT

Figure 84.31 Positive anterior drawer test demonstrating ligamentous insufficiency of the anterior talofibular ligament.

report symptoms of ankle instability. The reason for this is probably compensation of the ligamentous laxity by mu scle power and a good proprioceptive reflex. 11 6 Therefore an anterior d rawer test is never performed during the standard examination but only when the history wa rrants it. The conservative treatment of this form of instability consists of proprioceptive training, so that a good reflex will replace the function of the insufficient ligament. Mechanical devices designed to prevent ankle sprain during high-risk sporting activities (e.g. soccer, basketbal l) are: wrapping the ankle with tape or cloth, orthoses, high-top shoes, some combination of these methods. Appropriately applied braces, tape or orthoses should not adversely affect performance.120-122 If necessary, surgical repair of the torn ligaments may be advised. 123, 1 24 The results of late surgical repair are goOd .125, 1 26

end of the block from touching the floor. The next step in regaining proprioception is training on a 'wobble board', first in a standing position, later with tiptoeing, jumping or with some weights added to the wobble board.136 A recurrent varus sprain can also result from neuro­ logical weakness of the peroneal muscles, which are not strong enough to prevent inwards rotation of the ankle. It must be remembered that the first complication of an upper motor neurone lesion is very often a recurrent varus sprain at the ankle. Another condition leading to recu rrent ankle sprains on a basis of weak peroneal muscles is sciatica with a fifth lumbar root pal sy. Patients with a palsy of the fifth root should therefore be warned to protect the ankle until the palsy has recovered. The best way to do this is to wear a floated heel at the outer border of the shoe. Many running shoes designed for athletes have a built-in floated heel that prevents an inversion movement at the heel. It is a remarkable fact, however, that in some condi­ tions in which there is serious weakness of the peroneal muscle, as in peroneal atrophy, the ankle will very rarely be repeatedly sprained.

Treatment.

Functional instability

Cyriax127 first introduced the concept of functional insta­ bility in 1 954 and experimental support was provided by Freeman in 1 965.128 , ] 29 This concept views instability after an ankle sprain as being merely the result of a failure of active protection by the muscles of leg and ankle, rather than the result of rupture or elongation of the lateral ligamentsPO,131 The sprain causes neurological damage at ligaments and capsule, which results in a prolonged propriosensory reflex. The increase in the peroneal reaction time is then responsible for inadequate protection against further sprain0J32, 133 However, arthromuscular reflex can be trained by movement and by coordination exercises on a ' wobble board'.134,135 The re-education process is started on a see-saw block or a tilting board cu rved in one plane. While maintaining equilibrium on one leg, the patient tries to prevent either

Differential diagnosis of instability

Recurrent ankle sprains and fear of the ankle 'giving way' must be distinguished from a number of other disorders at the outer side of ankle and foot which give rise to sudden pain, clicks and twinges. •

•

If there is a history of previous sprain, apart from a chronic peroneal tendinitis, the differential diagnosis is a chronic ligamentous adhesion (see Table 84.7). If there is no clear history of previous ankle sprains, instability must be differentiated from loose bodies in the ankle and subtalar joints, 'snapping peroneal tendon', chronic peroneal tendinitis and jumper 's sprain.

EVERSION SPRAIN An eversion sprain at the ankle is rare. When this condi­ tion is encountered, the foot should always be examined in an endeavour to discover why the sprain has occurred.

MECHANISM The deltoid ligament is strong. The position of the ankle and foot is such that excessive eversion movement does not take place unless the patient already stands with a valgus deformity at the heel. Alternatively, a st;ong valgus movement can produce bone damage rather than a ligamentous lesion. The deltoid ligament is so strong

CHAPTER 84 - DISORDERS OF T H E A N K LE A N D SU BTALAR J O I NTS 1 23 1

Table 84.7 Differential diagnosis and treatment of recurrent disability a t the outer side o f the foot Instability

Chronic adhesions

History

Ankle turns over easily and is subjected to a succession of minor sprains, with disability for some days Fear of the ankle 'giving way'

Foot is adequate for ordinary purposes but tends to swell and ache after vigorous or prolonged use No sudden aggravation or twinges

Examination

Between the attacks 1 Anterior talofibular ligament: Normal routine examination Sometimes excessive range of inversion End-feel normal or 'empty' Positive anterior drawer test 2 Unstable mortice: Reproduction of click and pain during strong varus movement at ankle Radiography shows increased distance between the two malleoli during forced varus 3 Defective propriosensory reflex: Normal clinical examination L5 palsy or upper motor neurone lesion Weak peroneal muscles

Treatment

1 &3 2

3

Wobble board training, floated heel, taping or surgery Sclerosing injections into the distal tibiofibular ligament over 3 consecutive weeks, or surgery Floated heel

that eversion injury tends to cause avulsion of the tibial malleolus rather than tearing of the ligament.

DIAGNOSIS The anterior fasciculi of the deltoid ligament are stretched during a combined plantiflexion-eversion movement. Palpation reveals the localization of the lesion, which invariably lies at the ligamentoperiosteal junction along the inferior border of the medial malleo­ lus. Simu ltaneous posterior tibial tendinitis often occurs with a sprain of the deltoid ligament. If this is the case, resisted inversion is also painful. An avulsion frac­ ture should be suspected when a strong varus move­ ment also causes significant pain at the inner side of the ankle.

TREATMENT Sprains of the anterior and middle fasciculi of the deltoid ligament are likely to continue causing pain for many months, or even years. The reason is that the patient, who stands with the heel in valgus deformity, overstretches

2

Adhesions of talofibular and calcaneocuboid ligaments: Pain at outer side of ankle and foot during full inversion and plantiflexion Slight limitation End-feel more tense than on the opposite side Resisted movements are negative Chronic tendinitis of peroneal muscles: Passive inversion during plantiflexion hurts at outer side of ankle and foot End-feel normal Pain during resisted eversion

Adhesions rupture by manipulating the ankle and foot after vigorous deep trans­ verse friction at the exact location 2 Deep transverse friction 3 times a week, for 2-4 weeks The patient should not use the foot more than strictly necessary until cure is complete

the damaged tibionavicular or tibiocalcaneal ligament each time the foot is put on the ground. Because each step causes a renewed strain, the fascicular tear never has a chance to heal. The 'chronic' lesion is caused by repeated traction; consequently, the worst possible treatment is manipulation, which overstretches the inflamed liga­ ment. It is entirely wrong to compare this lesion with chronic adhesions at the lateral side of the ankle. Treatment consists initially of relief from tension. Thus, a support (1-2 cm thick) must be fitted under the heel and the inner midtarsal area. This gives the calcaneus a neutral position and prevents further tension on the liga­ ments. Although preventing the ligament from further overstretching, it does not always cure the existing inflammation. Therefore, some triamcinolone should be injected into the affected area, quickly reducing the inflammation, so leading to cure. Massage is totally ineffective in this condition. Technique: infiltration. The patient lies supine with the hip and leg rotated outwards. The foot is held in eversion and slight dorsiflexion, rendering the medial malleolus more prominent. The precise site and extent of the painful area is determined by careful palpation.

1 23 2 S ECTIO N FOURTEEN - T H E LOWER LEG, ANKLE A N D FOOT

A 2 ml syringe is filled with 20 mg of triamcinolone and fitted to a thin needle, 2.5 cm long. A point is chosen about 2 cm below the medial malleolus. The needle is inserted here and pushed upwards through the ligament until it hits bone (Fig. 84.32). By a series of partial with­ drawals and reinsertions, droplets of the suspension are injected along the affected extent of the ligamento­ osseous junction, each time with the needle making

contact with bone. Because the deltoid ligament is a thick structure, the infiltrations should be made superficially and deeply. After the injection, the ankle is likely to be sore for 24-48 hours. Meanwhile the patient should use the affected foot for weight bearing as little as possible. The differential d iagnosis of lesions at the heel and ankle is summarized in Table 84.8.

Table 84.8 Differential diagnosis of lesions at the heel and ankle

Posterior pain

Disorder

Diagnosis

Achilles tendinitis

Pain during rising on tiptoe Differentiate 4 types by palpating insertion, localizing sign and passive plantiflexion

Deep transverse friction Alternative: triamcinolone

Achilles tenovaginitis

Discrepancy between symptoms and signs Warm, swollen and tender to the touch

Medication Triamcinolone

Subachilles bursitis

Painful passive plantiflexion

Triamcinolone

Dancer's heel

Painful passive plantiflexion Some laxity of plantiflexion movement

Triamcinolone

as trigonum periostitis

Painful passive plantiflexion Limitation of plantiflexion (Painful resisted flexion of big toe)

Triamcinolone Surgery

Subcutaneous bursa

Normal examination Painful palpation

Triamcinolone Better shoes Surgery

Subcutaneous nodules

Normal examination Palpation of small, hard, tender nodules

Subcutaneous tenotomy

Plantar fasciitis

Typical history and localization Normal functional examination Painful palpation

Horizontal, raised heel Triamcinolone

Painful heel pad

Typical history Normal functional examination Painful palpation

Procaine

Sprain of posterior talofibular ligament

Passive plantiflexion and eversion hurts at the outer posterior side

Triamcinolone

Tendinitis of tibialis posterior

Painful resisted inversion and resisted plantiflexion Localization behind the medial malleolus

Deep transverse friction

Calcaneal apophysitis

Boys aged 1 2-16 years Intermittent pain Normal functional examination

Rest

Treatment

CHAPTER 84

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D I SORDERS OF T H E ANKLE A N D SU BTALAR JOI NTS 1 233

Table 84.8 Differential diagnosis of lesions at the heel and ankle (continued)

Lateral pain

Anterior pain

Medial pain

Pain in the ankle

Disorder

Diagnosis

Treatment

Peroneal tendinitis

Painful passive inversion Painful resisted eversion

Deep friction Alternative: triamcinolone

Mucocele of peroneal tendons

Painful passive inversion Painful resisted eversion Palpable, fluctuating swelling

Aspiration Triamcinolone

Snapping ankle

Same as peroneal tendinitis Palpation of moving tendon during plantiflexion-dorsiflexion

Surgery?

Jumper's sprain

Typical history Normal functional examination Additional test: valgus during dorsiflexion

Tramcinolone Prevention

Chronic adhesions of lateral ligament

History of varus sprain Painful inversion Changed end-feel

Manipulation

Sprain of posterior talofibular ligament

Passive eversion and plantiflexion cause pain at the posterolateral side

Triamcinolone

Ankle instability (lateral ligament)

History of varus sprain and fear of the ankle 'giving way' Laxity during passive inversion Positive anterior drawer sign

Wobble board training Surgery

Sprain of the anterior tibiotalar ligament

Previous plantar sprain? Painful passive plantiflexion

Deep friction

Anterior periostitis

Painful passive dorsiflexion

Triamcinolone

Tenosynovitis of the extensors of the toes

Painful passive plantiflexion Painful resisted dorsiflexion of the toes Crepitus/fluid

Deep friction Triamcinolone

Tendinitis of tibialis posterior

Painful resisted plantiflexion and resisted inversion

Triamcinolone Deep friction

Tendinitis of flexor hallucis longus

Painful resisted plantiflexion and resisted inversion Painful resisted flexion of the big toe

Triamcinolone Deep friction

Sprain of deltoid ligament

Painful passive eversion and plantiflexion

Triamcinolone and support

Unstable mortice

Pain and click during strong varus

Sclerosing injection Surgery

Psoriatic arthritis of the ankle joint

Capsular pattern Warmth Fluid

Triamcinolone

Haemarthrosis of the ankle

Trauma Nocturnal pain Capsular pattern Tender

Aspiration

Osteoarthrosis of the ankle

Capsular pattern Hard end-feel Crepitus

Arthrodesis

1 234 SECTION FOURTE E N - THE LOWER LEG, ANKLE A N D FOOT

Table 84.8 Differential diagnosis of lesions at the heel and ankle (continued)

Pain in the ankle

Disorder

Diagnosis

Treatment

Immobilizational stiffness of the ankle

After immobilization Limitation of fiexion and extension

Mobilization

Loose body in the ankle joint

Twinges (during walking downstairs) Normal clinical examination

Manipulation Root's shoe

Immobilizational stiffness of subtalar joint

Immobilization Marked limitation of varus and valgus No muscle spasm

Mobilization

Osteoarthrosis at the subtalar joint

After a fracture Limitation of varus Hard end-feel

Arthrodesis

Loose body in the subtalar joint

Twinges Fixation in valgus or full range of movement

Manipulation

Subacute traumatic subtalar arthritis

Previous sprain or foot injury Limitation of varus by muscle spasm

Triamcinolone Immobilization

Monoarticular subtalar arthritis

No injury Capsular pattern and muscle spasm Joint is warm, swollen and tender

Triamcinolone

Psychogenic pain

Fixation of the subtalar joint in varus

Figure 84.32

Infiltration of the deltoid ligament.

CHAPTER 84 - DISORDERS OF T H E ANKLE A N D SU BTALAR J O I NTS 1 23 5

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63. Stephens MM, Sammarco GJ. The stabilizing role of the lateral

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sprains. Acta Chir Scand 1964;128:483. 66. Prins JG. Diagnosis and treatment of injury to the lateral liga­ ment of the ankle. Acta Chir Scand 1978:486. 67. Fallat L, Grimm DJ, Saracco JA. Sprained ankle syndrome: prevalence and analysis of 638 acute injuries. J Foot Ankle Surg 1 998;37(4):280-285. 68. van Dijk CN, Molenaar AH, Cohen RH et al. Value of arthrog­

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ankle instability. Clin Orthop 1968;56: 1 69-178. 75. Frost HM. Does the ligament injury require surgery. Clin Orthop 1 974;103:49.

530-535. 88. Linde F, Hraas I, Jurgensen U, Madsen 1. Early mobilizing

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sies. Ned Tijdschr Geneeskd 1978;122:1612-1618. 92. Brostrom L. Sprained ankles. Treatment and prognosis

in recent ligament ruptures. Acta Chir Scand 1 966;132: 537-550. 93. Rens van THJG. Rupturen van de laterale enkelbanden; oper­

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bei der frischen aussenbandruptur des oberen sprunggelenks. Unfallchirurgie 1991 ;94:99-104.

'

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116. Brostrom L. Sprained ankles. III. Clinical observations in recent ligament ruptures. Acta Chir Scand 1 965;130:560-569. 117. Castaing J, Delplace J. Entorses de la cheville. Interet de l'etude de la stabilite dans Ie plan sagittal pour de diagnostic de gravite. Recherche radiographique du tiroir astralgien anterieur. Rev Chir Orthop 1 972;58:51-63. 1 1 8. Laurin C, Mathieu J. Sagittal mobility of the normal ankle. Clin Orthop 1975;108:534-550. 119. Karlsson J, Eriksson BI, Renstrom PA. SubtaJar ankle instabil­ ity. A review. Sports Med 1 997;24(5):337-346. 120. Robbins S, Waked E. Factors assocaited with ankle injuries. Preventive measures. Sports Med 1998;25(1):63-72. 1 2 1 . Thacker SB, Stroup DF, Branme CM et al. The prevention of ankle sprains in sports. A systematic review of the literature. Am j Sports Med 1999;27(6);753-760. 122. Quinn K, Parker P, de Bie R, Rowe B, Handoll H . Interventions for preventing ankle ligament injuries. Cochrane Database Syst Rev 2000;2:CD00001 8. 123. St Pierre R, Allman F, Bassett FH et at. A review of lateral ankle ligamentous reconstruction. Foot Ankle 1982;3:114-123. 124. Saltrick KR. Lateral ankle stabilization. Mod ified Lee and Christman-Snook. Clin Podiatr Med Surg 1991;8(3):579-600. 125. Snook GA, Christman 00, Wilson TC. Long-term results of the Christman-Snook operation for reconstruction of the lateral ligaments of the ankle. J Bone joint S u rg 1985;67A:1-7. 126. Colville MR. Surgical treatment of the unstable ankle. J Am Acad Orthop Surg 1998;6(6):368-377. 127. Cyriax JH. Textbook of Orthopaedic Medicine, vol. I. Diagnosis of Soft Tissue Lesions, 2nd edn. Cassell, London, 1954. 128. Freeman MAR. The etiology and prevention of functional instability of the foot. J Bone Joint Surg 1965;47B:678-686. 129. Freeman MAR. Instability of the foot a fter injuries to the lateral ligament of the ankle. J Bone joint Surg 1965;47B:669-677. 130. Hertel J. Functional instability following lateral ankle sprain. Sports Med 2000;29(5);361-371. 1 3 1 . Konradsen L, Olesen S, Hansen HM. Ankle sensorimotor control and eversion strength after acute ankle inversion injuries. Am J Sports Med 1998;26(1):72-77. 132. Konradsen L, Bohsen Ravn J. Ankle instability caused by prolonged peroneal reaction time. Acta Orthop Scand 1990; 61(5):388-390. 133. Konradsen L, Ravn JB. Prolonged peroneal reaction time in ankle instability. Int j Sports Med 1991;12(3):290-292. 134. Freeman MAR. Coordination exercises in the treatment of the functional instability of the foot. Physiotherapy 1965;51:393-395. 135. Tropp H. Functional instability of the ankle jOint. Thesis, University of Linkoping Medical Dissertations, Linkoping, Sweden, 1985. 136. Rozzi SL, Lephart SM, Sterner R, Kuligowski L. Balance train­ ing for persons with functionally unstable ankles. j Orthop Sports Phys Ther 1 999;29(8):478-486.

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Disorders of the midtarsal joints

CHAPTER CONTENTS

1242

The capsular pattern

Subacute arthritis in adolescence Subacute arthritis in middle age Rheumatoid arthritis

1242 1243

1243

1243 1243

Non-capsular patterns Midtarsal strain

Midtarsal ligamentous contracture Aseptic necrosis 1247 Navicular stress fracture 1247

1246

Cuboid rotation 1247 Midtarsal arthrosis 1248 Lesions of the cuneiform-first metatarsal joint Osteoarthrosis Gout 1249 Loose body

1248

1249

1248

The talonavicular and calcaneocuboid joints and the tarsometatarsal joints comprise the midtarsal joints. Functionally, they act as one structure. Movement is possi­ ble in six directions: dorsiflexion-plantiflexion, adduc­ tion-abduction, pronation-supination. It is important that the ankle and subtalar joints are stabilized when these movements are performed; this is achieved by dorsiflexion in the ankle joint and strong valgus pressure at the heel. Because of the obliquity of the joint surfaces and the greater mobility of the talonavicular joint, dorsiflexion is usually accompanied by some abduction, whereas plantiflexion induces adduction. At the distal (Lisfranc's) joint, considerable rotation round the second metatarsal shaft is possible (Fig. 85.1). Because of the specific structure of the joint line, plantiflexion of the metatarsals will always be

Figure 85.1

At Lisfranc's joint rotation round the second metatarsal shaft is possible. Because of the specific joint line, plantifiexion of the metatarsals is always accompanied by a movement towards the second metatarsal.

1239

1240 SECTION FOURTEEN - THE LOWER LEG, ANKLE AND FOOT

accompanied by a movement towards the second metatarsal. Therefore a plantiflexion movement at the midtarsal joint increases the curvature of the anterior arch, whereas dorsiflexion is associated with flattening.

The capsular pattern at the midtarsal joints is increasing limitation of adduction, supination, plantiflexion and dorsiflexion (Fig. 85.2). The mid foot finally fixes in an abducted and pronated position, because of a spasm of the peroneal muscles.

SUBACUTE ARTHRITIS IN ADOLESCENCE

The sign that first draws attention to this disorder is spasm of the peroneal muscles. Therefore it has been called 'spasmodic pes planus', which is a misnomer, because it is not the spasm but the underlying capsulitis that causes the pain. Spasm is never primary but results from inflammation of the joint. The arthritis is caused by overuse at the midtarsal joints. It is now an uncommon condition that occurs only in boys aged between 12 and 16 years. Cyriax men­ tioned the cause as being overuse, resulting from stand­ ing for long periods, which used to happen in the transition from school to work. Both the midtarsal joints and the talocalcaneal joints are affected. The condition is usually bilateral. The first sign that draws attention to the disorder is that the boy has a clumsy gait, which does not go unnoticed by his parents. There is also some discomfort on standing.

Figure 85.2

The capsular pattern at the midtarsal joints

Walking and rmming do not cause pain and there is also complete absence of pain during sitting or lying down. Clinical examination Inspection reveals a long thin foot, sometimes with some degree of pes cavus. An eversion deformity at the heel and the midfoot are seen to be maintained by a spasm of the peroneal and extensor digitorum longus muscles. In standing, the peroneal tendons are visible as a prominent tight band behind and below the lateral malleolus. Functional examination shows a limitation of varus at the subtalar joint and limitation of adduction and supination at the midtarsal joints. These movements are prevented by muscle spasm. In long-standing cases, contraction of the joint capsules may increase the limi­ tation of the already restricted movements. For diagno­ sis, it is vital to detect the muscle spasm of capsular contracture during clinical examination in the lying position. A radiological evaluation of ankle and foot reveals no abnormality. Natural history The natural history is for symptoms to subside and cease after 2 years. By that time the foot has become perma­ nently but painlessly fixed in the deformed position. A limp results. The disorder can also lead to later valgus sprains or lesions of the tibialis posterior and flexor hallucis longus tendons. Treatment In the early stage, the essence of treatment is relief of weight bearing and support for the joint. Cyriax:1 (pp. 436-438) advised that: 'The lad . . . requires (a) a sedentary job, (b) a bicycle, (c) . .. [an inner] wedge on the heels of his shoes and (d) strapping of the joint.' The patient is first told how his condition is provoked and he must understand that avoiding weight bearing is the important part of the treatment. He should never stand if he can help it: he must seek a sedentary job, should sit when at home and should use a bicycle rather than walk. To bring the heels towards a varus position, the shoes are fitted with inner wedges and non-elastic strapping is worn as often as possible. The patient must maintain this regime for 6-12 months until he regains a full range of movement at the subtalar and midtarsal joints. Recurrence is uncommon once this stage is reached. In late cases, the subtalar joint will have become fixed in a valgus position by considerable spasm of the per­ oneal muscles. Only slight movement can be obtain�d at the midtarsal joints. If no structural contracture of the lig­ aments about the talocalcaneal and midtarsal joints has yet occurred and the valgus deformity is only caused by

CHAPTER 85

peroneal spasm, immobilization in a plaster cast, with the foot held in varus position, can be tried. The cast, from below the knee to the toes, should be worn for 6 weeks to 2 months. To obtain this position, the peroneal nerve must temporarily be blocked at the point where it curls round the neck of the fibula. SUBACUTE ARTHRITIS IN MIDDLE AGE

The patients are usually overweight women in their 40s, 50s or 60s. Overuse is the common cause of the arthritis. Sometimes an isolated sprain is the cause. The pain, lim­ itation of movement and muscular spasm are less pro­ nounced than in arthritis in adolescence. The condition does not seem to have a natural history: without treat­ ment it appears to continue indefinitely but without much alteration. Cases that have persisted for 2 or 3 years are not uncommon. Usually the arthritis is unilateral. Clinical examination reveals a capsular pattern of both the subtalar and mid­ tarsal joints: the peroneal spasm restricts varus at the hindfoot and adduction-supination at the midfoot. The radiological appearances are normal. Treatment If only one joint is affected, infiltration with triamci­ nolone can be successful, provided prophylaxis against recurrence is given. If more joints are affected, which is usually the case, the following treatment is instituted: • Modified

rest and relative relief from weight bearing. Strapping the joints in varus and supination. • Tilting the heel in varus position by a medial wedge.

•

If all these measures are taken, the arthritis can be expected to cease after 6 months but the patient should guard against renewed overuse. RHEUMATOID ARTHRITIS

Rhematoid or reactive types of arthritis can attack the midtarsal joints. If the arthritis is severe, the patient can walk only with difficulty and pain at rest is so intense that sleep becomes disturbed. Apart from marked fixation in valgus and abduction­ pronation, clinical examination shows gross synovial thickening, warmth to the touch and tenderness. If the oedema allows, the synovial thickening can be palpated over the dorsum of the joint. A very effective local treatment is immobilization in a plaster case, which eases the pain within a few days; however, if the cast is removed too soon, the pain quickly returns.

-

DISORDERS OF THE MIDTARSAL JOINTS

1241

Spontaneous recovery takes 1 or 2 years. In this time the joint becomes fixed in abduction-pronation.

NON-CAPSULAR PATTERNS MIDTARSAL STRAIN

If an excessive strain is imposed on the midtarsal joints, for instance as the result of some deformity (e.g. plan­ taris), the power of the musculature becomes insufficient to maintain the longitudinal arches during weight bearing. After some time the midtarsal ligaments becomes stretched, elongate and undergo inflammatory changes, so that pain results. Elongation promotes exces­ sive movements at the midtarsal joints, which cause the plantar arch to flatten during weight bearing. As a result, the forefoot dorsiflexes and abducts, which causes the inner side of the foot to become prominent and further overstretches the calcaneonavicular ligament. In due course, the excessive motion of the joints and their poor alignment leads to inflammation of the capsule and to structural damage of the articular surfaces, which finally results in structural deformity and arthrosis. Mechanism To understand the mechanism of midtarsal strain, the ankle and foot should be seen as complex structures with an intimate interaction between position and function of their different components. Initially the body weight bears on the talus from a downwards thrust through the tibia. The talus is sup­ ported by the calcaneus, on which it lies in an oblique manner. The former therefore has a tendency to glide in a medial and forward direction, especially in patients with an equinus deformity at the ankle or in patients with too short plantiflexor muscles. In women who wear high and oblique heels, the talus also tends to be pushed forwards on the calcaneus (Fig. 85.3a). The forward and medial gliding of the talus imposes medial and downward pressure on the anteromedial cal­ caneal border. The medial pressure forces the calcaneus towards valgus which may be furthered by a shortening of the Achilles tendon (Fig. 8S.3b). The downwards pres­ sure of the talus evokes dorsiflexion at the talonavicular joint.2 This increases the depression of the longitudinal arch and can be responsible for greater stress on the plantar ligaments and the fascia plantaris (Fig. 8S.3c). The downwards pressure of the talus and the consequent dorsiflexion at the talonavicular joint will initiate a number of other events, which are the source of more deformity and trouble: •

Because of the obliquity of the joint surfaces, each dorsiflexion in the midtarsal joints is accompanied by

1242 SECTION FOURTEEN - THE LOWER LEG, ANKLE AND FOOT

tendon of the flexor hallucis longus, which is not only an invertor but, through its position under the sus­ tentaculum tali, also has a specific function as a stabi­ lizer of the anterior part of the calcaneus, also becomes strained (Fig. 85.4). The mechanism of midtarsal strain is summarized in Fig. 85.5. Clinical examination As midtarsal strain advances, three clinical grades can be distinguished.

(a)

Postural pain. The plantiflexion-dorsiflexion range of movement increases and therefore also the abduc­ tion-pronation range of the foot. Because of this laxity, the

Figure 85.3 Midtarsal strain: (a) movement of the talus forwards on the calcaneus, (b) medial pressure forcing the calcaneus towards valgus, (c) downwards pressure of the talus causes increasing depression of the longitudinal arch and increasing stress on the plantar ligaments.

•

some abduction. The downwards movement of the talus is thus at the origin of an abduction deformity in the midfoot. This dorsiflexed and abducted foot overstretches the inner ligaments (calcaneonavicular ligament and capsule of the talonavicular joint). Dorsiflexion at the midtarsal joint also causes spreading out and abduction of the metatarsals. Abduction is the result of obliquity of the joint line. Spreading out is caused by the specific cone-shaped form of the bases of the metatarsals, which move their heads away from the centre during extension (see p. 1165). This flattens the anterior arch and results in a splay foot.

Figure 85.4 The sustentaculum tali (2) is propped upwards by contraction of the fiexor hallucis longus (1); tibialis posterior (3).

Thus, on account of an initial forwards and medial glid ing of the talus, a number of events take place: •

•

•

•

Valgus of the calcaneus with possible shortening of the Achilles tendon. Dorsiflexion and abduction of the midfoot, with flattening of the longitudinal arch and tension in the plantar and medial ligaments. Flattening and abduction of the forefoot, with spreading of the metatarsal heads and loss of the anterior arch. In due course, there will also be some effect on the tendons: that of the tibialis posterior, the first invertor of the foot, suffers strain and becomes inflamed. The

Overstretching of: Hallucis longus muscle

Figure 85.5

Overstretching of: Calcaneonavicular ligament Posterior tibialis muscle

Flattening of anterior arch

Summary of the mechanism of midtarsal strain.

CHAPTER 85

foot becomes 'wobbly', but neither structural changes nor clear signs of overstretched tendons and ligaments appear. There is muscular fatigue and pain after long periods of standing or after prolonged walking. Clinical examination reveals only laxity in the midtarsal joints. Midtarsal 'strain'. This appears when the joint capsules and the ligaments become inflamed. On account of the excessive play and poor alignment of the joints, the pro­ tective muscular action of the tibialis anterior and flexor hallucis longus are overwhelmed and they start to become inflamed. There is pain during and after weight bearing. The deformity of the foot is functional only. No structural changes appear at this stage. Clinical examina­ tion reveals excessive mobility in the joints, together with pain at the extremes of range, especially rotation. Resisted inversion of the foot and resisted plantiflexion of the big toe may be painful, because of tendinitis of the tibialis posterior or of the flexor hallucis longus.

Because of abduction of the forefoot on the hindfoot, the medial side of the foot becomes prominent. Talonavicular arthrosis supervenes, with osteophytes at the dorsum and the inner side of the joint. In that the navicular bone is now permanently depressed, a painful and persisting over-stretching of the talonavic­ ular ligament results. Apart from the visible deformities at the inner side and the dorsum of the foot, the clinical findings are permanent fixation of the foot in abduc­ tion-dorsiflexion, some limitation of rotation with a hard end-feel and tenderness at the talonavicular ligament. Structural changes.

Treatment

The heel must be raised in a horizon tal way (Fig. 85.6) so as to allow the forefoot to adopt a more plantigrade position in relation to the talus when weight is borne. A slight medial wedge can be added to correct the valgus position of the heel. Attempts should be made to stretch the triceps muscle if there is shortening. Heel raising.

Exercises (faradic and resisted) should be given to the short plantiflexor muscles of the sole, especially to the adducExercises for the short plantiflexor muscles.

Figure 85.6 on the talus.

The horizontal raised heel on the right reduces the towards force

-

DISORDERS OF THE MIDTARSAL JOINTS

1243

tor hallucis, flexor hallucis brevis, flexor digitorum brevis and quadratus plantae. The main purpose is to make them adequate to take the strain and thus to relieve some tension on the ligaments. Exercises for the invertors should also be given; strengthening them protects the foot against further pronation-abduction. A strong and functional flexor hallucis longus muscle plays a role in 'propping' the talus upwards by lifting the sustentacu­ lum tali (Fig. 85.4). Mobilization of the joints. Mobilization of the midtarsal joints aims to allow a full range of motion to be painlessly achieved. During the initial stages, the range of move­ ment is excessive. Nevertheless, repeated strains, fol­ lowed by healing of minor ruptures, lead to the formation of painful adhesions. The self-perpetuating inflammation in these elongated ligaments is the main reason for the discomfort at the end of range. Therefore treatment also includes manipulation to break the ligamentous adhe­ sions. This is the only area of the body in which manipu­ lations are required at a joint that already has an excessive range of motion.

Technique: manipulation. The patient lies in a supine position on a high couch. The manipulator sits facing the patient's foot. Because great strength is required and the manipulator has to work without leverage, a good start­ ing position is vital. The heel of the ipsilateral hand is placed at the dorsum of the first metatarsal bone and the heel of the contralateral hand is placed at the plantar aspect of the fourth and fifth metatarsal bones. Both hands are clasped about the outer and dorsal aspect of the forefoot. The foot is pressed slightly towards dorsiflexion (Fig. 85.7). Rotation is now imparted to the forefoot by a swinging movement in the shoulders and elbows, which causes the upper hand on the inner side to press towards the manipulator and the outer hand to do the press away. This movement is repeated in a rhythmiC manner for a few minutes. Steroid infiltration. Sometimes there is marked and per­ sistent tenderness of the calcaneonavicular ligament, which calls for an infiltration with triamcinolone. The injection is repeated after 2 weeks.

Technique: infiltration. The patient lies in a supine posi­ tion on a high couch. The sustentaculum tali and the navicular bone are identified. Between them, the tender ligament can easily be palpated. A thin needle, 2 cm long, is fitted to a 2 ml syringe filled with triamcinolone. The palpating thumb remains on the tender ligament and the needle is introduced between the thumb and bone (Fig. 85.8). The point of the needle is then aimed to the calcaneal border of the ligament, where 1 ml is injected. Another 1 rnl is then infiltrated at the navicular insertion of the ligament.

1244 SECTION FOURTEEN - THE LOWER LEG, ANKLE AND FOOT

If the flexor hallucis longus or the tibialis posterior tendons are at fault, deep friction is indicated (see Ch. 83).

Deep friction.

If conservative management fails, the painful midtarsal joints are best stabilized by arthrodesis. In the past, triple arthrodesis was used extensively; nowadays more limited single-joint fusions are used which allow more preservation of the hindfoot motion, resulting in better function.3-6 A summary of midtarsal strain is outlined in Figure 85.9.

Surgery.

MIDTARSAL LIGAMENTOUS CONTRACTURE

Adhesions in the midtarsal joints may cause serious problems. They are likely to form in middle-aged patients after immobilization in plaster for fractures of the lower leg. History The patient is usually between 50 and 65 years of age and the usual complaint is that, some months or even years after the lower leg has been immobilized, there is still an inability to run or ski without immediate pain in the foot. Figure 85.7

Manipulation to break adhesions at the midtarsal joints.

Depression of the talus

J

Equinus deformity High and oblique heels Short triceps muscle

1

Valgus at the heel Dorsiflexion and abduction at the midtarsal joint Spreading of the forefoot

1

Hyperlaxity of the joint Sprains and adhesions in the medial ligaments Tendinitis of tibialis posteriori extensor hallucis longus Structural changes and arthrosis

1 Treatment A horizontal heel Faradism and training of the short plantiflexor and invertor muscles Mobilization of the midtarsal joints to break the adhesions (Infiltrations at the strained ligaments) (Deep friction to the strained tendons) (Surgery)

Figure 85.8

Steroid infiltration of the calcaneonavicular ligament.

Figure 85.9

Summary of the mechanism of midtarsal strain.

,

CHAPTER 85

Although the foot is good enough for normal daily pur­ poses, some sports remain impossible without problems. There are no twinges or pain at rest. Clinical examination The midtarsal movements, though considerably limited, are only slightly painful. The end-feel is normal; there is no muscle spasm. There are no visible structural changes from midtarsal arthrosis. Warmth is absent, as is swelling of the joint. The ligaments at the dorsum of the foot are tender to the touch. Treatment This ligamentous contracture seems to be resistant to manipulation. Even manipulation under anaesthesia does not lead to the slightest improvement. The only effective treatment is infiltration of all the tender liga­ ments with triamcinolone. When the lesion is very exten­ sive, treatment must be carried out over several sessions. Although the infiltration will not improve the range of motion, pain will cease almost immediately. The foot does not become completely normal, but sports again become possible.

ASEPTIC NECROSIS

Osteochondritis dissecans at the navicular bone appears in boys aged between 4 and 12 years and is known as Kohler's disease I. There is pain and limitation of the midtarsal movements. The diagnosis is made from a radiography or a bone scan? The course of the disease process is benign and self­ limiting.8,9 The treatment is symptomatic and consists of weight-bearing plaster casts over 3 months.lO With or without treatment, there is a spontaneous reconstitution of the navicular bone and an excellent recovery of func­ tion after an average duration of 15 months.ll,12

-

DISORDERS OF THE MIDTARSAL JOINTS

1245

CUBOID ROTATION

Subluxation of the cuboid bone occurs when a strong pull of the tendon of the peroneus longus muscle causes a rotation of the bone16 (see Fig. 85.10). The lateral side of the cuboid is tilted upwards and the medial side becomes depressed. The cuboid is locked in this subluxated posi­ tion and pain results. Newell and Woodle17 found this condition in some 4% of athletes complaining of pain in the midtarsal region. The condition seems to be more common in patients who have pronated feet. The patient, most often a long-distance runner, com­ plains of pain at the outer side of the foot during and after activity. Clinical examination reveals a full range of midtarsal movements with pain at the end of the range. The liga­ ments at the inferior aspect of the cuboid bone are tender. Treatment is manipulation. Technique: manipulation. 18, 19 The patient stands with the back to the manipulator and holds onto a couch or a chair. The knee is flexed to a right angle. The physician grasps the foot with both hands in such a way that the fingers are placed at the dorsum of the forefoot and the crossed thumbs over the plantar aspect of the cuboid (Fig. 85.11). The manipulation is now performed as a quick upwards 'whiplash', while the thumbs, at the plantar aspect, apply strong downwards pressure.

NAVICULAR STRESS FRACTURE

This lesion occurs in long-distance runners, in whom repetitive cyclic loading results in fatigue failure through the relatively avascular central position of the tarsal nav­ icular. According to Torg,13 The characteristic fracture is located in the central third of the bone. A navicular stress fracture produces chronic, diffuse and vague foot pain during activity. The navicular bone is tender to the touch and early diagnosis is made by ultra­ sound, which is a good screening test for stress fractures.I4 The fracture can be confirmed early by a bone scan.I5 Treatment consists of a plaster cast and non-weight bearing for 6 weeks.

Figure 85.10 peronei.

The relationship of the cuboid bone and the tendons of the

1246 SECTION FOURTEEN - THE LOWER LEG, ANKLE AND FOOT

During routine functional examination of the foot, movements at the cuneiform-first metatarsal joint cannot be distinguished from those at the talonavicular and cuneiform-navicular joints. If a lesion of the cuneiform-first metatarsal joint is suspected, the joint must be examined separately after the routine examination. The disorders that occur at this joint are: • • •

Osteoarthrosis Gout Loose body.

OSTEOARTHROSIS

Figure 85.11

Manipulation for cuboid rotation

The manipulator 's elbows should be close together and the arms, wrists and hands should be fully relaxed. In long-standing cases, or when the foot is pronated, it may be necessary to prevent recurrences with an orthotic device. MIDTARSAL ARTHROSIS

Arthrosis of the midtarsal joint can be the result of a navicular fracture, an old navicular apophysitis or an ordinary midtarsal strain. A fracture or apophysitis can lead to gross deformities with serious disturbances to the anatomy of the foot. If this is the case and serious trouble results, a steel support moulded accurately to the sole of the foot will minimize movements at the disorganized joints. If this is not fol­ lowed by improvement, arthrodesis can be considered. However, the diagnosis 'midtarsal arthrosis' is very often a misnomer because it is based only on deductions from radiological appearances. The common cause for the radiologically visible osteophytes at the dorsum of the talonavicular joint is a long-standing midtarsal strain. Once again, neither the osteoarthrosis nor the osteo­ phytes but rather the underlying ligamentous strain causes the trouble. If the ligaments are strained, treat­ ment for midtarsal strain must be applied whether there is radiological evidence of osteoarthrosis or not. -

LESIONS OF THE CUNEIFORM-FIRST METATARSAL JOINT

-

_.

The cuneiform-first metatarsal joint permits not only plantiflexion and dorsiflexion movement but also slight rotation around the base of the second metatarsal.

This condition usually results from a previous osteochon­ dritis (Cyriax:1 p. 439). There is a similarity with hallux rigidus, also known to be the result of osteochondritis.2o The patient is an adolescent and more girls are affected than boys. The condition is usually bilateral and the onset insidious. One day the patient finds that, if wearing tight shoes, localized pain arises at the site of small projections at the dorsal and medial aspect of the foot. There is no trouble unless something catches against the promi­ nences. Rarely, the onset is sudden and the patient says that both joints became tender and swollen for about a week. After this severe phase, there is a permanent and small prominence on each foot. There is a visible and palpable outcrop at the dorsum of each foot. If the condition is acute, there is also some swelling and local tenderness. Clinical examination is usually largely unrevealing except for slight stiffness of the range of plantiflexion-dorsiflexion. A radiograph confirms the diagnosis.

TREATMENT If the arthritis is acute, a few days' rest is advised with weight bearing only in a high-heeled shoe, no part of which should touch the joint. Because the condition is harmless and the recurrent pain is only from the pressure of lace-up shoes squeezing the skin against the osteo­ phytes, treatment is to prevent this pinching. For girls, it is easy to find shoes that have no part touching the joint; alternatively, a felt ring around the bony outcrops can be used. For boys this is sometimes more difficult to achieve and, if the inconvenience continues, the bony promi­ nences have to be removed surgically. It is important to note that gross osteoarthrosis of the cuneiform-first metatarsal joint may lead to fixation, � with considerable plantaris deformation of the first metatarsal (fixation in plantiflexed position). This may, in turn, result in metatarsalgia of the first metatarso-

CHAPTER 85

phalangeal joint or, more frequently, a lesion of the sesamoid-metatarsal joint. If this occurs, a support must

-

DISORDERS OF THE MIDTARSAL JOINTS

1247

be prescribed to take the weight off the head of the bone (see p. 1255).

Table 85.1 Differential diagnosis and treatment of disorders at the midfoot Presentation

Examination

Treatment

Subacute arthritis in

Boys

Capsular pattern with peroneal

Early cases - prevention:

adolescence

Clumsy gait/slight pain

spasm

Disorder

Sedentary job Raised heel Joint strapping Long-standing cases: Plaster cast Immobilization

Subacute arthritis in

Overweight women in their 50s

Capsular pattern with muscle

Modified rest

middle age

or 60s

spasm

Joint strapping and tilting the

Differential diagnosis: gout and

heel

rheumatoid arthritis

Triamcinoline infiltration

Midtarsal strain

Pain at the midfoot

Abduction and dorsiflexion in

Raising the heel, exercise to the

the midfoot

short plantiflexor muscles,

No muscle spasm

mobilization of the midtarsal

First stage:

joints

'Wobbly' foot with increased range Pain at the end of dorsiflexion/abduction Later stages: Structural deformity Strained ligaments Strained invertor muscles Midtarsal ligamen-

Patients in their 50s and 60s

Pain at the end of range

Infiltration of all the tender

tous contracture

Previous plaster immobilization

No muscle spasm

ligaments with triamcinolone

Pain during exercises

No increase in range of mobility

Stress fracture of

Long-distance runners

Normal functional examination

the navicular bone

Increasing pain during activity

Local tenderness and pain

Rest

during application of ultrasound Aseptic necrosis of

Boys of 5-12 years

Pain and limitation

Support

Diagnosis is established by the

the navicular bone

radiograph Cuboid rotation

Athletes, with midtarsal pain

Full but painful range of rotation

during running

movements

Manipulation

Tender ligaments at the inferior aspect of the cuboid bone Midtarsal arthrosis

After an apophysitis or fracture

Steel support

Gross deformities

Arthrodesis

Arthrosis at the

Teenagers with bilateral bony

Normal clinical examination

cuneiform-first

outcrop at the dorsum of the

Local tenderness

metatarsal joint

foot

Gout at the

Red, warm, swollen and

cuneiform-first

exquisitely tender joint

Prevention of pressure

Medication

metatarsal joint Loose body at the

Athletes

cuneiform-first

Sudden pain during a

metatarsal joint

sprint

Normal clinical examination

Sustained traction

Manipulation

Chronic ligamentous

After an ankle sprain

Pain during inversion/adduction

adhesions at the

Persistent lateral pain during

and supination

calcaneocuboid joint

and after exercises

1248 SECTION FOURTEEN - THE LOWER LEG, ANKLE AND FOOT

GOUT

It is not uncommon for gout to attack this joint, even before the metatarsophalangeal joint of the big toe.21 If there is sudden pain, warmth, reddening of the skin, pain at night and extreme tenderness of the joint, gout should be considered.

LOOSE BODY

Athletes sometimes complain of sudden twinges at the medial border of the foot during sprinting. These are

recurrent and appear race after race but cannot be repeated voluntarily. Between races, the foot is normal and pain is not present when the foot is examined. However, localiza tion shows the twinges not to arise from the ankle or the subtalar joint. When the patient rises on tiptoe, subluxation of the metatarsal bone on the cuneiform does not occur. Because of the typical history of sudden twinges and because the clinical examination is entirely negative, some internal derangement is very likely. Good results can be obtained by sustained traction on the big toe (up to 10 kg) for 30 minutes, two or three times a week. Differential diagnosis and treatment of disorders at the midfoot are summarized in Table 85.1.

REFERENCES 1. Cyriax JH. Textbook of Orthopaedic Medicine, vol 1, Diagnosis of

Soft Tissue Lesions, 8th edn. Bailliere Tindall, London, 1982. 2. Astion DJ, Deland JT, Otis JC, Kenneally S. Motion of the hind­ foot

after simulated arthrodesis. J Bone

Joint Surg 1997;

79A(2):241-246. 3. Schramm CA, Hein SC, Cooper PS. Triple arthrodesis. AORN J 1996;64(1) :31-52. 4. Donatto KC Arthritis and arthrodesis of the hindfoot. Clin

Orthop 1998;349:81-92. 5. Harper MC Talonavicular arthrodesis for the acquired flatfoot in the adult. Clin Orthop 1999;365:65-68. 6. Harper MC, Tisdel CL. Talonavicular arthrodesis for the painful adult acquired flatfoot. Foot Ankle 1nt 1996;17(11):658-661. 7. Bui-Mansfield LT, Lenchik L, Rogers LF et al. Osteochondritis dissecans of the tarsal navicular bone: imaging findings in four patients. J Comput Assist Tomogr 2000;24(5):744-747. 8. Borges JL, Guille JT, Bowen JR. Kohler's bone disease of the tarsal navicular. j Pediatr Orthop 1995;15(5):596-598. 9. Devine KM, Van Demark RE. Kohler's osteochondrosis of the tarsal navicular: case report with twenty-eight year follow up.

South Dakota J Med 1989;42(9):5-6. 10. Ippolito E, Ricciardi Pollini PT, Falez' F. Kohler's disease of the tarsal navicular: long-term follow-up of 12 cases. J Pediatr Orthop 1984;4(4):416-418.

11. Williams GA, Cowell HR. Kohler'S disease of the tarsal navicular.

Clin Orthop 1981;158:53-58. 12. Leeson

MC,

Weiner

DS.

Osteochondrosis

of

the

tarsal

cuneiforms. Clin Orthop 1985;196:260-264. 13. Torg JS et al. Stress fractures of the tarsal navicular. ] Balle Joint

Surg 1982;64:700-712. 14. Moss A, Mowat AG. Ultrasonic assessment of stress fractures.

BMJ 1983;286:1479-1480. 15. Hulkko A, Orava S, Peltokallio P, Tulikoura I, Walden M. Stress fracture of the navicular bone. Nine cases in athletes. Acta

Orthop Scand 1985;56(6):503-505. 16. Mooney M, MaHey-Ward L. subluxation: assessment

and

Cuboid plantar and dorsal treatment.

jOSPT

1994;20:

220-226. 17. Newell SG, Woodle A. Cuboid syndrome. Phys Sportsllled 1981;9(4):71-76. 18. Taplin GC Foot technique. ] Am Osteopath Assoc 1928;27: 606-608. 19. Jones LH. Foot treatment without hand trauma. J Am Osteopath

Assoc 1973;72:481-489. 20. Huskisson EC, Hart FD. Joint Disease: All the Arthropathies, 4th edn. John Wright, Bristol, 1987. 21. Dieppe PA, Calvent P. Crystals alld Joillt Disease. Chapman and Hall, London, 1983.

CHAPTER CONTENTS the Forefoot

1251

Short first metatarsal bone March fractures

1251

Fractures of the fifth metatarsal Splay foot 1253

1252

The first metatarsophalangeal joint The capsular pattern 1254

1253

Gout

Disorders of the forefoot and toes

1251

1254

Arthritis in adolescence 1254 Traumatic arthritis 1255 Arthrosis in middle age 1255

Rheumatoid arthritis 1255 Non-capsular patterns 1256 Metatarsalgia

1256

Sesamometatarsal lesions Hallux valgus 1256

THE FOREFOOT 1256

The outer four metatarsophalangeal joints

The capsular pattern 1257 Rheumatoid arthritis and gout 1257 Freiberg's osteochondritis 1258 Traumatic arthritis 1258 Osteoarthrosis 1258 Non-capsular patterns 1258 Chronic metatarsalgia 1258 Interdigital ganglion 1259

Pressure on the nerves in the forefoot

SHORT FIRST METATARSAL BONE 1257

1259

This is known as Morton's syndrome. Sometimes a short first metatarsal is related to pain, sometimes it is not. If the first metatarsal is too short and hypermobile, most of the body weight will be borne by the second metatarsal. Because of the hypermobility and shortening, the trans­ verse arch becomes depressed and metatarsalgia results (p. 1258).

MARCH FRACTURES

This condition was first described in 1855 by Breithaupt,l a Prussian military doctor, who stated that many soldiers developed painful swellings at the dorsum of their feet after long marches. He called this Schwellfuss but the cause remained unclear until Stechow2 proved that the condition is caused by stress fracture. The second and third metatarsal shafts are most often affected, followed by the fourth.3 Usually, the fracture lies at the neck of the bone although it can be anywhere along the shaft.4--{j Stress fractures seem not to occur in the first metatarsal. The lesion should be suspected when a patient presents with unilateral and localized warmth and oedema at the dorsum of the foot. Often the symptoms appeared after a long walk but sometimes there has been no specific pre­ cipitating activity. It is surprising that children are almost as liable to marching fractures as adults. Cyriax's8 (his p. 440) youngest patient was a 6-year-old boy. During the first weeks after the onset of pain, there is local warmth and oedema over the dorsum of the fore­ foot. The normal findings on functional examination of the ankle and midfoot contrast with tenderness at the forefoot. Because not only the bone but also the interosseous muscles at both sides are involved, the ten­ derness is more extensive than might be expected from the fracture itself. During the first few days, the fracture (usually a hair­ line crack) may not be revealed by routine radiography. 1 249

1 2 50 SECTION FOURTEEN - THE LOWER LEG, ANKLE AND FOOT

The diagnosis is confirmed after a few weeks, when the callus formation around the fracture becomes radiologi­ cally apparent. Earlier confirmation of the diagnosis is obtainable by either radionuclide bone imaging,9,10 or ultrasound examination.l1 -13

undergoes spontaneous cure and chronic pain can last for years. The only effective treatment for this condition is deep transverse friction for 15 minutes, three times a week, for about 2-4 weeks. After the massage, faradic and resisted flexor exercises are given to the toes. The results of this combined treatment are excellent.

DIFFERENTIAL DIAGNOSIS

Technique: friction. The patient lies supine on the couch. The therapist sits facing the foot and with the ipsilateral hand encircles the toes in such a way that the thumb lies at the dorsal aspect and the proximal interphalangeal joint of the flexed index finger presses under the metatar­ sophalangeal joints. The big toe is left free. The thumb keeps the toes flexed and the index finger presses upwards, so as to render the metatarsus convex. The shafts move apart and the muscle bellies lie closer to the surface. The middle finger of the other hand, rein­ forced by the index finger, is now placed in the groove between the two metacarpal bones (Fig. 86.1). Fingers, wrist and forearm are kept in one line and parallel to the metatarsal bones. Deep friction is imparted by rotating the fingers through an alternate pronation and supina­ tion movement of the forearm, so that the muscle is moved between the fingertip and the metatarsal shaft.

Localized swelling, warmth and tenderness in the fore­ foot can also occur in: •

Gout in one of the tarsometatarsal joints. A history of recurrent acute attacks of arthritis at the same joint or in other joints is helpful.

•

Rheumatic forms of arthritis, such as rheumatoid arthritis, psoriasis and reactive arthritis. These disorders affect multiple joints. The history is also longer than the usual 6 weeks of that of a march fracture.

•

•

Freiberg's arthritis at the second metatarsophalangeal joint. Although ischaemic epiphyseal necrosis of the base of the second metatarsal bone occurs in adolescence, the disease may be asymptomatic until adult life, when the deformity of the joint and the degenerative arthritis produce pain. Ringworm and erysipelas. Local cellulitis, caused by an infection of /3-haemolytic streptococci or fungi, can cause considerable redness, thickening and tenderness. In erisypelas, there is malaise, chills and fever, together with an increased erythrocyte sedimentation rate. In ringworm, there is considerable itching and inspection of the interdigital clefts very often reveals a small localized infection between two toes.

FRA CTURES OF THE FIFTH METATARSAL

TREATMENT

Three distinct fracture patterns occur in the fifth metatarsal: tuberosity avulsion fractures, Jones fractures, and diaphyseal stress fractures. Tuberosity avulsion frac­ tures are the most common and usually complicate an inversion sprain (see p. 1221). The majority heal with symptomatic care in a hard-soled shoe. The true Jones fracture is an acute injury involving the fourth-fifth intermetatarsal facet and is best treated with a

March fractures, whether partial or complete, always heal spontaneously in about 6 weeks. By that time, the bone is usually firm enough to be painless and mis-union need not be feared. Treatment consists of relative rest. Normal walking need not be forbidden during the period of union. Immobilization is achieved when the forefoot is firmly bound, so that the other metatarsals splint the broken bone. Because, even with a splinted fracture, weight bearing still hurts a little, it is up to the patient to do as much as can be stood. If the pain is too severe, a plaster cast can be applied for 4 weeks. If there is persistent pain after 6 weeks have elapsed, the interosseous muscles must be at fault. It is obvious that when there is a broken bone, the interosseous muscles will suffer abnormal stresses and become strained. Such a strain, whether the cause is a direct injury, a march fracture or as overstrain, hardly ever

Figure 86.1

Friction to the interosseus muscles.

CHAPTER 86

-

DISORDERS OF THE FOREFOOT AND TOES 1 25 1

non-weight-bearing cast immobilization for 6-8 weeks. Non-acute diaphyseal stress fractures of the proximal fifth metatarsal are also treated with relative rest over 6 weeks. Non-unions can be managed with operative fixation. 14

SPLAY FOOT

A splay foot is a broadened forefoot, with weakness of the intermetatarsal ligaments, associated with weakness of the intrinsic muscles. Very often splay foot starts with excessive dorsiflexion movement of Lisfranc's joint, which occurs when too much weight falls on the midfoot. This is particularly likely to occur in women who wear high heels. When excessive weight falls on the midfoot, the talus is pressed downwards, and the metatarsals undergo an upwards pressure, so that they are given excessive horizontal play and the transverse arch flattens. The result is a painful overstretching of the transverse interosseus ligament and an increase in weight on the middle metatarsal heads. Calluses will form on the plantar surfaces of the heads and bruising of the plantar aspect of the capsule of the metatarsophalangeal joints (so-called chronic metatarsalgia) results. In practice, splay foot is not a specific entity but usually accompanies a midtarsal strain. Treatment includes a high heel with a horizontal upper· surface, which prevents the forwards gliding of the talus and thus releases the forefoot (see Ch. 85), and energetic training of the short plantiflexor muscles of the toes. Localized splaying indicates a ganglion lying between two metatarsal heads. When the patient stands, an exces­ sive interval is seen between two toes and palpation reveals a semisolid tumour keeping the heads apart (see p. 1257).

Figure 86.2 The first metatarsophalangeal joint; colour indicates the location of the sesamoid bones within the tendons of the flexor hallucis brevis.

allow the hallux to function normally during the stance phase of gait.I6 In the final stage of forefoot contact, 40% of body weight is imposed on the joint and the big toe]7 (Fig. 86.3). During extension, the sesamoids are drawn from the head-neck junction of the first metatarsal to the distal head area. The average range of motion is 500.18 Apart from their function in weight bearing, the sesamoids also serve as a fulcrum that increases the mechanical advantage of the flexor hallucis brevis tendon. The clinical examination of the big toe is summarized in Box 86.1.

THE FIRST METATARSOPHALANGEAL JOINT

The capsule of the first metatarsophalangeal joint is rein­ forced on the plantar surface by a fibrocartilaginous plate that is attached distally to the proximal phalanx and proximally to the plantar aspect of the neck of the first metatarsal. This volar plate contains the two sesamoid bones, inserted in the tendons of the flexor hallucis brevis (Fig. 86.2). The flexion-extension movement is a rolling and sliding of the metatarsal head within the stable support made up of the base of the proximal phalanx and the volar plate. IS The joint is extremely important for normal gait. There must be 60-70% of extension with the first metatarsal to

Figure 86.3

The final stage of forefoot contact during walking.

1 252 SECTION FOURTEEN - THE LOWER LEG, ANKLE AND FOOT

Box 86.1 Clinical examination of the big toe

.-

Inspection Redness and swelling: gout Gross osteophytes: arthrosis Valgus deformity and enlarged medial portion of the metatarsal head: hallux valgus Ingrowing toe nails Dermatological conditions Functional examination Passive extension and flexion Normally the big toe can be extended to a right angle with the forefoot, whereas flexion is only 30-45°. Both end-feels are elastic

joint is swollen and exquisitely tender. The overlying skin is tense, warm and dusky red. The attack last 1-2 weeks, and asymptomatic periods of months or years commonly follow the initial acute attack.19 An acute attack can frequently be aborted by colchicine or by one of the non-steroidal anti-inflamma­ tory drugs.20-22 When attacks are frequent or other gouty complications such as tophi occur, lowering of blood uric acid is indicated.23

ARTHRITIS IN ADOLESCENCE

Passive abduction, adduction and rotations Resisted extension: extensor hallucis longus and brevis Resisted flexion: flexor hallucis longus and brevis

Palpation For tenderness, fluid and osteophytes

THE CAPSULAR PATTERN

The capsular pattern at the first metatarsophalangeal joint is slight limitation of flexion, together with marked limitation of extension (Fig. 86.4).

GOUT

The first metatarsophalangeal joint is usually the first joint to be affected in gout. The attack is characterized by a sudden onset of intense pain, frequently at night. The

Figure 86.4

The capsular pattern at the first metatarsophalangeal joint.

Early osteoarthrosis at the first metatarsophalangeal joint, mostly bilateral, occurs in adolescence and is the result of osteochondritis dissecans.24. It leads to the formation of a hallux rigidus in young adults. The teenage patient, nearly always male, develops large osteophytes at the dorsum of both first metatarso­ phalangeal joints. The onset is slow and there is no history of overuse or of injury. Initially the pain appears only during hyperextension of the big toe. Later, the joint gradually fixes in the neutral position, leading to a hallux rigidus. Pain at every step is the inevitable from stress on the rigid joint. Clinical examination shoes the big toe to be fixed in a neutral position. There is only a small range of extension and flexion. The end-feel is hard and large osteophytes can be palpated on the dorsum of the joint. Because the patient is unable to extend the big toe during the foot-off phase, treatment must aim to intro­ duce a forefoot movement that does not interfere with the mobility of the joint but nevertheless enables the heel to move upwards while the forefoot is on the ground. To do this, a 'rocker' is placed in or under a thick and solid sole, at the joint line (Fig. 86.5). Instead of extending at the first metatarsophalangeal joint, the forefoot will now rock during a normal gait. If this is not adequate, a steel plate in the sole prevents further stress on the rigid joint but the resulting gait is less natural,25

Figure 86.5

------

A 'rocker' fitted to the shoe.

----

CHAPTER 86

Surgery for hallux rigidus consists of resection of osteo­ phytes and metatarsal head (cheilectomy)26 or resection arthroplasty.27-29

TRAUMATIC ARTHRITIS

This results from a direct trauma or forceful hyperexten­ sion of the joint. This is the case in osteoarthrosis, in which a superimposed posttraumatic arthritis easily occurs. It is also encountered in certain sports, such as soccer and American footbalpO-33 Treatment consists of an intra-articular injection of 10 mg of triamcinolone and prevention of further overstretching.

-

DISORDERS OF THE FOREFOOT AND TOES 1 2 53

Technique: injection. The patient sits with the foot flat on the couch. The physician grasps the distal phalanx and pulls it in an axial direction, with a slight flexion compo­ nent. This distracts the joint surfaces and enables the joint line to be identified, which is not always easy to do in patients with large osteophytes: the depression between the osteophyte and the bone should not be mistaken for the joint line. A 1 ml syringe is filled with steroid suspen­ sion and fitted with a thin 2 cm needle. After identifying the joint line and the tendon of the long extensor, the needle is passed into the space between the two bones, medially to the tendon (Fig. 86.6) and the steroid is injected. The patient should be warned of severe after-pain for 12-24 hours but will be pain free afterwards. If care is taken in the future, a second injection will not be necessary.

ARTHROSIS IN MIDDLE AGE

Osteoarthrosis at the first metatarsophalangeal joint can also occur and provoke problems between the ages of 40 and 60 years. The degeneration and stiffness is not the result of a previous aseptic necrosis but has probably been induced by trauma or repetitive stresses. Sometimes a heavy weight falling on the joint or a fracture is the precipitating cause. Repetitive stresses during extension (as in women wearing high heels) can influence the degeneration. Deterioration is slow and insidious, and therefore symptoms may not arise for years. They appear only when the joint becomes overstrained.34 In other words, the source of the pain is not the osteoarthrosis as such but the superimposed posttraumatic arthritis. Symptoms there­ fore start when some dorsiflexion is lost: in men when 45° of extension range has been lost, in women who wear high heels when only 20 or 30° has been lost. The typical case is consequently a middle-aged man or woman who has pain at the big toe during and after walking. Clinical examination shows a painful and markedly limited extension of the big toe, together with slight limitation of flexion. The end-feel is hard. Osteophyte formation and some local tenderness can be palpated at the dorsum of the joint.35 Because the pain is the result of a posttraumatic arthri­ tis, it can be abolished by one intra-articular injection of triamcinolone. If the patient is careful in the future, wears appropriate shoes with thick, solid soles and avoids high heels, relapses are not to be expected. Good results can also be achieved by traction. Alternatively, mobilization of the metatarsophalangeal joint, using traction-transla­ tion techniques, can be recommended.36 In advanced cases, in which there is hallux rigidus, the use of a 'rocker' and a steel sole must be advised. If all conserva­ tive treatment fails, surgery can be undertaken.37

RHEUMATOID ARTHRITIS

This disease often affects the metatarsophalangeal joints. The usual signs and symptoms of an inflamed joint are seen. The patient has nocturnal pain and morning stiff­ ness. Clinical examination reveals a capsular pattern and a capsular thickening at a warm and swollen joint. Treatment is causative.

t

Figure 86.6

Intra-articular injection of the first metatarsophalangeal joint.

1 2 54 SECTION FOURTEEN - THE LOWER LEG, ANKLE AND FOOT

NON-CAPSULAR PATTERNS METATARSALGIA

Metatarsalgia at the first metatarsophalangeal joint is not as frequent as at the outer four toes. When it occurs, it is usually the result of an increase in the angle between the forefoot and the hindfoot. This is the case in a pes cavus deformity and also in osteoarthrosis at the cuneiform-first metatarsal joint (after a previous osteochondritis), which fixes this joint in plantiflexion and therefore increases the pressure on the plantar aspect of the first metatarso­ phalangeal joint during walking. The clinical signs are pes cavus deformity of the foot, with normal mobility and painless resisted flexion of the big toe. However, there is significant tenderness at the plantar aspect of the capsule of the first metatarso­ phalangeal joint. Treatment consists of an intra-articular injection of 10 mg of triamcinolone (see earlier). In a pes cavus defor­ mity, the patient must also wear a raised heel with a hor­ izontal upper surface (see Ch. 85). This measure relieves the excessive stress on the joint and prevents recurrences.

SESAMOMETATARSAL LESIONS

Traumatic periostitis of the sesamoid bone of the flexor hallucis longus usually results from local trauma, such as stepping barefoot on a sharp pebblestone or landing on the medial side of the extended joint.38,39 After the accident the patient feels pain at the inner aspect of the forefoot with each step. Clinical examination shows a full range of movement, sometimes with pain at the end of extension. Resisted flexion hurts at the plantar aspect and the sesamoid bone is tender to the touch, the exact point shifting with the position of the hallux.18 Clinical diagnosis can be confirmed with conventional radiography and MRI imaging.4o,41 Treatment consists of infiltration of the correct area with 10 mg of triamcinolone. Usually one infiltration is sufficient. Some authors advise orthotics42 as a prophyl­ actic measure but experience shows that this is never necessary. If conservative treatment is not followed by quick recovery, fracture43, 44 or posttraumatic osteochon­ dritis45 should be suspected. Immobilization in a plaster cast or surgical intervention is then required. Surgical treatment may include partial or complete resection of the sesamoid, shaving of a prominent tibial sesamoid or autogenous bone grafting for non-union.38 Alternatively, the pain can be caused by overuse, which sets up a traumatic arthritis at the sesamoid-first

Figure 86.7

I nfiltration of sesamoid lesions.

metatarsal jOint.46,47 This condition is similar to metatarsalgia of the big toe. Treatment is an infiltration with 10 mg of triamcinolone between the sesamoid and the first metatarsal, together with prevention by use of a raised horizontal heel. Technique: infiltration and injection. The patient lies supine on a high couch. The tender point is identified. Because the skin is usually thick and difficult to sterilize, the medial side of the metatarsophalangeal region must be scraped until the epidermis is clean. A 1 ml syringe is fitted to a thin needle and filled with 10 mg of triamci­ nolone. The insertion is made from the medial aspect. The thumb of the free hand is kept on the tender spot and the needle is advanced in the direction of the palpating thumb (Fig. 86.7), whether at the sesamoid bone or at the joint between sesamoid and metatarsal. Depending on the lesion, an infiltration or an injection is then made.

HALUX VALGUS

This is the most common deformity of the big toe. It has been estimated that about 25% of the population have it to some degree. There is no parallel between the degree of valgus and the severity of the symptoms, and many patients with severe deformity are free of symptoms. Much has been written about the aetiology of hallux valgus.48-50 Because hallux valgus also occurs in bare­ footed people who never wear shoes, there must be congenital factors predisposing to the deformity. The causative components seem to be multiple: the first metatarsal shaft is shorter than the second, there is a hypermobility of the first ray and the first intermetati�rsal angle is enlarged.51 All these factors contribute to the origin of a widely splayed forefoot (A in Fig. 86.8).52,53

CHAPTER 86

o 8 ..,..._ .,. ,..'"

-

DISORDERS OF THE FOREFOOT AND TOES 1 2 55

appropriate shoes: a wide shoe with a horizontal heel should be advised; sometimes a 'pouch' can be pressed out at the side of the metatarsal head. Local tenderness at the skin or at the inflamed bursa can often be treated suc­ cessfully with ichthammol ointment. Surgery is indicated when there is continuous pain or for cosmetic reasons.57-60 There is a choice of several procedures depending on the severity of the lesion and the age and mobility of the patient.61 ,62

THE OUTER FOUR METATARSOPHALANGEAL JOINTS THE CAPSULAR PATTERN

The capsular pattern at the outer metatarsophalangeal joints is more limitation of flexion than extension (Fig. 86.9). Figure 86.8

Aetiologies of hallux valgus (see text for details).

RHEUMATOID ARTHRITIS AND GOUT

Because of the shortness of the first metatarsal, the second toe takes most of the weight during the final phase of the step. If there is a muscular imbalance between the adductor hallucis and abductor hallucis, the big toe will deviate laterally (B) and undergoes a prona­ tion movement (C).54 This is accentuated by the contrac­ tions of the flexors and long extensor of the toe, which act like a bowstring and shift the tip of the big toe further into adduction (0). When this predisposed splayed fore­ foot is now forced into a high-heeled pointed shoe, exces­ sive weight is added and the first toe deviates increasingly and rapidly in a lateral direction. The pointed shoe increases the pressure at the medial aspect of the metatarsophalangeal joint, which results in an inflamed and painful bursa (tailor'S bunion).55, 56 The diagnosis is made on the typical appearance:

Rheumatoid arthritis affects the metatarsophalangeal joints symmetrically. In advanced cases, the toes become fixed in the clawed position of extension at the meta­ tarsophalangeal joint and flexion at the proximal inter­ phalangeal joint. Gout is less frequent at the outer toe joints than at the big toe. The acute redness and tenderness should always be differentiated from a march fracture.

The forefoot is broadened and the transverse arch flattened. • The big toe is angled towards the second toe and frequently overlies it. The medial portion of the first metatarsal head is enlarged. • The skin and the bursa over the medial aspect of the first metatarsophalangeal joint are inflamed and thickened. •

Treatment depends on the degree of disability. It is as well to remember that many patients with extreme defor­ mities have no pain at all. Because most of the pain stems from the compression of the enlarged forefoot in too narrow shoes, the primary conservative treatment is

Figure 86.9 joins.

The capsular pattern at the outer four metatarsophalangeal

1 256 SECTION FOURTEEN - THE LOWER LEG, ANKLE AND FOOT

FREIBERG'S OSTEOCHONDRITIS

This is an ischaemic epiphyseal necrosis of the head of the second metatarsal bone, first described by Freiburg in 19 14,63 and later by Kohler.64 Hoskinson65 showed that the third instead of the second metatarsal is involved in about 20% of cases. The disease occurs in adolescence, before the epiphyseal closure of the metatarsal head has been completed.66 The precise aetiology is unknown but it is assumed that the development is precipitated by an abnormally long second metatarsal bone, indirect trauma and changes in bone marrow pressure.67,68 Sometimes the disease is asymptomatic until adulthood, when defor­ mity of the involved metatarsal head and osteoarthrosis supervene and cause symptoms. If the condition itself causes symptoms, examination will show localized arthritis of the second (or third) metatarsophalangeal joint, with local swelling and warmth and limitation of flexion and extension. It takes a month from the onset of pain before the characteristic radiographic changes become visible. Therefore, in its early stages the lesion is difficult to diagnose and a scinti­ graph or MRI image may be needed to distinguish it from a march fracture of the metatarsal shaft.69,7o Spontaneous recovery from this subacute stage takes up to a year. By that time the metatarsal head is perma­ nently enlarged and palpation reveals a prominent ridge at the dorsal aspect of the metatarsal shaft. There is also some painless limitation of flexion and extension. Sometimes, and if no proper prophylactic measures are taken, metatarsalgia caused by the bony enlargement may supervene. Later on, when the patient is 40-50 years old, osteoarthrosis may complicate the picture and the joint becomes fixed in a manner analogous to hallux rigidus. Treatment consists of using orthotic metatarsal plat­ forms to release pressure on the second metatarsal head. If there is limitation of extension, a 'rocker', as in hallux rigidus, can be prescribed. In advanced cases, surgery may be necessary.72

TRAUMATIC ARTHRITIS

Traumatic arthritis at a metatarsophalangeal joint is rare. It can result from a direct blow or from indirect trauma, for instance during a hyperextension move­ ment.73 Recently, hyperplantiflexion injuries to the great toe sustained in beach volleyball players have been described. This injury is referred to as 'sand toe' and may result in significant functional disability.74 Untreated, the capsulitis can continue for months,

whereas one injection with 5 mg of triamcinolone can completely relieve pain within 2 days. OSTEOARTHROSIS

Local injury or a former Freiberg's osteochondritis can cause osteoarthrosis at the metatarsophalangeal joints. Limitation of flexion and extension with a hard end-feel result. Treatment consists of prescribing shoes with hard and thick soles, eventually fitted with a 'rocker' to render extension asymptomatic. NON-CAPSULAR PATTERNS CHRONIC METATARSALGIA

Pain in the plantar aspect of the forefoot is called metatarsalgia. Chronic metatarsalgia affects the middle three toes and arises when the metatarsal heads have to bear a disproportionate amount of the body's weight. AETIOLOGY

Scranton75 differentiates secondary and primary metatarsalgia. In the former , the lesion is the result of structural changes in the joint (e.g. Freiberg's disease, rheumatoid arthritis or gout). The latter occurs if there is any incongruence between load and load-bearing capacity. The aetiology of primary metatarsalgia is as follows. In a normal foot, only one-third of the body weight is borne by the forefoot. The transverse arch and the contraction of the long flexor muscles of the toes distribute the weight between the pads of the toes and the metatarsophalangeal joints. Because of the tautness of the anterior arch, the big toe and the outer toe take most of the weight. When too much weight falls on the forefoot, flattening of the anterior arch and insufficiency of the flexor muscles of the toes results in abnormal pressure on the plantar aspects of the second, third and fourth metatarsophalangeal jointS?6,77 In due course, a local capsulitis develops. This happens in the following conditions: •

•

•

Splay foot: the broadened forefoot, associated with weakness of the intrinsic flexor muscles leads to flattening of the anterior arch and some clawing of the toes. Plantar deformity: the dropped forefoot leads to too much pressure at the plantar aspects of the metatarsophalangeal capsules. High heels: If the shoe has a high heel with an oblique upper surface, the patient will stand on an

CHAPTER 86 - DISORDERS OF THE FOREFOOT AND TOES 1 257

•

•

•

inclined plane, sliding constantly downwards on tne forefoot. Too much weight is imposed on the forefoot, with chronic metatarsalgia as a result. It is not the high heel itself but the oblique upper surface which is the source of the trouble. High heels with a horizontal upper surface do not cause problems and are even beneficial to women with a plantaris deformity of the forefoot. Unfortunately, no such ready-made shoes exist. Pes cavus deformity: a pes cavus deformity is very often accompanied by extreme hyperextension at the metatarsophalangeal joints, caused by shortening of the extensor digitorum muscles together with ineffective intrinsic flexors, holding the toes clawed?S In such cases, the toes do not bear body weight at all and serious metatarsalgia results, with large callosities under the metatarsal heads, together with corns at the dorsal aspects of the interphalangeal joints. Weak flexor muscles: sometimes the short muscles in the sole of the foot are weakened after a long rest in bed during an illness. If too much weight is borne too soon for too long a time, metatarsalgia can result. Dancer's metatarsalgia: a dancer working en pointe may bruise the plantar aspect of the second, third and fourth metatarsophalangeal joints?9 To prevent this, most ballet shoes are fitted with a small semilunar pad, which ensures that the joints are protected and the body weight distributed as widely as possible.

SYMPTOMS AND SIGNS

There is pain at the plantar aspect of the forefoot on standing and walking, relieved by rest. Sometimes a callus will form, which increases the pressure on the metatarsal head and aggravates the irritation. Clinical examination shows pain at the end of dorsiflexion, sometimes at the end of both dorsiflexion and plantiflexion. Tenderness is noted under the metatarsal heads. Although the tenderness is described as being of the metatarsal heads, it is not the articular car­ tilage but the plantar aspect of the metatarsophalangeal joint that is at fault. The difference is important, because irreversible changes never take place and relief of too much weight bearing will always lead to full recovery. TREATMENT

The most important measure is to avoid excessive weight bearing at the forefoot: the high heel must have a hori­ zontal surface. This brings more weight onto the hindfoot than the forefoot and prevents the foot from sliding for­ wards. A support with its thickest part stopping just behind the heads of the metatarsals (metatarsal pad) must

be fitted into the shoe. This ensures that the shafts of the metatarsals bear more weight than the joints themselves. In a splay foot or after a long stay in bed, vigorous strengthening of the short flexor muscles of the toes by exercises is necessary, so that the toes flex properly at each step to take most of the body weight during walking. In long-standing cases, good results can be obtained by a single intra-articular injection of triamcinolone into the joint. Technique: injection. The patient lies supine. The joint is identified at the plantar and dorsal aspect; usually the joint line is more proximal than might be expected. A thin needle is fitted to a syringe filled with 0.5 ml of triamci­ nolone. By pulling at the toe and by moving the proximal phalanx in slight plantar flexion, the joint line becomes accessible to the needle. The needle is thrust downwards, lateral to the long extensor tendon. After 1 cm the tip of the needle is in the joint space and the steroid is injected. Some soreness is to be expected for about 24 hours. Good results follow after 2 days. If preventive measures are also taken, the relief is permanent.

INTERDIGITAL GANGLION

A ganglion arising from a flexor tendon sheath may arise between the toes at the dorsum of the foot. It can cause painful pressure, especially if small shoes are worn.so The diagnosis is obvious when a firm mass appears during standing. An excessive interval is then seen between the two toes and palpation reveals a semisolid tumour. Lying down permits the ganglion to recede. Because the mass is thick and composed of fibrolipomatous material, aspira­ tion often fails. Excision is indicated if problems persist.

PRESSURE ON THE NERVES IN THE FOREFOOT

Symptoms caused by pressure on nerves at the forefoot are very often regarded as metatarsalgia. The differential diagnosis relies on the fact that the patient describes sharp, unexpected and sudden twinges instead of contin­ uous pain during walking or running. During clinical examination, no signs of bruising of the plantar capsule of the metatarsophalangeal joints are discernible. Sometimes the symptoms can be reproduced by local pressure on a nerve. BRUISING OF THE SECOND DIGITAL NERVE

This is a rare condition, which is rather surprising, because the nerve passes forwards on the lateral side of the plantar

1 2 58 SECTION FOURTEEN - THE LOWER LEG, ANKLE AND FOOT

aspect of the first metatarsophalangeal joint, close to the surface and unprotected from external trauma. It can easily be palpated as a thick band, before it bifurcates just distal to the joint, to supply sensation at the adjacent borders of the first and the second toes. If there is repetitive injury, bruising will persist. Consequently, the patient gets sharp twinges during walking. The twinges will be followed by pins and needles and by a constant ache. During clinical examination the symptoms can be reproduced by local pressure on the bruised nerve. Treatment consists of wearing a thick rubber pad under the forefoot for 3-6 months.An alternative is the injection of triamcinolone suspension around the inflamed nerve: a needle is introduced at the dorsum of the foot between the first and second metatarsophalangeal joints and thrust in the direction of the affected area, until it is felt to impinge against the plantar skin, where 1 ml of the suspension is infiltrated. MORTON'S METATARSALGIA

This condition, first described in 1876,81 results from a neuroma at the interdigital nerve between the fourth and fifth toes (exceptionally between the third and fourth toes). The history is characteristic. The patient, usually a middle-aged woman, states that during walking she is suddenly seized by a sharp and unexpected pain at the outer side of the forefoot. She has to stop walking and characteristically take the weight off the foot and remove her shoe to rub and massage the painful area. After some minutes the pain ceases and she can con­ tinue to walk. The frequency of attacks is very difficult to predict, because sometimes there may be several

attacks a day or none during a year. Usually recurrences tend to become more frequent. Between the attacks the patient is unaware of the condition and there are no symptoms at all. Clinical examination is negative in most cases. Sometimes the symptoms can be reproduced by moving the heads of the adjacent metatarsal bones against each other during compression. Recently, ultrasound examina­ tion has been shown to be very sensitive in the detection of web space abnormalities.82,83 The cause was described by Betts in 1940,84 who stated that the painful condition results from a fusiform neuroma, about 1 cm long, of the fourth digital nerve proximal to its point of division.8s When the fibrous swelling is nipped between the adjacent metatarsal heads, or pulled against a swollen transverse ligament,86 sudden 'neuritic' pain results. Treatment consists of relieving the pressure on the neuroma by alternating the alignment of the metatarsal heads. For instance, the head of the fourth bone can be elevated by a small support (Fig. 86.10). This will keep the bones slightly out of line and prevent pressure on the nerve. Steroid infiltration seldom succeeds. When conser­ vative treatment fails, surgical excision of the neuroma may be required.87,88

Figure 86.10

Orthotic device for Morton's metatarsalgia.

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Metatarsal osteotomy versus excision arthroplasty. Clin Orlhop 2000;376:183-194. 63. Freiburg AH. Interaction of the second metatarsal bone. Slirg Gynecol Obslel 191 4;19:191. 64. Kohler A. Typical disease of the second metatarsophalangeal

joint. A,n ] RoentgenoI1923;10:705. 65. Hoskinson J. Freiberg's disease: review of long-term results. Proc R Soc Med 1974;67:10.

66. Ficat RP, Arlet J. Ischemia and Necrosis of Balle. Williams &

Wilkins, Baltimore, 1980.

67. Stanley 0, Betts RP, Rowley DI, Smith TW. Assessment of

etiologic factors in the development of Freibeig's disease. ] Fool Surg 1990;29(5):444--447. 68. Beito SB, Lavery LA. Freiberg's disease and dislocation of the

second metatarsophalangeal joint: etiology and treatment. Clin Podialr Med Surg 1990;7(4):619-631. 69. Manusov EG, Lillegard WA, Raspa RF, Epperly TD. Evaluation

of pediatric foot problems: Part r. The forefoot and the mid foot. Am Fam Phys 1996;54(2) :592-606.

70. Mandell GA, Harcke HT. Scintigraphic manifestations of infrac­

tion of the second metatarsal (Freiberg's disease). ] Nuc/ Med 1987;28(2) :249-251. 71. Helal B, Gibb P. Freiberg's disease: a suggested pattern of

management. Fool Ankle 1 987;8:94-]02.

1 260 SECTION FOURTE EN - THE LOWER L E G, ANKLE AND FOOT

72. Chao KH, Lee CH, Lin LC. Surgery for symptomatic Freiberg's

disease: extraarticul a r dorsal closing-wedge osteotomy in 1 3 patients followed for 2-4 years. A c t a Orthop Scand 1999;70(5):483-486. 73. Clanton TO, Butler JE, Eggert A. Injuries to the metatarso­

phalangeal joints in athletes. Foot Ankle 1986;7(3):162-176. 74. Frey C, Andersen GO, Feder KS. Plantarflexion injury to the metatarsophalangeal joint ('sand toe' ). Foot Ankle Il1 t 1996;17(9):576-581. 75. Scranton rE. Metatarsalgia. } Bone Joint Surg 1980;62A:723. 76. Herschel H, Van Meel PJ. Metatarsalgie. Ned Tijdschr Geneeskd 1982;126(45). 77. Bojsen Moller F, Lamoreux L. Metatarsalgia. Acta Orthop Scand 1979;50:47 1 .

81. Morton TG. Peculiar painful affection of fourth metatarso­

phalangeal articulation. Alii } Med Sci 1 876;71:37. JW, Noakes JB, Kerr D et al. Morton's metatarsalgia: sono­ graphic findings and correlated histopathology. Foot Ankle l i l t

82. Read

1999;20(3):153-161.

83. Oliver TB, Beggs 1. U ltrasound in the assessment of metatars­

algia: a surgical and histological correlation. Clill Radial 1998; 53(4):287-289. 84. Betts LO. Morton's metatarsalgia: neuritis of the fourth digital

nerve. Med J Aust 1940;1:514. U lrich 1, Dick W. Morton's intermetatarsal neuroma: morphology and histological substrate. Food Ankle Jilt

85. Morscher E,

2000;21(7):558-562. 86. Bosley CG, Cairney Pc. The intermetatarsophalangeal bursa. Its

78. Myerson MS, Shereff MJ. The pathological anatomy o f claw and

significance in Morton's metatarsalgia. f Balle Joint Surg

hammer toes. J Bone Joint Surg 1989;71A(1):45-49. 79. Brok AGM. Medische problemen bij ballet en andere dansvor­ men. Gelleeskd Sport 1983;16:135-140. 80. Kulund DN et al. Airplane insulation for flying feet. A thletic

1980;62B:184.

Trainillg "1 979;14(3):144-1 45.

87. Dereymaeker G, Schroven I, Steenwerckx A, Stuer P. Results of

excision of the interdigital nerve in the treatment of Morton's metatarsalgia. Acta Orthop Belg 1996;62(1):22-25. 88. Assmus H. Morton metatarsalgia . Results of surgical treatment in 54 cases. Nervel1arzt 1994;65(4):238-240.

SECTION FIFTEEN

Nerve lesions and entrapment neuropathies in the lower limb SECTION CONTENTS 87. Nerve lesions and entrapment neuropathies of the lower limb Introduction 1265 Sciatic nerve 1265 Lateral cutaneous nerve 1266 Femoral nerve 1267 Saphenous nerve 1267 Common peroneal nerve 1268 Deep peroneal nerve 1269 Superficial peroneal nerve 1269 Tibial nerve Plantar nerves

1269 1270

THIS PAGE INTENTIONALLY LEFT BLANK

CHAPTER CONTENTS Introduction 1265 Sciatic nerve 1265 Lateral cutaneous nerve 1266 Femoral nerve 1267 Saphenous nerve 1267 Common peroneal nerve 1268 Deep peroneal nerve 1269 Superficial peroneal nerve 1269 Tibial nerve 1269 Plantar nerves 1270

Nerve lesions and entrapment neuropathies of the lower limb INTRODUCTION The main symptom of pressure on nerves is paraes­ thesia. Depending on the level of the compression, paraesthesia is accompanied by pain and numbness. The combination of these three symptoms and their interrelation are of importance in localizing the site of compression.} Pressure on the distal spinal cord induces painless pins and needles in both feet, soon followed by numb­ ness, incoordination and abnormal reflexes. This mech­ anism has been discussed in the chapters on cervical and thoracic spine. Pressure on a nerve root causes segmental pain, paraesthesia at the distal aspect of the respective der­ matome and, if the pressure increases, motor and sensory deficit. For detailed descriptions of these pathologies, see the chapters on the lumbar spine. Pressure on the lumbosacral plexus causes little pain but increasing numbness and weakness. For instance, compression of the plexus by a neoplasm does not cause pain in the limbs but only sacral or coccygeal pain. However it does give rise to gross weakness of the muscles of one or both legs and feet. The effects of pressure on the peripheral nerves of leg and foot are discussed in this chapter.

SCIATIC NERVE Neurocompression syndromes of the sciatic nerve are not common. Some believe that the nerve can become com­ pressed between the fibres of the piriformis muscle (the piriformis syndrome2). If the nerve becomes damaged or is chronically irri­ tated, serious deafferentation pain can result and occurs in circumstances in which the sciatic nerve is locally bruised or has undergone damage after local injection of irritating substances.

Continuous and burning pain,

independent of posture, is then felt in the sensory dis­ tribution of the nerve. Local pressure on the nerve can

increase the pain considerably.3-4

1263

1264 SECTION FIFTEEN - NERVE LESIONS

LATERAL CUTANEOUS NERVE Entrapment of the lateral cutaneous femoral nerve is not uncommon and results in meralgia paraesthetica. The lateral cutaneous nerve is sensory only. It origi­ nates at

L2 and runs retroperitoneally to emerge at the

outer edge of the psoas and then crosses the iliacus muscle at the lateral border of the pelvis, which it follows to the anterior superior spine of the ilium. It then passes under the lateral aspect of the inguinal ligament to follow the fibres of the sartorius muscle. Its course and the location as it exits the pelvis are very variable. Aszmann et aJ.5 Investigated its relation to soft-tissue and bony landmarks in the inguinal region through dis­ section of

52 human anatomic specimens and identified

five different types: type A, posterior to the anterior superior iliac spine, across the iliac crest anterior

to

the

anterior

superior

(4%); type

iliac

spine

B,

and

superficial to the origin of the sartorius muscle but within the substance of the inguinal ligament

(27%); type

C, medial to the anterior superior iliac spine, ensheathed in the tendinous origin of the sartorius muscle

(23%);

type D, medial to the origin of the sartorius muscle located in an interval between the tendon of the sartorius muscle and thick fascia of the iliopsoas muscle deep to the inguinal ligament

(26%); and type E, most medial

and embedded in loose connective tissue, deep to the inguinal ligament, overlying the thin fascia of the iliop­ soas muscle and contributing the femoral branch of the genitofemoral

nerve

(20%). Other studies located 10-15 mm medial to the

the nerve most commonly at

anterior superior iliac spine but in some cases it was located as far medially as 46 mm. 6,7 A few centimetres below the anterior superior iliac spine it emerges

Figure 87.1

Course of the lateral cutaneous nerve.

shelf operations for acetabular insufficiencyl° and after the removal of bone from the iliac crest for a graft.ll However, most cases of meralgia

paraesthetica are

idiopathic, although some external causes such as tight trousers, 12 obesity,J3 the use of belts, corsets and trusses, or an overtight bandage round the pelvis14 after an oper­ ation or during pelvic traction can compress the nerve just medial to the anterior superior iliac spine. The symptoms are typical of any lesion of a small peripheral sensory nerve: pain, paraesthesia and numb­ ness, confined to its distribution. The patient typically

through the deep fascia and continues its course subcu­ taneously (Fig.

87.1).

The nerve supplies the anterolateral aspect of the thigh from the upper border of the trochanter to the level of the superior margin of the patella (Fig.

87.2).

The nerve can become trapped at any point along its course, although most cases result from nipping at the inguinal ligament or beyond the fascial tunnel, usually at the

point where the nerve becomes superficial.

Occasionally the symptoms stem from an abnormality in the pelvis, the typical example of which is meralgia during pregnancy (Cyriax:1 pp.

297-298), encountered

between the fourth and seventh months. In this condi­ tion, the symptoms are always unilateral and disappear spontaneously during the pregnancy. They have been ascribed to the pressure of a small fibromyoma against the nerve, close to where it emerges at the lateral border of the psoas. Meralgia paraesthetica has also been reported after pelvic osteotomies for Perthes' disease,B,9

10......-

_ __ _ _ _____ --

-----

Figure 87,2

Area innervated

by

the lateral cutaneous nerve.

CHAPTER 88 - NERVE LESIONS OF THE LOWER LIMB

1265

describes a burning or tingling sensation over the antero­ lateral aspect of the thigh. The edge is well defined and the centre is often completely anaesthetic. Clinical examina­ tion reveals the extent of anaesthesia, which has a clear edge. Tenderness to pressure can sometimes be evoked distal to the anterior superior iliac spine. In some cases, the paraestheSia can be aggravated by tapping the nerve. 15,16 Differentiation of meralgia paraesthetica from a second lumbar root lesion remains the greatest problem in diagnosis 17 and relies on the careful delineation of the paraesthetic area, the degree of numbness and NMR of the lumbar spine. 18 Although the L2 area and the area supplied by the lateral cutaneous nerve correspond well laterally, the second root also contributes to the innerva­ tion of the groin and the inner aspect of the thigh. Furthermore, in L2 root lesions the analgesia is very slight because of the overlap between L2 and L3,

Figure 87.3

Area innervated

by

the anterior cutaneous nerve.

whereas in lesions of the nerve there is almost full anaesthesia, with a clear-cut border. In

10 cm below the inguinal ligament. Local pressure or

external pressure at the fascial tunnel, it is sometimes

friction may cause pins and needles and cutaneous anal­

Treatment depends on the underlying cause.

sufficient to remove the cause. Should this simple action

gesia confined to the anterior aspect of the thigh, with a

fail, infiltration with anaesthetic at the point of contact is

clear-cut

indicated.

towards the centre of the area.

Technique: infiltration. A 10 ml syringe is filled with procaine

0.5% and fitted to a thin needle 5 cm long. A 5 cm below and medial to the anterior

border

and

almost

complete

numbness

Treatment is removal of the external pressure and pro­ caine infiltrations.

point is chosen

superior iliac spine. The needle is inserted and moved upwards along the anterior and medial side of the sar­ torius muscle. A fan-wise infiltration is made here.19 Two to four weekly infiltrations may be necessary. In intractable cases surgery can be considered.20 It should be remembered, however, that in about two­ thirds of cases the symptoms subside spontaneously over

2 years.21,22

SAPHENOUS NERVE The saphenous nerve is the largest cutaneous branch of the femoral nerve. It leaves the subartorial canal about

8-10 cm above the medial condyle of the knee. Some of the branches there provide innervation of the medial aspect of the knee. Another branch follows the sartorius muscle and becomes superficial just below the medial condyle of the tibia.27 It then runs down on the leg to

FEMORAL NERVE

follow the great sapheneous vein over the anterior aspect of the medial malleolus (see Fig.

87.6). Its terri­

tory of distribution is the medial side of the leg, the Although the femoral nerve can be compressed by differ­

medial malleolus and the medial border of the foot28

ent processes in the psoas region, the pelvis and the groin,

(see Fig.

87.5).

neither pain nor paraesthesia ever result.23 The symp­

Traction on the saphenous nerve as it leaves the sub­

toms are a vague numbness in the anterior crural area

sartorial canal may cause oedema, inflammation and thus

and increasing weakness of the psoas and quadriceps

compression29-31 (Fig.

femoris muscles. A new cause of femoral compression

nerve may also occur in

neuropathy has been reported during recent decades -

condyle.32,33 However, the usual site of compression is at

retroperitoneal bleeding resulting from anticoagulant therapy.24-26

the ankle, at the anterior aspect of the medial malleolus.

The anterior cutaneous nerve innervates the skin of the

87.4). Direct compression of the

Saphenous neuralgia is

front of the inner tibial

also

a

well-known

and

common complication after harvesting of great saphe­

front of the thigh as far as the upper border of the

nous vein -for coronary artery bypass grafting. The

patella (Fig.

main symptom is anaesthesia which may persist for a considerable time postoperatively.34-36

87.3). It can be compressed at the point

where it emerges through the fascia of the thigh, some

1266 SECTION FIFTEEN - NERVE LESIONS

2

_..--1'-

5

11'+----1>--1----

3

2

4 ---+--&\ 3 --+---. 6 ------+.\,\\

Figure 87.4 Localization of entrapment along the saphenous nerve: 1, leaving the subsartorial canal; 2, in front of the inner tibial condyle; 3, at the anterior aspect of the medial malleolus.

Paraesthesia over the inner aspect of the ankle and along the medial border of the foot, together with aching

7 --+fi--\-fA.�

Figure 87.6 Sites of compression and localization of infiltration of the superficial peroneal nerve (1), deep peroneal nerve (2), and saphenous nerve (3), the saphenous vein (4) and dorsal artery of the root (5) are also shown, (6) is the tendon of the tibialis anterior and (7) extensor hallucis longus.

and numbness along the subcutaneous border of the tibia, results from either a direct contusion or sustained compression. Combined plantiflexion and eversion of the foot or flexion of the hallux may stretch the nerve and cause sharp neuralgic twinges.37 Procaine infiltrations of the nerve, level with the ankle joint, are often curative. Ten ml of procaine infiltrated each week, over

3 consecutive weeks.

1% is

COMMON PERONEAL NERVE The common peroneal nerve emerges at the upper and lateral aspect of the popliteal fossa, through the fascia between the biceps femoris tendon and the lateral head of the gastrocnemius.38 It follows the biceps to the neck of the fibula where, under a fibrous edge beneath the origin of the peroneus longus, it divides into two branches. The superficial peroneal nerve continues under the peroneus longus, first along the fibula and then between peroneus longus and brevis.39 The deep peroneal nerve winds around the fibular neck and runs through the anterior compartment between the extensor hallucis and tibialis anterior muscles until it traverses the ankle deep to the inferior extensor retinaculum. Compression or elongation of the common peroneal nerve classically occurs where it winds round the lateral aspect of the neck of the fibula.4o Direct compression follows immobilization in an overtight plaster cast, frac­ ture of the neck of the fibula or externally from pressure of the fibular head against a hard surface such as the side of a desk. Elongation is frequent from sitting with the knees bent and the foot in full passive plantiflexi9n and inversion41 or from prolonged squatting.42 Long-standing compression causes atrophy and a drop foot. Slight and

Figure 87.5

Area innervated by the saphenous nerve.

temporary compression or elongation of the nerve leads

CHAPTER 88

-

NERVE LESIONS OF THE LOWER LIMB 1267

to 'neuropraxis' - a neurological deficit that recovers

dorsum of the foot47,48 (Fig.

sponraneously within the course of

pathy from tight boots or shoe straps has been called the

1-2 weeks. Chronic

87.6). Compression neuro­

recurrent entrapment of the common peroneal nerve has

anterior tarsal tunnel syndrome.49,50 A direct blow pro­

recently been described in long-distance runners.43,44

duces the same condition.

There is only slight pain and there is no paraesthesia

The patient complains of aching deep in the medial

during the period of compression. Clinical examination

and dorsal aspect of the foot and pins and needles at the

reveals numbness of the dorsum of the foot and four inner toes, together with weakness of the tibialis anterior, extensor hallucis longus and peroneal muscles, which combine to produce a drop fOOt.45 There is no specific treatment but, in stretch or after moderate compression, spontaneous recovery is the rule. The patient must then be told how to prevent recurrence. In recurrent and transient entrapment, neurolysis of the peroneal nerve as it travels under the sharp fibrous edge of the origin of the peroneus longus can be performed

adjacent borders of the big and second toes (Fig.

87.7).

The symptoms are typically worse on activity and relieved by rest.5 1 Examination demonstrates diminished touch percep­ tion in the web space between the first and second toes. A positive percussion sign (Tinel's sign) is usually found.52 Treatment consists of wearing better boots and three or four weekly procaine infiltrations around the nerve. Surgical intervention is seldom necessary.

and seems to give good results.46 When the condition is caused by the pressure of an overtight plaster or a direct

SUPERFICIAL PERONEAL NERVE

blow, drop foot is usually permanent. The superficial peroneal nerve emerges from the deep fascia at the junction between the middle and lower

DEEP PERONEAL NERVE

thirds of the leg. From this point it runs subcutaneously

Contusion of the terminal branch of the deep peroneal

third of the front of the leg and the dorsum of the foot,

nerve can occur at the anterior aspect of the ankle, where it is relatively unprotected between the tendons of the tib­ ialis anterior and the extensor hallucis longus, or at the

and is sensory only. It supplies the skin of the distal except the adjacent borders of the big and second toes. Entrapment can result from fibrosis after a direct blow53 or surgery for chronic lateral compartment syn­ drome.54 Transient tethering of the nerve during forced inversion and plantiflexion of the foot (ankle sprain) can also result in a momentarily stretch.55,56 The symptoms are pain, tingling and numbness over the dorsum of the whole foot and all the toes. Pressure or percussion (Tinel's sign) at the point of exit causes

\ \ \ \ \ \ 2 \ \ \ \ \ \ I I \ \ \ \ \ \ \ \ \ \ \ I \ I \I v Figure 87.7 Area within which sensory changes may be found in lesions of the deep (1) and superficial (2) peroneal nerves.

neuralgic pain and paraestheSia in the same area.57 Treatment consists of repeated injections with procaine at the site of compression. Should these fail, triamci­ nolone should be substituted. Fasciotomy and neurolysis relieve symptoms in only half of the cases.58,59

TIBIAL NERVE Entrapment of the posterior tibial nerve is most com­ monly seen at the medial aspect of the ankle and the midfoot in the so-called 'tarsal tunnel' .60 The tarsal tunnel is an osteofibrous space bordered by the medial malleolus, the medial aspect of the talus and calcaneus and the flexor retinaculum. It contains the tibialis poste­ rior, the flexor hallucis longus, the flexor digitorum longus and the arteria and posterior tibial nerve61 (Fig.

87.8). Consequently, compression of the posterior

tibial nerve behind the medial melleolus and under the flexor retinaculum has been called the tarsal tunnel syndrome.62,63

1268 SECTION FIFTEEN - NERVE LESIONS

3 ----+--+--l 9----+---\�

�\_-_+_--+-- 2

4 5 Figure 87.9 tibial nerve.

7

Area within which sensory changes may be found in lesions of the

8 6

be reproduced by inflating a pneumatic tourniquet around the affected ankle.75

Figure 87.8 The tarsal tunnel: 1, calcaneus; 2, talus; 3, tibia; 4, tibialis posterior tendon; 5, flexor digitorum longus tendon; 6, flexor hallucis longus tendon; 7, tibial nerve; 8, flexor retinaculum; 9, deltoid ligament.

Treatment is first by correction of the underlying dis­ order. Infiltration with procaine or triamcinolone can be tried. If these measures fail, surgical release of the flexor retinaculum is considered.76 However, the neurophysio­

The causes of compression are a space-occupying lesion (such as a bony exostosis), callus formation64 or an

logical and clinical outcome of surgical decompression is successful in less than half of the operations.77,78

inflamed and enlarged tendon sheath.65 Excessive valgus deformity of the calcaneus with tension across the flexor retinaculum

has

been

blamed.66

Diseases

such

as

PLANTAR NERVE S

rheumatoid arthritis, diabetes or a varicose vein have also been implicated.67-69

These are branches of the posterior tibial nerve, running

Patients with tarsal tunnel syndrome present with

behind the medial aspect of the tuber calcanei, under the

paraesthesia, burning pain and numbness in the plantar

abductor hallucis and quadratus plantae. In valgus defor­

aspect of the foot and the toes7o,71 (Fig.

87.9).

mity of the ankle they can be compressed between the

These symptoms are frequently exacerbated during

sharp calcaneal border and the shoe, to cause pain and

weight bearing, especially when valgus deformity causes

burning sensation in the heel and foot.79 Compression of

the compression.72 Many patients complain of nocturnal

the lateral nerve causes pain and paraesthesia at the outer

symptoms, which has been attributed to venous engorge­

side of the foot, medial nerve compression at the medial

ment because the symptoms disappear when the foot is

side.8o

elevated.

Symptoms can be

reproduced by strong

Treatment is correction of the valgus deformity and

plantiflexion and inversion of the ankles.73 Sometimes

infiltrations with triamcinolone.81 Should these conserva­

Tinel's sign is positive.74 Pain and paraesthesia may also

tive measures fail, surgery can be considered.82

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55. Kernohan I, Levack B, Wilson IN. Entrapment of the superficial

1997;11(3):195-199.

1998;19(11):753-756. 29. Lee BY, Lapointe DG, Madden JL. The adductor canal syn­

drome. Am J Surg 1978;65:465-466. 30. Romanoff ME, Cory PC, Kalenak A, Keyser GC, Marshall W K.

Saphenous nerve entrapment at the adductor canal. Am J Sports Med 1989;17:478-481. 31. Telment TD, Birch NC, Holmes MJ, Birch R, Goddard NJ. Knee

pain and the infrapatellar branch of the saphenous nerve. J R Soc Med 1998;91(11):573-575. 32. Mens JMA. Pseudo-artritis van de knie ten gevolge van com­

pressieneuropathie van de nervus saphenus. Ned Tijdschr Geneeskd 1987;131:1215-1218.

of the lower third of the leg. J R Soc Med 1984;77:72-73. Sports Med 1988;16:165-169.

peroneal nerve,

three

case

reports.

J

Bone

Joint

Surg

1985;67B:172-173. 56. Hayes DW Jr, Mandracchia VI, Webb GE. Nerve injury associ­

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and results of decompression. J Bone Joint Surg 1989;71B: 131-135. 59. Johnston EC, Howell SJ. Tension neuropathy of the superficial

33. Hemler DE, Ward W K, Karstetter KW, Bryant PM. Saphenous

peroneal nerve: associated conditions and results of release.

nerve entrapment caused by pes anserine bursitis mimicking stress fracture of the tibia. Arch Phys Med Rehabil 1991;72(5):

60. Oh SI, Meyer RD. Entrapment neuropathies of the tibial

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61. Heimkes B, Pose 1

P, Stotz S, Wolf K. The proximal and distal tarsal tunnel syndromes: an anatomical study. Int Orthop

ankle position on tarsal tunnel compartment pressure. Foot Ankle lnt 1999;20(11):721-726. 73. Mondelli M,Giannini F, Reale F. Clinical and electrophysio­

1987;11(3):193-196. 62. Lam SJS. Tarsal tunnel syndrome. Lancet 1962;2:1354. 63. Keck C. The tarsal tunnel syndrome. J Bone Joint Surg 1962;

logical findings and follow-up in tarsal tunnel syndrome. Electroencephalogr Clin Neurophysio 1998;109(5):418-425. 74. Hammerschlag WA, Goldner JL, Bassett FH. P osterior tibial

44A:180. 64. Puelo D, Knudsen HA, Sharon SM. Talar exostosis as a cause of

nerve entrapment: a thirty-three year review. Alii Ort/lOp Foot

tarsal tunnel syndrome. JAMA 1987;77:147. 65. Sammarco GJ, Stephens MM. Tarsal tunnel syndrome caused by the flexor digitorum accessorius longus. J Bone Joint Surg

75. Stearn OS, Joyce MT. Tarsal tunnel syndrome: a review of 15

surgical procedures. J Foot Surg 1989;28(4):290-294. P, Kerham W. Tarsal tunnel syndrome. ] Balle Joint Stlrg

76. Kaplan

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67. Baylan SP, Paik SW, Barnert AL, Ko KH, Yu J, PerselJin RH.

cJinkal and neurophysiological results of decompression.

Prevalence of the tarsal tunnel syndrome in rheumatoid arthri­ tis. Rheum Rehab 1981;20(3):148-150. 68. Oloff L, Jacobs AM, Jatte S. Tarsal tunnel sydrome: a manifesta­ tion of systemic disease. J Foot Surg 1985;22:302. 69. Gould N, Alvarez R. Bilateral tarsal tunnel syndrome caused by varicosities. Foot Ankle 1983;3:290. 70. Jackson DC. Tarsal tunnel syndrome in athletes. Am J Sports Med

J R Call Stlrg Edin 1998;43(1):35-36.

1991;1:61-65. 71. Menon J, Dorfman HD, Renbaum J, Friedler S. Tarsal tunnel

78. Turan I, Rivero-Melian C, Guntner P, Rolf C. Tarsal tunnel syn­

drome. Outcome of surgery in longstanding cases. Clin Orthop 1997;343:151-156. 79. Doxey GE. Calcaneal pain: a review of various disorders. J Orthop Sport Phys Ther 1987;9:25-32. 80. Henricson AS, Westlin NE. Chronjc calcaneal pain in athletes:

entrapment of the

calcaneal

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AI1I

J

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1984;12(2):152-154.

syndrome secondary to neurolemoma of the medial plantar nerve. A case report and review of the literature. J Bone Joint

81. Baxter DE, Pfeffer GB, Thigpen M. Chronic heel pain: treatment

Surg 1980;62:301-303.

82. Kenzora JE.

72. Trepman E, Kadel NJ, Chisholm K, Razzano L. Effect of foot and

rationale. Orthop Clin North Am 1989;20:563-569. The painful heel syndrome: an entrapment neuropathy. Bull Joint Dis Orthop lnst 1987;47(2):178-189.

SECTION SIXTEEN

Psychogenic pain

SECTION CONTENTS 88. Psychogenic pain 1275 Introduction 1275 Orthopaedic medicine and psychogenic pain 1275 Clinical examination in psychogenic pain 1277 Diagnosis of psychogenic disorders Treatment of psychogenic disorders

1280 1280

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SEGION CONTENTS Introduction

1275 Orthopaedic medicine and psychogenic pain 1275 Clinical examination in psychogenic pain 1277 1280 Diagnosis of psychogenic disorders Treatment of psychogenic disorders 1280

Psychogenic pain

INTRODUCTION Unless the patient has reasons for 'malingering' - the symptoms are simulated for compensation or litigation motives - pain is always indicative of some degree of dysfunction.' In most instances, the dysfunction is phys­ ical. Sometimes, however, the pain is devoid of any organic basis. If the patient has an unconscious belief in the reality of the symptoms a psychogenic disorder is likely. The pain is then labelled 'inorganic' or 'functional'. There is an emotional illness and, although no peripheral tissue damage exists, the pain is as distressing as is somatic pain. Pain is often the outcome of a combination of physical and psychological causes. It is a highly complex phe­ nomenon: psychological factors affect the way people experience and express pain;2 conversely, chronic pain often results in secondary personal difficulties.3,4 Because pain is an abnormal affective state (though called into being by physical changes in the body), a heightened awareness may increase the severity of the symptoms. The patient may then present with irrational complaints that obscure genuine factors.s The detection of disorders which have their origin in the patient's mind or from the desire to elicit sympathy or compensation is simple if the patient is examined by the methods set out in this book. However, it is more difficult to assess those who present with an organic lesion with psychogenic overlap. Here, much patience and clinical experience will be required to unravel the complicated clinical picture.

ORTHOPAEDIC MEDICINE AND PSYCHOGENIC PAIN IMPORTANCE OF IMMEDIATE DIAGNOSIS After the first attendance it is important to decide whether the patient does or does not have an organic lesion; this may be more difficult in an organic lesion with strong psychogenic overlap but, if the physician is alert, strong suspicion is usually aroused. For the sake of 1273

1274 SECTION SIXTEEN - PSYCHOGENIC PAIN

both patient and physician, psychogenic pain ought to be

should be accepted unconditionally but, conversely, not

detected at once. If active treatment is applied to a patient

every patient with a symptom that differs from the usual

who is dissembling or who is enmeshed in a compensa­

should be regarded as suffering from an imaginary dis­

tion claim, nothing but an allegation of making symp­

order. However bizarre the behaviour of the patient, the

toms worse can be expected. Also, in pain of 'inorganic'

examiner should always face the clinical situation with

origin, the treatment will be completely inefficient and

an open mind that takes note of and registers the state­

endless - the malady does not worsen but it never

ments and findings. The diagnosis is then substantiated

improves either. This is not only extremely discouraging to the physician and therapist but will also worsen the

by the discovery of positive inconsistencies. The most

patient's mental state. Conversely, it is unethical to regard the patient's symp­ toms as being devoid of organic basis simply because a treatment is unsuccessful. The label 'psychogenic pain'

important pitfalls are: • The manner of the patient • The obscurity of the history • The potential bias of the examiner.

can never become an excuse for the physician's failure; it

A patient with chronic pain who has seen several

can only be given at the first interview and before any

practitioners without benefit feels under suspicion or

treatment is instituted.

begins to have self-suspicion and develop the behaviour of a suspect. Strong emphasis on symptoms may occur

IMPORTANCE OF A POSITIVE DIAGNOSIS

with attention-seeking activity so as to convince the physician by exaggeration. However, it is not so much

The diagnosis 'psychogenic pain' should be made on the

the current performance of the patient that may con­

discovery of positive inconsistencies during orthopaedic

vince the physician that there is not an organic lesion

assessment and not as the result of supposition about

but the remarkable sequence of events and the unlikely

possible psychological factors, such as anxiety, depres­

sensations that are described.

sion, stressful life situation or family dissatisfaction. A

The examiner should also eschew the belief that a

pa tient regarded as psychoneurotic can develop a

history or pattern not encountered previously does not

genuine orthopaedic condition in parallel, and concentra­ tion on the psychological problem may distract the exam­

patient's symptoms remain within segmental bound­

iner from the organic cause of the pain. When there is an

aries, the complaints are consistent and the diagnostic

exist: unknown is not the same as inconsistent. If the

organic cause, thorough orthopaedic examination will

movements are the same at each examination, an organic

reveal a simple and consistent pattern that markedly

lesion is very likely. Although the examiner may not be

contrasts with the excessive nervous behaviour of the

able to make a diagnosis it must be obvious that here is a

patient. The mechanofunctional aspects of the body are

genuine, even though unfamiliar, disorder.

well defined and easy to interpret. In pain not of organic

A serious pitfall in the detection of psychogenic

origin, the findings are self-contradictory and, given

disorders is the bias of the examiner towards the

enough opportunity, the patient will sooner or later

patient. The doctor usually has initial sympathy for

demonstrate inconsistencies.

the patient who comes for help. However, dispassionate

To establish that there is not an organic basis for symp­

history and examination are essential. Only then is it

toms is extremely important in order to protect the

possible

patient from endless therapy or repeated surgery.

symptoms are psychogeniC. A great effort is sometimes

to

decide

whether

or

not

the patient's

However, to make an objective distinction between the

required to be completely objective but for the patient's

different types of inorganic pain - whatever names they

sake it is essential. It is even more difficult for a

are given - is extremely difficult and requires further

doctor employed by an insurance company to remain

(psychological) assessment. An orthopaedic physician

unbiased; a detailed clinical approach is vital to

should

beware of using diagnostic labels such as

'hysterical, hypochondriac, regressed'. Because such

establish facts and draw conclusions but is not partisan in a lawsuit (Cyriax:6 p.

454).

classification depends merely on the doctor 's sympathy

Sometimes nothing can be found during clinical exam­

or lack of it, it results in poor communication and engen­

ination. Although the patient has a clear and well-defined

ders negative perceptions of the patient and a sense of

complaint, the functional examination remains com­

pessimism regarding the prognosis.

pletely normal. If nothing can be found to account for pain, the decision that the symptom is psychogeniC should not be taken lightly. It is possible that the

PITFALLS FOR THE EXAMINER

examination has not been sufficiently precise to dete'ct the

The examiner must try to keep a balance between exces­

organic disorder or the lesion is organic but not of orthopaedic origin. After serious internal disorders have

sive scepticism and naIve trust. Not every statement

CHAPTER 88 - PSYCHOGENIC PAIN 1275

been excluded, it is then fair to admit to the patient that one has failed to arrive at a diagnosis.

Sometimes suspicion arises when none of the current and recognizable patterns emerges - the 'inherent likeli­ hoods' (see Ch.

3). The lack of inherent likelihoods

should put the examiner on guard. The patient is then

CLINICAL EXAMINATION IN PSYCHOGENIC PAIN

allowed to go on talking so that contradiction of earlier statements may emerge.

Diagnosis follows the demonstration of positive inconsis­ tencies during both the history and clinical examination. Sometimes the history contributes to the diagnosis, some­ times the examination will be the criterion but usually it is the overall picture - the combination of history and clinical

examination

-

that

is

most

informative.

Inconsistencies may be found between symptoms, between signs and between symptoms and signs.

INSPECTION The patient is observed on entering the room and sitting down. Walking, sitting and undressing may demon­ strate that certain muscles are not paralysed and estab­ lish that a degree of movement exists at the joints of the lower limb. The facial expression should be compared with the degree of alleged suffering. The face of a well-nourished and healthy patient does not correspond

HISTORY

with the contention: 'I haven't had a wink of sleep in

The examiner first listens to the history as related by the patient. Some accounts immediately draw attention to a possible existence of psychogeniC pain or at least to a good deal of over-reaction. The patient describes symp­ toms in a melodramatic way: 'a spear going through my back'; the pain is 'dreadful, torturing, agonizing'. The patient's story is not a clear description of the symptoms but one of intense suffering, increasing disability and of ineffective treatments received? The examiner then asks precise questions, such as when did the pain start; how did it start; where was the pain first; to where did it spread? This technique of que�­ tioning is extremely helpful in defining the psychogemc causes. A patient with a genuine lesion may have difficulties in explaining himself, may be garrulous or apathetic, sullen or rambling, and fail to give a coher�nt account. The invitation to give precise answers to preCIse

�

�

two months'. If a limp is present, it should also be studied. The movement must be analysed and compared with the degree of dysfunction found during functi0r:al examination. Joints behave in a typical way when dIS­ eased and create a characteristic gait. PsychogeniC stiff­ ness results in fixation in completely different positions which are, strange enough, completely opposite: an arthrotic knee causes loss of extension, whereas in psychogenic disorders full extension is present; gro�s arthritis fixes the hip in full lateral rotation, psychogemc disorders in full medial rotation. In serious psychogenic disorders leading to fixation of joints, the 'wrong' joint is often held fixed: 'acute shoulder pain' with the shoulder girdle elevated and the neck flexed towards the pain; 'lumbar pain' with a gross deviation in the thoracic and cervical area.

questions will produce pleasure that at ast a doctor w ll listen with interest and patience. A conSIstent report wlll then almost always be obtained, which quickly suggests the organic nature of the lesion. The response of patients with psychogenic symptoms is in strong contrast: because they do not know exactly what to say and refuse to commit themselves, precise answers are avoided. Pressed to described the exact position of the symptoms they take refuge in very vague but exaggerated state­ ments such as 'whole leg pain', 'whole leg numbness' and 'the whole leg giving way'. No position makes the pain better, or it comes and goes in the most improbable way. There is a tendency to embark quickly on the degree of suffering and the way the pain has influenced social, family or sexual life. When brought back to the point, there is reluctance to supply answers, which may even turn to irritation when the examiner continues with precise questions on the exact position of the pain, its variation and its spread.

tIV�

Practitioner's checklist

Positive inconsistencies during the history:

• The patient's appearance does not fit with the alleged degree of suffering.

.

.

.

• Symptoms occupy an inconsistent area of skin: pain In the whole leg, spreading from the skull, over the scapula to the buttock and the limb, or affecting one half of the body

• The patient cannot describe the localization and radiation of pain, or the pain always has different loca I izations

• The sequence of symptoms, the variation and the

. spread of pain or the development of paraesthesia

�o

not fit 'inherent likelihoods'. (Remember that what IS inconsistent to the examiner is by no means so to the

patient: ridiculous statements can be maintained by the . complainer, despite being functionally or anatomically completely impossible)

1276 SECTION SIXTEEN - PSYCHOGENIC PAIN

FUNCTIONAL EXAMINATION In practice, functional examination is a better procedure

Positive inconsistencies in the functional examination

to confirm or reject the diagnosis of psychogenic pain.

Fixation of the joint in a position opposite to the capsu­

Sometimes a nervous patient suggests a psychogenic

lar pattern. In psychological disorders the hip is fixed in

component but the examination reveals a clear and

medial rotation, the knee in extension and the subIatar

consistent pattern. Conversely a patient who recounts a

joint in varus.

perfect plausible history may show a clinical pattern highly suspicious of psychogeniC pain. There may be inappropriate, 'acting' behaviour:8 the patient twitches or rolls about or rubs the painful area during the examination, in the meantime trying to confirm the degree of suffering by grimaces, sharp intakes of breath, groans and sighs.9 It should be stressed, however, that acting behaviour is not proof of psychogeniC pain. The patient may be so desperate in seeking attention that there is over-reaction. Although the performance may irritate the examiner, it should not alone be sufficient reason to regard the patient as not having an organic lesion.1° Not the behaviour of the patient but the existence of inconsistencies leads to the diagnosis of inorganic pain. The functional examination is started at a joint as far away as possible from the allegedly painful area: if the shoulder is said to hurt, the wrist and elbow are exam­ ined first; in supposed cervical pain, the thoracic spine and lumbar spine are tested first. The patient makes the assumption that, after the time-consuming history, the examiner will immediately start with those movements that usually cause pain and only few will resist the invitation to fake. During an examination performed by the methods described in this book, a patient who is dissembling makes contradictions. A request is made for simple answers (it hurts; it does not hurt) regarding a large series of movements, which makes it difficult for the

Movements hurt at an impossible site. Flexion and extension of the knee provoke pain in the hip; pain in the

back limits movements of the arm. Repeat examination. A completely different pattern emerges during repeat examination. The discrepancy between limitation in one direction and the completely normal movements of its components.

Elevation of the arm is impossible but elevation of the shoulder girdle and scapulohumeral abduction are of full range. Discrepancy

between

the

results

of

the

same

movement carried out in different ways. The patient

presents with straight leg raising grossly limited by pain but can sit up with the legs out straight (Fig.

88.1).

A painful resisted extension of the wrist may prove to be painless if the test is carried out with the wrist in supination (Fig.

88.2).

Discrepancy between what the patient can do and the physical signs. A patient who sits normally must be

able to flex the hip to

90°. Normal heel-to-toe walking

may be observed but resisted dorsiflexion of the foot is apparently weak. Detection of alleged weakness. There are several ways

to detect alleged weakness: • Discrepancy between the bulk of a muscle and weakness

patient to work out quickly which movements might be

during manual testing: as weakness leads to atrophy, a

expected to be painful and which not. Random answers

long-standing dysfunction always results in a

are therefore given, forming a pattern that is not consis­ tent with any one lesion. If the whole examination is repeated, the answers then form a completely different

decrease in muscle bulk. • Weakness in manual testing which is not seen in other

activities: if the patient can move on and off the couch

pattern. Alternatively the patient may state that every

without help, there must be some strength in the

movement is painful. Suspicion also arises when the

flexors of the hip (Fig.

patient defers an answer or asks for the movement to be

may be found to be absent when the same movement

done again, so gaining time to formulate a reply.

is performed in another position: resisted knee flexion is weak with the patient prone but strong in the

Patients without psychogenic pain say straight away that a particular movement hurts whereas another is painless. When the physician suspects a psychogeniC cause,

88.3). Alternatively a weakness

supine position. • 'Cogwheel weakness' is found: the patient, when asked to

perform strong isometric contraction, does not fully

attempts should be made to uncover more and more

cooperate and the examiner can feel that the

inconsistencies, further confirming an inorganic basis.

contraction is actively countered by antagonist

Movements are tested again or in a different way, and

muscle activity. This results in a sequence of

movements not relevant to the alleged site of the pain are

contractions and relaxations, which gives a typical

added to the basic set.

cogwheel sensationY

CHAPTER 88

-

PSYCHOGENIC PAIN 1277

Figure 88.2 Pain on resisted extension of the wrist is a false sign if the test repeated with the wrist in supination is negative.

Figure 88.1 Limitation of straight leg raising by pain can be demonstrated to be false if the patient can sit up with the legs straight.

• Unwillingness to cooperate can sometimes by

demonstrated by active antagonist contractions distal to the tested joint: thus weak dorsiflexion of the foot is

accompanied by visible contractions of the toe flexors (Fig.

VII�

88.4).

I

Practitioner's checklist

LiM

-

Positive inconsistencies in the functional examination:

• Fixation of the joint in a position opposite to the capsular pattern

• Movements hurt at an impossible site • Repeat examination gives a different pattern • Discrepancy between limitation in one direction and normal movements of its components

• Discrepancy between results of the same movement carried out in different ways

• Discrepancy between what the patient can do and the physical signs

• Weakness is demonstrated not to be genuine

Figure 88.3 Weakness on testing the flexors of the hip is not compatible with ability to get off the couch without help.

1278 SECTION SIXTEEN - PSYCHOGENIC PAIN

patient deliberately assumes the symptoms - to deceive, to evade responsibility or to derive gain - the label of 'malingerer' is applied. However, no objective method of differentiation exists and sometimes one label, sometimes another, is used, depending on the examiner's sympathy or the lack of it (see Box

88.1).

The patient who tries to reproduce symptoms or signs of an orthopaedic problem may do so in a number of ways: there may be pretence or perseveration. Pretence is used when the patient fabricates symptoms and signs; perseveration when signs and symptoms, once present, have now ceased to exist but are continued by the patient. Patients who exaggerate their condition are a particu­ lar problem: the symptoms and signs are magnified to represent more than they really are. Again the process may be conscious or unconscious. It is, for instance, quite possible that the patient tries so desperately to convince the examiner of a problem that overemphasis occurs.12 The symptoms and physical signs, though largely correct in quality, are then excessive in quantity. Alternatively, the patient may have psychological prob­ lems but also develops a painful physical condition. In such a case, the pain generates such emotional distress that the consistent clinical pattern is overshadowed by emotional behaviour and excessive excitability. Much time, clinical experience and several repetitions of the examination may then be required to make a proper diagnosis, free from psychogenic overtones.

TREATMENT OF PSYCHOGENIC DISORDERS ORGANIC PAIN WITH PSYCHOGENIC OVERLAY Figure 88.4

In a genuine attempt to dorsiflex the foot against resistance the toes are straight (left) but contraction of the flexors is seen when the patient is uncooperative (right).

DIAGNOSIS OF PSYCHOGENIC DISORDERS The orthopaedic approach to suspected non-physical dis­ orders is pragmatic: two questions need to be answered once clinical assessment is complete: • Is there a genuine physical basis for the disability or not? • If the pain is devoid of any organic basis, is it an

unconscious (psychogenic) or a conscious process? The answer to the first question is easy to ascertain, but the second is difficult because there are no clinical orthopaedic methods to make the distinction. If the patient is regarded as 'sincere' and possessing an uncon­ scious belief in the condition, psychogenic pain is diag­ nosed - the patient is mentally ill. If it is believed that the

Because a real - though minor - pain is present, the organic lesion should be treated first. Often the relief of

Box 88.1 Diagnostic possibilities in apparent psychogenic pain Organic lesion Organic lesion with psychogenic overlay Organic pain in neurotic patients Exaggeration: Conscious (gain) Unconscious

Absence of organic lesion Pure psychogenic pain Neurosis Hysteria Depression Malingering Pretence Perseveration

CHAPTER 88

-

PSYCHOGENIC PAIN 1279

the physical lesion, by depriving the patient of the basis

diagnosis difficult to accept. Some are upset, reject the

of the malady, is curative alone. However, treatment

diagnosis and probably degrade the competence of the

should be adapted to the psychological condition of the

physician. It is therefore better to state the diagnosis and

patient. It is best to carry out the treatment techniques

the reasons for arriving at it in the presence of the patient's

gently and carefully, in order not to provoke too much in

nearest relatives. It is remarkable how many relatives

the way of reactions. Only little should be done at once:

immediately agree that the point of view is correct.

for example one or two manipulative manoeuvres, or

Usually, they have suspected a psychogenic background

should also be warned, preferably in the presence of

but their assumption has never been supported by frank and objective medical statements. Once the relatives

10 instead of 20 minutes of deep friction. The patient

relatives, of a possible temporary increase in pain after

know the situation, they can start to help the patient in a

each treatment session.

positive way or at least provide protection from further useless and endless physical treatment or even surgery.

ABSENCE OF ORGANIC PAIN

Another tactic for the phYSician is to declare, after the patient's confidence has been won by a sympathetic and

Active physical treatment should never be given to

benevolent attitude demonstrated during history and

patients whose pain does not have an organic basis. Not

clinical examination, that an attempt must be made to

only is it useless but, if the patient's emotional pain gets

put matters on the road to recovery. The patient is sent to

worse, the treatment will be blamed for this. In contrast,

the phYSiotherapist who applies daily electrical stimula­

2 weeks. The

it is very difficult to explain to a patient with psychogenic

tion to 'all the affected muscles' over

pain that the complaints are devoid of a physical basis.

demonstration of normal contraction is then accompa­

The most unfortunate form of explanation is a straight­

nied by praise from the therapist who reassures the

forward declaration that there is nothing wrong and that

patient that the muscles and nerves are normal but that

the sufferer is fit to return to normal activities including

there is a block to transmission of the message. The

work. Such a statement only induces an added determi­

treatment, it is then suggested, will be addressed to

nation to prove by more exaggeration that the disability

releasing this block. Thereafter, the patient practises the

is physical. Some method must be found to induce a

hitherto impossible or painful movements. The role of

change in attitude without loss of face, in that there is

the physiotherapist is essential: to be encouraging and

never willingness on the patient's side to admit to him- or

sympathetic and try to establish a good relationship. The

herself to others that the disease is not organic.

expression 'psychogenic pain' should never be used; the

Communication of the absence of physical causes must

lesion from which the patient is suffering is a 'functional

be done with tact, diplomacy and in an understanding

block'. Patients usually accept the diagnosis and such

and sympathetic manner. One possibility is to say that an initial minor disorder, for unknown reasons, has triggered such a change in emotional tone that the latter has started to live its own life, although the original source of pain has now long vanished. In spite of this tactic, most patients find the

supportive treatment, with positive enforcement, is often highly successful. In a series of

107 patients regarded as

suffering from purely psychogenic symptoms (therefore

76 declared them­ 3 weeks' supportive electrical treatment (Cyriax:6 p. 460). compensation cases were excluded)

selves well and returned to work at the end of

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8 McCullogh JA, MacNab I. Sciatica and Chylllopapain, Williams &

The Lumbar Spine and Back Pain, 2nd edn. Pitman Medical, Kent, 1980:265.

Wilkins, Baltimore, 1983:89. 9 Keefe FJ, Hill RW. An objective approach to quantifying pain behaviour and gait patterns in low back pain patients and

2 Melzack R. The Puzzle of Pain. Penguin, Harmondsworth, 1973. 3 Mersky H, Boyd D. Emotional adjustment and chronic pain. Pail1 1978;5:173.

controls. Pain 1985;21:153-161. 10 Leavitt F, Sweet JZ. Characteristics and frequency of malig­

4 Magno G. Chronic low-back pain and depression: an epidemio­

nancy among patients with low back pain. Pnill 1986;25:

logic survey. Acta Psychiatr Scand 1984;70:614-617. 5 Menges LJ. Chronic low-back pain. A medical-psychological report. Soc Sci Med 1983;17:747-753. 6 Cyriax JH. Textbook of Orthopaedic Medicine, vol 1, Diagnosis of Soft Tisslle Lesiol1s, 8th edn. Bailliere Tindall, London, 1982. 7 Leavitt F, Garron DC, D'Angelo CM, McNeill TW. Low back pain in patients with and without demonstrable organic disease. Pain 1979;6:191-200.

357-364. 11

Withrington RW, Wynn Parry CB. Rehabilitation of conversion paralysis. J Bone Joint Surg 1985;67(B):635-637.

12 Roberts AH, Reinhardt L. The behavioural management of cmonic pain. Long-term follow up with comparison groups. Pain 1980;8:151-162.

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Appendix

TEACHING FACILITIES *Tuition in Orthopaedic Medicine is available

from

Orthopaedic Medicine International (OMI). Coordination: Pierre Bisschop Kerkstraat 48 A B-9910 Knesselare Tel: 3293743250 Fax: 329 374 78 12 Mobile: 3247639 76 72 e-mail: pierre.bisschop@sky net.be So far, OMI has developed in the following countries: Belgium,

Luxembourg,

UK,

Germany,

Switzerland,

Norway, Sweden, Denmark, Italy, Brazil, Canada and USA.

'Online courses in Orthopaedic Medicine can also be downloaded from: http://www.orthom.com 1281

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SUBJECT INDEX Note:

Cross-references in italics are either general cross-references, or refer to other subentries within that same main entry (the main entry term is not repeated to save space). Page numbers in italics refer to illustrations/ tables. This index is in letter-by-letter order, whereby spaces and hyphens between words are ignored in the alphabetisation e.g. dural tests precedes dura mater

abdominal aorta anatomy 980 aneurysnl 660, 867 abdominal colic 660 abdominal muscles 589-591, 590, 591 lesions 665-667 oblique 838 strengthening exercises, lumbar instability treatment 842-843 disc stability not affected by 756, 843, 926 abdominal neoplasms 1025 abdominal surgery, traction contraindication 897 abdominal wall 1 6, 589-591 anatomy 589-591 disorders 665-667 see also thoracic cage, disorders muscles see abdominal muscles pain 593 thoracic pain vs 594 referred pain to 6, 655-662 'abduction lurch' 978, 1029 abductor hallucis 1 1 69 abductor pollicis longus tendon 477, 525 infiltration technique 526, 527 mechanical tenovaginitis 524-525 tenosynovitis 524-526, 525 abscess dental 680 epidural 865 ischiorectal 1009 pterygoid muscles 696 retropharyngeal 184 sternoclavicular joint 405 subcutaneous, shoulder 316 subphrenic 659 temporomandibular joint (TMJ) 695 acceleration-deceleration exercises, glenohumeral instability treatment 342-343, 343 acceleration injury see whiplash-associated disorders accessory atlantoaxial ligaments 141 accessory tests 75-76, 76 see also individual allatomical structures

acetabular fossa 973-974 acetabular labrum 974 tears 1037 acetabular notch 973

acetabulum anatomy 973, 973-974, 974 'false' 1 045 Achilles bursa 1 206-1207, 1 207 Achilles bursitis 1206-1207 Achilles tendon anatomy 1 1 66, 1 1 67 deep friction 1 1 87-1190 anterior 1 188-1189, 1 1 89 medial / lateral edges 1 1 88, 1 1 89 pinch grip technique 100, 1 0 1 pronation-supination 100, 1 0 1 results 1 1 90 tenoperiosteal insertion 1 1 89, 1 1 90 high rupture 1 1 84 insertion 1 166, 1 1 67 rupture 52, 1191 conservative treatment 1191 differential diagnosis 1191 examination 71, 1 1 74 healing 52 rising on tiptoe test 1 1 74 surgical repair 1 1 91 treatment 1 1 9 1 weakness d u e t o 1 1 91 steroid injection technique 1 1 87, 1 1 88 Achilles tendoni tis 1 1 86-1190 causes 1 1 86 history and clinical examination 1186-1187 peritendinitis 1 187 prevention 1 1 90 site of lesion 1 186 tendinosis 1 1 87 treatment 1 187-1190 deep friction see Achilles tendon rest, ice and elevation 1187 steroid injection 1 187, 1 1 88 surgery 1187 Achilles tenovaginitis 1 1 90 ankylosing spondylitis 1 1 90 rheumatoid 1 1 90 xanthomatous 1 1 90 acromial impingement syndrome 380 acromial ligament, acromial 'hooks' 350 acromioclavicular joint 277, 280, 280 anatomy 387-388, 388 ankylosing spondylitis 322, 398 ankylosis 398, 407 arthrosis 331 C4 origin 292, 293 capsule 387

dislocations, grades 327-328, 328 extra-articular ligaments 387-388 injury 327 movements 388 osteophytes in elderly 329 overuse 327 rheumatoid arthritis 322 sprains see acromioclavicular sprains stabilization 327 acromioclavicular ligaments 387-388 infiltration 329, 329, 330 acromioclavicular sprains 327-331, 405 deformity due to 330 differential diagnosis 328, 332, 333 functional examination 327 painful arc 327, 360, 380 pain on resisted adduction 360 recurrence 330 symptoms and signs 327-328 treatment 328-330 without displacement 327, 328 acromion 278, 278 changes with rotator cuff disease 350 hooked 281 , 350, 356 metastases 380 normal 356 warning signs in metastases 380 acromioplasty 352 actin 42, 42 active movements functional examination 71, 71 arm 1 57, 157 neck 152, 1 53 scapular 155, 157, 1 5 7 shoulder 295, 296 temporomandibular joint 681 , 681, 682 impairment 81-83, 82 cervical spine 169-170, 1 70, 1 80 in isolation 81-83 with passive movements 81, 169-1 70, 1 70 patterns 81 with resisted movements 81 interpretation 81-83 normal range of joints 114 therapeutic 94, 1 14-115 see also individual joints

acute ischaemic syndrome, upper limb 548 acute lumbar lumbago see lumbago acute thoracic lumbago see thoracic lumbago, acute 1283

1284 INDEX

adductor hallucis 1169 adductor longus muscle anatomy 978 injury, pain 1 026 differential diagnosis 1026 injection 1027-1028, 1028 treatment 1 026-1028 musculotendinous junction, deep friction 1027, 1 027 tenoperiosteal junction, deep friction 1027, 1 027 adductor pollicis muscle, lesions and friction for 536, 537 add uctor reflex test 1025 adhesion(s) after ankle sprains 1220-1221 calcaneocuboid ligament 1220-1221 capsular 55 grade B mobilization 1 04 formation after rest 45, 46 knee intra-articular 1 093 medial collateral ligament, manipulation 1 1 06, 1106-1107, 1 1 07 posttraumatic 1101 ligamentous see l igamentous adhesions muscle 1185 postoperative intra-articulal� grade C mobilization 1 04 prevention by deep transverse friction 95-96, 96 in ligament lesions 53, 56 in overuse tendinous lesions 50 rupture by deep transverse friction 95-96, 96, 96, 98 grade C mobilization 105 manipulation of medial collateral ligament 1 1 06, 1 1 06-1107, 1 1 07 talofibular ligament 1220-1221 tenoperiosteal, rupture by grade C mobilization 105 adhesion-cohesion mechanism 336 Ad nerve fibres 4, 26 adolescents anterior lumbar disc displacement 733, 735, 735 arthritis first metatarsophalangeal joint 1 252-1 253 midtarsal jOints 1240-1241 kyphosis 642 loose bodies in elbow 440 postviral torticollis 1 83 scoliosis 646 adrenal cortex, suppression, corticosteroid side effect 124 adrenaline (epinephrine) anaphylactic reaction to local anaesthetics 121, 122 inhalation 121 Adson's test 550 modified 550 afferent nerve fibres 5

age annulus fibrosus tears see annulus fibrosus articular cartilage changes 41 cervical spine problems 147, 1 76-1 77, 197 facet joint laxity 737, 776 history-taking 64-65 intervertebral joint changes (lumbar) 738, 738 low back pain 734, 734-735, 985 lumbar disc changes see lumbar disc(s) lumbar spine changes see lumbar spine lumbar spine disorders 801-802, 802 nucleus pulposus changes 1 76, 706 rotator cuff tendon degeneration 350 sacroiliac joint changes 957 shoulder pain 292 thoracic wa rning symptoms / signs 636 see also elderly alar ligaments 140 algodystrophy (Si.ideck's atrophy) 538-539, 812 algoneurodystrophic process 313 a lIergic reactions local anaesthesia causing 118-119, 120-121 see also anaphylactic reaction allodynia 26 a-efferen ts 42 AMBRII syndrome 337 amides, anaesthetic 119 aminophylline 121, 122 amplitude of movement 72-73 amyotrophic lateral sclerosis cervical spondylotic myelopathy vs 204 dorsal interosseous muscle weakness 536 T1 nerve root compression vs 191 amyotrophic neuritis see neuralgic amyotrophy anaesthesia, local see local anaesthesia analgesia, cutaneous C7 nerve root compression 1 89 cervical nerve root pain 186 anaphylactic reaction clinical features 120-121, 1 2 1 corticosteroid side effects 125 local anaesthesia 1 20 treatment 121, 1 2 1 , 1 2 2 anatomical snuffbox 477 tenderness 500 anatomy see individual allatomical structu res/reg ions

anconeus 421 anconeus compartment syndrome 452 aneurysm abdominal aorta 660, 867 cerebral, leaking 680 d issecting, of thoracic aorta 656 subclavian artery 546, 548, 548 thoracic aorta 656 aneurysmal bone cyst cervical spine 213 lumbar spine 860 angina pectoris 108 C8 nerve root compression vs 190 pain 16, 656

angiography, thoracic outlet syndrome 551 angle of Louis see Louis, sternal angle ankle jerks see ankle reflex ankle joint 1157-1260 anatomy 1161-1 1 62 chronic problems 1220-1221 clinical examination 1171-1179 history-taking 1 1 71 , 1 1 71-1172 interpretation 1 1 81-1 1 82 differential diagnosis of lesions 1 232-1234 d isorders 1 203-1209, 1203-1239 capsular pattern 1 203, 1 203-1 204, 1 209 differential diagnosis 1 232-1234 non-capsular pattern 1204-1209, 1 209 summary 1 209 dorsiflexion, testing 1174, 1 1 74 see also foot functional examination ligamentous tests 1174-1175, 1 1 75 tests 1174, 1 1 74 see also II nder foot 'giving way' 1227, 1229, 1230 haemarthrosis 1204 immobilizational stiffness 1204 injection / aspiration tecllnique 1204, 1205 instability 1227-1230 differential diagnosis 1230, 1231 functional 1230 insufficiency of anterior talofibular ligament 1 229, 1229-1230, 1230 sclerosing injections 1 228, 1228-1229 treatment 1231 unstable mortice 1 228, 1228-1229 inversion sprains see ankle sprains l igaments see ankle ligaments loose bodies 1 204-1205 differential diagnosis 1205 treatment 1205, 1 206 movements, terminology 1159 muscles and tendons 11 66-1 170 normal movement 1162, 1 1 62, 1 203 osteoarthrosis 1 204 pain anterior / medial, causes 1 233 differential diagnosis 1 233-1234 disorders causing 1 209, 1 232 lateral, causes 1 233 posterior 1208, 1 232 plantiflexion, testing 1174, 1 1 74 resisted eversion 88 rheumatoid conditions 1204 'snapping' 83, 1197 'soccer' 1206 twinges 1204 ankle ligaments 1 163, 1 1 63 anatomy 1163, 1 1 63, 1 1 64 d isorders 1216-1217 see also ankle sprains lateral 1163, 1 1 63 testing 1174, 1 1 75 medial 1163, 1 1 64 testing 1 1 75, 1 1 75 testing 1174-11 75, 1 1 75 see also individllal ligaments

ankle pulse, absence 827

INDEX 1285

ankle reflex (jerk) absence 827-828 bilateral 765 sciatica 765 testing 827-828, 828 ankle sprains 37, 1204, 1206, 1216-1217 early mobilization 52 eversion 1230-1234 diagnosis 1231 mechanism 1230-1231 treatment 1231-1234 grading of severity 1217, 1 2 1 8 haemarthrosis 1219 inversion 1217-1230 adhesions after 1220-1221 chronic 1220 clinical examination 1219, 1220-1221 diagnosis 1219 differential diagnosis 1 222 investigations 1219-1220 ligamentous and tendinous disorders 1217, 1219, 1 2 1 9, 1 222 malleolar fractures with 1217, 1 2 1 8 mechanisms 1 2 1 7, 1217-1218 natural history 1218-1 219 Ottawa rules (X-rays) 1217-1218 plantiflexion affecting site 1217 radiography 1219-1220 sites 1217, 1 2 1 8 treatment 1221-1227 acute stage 1222, 1 223 chronic stage 1223 deep friction 1 224-1226, 1 225, 1 226 early mobilization 1221-1 222 infiltration 1223-1227, 1 224 manipulation contraindications 1 227 manipulation of adherent ligaments 1226-1227, 1 227 subacute stage 1 222-1223, 1 223 warning signs 1219, 1 2 1 9 recurrent varus 1 227-1230 see also ankle, instability varus 1217, 1 2 1 7 see also ankle sprains, inversion ankylosing hyperostosis (Forestier's disease; vertebral hyperostosis) 862-863 clinical examination 817 ankylosing spondylitis Achilles tenovaginitis 1190 acromioclavicular joint 322, 398 anterior longitudinal ligament 670 referred pain from 90 back pain 802 cervical spine 216 injection / infiltration 270, 270-271 manipulation (slow stretching) 268 costotransverse joints 650, 670 costovertebral joints 650, 670 cricoarytenoid joint 216 diagnosis 958 hip 1 000-1001 HLA-B27 association 960 incidence 669, 957-958

inflammatory stage, cervical manipulation contraindication 251 joints involved 958 juvenile 315-316 lumbar pain 801, 805, 861-862, 862 history 807, 862 lumbar spine 861-862 articular vs dural signs 853 diagnosis and features 862 functional examination (standing) 815-816, 8 1 7 warning signs 854 manubriosternal joint 662, 670 natural history 958 New York criteria, modified 958 prognosis 960 radiography 670 sacroiliac joint 669, 670, 957-960 fusion 945 grading of changes 959, 959 natural history 960 treatment 960 sacroilitis 958-960 shoulder 315-316 spinal manipulation contraindication 110 sternoclavicular joint 322, 398 temporomandibular joint 694-695 thoracic spine 669-670 facet joints 670 thorax 669-671 investigations 670 treatment 670--671 ankylosis acromioclavicular joint 398, 407 sternoclavicular joint 398, 407 annulus fibrosus 137 age-related changes 176, 731, 745 lateral tears 176 radial fissures 731, 745 cervical disc displacement acute torticollis 183 traction contraindication 264 see also cervical disc displacement displacement, manipulation indication 109, 877-878 lamellae 705, 706 lumbar disc displacement annular lumbago 746-747, 747, 750 manipulation indication 877-878 nuclear protrusion vs 896, 897 sudden backache 751, 803 treatment 756 lumbar discs 705, 706 posterior bound zone with nucleus, nutrient deficiency 731 anorectal abscess 1009 antalgic gait 949 anterior capsular contracture 324-325 anterior cerebral artery 228, 229 anterior compartment, lower leg 1160, 1 1 60, 1 1 94 tight fascia syndrome 1193-1194, 1 1 94 anterior cruciate ligament 1 057-1058 acute complete rupture, treatment 1122-1123

infiltration 1111, 1 1 1 2 injuries 1100 rehabilitation evaluation 1 1 27 rehabilitation programme 1 1 26 summary 1 1 1 5 mechanical response to load 38 reconstruction, evaluation 1 12 7 sprains 1 1 02, 1111 tears 1110-1111 causes 1110 diagnosis 1111 rehabilitation 1123 treatment 1111, 1122-1123 anterior cutaneous nerve 1265 innervation area 1 265 anterior drawer test anterior talofibular ligament integrity 1179 insufficiency of anterior tibiofibu lar ligament 1 229-1 230, 1 230 knee 1067, 1 068, 1118-1119, 1 1 1 9 shoulder dislocation 338, 340 anterior gapping test 950, 950, 959 anterior horn disorders 83 anterior inferior iliac spine 981 anterior interosseous nerve, forearm 566 compression 568 'anterior knee pain' 1138, 1 153 anterior longitudinal ligament ankylosing spondylitis 90, 670 cervical spine 141, 1 4 1 lumbar spine 7 1 1 , 71 1 , 838 referred pain 597 thoracic spine 583, 583 anterior periostitis (ankle) 1208 anterior sacroiliac ligament 942 anterior scalene muscle 547 anterior serratus see serratus anterior muscle anterior spinal artery, ischaemia 201 anterior superior iliac spines (ASIS) 981 avulsion fracture 1025 anterior syndrome, cervical spondylotic myelopathy 201 anterior talofibular ligament 1163, 1 1 63 insufficiency 1 229, 1 229-1230, 1 230 anterior tarsal tunnel syndrome 1267 anterior tibialis muscle see tibialis anterior anterior tibialis tendinitis 1195 anterior tibial tuberosity 1 058 anterior tibiofibular ligament, insufficiency 1229-1230, 1 230 anterior tibiotalar ligament, sprain 1206 anterolisthesis 1 77 spinal cord narrowing 201 anteroposterior glide, cervical manipulation 259, 259, 261 antibiotics, septic arthritis of shoulder 316 anticoagulants carpal tunnel syndrome and 569 epidural anaesthesia contraindication 907 spinal manipulation contraindication 109-110, 600, 623, 879 cervical spine 251 lumbar spine 879 thoracic spine 600, 623 antihistamines 121, 122

1286 INDEX

anti-inflammatory effects, corticosteroids 122, 125 anti-inv Hammatories 244 anus, paraesthesia 807 anxiety attack, local anaesthetic side effect 120 aorta abdominal see abdominal aorta aneurysm (abdominal) 660, 867 dissecting aneurysm 656 lesions, referred pain to back 867 referred pain from 597, 656, 867 thoracic, aneurysm 656 aortic graft, spinal manipulation contraindication 879 apical ligament 140 apical lung cancer see Pancoast's tumour apical tuberculosis, costocoracoid fascia li mitation 408 aponeurosis erector spinae 713, 713 forearm 421 palmar 480 apophyseal joints see facet joints apophysitis calcaneus 1190-1191 iliac 1029 tibial tuberosity 1137 appendicitis, acu te, referred pain 660 appendix, referred pain fro m 598, 660 apprehension, definition 335 apprehension test midcarpal instability 509 recurrent anterior dislocation of shoulder 337-338, 338 recurrent posterior dislocation of shoulder 338, 339 arachnoid cysts, lumbar spine 865 arachnoiditis, lumbar spine 865 arachnoid membrane 25, 143, 718 arcade of Frohse see radial tunnel (arcade of Frohse) arm discoloration 657 immobilization, arthritis in shoulder after 312 lower, pain due to biceps 448 movements see arm movements oedema 657 pain see arm pain reflexes, testing 1 60-161, 1 61 sensory conduction tests 159, 1 60 weakness cervical spondylotic myelopathy 201 osteophytic root compression 199 arm elevation 157, 1 57, 283 active pain 412 stress fracture of first rib 411 definition 319 functional examination / testing active movements 295, 296 passive movements 295, 296 glenohumeral instability 337 initiation by deltoid muscle 359

limitation active with normal passive elevation 322-324 cervical spine disorders 1 72-173, 218 differential diagnosis 3 1 9 interpretation 1 72-173 painless in mononeuropathy of spinal accessory nerve 544 passive, causes 319-322 passive with normal scapulohumeral abduction 322 passive with scapulohumeral abduction limited 31 9-322 psychogenic 321-322 shoulder disorders 319-324 supraspinatus tendon rupture 359 see also subdeltoid bursitis muscles involved 285, 285, 359 painful arc see painful arc shoulder examination 295-296, 296 supraspinatus tendinitis causing pain 354 see also shoulder, abduction arm movements active 157, 157 cervical nerve root pain 186 elevation see arm elevation examination 1 57, 157-1 61, 1 58 interpretation 169, 1 72-1 73, 1 73 l i mitations 1 72-173 acute torticollis 1 83 elevation see arm elevation painful 1 72 pronation-supination 474 resisted 158, 1 58 flexion 374, 374 horizontal abduction 412, 4 1 2 neurological weakness 173 positive, interpretation 1 73 weakness 1 73 arm pain biceps strain 447 C5 origin 186, 293, 319, 333 causes 293, 294 examination 294 posterocentral cervical disc displacement 196 unilateral cervical root pain 186 arthri tis at first metatarsophalangeal joint in adolescence 1 252-1253 iatrogenic infectious 123 reactive see reactive arthritis rheumatoid see rheumatoid arthritis sacroiliac see sacroiliac joint septic see septic arthritis subacute, at midtarsal joint see under midtarsal joints traumatic see capsulitis; traumatic arthritis arthritis deformans juvenilis see Perthes' disease arthrodesis, spinal 931 arthrography ankle sprains (inversion) 1 220 facet 833 shoulder 301

arthroscopy 80 capsulotomy, traumatic arthritis of shoulder 312 hip joint 995 loose bodies elbow 441 knee 1089 meniscal injuries (knee) 1085 shou Ider 301 arthrosis acromioclavicular joint 331 cervical see cervical spondylosis corticosteroid infiltration 123 elbow 439, 440 facet joints, cervical spine 1 98, 198-199, 1 99, 269-270 fingers 534 at first metatarsophalangeal joint in middle age 1253 midtarsal joints 1246 radioulnar joint, lower / distal 496 scaphoid 504 sternoclavicular jOint 405 temporomandibular joint 692-693 thumb see thumb trapezium-first metacarpal joint 484 wrist 501, 504 see also haemarthrosis; osteoarthrosis articular cartilage 39-41 age-related changes 41 cells 39-40 characteristics 40-41 collagen fibre structure / position 40, 40 composition 39-40 effect of load 40, 40 loss, knee 1079 zones 39, 39-40 see also cartilage articular crepitus 79 articular patterns see individual joints aseptic care, infiltration / injections 117 aseptic necrosis see avascular necrosis aspiration, diagnostic 80 astrocytoma, cervical spine 218 athletes atraumatic osteolysis of distal clavicle (AODC) 331 elbow ligamentous disorders 444 see also sports atlantoaxial area, vertebral artery course 229, 229 atlantoaxial joint 139 anterior subluxation in rheumatoid arthritis 215, 216 fractures and dislocations 212, 215 subacute arth ritis 198 subluxation 215, 216 atlanto-occipital membrane 140 atlas anatomy 1 35-136, 136 dislocations 2 1 2 fractures a n d dislocations 212, 2 1 5 ' atraumatic osteolysis of distal clavicle (AODC) 330-331 atypical facial neuralgia 680

INDEX 1287

at; riculotemporal nerve 678, 678 ausQultation, thoracic outlet syndrome 550 avascu lar necrosis (osteonecrosis/ aseptic necrosis) 125 hip see hip joint, aseptic necrosis humeral head 317 knee, spontaneous 1089 lunate bone see Kienbock's disease midtarsal joints 1 245 scaphoid 500 shoulder 317 differential diagnosis 334 avulsion fractures anterior superior iliac spine 1025 at apophysis of lesser trochanter 1025 greater trochanter 1029 hip, in children 1046-1047 axial ligament 942 see also interosseous ligament axillary artery, pseudoaneurysm 546 axillary crutches, radial nerve lesions 558 axillary nerve 288, 288, 556-557 anatomy 556, 556 posterior cord of brachial plexus 545 d isorders 556-557 innervation 556, 556 palsy 360 differential diagnosis 1 88 axillary pain 361 axis anatomy 136, 136 fractures and dislocations 212, 2 1 5 subaxial subluxation 216 axons 23-24, 24 regeneration 26 Wallerian degeneration 27 'waviness' in peripheral nerves 41 axoplasma 4] 8

Babinski's sign 160, 605 cervical disc displacement 181, 196 cervical spondylotic myelopathy 202 negative/positive reactions 827 testing 827, 827 Babinski-Weill test 234 back flattened 810 'keep your back hollow' 710, 922 positions 922 muscles, stability of disc not increased by 756, 926 pain see backache; low back pain pain referred to 816, 867-868 'physiological position' 921, 922 'sprung' 782 stiffness 669, 776-777 backache age of onset 739 central, shifting pain 66, 66 costs 874-875 definition 699 diagnostic epidural injection 904 diffuse, postural syndrome 777, 777

discodural (lumbar) see low back pain, discodural lumbar see low back pain; lumbar pain onset 65, 66 phenol infiltration 126 posterior facet joint syndrome 109 summary 849 as symptom not diagnosis 700 thoracic see thoracic backache treatments 701 warning signs 851-855 see also low back pain 'backpack injuries', long thoracic nerve 553 back rests, chairs 923, 923 back schools 701 lumbar spinal stenosis treatment 790 postural syndrome treatment 778 principles 902 bacterial infections, deep transverse friction contraindication 98 Baker's cyst, rupture 1184 balance training, rehabilitation after knee instability 1 1 24-1125 ball-and-socket joint, humeroradial 418 ball games, disc lesions 926 bamboo spine 670, 862 Barany's test 234 Barlow's sign 1044 Barlow's test 1 043, 1044, 1 045 basal spinal nucleus, gateway synapse 4, 5 basilar artery 145, 229, 230 basilar ischaemia, cervical manipulation contraindication 251 Batson's plexus 861 bed, correct posture 925, 925 bed rest acute lumbago 750 low back pain increase 752 traction comparison 896 Beevor's sign 609-610, 621 Bell's palsy 680, 681 belt, sacroiliac 962, 963 Bence-Jones proteins 861 bending, forward lateral recess stenosis 793 low back pain 751 l umbar disc pressures 708, 708, 733 nuclear lumbago 747, 748 pelvic rotation 818 posterior movement of nucleus 922, 922 vertebral canal lengthening 715, 715

see also 'flexion' under specific join ts; lumbar spine; thoracic spine bent finger syndrome 776 biceps brachii anatomy 420-421, 421 disorders 447-451 distal i nsertion deep friction 450, 450 infiltration 449, 449 lesion and pain 427 rupture 451 function 286 lesions 87, 371, 372 muscle belly 448, 448

movements due to 421, 422 musculotendinous j unction 421 pain at elbow 448-450 lower arm 448 at mid-arm 447-448 at shoulder 447 painful resisted flexion of elbow 447-451 partial rupture, C6 nerve root compression vs 1 89 sites of lesions 421, 448 strain, pain at mid-ann 447 biceps femoris, anatomy 977, 977, 1 060 biceps jerk, absent 1 6 1 , 188 biceps reflex, testing 160 biceps tendinitis 444 C6 nerve root compression vs 189 lower limb 1145 biceps tendon (lower limb) lesions vs upper tibiofibular joint lesions 1 146 massage 1145, 1 1 46 tendinitis 1145 biceps tendon (upper limb) avulsion/ rupture 451 dislocation 373 lesion at glenoid origin 371-372, 372 treatment 372, 372 lesions 371, 372 long head 286, 420 intra-articular lesion 372 lesion in sulcus 372-373 painful arc 381 as part of rotator cuff 350 rupture 447 snapping 373, 382 tendinitis 360, 381 rupture 373 short head 286, 420 tenoperiosteal junction 421 lesions and treatment 42 1 , 449, 449-450, 450 bicipital radial bursitis 445 bicycling, after knee instabil ity treatment 1 1 25 big toe see toe, big bilaminar zone, temporomandibular joint 676 bile d ucts, referred pain from 597-598, 660 biofeedback, dual channel electromyography 1 1 5 'blackbird's sign' 151, 1 84 bladder diseases, pain referred to back 867 bleeding, into joints 78 see IIlso haemarthrosis bleeding disorders, spinal manipulation contraindication 1 09-1 1 0, 600, 623 blood flow increased, inflammation 44 vertebrobasilar system 230, 230-231 blood pressure, thoracic outlet syndrome 550 blood supply cervical spine 1 45, 1 46, 228, 228-230 hip joint 980, 980

1288 INDEX

blood supply (continued) knee 1060-1061 scaphoid 500, 501 shoulder 288, 288 temporomandibular jOint 678, 678 thoracic spinal cord 584 vertebrobasilar system 228, 228-230 blood vessels, formation during tissue repair 44-45 bone aneursymal cyst see aneurysmal bone cyst disorders, lower leg 1 1 83 formation heterotopic 49, 450 Paget's disease 651 lesions, radiographic diagnosis 113 ligament attachment 37, 38 Pagetoid 651 pain 20, 88, 1 66 resorption atraumatic osteolysis of distal clavicle 331 Paget's disease 651 subchondral 1001 tendon insertion 43, 50 see also tendon(s) bone scans aseptic necrosis of hip 1010 cervical spine lesions 1 62 cervical spine metastases 215 osteitis pubis 1 038 pyogenic osteomyelitis (thoracic) 648 bone-to-bone end-feel 73, 216 bony lesions, pain 88, 166 Bornholm disease, referred pain 658 Bouchard's nodes 534 bowel problems, thoracic spinal cord compression 621 'bowstring' sign 824 brace scoliosis treatment 647, 647 see also bracing and taping brachial biceps see biceps brachii brachiaJis muscle anatomy 420, 42 1 deep friction 450 heterotopic ossification 450 lesions 371, 450-451 brachial neuritis see neuralgic amyotrophy brachial pain cervical manipulation contraindication 251 traction causing 264 brachial plexus 25, 545-553 acute neuropathy see neuralgic amyotrophy acute/subacute neuritis 552 anatomy 545, 545 compression 28 medial branches in thoracic outlet syndrome 547-548 thumb weakness 529 cords 545, 545 disorders 545-553

idiopathic neuropathy see neuralgic amyotrophy innervation 546 lesions, paraesthesia 151 metastases in 546 palsies 546, 546 peripheral nerves 545, 545 plexitis 556 see also neuralgic amyotrophy space-occupying lesions 546 thoracic ou tlet syndrome see thoracic outlet syndrome (TOS) traction palsy, C8 nerve root compression vs 190 traumatic disorders 546 trunks and divisions 545, 545 brachioradialis muscle anatomy 420, 42 1 lesions 451 brachioradialis reflex, testing 160, 1 6 1 bracing and taping golfer'S elbow 468 trial in lumbar segmental instability diagnosis 842 type II tennis elbow 463, 463 see also brace Bragard's test 823 brainstem compression 216 modulation of pain 6 breast cancer 316 breathing, pain on 549, 600 bronchia l carcinoma bilateral weakness of wrist 513 C7 nerve root compression vs 190 cervical extradural tumours 218 referred pain 656 see also Pancoast's tumour bronchitis, referred pain 656 Brown-Sequard syndrome 621 bruxism 681, 695 bupivacaine 119 bursa 41 Achilles 1206-1207, 1 207 corticosteroid infil tra tion 1 23 elbow 425, 426 inflammation 443, 444-445, 445 gluteal see gluteal bursae hip 979 referred pain from 987 under iliotibial tract 1095 ischial 979, 981 lateral tibial condyles 1095 prepatellar 1054 psoas see psoas bu rsa shoulder 282, 282-283 subacromial see subacromial bursa subcoracoid see subcoracoid bursa subdeltoid see subdeltoid bursa synovial 41 trochanteric 979, 1018, 1 0 1 8 bursa i I iopec tinea see psoas bursa bursal crepitus 79 bursitis Achilles 1 206-1207

acute subdeltoid 86 conewise infiltration 117 crepitating 335 deep transverse friction contraindication 98 elbow 443, 444-445, 445 epicondylar and radiohumeral 445 gluteal see gluteal bursitis hip see hip joint. bursitis ischial 1019, 1031 �lee 1 094-1096, 1 096 olecranon 445 patellar 1095 pes anserinus 1095-1096 prepatellar 1095 psoas see psoas bu rsi tis radiohumeral 445 septic elbow 445 hip 1008-1009 subacromial, fanwise infiltration 117 subcoracoid see subcoracoid bursitis subcutaneous 1216 subdeltoid see subdeltoid bursitis trochanteric 1018-1 019 bursoscopy, shoulder 301 burst fractu re, vertebral body 643 buttock 971-1050 claudication 827 clinical examination 985-996 interpretation 997-998 see also Linder hip joint dermatome and myotome 16, 1 6 lesions 1007-1019 straight-leg raising limitation 763, 822 pain see buttock pain referred pain from 986, 987 referred pain to 986, 986, 987 discodural backache 751 'buttock, sign of' 855, 964, 1007, 1 008 characteristics 1008, 1008 disorders with 1007-1010 buttock muscles contraction, testing 829, 829 referred pain from 986 buttock pain 985, 1023 causes 819 non-orthopaedic 986 functional examination 817, 819 history-taking 987-988 psychogenic 1019 sciatica 761 see also gluteal pain buttonhole deformity 534

c calcaneocuboid joint 11 64, 1 1 64, 1 239 calcaneocuboid ligament adherent/ adhesions 1220-1221 manipulation 1226-1227, 1 227 deep friction 1225-1226, 1226 infiltration technique 1224, 1224 sprains 1217

INDEX 1289

calcaneofibular ligament 1 163, 1 1 63 damage during inversion sprains 1217 deep friction 1225, 1226 infiltration technique 1223-1224, 1 224 calcaneonavicular ligament 1 1 63 steroid infiltration in midtarsal strain 1243, 1 244 calcaneus 1162, 1 1 62 apophysitis 1190-1 191 subcutaneous bursitis 1216 subcutaneous nodules 1216 calcification cartilage 41 collateral ligament of elbow 444 corticosteroid side effect 124 pericapsular 124 rotator cuff tendons 350, 352-353 soft tissues, deep transverse friction contraindication 98 tendons 51 calcitonin, lumbar spinal stenosis treatment 790 calcium pyrophosphate crystal deposition see pseudogout calf ache, primary posterolateral displacement of lumbar disc 761 referred pain to 1 184 calf muscles deep venous thrombosis 1184 short 1191-1192 plantar fasciitis 1213 stretching, grade B mobilization 104 weakness 1 1 99 canoeing, disc lesions 926 capillaries, repair of connective tissue 44-45 capitate 474 subluxation 502 capsular (elastic) end-feel 73 capsular inflammation, manipulation contraindication 1 05 capsular pattern passive movement limitation 84

see nlso individllnl joints capsular stretching 1 04 cervical facet joint arthrosis 268 cervical non-discogenic disorders 267-269 heat before 1 04 lateral rotation of shoulder 325, 325 traumatic arthritis of shoulder 308-309, 309 force used 309 sequence and duration 309 technique 308-309 warning 308 capsules (joint) 37-39 acromioclavicular joint 387 deep transverse friction 98 facet joints of lumbar spine 710 glenohumeral jOint 279, 305 see nlso glenohumeral joint grade C mobilization 104 hip see hip joint

immobilization effect on healing 46, 47 inflammation, manipulation contraindication 105 innervation 37 knee 1056-1057 lesions 54-56 forced movement contraindication 55 mobilization effect on healing 47, 47 overstretching, prevention 37 sacroiliac joint 942-943 sensory receptors 36 sternoclavicular joint 281 , 388 stretching see capsular stretdling capsulitis (synovitis) 54, 84 forced movements contraindications 55-56, 56 temporomandibular joint 681 traumatic 55 see aLso traumatic arthritis capsuloligamentous disorders, cervical spine 204, 227 manipulation 268 capsuloligamentous structures 37 caput ulnae syndrome 496 carbolic acid 125 carboxymethylcellulose 125 cardiac arrest, side effects of local anaesthesia 120 cardiac insufficiency, traction contraindication 897 cardiovascular system, side effects of local anaesthesia 120 carotid arteries 228 carpal bones 474, 474 fracture 499, 501 instability see carpal instability subluxation 502-503, 503, 504 manipulation techniques 502-503, 503, 504 see also scaphoid; trapezium; wrist; other

specific bones carpal instability 507 aetiology 507 clinical diagnosis 508, 508-509, 509 epidemiology and classification 507-508 carpal ring concept 508 carpal tunnel anatomy 478, 478-479, 566, 568, 568 median nerve route 478, 568, 570 tendinous structures 478, 478-479 carpal tunnel syndrome 28, 481 aetiology 568-569, 569 clinical features 569-570 diagnostic infi ltration 571 differential diagnosis 571 C6 nerve root compression vs 189 cervical disc lesion vs 571 thoracic outlet syndrome vs 550, 551, 571 full syndrome 568, 569 historical background 568 inspection and examination 570, 570 partial syndrome 568, 569, 572-573 recurrence 569, 572 technical investigations 571

treabnent 571-572, 572 steroid injection 571-572, 572 see nlso median nerve carpometacarpal joints anatomy 476 first see thumb carrying loads, correct posture for 924-925, 925 car seats, position 923-924, 924 cartilage 39-41 calcified 41 characteristics 40-41 destruction, corticosteroid side effect 123 fibrillation, hip osteoarthrosis due to 1001 fibroelastic 40, 41 fragment, subluxation 77-78 hyaline 40 immobilization effect on healing 46, 47 mobilization effect on healing 47, 47 nutrition and water transport 40 plastic deformation 40 see nLso articular cartilage cartilaginous endplate, lumbar disc 704, 705 catecholamines, pain modulation 6 cauda equina anatomy 714 compression massive posterior displacements of disc 733, 734 spinal manipulation complication 112 tumour 865 cauda equina syndrome posterior disc displacement causing 733, 734 spinal manipulation contraindication 1 1 0, 879 surgery 928 causalgia (Sudeck's atrophy) 538-539, 812 central nervous system, side effects of local anaesthesia 1 19-120 central transmission, pain 5-6 cerebral aneurysm, leaking, pain referred to temporomandibular joint 680 cerebral arteries 228 posterior 145 cerebraI cortex depression, side effects of local anaesthesia 119, 120 pain modu lation 6 pain perception 5, 7 stimulation, side effects of local anaesthesia 119-120 cerebral palsy, short plantiflexor muscles 1191-1192 cerebrospinal fluid 24 thoracic neurofibroma 638 cerebrovascular disorders cervical spondylotic myelopathy vs 204 spinal manipulation complication 1 1 2 cervical collars 266, 271 cervical derma tomes 1 0, 11, 1 2 C1 a n d C 2 1 87, 1 97 C3 1 8 7 pain 1 87, 219 C4 and C5 1 88, 292, 293, 327

1290 INDEX

cervical dermatomes (continued) C6 and C7 1 89 C8 1 90 cervical disc(s) 137, 1 37 age-related lesions 1 76 degeneration 1 76 consequences 1 76-1 77 radiography 1 77 functions 138 mushroom phenomenon 200, 200 pain 148, 1 67 displacements/protrusion 1 7, 1 78 protrusion see cervical disc displacement cervical disc displacement 1 77-178 by age group 1 78, 1 78 annular, traction contraindication 264 carpal tunnel syndrome vs 571 cartilaginous 1 77 circular 1 76-177 common syndromes 1 81-192, 1 92 T1 and T2 nerve root compression 190-191 torticollis see torticollis, acu te unilateral pain in neck/ trapezius/ scapular area 1 84-185, 1 85 unilateral root pain see cervical nerve roots; cervical root pain effect on blood flow in vertebral arteries 231 examination and history-taking see under cervical spine examination findings 1 78-181 articu lar symptoms/ signs 1 79-180, 1 80, 250 cord symptoms/ signs 181, 1 81 , 250 dural symptoms 1 78-179, 1 79, 250 interpretation for safe manipulation 250 root symptoms/signs 180-1 81, 1 81 intradural extramedullary tumours vs 2 1 7, 2 1 7 less common syndromes 192-197 central pain in acute torticollis 192 central pain in neck/ trapezius/ scapula 192, 196-197 nuclear 251 acute torticollis 251, 261-262 continuous traction in bed 265 head suspension (traction) indication 263-264 manipulation futility 252 osteophytic root compression vs 1 99, 199-200 pain 1 7, 1 78, 1 84-185, 595, 595, 615 referred to thoracic cage 661 in thoracic region 595 painful arc vs or with 382 partial articular pattern of internal derangement 180, 1 80 posterocentral 1 77, 1 8 1 , 192, 1 96 bilateral root pain with 253 central neck pain 252 continuous traction in bed 265 diagnOSis and differential diagnosis ] 96-197

extrasegmental pain referred to thorax 661 head suspension (traction) 264 history and examination 196 manipulation after whiplash injury 244 manipulation course 261-262, 262-263 manipulation indications 252 rotational manipulation contraindicated 251 spinal cord narrowing 201 symptoms/signs 241 treatment 197 unilateral cervicoscapular pain 252, 261-262 whiplash injury 241 see IIlso discodural interaction; dural pain posterolateral 1 77-178, 1 81 primary/ secondary 1 77-178 root pain with, manipulation futile 252 root pain without neurological deficit 253, 263 segmental pain referred to thorax 661 shoulder pain 292 whiplash injury 241 see IIlso cervical nerve roots; disco radicular interactions prophylaxis 266-267 recurrent 266-267 stabilization by traction 264 reducible and irreducible 253-254, 254 spontaneous recovery 267 stages/evolution 1 78, 1 78 thoracic disc lesion differences 594 thoracic outlet syndrome vs 551 treatment 247-267 collars 266 epidural injection 266 injection at nerve root 265, 266 manipulation see cervical manipulation surgical 267 traction 263-265 see also traction u ntreated, risks 249 whiplash injuries 241 cervical lordosis, age-related change 1 77 cervical manipulation 247-263 arguments against use 248 capsular stretching and 267-269 complications 248 consent for 253-254 contraindications 250-252, 252 controversy 247-248 dangers and risks 248-249 dangers of not manipulating 249 evidence and results 249 futility/ failures 251-252 indications 252-253, 253 nerve root compression 1 9 1 for non-discogenic disorders 267-269 quick vs slow stretching 268, 268 types/ tedmiques 268-269 precautions 249-252 procedure 260-263 assessment of progress 261

courses 261-263 repetitions 261 prognosis and reducibility criteria 253-254, 254 techniques 254-260 anteroposterior glide 259, 259, 261 choice 260-261 circumduction during traction 256, 260 for discogenic disorders 254-260 forced rotation 268, 269 forced side-flexion 269, 269 lateral gliding 259-260, 260, 261 for non-discogenic disorders 268-269, 269 patient position and fixation 254-255, 255 position of assistant/ manipulator 254-256, 255 rotation during traction 257, 257, 258, 260 side flexion during traction 258, 258, 261 straight pull 257, 257, 260, 268 traction with leverage 260, 260, 261 traction wi th see traction warning signs 250 whiplash injury 244 without traction, non-discogenic disorders 268 cervical nerve roots 144-145, 145 anatomy 144-145, 145 C1 lesions 1 61 , 187, 1 93 C2 lesions 1 6 1 , 187, 1 93 shoulder girdle limitations 408 C3 lesions 1 61 , 1 87, 1 93 C4 lesions 1 88, 1 93, 202 acromioclavicu lar joint and 292, 293 pain in thorax 595 shoulder girdle limitations 408 C5 lesions/ compression 1 6 1 , 188, 1 94 differential diagnosis 188-189 medial rotation weakness 371 osteophytic 1 99 osteophytic palsy 188 palsy 324, 360, 368, 373-374, 451, 546 resisted flexion of elbow 373-374 testing 158 traction injury 188 weakness and spasticity 202 weakness of resisted extension of wrist 465-466 C6 lesions 1 61 , 181, 189, 1 94 medial rotation weakness 371 pain 189 palsy 546 palsy and resisted flexion of elbow 374, 451 palsy and weakness on extension of wrist 513 tes tin g 158 weakness of resisted extension of wrist 465-466 weakness of resisted flexion of wrist 468 weakness on resisted elbow extension 374

INDEX 1291

C7 lesions 161, 181, 189-190, 1 94 -arm pain 189, 292 arm weakness 173 elbow extension weakness 189 palsy 324, 363-364, 453, 546 palsy and weakness on extension of wrist 513 palsy and weakness on flexion of wrist 516 testing 158 weakness of resisted extension of wrist 465-466 weakness of resisted flexion of wrist 468 weakness on resisted elbow extension 374 C8 lesions 1 6 1 , 190, 1 95 compression and thumb weakness 529 lower brachial plexus palsy 546 pain 190, 253 palsy and weakness on extension of wrist 513 palsy and weakness on flexion of wrist 516 testing 158 compression by disc protrusion see cervical disc displacement intradural extramedullary tumours 218 by neu roma 200 osteophytic 1 99, 199-200 osteophytic vs disc protrusion 1 99, 199-200 symptoms 1 77, 180-181 by tumour/ metastases 200 derma tomes associated 1 87, 1 88, 1 89, 1 90, 191 injections 265, 266 lesions 145 tennis elbow association 455 neurological deficit by level 1 6 1 pain see cervical root pain parenchymal lesions 145, 250 symptoms/ signs, disc displacement 180-1 81, 1 8 1 syndromes 187-192, 1 93-195 examination and diagnosis 186-187 history and inspection 186 natural history 191 order of frequency 187 recurrence 192 spontaneous cures 191, 267 symptoms/ signs 186, 187 treatment 191-192 cervical neuroma 292 cervical rib compression by, thumb weakness 529 definition 548, 551 detection 551 dorsal interosseous muscle weakness 536 neurocompression by 548 rudimentary 548 T1 nerve root compression vs 191 thoracic outlet syndrome due to 548 see also thoracic outlet syndrome (TOS)

cervical rib syndrome 548 cervical root pain 148 age associated 147 causes 1 85, 185-186 du ration 253 intradural extramedullary tumours 217, 218, 2 1 8 manipulation course 263 futile conditions 251 indications 253 posterolateral development, manjpulation futility 252 scapular pain and 186, 253 spinal manipulation 113 swift progression, marupulation futility 252 symptoms/ signs 186, 1 86 chronology 1 86, 253 treatment, injections 265, 266 unilateral 185-192 manipulation course 263 spontaneous recovery 267 see also cervical nerve roots with neurological deficit, manipulation futility 251 without neurological deficit continuous traction in bed 265 manipulation 253, 263 cervical scoliosis, acute torticollis vs 1 83 cervical spinal canal 142-143 consequences of disc ageing 1 76-177 infections 216-217 narrowing 200-204 mechanisms 201, 201 prevention 204 see also cervical spandylotic myelopathy space-occupying lesions 217, 2 1 7, 218 tumours 2 1 7, 217-218 cervical spinal cord 200 compression 202, 250, 543 spinal manipulation complication 112 spinal manipulation contraindication 110, 251 see also cervical spondylotic myelopathy injuries after motor vehicle accidents 241 paraesthesia due to 151, 543 symptoms/ signs of disc displacement 181, 1 8 1 , 196 cervical spinal nerves, ventral rami, in brachial plexus 545, 545 cervical spine 133-273, 138, 1 38 ageing 147, 1 76-1 77, 197 anatomy 1 35, 135-146 blood supply 145, 1 46, 228, 228-230 bones 135-1 37, 1 36, 1 3 7 intervertebral discs 137, 1 3 7 joints 137-139, 1 38 ligaments 139-142, 1 40, 1 41 muscles 142, 1 42, 1 43 nerve roots 144-145, 1 45 nervous structures 142-144, 1 43, 144 ankylosing spondylitis 216

arthrosis see cervical spondylosis C1 and C2 vertebra 135-136, 136 C3-C7 vertebrae 136, 1 36-137, 1 3 7 C7 vertebra 137, 1 3 7 metastases 190, 215 traction fracture of spinous process 406, 411 capsuloligamentous disorders 204, 227 clinical examination 147-163 interpretation 165-173 technical investigations 16]-]62 false negatives 1 62 see also functional examination/ testing

(below) clinical standards for premanipulative testing 232-233, 249 deformity, cervical manipulation contraindication 251 degenerative changes ] 75, 1 76-1 77 degenerative disorders 197-204 diagnOSiS 197 post-traumatic osteoarthrosis 1 99-200 spondylotic myelopathy see cervical spondylotic myelopathy subacute atlantoaxial arthritis 198 see also cervical spondylosis discogenic lesions see cervical disc displacement disorders with symptoms on shrugging of shoulders 205 facet joints see facet join ts fractures and dislocations 21 ] -212 whiplash injury 241 functional examination 152-16] arm tests 1 57, 157-1 61, 1 58 interpretation ] 69-1 72 manipulation precautions 249-250 scapular movements 155, 157, 1 57 testing reflexes 160, 1 6 1 i n thoracic outlet syndrome 550 see also neck movements history-taking 147-1 51, 1 52, 161, 175 interpretation 1 65-168 marupulation precautions 249-250 hyperflexion injury 239, 241 hypermobility, spinal manipulation contraindication 1 1 0 innervation 145, 1 45 inspection 151-152 intraspinal tumours 2 1 7, 217-218 joints 1 37-139, 1 38 C1 and C2 138, 138 C2 to C7 1 38, 138-139 facet see facet joints lengthening 143 lesions, paraesthesia ('pins and need les') 1 50, 150-1 51, 1 68, 181, 543 ligaments 139-142 injuries, whiplash 241, 244 lower anatomy 1 36, 1 36-137, 1 3 7 fractures 2 1 2 ligaments 1 4 1 , 141-142 metastases 215 manipulation complication 1 1 2

1292 INDEX

cervical spine (continued) mechanical disorders 1 75, 1 75-209 disc displacements 1 77-178 treatment 247-267 see also cervical disc displacement movements 138, 139, 139 facet joints 1 40 see also neck movements non-mechanical disorders 21 1-221 arthritis and ankylosing spondylitis 215-216 cervicoscapular pain in shoulder girdle disorders 219 classification 211 infections 216-217 osseous disorders 211-215, 2 1 5 positive signs on neck examination 218-219 pain 147-150 acute, subacute or chronic 148 disc lesions 1 67 duration 168 early morning 1 68 evolution 148, 167, 1 67 factors influencing 167-168 interpretation 165-168 ligamentous conditions 1 67 localization 148, 1 65-166 multisegmental 149, 1 49, 1 66 onset 148, 1 66, 1 66-167 in pectoral area 150 recurrent 148 referred see below remission 149 on resisted neck movement 204-205 in scapular area 150, 1 50 shifting 167, 1 80-1 81 spreading and expanding 1 67 sudden or gradual 166-167 symptoms associated 168 in upper limb 150 see also cervical root pain; dural pain; headache; neck pain paraesthesia 1 50, 1 50-151, 1 68 interpretation 1 68 referred pain 149, 1 49, 166, 1 66 to elbow 455 to trapezius 412 rheumatoid arthritis 215-216 symptoms of lesions 147-151 current, in history-taking 149-150 thoracic spine differences 593-594 treatment 247-273 discogenic disorders see cervical disc displacement non-discogenic disorders 267-271 tuberculosis 216 tumou rs 212-215 benign 212-213, 2 1 5 malignant 213-215, 2 1 5 metastases 190, 2 1 4, 214-215 primary 212, 213-214 warning signs 212, 2 1 3, 2 1 4 upper anatomy 135-136, 136

arthrosis 187 fractures/ dislocations 212 metastases 214 warning signs 1 65, 170, 1 71, 250 disc displacement 180 intradural extramedullary tumours 218 tumours 212, 2 1 3, 2 1 4 see also warning signs cervical spondylosis (arthrosis; spondylarthrosis) 197-199 at facet joints 1 98, 198-199 manipulation 268 symptoms/signs 197 cervical spondylotic myelopathy 197, 200-204 assessment scale 203 classification (Nurick's) 202-203, 203 diagnosis 202-203 differential diagnosis 203-204, 204 mechanical vs vascular cause 201 natural h istory 203 summary 204 symptoms/ signs 202, 202-203 syndromes 201 treatment 204 see also cervical spinal canal, narrowing cervical sprain see whiplash-associated disorders cervical strain see whiplash-associated disorders cervicobrachial pain, thoracic outlet syndrome 551 cervicoscapular pain 1 84, 1 85, 1 86, 1 92 bilateral, manipulation 252, 262-263 progression, manipulation futility 252 shoulder girdle disorders 219 unilateral, manipulation 252, 261-262 cervicothoracic junction, pain 406 chairs anterior inclination of seat 923, 923 back rest position 923, 923 for correct sitting posture 922-923, 923 lumbar support position 923, 923, 924 Charley Horse 1131 chemical denervation, phenol effect 126 chemical radiculitis, sciatica 759 chemical rhizotomy, postthoracotomy pain 664 chemical sclerosis, postural syndrome treatment 778 chemonucleolysis, lumbar disc lesions 929 chest deformities 642-647 chest pain causes 655, 656, 662 referred to arm 655, 656 see also angina pectoris children acute limitation of supination/extension of elbow 443 acute torticollis 183 disci tis (thoracic) 649 'growing pains' 1 1 83 hip disorders see under hip joint scoliosis 646, 810

chin, forward protrusion 681, 682 chiropraxy 109, 877 historical aspects 1 06 manipulation complications 248 manipulation controversy and 248, 877 neurological complications 112 cholecysti tis, referred pain 660 choledocholithiasis, referred pain 660 chondroca lei nosis hip joint 1001 knee 1 080, 1081 menisci (knee) 1 087 shoulder 316 chondrocytes 39-40 zones 39 chondroitin sulphate 39 chondromalacia patellae 1138, 1 1 43 see also patellofemoral pain syndrome (PFPS) chondrosarcoma cervical spine 214 lumbar spine 860 chondrosternal joints, referred pain 597 Chopart's joint 1164, 1 1 64 chordoma cervical spine 214 lumbar spine 860 sacrococcygeal 964 circle of Willis 145, 228, 229, 230 circulation, lumbar spine examination 827 circumduction, cervical manipulation 256, 260 classification cervical spine, non-mechanical disorders 211 cervical spondylotic myelopathy (Nurick's) 202-203, 203 cubital tunnel syndrome 564 glenohumeral subluxations 32-5 headache 223-224 Kellgren, hip osteoarthrosis 1003 knee sprain 1100, 1 1 00 Lichtman, carpal instability 508 ligamentous lesions 53 lumbar segmental instability 839-840 lumbar spine disorders 739 nystagmus 231, 231-232 scaphoid fracture 500 shoulder arthritis 306, 307 tendinous lesions 50 tennis elbow 455 ulnar nerve entrapment 564 whiplash-associated disorders 240, 240 claudication, buttock 827 claudication pain 1 90 neurogenic vs vascular 789, 789, 793 see also intermittent claudication clavicle anatomy 279, 387 thoracic outlet and 547 displacement 328 distal, atraumatic osteolysis 330-331 infiltration at ligament insertion 332, 332 lesions 332

INDEX 1293

movements 389 pain 403 rotation 393 claw hand 564 claw spurs 736, 736, 738 clay-shoveller's fractures 212, 323 clicks 79 clinical approach 90 clinical diagnosis see diagnosis clinical evaluation 63-80, 8 1 accessory tests 75-76, 76 diagnostic infiltration/aspiration 80 functional testing see functional examination/ testing history-taking 64-69 inspection 69-70 palpation 77-79 preliminary examination 70, 70 spinal manipulation complication avoidance 113 technical investigations 80, 80 clinical features see signs; symptoms clinical trials infiltration for tennis elbow 459 spinal manipulation 110-1 11 C nerve fibres 4, 26 damage, pain 26 coagulopathy, spinal manipulation contraindication 109-11 0 Cobb's angle 645, 646, 646 coccygeal pain 803, 967 referred 968 coccygectomy 969 coccygodynia idiopathic 968 local 968-969 postpartum 968 psychogenic 969 referred 968 treatment 968-969 types 968 coccyx 967-969 anatomy 967 clinical examination, interpretation 955-956 disorders 967-969 steroid infiltration 968-969, 969 tumours 968 'cocktail party syndrome' 777, 804 'cogwheel' phenomenon 79 'cogwheel weakness' 1276 cohesion-adhesion forces 336 cold extremities, assessment 78 cold therapy, acute muscular tears/ strains 48 collagen 34 bundles 35 epineurium 23 fibrils and fibres 34, 36 arrangement in cartilage 40, 40 articular cartilage 40, 40 ligaments 38 loss, tendinosis 51 proteoglycan aggregate interactions 34 structure 34-35

synthesis 34, 35, 35 connective tissue repair 44, 45 healing of ruptured tendons 52 in tendon 43, 43 tensile strength 36 type I 35 type II 35 syntheSiS 39 type III 36 'collar on the Scottie dog's neck' 856, 856 collars, cervical 266, 271 collateral ligaments see individual collateral

ligaments Co lies' fracture 505 carpal tunnel syndrome after 569 mal-united 496 tendon ruptures with 528-529 colon distension 660 lesions, pain referred to back 868 referred pain from 598 columnar concept, Navarro's 507-508 common carotid artery 228, 281 common flexor tendon, sites of lesions 466, 466 common palmar digital nerve, compression 572 common peroneal nerve 1266 branches 1266 compression and entrapment 1266-1267 course 1266 compartments, leg see lower leg compensation claims capsuloligamentous disorders of cervical spine 204 whiplash injuries 241, 242 competition, return to, after knee instability treatment 1125-1126 complex regional pain syndrome 538 computed tomography (CT) bulge in sciatica inadequate for diagnosis 759, 768 carpal tunnel syndrome 571 cervical spine lesions 162 low back pain 700 lumbar spine 834 pyogenic osteomyelitis (thoracic) 648 shoulder 301 temporomandibular joint disorders 684 thoracic neurofibroma 638 thoracic outlet syndrome 551 thoracic spine disorders 610, 612 'concavity compression' 287, 287 concussion headache after 226-227 whiplash-associated disorders after 242-243 congenital dislocation of hip see hip joint, congenital dislocation connective tissue 33-58 cells 33, 35 components 35 extracellular matrix see extracellular matrix (ECM) functions 33

innervation 36-37 irregular types 36, 37 regeneration 44, 95 fibre orientation by deep transverse friction 95 phases 95 regular types 36, 37 remodelling 45, 95 repair, steroids effect 44, 45, 1 22 repair process 44-45 deep transverse friction role 95-96 lack of movement effect 45 stages 43-44, 44, 95 strength, exercise effect 47 structure/composition 33 structures containing 37-43 cartilage 39-41 joint capsules and ligaments 37-39 muscle 42, 42-43 nerves 41, 41 synovial bursa 41 synovial membrane 39 tendons 43, 43 trauma 43-56 immobilization effect on healing 46-47, 47 inflammation 43, 44 mobilization effect on healing 47, 47 repair or regeneration 44 stages of repair 43-44, 44 treatment 47-56 see also ligamentous lesions; muscular lesions; tendinous lesions vascularization 36 conoid ligament 282 anatomy 387 lesion 406 pain 597 sprains 331-332 differential diagnosis 325 consent, patient's, cervical manipulation 253-254 constant-length phenomenon 86, 981 contractile tissues 61, 61-62, 62 functional testing 6 1 , 61-62 contracture after mastectomy 322 anterior capsular 324-325 costocoracoid fascia see costocoracoid fascia Dupuytren's 313, 538 extensor hall ucis longus 1193 ischaemic, thumb 529 Volkmann's 86 contusion deep peroneal nerve 1267 muscular 48, 49 quadriceps muscle 1131 ribs 597 thigh 1131 conus medullaris 714 compression, by tumours 640 convergent pattern lumbar spine movements 8 1 5 neck movements 1 70

1294 INDEX

convergent pattern (continued) pain in arthrosis of cervical facet joints 198, 1 98 convulsions, side effects of local anaesthesia 119, 120 Cooper, ligament of 418, 4 1 9 coordination exercises 115 coracoacromial arch 280, 281 changes with rotator cuff disease 350 coracoacromial ligament 281, 387 coracoacromial roof 281 , 287, 387 coracobrachialis muscle 287 lesions 374 coracoclavicular ligaments 280, 281-282, 327, 332, 387-388 rupture 328 sprains 331-332 differential diagnosis 332, 334 infilh·ation 332, 332 see also conoid ligament; trapezoid ligament coracohumeral ligament 373 coracoid process 278, 278 infiltration at ligament insertion 332, 332 lesions 332 cornua coccygeal 967 sacral, epidural anaesthesia landmark 908, 908-909 coronary ligaments, knee 1 055, 1058, 1 058 injuries 1108-1 110 deep friction 1109-1 110, 1 1 1 0 diagnosis 1 1 08 infiltration 1 1 09-1 110, 1 1 1 0 summary 1 1 1 5 treatment 1 1 09-1 110 medial and lateral 1109-1110, 1 1 1 0 meniscal injuries v s 1108, 1109 sprains 1 086, 1108-1 110 coronoid fossa 418, 419 coronoid process temporomandibular joint 675, 676, 684 ulna 419 corporotransverse ligament 793 cor pulmonale 670 corticospinal tract 82, 84 corticosteroid(s) 121 actions 121 for anaphylactic reaction to local anaesthetics 122 mechanism of action 122 types 121-122, 1 2 2 see also hydrocortisone; steroids corticosteroid infiltration 121-125 agents used 121-122, 1 2 2 contraindications 1 2 6 criteria o f ideal steroid 121 deep transverse friction vs 97 indications 122-123, 125 intrafascicular (peripheral nerves) 124 intrasynovial 122 ligamentous lesions 54 monoarticular steroid-sensitive arthritis of shoulder 314, 3 1 5 overuse tendinous lesions 50-51

side effects general 124--125 local 123-124 two joints 124 weakening of tendons 97 see also triamcinolone infiltration costal angle 586 costochondral joints perichondritis (Tietze's syndrome) 597, 662-663 referred pain 597 costochondritis 597 costoclavicular ligament 281 anatomy 388 costocoracoid fascia 282, 282 anatomy 391 apical tuberculosis affecting 408 con tra ctu re 322 idiopathic 406, 407-408 disorders 407-408 haematoma 408 postradiation therapy effect 408 referred pain 597 shortening 322 tumours 408 costotransverse joints 390 anatomy 586 ankylosing spondylitis 650, 670 arthritis 650 first, sprain 405-406 injections 650 referred pain 597 costotransverse ligament 390 costovertebral joints 581 anatomy 390, 390, 586 ankylosing spondylitis 650, 670 arthri tis 650 referred pain 597 costoxiphoid ligaments 585 coughing arm pain 218 pain exacerbation 150, 600 acute annular lumbago 746 arthri tis of costovertebral/costotransverse joints 650 cervical spine lesions 150, 168, 250 low back pain 804, 804 lumbar spine disorders 804 sacroiliac joint lesion 949 thoracic intraspinal tumours 639 pain in neuralgic amyotrophy 552 counternutation definition 944 sacroiliac joint 943-944, 944, 944 counterpressure, deep transverse friction 100, 1 00 crack, on active movement 83 cracking joints 83 cranial nerve XI see spinal accessory nerve cranial settling 215, 216, 2 1 6 cranial shear test 951 creep deformation 38 ' creeping tendon failure' 359 cremasteric reflex 610

crepita ti ng bu rsi tis 335 crepitus articula r 79 bursal 79 hand and wrist 488 muscular 79 osseous 79 palpation 78-79 scapular elevation 408-409 scapulothoracic 79 shoulder 317 shoulder girdle 1 72 elevation 397, 408-409 'silken' 79 temporomandibular joint 681, 693 tendinous 79 tenosynovitis 51 wrist movements 488, 524 cricoarytenoid joint ankylosing spondylitis 216 rheumatoid arthritis 216 crisp end-feel 74 crossed hands method, thoracic manipulation 627, 627 ' cross-talking' nerve fibres 26 cruciate ligaments 1057-1058 sprains, corticosteroid infiltration 123 see also anterior cruciate ligament; posterior cruciate ligament cruciform ligament 140, 141 crural pain, posterior, sacroiliac arthritis 959 crutches, radial nerve lesions 558 crystal-induced arthritis corticosteroid side effect 124 see also gout; pseudogout crystal synovitis elbow 439 knee 1080 shoulder 316 cubital tunnel 424, 424, 561 , 563, 563 ulnar nerve entrapment 562 cubital tunnel synd rome 562-565 aetiology 563 classification 564 clinical features 562, 563-564 diagnosis 563-564 treatment 564, 565 cubitus valgus 563 cuboid bone relationship to tendons of peronei 1245 rotation 1 245-1246 treatment 1245-1246 'cuff arthropathy' 318 cuneiform-first metatarsal joint 1246 lesions 1246-1248 gout 1248 loose body 1248 osteoarthrosis 1246-1247 cupulae 227 Cushing's syndrome 121 iatrogenic 1 24-- 1 25 cyclist's palsy 536 Cyriax, E., oscillatory techniques 106 Cyriax, J.H. (quotations and views) anaphylactic reaction risk 120

INDEX 1295

axillary nerve disorders 557 bu'tto ck pain 985 causes of low back pain 700 cervical disc displacement 1 77, 178, 192 cervical manipulation advice 254 deep transverse friction 98-99 deep transverse friction and pain relief 95 dennatomes and myotome discrepancies 15-16 directions of lumbar discal tissue 732-733 dural concept 743-746 early mobilization after ankle sprains 1221 end-feel 73 entrapment syndromes 27 epicondylar bursitis 445 examination inadequacy and errors 80 extrasegmental reference of dural pain 1 7 functional instability o f ankle 1230 history-taking 63 impingement syndrome 380 'incomprehensible bursitis' 333 lateral elbow pain examination 560 ligamentous lesion treatment 53 mobility of nerve root sheath 719 mushroom phenomenon 735, 735 myositis ossificans (elbow) 451 myosynovitis 49 painful arc on shoulder elevation 354 pain on passive supination of wrist 512 postural thoracic outlet syndrome 549 principles of treatment 93, 94 procaine use 118 referred pain as error in perception 6-7 referred tenderness 19, 526 rules of referred pain 8 self-perpetuating inflammation 45 shoulder examination 291 shoulder sti ffiless 306 spinal manipulation 106, 108, 109, 876 migraine 225 spondylolisthesis pain 857 tennis elbow types 455 thoracic outlet syndrome 547-548 'transmitted stress' 360 type II tennis elbow 458, 459, 460 cyst aneurysmal bone see aneurysmal bone cyst arachnoid, lumbar 865 Baker's, rupture 1184 intraspinal synovial 865 knee 1094-1096, 1 096 menisci (knee) 1 086-1087, 1096 ovaries 661 popliteal 1096

daily activities, low back pain 802 dancer's heel 1207, 1207-1208 dancer's metatarsalgia 1257 'dashboard injuries' 1113, 1137 de-afferentation pain see neuropathic pain

deep cervical artery 229-230 deep friction see deep transverse friction deep inspiration pain exacerbation 600, 619 rib fracture 663 thoracic lumbago pain 619 thoracic spine examination 601, 602 deep lumbar fascia, injection technique 919, 920 deep peroneal nerve 1266 disorders areas in which sensory changes occur 1 266 contusion and compression neuropathies 1267 infiltration 1 266 sites of compression 1 266 deep radial nerve 424-425, 425, 482 deep transverse friction (deep friction) 94-102 abductor pollicis longus tenosynovitis 524, 525 Achilles tendon see Achilles tendon acromioclavicular sprain 329-330, 331 acute muscular tears/ strains 48 adductor longus injury 1 026-1027, 1 027 adhesion prevention/rupture 95-96, 96 ankle sprains 1223 biceps lesions (muscle belly) 448, 448 biceps tendon (brachii ), distal insertion of 450, 450 biceps tendon (femoris) 1145 brachialis muscle 450 calcaneocuboid ligament 1225-1226, 1226 calcaneofibular ligament 1225, 1 226 cervical non-discogenic disorders 269-270 cervical spine 269-270, 270 chronic muscular tears 49 coccygodynia 968 connective tissue repair 95-96 contraindications 98, 98 coronary ligaments 1 1 09-1 110, 1 1 1 0 corticosteroid infiltration v s 97 diagnostic 96 diaphragmatic lesions 665, 666 dorsal carpal ligaments 506, 506 duration/intensity and frequency 97-98, 99, 102, 1 03 extensor carpi radialis longus/brevis lesions 511, 5 1 1 extensor carpi ulnaris lesions 512, 512 external oblique muscle 667, 667 flexor carpi radialis tendon 514, 5 1 4 flexor carpi ulnaris tendon 515, 515 flexor digitorum profundus tendon 516, 516 gastrocnemius muscle 1 1 85, 1185-1186 golfer'S elbow 468 hamstrings 1145, 1 1 45 hamstring tendons 1031, 1 03 1 iliotibial tract 1028, 1 029 indications 94, 96-98, 98, 1 03 infrapatellar tendon 1134-1135, 1 1 36 infraspinatus tendon 365-366, 366 inverter muscles of foot 1195, 1 1 95

lateral collateral ligament (knee) 11 08, 1 1 08 latissimus dorsi muscle lesions 363, 364 ligament lesions 53 long head of biceps 372-373, 373 malleolus 1 1 98, 1 1 98 medial collateral ligament injuries (knee) 1 1 04-1105, 1 1 05, 1 1 22 midtarsal strain treahnent 1244 before Mill's manipulation 460, 460 for mobilizations/ manipulation 96 mode of action 94-95 muscular contusion treatment 48 pain relief 95, 96 pectoralis major muscle lesions 362-363, 363 peroneal tendons 1198, 1 1 98 popliteus muscle 1147, 1 1 48 posterior thoracic wall 409, 409 pronator teres muscle 454, 454 quadriceps 11 32, 1 132 quadriceps expansion (at patella) 1 1 34, 1 1 36 rectus abdominis muscle 666, 667 rectus femoris tendinitis 1030, 1 030 serratus anterior muscle 412, 4 1 3 sprained intercostal muscle 664-665, 665 sprained ligament treatment 54 steroid injections vs 94 subclavius muscle 413, 4 1 3 subscapularis tendon lesions 369-370, 370 supinator brevis muscle 453, 454 suprapatellar tendon 1133-11 34, 1 1 34 supraspinatus, musculotendinous lesions 358, 358 supraspinatus tendinitis 356-358, 357 talofibular ligament 1224-1225, 1225, 1 225 technique 94, 98-1 02 counterpressure 100, 1 00 direction of friction 98, 1 01 finger/ skin movement avoidance 100-1 01 hand movements 99-100 pain avoidance 102 patient position 99 pinch grip 100, 101 pressure amount 102 pronation-supination 100, 1 0 1 site identification 98 summary 1 02 sweep 1 01 therapist's position 99 to-and-fro- movements 99, 99-100 temporomandibular joint 693, 693 terll1 i s elbow type I 457, 458 type III 463, 464 tenosynovitis 51, 97 tensor fasciae latae 1028 therapeutic 96-98 joint capsules 98 ligaments 97-98 muscle bellies 96-97, 97 musculotendinous junctions 97 tendons 97

1296 INDEX

deep transverse friction (continued) thumb arthrosis 523, 523 tibialis anterior muscle 1193, 1 1 94 tibialis muscle 1 1 95, 1 1 95, 1 1 96 tibialis posterior 1195, 1 1 96 transverse movement 96 traumatic hyperaemja induction 96 triceps muscle ! tendon 452, 452 deep transverse massage, cervical spine 269-270, 270 deep venous thrombosis 1 1 84 deformities grade A mobilization 103 inspection 69 degenerative disease glenohumeral joint 317-318 spine see cervical spine; lumbar spine Dejerine-Klumpke paralysis 546 De Kleyn-Nieuwenhuyse test 234, 235 deltoid area pain 333 pins and needles 557 deltoid Ligament 1 1 62, 1 230 anatomy 1163 eversion sprains 1 230-1 231 infiltration 1231-1 232, 1 234 deltoid muscle antagonists, strength ! propriocepsis training 342 disorders 353 functions 359 innervation 556 lesion in muscle belly 353 pain on resisted abduction of shoulder 353 testing 353, 353 parts 285 shoulder abduction 285, 285, 295, 296 weakness 324 'deltoid of the hip' 978 dens see odontoid process dental abscess 680 dental infections 680 dentate ligaments 143 depigmentation, skin 124 depression 808 inspection 808-8 1 2 de Quervain's disease 524-526 pain and testing 525 tenderness 78, 526 'derangement syndrome' 902 dermatitis, local anaesthesia 120 dermatomes 8, 10-15 arm 12 cervical see cervical derma tomes definition 8, 1 0 foot 1 4 h i p and bu ttock 986, 986 leg 1 3, 1 4, 1 5 lumbar see lumbar dermatomes migration during development 9, 1 0 myotomes discrepancy 15-16 overlap between 10 sacral 11, 1 4, 15 thoracic see thoracic derma tomes dermatomic zones 6

devil's grip, referred pain 658 dexamethasone 124 dextrose-phenol-glycerol lumbar segmental instability treatment 843-844 postural syndrome treatment 778 dextrose prolotherapy 125 thumb arthrosis 522 diabetes mellitus monoarticular steroid-sensitive arthritis 313, 314 neuropathic arthropathy of shoulder 318 pyogenic osteomyelitis (thoracic) 648 d iagnosis deep transverse friction for 96 difficulties 89-91 non-orthopaedic disorders 90 double lesions 90 epidural anaesthesia for see epidural local anaesthesia erroneous confirmation, by spinal manipulation 108 importance of precision 59, 93, 1 1 6 by infiltration o r aspiration 80 interpreta tion of tests 80-91 principles of procedure 60, 60--63 soft tissue lesions 59-92 importance 59 tentative, confirmation by accessory tests 76 warning signs see warning signs diaphragm 588, 588 anatomy 588, 588 contraction 588 deep friction 665, 666 dermatome migration 1 0 irritation, pain 659 lesions 665 referred pain from 597, 598, 659, 659, 665 to shoulder 292 diaphragmatic hernia 659 diaphyseal fractures 1251 diarthrodial joints 139 diazepam, treatment of local anaesthetic side effects 120 differential diagnosis 76 diffuse idiopathic skeletal hyperostosis (DISH) see ankylosing hyperostosis digastric muscle 677 digital flexor tendons localized swelling 51-52 swelling, carpal tunnel lesion 572 digital nerves 566 director cells 33 disability, functional see functional disability disc, intra-a rticular acromioclavicular joint 387 radioulnar joint 473 sternoclavicular joint 388 disc(s) (intervertebral ) ageing 729 cervical discs 1 76 see also lumbar disc(s)

cartilage 706 cervical spine see cervical disc(s) composition 41 disease, terminology 729 innervation of border 744 insensibility, clinical evidence 743 lesions age-related 1 76 cervical see cervical disc displacement lumbar see lumbar disc lesions! displacements progressive compression of nerve roots 29, 29 thoracic see thoracic disc lesions lumbar see lumbar disc(s) nutrition see under lumbar disc(s) protrusion annular see annulus fibrosus manipulation see manipulation (spinal) nuclear see nuclear disc protrusion structure 137 thoracic see thoracic disc(s) discectomy lumbar 929 indications 929-930 percu taneous ! suction 929 disci tis definition 738 lumbar 864 postoperative (thoracic) 649 thoracic 649 discodural backache see low back pain, discodural discodural interaction 1 8 1 assessment before treatment 874 cervical 1 77 acute torticollis 182-183 pain in thoracic region 595 signs 1 80, 250 treatment 247-263 whiplash injury 241, 243 see also cervical disc displacement; dural pain cervicogenic headache 226 history-taking 806 lumbar morning pain 805 pain 800 painful limitation to flexion 818 pain in thoracic region 596 pain mechanism 745 partial articular pattern with 815 position (in spine) 746 postu re effect 804 see also low back pain; lumbago; lumbar pain lumbar segmental instability 840 mechanism 745 pain characteristics 752 mechanism 745 prevention 843, 921-926 recurrence 921 straight-leg raising as indicator 715-716, 748, 749

INDEX 1297

surgery for 928-930 thoracic 594, 595, 616, 618 referred pain 594 see also dural concept; dural pain; dura mater discodural pain see dural pain discogenic disorders see cervical disc displacement; lumbar disc lesions/displacements; thoracic disc lesions discography, lumbar spine 833-834 discoid lateral meniscus (knee) 1082, 1 082 discoradicular interactions 181 assessment before treatment 874 cervical 1 77-1 78, 1 92 diagnosis 250 injections 265, 266 natural history 191 pain evolution 167, 1 85, 1 85-186 pain in thoracic region 595 pain remission 168 posterocentral with bilateral root pain 253 syndromes 1 92 treatment 1 9 1 , 191-192, 247-263 see also cervical disc displacement whiplash injury 241, 243 see also cervical nerve roots; cervical root pain lumbar course of paiJl 804 nerve root fibre disturbances (sciatica) 759 pain in thoracic region 596 see also lumbar disc lesions/displacements; lumbar nerve root(s), pain; sciatica nerve root signs (Ll-S4) 760, 766-767 neurofibroma/schwalilloma vs 2 1 7 signs/symptoms 760 sequence 803, 807 spontaneous recovery 765 surgery for 928-930 thoracic pain 594, 595-596 referred pain 594, 595-596 treatment strategies 769, 769 discoradicular sciatica see sciatica dislocation atlas and axis 212, 2 1 5 defini tion 335 fingers 535 patella 1141-1142 sternoclavicular joint 407 temporomandibular joint 692, 692 see also glenohumeral joint; hip joint; shoulder dissecting aneurysm of thoracic aorta 656 distal radioulnar joint see radioulnar joint, lower/ distal distraction techniques capsular lesions 55 hip osteoarthrosis treatment 1 005-1007 monoarticular steroid-sensitive arthritis of shoulder 314

temporomandibular joint 691 traumatic arthritis of shoulder 309-310, 310 divergent pattern lumbar spine movements 8 1 5 neck movements 1 70 pain in arthrosis of cervical facet joints 198, 1 98 Oix-Hallpike test 234-235 dizziness 227, 233 provocation tests 235, 236 see also vertigo dorsal carpal ligaments 475, 475 deep transverse friction 506, 506 rupture 506 sprains 506, 506 dorsal interosseous muscles foot 1 1 69-11 70, 1 1 70 hand 480, 480 disorders 535-536 friction technique 535-536, 536 functional examination 488, 488 muscle belly lesions 535, 535 pain 535-536 sites of lesions 535 weakness 536 dorsal interosseous tendon, friction technique 535-536, 536 dorsalis pedis artery, feeling pulse 828 dorsal ligaments, wrist see dorsal carpal ligaments dorsal root ganglia 4, 716 dorsaJ scapular nerve 545 dorsiflexion big toe, L4/L5 nerve root test 825, 826 foot/lower limb see foot dorsi flexors, lower leg 1 1 67, 1167-1168, 1 1 93 lesions 1 1 93, 11 93-1194 drawer tests see anterior drawer test; posterior drawer test drop attacks 197 cervical manipulation contraindication 251 drop foot lumbar nerve root compression 764 spinal surgery indication 929 drop hand 559 drugs, pain modulation by reticular formation 6 'drummer boy palsy' 526 50's in vertebrobasilar insufficiency 235 Duchenne-Trendelenburg syndrome 978 duodenal u lcer, referred pain 659, 868 duodenum, referred pain from 597, 659, 659 Dupuytren's contracture 313, 538 dural concept 700, 743-774 definition 743, 745 duality of dural pain mechanism 744, 744-745 evidence 743-744 hypothesis 743-746 natural history of ageing discs 745-746 see also dural pain; dura mater

dural nerves 1 7 discodural interaction diagnosis 250 dural pain 1 7-18, 18, 1 9, 67 active elevation of shoulder 397-398 cervical 595 posterocentral disc displacement 196 chronology 744 deep inspiration a ffecting 600 extrasegmental reference 17, 18 segmental radicu lar pain vs 759, 803 history-taking 67, 600 inflammatory natu re 744-745 lumbar acute l u mbago 733, 733-734, 746-748, 747 L5 protrusion 747 lower back pain 700, 744 mechanical nature 744 mechanism 1 7, 144, 148-149, 585, 71 6 dual 744, 744-745 multisegmental 1 7, 1 8, 1 9, 166, 585, 595 cervical spine 1 79, 250 lumbar spine 745 thoracic spine 585, 595, 616, 618 radicular pain in limb vs 761, 803 referred, in sciatica 761, 803 segmental 17, 148, 166 thoracic 594, 595, 595, 618 tumours causing 637, 638 dural reference definition 1 7 see also dural pain dural sac 714, 791 dural sheath 25, 28, 145 innervation 71 9, 71 9-720 lumbar region 71 8, 718-720, 734 mobility and sensitivity 145, 719-720 pain 145 stretching pain due to 719 see also straight leg raising (SLR) test dural signs/ symptoms 601, 745 articular signs discrepancy 853-854 cervical disc displacement 1 78-179, 1 79 lumbar disc displacement 716, 734 low back pain 753-754 mobility alterations (sign) 759, 759 sciatica 759 segmental pain (symptom) 759 lumbar neurofibroma/ meningioma 865 pain exacerbation on coughing see coughing pain on neck flexion during straight-leg raising 823 see also neck movements; straight leg raising (SLR) test thoracic disc displacement 616-617, 6 1 8 dural sleeve 716, 717, 734 bruised clinical examination 816 epidural anaesthesia for 906 sciatica 761, 906 desensitization 874 referred pain (sciatica) 744, 759, 760 see also dural sheath; dura mater

1298 INDEX

dural tests acute lumbago 748-749 neck flexion 1 79 thoracic spine 601-603 dura mater 1 7-18, 1 8, 36, 143, 1 44, 714-716 ad herent, cervical manipulation contraindication 251 anatomy 584, 714, 714-716 attachments 745 with posterior longitudinal ligament 744 bruising 754-755 clinical examination 816 diagnosiS 778 therapeutic epid ural anaesthesia 904 treatment 757 see also dural sleeve cervicogenic headache referred from 226 compression 406 cervical disc displacement 1 79, 181, 250 referred tenderness 78, 1 79 desensitization 874 effect of pressure on 19 inflammation 754 innervation 144, 1 44, 148, 584, 716 anterior region and sensitivity 716, 716 evidence for dural pain 744 low back pain 700 lumbar region, anatomy 714, 714-716 mobility 1 43-144, 145, 71 5, 715-716 testing by straight leg raising 820-821 pain see dural pain sensitivity 144, 145, 716 clinical evidence 743-744 see also dural concept; dural pain thoracic spine 584, 584

see also elltries begillnillg intradural dysaesthesia 26 dysfunction syndrome see posterior dysfunction syndrome dysphagia, cervical spine tumours 214 dyspnoea 657, 658, 659

eccentric training 115 effleurage, sprained ligament treatment 54, 1222 effusion 78 elastic end-feel 73, 73, 295 elastin 34 elastofibroma, scapula 408 elbow 415-470 anatomy 4] 7-426 bursae 425, 426 joints 4 1 7-418 ligaments 418-419, 4 1 9 muscles a n d tendons 420-423 nerves 424, 424-425 arthrosis 439, 440 biomechanics 419-420 bu rsitis 443, 444-445, 445 capsulitis, forced movement contraindication 55-56

clinical examination 427-433 accessory tests 431, 431-433 history-taking 427-428 inspection 428 interpretation 435 palpation 431 summary 433 crystal synovitis 439 dislocation 444 median nerve damage 567 disorders of contractile structures 447-470 disorders of inert structures 437-446 limitation of movement 437-443 normal range of movement 443-445 extension 419, 420 acute limitation in children 443 end-feel 73 limitation in isolation 440, 440-443 limitations 437-440 muscles involved 286, 286-287, 421, 421 passive 428, 429 resisted see elbow, resisted extension weakness in C7 nerve root com pression 189 extensor muscles 421, 421, 423 see also triceps brachii flexion 419, 420, 421 limitation in isolation 440, 440-443 limitations 437-440 muscles involved 286, 286, 420-421, 421 pain 445 passive 428, 429, 445 resisted see elbow, resisted flexion rest, in traumatic arthritis treatment 438 test, cubital tunnel syndrome 564 flexor muscles 420-421, 421 sites of lesions 466, 466 see also biceps brachii; brachialis muscle fractures 438 full range of movement, disorders with 443-445 functional examination 428-431 passive movements 428 resisted movements 428-430, 430 resisted tests on wrist muscles 430-431, 431 golfer'S see golfer'S elbow gout and pseudogout 439 haemarthrosis 439 l a teral epicondylitis see tennis elbow ligamentous lesions 444 limited range of movement 437-443 capsular pattern 437, 437-440, 464 non-capsular pattern 440, 440-443, 464 see also tennis elbow 'little league' 444 locking 440 loose bodies 439, 440-443, 441 adolescents 440 arthrotic joint in old/middle age 443 cartilaginous fragments 441 manipulative reduction 441-442, 442, 443 normal joint in adulthood 441-443, 442

monoarticular steroid-sensitive arthritis 439 movements 419 examination in shoulder examination 294

see also individual movemellts above/below muscles controlling wrist movements 422, 422-423, 423 neuropathic arthropathy 439 open injuries 440 overextension 419 overuse 439 tennis elbow 455-456, 456 pain 427-428, 438 biceps lesion 448-450 full passive supination 443-444, 444 lateral 452, 464-465, 560 examination 560 in radial tunnel syndrome 560 olecranon bursitis 445 resisted flexion 447-451 passive movements 428, 429 pronation 420, 420 limitation 443 passive 428, 429 pain 444-445, 449 pronator muscles 422, 422 'pulled' ('nursemaid's') 443, 444 referred pain 427 from cervical spine (tennis elbow) 455 resisted extension 158, 298, 299, 374, 429, 430, 451-453 pain 451-452 painful arc with 452 weakness 453 resisted extension of wrist and see tennis elbow resisted flexion 158, 1 59, 298, 299, 371-374, 374, 429, 430 biceps lesions 447-450 brachialis muscle lesions 450-451 brachioradialis muscle lesions 451 pain 371-373, 447-451 painless weakness 373-374 weakness 451 resisted flexion of wrist 466, 466-468 see also golfer'S elbow resisted pronation 429-430, 430, 467 pain 454 resisted supination 430, 430, 453-454 in extension 432 pain 453-454 rheumatoid arthritis 439 septic arthritis 440 supination 420, 420, 421 acute limitation in children 443 passive 428, 429 pain 443-444, 444 resisted see elbow, resisted supination supinator muscles 422, 422 swelling 428, 438 tennis see tennis elbow traumatic arthritis 437-438, 438 valgus instability 444 valgus position (physiological) 419, 419

INDEX 1299

valgus/ varus stress 444 elderly acromioclavicular joint osteophytes 329 anterior erosion of thoracic spine 645, 645 benign positional paroxysmal vertigo 235, 236 cervical disc displacement 1 78 cervical manipulation 261 lateral recess stenosis 649, 793-794, 802 loose bodies in elbow 443 morning headache 147, 197-198, 226 manipulation 268 pain after spinal manipulation 111-112 posterocentral cervical disc displacement 196 postural thoracic outlet syndrome 549 sciatica see sciatica septic arthritis of shoulder 316 spondylosis, painful lirnitation of lumbar spine extension 816 spontaneous haemarthrosis of knee 1081 supraspinatus tendon rupture 359, 360 electrical stimulation chronic muscular tears treatment 49 rehabilitation after knee instability 1 1 24 tennis leg treatment 1 185-1186 therapeutic 115 electrodiagnosis, lumbar spine disorders 834 electromyography carpal tunnel syndrome 571 cervical spine lesions 162 lumbar spine disorders 834 patellofemoral pain 1139 sacrospinalis muscle in sustained traction 896 thoracic outlet syndrome 551 embryogenesis 9 abdominal organs 16 nociceptive mechanism for referred pain 8-10 emotional experience of pain 5, 67 emphysema, mediastinal 658 empty end-feel 74, 216, 319 end-feel 68, 73 bone-to-bone 73, 216 bony block, passive movement limitation 84 elastic 73, 73, 295 empty 74, 216, 319 hard 55, 73, 73 pain relationship 74, 74 palpation 79 pathological 73, 73-74 physiological 73 soft 73, 73 spinal manipulation 107, 113 unilateral pain in neck/ trapezius 184 endocrine d isorders, carpal tunnel syndrome due to 569 endocrine system, corticosteroid side effects 124-125 endometriosis 867 endomysium 42 endoneurium 25

endothelial cells, inflammation 44 entrapment neuropathies 26, 68 lower linlb 1261-1270 upper limb 28, 541-578

see also individual nerves entrapment phenomena clinical features 26-27 long-duration, effects 27 peripheral nerves 28 syndromes 27-30 eosinophilic granuloma cervical spine 213 lumbar spine 859-860 ependymoma, cervical spine 218 epicondylar bursitis 445 epidemic myalgia, referred pain 658 epidural abscesses, lumbar 865 epidural haematoma, lumbar 865 epidural local anaesthesia 903-914 acute lumbago 757, 806, 904 aim 903 caudal, sciatica 770 cervical disc displacement 266 diagnostic 903 indications 903-904 lumbar disc lesions 832-833 sacroiliac joint lesions 953 failure 915, 915 follow-up 913 intervals between 913 intrasacral 903 low back pain 904-905 lumbago (hyperacute) 904 lumbar spine disorders 903-914 lumbar spine examination 832-833 mechanism of action 903, 913-914 separation hypothesis 913-914 results 914 sciatica 769-770, 903, 905-907 side effects and dangers 907-908 structures penetrated 903 technique 908, 908-913 after care 912-913 landmarks 908, 908-909 misplaced needle 9 1 1 , 911-912 needle introduction 909-911, 910 preparation 909, 9 1 0 procaine injection 9 1 1 , 911-912, 9 1 2 therapeutic contraindications 907 indications 904-907, 907 epidural space, anatomy 721 epigastric pain 636 epimysium 42 epinephrine see adrenaline (epinephrine) epineurium 23, 25, 41 nerve root 720 epiphysiolysis 1046 epitendineum see tendon sheath equilibrium disturbances 232 examination 233-234 equinus deformity, cerebral palsy 1191 Erb-Duchenne's paralysis 546 erector spinae 713, 713 aponeurosis 713, 713

lumbar 838 strengthening exercises 842 see also sacrospinalis muscle ergonomics 921 correct sitting position 922-923, 923 correct standing posture 924, 925 erythrocyte sedimentation rate pyogenic osteomyelitis 648 septic arthritis of shoulder 316 temporomandibular joint disorders 684 ever tors, foot see foot evolution, spine 703-704 Ewing's sarcoma, cervical spine 214 examination 63-80 interpretation 80-91 see also functional examination / testing preliminary 70, 70 see also clinical evaluation exercise(s) extension of spine under passive traction 926, 926 harmful for lumbar discs 843, 926 lumbar segmental instability treatment 842, 843 to prevent lumber spine disorders 756, 843, 926, 926 rehabilitation after knee instability treatment 1124, 1 1 25 retrain co-contraction of transversus abdominis and multifidus 843 temporomandibular joint 691-692 thoracic outlet syndrome treatment 551-552 expanding lesions, pain 66, 66 expanding pain 66, 66 cervical spine 1 67 lumbar spine 852 extension exercise, of spine under passive traction 926, 926 extensor carpi rad ialis brevis anatomy 422, 422, 510 infiltration of muscle belly 463-464, 466 lesions 510-511 infiltration and deep friction methods 511, 5 1 1 referred pain 427 tennis elbow 456, 463-464 overuse i n tennis elbow 455 stretching by Mill's manipulation 459-461, 460, 461 tendon 477 tenoperiosteal lesion 464-465 extensor carpi radialis longus anatomy 422, 422, 5 1 0 lesions 510-511 infiltration and deep friction methods 511, 5 1 1 tennis elbow 456 tendon 477 extensor carpi ulnaris muscle anatomy 423 disorders 512 isometric contraction 524-525 lesion 465, 466

1300 INDEX

extensor carpi ulnaris tendon 478 anatomy 511 lesions 511-512 deep friction and infiltration 512, 512 posttraumatic rupture of subsheath 51 2 sheath 474 tenosynovitis 496-497 extensor carpi ulnaris tenosynovitis, mechanical vs rheumatic 5 1 2 extensor digiti minimi tendon 478, 496, 496 extensor digitorum communis, anatomy 423 extensor digitorum longus anatomy 1 1 67-1168 tenosynovitis 1 1 93 extensor digitorum muscle, lesions 465 extensor digitorum tendons 477 rupture (mallet finger) 537-538 extensor d igitorum tenosynovitis 513 extensor hallucis longus 1 167 adherence 1 1 93 ischaemic contracture 1 1 93 tenosynovitis 1 1 93 extensor indicis proprius tendon 477 lesions 512-513 extensor muscles elbow 421, 421, 423 hip joint 976, 976-978 knee see knee lumbar spine 713, 713-714 wrist and fingers 422, 422-423

see also individual flexors/joints extensor pollicis brevis tendon 477, 525 infiltration technique 526, 527 mechanical tenovaginitis 524-525 tenosynovitis 524, 525 extensor pollicis longus tendon 477 lesions 526 rupture 528-529 tenosynovitis 524, 525 extensor tendons hand 477, 477-478 wrist vs fingers 5 1 0

see also individual tendons external carotid artery 228 external intercostal muscles 587, 588 external oblique muscle 589-590, 590 deep friction 667, 667 lesions 666-667 external rotation-recurvatum test, knee 1121, 1 1 2 1 extra-articular end-feel 73 extracellular matrix (ECM) 34-37, 35 fibrous elements 34-36 non-fibrous ground substance 34 extracorporeal shock wave therapy, type II tennis elbow 463 extradural haematoma, thoracic spine 641 extradural lesions, lumbar 864-865 extradural neoplasms cervical spine 218 lumbar spine 864-865 extrasegmental pain 1 7, 1 8 referred t o thorax 661 segmental radicular pain vs 759, 803 extraspinal nerve root 25

extrinsic muscles foot 1 1 59-1160, 1 1 99 hand 476, 477-479 exudative phase, inflammation 44 eye movements, nystagmus see nystagmus

facet arthrography 833 facetectomy, for lateral recess stenosis 930-931 facet joints cervical spine 1 39, 1 40 arthrosis 1 98, 198-199, 1 99, 269-270 manipulation 268 consequences of disc ageing 1 76 convergent/ divergent pain pattern 198, 1 98 deep transverse friction 269-270 movement 1 40 rheumatoid arthritis 199 whiplash injuries 241, 244 hypertrophy, straight-leg raising 763 laxity, age-related 737, 776 lumbar spine ageing effects 710, 736-737, 788 anatomy 710, 710-711 arthropathy 779 capsular inflammation 8 1 8 capsular lesions causing pain 8 1 5 capsule innervation 779 capsule types (l / II) 776 excessive rotation 779, 780 functions 710 hypertrophic osteoarthrosis 791 inflammation 779 joint capsules 710 L4-L5 71 1 L5-S1 71 1 lesions 779, 800 see also facet joint syndrome 'menisci' 710 overstretching of posterior capsules 776, 777 pain on palpation 780 posterior capsule injection technique 91 8-919, 9 1 9 radiological signs of degeneration 738 reference of pain in lesions 780, 780 posterior dysfunction syndrome 815 thoracic spine 581 , 583-584 ankylosing spondylitis 670 arthritis 650-651 degeneration 641, 650-651 pain 597 sclerosant infiltration for disc lesion prevention 632, 632-633 superior and inferior articular processes 583-584 triamcinolone injection 650-651, 651 'three-joint complex' with discs 736 facet joint syndrome 779 clinical examination 780 history 780 summary 781

facial nerve (cranial nerve VII) 678, 678 facial pain, referred 149-150 facial palsy, idiopathic peripheral (Bell's) 680, 681 falls cubital tunnel syndrome 563 glenohumeral instability 337 infraspinatus tendon rupture 367 partial carpal tunnel syndrome 572 supraspinatus tendon rupture 359 'far out' syndrome 793, 857 fasciculation, muscle 29 fasciculi muscle 42 nerve 23, 24, 25, 41 nerve root 720 fasciitis plantar see plantar fasciitis traumatic, costocoracoid and ribs 408 fat necrosis 1 24 fat pads, facet joints of lumbar spine 710-711 fear, local anaesthetic side effect 120 femoral artery 980 femoral condyles, anatomy 1053, 1053, 1054 femoral epiphysis, slipped 1046 femoral head anatomy 973, 974 osteonecrosis see hip joint, aseptic necrosis femoral hernia 1 038, 1 038-1039 femoral neck fracture, avoidance in elderly 1015 stress fracture 1012, 1036-1037 treatment 1037 femoral nerve anatomy 979, 980 compression 1 265 saphenous branch see saphen{)us nerve femoral prosthesis 1010 loose 1010 femoral pulse, feeling 828, 994 femoral stretching test crossed 829 false-positive 828 femoral triangle, anatomy 981 femur distal 1053 attachment to knee joint capsule 1057 metastases 88, 1025 upper neoplasm 1009, 1025 osteomyelitis 1009 fetus, spine 703, 703-704 fibres of Sharpey 705 fibrillation, cartilage, hip osteoarthrosis due to 1001 fibrinogen, inflammation 44 fibroblasts 33 collagen synthesis 34, 35, 35 epineurium/ perineurium 23, 41 proliferation in tissue repair 44 phenol effect 126 steroids effect 122 role in wound repair 33

INDEX 1 301

fibrocartilage 37 fibrositis 1 9 fibular coJlateral ligament manipulation after ankle sprains 1226-1227, 1227 sprains 1217 Ficat and Arlet staging, hip osteonecrosis 1 0 1 1 , 1011-1012 ' figure-of-eight' bandage 407 filum terminale 714 finger escape sign 202 fingers 431, 43 1 adduction, resisted 158, 1 60 arthrosis 534 chip fracture 534 dislocation, unreduced 535 disorders 533-539, 538 disorders of contractile structures 535-538 dorsal interosseous muscles 535-536, 536 flexor tendons 536 tendon ruptures 537-538, 538 thenar muscles 536, 537 trigger finger 536-537, 537 disorders of inert structures 533-535 capsular pattern 533-535 history-taking 533 non-capsular pattern 535 extension, resisted 431, 432 extensors 422, 422-423 wrist extensors differentiation 5 1 0 flexion, resisted 431, 432 flexor muscles 423, 423 wrist flexors differentiation 513 flexor tendons 478 tenosynovitis 536 functional examination 488, 488, 490-491, 491 passive movements 490-491 resisted movements 491 gout 535 mallet 537-538, 538 morning stiffness 534 muscle and tendon strains 535-538 overuse problems 535 palpation 491 posttraumatic pain 538-539 radial deviation, assessment 491 resisted extension / flexion 489, 490, 491 resisted separation 488, 489 rheumatoid arthritis 534 squeezing together 488, 488 traumatic arthritis 534 trigger 51-52, 536-537, 537 ulnar deviation assessment 491 rheumatoid arthritis 534 Finkelstein's test 525 first rib syndrome 548 shoulder elevation exercise 552, 552 see also thoracic outlet syndrome (TOS) Fischgold and Metzger measurement 216 fish vertebrae 644, 644 flexion, forward see bending, forward;

individunl spinal regions

flexor carpi radialis anatomy 423, 423, 5 1 4 deep transverse friction a n d infiltration 514, 5 1 4 lesions 513-514 tendon 478 flexor carpi ulnaris muscle, anatomy 423, 423 flexor carpi ulnaris tendon 478 anatomy 5 1 5 lesions 514-515 flexor digitorum longus tendon 1 1 66, 1 1 67 rupture 538 flexor digitorum profundus tendon deep transverse friction 516, 5 1 6 d isorders 515-516 flexor hallucis brevis 1 166, 1 1 69 flexor hallucis longus 1 1 66 anatomy 1 1 66, 1 167 toe contraction 1 1 66, 1 1 66 flexor muscles elbow 420-421 , 421 sites of lesions 466, 466 fingers 478 foot 1 1 66, 1 1 67 hand 478, 478-479 hip 975-976, 976 lumbar spine 714 weak, metatarsalgia due to 1257 wrist and fingers 423, 423 wrist vs fingers 5 1 3 see also flexor tendons; individual

flexors/joints flexor pollicis longus muscle, anatomy 423, 423 flexor pollicis longus tendon 479 anatomy 527 friction 527, 528 infiltration technique 526-527, 527 pain on resisted flexion 526-527 tenosynovitis 526-527, 527 flexor retinaculum (transverse carpal ligament) 478, 480, 568 flexor tendons fingers 478 rupture 538 tenosynovitis 536 hand 478, 478-479, 479 see also flexor muscles flushing, corticosteroid side effect 125 foot 1 157-1260 abduction-adduction 1 159, 1 1 68 testing 1 1 76-1178, 1 1 77 anatomy 1 1 61-1166 segments and bones 1 1 61 , 1 1 6 1 anterior segment see forefoot arches 1 1 61 , 1 1 65 anterior 1 1 65, 1 1 65 longitudinal, i nspection 1 1 72 muscular support 1 1 69 clinical examination 1 1 71-1179 history-taking 1 1 71 , 1 1 71-1172 illSpection 1 1 72-11 73 interpretation 1 1 81 - 1 1 82 derma tomes 1 4

dorsiflexion 1 1 62 anterior periostitis 1 208 pain 1 1 93-1194 resisted, L4 nerve root test 825, 826 dorsiflexors 1 167, 1 167-11 68, 1 193 lesions 1 1 93-1194 see also under lower leg drop see drop foot eversion 1 1 59 resisted, L5 / S 1 nerve root test 825-826, 826 evertor lesions 1 1 97-1199 pain 1 1 97-1198 weakness 1 1 98-1199 extension, testing 1 176-1178, 1 1 77 fascia 1 170, 1 1 70 flexion, testing 1 176-1178, 1 1 77 functional examination 1 1 73, 1 1 73-1179 accessory examination 11 79, 1 1 79 ligamentous tests 1 1 74-11 75, 1 1 75 mobil i ty at subtalar joint 1 1 75, 1 1 76 normal but pain 1 1 79 passive movements (midtarsal) 1 176-1178, 1 1 77 resisted movements 1 1 78, 1 1 78-11 79 rising on tiptoe 1 1 73, 1 173-1] 74 functional terminology 1 1 59 inversion 1 1 59 invertor lesions 1 1 95-1197 pain 1 1 95-1197 weakness 1 197 invertor muscles, deep friction 1 1 95, 1 1 95 ligaments testing 1 174-11 75, 1 1 75 see also ankle ligaments middle segment see midfoot movements summary 1 1 73 terminology 1 1 59 muscles anatomy 1 1 66-1170 extrinsic 1 1 59-1160, 1 1 99 intrinsic 1 1 69, 1 1 69-1 1 70 neurological weakness 1 199, 1 1 99 oedema 827 pain 1 1 72 normal movements 1 1 79 plantifiexion 1 1 59, 1 1 62 indirect 1 1 69 inversion sprains 1 2 1 7, 1 2 1 7 sprain o f anterior tibiotalar ligament 1206 testing 1 1 73, 1 1 73-1 1 74 plantiflexors 1 1 66, 11 66-1167, 1 1 79 see also plantiflexors posterior segment see ankle pronation 1 159, 1 1 68 testing 1 1 76-11 78, 1 1 77 referred pain from 1171 referred pain to 1 171 sole, muscles 1 1 69 splay see splay foot supination 1 1 59, 1 1 68, 1 2 1 7 testing 1 1 76-11 78, 1 1 77

1 302 INDEX

foot (continued) tendons anatomy 1166-1170 dorsiflexors 1 1 67, 1 1 67-1168 evertors (abduction, pronation) 1 1 68, 1168-1169 functional axes 1 1 66 inverts (adduction, supination) 1 1 68, 1 1 68 at medial malleolus 11 67, 1 1 67 plantiflexors 1 1 66, 1 1 66-1167 valgus movement 1 1 59 assessment 1 1 75, 1 1 76 under dorsiflexion 1 1 79 varus movement 1159, 1 2 1 7 assessment 1 1 75, 1 1 76 warm, unilateral (warning sign) 855 see also ankle; toe(s) footwear high heels, metatarsalgia due to 1 256-1257 inspection 1 1 72 plantar fasciitis treatment 1213--1 214, 1 2 1 4 'rockers' see 'rocker' foraminal encroachment 792-793, 793 ' forbidden' area 812, 8 1 2, 852 pain in 812, 852, 858, 861, 862 forced movements contraindications 105 capsular lesions (capsulitis) 55-56, 56, 105 see also manipulation; mobilization forearm, pain 483 radial tunnel syndrome 560 T1 nerve root compression 190 forefoot anatomy 1161, 1 1 6 1 , 1 1 65-1166 disorders 1 249-1251 fifth metatarsal fractures 1250--1251 final stage of contact during gait 1 251 march fractures 1249-1250 see also march fractures pressure on nerves 1257-1258 bruising on second digit nerve 1 257-1258 Morton's metatarsalgia 1 258 see also Morton's metatarsalgia short first metatarsal bone 1249 splay foot 1251 see also splay foot tendons 1 1 65-1166 see also foot; metatarsal bones; metatarsophalangeal joints Forestier disease (vertebral hyperostosis) see ankylosing hyperostosis forward bending see bending, forward fractures clay-shoveller's 212, 323 corticosteroid side effect 125 hangman's 212 Jefferson's 212 lumbar vertebrae see lumbar vertebrae odontoid process 212 pathological acute subdeltoid bursitis vs 320 cervical spine 212 lumbar vertebrae 853

vertebral bodies 643-644 spinal manipulation complication 112 stress see stress fracture traction, cervical spine 212 u nstable, spinal manipulation contraindication 110

see also individual bones ' freezing arthritis', shoulder 313 Freiberg's osteochondritis 1256 friction dorsal interosseous muscle/ tendon 535-536, 536 flexor pollicis longus tendon 527, 528 forefoot march fractures treatment 1250, 1 250 thenar muscles 536, 537 'frozen' shoulder 306, 307 functional disability, history-taking 68 functional disorders 93 functional examination / testing 70-75 aims 71, 81 definition and function 61 i n diagnosis 60-61 inadequacy and errors 80 inert and contractile tissues 61-62 inherent likelihoods 60 interpretation 80-91 active movements 81-83 cervical spine 165-173 passive movements 83-87 movements 71-75 patterns 81 see also active movements; passive movements; resisted movements nature of questions during 71 negative, accessory tests after 76 palpation vs 60-61 physiological movements used 61 procedure / principle 70-71 selective tension principle 61 summary 81

see also individual anatomical regions ' functional unit of Junghans' 705, 705

G Gaenslen's test (pelvic torsion) 810, 951, 952 gait abnormalities 69 antalgic 949 disturbances cervical disc displacement 181 cervical spondylotic myelopathy 202, 203 forefoot final stage of contact 1 251 hobbling 1008 importance of first metatarsophalangeal joint 1251 inspection 988 meniscal lesions (knee) 1084 short plantiflexor muscles 1192 Trendelenburg 1029 see also walking gallbladder inflammation 219 referred pain from 597-598, 598, 660, 660

g-efferen ts 42 ganglion 507 differential diagnosis 502 treatment 507 ulnar nerve compression 563 gaps, palpation 78 Gardener's palsy 27 gas, in lumbar discs 738 gastric lesions, referred pain from 597, 598, 659, 659, 868 gastric tumours, referred pain 659 gastric ulcer adherent to lumbar spine 868 referred pain 659 gastritis, referred pain 659 gastrocnemius 1161 anatomy 1059, 1166 deep friction 1 1 85, 1185-1186 infiltration in tennis leg 11 85, 1 1 85 lesions 1147-1148 medial, swelling / haematoma 1184 stretching 1192, 1 1 92 tears / strain injuries 48, 1183 gastrointestinal diseases, pain referred to back 868 gate control theory of pain 5, 5-6, 26, 95 gaze deviation (nystagmus) see nystagmus geniohyoid muscle 677 genitalia, paraesthesia 807 genitourinary diseases, referred pain to back 867-868 giant cell tumour, cervical spine 213 Gillett test 949, 950 'giving way' of joints 53 ankle joint 1227, 1229, 1 230 knee see knee glandular fever 184 glenohumeral joint 277, 279-280 apprehension 335 arthritis early, differential diagnosis 325 pain 292 capsule 279, 305 joint stability 336 lesions 305 cohesion-adhesion forces 336 congruence 336 degenerative disease 317-318 dislocation 335 recurrent anterior, test 337-338, 338 recurrent posterior, test 338, 339 see also shoulder, dislocation effusion 294 instability 279, 335-344 accessory tests 337-341 atraumatic 337 causes 335 definition 335 diagnosis 341 functional examination 337-341 history-taking 337 inferior 341 posterior 341 recurrent 335 surgery 344 treatment 341-343

INDEX 1303

see also glenohumeral joint, dislocation insufflation with fluid 312 movements 283, 389 enlarged range 337-341 normal range 283, 335 see also shoulder, muscles and tendons pain 337 stability 335-336, 359 dynamic factors 336, 336, 337 factors affecting 335-336 rotator cuff role 287, 350 static; factors affecting 335, 336 subluxations 335 chronic 317-318 classification 335 features of 'attack' 337 momentary 337, 341, 382 painful arc with 337 traumatic arthritis after 307 tests 283, 296-298, 297 passive lateral rotation 296-297, 297 passive medial rotation 297, 298 passive scapulohumeral abduction 296, 297 tuberculosis 31 6-31 7 glenohumeral ligaments 279-280, 335 stability of joint 336 glenoid 278, 278, 359 long bicipital tendon lesion at 371-372, 372 musculotendinous 359 osseous 359 glenoid cartilage, thickness 336, 336 glenoid fossa 278, 278 glenoid labrum 279 function 336, 336 glucocorticoids 121 see also corticosteroid(s) gluteal arteries 980 gluteal bursae 979 anatomy 1017, 1 0 1 7 gluteal bursitis 987, 1017-1018 clinical examination 1017 diagnostic injection of anaesthetic 1017-1018, 1 0 1 8 pain o n resisted extension of h i p 1026 gluteal muscles 1 6 spasm 811 gluteal pain causes 1025, 1026 unilateral diagnosis 959 sacroiliac lesions 949, 958 see also buttock pain gluteus maximum muscle anatomy 976-977, 977 coccygeal fibres 967 irritation 968 examina tion 978 pain 1025-1026 'gluteus medius lurch' 1029 gluteus medius muscle anatomy 977, 978, 978 injury 1028 gluteus minimus muscle 978 injury 1028 glycoproteins 34

glycosaminoglycans 34 golfer's elbow 454, 466-468 C7 nerve root compression us 190 refractory 468 sites of lesions 466, 466--467 treatment 467, 467--468 gout ankle 1204 carpal tunnel syndrome due to 569 cuneiform-first metatarsal joint lesion 1248 elbow 439 fingers 535 hip joint 1001 knee 1080 metatarsophalangeal joints first 1252 outer four 1255 sacroiliac joint 957, 961 temporomandibular joint 694-695 gouty arthritis, acute subdeltoid bursitis us 320 gracilis muscle, anatomy 978, 1059 granulation 44, 44 steroid injections during 54 granulation tissue 45 granuloma, eosinophilic see eosinophilic granuloma gravity, centre of, sacroiliac joint 942, 942 greater trochanter, avulsion fracture 1029 'grind test', thumb arthrosis 522 grip and release test 202 Grisel's syndrome 1 84 groin, dermatomic overlap 1 036 'groin disruption' 1 039-1040 groin hernia 1 038-1039 groin injury 1035 groin pain 1 023, 1035-1041 clinical examination 1036 interpretation 1 036-1040 history-taking 1035 lesions causing 1036-1040, 1 03 7 sciatica 761 terminology 1 035, 1 036 ground substance, non-fibrous 34 'growing pains' 1 1 83 Guyon's tunnel 479, 479, 561 anatomy 479, 479, 561, 565, 565 ulnar nerve in 481, 561 ulnar nerve entrapment 562, 565-566 gymnastics, shoulder girdle muscle injuries 363

haem angioma cervical spine 213 lumbar spine 859 haemarthrosis 54 ankle 1204, 1219 elbow 439 hip, children 1045-1046 knee 1081 spontaneous of elderly 1081 posttraumatic, of knee 1081 shoulder 293, 316

haematoma costocoracoid fascia 408 deep transverse friction contraindication 98 epidural, lumbar 865 extradural, thoracic spine 641 intramuscular 48 medial gastrocnemius 1 1 84 subsynovial, knee 1 093-1094, 1094 haemophilia carpal tunnel syndrome 569 hip haemarthrosis 1045-1046 knee haemarthrosis 1081 shoulder haemarthrosis 293, 316 haemorrhage psoas bursitis 1016-1017 quadriceps muscle 1 1 32 subdeltoid bursitis 321 Haglund's disease 1216 hair, lumbar spine inspection 811 hallux rigid us 1256 hallux valgus 1 254-1255 aetiologies 1 254-1255, 1 255 diagnosis 1255 treatment 1255 hamate 474 hamstring muscles 1 030 accessory tests 76 anatomy 977, 977-978 deep friction 1145, 1 1 45 functions 1144 knee flexion 1 059-1060, 1 060, 1 1 44 lesions 1 1 44 straight-leg raiSing limitation 763, 822 muscle strength imbalance with quadriceps femoris 1030-1031 procaine infiltration 1 1 44-1145 reflex contraction 720 strains 48, 1 030-1031, 1144-1145 treatment 1144-1145 tears 48 thigh extension 1144 tightness, straight leg raising test 822 see also biceps femoris; semimembranosus muscle; semitendinosus muscle hamstrings syndrome 1030-1031 differential diagnosis 1031 treatment 1 031 hamstring tendons deep transverse friction 1031, 1 03 1 infiltration technique 1031 hand anatomy 473--482 extrinsic muscles and tendons 476, 477--479 intrinsic muscles 477, 479, 479--480 joints and ligaments 473--4 76 nerve structures 480--482 claw 564 clinical examination 483--491 accessory tests 489, 490 history-taking 483--484 inspection 484 interpretation 493-494 palpation 488

1 304 INDEX

hand (continued) summary 491 colour 484 cyst 484 dermatome and myotome 15 disorders 533-539, 538 drop (porter's) 559 extensor tendons 477, 477-478 flexor tendons 478, 478-479 functional examination 484, 484-486 intrinsic muscles 488, 488 mal-united fracture 484 pain 533 sensory nerve supply 566 swelling 484 wasting of intrinsic muscles 564 weakness, carpal tunnel syndrome 570 see also fi ngers; wrist hangman's fracture 212 hard end-feel 55, 73, 73 head dermatomes and myotomes 15 injury, whiplash see whiplash-associated disorders positions, effect on blood flow in vertebral arteries 230, 230-231 headache 149-150, 223-227 cervical spondylosis 197 cervicogenic 225-227 diagnostic criteria 225-226, 226 chronic daily 223 classification 223-224 cluster 149, 224, 225 pain referred to temporomandibular joint 680 early morning 147, 149 migraine see migraine morning (matutinal) in elderly 147, 197-198, 226 cervical spondylosis causing 1 97 manipulation 268 mul tisegmental 149, 1 49 non-cervicogenic 224-225 postconcussional 226-227 prevalence 223 primary disorders 224 segmental 1 49, 1 49 tension-type (stress) 223 clinical features 224 unilateral 226 healing acute muscular tears / strains 48 connective tissue injuries 44, 44-45 immobilization effect 46-47, 47 promotion by grade A mobilization 103 heart disease, C3 dermatome pain 1 87, 219 insufficiency, traction contraindication 897 referred pain from 597, 598, 655, 655-656 heart attack, differential diagnosis 548 heartburn 658 heat before capsular stretching 104 knee 1071, 1 088

Heberden's nodes 534 heel dancer's (posterior periostitis) 1 207, 1207-1208 differential diagnosis of lesions 1232-1234 high (shoes), metatarsalgia due to 1256-1257 painful conditions 1213-1216 differential diagnosis 1 232-1234 raised midtarsal strain treatment 1 243, 1 243 tennis leg treatment 1185 heel pad, anatomy 1 1 70, 1 1 70, 1214-1215, 1215 heel pad syndrome 1 214-1216 tenderness site 1215, 1 2 1 5 treatment 1215-1216, 1 2 1 6 hepatitis, acute, referred pain 659 hernia diaphragmatic 659 groin 1 038-1039 hiatus 897 inguinal 591 'sports' 1 039 herpes zoster 664 differential diagnosis 189 lumbar pain 864 oticus infection 680 thoracic pain 596, 661 heterotopic ossification 49 brachialis muscle 450 hiatus hernia 897 high heels, metatarsalgia due to 1 256-1257 high-velocity, short-lever, manipulation (spinal) 108-109 hinge joint humeroulnar 418 knee as 1 053, 1 054 hip joint 971-1050 abduction 982, 982 passive 990, 990 resisted see hip joint, resisted abduction abduction brace 1043, 1045 abductor muscles 978, 978 re-education in osteoarthrosis 1007 see a/so gluteus medius muscle adduction 982, 982 passive 989-990, 990 passive with flexion 994 resisted see hip joint, resisted adduction adductor muscles 978-979, 979 see also adductor longus muscle anatomy 973, 973-974 blood vessels 980, 980 bursae 979 capsule and ligaments 974-975 muscles 975-979 nerves 979-980 topographical 981 ankylosing spondylitis 1000-1001 arthroscopy 995

aseptic (avascular) necrosis 1010-1012, 1012 diagnosis 1010 pathogenesis 1010 staging 1 01 1 , 1011-1012 treatment 1012 bursitis 994 gluteal 1017-1 018 ischial 1019 psoas see psoas bursitis septic 1 008-1009 trochanteric 1018-1019 capsule anatomy 974-975 hip osteoarthrosis aetiology 1001-1002 laxity in children 1 044 rigidity 1002 stretching 1 004, 1004-1005 capsulitis, forced movement contraindication 56 chondrocalcinosis 1001 clinical examination 985-996, 994 accessory tests 994, 994 history-taking 987, 987-988 inspection 988-989 interpretation 997-998 palpation 994 technical investigations 994-995 congenital dislocation 1043-1045 incidence and aetiology 1 043 tests and investigations 1044, 1 044-1045, 1 045 treatment 1045 diagnosis of disorders 985 disorders in children 1043-1048 arthritis 1 045-1046 avulsion fractures 1 046-1047 congenital limitation of extension 1045 dislocation see hip joint, co:1genital dislocation Perthe's disease see Perthes' disease disorders of contractile structures 1023-1033, 1 032 disorders of inert structures 999-1022 capsular pattern 999, 999-1007 non-capsular patterns 1 007-1 019 extension 982, 982 congenital limitation 1045 forced, osteoarthrosis treatment 1004-1005, 1 005 passive (prone) 991-992, 992 resisted see hip joint, resisted extension sustained active 994, 994 extensor muscles 976, 976-978 re-education in osteoarthrosis 1007 see also gluteus maximum muscle; hamstring muscles flexion 981, 982 forced, osteoarthrosis treatment 1004, 1 004 passive 989, 989 buttock sign 1 008, 1 008 passive with adduction 994 resisted see hip joint, resisted flexion testing 82 1

INDEX 1305

flexor muscles 975-976, 976 -see also il iopsoas muscle; rectus femoris; sartorius muscle functional examination 820, 82 1 , 985, 989-994 basic 989-994 preliminary 989 prone 991-994 supine 820, 82 1 , 989-991 tests 989 gout 1001 haemarthrosis, children 1045-1046 internal derangement 1012-1015 symptoms/ signs 1013 see also hip joint, loose bodies internal rotation, straight-leg raising 719 intra-articular injection technique 1 000, 1000 lateral rotation 982, 983 bilateral resisted (prone) 992, 993 passive (supine) 989, 990 reduction of loose body 1013-1014, 1015 testing 821 lateral rotator muscles 979, 979 ligaments 974, 974-975, 975 loose bodies 1012, 1013 reduction 1013-1015, 1014, 1015 medial rotation 982, 983 bilateral resisted (prone) 993, 993 forced, osteoarthrosis treatment 1005, 1 005 passive (prone) 992, 992 passive (supine) 989, 990 reduction of loose body 1013, 1014 testing 82 1 medial rotator muscles 979, 979 monoarticular arthritis, middle-aged persons 1001 monoarticular steroid-sensitive arthritis 1000 movements 981-983 ligaments 975 limitations in osteoarthrosis 1002-1003 muscles involved 975, 975-979, 976 passive (prone) 991-992, 992 passive (supine) 989-990, 990, 991 resisted 990-991, 991, 992-994, 993, 1023-1025

see also en tries below muscles 975-979, 976 con tou r inspection 988 examination 978 hyperactive, stretching 1007 inhibited, activation 1 007 osteoarthrosis aetiology 1002 re-education in osteoarthrosis treatment 1007 osteoarthrosis 988, 1 001-1007 aetiology 1 001-1002, 1002 idiopathic (primary) 1001 Kellgren classification 1003 radiography 1003 secondary 1001

symptoms and signs 1 002-1003 osteoarthrosis treatment 1 003-1007, 1 004 capsular stretching 1 004, 1 004, 1 004-1005 intra-articular injections 1007 muscle re-education 1007 surgery 1007 traction 1 005-1007 pain 985 history-taking 987-988 internal derangement causing 1013 osteoarthrosis 1002 psychogenic 1019 summary 1 049-1050 passive movement limitation, capsular pattern 84 passive rotation 989, 990 polymyalgia rheumatica 1001 position, inspection 988 referred pain from 986-987, 987 referred pain to 986, 986, 987 resisted abduction 991, 992, 1028-1029 pain 1 028-1029 pain and weakness 1 029 painless weakness 1029 resisted adduction 991, 992, 1026-1028 pain 1 026-1028 resisted extension 991, 991 , 1025-1026 pain 1025-1026 painless weakness 1026 resisted flexion 990-991, 991, 1023-1025 L2 / L3 nerve root test 825, 825 pain 1 023-1025 pain and weakness 1025 painless weakness 1025 resisted lateral rotation 1029 bilateral 992, 993 resisted medial rotation 1029 bilateral 993, 993 rheumatoid conditions 1000-1001 septic arthritis 1001 symptoms 987, 987-988 tend initis 994 total replacement 1007 loose prosthesis 1 010 types of prostheses 1007 transitory arthritis, children 1 045 traumatic arthritis 999-1000 tuberculous arthritis 1001 children 1 045 twinges 1013 histamine 44 histocytosis-X 213 history-taking 63-69, 799-800 cervical spine lesions see cervical spine dural pain 600 elbow d isorders 427-428 finger / hand disorders 533 form of questions 63, 799 hip and buttock disorders 987, 987-988 knee 1 064, 1 064-1065 lower leg, ankle and foot 1 1 71 , 1 1 71-1172 lumbar spine see under lumbar spine

procedure 64-69 shoulder 292, 292-294 shoulder girdle disorders 395 spinal manipulation complication avoidance 1 1 3 summary 6 9 temporomandibular joint 680-681 tennis elbow 456 thoracic spine / abdominal problems 599-600 unlikelihoods 801 vertigo 233, 236 wrist and hand 483-484

see also specific conditions, anatol11ical sites HLA-B27, ankylosing spondylitis association 960 hoarseness 657 hobbies, history-taking 64 Hoffman's reflex 202 Hofmann complex 714 'hornblower' s sign' 367 Horner's syndrome 149, 190, 215 brachial plexus dysfunction 546 features 551, 657 in Pancoast's tumour 657 horse riders' sprain 1026 Horton's neuralgia see headache, cluster housework, correct posture 924, 925 humeral head, osteonecrosis 31 7 humeral trochlear hypoplasia 563 humeral tuberosities, painful arc and 379 humeroradial joint 4 1 7, 417-418, 4 1 8 function a n d anatomy 418, 4 1 8 humerou lnar joint 4 1 7, 4 1 7-418, 4 1 8 function and anatomy 418, 4 1 8 humerus anatomy 279, 2 79, 419 biomechanics 419 epicondyles 418 medial epicondyle 423 muscles originating at 423, 423 rotation by rotator cuff muscles 287 hyaline cartilage 40 hyaluronan 34 secretion by synovial intimal cells 39 hyaluronic acid, knee osteoarthrosis 1079 hydraulic distension, traumatic arthritis of shoulder 312 hydrocortisone historica I use 121 intra-articular injections complications/ side-effects 312 traumatic arthritis of shoulder 310, 311 see also corticosteroid(s) hyperacute lumbago see lumbago, acute lumbar hyperaemia, traumatic, induction by deep friction 96 hyperextension-hyperflexion injuries, neck see whiplash-associated disorders hyperextension injury see whiplash­ associated disorders hyperglycaemia, corticosteroid side effect 124

1306 INDEX

hyperkyphosis (thoracic spine) 601 , 619, 632, 642-645, 8 1 0 ankylosing spondylitis 669 anterior erosion 645, 645 definition 643 juvenile 642 thoracic postural pain syndrome 631, 644-645, 645 see also wedge fracture hyperlordosis see lumbar lordosis, excessive hypermobility 87 assessment 79 normal end-feel 73 spinal manipulation contraindication 1 1 0 tests 1 1 0 hyperostosis age-rela ted 1 76 ankylosing (vertebral / diffuse idiopathic skeletal ) see ankylosing hyperostosis sternoclavicular joint 407 hypertension, pulmonary, referred pain 658 hypertrophic osteoarthrosis, facet joint (lumbar) 791 hyperventilation, thoracoabdominal features 661 hypomobile segment, spinal manipulation 1 07, 1 08 hypomobiJity, assessment 79 hypotension epidural anaesthesia side effect 907 side effects of local anaesthesia 120 treatment 1 20 hypothenar muscles 479 hypothyroidism, carpal tuIUlel syndrome 569 hysterical torticollis 1 84 hysterical trismus 696

iatrogenic Cushing's syndrome 1 24-125 iatrogenic infectious arthritis 1 23 ice, Achilles tendonitis treatment 1 1 87 idiopathic frozen shoulder 313 iliac apophysitis 1 029 iliac arteries 980 iliac crest pal pa tion 8 1 1 reduction of space between thoracic cage and 809-81 0 iliofemoral ligament of Bertin 974, 974 ilioinguinal nerve, anatomy 1 040, 1 040 ilioinguinal neuralgia 1 040 ilioinguinal region, anatomy 590-591 iliolumbar ligaments anatomy 712-713, 713, 781 , 942-943 development 712-713, 71 3 functions 713, 781 injection technique 920, 920 lesion / strain 781-782, 800 history and clinical examination 781 -782 pain reference 782 provocative test and treatment 782 sclerosant injections 964, 964

strain 8 1 8 iliopsoas muscle 975 anatomy 975, 976 iliopsoas tendon, anatomy 980 iliotibial band (tract) 977 anatomy 978, 1 1 43-1144 bursa under 1 095 deep friction 1028, 1 029 sprains 1 028 strained 1 143-1144, 1 1 44 iliotibial band friction syndrome 1 1 44 diagnosis and treatment 1 1 44 iliotibial tract see iliotibial band (tract) ilium anatomy 941 anterior superior spines, sacroiliac joint testing 820, 820 apophysitis 1 029 neoplasm 1009 see also sacroiliac joint imaging lumbar spine 833-834 see also radiography; other specific

techniques immobilization 642 adverse effects on muscle 46 ankle sprains (inversion) 1218 ankle stiffness 1204 degeneration of discs 922 effect on healing 46-47, 47 ligament ruptures 52-53 ad verse effects 53, 97 self-perpetuating inflammation and 45 subtalar joint stiffness 1 2 1 1-1212 immobilizational arthritis, shoulder 312-313 after supraspinatus tendon rupture 360 immune system, corticosteroid side effects 1 25 impingement syndrome 380 incoordination cervical spine lesions 1 5 1 history-taking 68 indometacin, ankylosing spondylitis 960 inert tissues 6 1 , 61-62, 62 inferior iliac spines, epidural anaesthesia landmark 908, 908-909 inferior subscapular nerve, anatomy 545 infil tra tion 1 1 5-127 aim 1 1 6 contraindication 1 1 6 definition 1 1 6 diagnostic 80 dynamic 1 1 7 conewise 1 1 7, 1 1 7 cylindrical 1 1 7, 1 1 8 fanwise 1 1 7, 1 1 8 follow-up and after-care 1 1 8 injection comparison 1 1 6 needles 1 1 6, 1 1 6 patient position 1 1 7 principles 1 16-11 8 static 1 1 7-118, 1 1 8 techniques 1 1 7, 1 1 7-11 8, 1 1 8 therapeutic 94

types of prod ucts see corticosteroid infiltration; local anaesthesia; phenol; triamcinolone infiltration inflammation 43, 44 acute muscular tears / strains 48 cells involved 44 chronic 45 clinical signs 44 exudative phase 44 joint capsules 54, 55 pain 67, 67 self-perpehlating 45-46, 46 arthrosis at cervical facet joint 1 98 tendinous lesions 50 inflammatory disorders 68, 68-69, 93 rheumatoid vs reactive pattern 68 temporomandibular joint 681, 694-695 inflammatory mediators 44 infraclavicular fossa, palpation 355 infra patellar pad 1 057 infrapatellar tendinitis 1 064, 1 1 32, 1 133, 1 1 36-1137 infra patellar tendon deep friction 1 1 34-1135, 1 1 36 infiltration 1 1 35-11 36, 1 137 lesions 1 1 36-1137 infraspinal fossa 278, 278 atrophy of infraspinatus muscle 367 infraspinatus muscle 286 exercises, glenohumeral instability treatment 342, 342-343 innervation 554, 555 lateral rotation of shoulder 364 lesions 364-366, 365 paralysis, in neuralgic amyotrophy 368, 553 rupture, differential diagnosis 1 88 weakness and wasting 368 neuralgic amyotrophy 368, 553 infraspinatus tendinitis clinical signs 367 differential diagnosis 1 88, 334, 366 painful arc 381 infraspinatus tendon 280 deep transverse friction 1 00 irreparable degeneration 367 lesions 364-366 sites 365 treatment 364-365, 365 partial rupture 367 rupture 324 active movement therapy 114 total rupture 367-368 inguinal canal 590 anatomy 1 039 palpation 1 039 inguinal hernia 591, 1 038, 1 038-1039 direct and indirect 1038 treatment 1039 inguinal ligament 590 inherent likelihoods 60 injection 1 1 5-127 cervical nerve root 265, 266 cervical non-discogenic disorders 270, 270-271

INDEX 1307

definition 115-116 infiltration comparison 116 intra-articular see intra-articular injections lumbar spine disorders 903-921 needles 116, 1 1 6 principles 116-1 18 therapeutic 94 types of drugs see corticosteroid infiltration; local anaesthesia; sclerosant infiltration see also infiltration innervation connective tissue 36-37 joints see specific joints inspection 69-70 instability 79 history-taking 68 instability catch 841 intercarpal ligaments 475, 476 stretching 507 interclavicular ligament 388 intercosta I muscles anatomy 587-588, 588 deep friction 664-665, 665 external 587, 588 internal 587, 588 sprains 663, 664-665 pain 597 intercostal nerves, anatomy 585, 585 interdigital ganglion 1257 intermittent claudication 641 gluteal pain 1026 leg pain 1184 neurogenic vs vascular 789, 789, 793 testing 827 see also claud ication pain internal carotid artery 228 internal derangement 93 hip see hip joint knee 1082-1092 partial articular pattern, cervical disc displacement 1 80, 180 passive movement limitation 86 proportionate vs disproportionate 86 recurrence of symptoms 66 symptoms 67, 68 temporomandibular joint 691-692 internal oblique muscle 590, 590 International Headache Society (IHS) 224, 225, 226 interosseous ligament anatomy 942 sc\erosant infiltration 963, 963 interosseous membrane, elbow 419 interosseous muscles dorsal see dorsal interosseous muscles palmar see palmar interossei interosseus tendon lesion, deep transverse friction 97 interphalangeal joints anatomy 476 arthrosis 534 capsulitis, forced movement contraindication 56

movements 476 passive movements 490 swelling, rheumatoid arthritis 534 interpretation, of examination see functional examination / testing 'intersection syndrome' 524 interspinous ligaments 139, 142, 1 42 lumbar spine 711, 7 1 1 , 712, 782-783, 838 injection technique 918, 918 lesions 782-783, 783 overstretched 782 wedge fracture 643 rupture 782 sclerosant infiltration, thoracic d isc lesion prevention 632, 632 intertransverse ligament 142, 1 42 lumbar spine 712 intertubercular transverse l igament, rupture 373 intervertebral discs see disc(s) (intervertebral ) intervertebral facet joints see facet joints intervertebral foramen cervical spine 143, 1 43 consequences of disc ageing 1 76-177 lower cervical 137 lumbar spine 717, 718 ageing effects 737 normal vs stenosis 790, 790 stenosis see lateral recess stenosis thoracic spine 582, 585 tumours within 637 intervertebral joints 1 40 cervical spine 1 38, 1 40 lumbar spine, age-related changes 738, 738 osmotic system lumbar discs role 706-707 proteoglycans role 707 intervertebral space age-related height reduction 1 76 lumbar spine 704 reduction, thoracic 649 intra-abdominal region, pain 16 intra-articular injections complications / side-effects 312 hip osteoarthrosis 1007 knee 1080, 1 080 radiouLnar joint, lower / distal 496, 496 temporomandibular joint 693, 693 traumatic arthritis of shoulder 310-312, 311 see also hydrocortisone; triamcinolone intradural extramedullary tumours see intraspinal tumours intradural lesions, lumbar 865-867 intradural spinal tumours 865-867 intramedullary tumours, cervical spine 218 intraneural oedema, sciatica 759 intraspinal lesions, lumbar region 864-867 intraspinal roots see nerve roots, intraspinal intraspinal space-occupying lesions, straight leg raising (SLR) test 821-822

intraspinal tumours cervical 2 1 7, 21 7-218 extrad ura\, cervical 218 intradural 865-867 intradural extramed ullary cervical 2 1 7, 21 7-218 warning signs 2 1 8 intramedullary, cervical 2 1 8 thoracic see thoracic spinal canal see also spinal tumours intrathoracic region, dermatome and myotome 15-16 intrinsic muscles foot 1 1 69, 1 1 69-1170 hand see hand invertor lesions, foot see foot investigations 63 ischaemia anterior spinal artery 201 basilar, cervical manipulation contraindication 251 mesenteric 661 ischaemic contracture, thumb 529 ischaemic heart disease, referred pain from 655, 655-656 ischaemic necrosis see avascu lar necrosis ischial bursa 979, 981 ischial bursitis 1019 hamstrings syndrome vs 1031 ischial tuberosity 981 ischiofemoral l igament 974 ischiorectal abscess 1009 isokinetic contractions, rehabil itation after knee instability treatment 1125 isometric contraction 61 glenohumeral instability treatment 341 indications 1 1 4 painful neck movement 1 71 rehabilitation a fter knee instability 1124 isometric testing, neck movements 171 isotonic contractions glenohumeral instability treatment 341 indications 114-115

Jaffe and Lichtenstein, villonodular arthritis of 1080 Jefferson's fracture 212, 2 1 5 Jendrassik's grip (reinforcement) 233, 234 jerk test, knee instability 1 1 20, 11 20-1 121 joint capsules see capsules (joint) joints bleeding into 78 controlled by muscles, ligament lesion treatment 54, 56 cracking 83 d isorders, corticosteroid infiltration 122-123 intra-articular d isplacement, grade A mobilization 103 locking 68 grade A mobilization 1 03 normal range maintenance active movements 114

1 308 INDEX

joints (continued) grade B mobilization 1 04 not controlled by muscles ligament lesion treatment 54, 56 manipulation contraindication 105 passive movement limitation 84 swelling 65, 78 see also individual joints and conditions

Jones fractures 1 250-1 251 jugular incisura 585, 586 'jumper's knee' 1132 jumper's sprain 1 208-1 209, 1 209 J unghans, functional unit of 705, 705 juvenile ankylosing spondylitis 315-316 juvenile hyperkyphosis (thoracic spine) 642 juvenile kyphosis, vertebral ring epiphysis growth interference 642

Kellgren classification, hip osteoarthrosis 1 003 keratan sulphate 39 Kernig's sign 716 kidneys, referred pain from 598, 599 Kienbock's disease 504 di fferential diagnosis 502, 504 Kiloh-Nevin syndrome 568 'kissing spines' 782 Kleinman's shear test 509, 509 knee 1 051-11 56 abduction stress test 1117, 1 1 1 7 aching, in patellofemoral pain syndrome 1 142 adhesions 1093 anatomy 1053-1061 articular surfaces 1 053-1054 blood vessels 1060-1061 joint capsu le 1056-1057 lateral aspect 1 1 47 muscles see knee, muscles nerves 1 060-1 061 , 1 063 posterior capsular reinforcements 1057-1058 synovial membrane 1057 tendons 1 058-1060, 1 059 see also menisci; patella anterior drawer test 1067, 1 068, 1118-11 1 9, 1 1 1 9 bursitis 1 094-1096, 1 096 chondrocalcinosis 1080, 1081 clinical examination 1 063-1073 accessory tests 1 0 72, 1 072-1073 history-taking 1 064, 1 064-1065 inspection 1 065-1066 interpretation 1 075-1 076 palpation see knee, palpation crystal synovitis 1080 cysts 1 094-1096, 1 096 deformities 1072 degeneration 1078, 1 084 disorders of contractile structures 1 1 31-1148 extensor mechanism 1131-1 138

flexor mechanism 1144-1148 patellofemoral d isorders 1138-1143 disorders of inert structures 1 077-1098 capsular pattern 1 077, 1 077-1082, 1 082, 1 1 56 differential diagnosis 1 082, 1 1 56 ligaments 1099-1130 non-capsular pattern 1 082-1096, 1088, 1 1 56 see also knee ligament(s); menisci, knee extension 1 066, 1 067 meniscal movement 1056 resisted 993, 994 testing 829, 829 extensor mechanism disorders 1131-1138 extensor muscles 1058-1059, 1 059 external rotation-recurvatum test 1121, 1121 flexion 1066, 1 067 meniscal movement 1056 passive, testing 828, 828 resisted 993, 993 testing 829, 829 flexor mechanism disorders 1144-1148 flexor muscles 978, 1059-1060, 1 060 see also hamstring muscles fluid in 1070-1071 eliciting fluctuation 1070-1071, 1071 testing 1070-1071 forces causing ligament lesions 1 099 functional examination 1 066, 1 066-1070 ganglia 1072 giving way 1064, 1 084, 1 1 02 chronic ligamentous lesions 1101 quadriceps ruptu res 1131 gout 1080 haemarthrosis 1081 heat 1071, 1088 as hinge joint 1 053, 1 054 hyperextendable 1 1 39 immobilization effect on healing 46 instability see knee ligament instability intercondylar spines 1 054 internal derangements 1082-1092 symptoms / signs 1 082 intra-articu lar adhesions 1093 intra-articular injection technique 1080, 1 080 'jumper's' 1132 Lachman's test 1067, 1 068, 1118, 1 1 1 8 lateral (axial) rotation 1 068 assessn1ent 1066 meniscal movement 1056 lateral shearing strain 1069, 1 069 lesions, differential diagnosis 1 1 53-1 1 56 ligaments see knee ligament(s) locking 1 064, 1082 extension, loose bodies 1087 vertical meniscal tears 1083 loose bodies 1 087 diagnostic test 1087 differential diagnosis 1080, 1 087, 1089 in1pacted 1092 in osteoarthrosis see be/ow treatment 1087

vertical meniscal tears vs 1087 young patients 1 087 loose bodies in osteoarthrosis 1 080, 1 088-1092 differential diagnosis 1 089, 1 089 history and examination 1088 manipulation 1 089-1092, 1 090, 1 091 special investigations 1 088-1089 treatment 1089-1092 loss of cartilage 1079 medial rotation 1 068 assessment 1 066-1067 meniscal movement 1056 medial rotators 978 medial shearing strain 1 068-1069, 1069 monoarticular steroid-sensitive arthritis 1080, 1 089, 1089 movements 1 054, 1066-1069 flexion-extension 1053, 1053 normal limits 1 077 primary 1066 resisted 1 069-1 070 secondary 1 066-1069 muscles 1058-1 060, 1 059, 1 060 ilmervation 1060, 1 060 summary (functions) 1 060 osteoarthrosis 1 078-1 079, 1 079 clinical features 1079 crepitating 1088 differential diagnosis 1 089 loose bodies with see knee, loose bod ies (above) prevalence 1079 treatment 1079 osteonecrosis, spontaneous 1 089 pain anterior 1138, 1 1 53 capsular pattern 1 1 56 differential diagnosis 1 1 53-1 1 55 history-taking 1 064-1065 lateral, di fferential diagnosis 1 1 54-1 1 55 loose bodies in osteoarthrosis 1 088 medial, di fferential diagnosis 1 1 54 non-capsular pattern 1 1 56 osteoarthrosis 1079 posterior, differential diagnosis 1 1 55 painful arc 1066 palpation 1 0 70, 1 070-1072 for fluid 1070-1071, 1 071 for heat 1071 moving joint 1 072 passive abduction test 1 1 1 7, 1 1 1 7 passive adduction test 1118, 1 1 18 passive rotation, bilateral 1 072-1073 plicae synoviales 1092-1093 posterior capsular strain 1094 posterior drawer test 1067-1068, 1 068, 1119-1 120, 1 1 20 posttraumatic adhesions 1101 prone rotation test 11 19, 1 1 20 pseudogout 1080 reactive arthritis 1078, 1 078 referred pain from 1064 referred pain to 1 063-1064

INDEX 1309

resisted extension 1029-1030, 1069-1070, 1070 pain 1029-1030 resisted flexion 1030-1031, 1070, 1 070, 1144 differential diagnosis 1 1 48 pain 1030-1031 painless weakness 1031 resisted movements 1 069-1070 resisted rotation, interna l / external 1073, 1073 rheumatoid arthritis 1078, 1078, 1184 septic arthritis 1081-1082 'snapping' 1082 sprain 1100 classification 1100, 1100 symptoms 65 see 11/50 knee ligament(s), injuries/ lesions 'sprain without a sprain' 1088 squatting, palpation during 1073 stability tests 1072-1073 stabilization, by vastus medius obliquus 1 1 38, 1138-1139 subsynovial haematoma 1093-1094, 1 094 swellings 1065-1066 synovial thickening / swelling 1072, 1 072 tenderness 1072 trauma 1064 traumatic arthritis 1077-1078, 1087, 1094 coronary ligaments 1108 medial collateral ligament injuries 1103 twinge 1064, 1082 loose bodies in osteoarthrosis 1088 plica synovial is syndrome 1092 valgus 1139 valgus strain 1066, 1067 valgus strain test 1117, 1 1 1 7 varus 1139 varus movement, pain 1 088 varus strain 1066, 1067 varus strain / stress test 1118, 1118 villonodular synovitis 1081 knee jerks, sciatica 765 knee knob 1137 knee ligament(s) 1057-1058, 1100 chronic sprains 1101 instability vs 1 1 02 disorders 1099-1130 injuries / lesions 1099 acute or chronic 1101 classification 1100, 1 1 00 diagnosis 1100-1101 early mobilization 1101-1102 examination 1101 forces causing 1099 history 11 00, 1100-1101, 1101 immobilization not recommended 1100 serious vs less serious 1101 summary 1115 treatment 52, 1127 treatment principle 1101-1102 sprains 1102-1113

see also illdividual liglll11ents

knee ligament instability 1113-1127 acute 1117 treatment 11 21-1123 anterior cruciate ligament sprains 1111 anterolateral rotatory 1116, 1 1 1 7 anteromedial rotatory 1116, 1 1 1 7 chronic ligamentous sprains vs 1 1 02 chronic stage 1117 conservative treatment 1123 degree of 1115, 1 1 1 6 functional examination 1117-1 121 posterola tera I rota tory 1116, 1 1 1 7 rehabilitation 1122, 1 1 23 strength training phase 1125 rehabilitation after surgery 1124-1126 assisted ambulatory phase 1124 early strength training phase 1 1 24-1125 return to sport after 1 1 25-1126 rotatory 1115-111 7, 1 1 1 7 straight 1115, 1 1 1 6 tests 1 1 1 7, 1117-1121, 1 1 22 treatment 1121-11 27, 1127 conservative 1121-1123 types 1114-1117 knee reflex test 827, 827 Kohler's disease I 1245 kyphosis adolescents 642 angular 810 inspection 69, 601, 810 intradiscal pressure increases 745-746 thoracic spine 581, 601 angular 642 apex at T7 585 exaggerated 810 see also hyperkyphosis

labrum acetabulare see acetabular labrum labrum glenoidale see glenoid labrum Lachman's test 1 067, 1068, 1118, 1 1 1 8 laminae lumbar vertebrae 704-705 thoracic spine 582 laminectomy cervical extradural tumours 218 for lateral recess stenosis 930-931 lumbar disc lesion recurrence 896 manipulation not useful a fter 880 root pain after, nerve root block indication 915 sacral nerve root compression 749 thoracic disc lesion treatment 631 urgent, 53 and 54 sacral root palsy 929 landmarks epidural local anaesthesia 908, 908-909 thoracic cage 589, 589 thoracic nerve root pain 596, 596 Lane's test 509 lateral calcaneocuboid ligament 1 1 65, 1 1 65 lateral collateral ligament (elbow) 418, 4 1 9 lesions 444

lateral collateral ligament (knee) 1 057 injuries 11 07-1 1 08 deep friction 11 08, 1 1 08 diagnosis 11 07-1 108 summary 1 1 1 5 treatment 1 1 23 lateral collateral ligament ( temporomandibular joint) 675-676 lateral cutaneous nerve anatomy 979-980, 980 course 1264, 1 264 entrapment 1 264-1265 see also meralgia paraesthetica innervation area 1 264 lateral epicondylitis see tennis elbow lateral flexors, lumbar spine 714 lateral gliding, cervical manipulation 259-260, 260, 261 lateral gutter syndrome see lateral recess stenosis lateral hamstring, anatomy 1060 lateral Ligaments, ankle functional testing 61 passive movement limitation 85 lateral malleolus 1 1 62, 1 1 62 lateral medullary infarction (Wallenberg's syndrome) 230, 230 lateral pectoral nerve, anatomy 545 lateral pterygoid muscle, anatomy 677, 677, 694 ' lateral pull sign' 1141, 1141, 1142-1 143 lateral raphe 714 lateral recess 716 ageing effects 737 anatomy 791, 791 lateral recess stenosis 791-795, 800 bilateral 853 definition 788 foraminal encroachment 792-793, 793 history 807 nerve root block indication 915 pathology 791 -793 pedicular kinking 792, 793 pelvic tilting exercises 928 postsurgical fibrosis/ stenosis 793 radiography 794-795 sciatica vs 761 straight-leg raising 763 subarticular entrapment (of nerve root) 791-792 symptoms / signs 793-794, 810 terminology 791 thoracic spine 649-650 treatment 795 surgery 930-931 lateral root ligament 718, 718 ' lateral snapping hip syndrome' 1028 latissimus dorsi muscle 285 dermatome migration 10 glenohumeral stability 336 lesions 363, 413, 665 strength / propriocepsis training 342 testing 361 'lawn tennis arm' see tennis elbow

1 3 10 INDEX

laxity of ligaments see ligamentous laxity lead poisoning bilateral weakness of wrist 513 C7 nerve root compression vs 189 radial nerve disorders 558 ulnar nerve disorder 564 leg(s) ache, flexion, sciatica 762 crossed-over, rotational lumbar manipulation 882-883, 883 derma tomes 1 3, 1 4, 1 5 length inequality ind ications for correction 810 static scoliosis 810 lower see lower leg nerve supply saphenous nerve 1 266 see also thigh, nerve supply pain alternating 804 bilateral 803 di fferential diagnosis 1 1 99 lumbar spinal stenosis 789 neuralgic amyotrophy 867 spondylolisthesis 857 see also lower leg; lower limb Legg-Calve-Perthe' disease 1 045, 1046 aetiology 1 046 lesser trochanter, avulsion fracture at apophysis 1025 leu kocytes 33 levator scapulae muscle 336, 411 anatomy 393 lesions 411-412 leverage, spinal manipulation 107 cervical, traction with 260, 260, 261 Lewis's substances 95 Lhermitte's sign 30, 151, 202, 602 cause 602 thoracic intraspinal tumours 639 Lichtman classification, carpal instability 508 lidocaine 119 epidural anaesthesia preparation 909 postural syndrome treatment 778 lifting correct posture for 924-925, 925 low back pain 751 lumbar disc pressures 708 nuclear lumbago 747, 748 'I i ft-off' signs 371 ligament(s) 37-39 ageing effect cervical spine 176 lumbar spine 736 attachment to bone 37, 38 cervical spine 139-142 composition 38 dynamic, rotator cuff 287, 287 fu nctions 38 immobilization effect on healing 46, 47 intracapsular 54 lumbar see lumbar ligaments mechanical response to loads 38 overstretching 54

as regular connective tissue 37 rupture 38, 39 corticosteroid side effect 124 sclerosant infiltration 126 sensory receptors 37 thoracic spine 583, 583

see also illdividual ligaments ligament injuries chronic, deep transverse friction 98 corticosteroid infiltration 123 deep transverse friction 97-98 sprains acute, deep transverse friction 97 grade A mobilization 1 03 infiltration therapy 1 1 8 see also ligamentous lesions; individllal

ligaments ligamentous adhesions active movement therapy 114 medial collateral ligament (knee), manipulation for 1 1 06, 1106-1107, 1 1 07 passive movement limitation 85-86 rupture by grade C mobilization 105 ligamentous concept 775-785, 778, 840 diagnosis before treatment 874 disorder prevention 926-927 lumbar segmental instability and 840 mechanism of ligamentous pain 775-776 posterior dysfunction syndrome 779-783 postural syndrome 775-779 ligamentous conditions, cervical spine pain 167 ligamentous dysfunction syndrome see posterior dysfunction syndrome ligamentous hypertrophy, spinal cord narrowing 201 ligamentous laxity 54 clicks 79 dural concept 745 passive testing 73 prevention after injury 54 radioulnar joint, lower / distal 496 ligamentous lesions 52-54 acute and chronic, treatment 52-54, 56 grades and classification 53 incomplete ruptures 53 lumbar, prevention 926-927, 927 micro-tears 53 rationale for treatment 52-54 ruptures/ complete tears 52-53, 53 'sprains' 53 treatment 54 treatment methods 53-54, 56 surgical 54 see also ligament injuries ligamentous pain, lumbar 775-776, 800, 840 age of onset 802 see also posterior dysfunction syndrome; postural syndrome ligamentous postural syndrome see postural syndrome ligamentous sclerosis 632-633 thoracic postural pain syndrome 644

ligamentum flavum 139, 141, 142, 589 anatomy 712, 712 hypertrophy 787, 789 ligamentum nuchae 139, 141, 141 ligamentum patellae tendinitis 1136-1 137 see also infrapatellar tendon ligamentum teres, anatomy 974, 974, 975 lignocaine see lidocaine limb, formation / development 8, 9 limitation of movement active movements 81-83 history-taking 68 passive movements 83-87 testing 72-73 proportionate vs disproportionate 72-73, 85 resisted movements 87-89, 89

see also illdividltnl joillls, spillal regions linea alba 591 Linscheid's test 509, 509 Lisfranc's joint 11 64, 1 1 64, 1239, 1239-1240 movements 11 64-11 65, 1 1 65 ' little league elbow' 444 liver, referred pain from 597-598, 659-660, 660 load-and-shift manoeuvres, shoulder dislocation 338, 340 load-deformation curve 38, 38 loading controlled cyclic passive, of tendons 52 effect on articular cartilage 40, 40 effect on ligament healing 52 mechanical response of ligaments 38 local anaesthesia acute muscular tears/ strains 48 diagnostic 80 gluteal bursitis 1017-1018, 1018 psoas bursitis diagnosis 1016, 1 0 1 6 epidural see epidural local anaesthesia evidence of role of dura in lumbar pain 744 infiltration / injection 116, 118-121 amides 119 cervical disc displacement 266 dosages 1 1 9 facet joint syndrome diagnosis 780 hyperacute lumbago 750-751 lower leg in tennis leg 1185, 1 1 85 side effects see below side effects 119-121, 1 2 1 allergic reactions 118-119, 120-121 psychogenic 119 toxic reactions 119-120 treatment 120, 121 types 118-119 see also lidocaine; procaine long bicipital tendon, lesions 371-372, 372 long thoracic nerve 553-554 anatomy 545, 553, 553 disorders 553-554 innervation 553, 554 mononeuritis 218 differential diagnosis 188 examination 71

INDEX 1 3 1 1

testing 323, 323 rTlQnoneuropathy 553, 554 palsy 323 testing 554, 609, 609 traumatic palsy 553-554 tests 554 longus colli muscle, lesions 205 loose bodies ankle joint see ankle joint clicking 79 cuneiform-first metatarsal joint 1248 elbow see elbow hip joint see hip joint, loose bodies knee see knee manipulation 94 midtarsal joints 1 248 passive movement impairment 86 reduction, grade A mobilization 103 shifting pain 66 subtalar joint 1205, 1212-1213, 1 2 1 3 symptoms 67, 79 ulnar nerve 563 lordosis cervical, age-related change 1 77 hyperlordosis see lumbar lordosis, excessive lumbar see lumbar lordosis Louis, sternal angle 585 pain at 662 low back pain 699, 762, 802-806 age-related syndromes 734, 734-735, 985 bilateral 803 causes 699 intervertebral discs 700, 751

see also discoduml (below) central 803 chronic 754 epidural anaesthesia results 914 chronology 744 compensation and costs 700 continuous 801 costs 874-875 definition 800 discodural 751-757, 803 centralization 751 clinical examination 752-754 duration of pain 805 history 751-752, 807 increased during/ aiter bed rest 752, 755 intermittent 754 intractable, epidural therapy 904 manipulation 878 indications 878 success rate 881 mechanism 751 natural history 754 nocturnal / morning 752, 755 nuclear self-reducing disc 755 onset (sudden) manipulation for 878 vs slow onset 751, 803 posture/ movement relationship 751-752 questions before treatment decision 755 recurrent 754, 756

referral to bu ttocks 751 shifting pain 751 site of pain 751 sitting effect 751, 752 summary 757, 849 treatment 755-757 therapeutic epidural anaesthesia 904-905 types 754-755 see low back pain, discodural early morning 752, 755, 805 therapeutic epidural anaesthesia 904-905 episodic 805 history-taking 800-801 course / sequence 803, 804 duration 805 factors influencing 804-805 localization 802-803 onset of pain 803 previous attacks 805 reminders 802 summary 806 typical for specific diseases 807 incidence 699 increasing a fter lumbar surgery 853 increasing in sciatica 762 ineffective diagnosis/ treatment 700 ligamentous 775-776 see also posterior d ysfu nction syndrome; postural syndrome lumbar disc degeneration relationship 739 malignant diseases causing 803, 860, 861 metastatic 861 manipulation success rate 881 neuromuscular control deficits 838-839 nocturnal 752, 755, 805 therapeutic epidural anaesthesia 904-905 non-organic (functional ) 800 organic disorders causing 800, 800-801 activity-related 800, 800 non-activity-related 800, 801 osteoporosis 858 pain-free intervals 806 pathogenesis/ origin 800, 800-801 posterior arch lesions causing 775 posterior displacement of lumbar disc 733, 733, 751 see also low back pain, discodural posture / movements a ffecting 751-752, 804 pregnancy 867-868 therapeutic epidural anaesthesia 905 prevention 921-928 extension exercise under passive traction 926, 926 see also lumbar spine, disorder prevention pyogenic vertebral osteomyelitis (lumbar) 863 recurrence 754, 756, 921 referred 800, 801 sacroiliac joint as source 943

before sciatica 744, 760, 804 shifting 751 , 804 spondylolisthesis causing 857 summary 849 su rgery 875, 928 technical investigations, role 700 treatment scheme 875 types 754-755 unilateral 803 clinical examination 8 1 7 warning signs 801, 851-855 see aLso lumbar pain lower brachial plexus palsy 546 lower leg 11 57-1260 anatomy 1159-1160, 1 1 60 anterolateral compartment 1160, 1 1 60, 1 1 94 muscles 1160 tight fascia syndrome 1 193-1194, 1 1 94 clinical examination 1 1 71-1 1 79 history-taking 1 1 71 , 1 171-1 1 72 inspection 1 1 72-11 73 interpretation 1 1 81-1182 disorders 1183--1202 bone 1 1 83 tennis leg see tennis leg dorsiflexor lesions 1 1 93, 1193-1194 pain 1 1 93-1194 weakness 1 1 94 dorsiflexors 1 1 67, 1 1 67-1 1 68 evertor lesions 1197-1 199 invertor lesions 1195-1 197 pain 1 1 95-1 1 97 weakness 1 1 97 lateral compartment, muscles 1 1 60 pain, differential diagnosis 1 1 99 plantiflexor lesions 1183-1193 pain 11 83-1191 short muscles 1191-1192 weakness 1191 see also Achilles tendonitis plantiflexors 1 1 66, 1166-11 67 posterior compartment, muscles 1160-1161 see also foot; leg(s) lower limb dermatomes and development 9 nerve lesions/ entrapment neuropathies 1261-1270

see also individual nerves neurological examination 6 1 0 weakness, thoracic spinal cord compression 621 see also ankle joint; foot; leg(s) lower motor neurone lesion, paralysis 202 l u mbago 19 acute lumbar 1 9, 746-751 annular 746-747, 747 manipulation 878 treatment 750 causes 748 clinical examination 748-749 inspection 69, 748, 810 kyphotic posture 810 passive movement impairment 86

1 3 12 INDEX

lu mbago (continued) spinal movements 86, 748, 749, 806, 814, 8 1 4-815 straight leg raising test 748-749, 822, 824 definition 699, 746, 800 with deviation, McKenzie's technique 902 differential diagnosis 848 history 746-748 hyperacute 749 manipulation not possible 880 therapeutic epidural anaesthesia 904, 914 treahllent 750-751 mixed 748 natural history 749 nuclear 747, 747-748 causes ! mechanism 748 treatment 750, 880 pain onset 803 posterior d isc displacement 733, 733-734 radicular pain vs 746, 803 recovery 805 recurrences 749 spinal manipulation complication avoidance 113 summary 750, 848 traction contraindication 897 treatment 749-751 epidural anaesthesia 904 epidural injection method 757, 806 grade A mobilization 1 03 maintenance of reduction 756-757 manipulation success rate 881 McKenzie's technique 902 twinges 746, 806, 897 without deviation, McKenzie's technique 902 acute ' thoracic' 600, 619-620 definition 699 sternal 620 lumbar aching 776 lumbar dermatomes 10-11, 12, 1 3, 1 4, 986, 986 L3 1 0-11, 1 71 3 lumbar d isc(s) ageing 705-706, 729-741 displacements see lumbar disc lesions! displacements dural concept in natural history 745-746 invasion by vessels and connective tissue cells 731 mechanism 730-731 protection against displacements 735 ruptures 731 structural changes 731 of surrounding tissues 736-737 see also lumbar disc(s), degeneration age-related changes 705-706, 707 anatomy 705-710, 706 behaviour 706-710 biomechanical properties 708-710

effect of external loads on hydration 707, 707-708, 708, 730 as osmotic system 706-707, 707 biconvex 736 biomechanics 708-710 asymmetrical vs symmetrical loading 709, 709, 733 cartilaginous endplate 704, 705, 706 cervical vs 137, 1 3 7 composition 706-707 degeneration 729, 776 age of onset 729 deflation of intradiscal pressure 746 flexion-extension movement changes 737, 737 by immobility 922 lateral recess stenosis and 792 macroscopic changes 731 macroscopic grades 731, 732 natural history 738 pedicular kinking 792, 793 symptom relationship 739 vicious cycle 730, 731 see also lumbar disc(s), ageing; lumbar disc lesions! displacements dehydration-hydration 730, 730 curve and shift with ageing 730, 731 dehydration-hydration point 707-708, 708 fluid content 707, 730 diurnal changes 752 effect of loads 707-708, 708, 730 functions 706 gas in 738 infections 864 innervation 706 innervation of border 744 intradiscal pressure 'deflation' 746 traction mechanism of action 895-896 intradiscal pressure increase 733, 735, 745 by exercise 756, 843, 843, 926 nocturnal backache 755 sciatica mechanism 757 loss of height 710, 730, 736, 776, 840 loss of volume 730, 736, 776 mushroom phenomenon 735, 735, 792, 792 normal, flexion-extension movements 737, 737 nutrition 705, 707, 708, 730 deficiency in posterior boundary zone 731 loading ! deloading as pump 708 oncotic pressure 745 pressures 708 effect of changing posture 708, 730, 733 forward bending 708, 708, 733 lifting effect 708 normal sitting, standing and walking 707-708, 708, 730

see also intradiscal pressure (above) shrinkage, sciatica 765-766 spinal height decrease (ageing) 710, 730 stability not affected by back muscle strengthening 756, 843, 926 'three-joint complex' with facet joints 736

turgor loss 730, 736, 776 vascular buds 706 weak zones 709-710 lumbar discectomy 929 lumbar disc lesions ! displacements 731-736 annular 746 vs nuclear 896, 897 see also annulus fibrosus anterior displacement adolescents 733, 735, 735 elderly 735, 735 backwards shift, effects 704, 709 bilateral sciatica and 853 circular displacement 736 contained vs non-contained herniations 895 diagnosis 763-764 diagnostic epidural local anaesthesia 832-833 effect of various sports 926 exercises not preventative 756, 843, 926 first, protrusion, traction 896 fissures of annulus 731 fourth lumbar, drop foot, surgery indication 929 indeterminate, traction 896 L5-S1 protruSion, history-taking 64 lack of pain 731-732 large, traction contraindication 898 manipulation not possible 880 nerve root compression 720 see also lumbar nerve root(s) nuclear 705, 731, 733, 747-748 arUlular vs 896, 897 see also nuclear disc protrusion pain 615 posterior displacements 733, 733-734 acute lumbago 733, 733-734, 746 annular 746 backache 733, 733, 751 cauda equina syndrome 733, 734 maintenance after reduction 756-757 massive 733, 734 nuclear 747-748 posterior longitudinal ligament tension 733, 734, 744, 749, 75� 792 pos ture effect 733 sciatica mechanism 757-758 trea tmen t 755-757 see also l umbago, acute lumbar posterior weaknesses 709, 71 0 posterocentral displacement, referred pain to abdomen 662 posterolateral displacements 734, 734-735 age-related syndromes 734, 734-735 pain and postural deviation 806 passive knee flexion test 828 primary 734-735, 761, 804 epidural anaesthesia for 906-907 manipulation not useful 880 traction for 896-897 referred pain 662 sciatica mechanism 757-758 secondary protrusion 734, 758, 760-761

INDEX 1 3 1 3

spontaneous reduction in sciatica 765 straight-leg raising 763 sym ptoms / signs 760 therapeutic approach 897 prevalence of herniation 80 prevention 631, 921-926 by correct posture 631, 710 posterior longitudinal ligament role 709, 711 see also lumbar spine, disorder prevention prolapse (herniation) 733 protection against 735 protrusions 733 spinal segmental innervation testing 825 referred pain, to thorax 596 repair by traction 896 sacroiliac pain vs 820 sciatic scoliosis 810 second, protrusion differential diagnosis 867 traction 896 self-reducing 804, 816 manipulation not useful 880 size and position 732, 733 spondylolisthesis with 856-857 straight leg raising (SLR) test 822 stages, size of protrusion 823 surgery 928-930 third 817 traction effect 895, 895-896 types related to age 732-733 vertical displacements 735-736 lumbar disc space, infections 864 lumbar fascia, deep, injection technique 919, 920 lumbar instability 837-846 arthrodesis for 931 definitions 837-838 see also lumbar segmental instability lumbar ligaments anatomy 838 disorder prevention 926-927 function 775 injection 918-921 lesions, lumbar segmental instability and 840 pain due to 775-776, 926 postural strain 775 see also posterior dysfunction syndrome; postural syndrome lumbar lordosis development 703, 703-704 excessive (hypedordosis) 809 congenital limitation of extension of hip 1045 correct posture for 926-927, 927 prevention 926-927 fixation during flexion 818 increased, inspection 810 physiological 922 importance 704, 710, 922, 922 mechanism 922, 922 as 'physiological position' 921

lumbar manipulation 755, 756, 875-893 advantages 881 antideviation techniques 890-891 rotation-distraction 890-891, 891 side bending 890, 890 side gliding 891, 892 cau tion 806 contraindications 879-880 absolute 879, 879-880 relative 880 controlled trials 876 dangers 881 extension technique 885-890 central pressure 886, 888 unila teral distraction 889-890, 890 unilateral pressure 887-888, 889 failure, epidural anaesthesia indication 907 indications 878, 878-879, 879 oscillatory and sustained, nuclear disc protrusion 902 principles 876-877 procedure 891-893 progress assessment 892-893 repetition 893 rotation technique 881-885 leg crossed-over with side flexion 883-884, 884 legs crossed-over 882-883, 883 reverse rotation with thigh 885, 887 reverse stretch 885, 886 stretch 882, 882 sel f-correction after 891, 893 side effects and precautions 881 success rate 881 symptoms/ signs favouring 878 techniques 881-891 choice / selection 891-892 traction during 877

see also specific techniques above lumbar nerve root(s) adherent, neuroma vs 866 anatomy 714-715, 716-721, 71 7, 71 7-721 course 717 structure 720 atrophy 763, 768-769 neuroma vs 866 behaviour 718 boundaries 716-717 bruised, in sciatica 770 compression 720, 787 lateral recess stenosis 791 mechanism 720, 720 paraesthesia 807 signs/ symptoms 720-721, 72 1 signs / symptoms by level 723-724,

766-767 conduction, testing 764-765 definition 716 dural sheath (sleeve) 717, 718, 71 8 anatomy 71 8, 718-720 innervation 71 9, 719-720 see also dural sheath; dural sleeve examination 720 infiltrations 770

inflammatory response, sciatica 758-759 ischaemic atrophy 720 L1 compression 721 referred pain 662 signs / symptoms 723, 760, 766 L1 deficit, non-mechanical disorder 854 L2 conduction testing 825 deficit, non-mechanical disorder 854-855 palsy 764, 825, 1025 L2 compression 721 referred pain 662 signs / symptoms 723, 760, 766 L2 syndrome, nerve root blocks 915 L3 71 7 conduction testing 825, 829, 829 palsy 764, 825 posterolateral displacement in sciatica 759 L3 compression 721 , 762 referred pain 662 signs / symptoms 723, 760, 766 L3 syndrome, nerve root blocks 915 L4 717 conduction test 825 disc protrusion effect 717 palsy 764 posterolateral displacement in sciatica 759 L4 compression 721 signs/ symptoms 723 , 760, 766 L5 71 7 conduction test 825 posterolateral displacement in sciatica 759 L5 compression 71 7, 721 l a teral, lateraI recess stenosis 793 signs/ symptoms 723, 760, 766 mobility, testing 763-764 motor and sensory rootlets 71 6 motor / sensory deficits 720 movement during straight-leg raising 715, 715 multiple, involvement 854 neurological deficits 720, 721 by level 721 pain duration 805 epidural anaesthesia for 905, 914 increasing in neurofibroma / meningioma 865 intractable, surgery indication 929-930 lateral recess stenosis 793, 794 long duration epidural anaesthesia 906 manipulation 880 posterolateral displacements 734 sciatica 758, 758, 804, 854, 906 palsy recurren t scia ti ca after 906 surgery vs non-surgical treatment 928 parenchymal findings in sciatica 759-760 sheath, inflammation, epidural anaesthesia for 906

1 3 14 INDEX

lumbar nerve root(s) (continued) signs in discoradicular interactions 760, 766-767 sleeve see dural sleeve tests, in sciatica 763-765 triamcinolone infiltration, lateral recess stenosis 795 lumbar nerve root blocks 914-918 ind ications 915 technique L2-L5 roots 915-917, 9 1 6 5 1 sacral root 91 7, 917-918 lumbar nerve root canal space-occupying lesions 763 stenosis 787 retrolisthesis causing 840-841, 841 lumbar osteoarthrosis 787 lumbar pain ankylosing spondylitis see ankylosing spondylitis clinical syndromes 746-770, 800 see also low back pain; lumbago; sciatica continuous 852-853 of dural origin 743-746 evidence of role of dura 744 see also dural concept; dural pain end of movement (standing) 815 in forbidden area 812, 8 1 2, 852, 852, 858, 861 , 862 i ncreasi ng / expanding 852 warning sign 852, 860 neck flexion, dural mobility and 715, 715-716 origin (sites) 588, 800 partial articular pattern 814, 8 1 4 pathogenesis 800-801 referred 800, 816, 867-868 rheu matoid arthritis 801, 862 straight-leg raising, dural mobility and 71 5, 715-716, 748-749 warning signs/ symptoms 801, 851-855, 860 see also low back pain lumba r-pelvic rhythm 8 1 8 normal, reversal 841, 841 lumbar postural syndrome see postural syndrome lumbar puncture needle, insertion method 909-911, 9 1 0 lumbar segmental instability 837, 837-838 anatomical aspects 838-839 contractile structures 838 inert structures 838 neuromuscular control 838-839 classification 839-840 definition 838 degenerative 839, 839 diagnosis 841-842, 842 discodural interactions and 840 ligamentous lesions and 840 misuse of term 841 rotational 840 stenotic concept and 840-841 translational 840

treatment 842-844 arthrodesis 931 exercises 842-843 sclerosant infiltration 843-844, 844 surgery 844 vulnerability to trauma 840 lumbar spinal canal ageing effects 737 anatomy 704, 714 anterior and posterior walls 714 space-occupying lesion 804 stenosis see lumbar spinal stenosis lumbar spinal cord 716 compression 807 testing integrity 827 tumours 865-867 lumbar spinal stenosis 787-788, 788-790, 800 bilateral sciatica due to 853 clinical examination 816 definition 788 degenerative 788, 789, 790 developmental 787-788, 788, 790 leg pain 789 pathological changes 788-789 pelvic tilting exercises 928 posture adopted 789-790, 927 prevention 927-928 radiography 790, 790, 791 surgery for 930-931 symptoms/ signs 789-790, 810 treatment 790, 927 see also la teral recess stenosis lumbar spine 697-937 ageing 729-741 lateral recess stenosis and 793-794 natural history 738 postural pain 776-777 radiological changes 738, 738 see also lumbar disc(s), ageing anatomy 703-738 contractile structures 838 inert structures 838 neuromuscular control 838-839 posture and 703-704 ankylosing spondylitis see ankylosing spondylitis biped vs quadriped 704, 729 clinical examination 799-836 accessory tests 831-832 epidural local anaesthesia 832-833 palpation 830, 830, 831 technical investigations 833-834

see also il1spection, junctional examil1ation (below) computed tomography (CT) 834 concepts 847, 848 see also dural concept; ligamentous concept; stenotic concept degeneration 700, 776-777 discs see lumbar disc lesions/ displacements ligamentous 775-785 natural history 738 phases 839, 839

stenotic concept 787-797

see also ligamentous concept; lumbar disc(s); lumbar spinal stenosis 'degenerative instability' 839, 839 primary and secondary 839, 839 translational 840 degenerative vertebral slippage 788 development 703, 703-704 discs see lumbar disc(s) disorder prevention 921-928 discodural interactions 631, 710, 921-926 extension exercise under passive traction prevention 926, 926 lifting and carrying positions 924-925, 925 ligamentous disorders 926-927 posture in bed 925, 925 primary / secondary 921 sitting posture 922-923, 923, 924 standing posture 924, 924 stenotic disorders 927-928 tertiary 921 disorders activity-related 800, 800 age-related 801-802, 802 classification 739 pathogenesis 800-801 see also ligamentous concept; lumbar disc lesions/ displacements; lumbar spinal stenosis extension examination standing 812, 812, 813, 816-817 interpretation 816-817 limitation in lateral recess stenosis 794 limited in acute lumbago 748, 749 limited in facet joint syndrome 779 low back pain examination 752 pressures towards, on palpation 830, 830 resisted, in prone position 832, 832 scia tica 762 extradural lesions 864-865 facet joints see facet joints fasciae 713, 713-714 flexion in acute lumbago 748 control by supraspinous ligament 782 examination standing 812, 818-819 interpretation 818-819 low back pain examination 752 muscles involved 818 pain at end of range 818 with rigid lumbar segment 854 sciatica 762-763 forward bending / lifting, nuclear lumbago 747, 748 fractures see lumbar vertebrae functional examination 812-831 prone position 827-829, 830, 831 psychogenic symptoms and 832, 832 standing position see lumbar spine, standing examination summary 83 1

INDEX 1 3 1 5

supine position see lumbar spine, supine examination warning signs 8 1 9, 827, 830 fusion 844 gastric ulcer adherent 868 history-taking 799-808 age and daily activities 801-802, 802 importance of good history 800 pain see low back pain paraesthesia ('pins and needles') 806-807 patient's reaction 808 problem-solving 801 routine of 802-808 Sl nerve root compression 807 hyperextension 783 facet joint syndrome 780 importance of diagnosis 873-874 importance of lordosis 704, 710, 922, 922 innervation 721-722 inspection 808-812 acute lumbago 748 normal 808, 808 pathological 808-812, 809 instabiiity see lumbar segmental instability intervertebral height decrease 710, 730, 776, 777 intervertebral space, normal 777, 790 intraspinal space-occupying lesions 821-822 lateral deviation 810, 811 acute lumbago 748 on flexion 819 see also scoliosis ligaments 711-713 magnetic resonance imaging (MRI) 834 malalignment, in segmental instability 841-842 malignant disease 801 history 807 manipulation complication 112 mechanical disorders 847-850 diagnosis before treahnent 874 differential diagnosis 847-850 see also low back pain; l umbago; sciatica movements 8 1 2 acute lumbago 748, 749 anterior / posterior translation during 842, 842 full articular pattern (standing) 815-816, 8 1 6 full range without pain (standing) 816 interpretation 816 L5-S1 joint 713 low back pain examination 752 neutral zone concept and 837-838 partial articular patterns 749, 753, 8 1 4, 814-815, 816 range (ROM) and zones 837-838 rota tiona I 838 sciatica examination 762, 762-763 muscles 713, 713-714 inspection 811

sprain 831-832 stability not a ffected by strengthening 756, 843, 926 stabilizing effect 838 non-mechanical (non-activity) disorders 700, 851-871, 855 infectious 863-864 intraspinal lesions 864-867 osseous 857-861 rheumatological 861-863 warning signs/ symptoms indicating 851--855 pain see lumbar pain painful arc 753, 754, 814 examination 814, 815 on flexion 819 painless click 815 on side flexion 818 straight leg raising (SLR) test 764, 823 plain radiography 833 referred pain 800, 816, 867-868 Reiter's syndrome 862 restabilization phase 839, 839 rheumatoid arthritis 862 rotational instability 840 sclerosant infiltration 126 technique 920-921 side flexion 813, 813-814 age-related reduction 8 1 4 examination standing 8 1 2 , 812-813, 813

gross / bilateral linlitation 854 gross limitation away from painful side 854, 854, 867 interpretation 817-818 limited in acute lumbago 748 low back pain examination 752 muscles involved 8 1 7 pain at e n d 818 painful limitation 863 painless / painful limjtation 8 1 7 resisted 832, 832 sciatica 762 warning sign 817 spondylolysis see spondylolYSiS stabilizing support 775, 838 decrease in segmental instability 838 neuromuscular control 838-839 passive (inert) and active (contractile) 838 standing examination 812, 812-819 findings 8 1 4, 814-816 interpretation 816-819 summary 831 warning signs 8 1 9 stenosis see lumbar spinal stenosis stiffness 776--777 mechanism 839 supine examination 819-827 circulation examination 827 motor conduction tests 825, 825--826, 826

sensory conduction test 826, 826--827 spinal cord integrity testing 827

spinal segmental innervation testing 824-827 summary 831 warning signs 827 see also straight leg raising (SLR) test surgery, increasing backache after 853 symptom localization 800 see also low back pain; lumbago, acute lumbar; sciatica thoracic spine differences 593-594 treahnent 873-937 injections 903-921 placebo and 'central' effect 873 questions to ask before 874-875 surgery see spinal surgery see also lumbar manipulation; traction, lumbar tumours 820-821, 859-861 benign 859-860 malignant (primary) 860-861 metastatic 861 vertebrae see lumbar vertebrae lumbar stenosis see lumbar spinal stenosis lumbar support car seats 923-924, 924 chairs 923, 923, 924 lumbar traction see traction lumbar vertebrae anatomy 704-705, 705 benign tumours 859-860 biconcave fish mouth 858 endplates age-related structural changes 731 - permeability 730 sclerosis 730, 736 forward displacements 842 fractures 858-859 crush, of vertebral body 858 fatigue, of pars interarticularis see spondylolYSiS pathological 853 stress, lumbar pedicle 859 transverse processes 818, 831, 859 Ll, tumours 640 laminae 704-705, 71 2 osteomyelitis 863 pedicles 704 slipped see spondylolisthesis 'squaring' 862 tuberculous osteomyelitis 863-864 vertebral bodies see vertebral bodies see also lumbar spine l umbosacral junction, stability, iliolumbar ligament role 713 lumbosciatic pain treatment scheme 875 see aLso low back pain lumbrical muscles 479 l unate bone 474 aseptic necrosis see Kienbock's disease subluxation 502, 569 lung apical tumours 657 see also Pancoast's tumour carcinoma, referred pain 656

1 3 1 6 INDEX

lung (continued) lesions, shoulder pain 219, 657 referred pain from 597, 656-657 superior sulcus 657 carcinoma see Pancoast's tumour lupus erythematosus, temporomandibular joint 694-695 lying, correct posture 925, 925 lymphatic vessels, connective tissue 36 lymphocytes 33 inflammation 44 lymphoma, cervical spine 214

macrophage 33, 44 magnetic resonance imaging (MRI) aseptic necrosis of hip 1010-1011 carpal tunnel syndrome 571 cervical spine lesions 1 62 low back pain 700 lumbar spine 834 rheumatoid arthritis of wrist 501 shoulder 301 temporomandibular joint disorders 684 thoracic neurofibroma 638 thoracic outlet syndrome 551 thoracic spinal cord compression 621 thoracic spine disorders 610, 612 malingering lumbar spine examination supine 819, 824 whiplash-associated disorders 242 see also psychogenic problems malleoli deep friction above/ below 1 1 98, 1 1 98 fractures 1 2 1 7, 1 2 1 8 medial 1 167 mallet finger 537-538, 538 Mallory-Weiss syndrome 658 mandible anatomy 675, 676 biomechanics/ movements 677-678 body and ramus 675, 676 deviation, examination 681, 682 resisted 683, 683 grinding movements 677 mandibular neck 675 manipulation (grade C mobilization) adherent lateral ligaments of ankle 1226-1227, 1227 carpal subluxation 502-503, 503, 504 chronic ankle sprain 1223 cuboid bone rotation treatment 1 245-1246, 1 246 indications 1 04 intra-articular adhesions of knee 1 093 loose body reduction ankle joint 1205, 1 206 elbow 441-442, 442, 443 hip 1013-1015, 1 0 1 4, 1 0 1 5 �1ee 1089-1092, 1 090, 1 09 1 subtalar joint 1212-1213, 1 2 1 3 medial collateral ligament injuries (knee) 1 1 06, 11 06-1 107, 1 1 07

midtarsal strain treatment 1 243, 1 244 reduction dislocation of temporomandibular meniscus 692, 692 luxation of condyle (temporomandibular) 694, 694 mensical displacement (knee) 1 085-1086 subtalar joint 1212, 1 2 1 2 techniques 94, 105 contraindications 105 definition 1 02, 105 indications 94, 105 preparation, by deep transverse friction 96 ' thrust' 1 02, 105, 107 traumatic arthritis of shoulder 310 manipulation (spinal) 1 05-114, 1 08 aims 1 1 3-114 cervical spine see cervical manipulation clinical trials 1 1 0-111, 249 complications 1 11-114 prevention 1 1 2-114, 1 1 4 b y spinal level 1 1 2 contraindications 107, 1 09-110, 1 1 0, 1 1 3, 600 cervical 250-252, 252 l u mbar 879, 879-880 definition 876-878 disc protrusion action 109 complication avoidance 1 1 3 end-feel 107, 1 1 3 erroneous confirmation of diagnosis 108 evaluation of effectiveness 1 1 0-111 historical aspects 106, 875-876 indications 1 09 cervical 252-253, 253 l u mbar 878, 878-879, 879 indiscriminate use 106 long-lever, and effects 877, 877 lumbar backad1e see lumbar manipulation migraine 225 mode of action 109 morning headache in elderly 197-198 non-specific long-lever 108 non-vestibular vertigo 236 not under anaesthesia 1 1 0 objective 876-877 orthopaedic medicine technique 1 06-107 overtreatrnent avoidance 114 pain a fter 1 11-112 pain relief 1 1 1 premanipulative testing 232-233, 249, 254 protocol 250 principles 876-877 procedures induded 105 reassessment after 1 07, 1 1 4 sciatica 769 selectivity 107-109 of diagnosis 1 07-108 of manipulation 1 08-109 segmental mobility tests 107

short-lever high-velocity 108-109 thoracic see thoracic manipulation 'thrust' 107, 108, 1 1 1 traction during 106-107 lumbar 877 manipulative schools 877 manual therapy manipulation controversy and 248 patient dependency 1 09 spinal 106 manubriosternal joint ankylosing spondylitis 670 arthritis 662 pain 597, 662 manubrium 585 pain 662 march fractures 1249-1250 diagnosis 1249-1250 differential diagnosis 1250 treatment 1250, 1 250 Martin-Gruber anastomosis 424, 565 massage acute muscular tears/ strains 48 deep transverse see deep transverse friction masseter muscle, anatomy 676, 677 mast cells 33, 44 mastectomy, contractu re after 322 McGregor line 216, 2 1 6 McKenzie, R., spinal manipulation 106, 109 McKenzie's techniques 902-903 acute annular lumbago 878, 902 manipulation controversy and 248 nuclear disc protrusion reduction 902-903 nuclear lumbago 750 McMurray intertrochanteric osteotomy 1007 McMurray test 1 084, 1085 mechanoreceptors, lumbar discs 706 mechanoreceptor transmission 5, 6, 26 medial collateral ligament (elbow) 418, 419 rupture 444 medial collateral ligament (knee) 1057, 1 057 adhesions, manipulation for 1 1 06, 1106-1107, 1107 bursitis 1 095, 1 095 calcification' 1093, 1 1 03-1104 complete tears, rehabilitation 1122 injuries 1 1 00 diagnosis 1 1 03-1104 instability due to 1121-1122 mechanism 1 1 03 natural history 1 1 03 rehabilitation 1 1 22 sprains 53, 11 02-110� 1 1 03 summary 1 1 07, 1 1 1 5 passive movement limitation 85 treatment of injuries 11 02, 1 1 04, 1 1 04-1107, 1 121-1122 acute 11 04, 1 1 04 deep friction 1 1 04-1105, 1 1 05, 1 122 infiltration and cold compression 1 1 04, 1 1 04

INDEX 1 3 1 7

manipulation 1 1 06, 1 1 06-1107, 1 1 07 , subacute and chronic stages 1105 medial collateral ligament (temporomandibular joint) 676 medial cutaneous nerve, of forearm 424 anatomy 545 lesions 573 medial epicondylar stress lesion 444 medial epicondylitis see golfer'S elbow medial ligamentous complex, knee 1057 medial malleolus, tendons 1167, 1 1 67 medial pectoral nerve, anatomy 545 medial pterygoid muscle, anatomy 676, 677 medial radiocarpal drawer test 509 median nerve 566-573 anatomy 424, 425, 480, 481, 566, 567 brachial plexus cords forming 545 in carpal tunnel 478, 568, 570 anomalies 424 branches 567 compression C6 nerve root compression vs 189 carpal tunnel see carpal tunnel syndrome causes 568-569, 569 corticosteroid infiltration 123 at lower arm and elbow 567-568 T1 nerve root compression vs 191 thoracic outlet syndrome vs 551 thumb weakness 529, 570 by tumours 569 disorders / lesions 567-573 at carpal tunnel see carpal tunnel syndrome at forearm 568 lower arm and at elbow 567-568 innervation 566, 566 neurolysis 572 palsy 424 median nerve syndrome, clinical features 567 median perineuritis 568 see also carpal tunnel syndrome mediastinal disorders, referred pain 658 mediastinal emphysema 658 mediastinal tumours, referred pain 658 mediastinitis, acute 658 medication, cervical spine history-taking 151 medicolegal cases, diagnostic epidural injection 904 medulla oblongata, blood supply 230 'medullary feeders' 584 membranous labyrinth 227 memory, long-term, of pain 5, 7 meningeal irritation 716 meningioma cervical 217, 2 1 7 lumbar 865-867 meningitis, acute torticollis vs 184 meningovertebral ligaments, ventral 714 meniscectomy, knee 1086 menisci anatomy / composition 41, 1 055, 1 055 facet joints of lumbar spine 710

knee anatomy 1 055, 1 055-1056 chondrocalcinosis 1087 congenital anomalies 1082-1083 cysts 1 086-1087, 1096 discoid, Wrisberg ligament type 1082, 1 082 discoid lateral 1082, 1 082 displacements manipulation 1 085-1086, 1 086 natural history and pain 1086 ruptures with 1084 insensitivity to pain 1055 lesions 1082-1087 coronary ligaments injuries vs 1108, 1 1 09 medial displacement, manipulation 1 085-1086, 1 086 vertical tears 1083 metabolic disorders affecting 1087 movements 1055-1056, 1 056 surgery 1086 tears / ruptures 1078 arthroscopy 1085 arthroscopy vs clinical diagnosis 1085 bucket-handle 1083 diagnosis 1 084, 1 084-1085 differential diagnosis 1 087 with displacement 1084 horizonta l / posterior cracks 1083, 1083-1084 surgery 1086 treatment 1085-1086 types 1 083 vertical see vertical tears (below) without displacement 1 084, 1 084-1085 testing 1072 traumatic lesions 1083-1086 vertical tears 1 083, 1 083 anterior cruciate deficiencies and 1111 loose bodies vs 1087 mechanism of injury and history 1083 sternoclavicular joint 281 temporomandibular joint see temporomandibular joint (TMJ) ulnocarpal 473 menstrual irregul arities, corticosteroid side effect 125 mental state manipulation contraindication 880 therapeutic epidural anaesthesia indication 905 traction contraindication 898 meralgia paraesthetica 28, 1 264-1265 differential diagnosis 1265 symptoms 1 264-1265 treatment 1265 mesenteric ischaemia 661 metabolic disorders, affecting menisci (knee) 1087

metacarpal gliding, test 509 metacarpal ligament, rupture 506 metacarpophalangeal joints anatomy 476, 476 capsulitis, forced movement contraindication 56 movements 476, 476 passive movements 490 pain 535 metastases bilateral sciatica due to 861 brachial plexus 546 cervical spine 1 90, 2 1 4, 214-215 femur 88, 1 025 lumbar spine 861 rib 664 scapula (warning sign) 408 shoulder 31 7 thoracic spine 190, 215, 639 thoracolumbar junction 639 metatarsal bones fi fth, fractu res 1250-1251 first cuneiform joint see cuneiform-first metatarsal joint short 1249 shafts 1165 metatarsalgia 1254 chronic 1 1 92, 1251, 1256-1257 dancer's 1257 strengthening of muscles, active movement therapy 115 metatarsal joints, cuneiform- see cuneiform-first metatarsal joint metatarsophalangeal joints first 1 25 1 , 1251-1255 arthritis in adolescence 1 252-1253 arthrosis in middle age 1 253 capsular pattern 1 252, 1 252-1255 gout 1252 hallux valgus 1 254-1255 importance in gait 1251 metatarsalgia 1254 rheumatoid arthritis 1253 sesamometatarsal lesions 1254 traumatic arthritis 1253 see also hallux valgus outer four 1255-1258 capsular pattern 1 255, 1 255-1256 chronic metatarsalgia 11 92, 1251, 1256-1257 Freiberg's osteochondritis 1256 gout 1255 interdigital ganglion 1257 non-capsular pattern 1 256-1258 osteoarthrosis 1256 pressure on nerves in forefoot 1257-1258 see also Morton's metatarsalgia rheumatoid arthritis 1255 traumatic arthritis 1256 methylparaben 120 microdiscectomy, lumbar 929 midcarpal instability, testing 509 midcarpal shift test 509

1 3 1 8 INDEX

midclavicular pain 406 midd le-aged persons arthritis of midtarsal joints 1241 arthrosis at first metatarsophalangeal joint 1253 loose bodies in elbow 443 posterocentral cervical disc displacement 196 postural thoracic outlet syndrome 549 middle brachial plexus palsy 546 middle cerebral artery 228 midfoot anatomy 1 1 61, 1 1 6 1 bones 1164 differential diagnosis and treatment of d isorders 1 247 ligaments 11 65, 1 1 65 passive testing 1176-11 78 resisted movements 11 78, 1 1 78 see also foot midtarsal joints 1164, 1 1 64 arthrosis 1246 aseptic necrosis 1245 cuboid rotation 1245-1246 cuneiform-first metatarsal joint lesions 1 246-1248 disorders 1 239-1248 capsular pattern 1 240, 1 240-1241 differential diagnosis and treatment 1 247 non-capsu lar pattern 1241-1246 ligamentous contracture 1244-1245 mobilization, strain treatment 1243 manipulation 1 243, 1 244 navicular stress fracture 1245 passive tests 1 1 76-1178 rheumatoid arthritis 1241 strain 1241-1 244, 1 242, 1 244 clinical examination 1242-1243 inflammation 1243 mechanism 1241-1 242, 1 242 postural pain 1242-1243 structural changes 1243 treatment 1243-1244 subacute arthritis in adolescence 1240-1241 in middle age 1241 sustentacu lum tail 1 242 migraine 149, 223-224, 224-225 diagnostic criteria 224, 225 manipulation under traction 267 neurovascular disorder theory 225 ophthalmoplegic 680 prevalence 223, 224 spinal manipulation 225 therapy 225 triggers 224-225 vascular theory 224-225 Mill's manipulation 459-461, 460, 461 contraindications 460 deep transverse friction before 460, 460 technique 460-461, 461 mineralocorticoids 121 mitral valve prolapse, referred pain from 656

mobilization definition 102 effect on healing 47, 47 ligamentous lesions 53 grade A 94, 102 indications 103 grade B 94, 102 indications 104-105 grade C see manipulation indications 94, 1 03-105 methods in ligament lesions 53 preparation, by deep transverse friction 96 traumatic arthritis of shoulder 308-310, 309, 3 1 0 monoarticular arthritis hip joint 1001 of unknown origin, arthrosis of cervical facet joints us 199 monoarticu lar steroid-sensitive arthritis corticosteroid infil tration 122 elbow 439 hip 1000 knee 1080, 1089, 1 089 manubriosternal 662 radioulnar joint, lower / distal 496 shoulder 3 13, 313-315 temporomandibular joint 694 mononeuropathy see illdividual Ilerves morning backache 755 cervical spine 168 nuclear self-reducing protrusions 931 therapeutic epidural anaesthesia 904-905 morning stiffness fingers 534 shoulder 315 mortice test (tibiofibular ligaments) 1 1 75, 1 1 76 Morton's metatarsalgia 1258 treatment 1258, 1 258 Morton's syndrome 1249 motion sickness 233, 235 motor conduction testing, lumbar spine 824-827 prone position 829, 829 supine position 825-826 motor deficit cervical spondylotic myelopathy 202, 202 nerve root compression 29 sciatica 759-760, 768 motor fibres 42-43 motor unit 43 motor vehicle accident patellar fractures 1137-1138 posterior cruciate ligament injuries 1 112-1113 whiplash injuries 239 mouth closing 677, 681, 682 difficulties 681 resisted 683, 683 opening 677, 681, 681 limitation 696 resisted 682, 683 reciprocal clicking on opening / closing 691

movement absence of pain 89 excessive range 73 functional examination 7] -75 limitation see limitation of movement normal range 71 see also active movements; passive movements; resisted movements mucocele, peroneal 1197-1 198 multifidus muscle 713, 713, 838 co-contraction exercise with transversus abdominis 843 reflex arc with supraspinous ligament receptors 838-839 stabilizing role to spine 838, 843 mul ti pie myeloma cervical spine 214 lumbar spine 860-861 radiography 861 thoracic spine 639 multiple sclerosis, cervical spondylotic myelopathy us 203 multisegmental pain C3 nerve root lesion 187 C4 nerve root compression 188 cervical spine 166, 1 79, 1 79 cervicogenic headache 226 dural see dural pain headache 149, 149 multisegmental tenderness, cervical disc displacement 179 muscle adhesions 1185 atrophy 42 centripetal / centrifugal migration 9-10 connective tissue 42, 42-43 contraction 42 pain due to 88-89 fasciculation 29 fasciculi 42 guarding 74, 251 healing, adverse effects of steroids 49 hypertrophy 42 immobilization effect on healing 46, 47 lesions, inspection 70 in limb formation 9 mobilization effect on healing 47, 47 nerve supply 42-43 paralysis, grade B mobilization of joint 104 power, absence 75 'pull' injuries 48-49 rupture, palpation 78 strain injuries 48-49 strength, decreased by immobilization 46 strengthening active movement therapy 115 back/ abdomen, lumbar disc stability not a ffected by 756, 843, 926 stretching, grade B mobilization 104 structure / organization 42, 42 tears, aims of treatment 1185 wasting, paraspinal muscles 811

see also illdividual muscles

INDEX 1 3 1 9

muscle belly btoadening, treatment of acute muscle tears 48, 49 conewise infiltration 117 deep transverse friction 96-97, 97 myosynovitis 49 partial rupture, infiltration therapy 118 muscle cells (myofibrils) 42, 42 muscle spasm 48 annular lumbago 746, 747 in arthritis, grade B mobilization 104 end-feel 74 ligament laxity 54 lumbar spine inspection 811 manipulation contraindication 105, 880 peroneal 1198 spinal manipulation action 109 warning sign in lumbar spine 854 warning sign in thoracic spine 637 muscular coordination, exercises 115 muscular crepitus 79 muscular end-feel 73 muscular lesions cervical spine, whiplash 241, 244 contusions 48, 49 delayed soreness 47-48 prevention 48 localization and treatment 52 minor tears (strain injuries) 48-49 acute 48 chronic 48-49 treatment 48 myosynovitis 49 tears deep transverse friction 96 isotonic contractions 1 1 4-11 5 treatment aims 96 treatment 47-50 types 47-50 muscular training programmes lumbar instability treatment 843 see also exercise(s) musculocutaneous nerve 545 anatomy and innervation 573, 573 lesions 573 musculotendinous junction, deep transverse friction 97 musculotendinous lesions, neck 204-205 musculotendinous unit 62 mushroom phenomenon cervical disc 200, 200 lumbar disc 735, 735, 792, 792 myalgia, temporomandibular joint (TMJ) 695 myelin sheath 23-24, 24 damage 27, 41 myelography contrast, lumbar spine 833 thoracic neurofibroma 638 thoracic spinal cord compression 621 myeloma see multiple myeloma myelopathy cervical spondylotic see cervical spondylotic myelopathy paraesthesia due to 151

myeloradiculopathy, cervical 201 , 202 mylohyoid muscle 677 myofascial pain syndromes 19 myofibrils (muscle cells) 42, 42 myofibroblasts 44 myofibrositis 19 myofilaments 42, 42 myopathy C5 nerve root lesion vs 189 painless weakness of upper limb 368 steroid 125 myosin 42, 42 myositis ossificans 49-50, 56 brachialis muscle 450 quadriceps rupture complication 1131 myosynovitis 49, 96 abductor pollicis longus 524 extensor pollicis longus / brevis 524 tibialis anterior muscle 1193 myotendinal junctions 42 myotome 8 derma tomes discrepancy 15-16

Navarro's columnar concept 507-508 navicular stress fracture, in midtarsal joints 1245 neck muscles 142, 1 42, 1 43 musculotendinous lesions 204-205 pain see neck pain pain referred to temporomandibular joint 680 soft tissue injuries see whiplash­ associated disorders stiff acute torticollis 183 postviral torticollis 1 84 structures causing cervicogenic headaclle 226 unilateral pain see torticollis, acute neck movements 617 in cervical disc displacement 180, 1 80 clay-shoveller'S fracture 212, 323 effect on blood flow in vertebral arteries 230, 230-231 9��oo l � 1� 1� 1 � 1� 1 � vertigo examination 233 favourable signs 253 flexion 138, 139, 1 39, 152, 1 53, 155, 1 55 acute lumbago 748 avoidance, indications 196 cervical disc displacement 1 79 cervical spine lengthening 143 dural mobility 715, 715, 719 low back pain and 753-754, 814 lumbar spine examination 814 pain in thoracic area 180, 617 pain in thoracic neurofibroma 638 paraesthesia 602 rheumatoid arthritis 215 during straight-leg raising 823, 824 thoracic spine examination 601-602, 602 twinges in nuclear lumbago 747

flexion a n d rotation 1 3 9 functional examination 152-155 active movements 152, 1 53 asymmetrical pattern 152, 1 54, 1 70, 1 70 full articular pattern 152, 1 54, 169, 1 70, 1 70 neurological conditions 218-219 passive movements 152, 154, 154-155, 1 69 resisted movements 155, 1 56 shoulder disorders 294, 294 thoracic spine disorders 601 -602, 602 interpretation 1 69, 1 69-172 lateral flexion 1 53, 155, 1 55 inspection 1 51 in migraine 225 painless weakness 1 71 passive / resisted, pain in septic arthritis 405 positive active and passive movements 1 69-170 convergent / divergent pattern 1 70 full articular pattern 152, 1 54, 1 69, 1 70, 1 70 limitation patterns 169-170, 1 70 painful limitation 169, 1 70 painless limitation 1 70 pain patterns and end-range pain 170 partial articular pattern 152, 1 54, 1 70, 1 70 positive active and resisted movements 1 71 , 1 71-172 proprioception disturbances 235-236 provocation tests for dizziness 235 resisted, pain 204-205 resisted extension 75 rotation 138, 139, 139, 152, 1 53, 1 54, 1 54 effect on blood flow in vertebral arteries 230, 230-231 signs in whiplash injury 243 testing 152-155 unfavourable signs 253 manjpulation futility 252 neck pain 1 50, 1 50 acute brachial plexus neuropathy (neuralgic amyotrophy) 368, 552 bilateral 192, 196-197 causes 197 central 192, 1 96-197 acute torticollis (symmetrical ) 192 see also cervical disc displacement, posterocentral; discodural interaction cervical spine tumours 212, 213, 214 cervical spondylosis causing 197 chronic, manipulation indication 252 facet joint arthrosis 1 98 history-taking 147-150 local 166 morning 197 nocturnal cervical spinal metastases 214, 2 1 4 tumours of cervical spine 212, 213 resisted neck movements 204-205

1320 INDEX

neck pain (continued) rheumatoid arthritis 2 1 6 sternoclavicular joint disorders 403, 404 thoracic cage problem 600 unjlateral 1 82, 1 84-185, 1 85 acute torticollis (asymmetrical) 1 83, 184 see also cervical nerve roots whiplash injury 243 needles, injections / infiltration 1 1 6, 1 1 6 nerve bundle 23 nerve conduction tests acute lumbago 749 lumbar spine 824-827 nerve damage, corticosteroid side effect 124 nerve fibres Ad group 4, 26 a fferent 5 anatomy 23-24 C group 4, 26 conduction velocities 4 'cross-talking' 26 fasciculi 23, 24, 25 small myelinated 4 unmyelinated 4 nerve impu lses, a fferent nociceptive system 4, 4-5 nerve lesions lower limb 1261-1270 upper limb 28, 541-578

see also individual nerves nerve pain 26 nerve plexus 24 anatomy 25 fasciculi 25 lumbosacral 1 8 pressu re, effect 28, 68, 1 5 1 , 543 see also bradlial plexus nerve root blocks, lumbar see lumbar nerve root blocks nerve roots 24-25 anatomy 720 cervical see cervical nerve roots compression, effects 28-29, 68, 543 see also paraesthesia extraspinal 25 intraspinal 24, 24 compression, effects 28-29 extra thecal 25, 28 intrathecal 24-25 lesions 83, 145 lumbar see lumbar nerve root(s) pain see root pain peripheral nerve comparison 720 progressive compression 29, 29 thoracic see thoracic nerve roots nerve root sheath 25 nerves afferent 5 anatomy 23-26, 24 connective tissue surrounding 41, 41 corticosteroid infiltration 1 23 disorders, deep transverse friction contraindication 98 hip joint 979-980

mechanjcal compression see entrapment neuropathies monofascicular 23, 25 multifascicular 23, 25 pressure on 23-30, 41 clilucal effects 26-27 clirucal syndromes 27-30 duration and interval before relief 28 summary 29 terminology 26 terminology 26 tolerance to tension 41 nerve supply connective tissue 36-37 muscle 42-43 tendons 43

see also specific joints nerve trunks 24 anatomy 25 compression, thoracic outlet syndrome 548 pressure, effect 28, 68, 151, 543 neuralgia atypical facial 680 Horton's see headache, cluster ilioinguinal 1040 saphenous 1265 neuralgic amyotrophy 219, 552 clinical features 368, 552, 553 d ifferential diagnosis 1 89, 867 treatment 553 neurilemmoma, terminology 637 neurinoma, terminology 637 neuritis 26, 27 intrinsic, paraesthesia in cervical spine 168 thoracic pain 596 neurofibroma cervical spine 217, 2 1 7 lumbar spine 865-867 pain 168 radicular pain 147 thoracic spine 637, 637-638, 638, 640 warning signs 638 neurogenic pain 26, 2 7 neurological complications cervical spine fractures 212 cervical spine manipulation 112 neurological deficits discoradicular d isorders with, epidural anaesthesia for 905-906 nerve root compression cervical 181, 1 9 1 lumbar 720, 721 thoracic 594 see also cervical nerve roots; lumbar nerve root(s) pain discrepancy (wanUi1g sign) 854 spinal manipulation complication 1 1 2 spinal manipulation contraindication 1 1 0, 622 neurological infections, epidural anaesthesia contraindication 907 neurological signs thoracic spinal cord compression 621 warnmg, thoracic 637

neurological weakness 75 arms 1 73 Pancoast's tumour 657 painless on resisted abduction of shoulder 360 resisted lateral rotation of shoulder 368 shoulder girdle 408 neurologic pain 26, 27 neurolytic action, phenol 126 neuroma 26 cervical 292 lumbar 865-867 differential diagnosis 866, 866-867 osteophytic root compression (cervical) vs 200 neuropathic arthropathy elbow, differential diagnosis 439 shoulder 318-319 neuropathic pain 26, 27 neuropathies, entrapment see entrapment neuropathies neuropraxis 27 neurosis, low back pain, therapeutic epidural anaesthesia 905 neurotransmitters, dura mater sensitivity and 716, 744 neurovascular complications, corticosteroid infil tra tion 124 neutral zone concept 837-838 neutrophils, inflammation 44 nociceptive pain 26, 27, 27 patellofemoral disorders 1139 pressure on peripheral nerves 28 nociceptive system afferent 4, 4-5 inhibition 6, 26 distraction technique 309 nerve endings 23 peripheral 3-4, 4, 26 receptors 4, 27 inhibition 95 for referred pain 7-8, 8-10 segmental organization 7, 8 nocturnal pain capsular, manipulation contraindication 1 05 carpal tunnel syndrome 569 cervical spine 1 68 metastases causing 214 tumours causing 212, 213 low back (backadle) 755, 805 therapeutic epidural anaesthesia 904-905 pyogenic osteomyelitis (thoracic) 648 sciatica 760, 769-770 spinal manipulation complication avoidance 1 1 3 thoracic extra- / intra-spinal tumours 639 non-steroidal anti-inflammatory drugs , (NSAIDs) complications 1 1 1 knee osteoarthrosis 1079 side-effects 1079

------- ---- -----

INDEX 1321

nuclear disc protrusion 747-748, 901 cervical acute torticollis 183 see also cervical disc displacement lumbar annular protrusion vs 896, 897 clinical features 896 low back ache 751 maintenance after reduction 756 manipulation indication 877-878 manipulation not useful (cases) 880 nuclear lumbago 747, 747-748, 750 self-reducing 755 slow onset of symptom 751, 803 traction indication 896 treatment 756 reduction methods 901-903 McKenzie's techniques 902-903 oscillatory and sustained manipulations 902 traction see traction, lumbar self-reducing, arthrodesis for 931 spinal traction 1 04-105, 895-901 see also traction, lumbar nuclear elf-reducing disc 755 nucleus pulposus 137, 746, 747 ageing 1 76 age-related changes 1 76, 706 air pockets in 738 dehydration 731 external loads causing 707-708, 708 effect of loading on 708-710, 709 asymmetrical vs symmetrical 709, 709

herniation biconvex discs 736 Schmorl's nodes 735-736, 736 importance of lumbar lordosis 710, 922, 922

lumbar discs 705-706, 706, 731 posterior bound zone with annulus, nutrient deficiency 731 posterior migration and effects 704, 709 numbness carpal tunnel syndrome 569 localization / sites 28 lumbar disc posterolateral protrusion 806 nerve root compression, cervical 1 8 1 pressure on nerve trunks / plexus 28 pressure on peripheral nerves 28 sciatica 760, 768 thoracic spinal cord compression 621 Nurick's classification (cervical spondylotic myelopathy) 202-203, 203 'nursemaid's elbow' 443, 444 nutation definition 944 sacroiliac joint 943-944, 944, 944, 945 nystagmus 228, 231-232 classification 23 1 , 231-232 examination 234-235 pathological 231-232 physiological 231

slow and quick phases 231, 234 spontaneous 231, 232, 234 types 231-232

objectivity, in diagnosis 63 oblique cord 418-419, 4 1 9 oblique muscle abdominal 838 lesions 666-667 obturator hernia 1024-1025 Trendelenburg test 994 obturator nerve 1025 anatomy 980 occipitoatlantoaxial joint complex 137-138, 138

ligaments 140, 140-141, 1 4 1 movements 138, 1 38 occupations history-taking 64-65 low back pain 802 odontoid process 135-136, 1 36 fractures 212 protrusion 216 subluxation 215, 216, 2 1 6 oedema arm 657 foot 827 intraneural, sciatica 759 intraradicu lar 27 oesophagitis, reflux 658 oesophagus malignant tumours 659 perforation 658 referred pain from 597, 598, 658, 658-659 rupture 659 spasm 658 olecranon 418 fracture 438, 453 C7 nerve root compression vs 190 olecranon bursitis 445 olecranon fossa 418, 419 olecranon process 419 Ongley's solution 962-963 Oppenheimer extensor plantar response 202 Oppenheim's sign 610 optical system 227 optohlnetic nystagmus 231 orgaruc lesion diagnosis 1 273-1274 treatment 1 278-1279 orthopaedic disorders categorization 93 combined aetiology 93 orthopaedic medicine manipulation vs cruropraxy and osteopathy 248, 877 principles 877-878 psychogenic pain integration see psychogenic pain orthotic device, Morton's metatarsalgia treatment 1 258 Ortolani's sign 1044

Ortolani's test 1 043, 1 044, 1044 oscillatory techniques 106 lumbar nuclear disc protrusion 902 thoracic disc lesions 630 unilateral pain in neck / tra pezi us / sca pula r a rea 184 Osgood-Schlatter disease ] 064, 1 1 37 Osgood's disease (calcaneal apophysitis) 1190-1 191 osseous crepitus 79 ossification, deep transverse friction contraindication 98 osteitis deformans see Paget's disease osteitis pubis 666, 1026, 1 038 clinical features and diagnosis 1038 treatment 1 038 osteoarthrosis (osteoarthritis) ankle 1204 capsular stretching 1 04 costotransverse joints 650 costovertebral joints 650 cuneiform-first metatarsal jOint lesion 1246-1247 facet joints (lumbar) 737 hip see hip joint as 'joint failure' 1002 knee see knee metatarsophalangeal jOints 1256 patella 1 143 post-traumatic see post-traumatic osteoa rthrosis sacroiliac joint 961 shoulder 31 7-318 spinal, radiographic ' label' problem 833 spinal manipulation complication avoidance 113 subtalar joint 1211 see also arthrosis osteoblastoma cervical spine 213 l u mbar spine 859 osteoblasts, hyperactive 651 osteochondritis, Freiberg's 1256 osteochondritis dissecans aetiology 1087 elbow 440 history-taking 1 064 loose bodies in knee 1 087 loose body in article joint 1204 osteochondritis juvenilis 860 osteochondroma, cervical spine 213 osteochondrosis adolescent 69 anterior displacement of lumbar disc 733, 735, 735 tibial tuberosity see Osgood-Schlatter disease osteochondrosis syndromes 1 1 90 see aLso Legg-Calve-Perthe' disease osteoclasts, hyperactive 651 osteogenic sarcoma, warning signs in elbow 450 osteoid osteoma cervical spine 213 lumbar spine 859

1 322 INDEX

osteomyelitis lumbar spine 863 chronic afebrile 853-854 pyogenic vertebral 648, 863 thoracic spine 648-649 tuberculous vertebral 863-864 upper femur 1009 osteonecrosis see avascular necrosis osteopathy 107, 1 09, 877 historical aspects 106 hyper- / hypomobility assessment 79 manipulation controversy and 248, 877 patient dependency 109 osteophytes cervical nerve roots compression 1 99, 1 99-200 C1 and C2 nerve roots 1 87 formation, age-related 1 76 lumbar spine anterior displacement of discs 735 circu lar displacement of disc 736 claw spurs 736, 736, 738 traction spurs 736, 736, 738, 841, 842 vertebral bodies 736 mushroom phenomenon 735, 735 sacroiliac joint 945 spinal canal 249 subperiosteal 1 76 thoracic spine anterior erosion 645, 645 spinal canal narrowing 620 ulnar nerve compression 563 uncovertebral 200 wrist 501 osteoporosis 857-858 compressive fractures 643 corticosteroid side effect 125 fish vertebrae 644, 644 lumbar spine 857-858 manipulation contraindication 105, 110 wedge fractures of vertebral body 642, 643 osteosarcoma, cervical spine 214 osteotomy, McMurray intertrochanteric 1007 os trigonum, pinching 1208 otitis externa 680 otitis media 1 84, 680 otoliths 227 Ottawa rules (X-rays), ankle sprains 1217-1218 ovaries cyst 661 referred pain from 5 98, 599, 661, 661 overuse lesions 45 acromioclavicular joint 327 biceps tendinitis (femoris) 1 1 45 elbow 439 fingers 535 iliotibial band friction syndrome 1144 myosynovitis 49 quad riceps tendon 1132 radioulnar joint, upper 443-444 shin splints 1195-1197 sternoclavicular joint 405

tendinous lesions adhesion prevention 50 see nlso tendinitis tendons 50-51 tennis elbow 455-456, 456 thumb 521, 524

paediatrics see children Paget's disease 651 knee 1 078-1079 lumbar spine 858 thoracic spine 651 pain 3-30, 67 absence on movement 89 amplitude of movement affecting 73 bilateral 67 on breathing 549 burning 26 C5 20 capsular lesions 55 central transmission 5-6 cerebral cortex areas 5, 7 cervical disc displacement see cervical disc displacement cervical spine lesions see cervical spine constant, examination 63 deep 7-8 definition 3 delayed muscle soreness 48 descriptions 67 diminishing or worsening 65 dural reference see dural pain 'electric' shock, sinuvertebral nerve block 720 emotional disturbances related 5, 67 end-feel relationship 74, 74 entrapment neuropathy 27, 28 expanding see expanding pain extrasegmental reference see extrasegmental pain gate control theory 5, 5-6, 26, 95 ' growing pains' 1183 history-taking 67, 67, 147-150 inflammatory 67, 67 intensity 5 intermittent 65 localization 3, 6, 7, 66 history-taking 67 local vs referred 16-17, 20 long-term memory 5, 7 mechanical 67, 67 modulation 5-6 central 6 peripheral 5, 5-6 reticular formation inhibitory action 6 morning see morning backache multisegmental see multisegmental pain muscular contraction causing 88-89 nerve 26 nerve root compression 28-29 see nlso cervical root pain; lumbar nerve root(s) neuropathic 26, 27

nociceptive 26, 27, 27 onset 66 perception 3-6 see nlso nocicepti ve system ' perceptual component' 5 from peripheral nerves 26 on pinching of tissue 87 postmanipulation (spinal) 111-112 psychogenic see psychogenic pain radicular 29 recurrence 66 referred / reference see referred pain relief deep transverse friction 95, 96 spinal manipulation 1 1 1 renal / ureteral 867 resisted movements 75 strength vs 88 rules of segmental reference 6, 8, 25, 28 segmental see segmental pain severity 67 shifting 65-66, 66, 66 cervical spine 167, 180-181 low back pain 751, 804 neck 148 sciatica 66, 66 stretching causing 86, 86-87 subjectivity 3 superficial dysaesthetic 26, 27 tendinitis 51 'the' in diagnosis 62 passive testing 71-72 tolerance, spinal manipu lation action 109 twinges see twinges unilateral 67 very severe, diagnostic di fficulty 90 very slight, diagnostic di fficulty 89-90 painful arc (knee) 1066 painful arc (lumbar spine) see lumbar spine painful arc (shoulder) 72, 295-296, 296, 379-383 definition / diagnostic criteria 72, 87, 295, 379 deltoid muscle lesion excluded 353 disorders mimic�ing 382, 382 cervical disc displacement 180, 382 momentary subluxation of glenohumeral joint 341, 382 disorders of contractile structures 380-381 , 38 1 , 382 infraspinatus muscle lesions- 364 infraspinatus tendinitis 381 infraspinatus tendon rupture 367 subacromial bursitis 452 subscapularis tendinitis 381 supraspinatus tendinitis 354, 354, 380 tendinitis of long head of biceps 381 disorders of inert structures 380, 382 acromial metastases 380 acromioclavicular sprain 327, 360, 380 acute subdeltoid bursitis 320, 38Cl chronic subdeltoid bursitis 333, 380 double lesions causing 382 on elevation l'S medial rotation 379

INDEX 1 323

glenohumeral subluxation with 337 U1terpretation of examination 83 as localizing sign 87 painful resisted abduction and lateral rotation with 367 painful resisted abduction and lateral rotation without 366-367 passive medial rotation 298, 379 pathogenesis 379-380 painful arc (thoracic spine) 605 pain provocation tests, sacroiliac see sacroiliac joint palmar aponeurosis 480 contracture see Dupuytren's contracture palmar interossei 480 functional examination 488, 488 palmaris longus muscle 478 anatomy 423, 423 palmar l igaments 475 palmar subluxation, differential diagnosis 502 palpation 77-79 avoidance and unreliability 60-61 danger in very slight pain 89 examination (of) elbow 431 fingers 491 hand 488 hip joint 994 iliac crest 8 1 1 infraspinatus tendon lesion 364-365 lumbar spine 830, 830, 831 shoulder 295, 300 shoulder girdle 399 subscapularis tendon lesions 369 supraspinatus tenoperiosteal lesions 354-355, 355 temporomandibular joint 684, 684 tennis elbow 456 thoracic spine 600-601 , 610 wrist 488 moving joint 78-80 negative 78 stationary joint 77, 77-78 therapy, acromioclavicular sprain 328-329 palsies central vs peripheral 82, 82-83 functional 81 intrinsic (myogenic) vs extrinsic (neurogenic) 83 organic 81 radicular 83

see also individual nerve roots Pancoast's tumour 190, 656-657 brachial plexus dysfunction 546 clinical features and warning sign 408, 657, 657 differential diagnosis 656 limitation of shoulder movement 322, 657 referred pain to shoulder 292, 294, 657 thoracic outlet syndrome vs 551 pancreas carcinoma 868 referred pain from 598, 598, 660, 660

pancreatitis acute and subacute 660 chronic 660, 868 paraesthesia ('pins and needles') 26, 27, 67-68, 1263 arm 395 bilateral, spinal cord pressure 29 cervical spine lesions 1 50, 150-151, 1 68, 181, 543 interpretation 1 68 cubital tunnel syndrome 563 duration 28 hand 483, 533 history-taking, lumbar spine disorders 806-807 localization / sites 28, 68, 68 movement increasing 28 m u ltisegmental, cervical disc displacement 181, 250 multisegmental bilateral 68, 543 nerve root compression 29, 68, 543, 720, 807 cervical 151, 181, 186, 1 87

see also specific nerve roots nocturnal carpal tunnel syndrome 569 postural thoracic outlet syndrome 549 painless 807 parenchymal irritation 145 pressure on nerve trunks / plexus 28, 68, 151, 543 pressure on peripheral nerves 28, 68, 151, 543 cervical spine region 1 68 pressure on spinal cord 807 proximal extent, localization and behaviour 1 68 release phenomenon 28, 543 sciatica 759, 760 shoulder girdle 1 72 thoracic spinal canal stenosis 641 thoracic spinal cord compression 621 thoracic spine disorders 600 wrist 483 paralysis epidural anaesthesia adverse effect 907-908 lower motor neurone lesion 202 spastic, upper motor neurone lesion 202 parana sal sinusitis 680 paraspinal muscles, spasm / wasting 811 paravertebral mass, warning sign 637 parenchyma, nerve root lesions, cervical 1 45, 250 Parkinsonism, acute torticollis vs 184 parotitis 680 pars interarticularis fatigue fracture see spondylolysis weakness, causing spondylolisthesis 855, 856 pars interlaminaris 704-705 Parsonage-Turner syndrome see neuralgic amyotrophy passive extension thrust, thoracic spine 607, 607

passive movements 72 contractile tissues 62 criteria and aims 71, 71-74 examination 71 functional examination 71-74 amplitude of movement 72-73 pain 71-72 for spinal manipulation 107

see also individual joints impairment 83-87 with active movements 8 1 capsular pattern 84 excessive range see hypermobility extra-articular limitation 86 ful l articular pattern 84 full range 86-87 limited range 83-86 non-capsular patterns 85, 85-86 pain on pinching 87 pain on stretching 86, 86-87 partial articular 85, 85-86 patterns 81 with resisted movement 85, 87 impossible / absent 87 interpretation 83-87, 89 ligament lesions 53 sprained ligament treatment 54 therapeutic 1 02-114 see also manipulation; mobilization patella anatomy 1 054, 1054-1055, 1 058 bursa see prepatellar bu rsa clinical examination 1 139-1141, 1 141 inspection during active movement 1 041, 1 1 41 inspection in supine position 1040 inspection on sitting 1 139, 11 39-11 40, 1 140 inspection on standing 1 1 39 passive movements of patella 1040, 1141 Q angle see below flake fracture 1 143 fracture 1 1 37-1138 function 1 055 'grasshopper eyes' 1 1 42 ' lateral pull sign' 1141, 1 1 41, 1 1 42-1143 lateral tilting 1 142, 1 1 42 malalignment 1 065, 1 142 mobility 1040 osteoarthrosis 1 1 43 outfacing and infacing 1 139 passive movements 1040, 1 1 4 1 Q angle 1 040, 1 140 decreased 1141-1142 definition and normal 1040, 1 140 increased in patellofemoral pain syndrome 1 142 measurement 1 040 recurrent dislocation 1141-1142 recurrent subluxation 1141-1142, 1 1 42 rotation assessment 1 040 stabilization by vastus medius obliquus 1 138, 1 1 38-1139 tendinitis at 1 1 32 tendinous lesions at 1 064, 11 32-1136

1 324 INDEX

patella alta 1139 patellar bursitis 1095 patellar tap 1 070, 1 071 patello-femoral arthrosis 1 064 patellofemoral disorders 1 1 38-1143 arthrosis 1 1 43 clinical examination 1 1 39-1141, 1 14 1 see also under patella clinical features 1 141-1143 instability 11 41-1 1 42 mechanical theory 1 138, 1 1 38-1139 neural theory 1 1 39 pain 1 1 38, 1 1 39 recurrent dislocation 1 141-11 42 recurrent subluxation at patella 1 141-1142, 1 142 without subluxation 1 1 42, 1142-1143 patellofemoral pain syndrome (PFPS) 1 1 38, 1 1 42, 1142-1143 anatomical changes 1142-1143, 1 143 examination and treatment 1 143 pathological fractures see fractures pathological wedging, thoracic spine 642-645 patient education, lumbar segmental instability treatment 842 patient history, in psychogenic pain examination 1 275 patient position cervical manipulation 254-255, 255 cornua location 909 traction (lumbar spine) 899, 900 patients cooperation, for diagnosis 62-63 dependency 109 personality, in diagnosis 63, 874-875 posi tion, intil tra tion / injections 117 psychological state, manipulation 878 see also mental state Patrick's test 952-953, 953 Pecina's 'shoe wiping test' 1031 pectoralis major muscle 282, 284, 285, 361-363 lesions 361-363, 665 differential diagnosis 325, 361-362, 412 treatment 362-363, 363 passive stretching 325 rupture 363 spasm 322 lung cancer 656 strength / propriocepsis training 342 testing 361 pectoralis minor muscle anatomy 391, 391 lesions 412 sprains 413 pectoral nerves 545 pectoral pain 108, 150 pectoral region, dermatome and myotome 15 pectoroscapular area, pain 1 90, 407, 408 pedicles, lumbar vertebrae 704 pedicular kinking 792, 793 pediculolysis 859 pelvic harness 898-899

pelvic inflammatory disease 868 pelvic instability, peripartum 949 pelvic rotation, forward bending 818 pelvic tilt, lateral 810 sciatica 762 pelvic tilting exercises 927 ligamentous disorders prevention 926-927 lumbar spinal stenosis treatment 790 method 928 stenotic disorder prevention 927-928 pelvic torsion (Gaenslen's) test 810, 951, 952 pelvis bony d isorders 964-965 bony sites 1 046, 1 047 excess movement 988 torsion 945 tumours 964 peppering 1 1 7 pericarditis, referred pain from 656 perichondritis, costochondral joint (Tietze's syndrome) 597, 662-663 perimysium 42 perineal pain 803 perineum, paraesthesia 807 perineurium 23, 25, 41 periosti tis anterior (ankle) 1 208 lateral (jumper's sprain) 1 208-1209, 1 209 os trigonum 1208 posterior (dancer's heel) 1 207, 1207-1208 pubic symphysis see osteitis pubis wrist 507 peripheral nerves 23-24 anatomy 23, 24, 25-26 brachial plexus 545, 545 connective tissue 41 fasciculi 23, 24, 41 lesions 541 arm weakness 1 73 nerve roots comparison 720 pain originating from 26 pressure / compression effect 28, 68, 1 51, 543 prolonged damage, pain 26 weakness of foot due to 1 1 99 peripheral nervous system terminology 26 zones 24, 24 peripheral neuropathy carpal tunnel syndrome due to 569 pain to temporomandibular joint 680 peritendinitis, definition 1 187 peritoneum, parietal, referred pain 661 peritonitis, referred pain 661 peroneal muscles, spasm at midtarsal joint 1 240 peroneal nerve palsy 1 1 45 peroneal spasm 1 1 98 peroneal tendinitis 1 1 97 treatment 1 1 98, 1 1 98 peroneal tendons deep friction 1 1 98, 1 1 98 relationship to cuboid bone 1 245 peroneus brevis 1 1 68-1169, 1 1 69

peroneus longus 1 168-11 69, 1 1 69 personality, patient's cervical manipulation 254 in diagnosiS 63 Perthes' disease 1010, 1046 pes anserinus bursitis 1095-1096 lesions 1146 pes cavus deformity, metatarsalgia 1257 pH, effect on nociceptor sensitivity 4 phagocytosis, stimulation by deep transverse friction 95 Phalen's test 570, 570 modified 570 phenol 125 indications 126 mode of action 1 26 postthoracotomy pain treatment 664 preparations 1 2 6 side effects and complications 126-127 see also sclerosant infiltration phenol-dextrose-glycerol see dextrose-phenol-glycerol phenylbutazone, ankylosing spondylitis 960 phrenic nerve, irritation, referred pain to shoulder 292 pia mater 143 pillows, cervical disc displacement prevention 267 pinch grip, deep transverse friction technique 100, 101 'pins and needles' see paraesthesia piriformis syndrome 1263 pisiform bone 474, 478 ulnar nerve entrapment 566 pisohamate ligament 479 pisotriquetral disorders 515 pivot-shift test, knee instability 1 1 20, 1 1 20-1121 plantar calcaneonavicular ligament 11 63, 1 1 64, 1 1 65 plantar deformity, metatarsalgia 1256 plantar fascia 11 70, 1 1 70 origin, pain 1213 overstrained 1213 tears 1 214 plantar fasciitis 1213-1214 injection technique 1214, 1 2 1 5 treatment and shoewear for 1213-1214, 1214 plantaris muscle 1 1 61 plantar nerves 1268 compression 1268 plantar reflex, testing 160, 1 6 1 , 606, 606 plantiflexion, foot see foot plantiflexors foot / l ower leg 1 1 66, 1166-1167, 1179 lesions 1 1 83-1193 pain 1 1 83-1 191 short, exercises in midtarsal strain treatment 1243 short muscles 1 1 91-1192 plasma cells inflammation 44 tumours see multiple myeloma

INDEX 1325

plasmacytoma, solitary cervical spine 214 lumbar spine 860 plaster cast, Achilles tendon rupture treatment 1191 plastic deformation, cartilage 40 platelets, inflammation 44 pleura, referred pain from 597, 656 pleurisy (pleuritis), referred pain 656 pleurodynia, referred pain 658 plicae synoviales 1092 medial 1092, 1 093 plica mediopatellaris 1092 plica synovia lis syndrome 1092-1093 pneumonia, referred pain 656 pneumothorax acute, pain 657 warning sign 650 polyarthritis, monoarticular steroidsensitive arthritis of knee us 1080 polymyalgia rheumatica, hip 1001 popliteal cysts 1096 popliteal fossa 1 060, 1060-1061 popliteus muscle 1059-1060 anatomy 1146 deep friction 1147, 1 148 strains 1146-1147 popliteus tendon 1146 infiltration technique 1147, 1 147 porter's hand 559 postconcussional headache 226-227 postconcussional syndrome 204 manipulation 268 posterior apprehension test 337-338, 338 posterior arch lesions 775 clinical examination 815 posterior atlanto-occipital membrane 140 posterior cerebral artery 1 45, 230 posterior compartment syndrome 1184 posterior cruciate Ligament (peL) 1058, 1 058 complete ruptures, treatment 1 1 23 infiltration technique 1 113, 1 1 1 4 injuries / lesions 1111-1113 causes 1112 diagnosis 1112-1113 summary 1 1 1 5 treatment 1113, 1 1 23 rotatory stability of knee 1 1 1 5-1116 sprains 1102, 1112 posterior cutaneous nerve, forearm, lesions 559 posterior drawer test knee 1067-1068, 1 068 shoulder dislocation 338, 340 posterior dysfunction syndrome 776, 779-783 characteristics 776, 776 facet joints 779-781 , 815 see also facet joint syndrome iliolumbar ligaments 781-782 summary 849 supraspinous and interspinous ligaments 782-783 treatment, sclerosant infiltration 921 unilateral 818

posterior facet joint syndrome 1 09 posterior gapping test 950, 951 posterior inferior cerebellar arteries 230 posterior interosseous nerve, forearm 425 anatomy 557, 559 compression 559, 560 at elbow 560, 561 lesions 559-561 thumb weakness 529 posterior intralaminar fusion 857 posterior longitudinal ligament adherence to dura mater 196 cervical spine 141, 1 41 , 1 96 dura mater attachments 744 functions 709, 711 laxity 776 lumbar spine 711, 712 disc weakness and 709 flexion effect 927-928 postural syndrome 776 pressure on dura mater (annular lumbago) 747 stenotic disorder prevention 927-928 tension with posterior disc displacement 733, 734, 744, 749, 757, 792 traction effect 894-895 overstretching 644, 776 referred pain 597 thoracic spine 583, 583 tightening, by manipulation 756 posterior periostitis (dancer's heel) 1 207, 1207-1208 posterior primary ramus, lumbar spine 721, 722, 722 anatomy 721, 722, 722 medial and lateral branches 722, 722 posterior sacroiliac ligament 942 sclerosant infiltration 962-963, 963 posterior spinal arteries 230 posterior sternoclavicular syndrome 219, 403, 404-405 posterior superior i l iac spine (PSIS) 977, 981 posterior talofibular ligament 1 163, 1 1 63 anatomy 1 208 sprain 1208, 1 208 posterior thoracic wall, deep friction 409, 409 posterior tibial artery, feeling pulse 828 posterior tibialis muscle see tibialis posterior posterior tibial tendinitis 1195 posthoracotomy pain 664 postmenopausal women sternoclavicular joint arthrosis 405 thumb arthrosis 522 postpartum coccygodynia 968 postradiation therapy, costocoracoid fascia limitation 408 postsurgical fibrosis/ stenosis, lumbar spine 793 post-traumatic frozen shoulder 306 post-traumatic muscular lesions, cervical 269

post-traumatic osteoarthrosis, cervical spine 199-200 postural ligamentous pain see postural syndrome postural pain 777 age of onset 802 cause 776 postural syndrome 776-777 postural syndrome 776-779 characteristics 776, 776 clinical examination 777, 816 definition 776 differential diagnosiS 777-778 history and clinical features 777, 777, 804, 807 postural pain in ageing spine 776-777 summary 779, 849 treatment 778-779 posture asymmetrical, lumbar spinal disorders 808-809 in bed, correct 925, 925 correct, for keeping lumbar lordosis 922, 922 effect on lumbar spinal stenosis 789 effect on pressure and lumbar disc hydration 707-708, 708 hyper lordosis correction 926-927, 927 i nspection of hip and buttock 988 l i fting and carrying, correct positions 924-925, 925 low back pain affected by 751-752, 804 lumbar disc lesion prevention 710 lumbar spine anatomy and 703-704 thoracic disc lesion recurrence prevention 631 thoracic outlet syndrome treatment 551-552 see also sitting; standing Pott's disease 648-649 pregnancy carpal tunnel syndrome 569 final month, spinal manipulation contraindication 879 low back pain 867-868 epidural anaesthesia 905 sacroiliac joint 945 premanipulative testing see manipulation (spinal) prepatellar bursa 1 054 prepatellar bursitis 1095 pressure, on nerves see nerves prilocaine 119 procaine 1 1 6, 1 1 8-119 concentrations 119, 1 1 9 historical use 1 1 8 hypersensitivity 907 meralgia paraesthetica treatment 1 265 procaine infiltration/ injection chronic subdeltoid bursitis 334, 334 extensor carpi radialis brevis 463-464, 466 hamstring strains 1144-1145 heel pad syndrome 1215-1216, 1 2 1 6 low back pain 754

1 326 INDEX

procaine infiltration / injection (continued) lumbar nerve root blocks 9 1 7-918 mechanism of action 903 pectoralis major muscle lesions 362, 363 rectus abdominis muscle 666, 666 sciatica 770 supinator brevis muscle 453, 453 tennis leg 1 1 85, 1 1 85 see also epidural local anaesthesia prolotherapy 1 25, 522 pronation-supination, deep transverse friction technique 1 00, 101 pronator quadratus muscle 422, 422 pronator teres muscle 422, 422 deep friction 454, 454 lesions 454 pronator teres syndrome 567, 568 proprioception 115 disturbance cervical spine causing 235-236 cervical spondylotic myelopathy 202 reflex 228 proprioceptive neuromuscular facilitation (PNF) technique 1 1 5 definition a n d procedure 1 1 5 rehabilitation after knee instability treatment 1 1 25 proprioceptive system, anatomy 228 proprioceptive training 94 prostate, pain referred to back 867 proteinases 313 proteoglycans 34 aggregates 34, 34 articular cartilage 39 effects of negative charges 34 lumbar discs 706-707 osmotic system of intervertebral joints 707 structure 34, 34, 707 synthesis 707 pseudoclaudication lumbar spinal stenosis 789, 789 thoracic spinal stenosis 641 pseudocoxalgia see Perthes' disease pseudogout carpal tunnel syndrome due to 569 elbow 439 knee 1080 shoulder 316 pseudojoints 138 pseudo ulnar palsy 1 90 psoas bursa 979 anatomy 980, 1015-1016 clinical examination 1016 pain from 987 psoas bursitis 1015-1016 diagnosis/ differential diagnosis 1016 diagnostic infiltration of anaesthetic 1016, 1 0 1 6 haemorrhagic 1016-10 1 7 psoas muscle examination by resisted flexion 1 023 irritation 863 lesions 666 weakness 854, 861

psoas position 750 acute annular lumbago 747, 750 sciatica 760 traction 899 psoas tendinitis 1023-1024 psoas tendon, deep transverse friction 1 024, 1 024 psoriasis corticosteroid side effect 123 deep friction contraindication 98 sacroiliac joint 960 pso ria ti c arthri tis ankle 1204 spinal manipulation contraindication 110 temporomandibular joint 694-695 psychogenic pain 63, 93, 1271-1 279 clinical examination 1 275-1277 history 1275 inspection 1275 coccygodynia 969 diagnosis 1278 possibilities 1278 diagnostic epidural injection 903-904 functional exarnination 1 276-1277 inconsistencies 1276-1277, 1 2 77, 1 2 78 hip /buttock 1019 orthopaedic medicine integration 1273-1277 importance of immediate diagnosis 1273-1274 importance of positive d i agnosis 1 274 pitfalls for examiners 1274--1 275 treatment 1 278-1279 absence of organic pain 1279 explanations to patients 1279 organic pain with psychogenic overlay 1278-1279 physical 1279 whiplash-associated disorders 242 psychogenic problems 76, 81, 89 diagnostic difficulties 90 limitation, arm elevation 321-322 lumbar spine accessory tests 832 straight leg raising test 819, 824 side effects of local anaesthetics 119 thoracoabdominal features 661 psychological state of patients manipulation and 878 see also mental state psychoneurosis, painless weakness on resisted flexion of hip 1025 pterygoid muscles 676-677, 677 abscess 696 pubic bone fracture 1026 neoplasm 1 026 stress fracture 88 pubic ramus, stress fracture 1037-1038 pubic symphysis periostitis see osteitis pubis postpartum instability 1 038 pubic tubercles 981

pubofemoral ligament 974, 974 'pulled elbow' 443, 444 pulmonary embolism 658 referred pain 658 pulmonary hypertension, referred pain 658 pulmonary tumours referred pain to shoulder 292 see also Pancoast's tumour pulsation of arteries, assessment 78 pulse, thoracic outlet syndrome 550 pus 78 pyramidal tract 82, 84 pyrosis (heartburn) 658

Q angle see under patella quadrate ligament 418, 4 1 9 quadratus femoris muscle 979 quadratus lumborum muscle anatomy 714 lesion, pain at end of side flexion 818 quadriceps expansion (at patella) deep transverse friction 97, 1134, 1136 tendinitis 1133 quadriceps femoris, muscle strength imbalance with hamstrings 1030-1031 quadriceps muscle anatomy 1 058-1059 bell ies, ruptures 1131-1132 treatment 1132, 1132 contusions 1131 deep friction 1132, 1132 haemorrhage 1132 knee extension 1058 muscles included 1058 painless weakness 1030 quadriceps tendinitis 1132 localizations 1132, 1 1 33 staging 1 133 trea tm.en t 1133-1136 conservative / general 1 1 33 deep friction 1133-1134, 1 1 34, 1134-- 1 135, 1 1 36 infiltration 1134, 1 1 34, 1 135-1 136, 1137 quadriceps tendon deep friction 1133-1134, 1 1 34 lesions 11 32-1136 overuse phenomenon affecting 1132 ruptures 1136 quadriped vs biped 704, 729 Quebec Task Force (QTF) 239, 240 questions during functional examination 71 during history-taking 63

radial annular ligament 418, 4 1 9 radial collateral ligaments 475, 475 infiltration technique 505, 505 sprain 505 radial deviation, resisted 431, 432 radialis tunnel syndrome 465

INDEX 1 327

radial nerve 557-561 anatomy 424-425, 425, 481-482, 557, 557-558 branches 557 558 posterior cord of brachial plexus 545 compression, thoracic outlet syndrome vs 551 deep 424-425, 425, 482, 557 lesions 559 disorders / lesions 558-561 distal part of forearm 561 distal part of upper arm 559 proximal / middle of upper arm 558-559 upper part of forearm 559-561 innervation 558, 558 palsy 453, 559 C6 nerve root compression vs 189 weakness on extension of wrist 513 superficial 425, 425, 481 , 557, 561 lesions 559 radial nerve syndrome, clinical features 558 radial tunnel (arcade of Frohse) 425, 557, 559 anatomy 559 radial tunnel syndrome 425, 455, 560-561 type IV tennis elbow vs 560, 561 radiate ligament, of costovertebral joint 390 radicular canal 584, 716 anatomy 716-717, 717, 791, 791 length 717 pathological changes/ narrowing 791-793 radicular canal stenosis see lateral recess stenosis radicular pain 29, 744 age associated 147 dural pain in limb vs 761, 803 lumbar 757 annular lumbago vs 746 see also sciatica segmental, extrasegmental dural pain vs 759, 803 warning sign in lumbar spine 854 see also cervical root pain radiculopathy, cervical spondylosis causing 197 radiocarpal instability, testing 509 radiocarpal joint 474-475 radiocarpal ligaments dorsal 475, 475 stretching 507 radiography ankle sprains (inversion) 1219-1220 cervical spine degeneration 197 degenerative disc lesions 1 77 lesions 162 tumours 212 hip osteoarthrosis 1003 lateral recess stenosis 794-795 loose bodies in elbow 441 lumbar spinal stenosis 790, 790, 791 lumbar spine 833 age-related changes 738, 738

Paget's disease 651 pyogenic osteomyelitis (thoracic) 648 sacroiliac joint 953 sacroilitis 959, 959 scaphoid fracture 499, 500 scoliosis 646 shoulder 301 rheumatoid arthritis 315 spinal manipulation complication avoidance 113, 1 1 4 stress, ankle sprains 1 219-1220 thoracic neurofibroma 638 wedge fracture of vertebral body 643 whiplash-associated disorders 242 radiohumeral bursitis 445 radioulnar joint lower / distal 420 anatomy 473-474, 474 arthrosis 496 capsulitis, forced movement contraindication 56 disorders 495-498, 512 disorders of con tracti Ie structures 497 disorders of inert structures 495-497 capsular pattern 495, 495-496 non-capsular patterns 496-497 functional examination 484, 485 intra-articular injection 496, 496 ligamentous laxity 496 monoarticular steroid-sensitive arthritis 496 passive pronation 484, 485 passive supination 484, 485 painful at end of range 496-497, 512 resisted pronation / supination 497 rheumatoid arthritis 496 supination limited 496 painful 496-497 traumatic arthritis 495 see also triangular fibrocartilage complex (TFCC) upper 417-418, 4 1 8 function a n d anatomy 418, 4 1 8 sprain / overuse 443-444 radius distal end 474 fractures see Colles' fracture head fr a cture 438 'pulled' ('nursemaid's') elbow 443 Raynaud's syndrome 68, 484 thoracic outlet syndrome vs 551 razor back 810 reactive arthri tis knee 1078, 1 078 rheumatoid arthritis vs 68, 68-69 shoulder 315 sites / pattern 69 reactive neuromuscular control 115 rectal cancer, referred pain 868 rectus abdominis muscle 589, 590 deep friction 666, 667 infiltration technique 666, 666 lesions 666

rectus femoris 975 anatomy and function 975--976, 1058, 1059 lesions 666 tendinitis 1 024, 1 029-1030 tightness 829 rectus femoris tendon deep friction 1 030, 1 030 infiltration 1 030, 1 030 rectus sheath 591 recurrent character, in disorders 66 referred pain 3, 6-21 ankylosing spondylitis 90 bilateral 1 7 bursa, ligament o r tendon 20-21 C3 dermatome 187 cervicogenic headache 226 clinical consequences 8 Cyriax concept 8 deep 16-17, 20 definition 7, 8, 19 diagnostic difficulties 60, 61 diagnostic epidural injection 904 distal referral 16-17, 20 dural see dural pain; dural sleeve extensive, sites of lesions 20 factors determining / affecting 1 9-21, 20 depth of affected structure 20 nature of structure 20-21 position of affected structure 20 strength of stimulus 20 from joint capsule lesion 20-21 local pain vs 16-17, 20 mechanisms 6-8 embryogenesis role 8-10 as error in pain perception 6-7, 8 from musculoskeletal structures 595-597 root pain 8 rules of presentation 6, 8, 8, 8-10, 25, 1 66 low back pain 751 segmental 6, 8, 28 cervical spine 1 66 dura mater as exception 17-18 headache 149, 1 49 history-taking 65 not across midline 1 7 thoracic root pain 620 severity, history-taking 65 sites/ examples 6 soft tissue lesions 6-21, 166 visceral disease 16, 1 6 from visceral structures 597-599, 598, 655-661

see also specific anatomical regions referred tenderness 18-19 cervical disc displacement 1 79 de Quervain's disease 526 diagnostic difficulties 61 localized deep 78 reflex arc, supraspinous ligament receptors and multifidus 838-839 reflexes absent, thoracic spinal cord compression 621 changes in sciatica 759-760

1 328 INDEX

reflexes (continued) testing, arms 160-161, 1 6 1

see also individual reflexes reflex sympathetic dystrophy syndrome (RSD5) 538-539 regeneration, after trauma 44 Reiter's syndrome 960 back pain 802 lumbar spine 862 sacroiliac joint 960 shoulder 316 spinal manipulation contraindication 110 release phenomenon 28, 543 postural thoracic outlet syndrome due to 549, 552 relocation test, glenohumeral instability 338, 339 remodelling, connective tissue 45, 95 renal colic 867 renal infarction 867 resisted movements examination 62 impairment 87-89 with active movements 81, 1 71 all movements positive 88 'contractile tissue pattern' 87, 1 71 in isolation 87 in lesions of non-contractile structures 88-89 with other resisted movements 87-88 pain and strength relationship 88 pain on repetition 88 with passive movements 85, 87 patterns 81 interpretation 87-89, 89 negative 88 pain 62 passive testing 74-75, 75 strength 75

see also specific joints/anatomical structures respiratory depression, side effects of local anaesthesia 120 respira tory insu fficiency, traction contraindication 897 respiratory irritation, traction contraindication 897 rest ice and elevation, Achilles tendonitis 1 1 87 self-perpetuating inflammation and 45 thoracic disc lesion treatment 631 see also bed rest reticular formation, modulation of pain 6 retrolisthesis 1 77, 840 lumbar nerve root canal narrowed 840-841, 841 retropharyngeal abscess 1 84 retropharyngeal tendinitis 205 retrospondylolisthesis 737 rheumatoid arthritis Achilles tenovaginitis 1 190 acromioclavicular joint 322 ankle 1 204 cervical manipulation contraindication 251 cervical spine 215-216 facet joints 1 99

injection / infiltration 270, 270-271 cricoarytenoid joint 216 elbow 439 extensor capri ulnaris tenosynovitis 512 extensor digitorum tenosynovitis 513 fingers 534 knee 1078, 1078, 1184 lumbar pain 801, 862 lumbar spine 862 manubriosternal joint 662 metatarsophalangeal joints first 1253 outer four 1255 midtarsal joints 1241 radioulnar joint, lower / distal 496 shoulder 315 sites / pattern 69 spinal manipulation contraindication 110 sternoclavicular joint 322, 405 subtalar joint 1210 temporomandibular joint 694-695 thumb 521 wrist 501 rheumatoid disorders deep transverse friction contraindication 98 reactive disorders vs 68, 68-69 rhomboideus muscle 336 lesion 412 rib anatomy 586, 586-587, 587 attachment to sternum 587, 587 attachment to vertebrae 586, 587 articulation with thoracic spine 390, 390 contusion 597 disorders 663-664 first anatomy 547, 587 disorders 405-406 fracture 322-323, 406, 601 stress fracture 322, 411 fra ctures 663 differential diagnosis 663, 664, 665 first rib 322-323, 406, 411, 601 lower ribs 8 1 8, 831 pectoralis major muscle lesion vs 361-362 referred pain 597 length 587 lesion, differential diagnosis 76 long floating 663 lower, fracture 818, 831 metastases 664 oscillation 609, 6 1 0 second 587 tumours 664 rib-tip syndrome 663 riders' sprain 1026 riding, upper tibiofibular joint lesions 1145-1146 'rocker' Freiberg's osteochondritis treatment 1256 shoe fitting for arthritis 1 252 Romberg's test 233, 234 Roos' test 550, 550

root pain cervical see cervical root pain dura tion 148 lumbar see lumbar nerve root(s) passive testing 72 referred 8 shifting 66 spontaneous remission 168, 267 thoracic see thoracic nerve roots rotation/ extension test, premanipulative (cervical spine) 249 rotator cuff 280, 287, 287, 350, 350-353 arthropathy 350 disorders, coracoacromial arch changes 281 functions 287, 349, 350, 350 microvascular supply 350 muscles contraction together 336, 336 functions 287, 336, 349 glenohumeral stability 336, 336, 337 proprioceptive exercises 342, 342-343 selective contraction 336-337, 337 muscles included 287, 336, 349, 349 see also infraspinatus muscle; subscapularis muscle; supraspinatus muscle; teres minor tendons ad verse effect of steroid injection 352 age-related degeneration 350 calcification 350, 352-353 failure 350-351, 351 insertion 350 tendons included 283, 350 rotator cuff lesions 350-353 calcifying tendinopathy 350, 352-353 'creeping tendon failure' 359 diagnosis and treatment 352-353 failure 350-351, 351 incidence 351, 351-352, 352 pain 352 painless weakness 352 pathogenesis 350-351 tendinitis 350 rotator cuff tears 52, 318 full thickness 350, 358 incidence 351, 351-352, 352 asymptomatic 352 partial 350 surgical repair 352 rotator muscles, lumbar spine 714 rowing 926 Ruffini endings 36 rules of segmental reference of pain 6, 8, 25, 28, 166, 751 see also referred pain running 926 after knee instability treatment 1125 iliotibial band friction syndrome 1144

54 syndrome see cauda equina syndrome sacral cornua 908, 908-909 sacral derma tomes 11, 1 4, 15

INDEX 1 329

sacral epidural injections 908 see also epidural local anaesthesia sacral hia tus, loca tion 908, 909 sacral nerve roots 716 compression, signs / symptoms by level 724 neurological deficits by level 721 51 conduction testing 825-826, 829, 829 lesions, hamstrings syndrome vs 1031 nerve root block 9 1 7, 917-918 poslerocentral protrusion a ffecting 807 posterolateral displacement in sciatica 759 referred pain 1 2 13 signs/ symptoms 760, 767 51 compression clinical features 807 history 799-800 sacroilitis vs 958-959, 959 52 compression, sacroilitis vs 958-959, 959 conduction testing 829, 829 lesions, hamstrings syndrome vs 1031 posterolateral displacement in sciatica 759 signs/ symptoms 760, 767 53 palsy, surgery indication 929 signs/ symptoms 760, 767 54 compression 749 danger, manipulation contraindication 879 palsy, surgery indication 929 referred pain from, traction 897 signs/ symptoms 760, 767, 853 signs in discoradicular interactions 760, 766-767 sacral pain 803 sacral plexus 25 sacral thrust (downwards pressure) test 950-951, 951 sacral tumours, chordoma 860 sacrococcygeal chordoma 964 sacrococcygeal joint 967 sacroiliac arthritis 947, 957-961 defini tion 948 diagnosis 820 tests 959 differential diagnosis, 51 / 52 disc lesions 958-959, 959 disc lesions vs 958 gout 957, 961 osteoarthritis 961 pain 958 psoriasis 960 referred pain from sacroiliac joint 948, 948 Reiter's syndrome 960 51 and 52 pain 20 septic 960-961, 1010 tenderness over sacroiliac joint 959 see also sacroilitis sacroiliac belt 962, 963

sacroiliac distraction test 949, 962 sacroiliac joint 939-966 age-related changes 957 anatomy 941 , 941-946, 942, 957 articular surfaces 941 , 941-942 innervation 943 joint capsule 942-943 ligaments see sacroiliac ligaments muscles 943 ankylosing spondylitis see ankylosing spondylitis arthritis see sacroiliac arthritis biomechanics 943-944 blocked subluxation 961 centre of gravity and 942, 942 clinical examination 947-954 history-taking 949 interpretation 955-956 radiology 953 contralateral, straining during straightleg raising 823 diagnosis of lesions 947, 948, 953 d iagnostic epidural anaesthesia 953 disorders 947-948, 957-966 see also sacroiliac arthri tis; sacroiliac joint syndrome distraction test 819-820, 820 dysfunction 948 force closure 962 functional examination 819-820, 949-953 indication for tests 949 sacroiliac tests 949, 949-953 fusion, ankylosing spondylitis 945 gout 957, 961 instability 947 lesions straight-leg raising limitation 763, 822 straight-leg raising pain 822 mechanical lesions 961-964 see also sacroil iac joint syndrome osteoarthrosis 961 osteophytes 945 pain 961 differential diagnosis 820 history-taking 961 postural characteristics 961-962 on resisted abduction of hip 1 028-1029 sacroilitis 958 testing 820, 820 pain provocation tests 949-953, 952, 961 anterior gapping test 950, 950, 959 Patrick's test 952-953, 953 pelvic torsion (Gaenslen's test) 951, 952

posterior gapping test 950, 951 posterior shear (thigh thrust) test 951, 952

sacral thrust (downwards pressure) test 950-951, 951 Yeoman's test 951-952, 952 in pregnancy 945 psoriasis 960 range of movements 943-944 complex movements 944-945, 945

nutation-counternutation 943, 944, 944, 945 torsion of pelvis and 945, 945 referred pain from 948, 948, 987 referred pain to 948 Reiter's syndrome 960 rotation, assessment by Gillett test 949, 950 strain / sprain 947, 961 adductor longus injury vs 1026 belt for 962, 963 definition / concept 947, 948 diagnOSiS 962, 962 functional examination 949 palpation tests 949 treatment 962-964 see also sacroiliac joint syndrome subluxation 947 testing 819-820, 820 torsion of pelvis and 945 tumours 964 warning symptoms 964 unila teral pain / tenderness 947 testing 820, 820 sacroiliac jOint syndrome 957, 961 -964 clinical examination 962 history-taking 961-962 treatment 962-964 belt 962, 963 sclerosing injections 962-964, 963 sacroiliac ligaments anatomy 714, 942-943, 943 in cOUl1ternutation and nutation 944 force closure 962 lesions 800 sclerosant injections 962-964, 963, 964 tests 952 see also sacroiliac joint, functional examination sacroiliac strain, sclerosant infiltration 126 sacroilitis 957, 958-960 acute 948 pain on coughing 804 in psoriaSiS 960 radiology 959, 959 symptoms and signs 958-959 see also sacroiliac arthritis sacrospinalis muscle 713, 713 epidural anaesthesia landmark 909 lesion, pain at end of side flexion 818 spasm 811, 818 in sustained traction 896 see also erector spinae sacrospinous ligament, triangular 942 sclerosant infiltration 963-964 sacrotuberous ligament 942 sclerosant infiltration 963-964 sacrum anatomy 941 fractures 964-965, 1009 see also sacroiliac joint saddle anaesthesia 640, 807 5affar's classification, carpal instability 508 'sand toe' 1256 saphenous nerve 1265 course 1265

1 3 30 INDEX

saphenous nerve (continued) disorders entrapment localization 1 266 paraesthesia 1266 sites of compression and localization of infiltration 1 266 traction 1 265 innervation area 1 266 saphenous neuralgia 1265 SAPHO syndrome 407 sarcomeres 42, 42 injury 47 sartorius muscle 975 anatomy 1059 lesions 1 024 sartorius tendinitis 1025 Saturday night palsy 27, 453, 559 scaphoid 474 avascular necrosis 500 blood supply 500, 501 fracture 500 isolated arthrosis 504 scaphoid bell sign 508 scapholunate instability 508 scapula anatomy 278, 278-279 elevation crepitus 408-409 deep friction therapy 409, 409 fossae 278, 278 fracture, differential diagnosis 189 metastases (warning sign) 408 movements 389, 390 acromioclavicular sprain 327 active 155, 15� 1 57 examination 1 55, 1 57, 1 5 7, 294, 397 interpretation 169 pain, in thoracic disc lesions 617 painful in rib fracture 322 resisted 1 57, 157 pain see scapular pain snapping 408 winging 609 mononeuropathy of long thoracic nerve 553 scapular approximation 393 pain 409 in thoracic neurofibroma 638 resisted, pain 412 weakness 412-413 scapular area derma tomes and myotomes 1 5 metastases, differential diagnosis 189 scapular pain 15, 1 86 arm pain after 1 86, 253 C4 nerve root compression 1 88 central 192, 196-197 cervical disc lesion 382 crepitus in scapular elevation 408 levator scapulae muscle lesions 411-412 multisegmental 150, 1 50 unilateral 1 84-185, 1 85 scapulohumeral abduction normal with passive arm elevation limited 322

passive, limitation 319-322 resisted, limited 359 see also shoulder, abduction scapulohumeral reflex 202 scapulohumeral region, blood supply and nerves 288, 288 scapulohumeral rhythm 283 scapulothoracic crepitus 79 scapulothoracic gliding mechanism 278, 281, 390 anatomy 389-390 functional examination 398 scapulothoracic rhythm 283 scar tissue benefits of mobility 53 formation 45 ill-organized acute muscular tears / strains 48, 49 after rest 45 management 45-46 pain associated 26 strength and remodelling 45 deep transverse friction action 95 tendinitis 50 Scheuermann's disease 735 Schmorl's nodes 642, 735-736, 736 Schwarm cells, compression affecting 27, 41 schwarmoma cervical spine 217, 2 1 7 spinal accessory nerve 544 terminology 637 sciatica 11, 757-770 age of onset 802, 802 alternating 762 backache before 744, 760-761, 804 bilateral 761-762, 853 metastatic disease causing 861 S4 syndrome 879 chronology 744 'classical', clinical features 760-761 clinical examination 762-765 common / unfavourable patterns 762, 763

inspection 762 root tests 763-765 spinal movements 762, 762-763, 816, 817 straight leg raising test 763-764, 824 CT evidence of bulge inadequate for diagnosis 759, 768 definition 699, 800 differential diagnosis 761-762 duration excessive 853 elderly 761, 765, 770 epidural anaesthesia 906 manipulation indication 879 history 760-762, 807 inherent likelihoods 60 l u mbar nerve root atrophy 763, 768-769 mechanism 718, 757-760, 758 muscle spasm in 811 natural history 760-761, 765 neurological deficit, epidural anaesthesia for 905-906

pain 804 localization 760, 803 nocturnal 760, 769-770 radicular 854 on straight-leg raising 719 posture adopted in 762 posture affecting 760 progression 711-712 radicular pain 854 recurrence 769 after root palsy 906 referred pain from dural sleeve 744, 760, 761, 803 severity of symptoms, factors affecting 758, 758 shifting pain 66, 66 signs / symptoms 720, 760 sequence 760-761 spinal manipulation complication avoidance 113 spondylolisthesis causing 857 spondylolitic 857 spontaneous recovery 765, 805, 930 mechanisms 768 recurrence not likely 768-769 summary 770, 850 as symptom not diagnosis 700 temperature of leg 764-765 traction contraindication in 897 treatment 769-770 epidural anaesthesia 769-770, 903, 905-907, 9 1 5 importance of delay before surgery 768, 769, 930 manipulation indications 878, 878-879 manipulation not useful (cases) 880 manipulation or traction 769 manipulation success rate 881 unilateral, lateral recess stenosis and 793 warning signs 851-855 without neurological signs, epidural anaesthesia indications 906-907 scia tic nerve anatomy 980, 981, 982 neurocompression syndromes 1263 pressure on 28 straight-leg raising effect 763 sciatic pain, mechanism 744 scintigraphy see bone scans sclerosant infiltration 125-127 indications 126 golfer'S elbow 468 iliolumbar ligament lesion/ strain 782 ligamentous sclerosis, thoracic disc lesions 632, 632-633 lumbar segmental instability 843-844, 844

postural syndrome 778 recurrent low backache 756 sacroiliac joint syndrome / strain 962-964, 963 type II tennis elbow 461 unstable mortice (ankle) 1 228, 1228-1229 lower lumbar spine, technique 920-921

INDEX 1 3 3 1

mode of action 126 results 127 side effects and complications 126-127 see also phenol sclerotome 8 scoliosis acquired 646 cervical, acute torticollis vs 183 compensatory 647 congenital 646 defini tion 645 idiopathic 646, 809, 810 psychogenic 809, 810 sciatic 809, 810 types in lumbar disc displacement 810 secondary 646 sta tic 809, 810 thoracic 601, 645-647 non-structural 645, 647 structural 645, 646-647 treatment 646-647, 647 types 809 scrotum, dermatome and myotome 16 segmental instability, lumbar see lumbar segmental instability segmental mobility tests 107 segmental pain 166 cervical disc displacement 180-181 root syndromes 1 87-192 dural 1 7, 148, 166 referred see referred pain see also multisegmental pain selective tension, principles 61 self-perpetuating inflammation 45-46, 46 tennis elbow 455 semicircular canals 227 semimembranosus muscle, anatomy 977, 977, 1059 semispinalis capitas muscles deep transverse friction 269, 270 massage before manipulation 256, 256 semispinalis muscle lesions 205 semitendinosus muscle, anatomy 977, 977, 1059 sensory cortex, arrangement and pain 7-8 sensory deficit cervical spondylotic myelopathy 202, 202 nerve root compression 29 sciatica 759-760, 768 sensory feedback, proprioception 115 sensory nerves 7, 43 sensory receptors, connective tissue 36-37 sensory tests arm 159, 1 60 carpal tunnel syndrome 570 cubital tunnel syndrome 564 lumbar spine 824-827 tests 826, 826-827 separation hypothesis, epidural anaesthesia 913-914 sepsis, epidural anaesthesia contraindication 907 septic arthritis acute subdeltoid bursitis vs 320 elbow 440

hip joint 1001 knee 1081-1082 sacroiliac 960-961, 1010 shoulder 316-317 sternoclavicular joint 405 septic bursitis, hip 1 008-1009 serotonergic agonists, migraine 225 serratus anterior muscle 336, 390 anatomy 393 deep friction 412, 4 1 3 innervation by long thoracic nerve 553, 554 lesions 412 mononeuropathy of long thoracic nerve 553 weakness and wasting 368, 553 serratus posterior inferior muscle, sprain 665 sesamoid bones 1 1 65-1166 hand 476 pa tella 1054 periostitis 1254 sesamometatarsal lesions 1254 Sever's disease 1190-1191 sex differences, disorders 64 Sharpey, fibres of 705 Sharp-Purser test 216 Sharp'S and Purser's sign 216 shifting lesions, pain see pain, shifting Shimizu's reflex 202 shingles see herpes zoster shin splints 1195-1197 'shoe wiping test', of Pecina 1031 shoulder abduction 283 muscles 285, 285, 353 passive 296, 297, 380 resisted see shoulder, resisted abduction see also arm elevation; deltoid muscle; scapulohumeral abduction; supraspinatus muscle adduction 283 horizontal see shoulder, horizontal adduction muscles and tendons 283, 284, 284-285, 285, 361 resisted see shoulder, resisted adduction see also latissimus dorsi muscle; pectoralis major muscle; teres major; teres minor anatomy 277-289 blood vessels 288, 288 bones 278, 278-279, 279 bursae 282, 282-283 extracapsular ligaments 281, 281-282, 282 intracapsular ligaments 279-280, 281 joints 279, 279-281, 280 muscles / tendons see below nerves 285, 288, 288 ankylosing spondylitis 315-316 anterior capsular contracture 324-325, 325 arthritis 292 C5 pain 20

classifica tion 306, 307 differential diagnosis 188 early 328 aseptic necrosis 317 backward movement, thoracic spine examination 602, 602-603 capsular laxity 382 capsular lesions 305 fibrosis 313 capsular pattern of limited movement 305, 305-319, 306, 3 1 8 conditions 306-319, 307 magnitude and phases 306, 306 staging 306, 306 chondrocalcinosis 316 clinical examination 291 -302 accessory tests 295, 300, 300 diagnostic difficulties 291 history-taking 292 importance of precise diagnosis 292, 300 incomplete diagnosis 295 inspection 294 interpretation 303-304 palpation 295, 300 technical investigations 300-301 crepitus 317 crystal synovitis 316 degenerative diseases 317-318 dislocation acute subdeltoid bursitis vs 320 axillary nerve palsy a fter 1 88 see also glenohumeral joint, dislocation disorders of contractile structures 349-377 resisted abd uction 353-360 resisted adduction 360-364 resisted lateral rotation 364-368 rotator cuff see rotator cuff lesions

see also individual movernents below disorders of inert structures 305-348 excessive movement see glenohumeral joint, instability full movement see below limited movement see capsular pattern

(above); non-capsular pattern (below) painful arc 380 distraction, grade A mobilization 103 double lesions 291 elevation 157 exercise in first rib syndrome 552, 552 sustained in thoracic outlet syndrome 550, 550, 551 thoracic spine examination 602, 602-603 see also shoulder, shrugging external rotation, resisted 158, 1 58 flexion, muscles and tendons 287, 287 ' frozen' 306, 307 idiopathic 313 full range of movement, disorders with 326-335 acromioclavicu lar sprain 327-331 chronic subdeltoid bursitis 333-335 conoid and trapezoid ligaments sprain 331-332 crepitating bursitis 335

see also individual disorders

1 3 32 INDEX

shoulder (continued) functional examination / testing 61, 294-299 arm elevation 295-296, 296 interpretation 172, 1 72 painful arc 295-296, 296 painless / painful limitation 1 72 preliminary 294, 294-295 resisted movements 298, 298, 299 summa ry 295 see also arm elevation; glenohumeral joint; shoulder girdle functions 277 haemarthrosis 293, 316 height difference 397 history-taking 292-294 horizontal abduction of arm 412, 4 1 2 horizontal add uction 283 muscles 286 passive 300, 300, 404 in acromioclavicular sprain 327 pain 403, 404 resisted 353, 353, 362 horizontal extension 283 resisted 353, 353, 557 horizontal lateral rotation 325 immobilizational arthritis 312-313 impingement 287, 379, 379 impingement syndrome 380 instability see glenohumeral joint, i nstabi I i ty lateral rotation 283 muscles and tendons 286, 286, 364 passive 296-297, 297, 337 li mitations 324-326 painful 369 resisted see shoulder, resisted lateral rotation see also infraspinatus muscle; teres minor limited range of movement 305-326 capsular pattern see above non-capsular pattern see below painful 172, 291, 324 medial rotation 283 muscles and tendons 285, 285-286, 286, 368-369 passive 297, 298, 379 resisted see shoulder, resisted medial rotation see also subscapularis muscle; teres major metastases 3 1 7 monoarticular arthritis, differential diagnosiS 3 1 8 monoarticular steroid-sensitive arthritis 3 1 3, 3 1 3-315 age association 313, 314 functional examination 314 phases / stages 3 1 3, 314, 3 1 4 treatment 314-315 morning stiffness 315 movements 283, 283

see also specific 1I10Vemel1 Is above/below muscles and tendons 283-287 abductors/ abduction 285, 285, 353

adductors / adduction 283, 284, 284-285, 285, 361 balance and rotator cuff role 287, 350 elbow extension 286, 286-287 elbow flexion 286, 286 flexors / flexion 287, 287 horizontal adduction 286 lateral rotation / rotators 286, 286, 364 medial rotation / rotators 285, 285-286, 286, 368-369 origins / insertions 284 stabilizing vs effector types 349, 349 see also rotator cuff neuropathic destructive arthropathy 318-319 non-capsular pattern of limited movement 319-335 active elevation limited 319-324 active elevation limited with normal passive elevation 322-324 active / passive elevation and sca puloh u meral abd uction limited 3J 9-322 active / passive elevation limited but normal scapulohumeral abduction 322 passive lateral rotation limited 324-326 passive medial rotation limited 326 summary 327 osteoarthrosis 317-318 overactivity 293 pain 1 72, 291, 292, 294 acromioclavicular sprain 327 active / passive elevation 403-405 acute subdeltoid bursitis 319, 320 biceps disorder 447 history-taking 292-293 lesions causing 292 lung lesions 219 monoarticular steroid-sensitive arthritis 314 palpation for 300 pectoralis major muscle lesions 361 resisted abduction 353-358, 366-367 resisted abduction and lateral rotation 366-367 resisted adduction 360-363 resisted lateral rotation 364-367 septic arthritis 316 painful arc see painful arc passive movements 72 limitation, capsular pattern 84 polyarticular arthritis 3 1 8 primary tumours 3 1 7 reactive arthritis 315 referred pain from 292, 395 referred pain to 219, 292, 395, 597, 657, 665 Reiter's syndrome 316 resisted abduction 158, 1 58, 298, 298 differential diagnosis 355 pain 353-358, 366-367 with painful resisted lateral rotation 366-367 painful weakness 358-359

painless weakness 359-360 summary 361 resisted adduction 298, 298, 360-364, 362 pain 360-363 painful weakness 363 painless weakness 363-364 pectoralis major lesions 665 summary 364 teres minor role 364 resisted lateral rotation 298, 299, 364-368 pain 364-367 with painful resisted abduction 366-367 painful weakness 367 painless weakness 367-368 summary 368 resisted medial rotation 298, 299, 368-371 pain 368-370 painless weakness 370-371 summary 371 resisted movements 158, 1 58 rheumatoid arthritis 315 septic arthri tis 316-317 shrugging (active elevation) 322, 397 crepitus or paraesthesia 397, 408 disorders with symptoms 205 pain 403-405, 406 positive 1 72 sustained in thoracic outlet syndrome 550, 550, 551 thoracic spine examination 602, 602--603 snapping 83 stability 335-336 stage I inflammation 306, 306 stage III arthritis 306 grade A mobilization 103 sti ffness 306, 312 morning 315 traumatic arthritis 307-308 traumatic arthritis 307, 307-312 arthroscopic release 312 capsu lar stretching see capsular stretching distraction technique 309-310, 3 1 0 hydraulic distension 3 1 2 intra-articular injections 310-312, 3 1 1 manipulation under anaesthesia 310 natural history and phases 307-308 onset and pain 307 passive mobilization 308-310, 309, 310 prevention 308 thawing phase 308 treatment 308, 308-312, 3 1 2 tuberculosis 316-317 shoulder girdle rulatomy 387-393, 388 osteoligamentous structures 387-390 arm elevation test 157, 1 57 clinical examination 395-399 history-taking 395 inspection 396 interpretation 401--402 palpation 399 depression 393 resisted 399, 399

INDEX 1 3 3 3

disorders , cervicoscapular pain 219 summary 414 disorders of contractile structures 411--414 pain on resisted approximation 412 pain on resisted depression 413 pain on resisted elevation 411--412 pain on resisted protraction 412 disorders of inert structures 403--410 limitation of active elevation with weak resisted elevation 408 pai n / limitation of active / passive elevation 407--408 pain on active elevation / protraction 406 pain on active/ passive elevation 403--406 pain on active / passive scapular approximation 409 paraesthesia 408 elevation 393, 397 active see shoulder, shrugging crepitus 397, 408 passive 398, 398 resisted 399, 399 elevators 411 functional examination 396, 396-399, 397 active movements 396-398, 397 passive movements 398, 398-399 resisted movements 399, 399 innervation 390-393 joints included 277, 387 see also acromioclavicular joint; scapulothoracic gliding mechanism; sternoclavicular joint lesions, paraesthesia due to 151 movements 392, 393 gross limitation 407 muscles 336, 390-393 anterior 390-391, 391 posterior 391, 391, 392, 393 see also latissimus dorsi muscle; levator scapulae; rhomboideus muscle; serratus anterior muscle; trapezius muscle pain 395, 397 bilateral in pathological fractures 644 mononeuropathy of spinal accessory nerve 544 thoracic intraspinal tumours 638-639 protraction and retraction 393, 397 active 397 pain 406 passive 398, 398 resisted 399, 399 pain 412 symptoms referred from 395 symptoms referred to 395 shoulder-hand syndrome 315 shoulder joint see glenohumeral joint 'sign of buttock' see 'buttock, sign of' signs diagnostic procedure 60 unusual, accessory testing 76 warning see warning signs

sinusitis, paranasal 680 sinuvertebral nerve 25, 28, 144, 144, 145, 585 anatomy 721-722 branches 722, I dural pain mechanism 148, 585 dura mater innervation 716, 71 9, 71 9, 744 lumbar spine innervation 721-722 nerve root sheath innervation 71 9, 719-720 sinuvertebral nerve block 631, 719-720 sitting coccygodynia 968 correct position 922, 922-924, 923 chairs and positions 923, 923 effect on lumbar intradiscal pressure 707-708, 710 knee inspection 1065 patella inspection in patellofemoral disorder 1 139, 11 39-1140 postural syndrome treatment 778 pressure on discs 922-923 sit-up exercises, adverse effect on lumbar discs 756, 843, 843, 926 skin atrophy 124 folds, gluteal and groin 988 lumbar spine inspection 811 skin lesions corticosteroid side effect 124 deep transverse friction contraindication 98 inspection 70 skull, enlargement, Paget's disease 651 sleep, sitting up, thoracic neurofibroma 638 slipped femoral epiphysis 1046 small intestine, referred pain from 598 snap on active movement 83 long head of biceps 373, 382 snapping ankle 83, 1197 knee 1082 scapula 408 shoulder 83 sneezing, pain exacerbation 168, 600 acute annular lumbago 746 low back pain 804, 804 soccer ankle 1206 soft end-feel 73, 73 soft tissue injury 43-56 definition 43 neck see whiplash-associated disorders soft tissue lesions characteristics 59 diagnosis 59-92 importance 59 obstacles 60 inspection 70 need for precise description 59 referred pain 6-21, 166 soft tissues, inert and contractile 6 1 , 61-62 soggy end-feel 74 soleus muscle 1161 anatomy 1166 stretching 1192, 1 1 92

somatosympathetic reactions, local anaesthetic 119 somites 8 space-occu pying lesions brachial plexus 546 cervical spine 2 1 7, 217-218 lumbar spinal canal 804 lumbar spine (intraspinal) 821 -822 'spacer effect' 359, 359 spasmodic pes planus 1240 spasticity, cervical spine lesions 1 51 sphenomandibular ligament 676 spica cast, traumatic arthritis of wrist 501 spinal accessory nerve 543-544 anatomy 543-544, 544 disorders 408, 543-544, 544 innervation 544, 544 mononeuritis 218, 544 differential diagnosis 1 88 testing 324, 324 mononeuropathy 544 neuritis and weakness of scapular approximation 412--41 3 palsy 323-324, 544, 545 spinal accessory neuropathy, idiopathic 544 spinal anaesthesia, epidural anaesthesia adverse effect 907-908 spinal arteries 145 spinal arthrodesis 931 spinal canal cervical see cervical spinal canal lengthening during flexion 715, 715 lumbar see lumbar spinal canal osteophytes 249 stenosis see lumbar spinal stenosis; spinal stenosis thoracic see thoracic spinal canal spinal cord 24 anatomy 716 anterior horn, disorder 83 cervical see cervical spinal cord compression 29 cervical see cervical spinal cord lumbar 807 thoracic see thoracic spinal cord dorsal horn, sensory nerves 7 lesions, paraesthesia 68 lumbar see lumbar spinal cord mechanism of referred pain 7 thoracic see thoracic spinal cord spinal epidural haematoma, thoracic level 641 spinal fusion indications 844 scoliosis treatment 647, 647 spinal ganglion 144, 145 spinal joint, derangement, forced movements 55 spinal manipulation see manipulation (spinal) spinal membranes, cervical spine 143 spinal nerve(s) 24 brachial plexus anatomy 545, 545 cervical 137 compression, symptoms / signs 719

1 334 INDEX

spinal nerve(s) (continued ) course 25 extraspinal region 716 intraspinal intrathecal part 716 lumbar 716 monofascicu lar 25 thoracic 584-585, 585 spinal nerve root canal 716 spinal pain, spinal manipulation action 109 spinal rami 230 spinal reAex arcs 37 spinal rhythm, normal, reversal 841, 841 spinal rotational manipulation 106 spinal stenosis 29, 787, 787 absolute us relative 788 acquired 788 cervical see cervical spinal canal, narrowing degenerative 788 iatrogenic 788 idiopathic developmental 787-788 lumbar see lumbar spinal stenosis mechanisms 201, 201 spinal sti ffness 107 spinal surgery, lumbar 928-931, 929 arthrodesis 931 discodural / discoradicular interactions 928-930 decompressive surgery failure 930 indications 929, 929-930 failure and reason 928 incidence 928 indications 928 lateral recess stenosis 930-931 spinal stenosis 930-931 spinal h"act, anterolateral 4 spinal traction, indications 104-105 spinal tumours cervical spondylotic myelopathy us 204 lumbar 113 spinal manipulation complication avoidance 113 spinal manipulation contraindication 110 see also intraspinal tumours spine bamboo 670, 862 development 703, 703-704 evolution 703-704 metastases cervical 190, 2 1 4, 214-215 warning signs 861 normal shape 808, 8 1 8 see also cervical spine; lumbar spine; thoracic spine spinothalamic tract 4 anterior 228 spinous processes cervical vertebrae (lower) 137 fractu res 212 lumbar spine abnormal projections or shelf 830 palpation 830, 830 sacral 909 thoracic spine 582 assessment of 'most tender' 624-625

transverse processes relationship 582, 624, 624-625, 625 traction fracture, C7 or T1 406 splay foot 1251 metatarsalgia 1256 spleen, referred pain from 598, 660 splenic flexure, distension 660 splenius capitis muscle deep transverse friction 269, 270 lesions 205 massage before manipulation 256, 256 spondylarthrosis 1 76, 177 spondylitic spurs 736, 736, 738 spondylitis, tuberculous 863 spondylolisthesis 855-857 aetiology 855-856 age of onset 802 bilatera I sciatica us 853 clinical features 856-857 sciatic pain 857 definition 855 degenerative 855 arthrodesis for 931 cervical 201 lumbar 788, 789 dysplastic 855 excessive lordosis 809 grading 856, 856 history-taking 807 isthmic (spondylolisthetic) 855, 855 lumbar segmental instability 839 pathological 855 with secondary disc lesion 856-857 traumatic 855 treatment 857 arthrodesis 931 types 855 without disc lesion 816 spondylolysis 858-859 definition 855 grading 856, 856 spondylosis 1 76 cervical see cervical spondylosis sports adductor longus injury 1026 avulsion fracture of anterior superior iliac spine 1025 hamstring strains 1144 history-taking 64 prevention of lumbar disc displacement 926 quadriceps tendon lesions 1132 sports hernia 1039-1040 'sprained ankle' see ankle sprains sprains 53, 54 active movement therapy 114

see also specific sprains springy block end-feel 74 'sprung back' 782 squatting, knee examination during 1073 squeeze test, Achilles tendon rupture 1191 standing correct posture 924, 925 hyperlordosis prevention 926-927, 927 knee inspection 1065

lumbar spine examination 812-819 pain 804 lateral recess stenosis 792 Staphylococcus aureus infections 123 pyogeniC osteomyelitis 648, 863 shoulder 316 sternoclavicular jOint 405 stenotic concept 794 definitions 787-788 diagnosis before treatment 874 disorder prevention 927-928 lateral recess stenosis see lateral recess stenosis lumbar segmental instability and 840-841 spinal stenosis see lumbar spinal stenosis sternal angle of Louis 585 sternal lumbago 620 sternoclavicular arthritis 219 sternoclavicular joint 277, 281, 281 anatomy 387, 388-389, 389 ankylosing spondylitis 322, 398 ankylosis 398, 407 arthrosis 405 capsule 281, 388 disorders 403-405, 662 pai n / limitation of active / passive elevation 407 hyperostosis 407 injection 404, 404, 404-405 meniscus 281 movements 389 overuse 405 pain 597 rheumatoid arthritis 322, 405 septic arthritis 405 sprain 404 structures behind 389, 389 traumatic dislocation 407 anterior and posterior 407 sternoclavicular ligaments 388 sprain 404 sternoclavicular syndrome, posterior 219, 403, 404-405 sternocleidomastoid muscle 142 anatomy 391, 391 functions 143 innervation from spinal accessory nerve 544, 544 painful contraction 62 reflex spasm 184 spasm 151 sternum anatomy 585, 586 disorders / lesions 662 referred pain 597 fra cture 662 metastases 662 pain 600, 620 ribs attachment 587, 587 steroids arthropathy due to 123-124 avoidance, chronic muscular tears h"eatment 49

INDEX 1335

effect on connective tissue repair 44, 45, 122 effect on macrophage during repair 44 infiltration / injection adverse effects on tendons 352 arthrosis at first metatarsophalangeal joint 1253, 1 253 cervical disc displacement 266 coccygodynia 968-969, 969 deep transverse friction vs 94 midtarsal strain 1243, 1 244 rotator cuff lesions 352 suprascapular nerve entrapment 555, 556 type II tennis elbow 458 see also corticosteroid infiltration; triamcinolone myopathy due to 125 self-perpetuating inflammation management 45-46 steroid sensitive arthri tis see monoarticular steroid-sensitive arthritis 'stick palsy' 572 Stieda-Pellegrini disease 1093, 1103-1104 stomach, referred pain from 597, 598, 659, 659 straight leg raising (SLR) test 820-824 acute lumbago 748-749, 824 bilateral limitation acute lumbago 748-749 unilateral vs 764, 764 'bowstring' sign 824 'constant-length' phenomenon 86 contralateral sacroiliac joint straining 823 crossed 764, 764, 823 dural mobility 715, 715 dural sheath mobility 71 9 as dural sign 715-716, 748 effect of lumbar nerve roots 719 effect on sciatic nerve 763 historical backgrow1d 821 indications 820-821 internal rotation of hip 719 low back pain (lumbar) 715, 715-716, 753-754 long-standing limitation, traction 897 lumbar neurofibroma / meningioma 865 neck flexion with 823, 824 non-organic disorders 824 pain 72 sacroiliac strain 962 sciatica 719 painful arc 764, 823 positive results extraspinal lesions 82 1 , 822 intraspinal lesions 821 , 821-822 procedure 822, 822-824 psychogenic problems 819, 824 sacroiliac strain / disorders 962 sciatica examination 763-764, 824 significance 821-824 stages and features 823 unilateral vs bilateral limitation 764, 764 straight pull, cervical manipulation 257, 257 strapping of joints, sprained ligament treatment 54

strength, resisted movements, pain vs 88 stress fracture femoral neck see femoral neck first rib 322, 411 lumbar pedicle 859 navicular 1245 pubic bone 88 pubic ramus 1037-1038 wrist 507 stress reaction, wrist 507 stretching, capsular see capsular stretching stretching exercises, acute muscular tears/ strains treatment 48 stroke, cervical spine manipulation complication 112 stylohyoid muscle 677 styloiditis radii 524, 526 see also de Quervain's disease stylomandibular ligament 676 subacromial abrasion see subdeltoid bursitis, chronic subacromial bursa 280, 282, 282 infiltration 334, 334 subacromial bursitis, fanwise infiltration 117 subacromial gliding mechanism 277 subacromial joint 277 subacromial lesion, painful arc 296 subacromial space 280, 280, 380 subarachnoid space 143, 718 subarticular entrapment (of nerve root) 791-792 subarticular stenosis 791 subaxial subluxation 216 subchondral bone, hip osteoarthrosis aetiology 1001 subclavian artery 228, 288, 288 ill1 eurysm 546, 548, 548 compression, thoracic outlet syndrome 548, 548 thrombosis, C8 nerve root compression vs 1 88 subclavian nerve, anatomy 545 subclavian vein 288, 288 impairment/ thrombosis 548 subclavius muscle anatomy 391, 391 deep friction 413, 413 lesions 413 sprain 413 differential diagnosis 332, 334 subcoracoid bursa 283 infiltration 326, 326 subcoracoid bursitis 283, 325-326, 326 differential diagnosis 332, 334 treatment 326, 326 subcoracoid impingement syndrome 380 subcutaneous bursitis 1216 subcutaneous nodules, calcaneus 1216 subdeltoid bursa 280, 280, 282, 282-283 infiltration 334-335, 335 subdeltoid bursitis 283 acute 31 9-321 calcified deposit with 321, 321 differential diagnosis 320

painful arc 320, 380 recurrence 319 treatment 320, 320-321, 321 chronic 328, 333-335 clinical patterns 333, 333, 367 differential diagnosis 366 painful arc 333, 380 recurrence 335 treatment 334, 334-335, 336 haemorrhagic 321 pain 293 subluxation definition 335 reduction, grade C mobilization 1 05 subphrenic abscess 659 subscapularis muscle 285, 286, 369-370, 390 lesions 369-370 subscapularis tendinitis 297, 369 differential diagnosis 325, 332 functional testing 62 painful arc 381 treatment 369-370, 370 subscapularis tendon 280 rupture 370-371 substance P 333, 706 substantia gelatinosa (SG) 5 subsynovial haematoma, knee 1 093-1 094, 1 094 subtalar joint (talocalcaneal) anatomy 1 1 62, 1 1 62 disorders 1 209-1213 capsular pattern 1 2 1 0, 1 210-1211, 1 2 1 3 non-capsular pattern 1 211-1213, 1 2 1 3 summary 1 2 1 3 immobilizational stiffness 1 211-121 2 injection technique 1210, 1 2 1 1 inversion sprains 1217 ligaments 1163, 1 1 63 loose bodies 1 205, 1212-1213, 1 2 1 3 manipulation 1212, 1 2 1 2 mobility assessment 1 1 75, 1 1 76 movements 1 1 62, 1 209, 1 2 1 0 osteoarthrosis 1211 rheumatoid disorders 1210 subacute traumatic arthritis 1210 varus / valgus movements, assessment 1 1 75, 1 1 76 suction discectomy 929 Si.ideck's atrophy 538-539, 812 sulcus sign 336, 338, 341, 341 superficial flexor digitorum, anatomy 423, 423 superficial peroneal nerve 1 266, 1267 disorders areas of sensory changes 1 266 compression sites and infiltration 1 266 entrapment 1267 superficial radial nerve 425, 425, 481 superficial temporal artery / veins 678, 678 superior facet syndrome see lateral recess stenosis superior pulmonary sulcus 657 superior sulcus tumour, of lung see Pancoast's tumour superior thoracic aperture 585

1336 INDEX

supinator brevis muscle 422 anatomy 559, 559 infiltration and deep friction 453, 453-454 lesions 453-454 radial tunnel syndrome and 560 suprahumoral gliding mechanism 280 suprahyoid muscles 677 suprapatellar tendon deep friction 1133-1 134, 1 1 34 infiltration 1134, 1 134 quadriceps ruptures above 1131 rupture 1136 tend ini tis 1 133 suprapubic pain 666 suprascapular nerve 288, 288, 554--555 anatomy 545, 554, 555 compression 368 disorders 554-555 entrapment 554, 555 injection technique 555, 556 innervation 554 mononeuritis 219 differential diagnosis 1 88 mononeuropathy 555 palsy 360 features and examination 368 traumatic, differential diagnosis 1 88 supraspinal fossa 278, 278, 285 supraspinal ligaments overstretched, wedge fracture 643 sclerosant infiltration, thoracic disc lesion prevention 632, 632 supraspinatus muscle 286 anatomy 285, 285 ann elevation 295, 296, 359 pain 354, 354 'critical zone' and hypovascular region 350 disorders 353-358 localization 354, 354 tenoperiosteal see supraspinatus tendinitis exercises, glenohumeral instability treatment 342, 343 functions 359 innervation 554, 555 rupture, differential diagnosis 188 in suprascapular nerve entrapment 555 wasting 368 weakness 324, 368 'supraspinatus outlet' 356, 356 supraspinatus tendinitis 353-358 calcification 356 clinical signs 367 deep transverse friction contraindication 98 differential diagnosis 1 88, 334, 366 musculotendinous lesions 358, 358 painful arc 354, 354, 380 recurrent 356 site of lesions 354, 354 tenoperiosteal lesions 354--356, 357 deep friction 356-358, 357 palpation 354--355, 355 triamcinolone infiltration 355-356, 356

supraspinatus tendon deep transverse friction 99 partial rupture 358 rupture 324 total rupture 359-360 treatment 360 supraspinous ligament 142, 782-783 lumbar spine 711, 711, 712, 782-783, 838 injection technique 918, 918 lesions 782-783, 783 mechanoreceptors, reflex arc 838-839 surgery Achilles tendonitis 1187 carpal tunnel syndrome 572 cauda equina syndrome 928 cervical disc displacement 267 cervical nerve root syndromes 192 cervical non-discogenic disorders 271 delay important in sciatica 768, 769, 930 for discodural interaction 928-930 for discoradicular interactions 928-930 extradural haematoma 641 glenohumeral instability 344 hip osteoarthrosis 1007 knee ligament see knee ligament instability lateral recess stenosis 930-931 low back pain 875, 928 lumbar segmental instability 844 lumbar spine see spinal surgery menisci, knee 1086 midtarsal strain treatment 1244 scoliosis treatment 647, 647 thoracic disc lesions 631 thoracic outlet syndrome 552 ulnar nerve entrapment 565

see also specific anatomical sites, procedures and conditions sustentaculum tail 1242 swallowing, painful 205, 679 swan neck deformity 534 swelling joints 65, 78 localized, palpation 78 swimming 926 symptoms 66-68 inherent l i kelihoods 60 initial, in history-taking 64 localization 65 onset 64 pain see pain progression, in history-taking 64, 65 recurrent 66 synchondrosis, sternum 585 syndesmophytes 862 synovial bursae 41 synovial cyst, intraspinal 865 synovial fluid 39, 43 hip osteoarthrosis aetiology 1002 synovial inflammation, shoulder 306 synovial joints 37, 38 capsule see capsules synovial membrane 37, 39 cell types (A and B) 39 intimal cells 39

thickening 78 synovial sheath 43, 43 synovitis see capsulitis synovi tis-acne-pustu losis-hyperostosis-ost eitis (SAPHO) syndrome 407 syringomyelia 318

tailor's bunion 1255 talar tilt 1219-1220 talocalcaneal joint see subtalar joint talocalcaneonavicular joint 1163, 1 1 63 talofibular ligament adhesions 1 220-1 221 deep friction 1224--1225, 1225, 1 225 infiltration technique 1 223-1224, 1 224 talonavicular joint 1239 anatomy 1164 mobility 1164, 1 1 64 talus 1161 anatomy 1 1 6 1 , 1161-1162, 1 1 62 dome, transchondral fracture 1204 taping see bracing and taping tardy ulnar neuritis 563 tarsal bones, anatomy 1164 tarsal canal 1162, 1 1 63 tarsal tunnel 1 267, 1 268 tarsal tunnel syndrome 1267 anterior 1267 tarsometatarsal joints 1165, 1 239 technetium bone scans see bone scans technical investigations 63, 80, 80 tectorial membrane 140 teeth grinding 681, 695 infections 680 loss, temporomandibular joint arthritis 695 wear and tear 681 temperature, of joints, assessment 77-78 see also heat temporal arteritis, pain referred to temporomandibular joint 680 temporal bone, anatomy 675 temporal is muscle, anatomy 676, 677 temporomandibular joint (TMJ) 673-696 abscess 695 anatomy 675-678 bones 675, 676 joint capsule and ligaments 675-676, 676 meniscus (disc) 675, 676 muscles and tendons 676-677, 677 nerves and blood vessels 678, 678 nociceptive innervation 676 ankylosing spondylitis 694-695 arthritis due to molar tooth loss 695 arthrosis 692-693 biomechanics/ movements 677-678 abnormal 689 distraction techniques 691 clinical examination 679-685 history-taking 680-681 inspection 681

INDEX 1 33 7

interpretation 687 palpation 684, 684 technical investigations 684 crepi tus 681, 693 deep friction 693, 693 disorders 689-696, 690 causes 689 of contractile structures 690, 695-696 of inert structures 689-695, 690 prevalence 689 functional examination 681-683 active movements 681, 681, 682 resisted movements 682-683, 683 hypermobility 689, 692 hypomobility 689 infections 695 inflammatory disorders 681, 694--695 internal derangement 691-692 intra-articular injection 693, 693 locking 680-681 luxation of condyle 694, 694 meniscus (disc) anatomy 675, 676 displacement 691, 691 fixed dislocation 692, 692 rupture 692 morning stiffness 694 myalgia 695 pain 679-680, 689, 695 painful clicks 679 reciprocal clicking 691 referred pain from 679 referred pain to 680 repetitive microtrauma 689, 691 rheumatoid arthritis 694-695 swelling 681 sympathetic arthritis 695 synovial disorders 694--695 synovitis 681 upper and lower compartment 676 see also mouth tenderness associated, sites 78 mu ltisegmental, cervical disc displacement 1 79 palpation 78 referred see referred tenderness tender spot, cervical disc displacement 1 79 tendinitis 50-51 acute traumatic lesions 50 corticosteroid infiltration 123 inherent likelihoods 60 overuse deep transverse friction 97 shoulder 293 resisted movements 75 retropharyngeal 205 shoulder 293 ,

see also specific forms of tendinitis tendinosis 50, 51 definition 1 1 87 tennis elbow 455 tendinous body lesions cylindrical infiltration 1 1 7 deep transverse friction 97

tendinous crepitus 79 tendinous insertions, static infiltration technique 1 1 7 tendinous lesions 50-52 classification 50 corticosteroid infiltration 123 deep transverse friction 97 localization and treatment 52 persistent pain 51 symptoms 67 tendon(s) 43 calcification 51 composition/ structure 43, 43 degenerative condition (tendinosis) 50, 51 function 50 healing 52 passive loading after 52 insertion into bone 43, 50 collagen changes in tendinosis 51 local swellings 51-52 nerve supply 43 overuse (chronic) lesions 50-51 regeneration, tendinosis 51 as regular connective tissue 37 ruptures/ tears 50 acute 52 complete 52 corticosteroid side effect 124, 1 25 deep transverse friction 97 healing and strength after 52 palpation 78 tension / exercise effect 43 tendon reflexes, absent, thoracic spinal cord compression 621 tendon sheath 43 hand 477, 477-478 lesions affecting 51 see also tenosynovitis telmis elbow 454-464 accessory tests 76 C6 nerve root compression vs 189 C7 nerve root compression vs 1 90 cervical spine involvement 455 classification 455 clinical examination 456, 457 clinical features 428, 456 definition and terminology 455 functional examination 456 historical aspects 454-455 history-taking 456 inherent likelihoods 60 limitation of extension 443 localizations 456, 457 pain / twinges 456 palpation 456 pathology 455-456 symptoms 67 synonyms 454-455 type I (supracondylar) 456-457, 458 type II (tenoperiosteal) 457-463 bracing and taping 463, 463 deep transverse friction 96 extracorporeal shock wave therapy 463 Mill's manipulation see Mill's manipulation

natural evolution / spontaneous cure 458, 458 refractory, treatment 461-463 sclerosant infiltration 126, 461 tenotomy 461-463, 462 triamcinolone infiltration 458-459, 459 type III (tendinous) 463, 464 type IV (muscular) 463-465 deep transverse friction 97 radial tunnel syndrome vs 560, 561 tennis leg 1 1 83-1186 Achilles tendon rupture vs 1191 differential diagnosis 1184 examination 1184 summary 1 1 86 treatment 1184-1186 deep friction and electric contractions 1 1 85, 1 1 85-11 86 infiltration (local anaesthesia) 1185, 1 1 85 surgery avoidance and scar problem 1184--1 1 85 tenography, ankle sprains (inversion) 1 220 tenoperiosteal adhesion, rupture by grade C mobilization 105 tenoperiosteal insertion lesions corticosteroid infiltration 123 vs deep transverse friction 97 deep transverse friction 97 injection therapy 1 1 6 tenoperiostitis, tibial tuberosity 1137 tenosynovitis 51 corticosteroid infiltration 123, 124 crepitus 79 deep transverse friction 51, 97 extensor digitorum 513 extensor digitorum longus 1193 extensor hallucis longus 1193 flexor digitorium profundus tendon 515, 516, 5 1 6 flexor pollicis longus tendon 526-527, 527 flexor tendons of fingers 536 muscular crepitus 79 upper limb 511-512 see also tenovaginitis tenotomy, type II tennis elbow 461-463, 462 tenovaginitis 51 abductor pollicis longus tendon 524--525 Achilles 1190 corticosteroid infiltration 123 extensor pollicis brevis tendon 524--525 rheumatoid abductor pollicis longus and extensor pollicis brevis 526 flexor digitorium profundus tendon 515 see also tenosynovitis tenovaginitis stenosans see de Quervain'S disease tension trajectories, articular cartilage 40, 40 tensor fasciae latae anatomy 976, 977, 978 deep transverse friction 1028 knee extensor 1 059, 1144 lesions 1028

1 338 INDEX

teres major 284, 285 testing 361 teres minor 280, 284, 286 innervation 556 lateral rotation of shoulder 364 lesions, pain 364 testicle carcinoma, pain referred to back 867 referred pain from 598, 599, 661, 661 torsion 661 trauma and pain 1 6 tetanus, warning sign 696 thalamic nuclear relay sites 4 thalamic nuclei, axons 5 thalamocortical projections 5 thalamohypothalamic system 5 'theatre, cocktail party syndrome' 777, 804 thecal sac neurocompression 648 thenar emi nence, muscular atrophy 570 thenar muscles 479 friction technique 536, 537 lesions 536 therapists 94 thigh contusions 1131 extension by hamstrings 1144 nerve supply anterior cutaneous nerve 1 265 lateral cutaneous nerve 1 264 thigh thrust test 951, 952 Thomas test 1013, 1037 thoracic aorta, aneurysm 656 thoracic backache 618-619 acute lumbago 600, 61 9-620 extradural haematoma 641 extraspinal tumours 639 manipulation 619 Paget's disease 651 postoperative, warning symptom 636 self-reducing lesion 619 see aLso thoracic spine, pain thoracic cage 585-589 bony structures 585-587, 586 contractile structures 587-589 muscles 588-589, 591 see also diaphragm; intercostal muscles disorders of contractile structures 664-667 disorders of inert structures 662-664 landmarks 589, 589 movements 589 muscles, disorders 664-665 razor back eminence 8 1 0 red uction of space between iliac crest and 809-810 referred pain 655-662 from musculoskeletal structures 661-662 from visceral structures 597-599, 598, 655-661

see also il7dividual organs thoracic derma tomes 10, 12, 1 3 T 1 1 90 T2 191 thoracic disc(s) 582, 583 dehydration 6] 9

thoracic disc lesions 61 5-634 cervical disc lesion differences 594 clinical features 594 clinical presentation 616-618 clinical types 6 1 8, 618-622, 6 1 9 acute lumbago (thoracic) 600, 619-620 thoracic root pain 620 see also thoracic backache; thoracic spinal cord, compression CT and MRI 612 degenerative 649 differential diagnosis thoracic neurofibroma 638, 640 thoracic spinal canal stenosis 641 tumours 640 discodural lesions 594, 595, 618 discoradicular lesions, pain 594, 595-596, 600, 620 dural pain 1 7-18, 594, 595, 600, 618 incidence / prevalence 615-616 lateral displacement and erosion 647, 648 nuclear protrusion 6 1 8, 622 paraesthesia 600 posterocentral protrusion 600, 616, 618 manipulation contraindication 622 referred pain 661 sustained traction treatment 631 thoracic postural pain syndrome 644 posterolateral protrusion 406, 582, 616, 619 pain 594, 595-596, 600, 620 primary and secondary types 620 rib fracture vs 663 unilateral band-shaped pain 662 postoperative discitis 649 recurrence prevention 631-633 ligamentous sclerosis 632-633 postural 631 referred pain from 595-596, 661-662 self-reducing 619, 622 sites 616 spontaneous recovery not found 594 symptoms and signs 616-617 articular 617, 6 1 8 cord compression 6 1 8 dural 616-617, 6 1 8 non-articu l ar patterns 617, 6 1 7, 619 pain 600, 615, 616, 617, 619, 620, 621 partial articular pattern 617, 619 T1 and T2 619 treatment 594, 622-633 bed rest 631 manipulation see thoracic manipulation nerve block 631 oscillatory 630 surgery 631 sustained traction 630-631 warning signs 621 thoracic harness 898 thoracic l umbago, acute 600, 619-620 thoracic manipulation 622-630 amount of force 624 contraindications 622, 622-623 absolute 622, 622-623

extension technique in prone position 624-627 central pressure method 625-626, 626 crossed hands method 627, 627 level identification 624, 624-625 rotation direction 625, 625 unilateral pressure method 626, 626 extension technique in supine position 627, 628 extension technique wanting (age) 624, 630 failure and reasons 630, 630 indications 622, 622 techniques 623-629 choice 630 traction principle / application 623, 623-624 for upper thoracic disc lesions 629, 629 longitudinal traction 629, 629 rotation method 629, 629 thoracic nerve roots 584-585 landmarks for origin of pain 596, 596 pain 620 lateral recess stenosis 649, 650 tumours causing 638 pain referred from 595 T1 585 stretching, test 607, 607-608, 619 T1 lesions 1 6 1 , 1 90-191, 1 95 compression 406, 616 dorsal interosseous muscle weakness 536 lower brachial plexus palsy 546 pain 595 palsy 1 90, 620 testing 158 T2 lesions 1 61 , 1 91, 1 95 compression 406, 616 pain 595-596 T3-T8 lesions 616 T9-T11 lesions 616 T12 585 palsy 620 thoracic neurofibroma 637, 637-638, 638, 640 thoracic outlet anat0l11Y 546-547, 547 synonyms 547 thoracic outlet syndrome (TOS) 28, 546-552 anatomical variety 548 postural variety differentiation 552 treatment 551, 551 C6 nerve root compression vs 189 C8 nerve root compression vs 190 carpal tunnel syndrome vs 550, 551, 571 differential diagnosis 551, 656 functional examination 549-550, 550 neurocompression 548 postural variety 548-549, 552 treatment 551-552 technical investigations 551 treatment 551 , 551-552 types 547-548 vascular compression 548 see also cervical rib

INDEX 1339

thoracic postu ral pain syndrome 644-645, 645 sustained traction treatment 63 1 , 645 thoracic spinal canal 584, 584, 584-585 innervation 585 osteophytes narrowing 620 stenosis 641 tumours 637-639, 638-639 metastatic 639 neu rofibroma 637, 637 638, 638, 640 zones 584 thoracic spinal cord 582 anatomy 584, 584 blood supply 584 compression 600, 618, 620-622 clinical features 621 extradural haematoma 641 functional examination 621 history 620-621 investigations 621-622 manipu lation contraindication 622-623 sustained traction treatment 63] symptoms / signs 61 R treatment 621 tumours 639 warning signs 621 critical vascular zone 584 diseases 621 vulnerability to damage 584, 620 thoracic spinal nerves 584-585 thoracic spine 579-671 anatomy 581, 581-585 facet joints 581, 583-584 intervertebral discs 582, 583 ligaments 583, 583 vertebrae 581 -582, 582 ankylosing spondylitis 669-670 anterior erosion 645, 645 clinical examination 593-61 2 accessory tests 607-610 history-taking 599-600 inspection and palpation 600-601, 610 summary 611 technical investigations 610, 612 disc lesions see thoracic disc lesions extension 589 active and passive 608-609, 609 limitation, warning sign 636 resisted 608, 609 extradural haematoma 641 facet joints see facet joints flexion 589 resisted 608, 608 rigid thoracic segment 636 thoracic postural pain syndrome 644 fracture, wedge, of vertebral body see wedge fracture fracture of transverse process 648 functional examination 601, 601 -607, 6 r I cord sign (plantar reflex) 606, 606 dural tests 601 -603, 602 passive movements 605, 605 prone 607, 607 resisted movements 605-606, 606 -

sitting 605-607 standing 601-604 trunk movements 603, 603-604 hyperkyphotic see hyperkyphosis (thoracic spine) infections 648-649 kyphosis see hyperkyphosis; kyphosis lateral erosion 647, 648 lateral recess stenosis 649-650 limited range of movement articular pattern 604, 604 partial articular pattern 604, 604, 650 lumbar / cervical spine differences 593-594 manipulation complication 112 metastases 190, 215 extraspinal (outside spinal canal) 639 intraspinal 639 morning stiffness 669, 670 movements 589 'side coupling' 589 neurological examination 609-61 0, 6 1 0 non-disc disorders / lesions 594, 635-653 warning signs/ symptoms 635-637, 636 Paget's disease 651 pain 593 abdominal wall pain vs 594 bilateral radiation of central pain 636 history-taking 599-600 lightning, on breathing 650 localization / sites 599-600 onset 599 standing, lateral recess stenosis 649 thoracic postural pain syndrome 644 tumours 599, 600 visceral vs musculoskeletal 593-594 warning symptom 599, 635-637, 636 see also thoracic backache passive extension thrust 607, 607 pathological wedging 642-645 see also hyperkyphosis (thoracic spine) postoperative disci tis 649 referred pain 593, 594-599, 600 from bones 596-597 dural 594, 595, 595 from joints and ligaments 597 from muscles 597 from musculoskeletal structures 595-597, 600 from nerves 596 from visceral structures 597-599, 598 rotation 589 limitation, warning sign 636 passive 605, 605 resisted 605-606, 606 scoliosis see scoliosis side flexion 589 away from painful side (warning sign) 604, 605, 617, 6 1 7, 6 1 8, 636 neurofibroma 638 limitation, warning sign 636 resisted 608, 608 spinous and transverse processes relationship 582, 624, 624-625, 625

squaring' erosion 670 Tl vertebra metastases 1 90 traction fractu re of spi nous process 406, 4rJ T12, tumours 640 tuberculosis 648-649 tumours 637-640 differen tial diagnosis 640 extraspinal 637, 639-640 intraspinal see thoracic spinal canal upper, metastases 2 1 5 vertebral collapse tuberculosis 649 see also hyperkyphosis (thoracic spine) vertebral tumours 597 warning sign s / symptoms 635-637, 636 wedge fracture see wedge fracture thoracodorsal nerve 545 thoracolumbar fascia 713, 713-714 thoracolumbar junction, metastases 639 thoracolumba r pain scoliosis 646 thoracic spine tumours 637 see also low back pain; thoracic spine, pain thoracotomy, pain after 664 thorax 585 ankylosing spondylitis 669-671 pain pectoralis major lesion 361 see also thoracic cage, referred pain 'three-joint complex' 736 thrombosis, subclavian artery / vein 548 thumb abduction, resisted 487, 488 adduction, resisted 487, 488 anatomy metacarpophalangeal joint 476 trapezium-metaca rpal joint 476 arthrosis 522 deep transverse friction 523, 523 intra-articular triamcinolone 522, 522-523 clinical examination 484, 497 interpretation 493-494 see also hand disorders 521-531 , 529 disorders of contractile structures 524-529 pain 524-528 weakness 528-529, 529 disorders of inert structures 521 -523 capsular pattern 521-523, 522 extension backward movement with 486-487, 487, 521 resisted 1 58, 1 60, 487, 487 pain 524-526 weakness in C8 nerve root compression 190 flexion, resisted 487, 487 pain 526-528 functional examination 484, 484-486, 486-488 muscles and tendons 487, 487-488

1340

INDEX

thumb (continued) ischaemic contractu re 529 nerve lesions 529, 529 overuse problems 521, 524 pain 522 passive movement 486-487, 487 resisted movements 487, 487-488 rheu matoid arthritis 521 swelling 522 tendon ruptures 528-529 traumatic arthritis 521 trigger 528, 528, 536-537, 537 weakness, carpal tunnel syndrome 529, 570 Z-shaped 534 see also trapezium-first metacarpal joint thumb-spica cast 501 tibia, attachment to knee joint capsule 1 057 tibial condyles anatomy 1 054 lateral 978 bursa 1 095 tibialis anterior 11 67, 1 168 deep transverse friction 1 1 93, 1 1 94 inversion of foot 1 1 95 myosynovitis 1 1 93 pain due to lesions 1 1 95 tibialis posterior 1 1 68 deep friction 1 1 95, 1 1 95, 1 1 96 lesions causing pain 1 1 95 tibialis posterior tendinitis 1 1 95 tibialis posterior tendon 1 1 66 rupture 52, 1 1 97 tibial nerve, disorders areas in which sensory changes occur 1 268 compression 1 268 entrapment 1 267 tibial tuberosity apophysitis 1 1 37 lesions at insertion 1 137 osteochondrosis see Osgood-Schlatter disease tibiocalcanean ligament 1 1 63, 1 1 64 damage 1 231 tibiofibular joint ankle 1 1 61-1 1 62 upper anatomy 1 061 lesions 1 1 45-1146 lesions vs biceps tendon lesions 1 1 46 tibiofibu lar ligaments anatomy 1 1 61-1 1 62 testing 1 1 75, 1 1 76 tibionavicular ligament, damage 1 231 'tide mark' 39 Tietze's syndrome 597, 662-663 tight fascia synd rome, anterior compartment 11 93-1194, 1 1 94 tilting board 1 1 5 Tinel's sign, testing 432, 433 Tinel's test 570, 570 tingling sensation see paraestheSia ('pins and needles')

tinnitus, manipulation under traction 267 tiptoe, rising on foot / ankle examination 1 1 73, 1 1 73-11 74, 1 1 83 lumbar spine examination 8 1 9, 819 weakness 1191, 1 199 to-and-fro- movements, deep transverse friction 99, 99-100 toe, big clinical examination 1 252 dorsiflexion, resisted, L4 / L5 nerve root test 825, 826 hallux valgus 1254-1255 muscles 1 1 69, 1 1 69 toe(s) disorders 1251-1 260 see also individual joints and bones

examination 1 1 79 gripping movements 1 1 65-11 66, 1 1 66 second, bruiSing of nerve 1257-1258 'toeing out' 988 tonsill i tis 1 84 torticollis acute 1 82-1 84, 1 85 asymmetrical pattern d ifferential diagnosis 1 83-184 examination and diagnosis 1 83, 1 83 history 1 83 inspection 69, 151, 1 83 spontaneous recovery 1 84, 267 summary 1 84 treatment 1 84 central pain with symmetrical features 192 cervical manipulation contraindicated 251 children 1 83 early cervical disc displacement 1 78 eosinophilic granuloma 213 flexion deformity with 252 manipulation course 261-262, 262, 262-263 pain 1 92 benign paroxysmal 1 84 congenital 1 83 hysterical 1 84 postviral in adolescents 1 84 spasmodic 1 84 spastic 1 84 tourniquet test, carpal tunnel syndrome 570 toxic reactions, local anaesthesia 1 1 9-120 traction 104-105 apparatus 898, 899 cervical disc displacements 263-265 as sole treatment 263-265 cervical manipulation with 1 06-107, 255-256, 263 benefits 255, 256 method 255-256, 256 for non-discogenic disorders 267-269 see also cervical manipulation continuous in bed, cervical disc displacement 265 grade B mobilization 104-105

head suspension 263-265 contraindications 264, 264 indications 263-264, 264 ted1l1ique 264, 264-265, 265 hip osteoarthrosis treatment 1 005-1007 manual 1 005-1006, 1 006 mechanical 1 006, 1006-1 007 historical aspects 875-876, 893-894, 894 intermittent 893-894 long-standing 265 lumbar 893-901 after-care 901 contraindications 897-898, 898 epidural anaesthesia indication 907 force and duration 899, 900 indications 896-897, 898 intervals between 899-900 non-useful (cases) 898 patient position 899, 900 procedure 898-901 release 901 results 901 paraesthesia induced by 264 sustained acute nuclear lumbago 880 disc lesions repair 896 effect on sta tu re 894 effects 894, 894-895 lumbar backache 756 lumbar manipulation with 877 mechanism of action 895-896 posterior longitudinal ligament tension 894-895 sciatica 769 thoracic disc lesions 630-631, 645 thoracic manipulation with 106-107, 623, 623-624 amount of force 624 longitudinal, upper disc lesions 629, 629 traction fracture, C7 or Tl spinous processes 406, 411 traction injury, C5 nerve root 1 88 traction palsy brachial plexus, C8 nerve root compression vs 1 90 C5 nerve root 1 88 traction spu rs calcaneus 1213 lumbar spine 736, 736, 738, 841, 842 ' transmitted stress', wrist 512 transverse acetabular ligament 974 transverse carpal ligament (flexor · retinaculum) 478, 480, 568 transverse foramen 228, 229 transverse friction massage, chronic (overuse) tendon lesions 50 transverse ligament 141 laxity 215 transverse processes lumbar vertebrae 704 fractures 818, 831, 859 thoracic vertebrae 582 fracture 648 spinous processes relationship 582, 624, 624-625, 625

INDEX 1341

transversus abdominis 590, 591 cel-contraction exercise with multifidus 843 stabilizing role for spine 838, 843 trapezium 474 movement (axes) 476, 476 trapezium-first metacarpal joint anatomy 476 arthrosis 484 see also thumb trapezius muscle central pain 192, 196-1 97 glenohumeral stability 336 innervation from spinal accessory nerve 544, 544 lesions and pain 412 shoulder elevation 411 strength testing 324 unilateral pain 184-185, 1 85 trapezius syndrome 88, 412 trapezoid ligament 281, 474 anatomy 387 lesion 406 pain 597 sprains 331-332 differential diagnosis 325 trauma 93 blood Aow change in vertebrobasilar system 231 traumatic arthritis distal radioulnar joint 495 elbow 437-438, 438 fingers 534 hip 999-1000 knee see knee metatarsophalangeal joints first 1253 outer four 1256 shoulder see shoulder subacute, subtalar joint 1210 thumb 521 wrist see wrist d isorders treatment, orthopaedic disorders 93-131 active movements 114-115 deep transverse friction see deep transverse friction injection and infiltration 115-127 see also infiltration; injection passive movements 102-114 see also manipulation; mobilization principles 93-131 techniques 94 Trendelenburg gait 1029 Trendelenburg's position 119, 120, 994, 1025 Trendelenburg's sign 1046 Trendelenburg test 994 triamcinolone anaphylactic reaction 125 arthrosis at first metatarsophalangeal joint treatment 1253, 1 253 bruising of second digit nerve treatment 1258 dose and concentration 116 infiltration see triamcinolone infiltration

injections at cervical nerve roots 265, 266 intra-articular injections elbow pain on passive supination 444 monoarticular steroid-sensitive arthritis (elbow) 439 monoarticular steroid-sensitive arthritis (shoulder) 314 thumb arthrosis 522, 522-523 traumatic arthritis of elbow 438, 438 traumatic arthritis of shoulder 310, 311 ligamentous lesion treatment 53 midtarsal joint subacute arthritis treatment 1241 midtarsal strain treatment 1243, 1 244 osteophytic root compression 200 sesamometatarsal lesion treatment 1 254, 1 254 triamcinolone acetonide 122, 125 triamcinolone hexacetonide 122 triamcinolone infiltration abductor pollicis longus tendon 526, 527 Achilles bursitis 1207 Achilles tendonitis 1187, 1 1 88 acromioclavicular ligaments 329, 329, 330 acute subdeltoid bursitis 320, 320, 321 adductor longus injury 1027-1028, 1 028 ankle joint 1 204, 1 205 ankle sprain treatment 1 223-1224, 1 224 anterior cruciate ligament 1 1 1 1 , 1 1 1 2 arthritis o f thoracic facet joints 650-651, 651 calcaneocuboid ligament 1 224, 1 224 carpal tunnel syndrome 571-572, 572 cervical nerve root syndromes 192 cervical non-discogenic disorders 270, 270-271 chronk metatarsalgia treatment 1257 coccygodynia 968-969, 969 coracoclavicular ligaments 332, 332 coronary l igaments 1109-1110, 1 1 1 0 cubital tunnel syndrome 564, 565 dancer's heel (posterior periostitis) 1 207, 1207-1208 deltoid ligament 1 231-1232, 1 234 de Quervain's disease 526 distal insertion of biceps tendon 449, 449 extensor carpi radialis longus/brevis lesions 511, 5 1 1 extensor carpi ulnaris lesions 512, 5 1 2 extensor pollicis brevis tendon 526, 527 facet joint syndrome 780-781 Aexor carpi radialis tendon 514, 5 1 4 flexor carpi ulnaris tendon 515, 5 1 5 flexor pollicis longus tendon 526-527, 527 golfer'S elbow 467, 467-468 hamstring tendons 1031 hazards 352 infrapatellar tendon 1 1 35-1136, 1 13 7 infraspinatus tendon 365, 365 infraspinatus tendon rupture 367 la teral recess stenosis 795

long bicipital tendon lesions 372, 372 medial collateral ligament injuries (knee) 11 04, 1 1 04 plantar fasciitis 1214, 1 2 1 5 popliteus tendon 1 1 47, 1 147 posterior cruciate ligament 1113, 1 1 1 4 postthoracotomy pain 664, 664 radial collateral ligament 505, 505 rectus femoris tendon 1030, 1 030 rheumatoid arthritis of wrist 501 rib-tip syndrome 663 rotator cuff lesions 352 sternoclavicular joint 404, 404, 404-405 subcoracoid bursitis 326, 326 subscapularis tendon lesions 369, 370 subtalar joint 1210, 1 2 1 1 suprapatel lar tendon 1134, 1 1 34 supraspinatus tendinitis 355-356, 356 supraspinatus tendon rupture 358, 360 temporomandibular joint 693, 693 trigger thumb 528, 528 type I I tennis elbow 458-459, 459 ulnar collateral ligament 505, 505 see also steroids triangular fibrocartilage complex (TFCC) anatomy 473-474, 474 disorders 497, 512 degenerative and traumatic 497 function 474 see also radioulnar jOint, lower / distal triceps brachii anatomy 421, 422 function 286 lateral head 421 lesions 374, 451-452 long head 421 medial head 421 musculotendinous junction, deep friction 452, 452 sites of lesions 422, 451 tendinitis, C7 nerve root compression vs 190 tenoperiosteal junction deep friction 452, 452 infiltration 451-452, 452 weakness C7 nerve root compression vs 189 neuralgic amyotrophy 553 triceps jerk, absent 1 6 1 triceps reflex, testing 160, 1 6 1 triceps surae 1166 short, Achilles tendonitis 1186 tear 1183 triceps tendon, tota l / partial rupture 453 trigeminal nerve lesion 187 neuri tis 680 trigger finger 51-52, 536-537, 537 trigger points 18 localization / sites 1 8-19 trigger thumb 528, 528, 536-537, 537 triptans 225 triquetral bone 474 triquetrolunate instability, testing 509, 509 trism us, hysterica 1 / m uscula r 696

1 342 INDEX

trochanteric bursa 979 anatomy 1 m 8, 1 0 7 8 trochanteric bursitis 1018-1019 trochlear palsy 1 84 trochoid joint 4 ] 8 Troiser and Elroy technique 269-270, 270 tropocollagen 34, 35 trunk combined flexion / twisting to be avoided 924-925, 925 extension, testing 608, 609 flexion-rotation, thoracic lumbago due to 619 movements 603, 603-604 resisted 608, 608 thoracic spine examination 603, 603-604 muscles 591 normal shape 808, 8 1 8 tubercu losis apical, costocoracoid fascia limitation 408 arthritis, hip ] om cervical spine 216 glenohumeral joint 31 6-31 7 thoracic spine 648-649 vertebral osteomyelitis 863-864 tuberosity avulsion fractures 1 250 tunnel of Guyon sec Guyon's tunnel turning sensations 233, 236 turning / stop turning test 235, 236 twinges 67 acute lumbago 746, 806, 897 ankle joint ] 204 causes 67 cervical spine pain ] 67, ] 68 disc displacement 1 79 elbow 428, 456 hip joint ] 0 1 3 neck movements 747 tennis elbow 456 two-point discrimination, cubital tunnel syndrome 564

ulna radial notch 420 styloid process, fracture 505 troch lear notch 419 ulnar collateral ligament 473, 475, 475 infiltration technique 505, 505 insu fficiency 444 sprains 505 ulnar deviation, resisted 43 1, 432 ulnar nerve 56]-566 anatomy 424, 424, 48 1 , 481 , 561 , 562, 563 dorsal and palmar branches 481 , 48 1 medial cord of brachial plexus 545 branches 561, 562, 565 com pression T1 nerve root compression us 191 thoracic outlet syndrome us 551 disorders / lesions 562-566 at elbow 562-565, 564 at wrist 565-566 see nlso cubital tunnel syndrome

entrapment 562 classification 564 at cubital tunnel see cubital tunnel syndrome thumb weakness 529 frictional neuritis, C8 nerve root compression us 190 innervation 561-562 loose bodies 563 neuritis 564 palsy 562, 563 aetiology 563 cubital tulmel syndrome 563, 564 pressure on, C8 nerve root compression us 1 90 recurrent dislocation 563 sensory supply to hand 561, 566 sheath, thickening 564 superficial and deep branches 561, 565 tardy ulnar neuritis 563 ulnar nerve synd rome, clinical featu res 562 ulna sag 509 ul nocarpal meniscus 473 ulnolunate ligament 473-474 u lnotriquetral ligament 473-474 ultrasound scanning congenital dislocation of hip 1044-1 045 hip joint 995 shoulder 301 umbilicus, pain 660 uncoarterioradicular junction 146, 146 u ncovertebral joints 1 36-] 37, 1 38-]39, 1 40 age-related changes 1 76 unlikelihoods, lumbar spine history-taking 8m Unterberger's test 233-234, 234 upper brachial plexus palsy 546 upper limb acute ischaemic syndrome 548 dermatomes and development 9 lesions, paraesthesia due to 151 movement, preliminary examination 70 nerve lesions / en tra pmen t neu ropath ies 541-578 see also illd ivid IInl nerves

pain, cervical spine lesions 150 see nlso arm; specific nnnioll1icnl sirtlcillres upper limb tension tests (ULTT) 1 79 upper motor neurone lesions 83, 202 upper tibiofibular jOint, anatomy 1061 ureters, referred pain from 598, 660 urethritis-arthritis-conjunctivi tis see Reiter's syndrome uric acid crystal deposition see gout urinary symptoms, thoracic spinal cord com pression 621 uterine disorders, pain referred to back 867

v vacuum phenomenon, gas in lumbar discs 738 Valsalva manoeuvre, pain 600 vasa vasorum 23

vascular disorders, intra-abdominal, referred pain 660-66] vascular injuries, cervical spine manipu lation complication 1 1 2 vascularization connective tissue 36 tendinous tissues 50 vascularized zones, 'critical' 50 vascular problems, spinal manipulation complication 1 1 2 vasodilatation, inflammation 44 vastus intermed ius ] 058 adherent 1 094, 1 1 32 vastus lateralis 1 1 39 vastus medius obliquus timing/ intensity and 11 43 vastus medius longus 1 ] 38 vastus medius obliquus 1138 patellofemoral pain syndrome ] ] 42, 1143 as stabilizer of patel la 1 1 38, 1 1 38-1 139 weakness 11 38 vertebrae see cervical spine; lumbar vertebrae; thoracic spine vertebral arch lumbar spine 704 thoracic spine 581 vertebral arteries ] 36, 228 anatomy 145, 146 anomalies 231 blood flow and factors affecting 230, 230-231 blood supply by 229-230 congenital anomalies 231 course and segments 229, 229 compression effect 231 damage, manipulation risk 249 diminished blood flow 230 symptoms relating to 1 51 vertebral bodies central zone 704 collapse cervical spine 2 ] 3 eosinophilic granuloma 2 ] 3 fractu re 642 burst 643 crush 858 upper cervical spine 241 see nlso wedge fractu re, vertebral body height, loss 643 lower cervical spine ] 36 lumbar 704 anatomy 704 erosion of posteroinferior aspect 765 osteitis, in ankylosing spondylitis 862 osteophytes 736 metastases 2] 5 space, sustained traction effect 894, 894 spu r formation 1 76 thoracic spine 58] anterior erosion of thoracic spine 645, 645 fracture 597 metastases 639 wedge fracture see wedge fracture wedging 858

INDEX 1343

vertebral canal see spinal canal vertebral foramen atlas 1 36 thoracic spine 582 vertebral fractures cervical spine 212 see also vertebral bodies vertebral hyperostosis of Forestier see ankylosing hyperostosis vertebral infections, spinal manipulation contraindication 1 1 0 vertebral-osteomyelitis 648-649, 863-864 vertebral ring epiphysis, growth, interference in juvertile kyphosis 642 vertebral tumours metastases cervical 190, 21 4, 214-21 5 thoracic see thoracic spine referred pa in 597 vertebra plana 213 vertebrobasilar system 1 45, 1 46 anatomy 228, 228-230 blood flow 230, 230-231 factors affecting 230-231 blood supply 228, 228-230 compressing factors 231 disturbances causing vertigo 235 insufficiency 151, 235 failure to detect before manipulation 248 vertigo 151, 227-236 acute and chronic 236 in acute torticollis 1 82 aetiology and classification 232-233 anatomy and 227-231 benign positional paroxysmal 235, 236 'cervical' 227 cervical joint dysfunction causing 235 cervical spondylosis 197 clinical examination 233-234, 236 interpretation 235-236 functional examination, risk factors 232-233 history-taking 233, 236, 236 non-vestibular 232 treatment 236 postural, manipulation under traction 267 technical investigations 235 temporomandibular joint disorders 681 therapy 236 types 233 vestibular 232, 235 central / peripheral 232 vestibular nuclei 227, 228 vestibular nystagmus 231 vestibular system 227, 227-228 central part 227-228 disturbances 235 peripheral part 227 villonodular arthri tis of Jaffe and Lichtenstein 1 080 'virhlal articulations' 389 viscera I reflex 5

visual disturbances, corticosteroid side effect 125 voice, hoarseness 657 Volkmann's contracture 86 volleyball, suprascapular nerve palsy 368 von Luschka, joints see uncovertebral joints von Recklinghausen's disease 637

walking foot-off phase, muscles/ tendons 1 1 66, 1 1 66

sacroiliac joint movements 945, 945 see also gait walking stick, partial syndrome of carpal tU11l1el 572 Wallenberg's syndrome 230, 230 Wallerian degeneration, axons 27 warmth of joint, assessment 77-78 warning signs 63, 1 1 3 see also specific anatomical regions

water transport, cartilage 40 Watson's test 508, 508 weakness active movement impairment 83 history-taking 68 neurological vs muscular 75 see also individual muscles

'weaver's bottom' (ischial bursitis) 1019, 1031 Weber's test, carpal tunnel syndrome 570 wedge fracture, vertebral body 642, 642-644, 643 high energy 642-643 pathological 643-644 warning signs 644 weightlifting, shoulder injuries 363 whiplash-associated d isorders 239-245 chronicity and costs of 243 classification 240, 240 clinical features 241, 242-243 definition 239 diagnosis 242-243 di fficul ties 242 incidence 240 mechanism 239 medicolegal consequences 241-242 natural history 243 pathology and types of lesions 241 prolonged disability avoidance 244 psychological problems 242 severe lesions 241, 242 technical investigations 242 therapy 243-244 time-course (since accident) 240, 243 whiplash injuries 1 5 1 , 239, 240 clay-shoveller's fracture 212 ' wobble board' exercises 1230 wound repair collagen type III role 36 fibroblasts role 33 stages 43-44, 44

Wrisberg ligament type, discoid meniscus 1 082, 1 082 wrist anatomy 473-482, 474, 474-475 joints and ligaments 473-476 muscles and tendons 476-480 nerves 480-482 clinical examination 483-491 accessory tests 489, 490 history-taking 483-484 interpretation 493-494 palpation 488 summary 491 crepitus 488, 524 dorsal ligaments see dorsal carpal ligaments extension carpal tunnel synd rome test 570 overuse in tennis elbow 455-456 passive 484, 485 resisted see below extensors 422, 422-423 finger extensors differentiation 5 1 0 flexion passive 484, 485 resisted see below flexors 423, 423 finger flexors differentiation 5 1 3 resisted movement 430, 43 1 sites of lesions 466, 466 functional examination 484, 484-486 passive movements 484-486, 485 resisted movemen ts 486, 486 immobilization 501 joints/bones included 473, 474 ligaments 475, 475 movement 475-476 axes 475, 475 muscles controll ing 422, 422-423, 423

pain dorsal 507 lower radioulnar joint disorders 495 posttraumatic 508, 509 radial side 525 ulnar-sided 497 radial deviation passive 484, 485 resisted 431 , 432, 456, 486, 486 referred pain 483 resisted extension 1 58, 1 59, 431, 43 1 , 486, 486, 5 1 0-513 fingers flexed 431, 43 1 , 489, 490 pain 5 1 0-51 3 weakness 465-466, 5 1 3 see also tennis elbow resisted flexion 1 58, 1 59, 466-468, 486, 486, 513-51 6 pain 466-468, 5 1 3-51 6 weakness 468 see also golfer'S elbow stiffness 501 supination, passive, pain at end of range 496-497, 512 swelling 484, 500

1 344 INDEX

wrist (continued) ulnar deviation passive 485, 486 resisted 431, 432, 456, 486, 486 see also carpal bones wrist disorders 499-519 arthrosis 501 isolated 504 of contractile structures 5 1 0-516, 5 1 6 pain o n resisted extension 51O-5l3 pain on resisted flexion 5 l 3-516 resisted extension 510-5l3 weakness on resisted extension 513 weakness on resisted flexion 5 1 6 degenerative arthritis 501 excessive range of movement 507-51 0 full range o f movement 504-507

ganglion 507 ligamentous lesions 504-506 periostitis and stress fractu re 507 of inert structures 499-510, 510 ligamentous instability see carpal instability limited range of movement 499-501 capsular pattern 499-501, 500 non-capsular pattern 502, 502-504 warning signs 499, 500 rheumatoid arthritis 501 traumatic arthritis 499-501 history and examination 500 treatment 501 un-united fracture 504 wrist impingement syndrome 507 wrist splint, carpal tunnel syndrome 57l

x xanthomatous tenovaginitis, Achilles tendon 1 1 90 xiphoid process 585, 588

Yeoman's test 951-952, 952

zinc sulfate 1 25 Z-line 42, 42 zygapophyseal joints see facet joints zygomatic arch 675, 676 zygomatic process 675